UAS Zoonosis

ZOONOSES
KHD – 302
Veterinary Medicine S1
LP RK
ZOONOSES-Intro_Soelih_2021 1
INTRODUCTION
DEFINISI
WHO 1966  Those diseases & infections which are
naturally transmitted between vertebral
animals
Since 90’s  Those disease & infections which are
naturally present in vertebral animals & man
They involve all types of agents: bacteria, parasites, viruses and
unconventional agents
DISEASE / INFECTION
AGENT
Inf, non inf, toxin
INDONESIA’s OIE Official Delelegate
Director General of Livestock Sevice & Animal Health
The Ministry of Agriculture
Building C, 6th Floor
Jl. Harsono - RM. No. 3 Building-C
Pasar Minggu
Jakarta 12550
THE MEANING OF ZOONOSES
FOR A VPH PRACTITIONERS
1. Epidemiology of communicable diseases which
are transmitted from vertebrate animals to man
2. Control management of zoonoses
Over 200 ZOONOSES have been described since many

centuries  90 % are from animal origin
HOW IMPORTANT ? 1. Dangerous

2. Economic losses
3. Effect to the public

CLASSIFICATION
I. SOURCE  1. ANTHROPOZOONOSES : VERTEBRATE  MAN
2. ZOOANTHROPONOSES : VERTEBRATE  MAN
3. AMPHIXENOSES : VERTEBRATE MAN
II. LIFE CYCLE OF THE CAUSATIVE AGENT  1. DIRECT ZOONOSES

2. CYCLO ZOONOSES
3. META ZOONOSES
4. SAPRO ZOONOSES
III. CAUSATIVE AGENT  1. BACTERIOSES

2. MYCOSES
3. CHLAMYDIOSES & RICKETTSIOSES
4. VIROSES
5. PARASITIC DISEASES
6. PRION DISEASES
LIFE CYCLE OF THE CAUSATIVE AGENT
VERTEBRATE VERTEBRATE
DIRECT ZOONOSES
MECHANICAL VECTOR
CYCLO ZOONOSES VERTEBRATE-1 VERTEBRATE-2
VERTEBRATE-3
invertebrate
invertebrate
META ZOONOSES VERTEBRATE VERTEBRATE
invertebrate
invertebrate
invertebrate
SAPRO ZOONOSES VERTEBRATE VERTEBRATE
invertebrate
Medical Dictionary (Stedman's)
Zoonosis
 Pronunciation: zō′ō-nō′sis
An infection or infestation shared in nature by humans and other animals.

[zoo- + G. nosos, disease]
 anthropozoonosis , cyclozoonosis , metazoonosis , saprozoonosis ,

zooanthroponosis Search...
Zooanthroponosis
Pronunciation: zō′ō-an′thrō-pō-nō′sis
 A zoonosis normally maintained by humans but that can be transmitted to
other vertebrates
 Examples : Amebiasis to dogs ; tuberculosis
Anthropozoonosis
 Pronunciation: an′thrō-pō-zō′ō-nō′sis
 A zoonosis maintained in nature by animals and transmissible to humans
 Examples : Rabies; Brucellosis
Amphixenosis
 Pronunciation: am-fiks′en-ō′sis
A zoonosis maintained in nature by humans and lower animals
 Examples : Streptococcoses & Staphylococcoses.
Cyclozoonosis
 Pronunciation: sī′klō-zō′ō-nō′sis
 A zoonosis that requires more than one
vertebrate host (but no invertebrate) for
completion of the life cycle
 Examples: various taenioid cestodes such as
Taenia saginata & T. solium
Metazoonosis
 Pronunciation: met′ă-zō′ō-nō′sis
 A zoonosis that requires both a vertebrate & an
invertebrate host for completion of its life cycle
 Examples : The Arbovirus infections of humans &
other vertebrates
Saprozoonosis
 Pronunciation: sap′rō-zō′ō-nō′sis
 A zoonosis, the agent of which requires both a vertebrate host and a
nonanimal (food, soil, plant) reservoir or developmental site for
completion of its life cycle.
 Combination terms may be used

 saprometazoonoses for fluke infections  when metacercariae
encyst on plants,
 Saprocyclozoonoses for tick infestations  the agents of which
complete part of their life cycles in soil.
[sapro- + G. zōon, animal, + nosos, disease]
World Organization for Animal Health
HQ in Paris
The OIE counts 167 Members
SHORT HYSTORY - 1
• In 1920 RINDERPEST occurred unexpectedly in

Belgium, as a result of zebus, originating from India
and destined for Brazil, transiting via the port of
Antwerp
• Despite the inevitable slowness of the negotiations
undertaken through diplomatic channels, twenty-
eight States obtained an "international agreement" on
25 January 1924. The ratification of this 1924
Agreement creating the Office International des
Epizooties (OIE) based in Paris eflects a desire clearly
expressed by the Secretary General of the League of
Nations.
• The International Committee of the Office held its first
General Session on 8 March 1927. Twenty-six
Delegates were present.
SHORT HYSTORY - 2
The United Nations, which replaced the League of

Nations in 1945, established two specialist
Agencies:
the Food and Agriculture Organization of the
United Nations (FAO) in 1946
the World Health Organization (WHO) in 1948.
Their aims partially covered those of the Office
The presence of these two Agencies called the
existence of the OIE into question and the
possibility of simply dissolving the organisation
was envisaged in 1946, and again in 1951.
Thanks to the opposition of numerous OIE
Member Countries and Delegates, the functions
of the Office were kept alive
SHORT HYSTORY - 3
• 1952 Official agreement between the OIE and the

FAO
• After the signing of the Treaty of Rome establishing
the European Community in 1957, the OIE lent its
support to the first attempts to harmonise animal
health legislation within the Community.
• 1960 Official agreement between the OIE and the
WHO
• 1924 – 2004 : The OIE counts 167 Members
• 2004 New Official agreement between the OIE and
the FAO
SHORT HYSTORY - 4
• On 30 January 1928, the first Conference met in

Geneva. Consisting of eight experts, it no
established the bases for an international
sanitary police. This latter stated that "only
sanitary documents emanating from nations with
correctly organised veterinary services can be
considered as providing importers with sufficient
guarantees".
One Health shall be achieved through
Mission Statement
Recognizing that human health (including mental

health via the human-animal bond phenomenon),
animal health, and ecosystem health are
inextricably linked, One Health seeks to promote,
improve, and defend the health and well-being of all
species by enhancing cooperation and
collaboration between physicians, veterinarians,
other scientific health and environmental
professionals and by promoting strengths in
leadership and management to achieve these goals.
Vision Statement
One Health (formerly called One Medicine) is
dedicated to improving the lives of all species—
human and animal—through the integration of
human medicine, veterinary medicine and
environmental science.
The One Health concept is a worldwide
strategy for expanding interdisciplinary
collaborations and communications in all
aspects of health care for humans, animals
and the environment.
The synergism achieved will advance health
care for the 21st century and beyond by
accelerating biomedical research
discoveries, enhancing public health efficacy,
expeditiously expanding the scientific
knowledge base, and improving medical
education and clinical care. When properly
implemented, it will help protect and save
untold millions of lives in our present and
future
Historic "One Health" 1st Step realized
July 15, 2008 -
One Health Task Force Recommendations Published…
Journal of the American Veterinary Medical Association
(JAVMA)
One Health Initiative Task Force Final Report at
http://www.avma.org/onehealth
Executive Summary JAVMA One Health Initiative Summary Report

http://avmajournals.avma.org/doi/pdfplus/10.2460/javma.233.2.259
"The convergence of people, animals, and our environment has created a
new dynamic in which the health
of each group is inextricably interconnected. The challenges associated with
this dynamic are
demanding, profound, and unprecedented. While the demand for animal-
based protein is expected to
increase by 50% by 2020,2 animal populations are under heightened pressure
to survive, and further loss of biodiversity is highly probable." .....
OIE Listed diseases Updated: 25/02/2011
Multiple Species Diseases Cattle diseases
•Anthrax •Bovine anaplasmosis
•Aujeszky's disease •Bovine babesiosis
•Bluetongue •Bovine genital campylobacteriosis
•Brucellosis (Brucella abortus) •Bovine spongiform encephalopathy
•Brucellosis (Brucella melitensis) •Bovine tuberculosis
•Brucellosis (Brucella suis) •Bovine viral diarrhoea
•Crimean Congo haemorrhagic fever •Contagious bovine pleuropneumonia
•Echinococcosis/hydatidosis •Enzootic bovine leukosis
•Epizootic haemorrhagic disease •Haemorrhagic septicaemia
•Equine encephalomyelitis (Eastern) •Infectious bovine
•Foot and mouth disease rhinotracheitis/infectious pustular vulvov
•Heartwater aginitis
•Japanese encephalitis •Lumpky skin disease
•Leptospirosis •Theileriosis
•New world screwworm (Cochliomyia hominivorax) •Trichomonosis
•Old world screwworm (Chrysomya bezziana) •Trypanosomosis (tsetse-transmitted)
•Paratuberculosis
•Q fever
•Rabies
•Rift Valley fever
•Rinderpest
•Surra (Trypanosoma evansi)
•Trichinellosis
•Tularemia
•Vesicular stomatitis
•West Nile fever
Sheep and goat diseases Equine diseases
Caprine arthritis/encephalitis African horse sickness
Contagious agalactia Contagious equine metritis
Contagious caprine pleuropneumonia Dourine
Enzootic abortion of ewes (ovine chlamydiosis) Equine encephalomyelitis (Western)
Maedi-visna Equine infectious anaemia
Nairobi sheep disease Equine influenza
Ovine epididymitis (Brucella ovis) Equine piroplasmosis
Peste des petits ruminants Equine rhinopneumonitis
Salmonellosis (S. abortusovis) Equine viral arteritis
Scrapie Glanders
Sheep pox and goat pox Venezuelan equine encephalomyelitis
Swine diseases
African swine fever
Classical swine fever
Nipah virus encephalitis
Porcine cysticercosis
Porcine reproductive and respiratory syndrome
Swine vesicular disease
Transmissible gastroenteritis
Avian diseases
Avian chlamydiosis
Avian infectious bronchitis
Avian infectious laryngotracheitis
Avian mycoplasmosis (M. gallisepticum)
Avian mycoplasmosis (M. synoviae)
Duck virus hepatitis
Fowl cholera
Fowl typhoid
Highly pathogenic avian influenza and low pathogenic avian influenza in poultry
Infectious bursal disease (Gumboro disease)
Marek's disease
Newcastle disease
Pullorum disease
Turkey rhinotracheitis
Lagomorph diseases Bee diseases

Myxomatosis Acarapisosis of honey bees
Rabbit haemorrhagic disease American foulbrood of honey bees
European foulbrood of honey bees
Small hive beetle infestation (Aethina tumida)
Tropilaelaps infestation of honey bees
Varroosis of honey bees
Fish diseases Mollusc diseases
•Epizootic haematopoietic necrosis •Infection with abalone herpes-like virus
•Epizootic ulcerative syndrome •Infection with Bonamia exitiosa
•Gyrodactylosis (Gyrodactylus salaris) •Infection with Bonamia ostreae
•Infectious haematopoietic necrosis •Infection with Marteilia refringens
•Infectious salmon anaemia •Infection with Perkinsus marinus
•Koi herpesvirus disease •Infection with Perkinsus olseni
•Red sea bream iridoviral disease •Infection with Xenohaliotis californiensis
•Spring viraemia of carp
•Viral haemorrhagic septicaemia
Crustacean diseases Other diseases

•Crayfish plague (Aphanomyces astaci) Camelpox
•Infectious hypodermal and haematopoietic necrosis Leishmaniosis
•Infectious myonecrosis
•Necrotising hepatopancreatitis
•Taura syndrome
•White spot disease
•White tail disease
•Yellowhead disease
Amphibians
Infection with Batrachochytrium dendrobatidis
Infection with ranavirus
"May there never develop in me the notion that
my education is complete
but give me the strength and leisure and zeal
continually to enlarge my knowledge."
- Maimonides -
Old Classification of Diseases Notifiable to the OIE
Updated: 25/01/2005
List A
Transmissible diseases that have the potential for very serious and
rapid spread, irrespective of national borders, that are of serious
socio-economic or public health consequence and that are of major
importance in the international trade of animals and animal products.
• Foot and mouth disease • Vesicular stomatitis
• Swine vesicular disease • Rinderpest
• Peste des petits • Contagious bovine
ruminants pleuropneumonia
• Lumpy skin disease • Rift Valley fever
• Bluetongue • Sheep pox and goat pox
• African horse sickness • African swine fever
• Classical swine fever • Highly pathogenic avian
• Newcastle disease influenza
List B
Transmissible diseases that are considered to be of socio-economic
and/or public health importance within countries and that are
significant in the international trade of animals and animal products.
Multiple species diseases Cattle diseases
• Anthrax • Bovine anaplasmosis
• Aujeszky's disease • Bovine babesiosis
• Echinococcosis/hydatidosis • Bovine brucellosis
• Heartwater • Bovine cysticercosis
• Leptospirosis • Bovine genital campylobacteriosis
• New world screwworm • Bovine spongiform encephalopathy
(Cochliomyia hominivorax) • Bovine tuberculosis
• Old world screwworm (Chrysomya • Dermatophilosis
bezziana) • Enzootic bovine leukosis
• Paratuberculosis • Haemorrhagic septicaemia
• Q fever • Infectious bovine
• Rabies rhinotracheitis/infectious pustular
• Trichinellosis vulvovaginitis
• Malignant catarrhal fever
• Theileriosis
• Trichomonosis
• Trypanosomosis (tsetse-transmitted)
List B
Sheep and goat diseases Equine diseases
• Caprine and ovine brucellosis • Contagious equine metritis
(excluding B. ovis) • Dourine
• Caprine arthritis/encephalitis • Epizootic lymphangitis
• Contagious agalactia • Equine encephalomyelitis (Eastern
• Contagious caprine and Western)
pleuropneumonia • Equine infectious anaemia
• Enzootic abortion of ewes (ovine • Equine influenza
chlamydiosis) • Equine piroplasmosis
• Maedi-visna • Equine rhinopneumonitis
• Nairobi sheep disease • Equine viral arteritis
• Ovine epididymitis (Brucella ovis) • Glanders
• Ovine pulmonary adenomatosis • Horse mange
• Salmonellosis (S. abortusovis) • Horse pox
• Scrapie • Japanese encephalitis
• Surra (Trypanosoma evansi)
• Venezuelan equine
encephalomyelitis
List B
Swine diseases Avian diseases
• Atrophic rhinitis of swine • Avian chlamydiosis
• Enterovirus encephalomyelitis • Avian infectious bronchitis
• Porcine brucellosis • Avian infectious laryngotracheitis
• Porcine cysticercosis • Avian mycoplasmosis (M. gallisepticum)
• Porcine reproductive and respiratory • Avian tuberculosis
syndrome • Duck virus enteritis
• Transmissible gastroenteritis • Duck virus hepatitis
• Fowl cholera
• Fowl pox
• Fowl typhoid
• Infectious bursal disease (Gumboro
disease)
• Marek's disease
• Pullorum disease
Lagomorph diseases Bee diseases
• Myxomatosis • Acariosis of bees
• Rabbit haemorrhagic disease • American foulbrood
• Tularemia • European foulbrood
• Nosemosis of bees
• Varroosis
List B
Fish diseases Mollusc diseases
• Epizootic haematopoietic • Bonamiosis (Bonamia exitiosus,
necrosis B. ostreae, Mikrocytos roughleyi)
• Infectious haematopoietic • Marteiliosis (Marteilia refringens,
necrosis M. sydneyi)
• Oncorhynchus masou virus • Mikrocytosis (M. mackini)
disease • MSX disease (Haplosporidium
• Spring viraemia of carp nelsoni)
• Viral haemorrhagic septicaemia • Perkinsosis (Perkinsus marinus,
P. olseni/atlanticus)
Crustacean diseases Other List B diseases

• Taura syndrome • Leishmaniosis
• White spot disease
• Yellowhead disease
Avian Influenza
ZOONOSIS - KHD 302

DEPARTMENT OF VPH
FACULTY OF VETERINARY MEDICINE
AIRLANGGA UNIVERSITY
3/24/2022 AI-Zoonosis_S1_Soelih_2021 1
INTRODUCTION
INFLUENZA  A Viral Non Food Borne Disease - ZOONOSIS

in animals, incl. bird & human  HPAI
Fam. ORTHOMYXOVIRIDEAE, RNA virus,4 generas:
1. Influenza Virus A  Human & Animals
2. Influenza virus B  Human
3. Influenza virus C  Human & pigs
4. Thogotovirus
* Virus Influenza Type A & B 
• Caustive agent of severe & fatal disease in MAN
• Avute Respiratory disease 
variation in clinical signs according to age
Epithel of Upper Respiratory Tract
• Natural reservoir  AQUATIC BIRDS Virus Influenza A

• Replication  mainly in the INTESTINUM
Viral shedding  FAECES & ORAL
Transmision  aerosol  dropplet
• Host  multiple species
INFLUENZA VIRUS
• RNA virus  8 SEGMEN GENOME
• VIRUS ENVELOPE has SURFACE
PROTEIN  HEMAGLUTININ &
NEURAMINIDASE
• 3 TYPE  A, B, C
• TYPE A  ANTIGENIC SCHIFT &
ANTIGENIC DRIFT
• TYPE B  ANTIGENIC DRIFT
• TYPE C  RELATIVELY STABLE
Courtesy of Linda Stannard, University of Cape Town, S.A.
CHARACTERISTIC of INFLUENZA VIRUS
Main Antigen is a surface

glycoprotein permukaan 
Hemaglutinin & Neuraminidase
• Hemagglutinin (HA) 
attach to the host cell
protective antibody
• Neuraminidase (NA) 
Remove neuraminic acid from
mucin & release from cell
Also 8 segmented code gene of
10 protein
CHARACTERISTIC of INFLUENZA VIRUS - A
18 HEMAGLUTININ H1- H18

11 NEURAMINIDASE  N1- N11
 H1-H16& N1-N9
M2 all in aquatic birds
 H17N10 in Bats found in
Guatemala
 H18N11 in Bats in Peru
M1NS1
PB1PB2 PA HANP NA M2NS2 NOMENCLATURE
A/Chicken/HK/5/98 (H5N1)
A/NY/7708/04 (HxNx)
Slide courtesy of Dr. David Wentworth
80-120 nm
H17N10 isolated from little yellow-shouldered bats, found in
Guatemala
1. Tong S, et al. (2012) A distinct lineage of influenza A virus

from bats. Proc Natl Acad Sci USA 109(11):4269–4274.
2. Li Q, et al. (2012) Structural and functional characterization
of neuraminidase-like molecule N10 derived
from bat influenza A virus. Proc Natl Acad Sci USA
109:18897–18902.
3. Zhu X, et al. (2012) Crystal structures of two subtype
N10 neuraminidase-like proteins from bat influenza A
viruses reveal a diverged putative active site. Proc Natl
Acad Sci USA 109:18903–18908.
H18N11 isolated from bats, found in Peru (Zhu et al. 2012)
It has been identified an influenza A virus from little yellow-
shouldered bats captured at two locations in Guatemala. It is
significantly divergent from known influenza A viruses.
The HA of the bat virus was estimated to have

diverged at roughly the same time as the known subtypes of
HA and was designated as H17.
The neuraminidase (NA) gene is highly

divergent from all known influenza NAs, and the internal genes
from the bat virus diverged from those of known influenza A
viruses before the estimated divergence of the known
influenza A internal gene lineages.
Attempts to propagate this virus in cell cultures and
chicken embryos were unsuccessful, suggesting
distinct requirements compared with known
influenza viruses.
Despite its divergence from known influenza A viruses

 the bat virus is compatible for genetic exchange
with human influenza viruses in human cells,
suggesting the potential capability for reassortment &
contributions to new pandemic or panzootic influenza
A viruses.
Classification (View hierarchy)
Viruses (Virus) → ssRNA viruses → ssRNA
negative-strand viruses →
Orthomyxoviridae → Influenzavirus A
(Influenza A virus) → Influenza A virus →
H17N10 subtype
Primary Descendants (View list)
Influenza A virus (A/little yellow-shouldered
bat/Guatemala/060/2010(H17N10));
bat/Guatemala/164/2009(H17N10))
http://www.oie.int/animal-health-in-the-world/update-on-avian-
influenza/2015/
UPDATE ON HIGHLY PATHOGENIC AVIAN INFLUENZA IN ANIMALS

(TYPE H5 and H7)
This page has been set up at the start of the epizootic of Highly
Pathogenic Avian Influenza due to H5N1 in South East Asia in late
2003, before its expansion later to other continents. It groups in a
single place for stakeholders interested by this important zoonotic
disease, all immediate notifications and follow-ups reports notified
by OIE Member Countries on Highly Pathogenic Avian Influenza due
to serotype H5N1 and other serotypes.
The graph gives the total number of outbreaks of Highly
Pathogenic Avian Influenza (subtype H5N1) in poultry since 2003. It
is kept up-to-date as soon as new outbreaks are notified to the OIE.
Last report received on 6 March 2015
VIRUS INFLUENZA A
• ANTIGENIC SCHIFT & ANTIGENIC

DRIFT PROTEIN HA & NA
• ANTIGENIC SCHIFT HA 
PANDEMI
• ANTIGENIC DRIFT HA & NA 
EPIDEMI
• BIASANYA  GEJALA FLU RINGAN
• KEMATIAN  karena KOMPLIKASI
PNEUMONIA
The three mechanisms used by influenza

viruses to adapt to their host ranges
A. ANTIGENIC DRIFT
B. REASSORTMENT
or ANTIGENIC SCHIFT
C. RECOMBINATION
Source : Webster RG and Hulse DJ. 2004. Microbial adaptation and change : avian
influenza. Rev. sci.tech.Off. int. Epiz. 2004, 23 (2) : 453 - 465

A. ANTIGENIC DRIFT  errors during the replication of

influenza v. which are unable to be repaired 
accumulate amino acid changes within the viral
genome  the existing strains being replaced by a
new antigenic variant  EPIDEMI
B. REASSORTMENT or ANTIGENIC SCHIFT  the
exchange of ribonucleic acid (RNA) segments
between 2 genotypically different influenza viruses
infecting a single cell  The generation of a novel
strain &/ subtype  PANDEMI
C. RECOMBINATION  2 different source of RNA
contribute to asingle influenza RNA segment
ANTIGENIC DRIFT  errors during the replication of influenza v. which are

unable to be repaired  accumulate amino acid changes within the viral
genome  the existing strains being replaced by a new antigenic variant
REASSORTMENT or ANTIGENIC SCHIFT  the exchange of ribonucleic acid

(RNA) segments between 2 genotypically different influenza viruses infecting
a single cell  The generation of a novel strain & subtype
RECOMBINATION  2 different source of RNA contribute to a single

influenza RNA segment
The genesis of a SINGLE GENOTYPE
AI Virus A/H5N1 in 2004
Li, K.S., Y. Guan, J. Wang, G.J.D. Smith, K.M. Xu, L.

Duan, A.P. Rahardjo, P. Puthavathana, C. Buranathai,
T.D. Nguyen, A.T.S. Estoepangestie, A. Chaisingh, P.
Auewarakul, H.T. Long, N.T.H. Hanh, R.J. Webby,
L.L.M. Poon, H. Chen, K.F. Shortridge, K.Y. Yuen, R.G.
Webster and J.S.M. Peiris. 2004.
Genesis of a highly pathogenic and potentially pandemic
H5N1 influenza virus in eastern Asia.
Nature, 430 : 209 – 213.
The genesis of a single H5N1 genotype in 2004
Gs/Gd/96-like viruses reassorted w/ viruses
from wild aquatic birds (genotype C) 
multiple genotypes appearing in 2001
Some 2001 H5N1 viruses transmitted from
domestic poultry back to wild aquatic birds 
a new set genotypes for 2002
In 2002  HA gene of H5N1 strain showed
significant antigenic drift  pronounced in the
genotype Z & Z+ viruses isolatd in late 2002 &
from human in early 2003
In 2004  these circulating viruses have
evolved to include only genotype Z
The colour coding of the schematically shown

virus particles  the virus lineages
A gap in the neuraminidase or non-structural
protein gene segments  a deletion
“ANTIGENIC DRIFT” Virus Influenza A
Aso called as “point mutation” of gene HA causing a “minor HA

changes”
• a continually process
• Immunity limited to 1 strain only
• Vaccine must test annually
• 6 – 8 months process (USA : 85 billion trivalent dose)
• Target  high risk people (inactive) & healthy people
(LAIV)
• Causing the seasonal flu epidemics
PHYLOGENETIC ANALYSIS of HPAI VIRUS
• Nucleoprotein v AI 5 host specific : classical
equine (15 years ago), recent equine, gulls, swine
& human
• Nucleoprotein & gene lineages v AI different
between virus isolate Eurasia & America 
Latitudinal Migrating Birds doesn’t contribute to
the virus distribution
• Longitudinal Migrating Birds  plays an important
role on the continuity of evolution of AI virus
• AI Virus  low speed of evolution rate, around
60 years the AI virus in the aquatic birds was
static
• Antigenic drift (NA) & antigenic shift (HA)
AVIAN INFLUENZA VIRUS - A
Low Pathogenic Avian Influenza Viruses (LPAI)
• Doesn’t cause a disease in WILD BIRDS
• Causes a mild infection in POULTRY
• Can mutates  HIGHLY PATHOGENIC VIRUSES
• Had been recognised  AI-OUTBREAK in the world
Highly Pathogenic Avian Influenza Viruses (HPAI)

• HIGH MORTALITY in POULTRY
• Subtypes H5 & H7
• HPAI determination  according to molecular & pathogencity
characteristics
Susceptible Animals to Avian Influenza Virus
No. Susceptible Animals SUBTYPES
& Human HEMAGGLUTININ NEURAMINIDASE
1. Aquatic Birds H1 – 15 N1 – 9
2. Ducks H1 -12 N1 – 9
3. Turkeys H1 -10 N1 – 9
4. Chickens H4, 5, 6, 7, 9, 10 N1, 2, 4, 7
5. Sea Birds H1 – 7, 9 - 16 N1 – 9
6. Pigs H1, 3,5 N1- 2
H1N1, H1N2, H3N2, H5N1
7. Horses H3,7 N7-8
H7N7, H3N8
8. Seawolf H10 N4
9. Harbour seals H3, 4, 7 N3, 5, 7
H7N7, H4N5, H3N3
10. Whale H3, 13 N2, 9
H3N2, H13N9
11. Fam. Felidae : Leopard, Tiger, H5 N1
Cats H5N1
12. Dogs H5 N1
H5N1
13. HUMAN H1-3, 5, 7 N1,2,7,8
H1N1, H2N2, H3N2, H5N1, H7N7
14. Yellow shouldered Bats H17, H18 N10, N11
• Causes Infection of Respiratory Tract & GI Tract of Birds
Usually doesn’t cause a disease in Wild Birds
Frequently genetic re-assortment
Morbidity & mortality in POULTRY
• Virus shedding through RESPIRATORY TRACT & FAECES

• By low temperature & low humidity  several days to week
• Survive in water
• Survie on the surface
• Should be desinfected to prevent its spread
VIRUS AVIAN INFLUENZA A
• TDK menyebabkan sakit pd UNGGAS LIAR
• Ada hubungannya dg INF RINGAN pd UNGGAS PIARAAN
• DPT BERUBAH  HIGHLY PATHOGENIC VIRUSES
• Ada hubungannya WABAH PENY FLU BURUNG di DUNIA

• TDK menyebabkan penyakit pd UNGGAS LIAR
• MORTALITAS TINGGI pd UNGGAS PIARAAN
• Determinasi HPAI berdasarkan kriteria secara molekuler &
pathogenitas
IMPACT of INFLUENZA
• Seasonal Epidmics in the 4 temperate regions
USA, Canada, Eropa, Rusia, Cina, Jepang, Australia, Brasil,
Argentina
• Year round in tropical area
In equator  Africa & Southeast Asia
IMPACT of INFLUENZA PANDEMI
INFLUENZA PANDEMI in 20th Century 
1. 1918 – 1919 “SPANISH FLU” A (H1N1)
Highst Fatality caused by INFLUENZA
> 500.000 in the USA & 50 million in the world
Most dead in several days of infection,otherwise died later
accompanied by complications
Almost a half of the deaths were healthy young & old people
H1N1 is still circulating until now since the outbreak in 1970
2. 1957 -1958 “ASIAN FLU” A (H2N2)
70.000 deaths in the USA
Started in China in late February 1957 & spread to the USA in
June 1957
3. 1968 – 1969 “HONG KONG FLU” A (H3N2)
Started in Hong Kong in the early 1968 & spread to the USA
at the end of the year
H3N2 is still circulating until now
THE CAUSATIVE AGENT OF INFLUENZA PANDEMI
1918 - 1919 “SPANISH FLU” Not yet know the
A (H1N1) virus origin  avian ??
STILL CIRCULATE TODAY
Virus has gene combination

1957 - 1958 “ASIAN FLU” of human influenza virus &
A (H2N2) avian virus influenza
HA, NA, PB1 = Avian
1968 - 1969 “HONG KONG FLU”

A (H3N2)
HA, PB1 = Avian
RECENTLY PANDEMI FLU
 H1N1  emerged in Mexico April 2009
 Structure of the virus is different from 1918-

1919 & the circulating H1N1 virus  this incl. 4
genes from European swine, Mexican Swine,
Human & Birds  Swine Flu
 WHOSince June 2009

 CFR  H1N1 MEXICO < H5N1
3/24/2022 AI-Zoonosis_S1_Soelih_2011
AI-Zoonosis_S1_Soelih_2021 31
Avian Antigenic “shift”
reassortant Pandemic
virus
Avian virus Quail/HK/G1/97 (H9N2)
Goose/Guangdong/1/96 (H5N1)
Teal/HK/W312/97 (H6N1)
Reassortment in humans
Avian virus Human virus
Model of the
emergence of a
pandemic
influenza virus Reassortment in swine Avian-Human
3/24/2022 AI-Zoonosis_S1_Soelih_2021 pandemic 32
reassortant virus
Reservoir of The New Influenza Virus A Subtype in
Human  Aquatic Birds (Ducks)
AVIAN INFLUENZA A HUMAN INFLUENZA A

H1 – H16 H1, H2, H3, H5, H7, H9
N1 – N9 N1,N2, N7, N8
HPAI INFECTION in HUMAN
The First Confirmed of HPAI Cases in Human following the
outbreak in Poultry
• H5N1 (Severe Respiratory Disease):
• 1997 HK  6 deaths / 18 cases
• 2003 HK  1 death / 2 cases
• 2003 – 2005 Vietnam, Thailand, Cambodia 
56 deaths /111 cases
• 2005  Indonesia 3 deaths / 4 cases
• H7N7 (mild infection, conjunctivitis):
• 2003 Holland  1 death / 89 cases
The victims were mainly poultry farm workers
• 2004 Canada (2 cases, no death)
PANDEMIC PHASE (WHO)
PUBLIC HEALTH ASPECTS of HPAI VIRUS
Characteristic of the H5N1 virus  INAKTIVE by

• 56 0 C / 3 h & 60 0 C / 3 min
• pH acid  pH 4
• Chemicals: oxidator, sod dodecyl sulphate,
lipid solvents, β-propiolactone
• Disinfektansia : formalin & Iodine
Survive in the animal tissues, faeces & water
PUBLIC HEALTH ASPECTS of HPAI VIRUS - 2
• Mutate frequently
– Antigenic drift
• Point mutations accumulated during
virus replication
– Antigenic shift
• Hybrid virus emerges when cell infected
with two different influenza viruses
– Human, avian, swine, equine
• Transfer of influenza virus to a
different species
AI Virus is type A Influenza virus  genetic

reassortment to novel mammalia virus
Sea Wolf–AI virus isolate, caused death due to
pneumonia  has the same HA & NA with a
turkey-isolate of several decades ago.
H5  poultry has an important role in the
epidemiology of influenza in human  2003 – 2007
167 deaths/277 cases (WHO 1 March 2007)
H7  1 death in 2003 (Holland)
THE EPIDEMIOLOGY OF HPAI
Highly contagious
Hosts  at the start only in chicken, turkey, but than
in almost all birds species
Source of infection  Faeces & Secretory of Respiratory
Tract.
Survive in faeces, tissues & water
Transmision 
Direct contact w/ sick birds  faeces
Contamination of feed, waterm equipments &
clothes
Broken eggs in the incubator
Reservoir  aquatic birds & sea birds
Air <<
Control & Prevention of HPAI
• Import restrictions
• Surveillance
• Appropriate biosecurity
– Control human traffic
– Introduction of new birds into flock
– Avoid open range rearing in waterfowl
prevalent areas
• Education of the poultry industry
• Prompt response to MP AI outbreaks
• Program Pengendalian Influenza pd Manusia

a) deteksi & identifikasi adanya varian virus influenza
baru pd saat yg tepat
b) menyeleksi strain virus yg cocok u/ vaksin
• Pengendalian Influenza pd Hewan
a) menunjang Program Pengendalian Influenza pd
manusia
b) Mengetehui ekologi v influenza yg berperan pd
kesehatan manusia & hewan
c) Determinasi secara molekuler adanya penularan pd
host lama & host baru
THERAPY  Amantadin, Oseltamivir

BIO SECURITY  eradicated & localised the virus
Hygienic & Sanitation precautions
1. Protecting the farm  avoiding contact to wild birds,
especially aquatic birds infected farm
2. Preventing the farm from unknown infected birds
3. Controlling any traffic  vehicle,human,equipment etc.
4. Washing & desifecting Procedure
5. “All in – all out”
Exotic  Biosecurity in an outbreak

• Stamping out totally
• Waste of cadaver & all poultry products
• Decontamination
• At least 21 days
• Central of the outbreak (5 km), buffer area (5 – 10
km) & free area >10 km
Endemic  Biosecurity  DEPOPULATION
Any question ???
ZOONOSES TRANSMISSION
DIVISI KESMAVET
MODES OF TRANSMISSION
• The two major categories of

transmission are
–direct transmission and
–indirect transmission (Table 1).
• DIRECT TRANSMISSION
• Contact between the infected animal and
the susceptible person can result in direct
transmission of a zoonotic disease.
• This can take place by touching the animal
or from droplet infection through the
animal’s coughing or sneezing.
• A person must be within 1 meter in front
of an animal for direct droplet
transmission to occur.
• The pathogen may stay on the person’s
skin, enter the body through breaks in the
skin or mucosal surfaces, be ingested, or
be inhaled.
• Plague is an example of a disease
contracted via direct transmission.
INDIRECT TRANSMISSION
• Indirect transmission includes any method of
transmission in which the infected animal and
susceptible person do not actually come in
direct contact.
• Some of these methods include:
INDIRECT TRANSMISSION
• Indirect transmission includes any method of
transmission in which the infected animal and
susceptible person do not actually come in
direct contact.
• these methods include:

• Transmission that involves contact between the
person and some inanimate object known as a
fomite. Animals contaminate objects with
pathogens, and people become infected when they
come in contact with the contaminated objects.
• Dermatophytes, skin infections, transmitted to
people via contact with contaminated bedding,
grooming tool etc.
• Hantavirus infection, via dust particles
contaminated, infect a person through the
respiratory tract
• Indirect transmission can also involve vectors. There
are two types of vectors—biological vectors and
mechanical vectors:
• Biological vectors are animals in which the
pathogen must go through part of its life cycle
before being passed on to a person : fleas, ticks,
flies, and mosquitoes.
• They can be reservoir hosts for a pathogen, as in
babesiosis.
• Mechanical vectors are animals that carry
pathogens to people but are not affected by the
pathogens : mosquitoes, ticks, flies, and pets.
• Insects and arthropods can be biological,
mechanical vectors also carrier for a pathogen.
• For example, flies can spread salmonellosis with
their feet.
• Vehicles of transmission are substances that are
normally brought into the body upon which a
pathogen has hitched a ride : water, air, and food.
• Water, contaminated with feces from an infected
animal, as in giardiasis.
• Air can be a vehicle if the person is standing >1 m
from an infected animal when it sneezes or coughs
and the pathogen becomes airborne on dust
particles or in droplets.
• Food transmission usually results in food poisoning.
PREVENTING ZOONOTIC DISEASES
• Methods such as thoroughly cooking meat,
boiling milk
• Quarantining sick animals
• Insecticides came into use in the 1940s and
helped protect against vector-borne diseases.
• Vaccines are available to protect animals and
people against some zoonotic diseases but not
all of them.
Classified persons at risk
• Group 1 (Agriculture): Farmers or other people in
close contact with livestock and their products.
• Group 2 (Animal-product processing and
manufacture): All personnel of abattoirs and of
plants processing animal products or by-products.
• Group I11 (Forestry, outdoors): Persons frequenting
wild habitats for professional or recreational
reasons.
• Group 4 (Recreation): Persons in contact with pets
or wild animals in the urban environment.
• Group 5 (Clinics, laboratories): Health care
personnel who attend patients, and health workers
(including laboratory personnel) who handle
specimens, corpses, or organs.
• Group 6 (Epidemiology): Public health professionals
who do field research.
• Group 7 (Emergency): People affected by
catastrophes, refugees, or people temporarily living
in crowded or highly stressful situations.
• Hazard : An act or phenomenon posing potential
harm to some person(s) or animal(s). The
magnitude of the hazard is the amount of harm
that might result, including the seriousness and
the number of people (and or animals) exposed.
• Risk : Adds to the hazard and its magnitude the

probability that the potential harm or
undesirable consequence will be realized.
• Risk assessment : The characterization of potential
adverse effects of exposures to hazards; includes
estimates of risk and of uncertainties in
measurements, analytical techniques, and
interpretive models. Quantitative risk assessment
characterizes the risk in numerical representations.
• Risk control assessment : Characterization of
alternative interventions to reduce or eliminate the
hazard and/or unwanted consequences; considers
technological feasibility, costs and benefits, and
legal requirements or restrictions.
• Risk management : The evaluation of
alternative risk control actions, selection
among them (including doing nothing),
and their implementation. The
responsible individual or office (risk
manager) sometimes oversees
preparation of risk assessments, risk
control assessments, and risk messages.
Risk management may or may not be
open to outside individuals or
organizations.
- Risk communication : An interactive process of
exchange of information and opinion among
individuals, groups, and institutions; often involves
multiple messages about the nature of risk or
expressing concerns, opinions, or reactions to risk
messages or to legal and institutional arrangements
for risk management.
- Risk message : A written, verbal, or visual statement
containing information about risk; may or may not
include advice about risk reduction behavior. A
formal risk message is a structured written, audio,
or visual package developed with the express
purpose of presenting information about risk.
• The International Office of Epizootics (OIE) has
developed a Disease Code List, distinguishing
diseases in domestic animals in relation to their
relative socioeconomic and public health
consequences! The diseases on that list of public
health consequence are zoonoses and all are
grouped into Lists A, B, and C, defined as follows:
• List A: Communicable diseases that have the
potential for very serious and rapid spread,
irrespective of national borders; are of serious
socioeconomic or public health consequence;
and are of major importance in the international
trade of livestock and livestock products. Reports
are submitted to the OIE as often as necessary to
comply with Articles of the International Zoo-
Sanitary Code (ISC). Examples: Newcastle
disease, Rift Valley fever, and vesicular stomatitis.
• List B Communicable diseases that are considered
to be of socioeconomic andor public health
importance within countries and are significant in
the international trade of livestock and livestock
products.
• Reports are normally submitted once a year,
although more-frequent reporting may in some
cases be necessary to comply with Articles of the
ISC. Exa: African trypanosomiasis, anthrax,
bovine tuberculosis, brucellosis,
campyloacteriosis, cysticercosis, dermatophilosis,
encephalomyelitis, echinococcosis/hydatidosis,
equine glanders, Japanese encephalitis,
leishmaniasis, leptospirosis, Nairobi sheep
disease, pasteurellosis, psittacosis, Q fever,
rabies, rodent tularemia, and trichinosis.
• List C Communicable diseases with important
economic influence at individual production
level. Examples: blackleg, botulism, other
clostridial infections, coccidiosis, contagious
pustular dermatitis (contagious ecthyma),
listeriosis, liver fluke, salmonellosis, swine
erysipelas, and toxoplasmosis.
CHIKUNGUNYA FEVER
Etiology :
 RNA genom virus (CHIK)
 genus Alphavirus (Arbovirus group A)
 famili Togaviridae.
 Memiliki hubungan antigenic dengan

Mayaro Fever, O’nyong-nyong , Ros
River dan Semliki virus (Sindbis).
Geographic distribution :
 Tersebar di daerah Sahara – Afrika, Asia
Tenggara, India dan Filipina (Tesh, 1992).
Kejadian pada Manusia :

 Endemic di pedesaan.
 Epidemi dapat terjadi di alam dan di kota

bila penduduknya peka
 Epidemi di Afrika Selatan pada tahun 1975,
1976 dan 1977 (Brighton et al, 1983)
 Ibadan, Negeria wabah pertama terjadi tahun
1969 pada anak-anak.
 Lima tahun kemudian wabah kedua terjadi
angka morbiditas tinggi pada anak-anak umur
< 5 tahun dan yang lebih tua memiliki kekebalan
perolehan.
 Penyakit ini dikelirukan dengan Dengue 

symptoma klinis mirip.
 Terjadi pada musim hujan ketika populasi
Nyamuk berkembang banyak
Kejadian pada Hewan :
 Antibodi thd virus CHIK ditemukan pada kera
hijau (Cercopithecus aethiops) dan baboon (Papio
ursinus) di Afrika Selatan.
 Studi serologis di Kruger National Park, Afrika

Selatan ditemukan 50 % kera hijau memiliki
antibodi thd virus CHIK (Kaschula et al, 1978)
 Daerah lain di Afrika, reaktor ditemukan pada

Colobus abyssinicus, chimpanzee, baboon Papio
dogueri.
Penyakit pada Manusia :
 Pernah disangka sebagai Dengue, karena baru
ditemukan tahun 1955.
 Masa inkubasi 4 sampai 7 hari.
 Gejala penyakit : sudden onset, demam,
menggigil, sakit kepala, anorexia, sakit pinggang,
konjungtivitis dan kadang2 adenopathy.
 Penderita (60 – 80 %)  lepuh kulit morbilliform
dan purpura pada kaki dan tangan.
Pengelupasan kulit dapat terjadi setiap 3 – 7
hari.
 Tanda klinis pada orang dewasa adalah
arthropathy  nama Chikungunya (jalan-
jalan hingga memar = bhs Swahili).
 Arthropathy  rasa sakit, pembengkaan dan

kekakuan pada metacarpophalangeal,
pergelangan tangan dan kaki, sendi siku,
bahu, lutut dan sendi metatarsal (Kennedy
et al, 1980).
 Arthropathy timbul 3 – 6 hari setelah
symptoma klinis pertama tampak, dan dapat
menderita hingga berbulan-bulan sampai
tahunan. Namun tidak ada yang mati karena
CHIK virus.
Penyakit pada Hewan :

 Symptoma klinis  belum ada konfirmasi
Sumber infeksi dan Cara Penularan :
 Siklus virus mirip Yellow fever yaitu antara Kera
di hutan dan nyamuk Aedes africanus dan A.
furcifer-taylori
 Kera Cercopithecus aethiops dan Papio ursinus

dgn titer viremia tinggi dapat menularkan virus
pada Kera Hijau yang lain melalui nyamuk
(percobaan lab oleh McIntosh, 1970)
 Epizootik terjadi pada kelomp kera dgn tingkat

kekebalan rendah dan terhenti penularannya
pada kelompok kera dgn kekebalan yang tinggi
 Orang didekat daerah hutan dpt tertular peny ini
 Ekosistem  epizootic pada kera di hutan akan
membunuh semua kera termasuk virusnya 
nyamuk tidak mengandung virus.
 Kera liar bukan reservoir bagi virus dan bila
terjadi wabah lagi ini disebabkan penularan dari
daerah lain.
 Kejadian epidemi karena Siklus Nyamuk –
Manusia – Nyamuk. Penderita dgn titer viraemia
tinggi menularkan virus pada orang yang peka
melalui nyamuk.
Diagnosis :
 Virus dapat diisolasi dari darah penderita
demam (percobaan virus yang diinokulasi
secara intra cerebral pada tikus atau
dibiakan pada sel VERO)
 Diagnosa serologis  pemeriksaan serum

darah penderita saat infeksi akut dan fase
penyembuhan dengan uji
haemagglutination inhibition, neutralization
dan complement fixation test
 Bila ada infeksi campuran antara virus CHIK
dengan O’nyong-nyong fever maka
identifikasi mengalami kendala baik isolasi
maupun diagnosa serologi karena kedua
virus ini secara antigenik sama.
 Perbedaannya hanya tergantung pada

tingginya titer antibody terhadap antigen
yang homolog (Filipe and Pito, 1973).
Kontrol :
 Pencegahan epidemi penyakit pada daerah
pedesaan  pemberantasan Aedes aegypti
 Vaksin yang diinaktifkan dgn formalin

berhasil pada tikus namun belum
diperbolehkan untuk digunakan pada
manusia (White et al, 1972).
DENGUE
Etiology:
Virus RNA Genus: Flavivirus
Family: Togaviridae
terdapat 4 serotype (1-4)
type homologkekebalan lengkap & tahan lama
type heterolog kekebalan sebagian & waktu
singkat
Geographic distribution:
 Daerah tropis di Asia, Afrika timur dan
barat, Polinesia & Micronesia, daerah
Carribia, Amerika tengah, Amerika selatan
Kejadian pd manusia:
 2 bentuk yi endemik & epidemik
 Wabah pertama terjadi thn 1963 di
kep.Caribbia dan menyebar ke Venezuela
disebabkan Dengue type 3.
 Wabah ke-2 terjadi 1969 disebabkan oleh
Dengue type 2 di kep. Caribbia , lalu menyebar
ke Colombia.
 Wabah ke-3 disebabkan oleh Dengue type 1,

thn 1977 di Jamaica dgn 60.000 penderita lalu
menyebar ke kep. Caribbia, Mexico, Amerika
Tengah dan Venuzuela.
 Wabah ke-4 terjadi thn 1981 oleh Dengue type

4, mulai dari San Bartolome (Antilles) dan
menyebar ke Caribbia
Kejadian pd hewan :
 Dengue merupakan penyakit manusia yang dibawa
oleh nyamuk genus: Aedes aegypti.
 Terdapat 2 siklus yi

1. siklus manusia
2. siklus hewan liar (kera-Aedes spp)  Aedes
niveus yang biasa hidup disekitar hutan.
 Di Malaysia 62,8 % kera, positif Arbovirus grup B

sedangkan 8% adalah Dengue  diisolasi dari 600
sera dari kera liar yang jauh dari populasi manusia.
Penyakit pada hewan :
 Kera yg ditularkan virus dengue secara buatan
tidak memperlihatkan gejala klinis penyakit.
Penyakit pada manusia :

 Umumnya penyakit bersifat akut dan demam
ringan.
 Masa inkubasi (saat digigit nyamuk hingga

timbul gejala klinis pertama) 5-8 hari.
•Kejadian ini mendadak dgn demam,menggigil,
sakit kepala, sakit bola mata, fotofobia, nyeri otot &
persendian.
•Kadang2 disertai nausea, vomit & radang

tenggorokan juga erythema dan 3 – 4 hari
kemudian timbul maculopapular & scarlatiniform
pada seluruh tubuh.
•Pembengkaan kelenjar lymphe.
•Demam diphasic, akhir hari ke 5 - 7 dan

kesembuhan terjadi bbrp minggu kmd. dgn tanda
fatique dan depresi.
 DHF  serius dan sering fatal, ditemukan di 12
kota tropis di Asia, terutama terjadi pada anak2
dengan 4 serotipe. Mula2 Dengue biasa, setelah
beberapa hari demam dan kemudian terjadi DSS
(perdarahan, sirkulasi gagal dan hipotensi).
 Pada anak2 karakterisasi DHF/DSS 
permeabilitas pembuluh darah abnormal 
problem koagulasi darah  diberi oksigen dan
cairan elektrolit untuk menggantikan cairan yang
hilang. Pada kasus schok yang berat diberikan
plasma darah.
 Pada dewasa  perdarahan, ptechia, echymoses,
kadang2 epistaksi. Jika hematokrit rendah 
transfusi darah.
Sumber infeksi dan cara penularan :
 Siklus terjadi antara manusia dengan nyamuk Aedes.
 Sumber infeksi adalah manusia pd saat viremia
 Setelah nyamuk mengisap darah penderita maka virus

akan masuk dan berkembang serta menginfeksi kelenjar
ludah nyamuk.
 Setelah 10 hari nyamuk dapat memindah kan penyakit

pada orang lain yg tidak kebal.
 Nyamuk Aedes aegypti bersifat anthropophilic yang aktif

pada siang hari. Vektor lain adl A. albopictus, A.
scutellaris dan terdapat pada saat musim hujan.
Diagnosis :
 Virus diisolasi dari darah penderita demam,
lalu dibiakkan pada kultur jaringan atau di
inokulasi kedalam thorax nyamuk.
 D/ HI test, CFT, Neutralization test.
Kontrol :
 Pencegahan thd wabah pembasmian
nyamuk A.aegypti.
DENGUE
Etiology:
Virus RNA Genus: Flavivirus
Family: Togaviridae
terdapat 4 serotype (1-4)
type homologkekebalan lengkap & tahan lama
type heterolog kekebalan sebagian & waktu
singkat
Geographic distribution:
 Daerah tropis di Asia, Afrika timur dan
barat, Polinesia & Micronesia, daerah
Carribia, Amerika tengah, Amerika selatan
Kejadian pd manusia:
 2 bentuk yi endemik & epidemik
 Wabah pertama terjadi thn 1963 di
kep.Caribbia dan menyebar ke Venezuela
disebabkan Dengue type 3.
 Wabah ke-2 terjadi 1969 disebabkan oleh
Dengue type 2 di kep. Caribbia , lalu menyebar
ke Colombia.
 Wabah ke-3 disebabkan oleh Dengue type 1,

thn 1977 di Jamaica dgn 60.000 penderita lalu
menyebar ke kep. Caribbia, Mexico, Amerika
Tengah dan Venuzuela.
 Wabah ke-4 terjadi thn 1981 oleh Dengue type

4, mulai dari San Bartolome (Antilles) dan
menyebar ke Caribbia
Kejadian pd hewan :
 Dengue merupakan penyakit manusia yang dibawa
oleh nyamuk genus: Aedes aegypti.
 Terdapat 2 siklus yi

1. siklus manusia
2. siklus hewan liar (kera-Aedes spp)  Aedes
niveus yang biasa hidup disekitar hutan.
 Di Malaysia 62,8 % kera, positif Arbovirus grup B

sedangkan 8% adalah Dengue  diisolasi dari 600
sera dari kera liar yang jauh dari populasi manusia.
Penyakit pada hewan :
 Kera yg ditularkan virus dengue secara buatan
tidak memperlihatkan gejala klinis penyakit.
Penyakit pada manusia :

 Umumnya penyakit bersifat akut dan demam
ringan.
 Masa inkubasi (saat digigit nyamuk hingga

timbul gejala klinis pertama) 5-8 hari.
•Kejadian ini mendadak dgn demam,menggigil,
sakit kepala, sakit bola mata, fotofobia, nyeri otot &
persendian.
•Kadang2 disertai nausea, vomit & radang

tenggorokan juga erythema dan 3 – 4 hari
kemudian timbul maculopapular & scarlatiniform
pada seluruh tubuh.
•Pembengkaan kelenjar lymphe.
•Demam diphasic, akhir hari ke 5 - 7 dan

kesembuhan terjadi bbrp minggu kmd. dgn tanda
fatique dan depresi.
 DHF  serius dan sering fatal, ditemukan di 12
kota tropis di Asia, terutama terjadi pada anak2
dengan 4 serotipe. Mula2 Dengue biasa, setelah
beberapa hari demam dan kemudian terjadi DSS
(perdarahan, sirkulasi gagal dan hipotensi).
 Pada anak2 karakterisasi DHF/DSS 
permeabilitas pembuluh darah abnormal 
problem koagulasi darah  diberi oksigen dan
cairan elektrolit untuk menggantikan cairan yang
hilang. Pada kasus schok yang berat diberikan
plasma darah.
 Pada dewasa  perdarahan, ptechia, echymoses,
kadang2 epistaksi. Jika hematokrit rendah 
transfusi darah.
 Siklus terjadi antara manusia dengan nyamuk Aedes.
 Sumber infeksi adalah manusia pd saat viremia
 Setelah nyamuk mengisap darah penderita maka virus

akan masuk dan berkembang serta menginfeksi kelenjar
ludah nyamuk.
 Setelah 10 hari nyamuk dapat memindah kan penyakit

pada orang lain yg tidak kebal.
 Nyamuk Aedes aegypti bersifat anthropophilic yang aktif

pada siang hari. Vektor lain adl A. albopictus, A.
scutellaris dan terdapat pada saat musim hujan.
Diagnosis :
 Virus diisolasi dari darah penderita demam,
lalu dibiakkan pada kultur jaringan atau di
inokulasi kedalam thorax nyamuk.
 D/ HI test, CFT, Neutralization test.
Kontrol :
 Pencegahan thd wabah pembasmian
nyamuk A.aegypti.
JAPANESE B ENCEPHALITIS
• Synonym Japanese Encephalitis type B
• Etiology Virus RNA
Genus Flavivirus (Arbovirus type B)
Fam Toga viridae
• Georaphic distribution Asia China,
Taiwan, Japan, Vietnam, pantai timur
Rusia, Laos, Birma, Korea, Filipina,
Malaysia, Singapura, Thailand, Indonesia,
Srilangka, India
• Kejadian pd manusia :
daerah tropis sporadis sepanjang tahun
epidemi musim hujan
• Di Jepang kasus setiap tahun kasus kecil
8000/thn
• Yg rentan umur 3 – 6 thn
• Infeksi tanpa gejala klinis
• Infeksi dgn gejala klinis 1 diantara 500-1000
serologis (+)
• Perbandingan inf dgn gejala klinis : Infeksi tanpa
gejala = 1 : 25 (org dewasa)
Kejadian pd hewan:
• Babi (sumber utama pembiakan virus)
• Asia (Jepang, Taiwan)
• Kerugian ekonomi tinggi kematian bayi
babi
• Titer Ab ditemukan pd kuda, sapi, burung,
bebek
Peny pd manusia umumnya subklinis (tanpa
symptoma neurologis)
Bentuk gejala klinis encephalitis mortalitas
20-50 %; masa inkubasi 4-14 hari timbul
hyperperexia, cephalalgia, muntah2,
manifestasi cerebral-meningeal kaku leher,
konfulsi-kebingungan, disorientasi, delerian,
paresis dan paralgia
Kesembuhan lama
Kematian ± hari ke-10
Peny pd hewan kerugian ekonomi tinggi akibat
aborsi dan kematian bayi babi (50-70 %)
fetus -mumifikasi
-hydrocephala
• Babi dewasa tidak ada gejala klinis atau
demam sebentar
• Virus tdpt pada semen
• Kuda tanpa gejala klinis
• Sapi; Kambing pyrexia, depresi, fotofobia,
tremor otot, inkoordinasi & ataxia
• Domba jarang terkena
Sumber infeksi & penularan
• Di Jepang & China vektor transmisi virus adl Culex
tritaeniorhincus menularkan pd burung; babi; sapi;
manusia
• Nyamuk berkembangbiak di sawah & air bersih.
Kadang2 pada Culides
Predeleksi dlm darah – hewan peliharaan,
- Burung,
- Manusia
Rentan anak2 < 3 thn
Diagnosis Isolasi virus dari – otak; - darah; -
cairan cerebrospinal  orang mati, hewan,
fetus babi
HI test, neutralization test, CFT pada fase
akut dan kesembuhan
Ab HI cepat terbentuk saat sakit
Ab CFT timbul minggu ke-3 s/d 4
Control vaksinasi (hidup, inaktif) manusia,
babi.
Nipah Virus Outbreak
• 1998-1999, Malaysia
– Respiratory and neurologic
syndrome in swine
– Encephalitis in humans
• More than 250 cases
• More than 100 deaths
– Initially mistaken for
Japanese encephalitis
– Discovered new Paramyxovirus
Nipah Virus
• Virus isolated in March 1999
• Quick national response with international
assistance
• 1.1 million pigs culled (out of 2.4 million
total)
• No new cases in Malaysia since 1999
Reservoir
• Flying foxes (fruit bats)
– Carry the virus
– Are not affected
– Virus found in
• Urine
• Partially eaten fruit
– Migratory
Photo courtesy of James Roth, Iowa State University
Nipah Field Investigations- Malaysia
Nipah Virus in Bangladesh
• Outbreaks of respiratory disease, high
fever, unconsciousness, vomiting,
headache
• 2002 to present
• Confirmed to be Nipah virus infection by
CDC
• Believed to be oral transmission from
contaminated fruit
Hendra virus
Emerged in Australia, 1994-1995
Killed 15 horses and 2 people
Horses
Peracute respiratory disease
Humans
Influenza-like disease
Severe respiratory distress
Meningoencephalitis
Picasso: Cat Catching a bird. http://www.people.hofstra.edu
Rabies Virus
• member of the Lyassavirus of the Rhabdoviridae.

• ssRNA enveloped virus, characteristic bullet-shaped appearance
with 6-7 nm spike projections.
• virion 130-240nm * 80nm
• -ve stranded RNA codes for 5 proteins; G, M, N, L, S
• Exceedingly wide range of hosts.
• There are 5 other members of Lyassavirus : Mokola, Lagosbat,
Duvenhage, EBL-1, and EBL-2.
• Duvenhage and EBL-2 have been associated with human rabies.
Rabies Virus
Structure of rabies virus (Source: CDC)
Rabies virus particles

Epidemiology
Rabies is a zoonosis which is prevalent in wildlife. The main

animals involved differs from continent to continent.
Europe fox, bats
Middle East wolf, dog
Asia dog
Africa dog, mongoose, antelope
N America foxes, skunks, raccoons,
insectivorous bats
S America dog, vampire bats
Pathogenesis
• The commonest mode of transmission in man is by the bite of a

rabid animal, usually a dog. Rabies is an acute infection of the CNS
which is almost invariably fatal.
• Following inoculation, the virus replicates in the striated or
connective tissue at the site of inoculation and enters the peripheral
nerves through the neuromuscular junction.
• It then spreads to the CNS in the endoneurium of the Schwann cells.
• Terminally, there is widespread CNS involvement but few neurons
infected with the virus show structural abnormalities. The nature of
the profound disorder is still not understood.
Laboratory Diagnosis
• Histopathology - Negri bodies are pathognomonic of rabies. However,
Negri bodies are only present in 71% of cases.
• Rapid virus antigen detection - in recent years, virus antigen detection
by IF had become widely used. Corneal impressions or neck skin
biopsy are taken. The Direct Fluorescent Antibody test (DFA) is
commonly used.
• Virus cultivation - The most definitive means of diagnosis is by virus
cultivation from saliva and infected tissue. Cell cultures may be used
or more commonly, the specimen is inoculated intracerebrally into
infant mice. Because of the difficulties involved, this is rarely offered
by diagnostic laboratories.
• Serology - circulating antibodies appear slowly in the course of
infection but they are usually present by the time of onset of clinical
symptoms.
Diagnosis of Rabies
Negri Body in neuron cell Positive DFA test (Source: CDC)

(source: CDC)
Management and Prevention
• Pre-exposure prophylaxis - Inactivated rabies vaccine may be

administered to persons at increased risk of being exposed to rabies e.g.
vets, animal handlers, laboratory workers etc.
• Post-exposure prophylaxis - In cases of animal bites, dogs and cats in a
rabies endemic area should be held for 10 days for observation. If signs
develop, they should be killed and their tissue.
• Wild animals are not observed but if captured, the animal should be
killed and examined. The essential components of postexposure
prophylaxis are the local treatment of wounds and active and passive
immunization.
• Once rabies is established, there is nothing much that could be done
except intensive supportive care. To date, only 2 persons with proven
rabies have survived.
Postexposure Prophylaxis
• Wound treatment - surgical debridement should be carried out.

Experimentally, the incidence of rabies in animals can be reduced by
local treatment alone.
• Passive immunization - human rabies immunoglobulin around the area
of the wound; to be supplemented with an i.m. dose to confer short
term protection.
• Active immunization - the human diploid cell vaccine is the best
preparation available. The vaccine is usually administered into the
deltoid region, and 5 doses are usually given.
• There is convincing evidence that combined treatment with rabies
immunoglobulin and active immunization is much more effective than
active immunization alone. Equine rabies immunoglobulin (ERIG) is
available in many countries and is considerably cheaper than HRIG.
Rabies Vaccines
The vaccines which are available for humans are present are inactivated whole
virus vaccines.
– Nervous Tissue Preparation e.g. Semple Vaccine - associated with the rare
complication of demyelinating allergic encephalitis.
– Duck Embryo Vaccine - this vaccine strain is grown in embryonated duck
eggs This vaccine has a lower risk of allergic encephalitis but is considerably
less immunogenic.
– Human Diploid Cell Vaccine (HDCV) - this is currently the best vaccine
available with an efficacy rate of nearly 100% and rarely any severe reactions.
However it is very expensive.
– Other Cell culture Vaccines - because of the expense of HDCV, other cell
culture vaccines are being developed for developing countries. However
recent data suggests that a much reduced dose of HDCV given intradermally
may be just be effective.
Control of Rabies
• Urban - canine rabies accounts for more than 99% of all human
rabies. Control measures against canine rabies include;
– stray dog control.
– Vaccination of dogs
– quarantine of imported animals
• Wildlife - this is much more difficult to control than canine
rabies. However, there are on-going trials in Europe where bait
containing rabies vaccine is given to foxes. Success had been
reported in Switzerland.
Avian Influenza
ZOONOSIS - KHD 302

DEPARTMENT OF VPH
INTRODUCTION
INFLUENZA  A Viral Non Food Borne Disease - ZOONOSIS

in animals, incl. bird & human  HPAI
Fam. ORTHOMYXOVIRIDEAE, RNA virus,4 generas:
1. Influenza Virus A  Human & Animals
2. Influenza virus B  Human
3. Influenza virus C  Human & pigs
4. Thogotovirus
* Virus Influenza Type A & B 
• Caustive agent of severe & fatal disease in MAN
• Avute Respiratory disease 
variation in clinical signs according to age
Epithel of Upper Respiratory Tract
• Natural reservoir  AQUATIC BIRDS Virus Influenza A

• Replication  mainly in the INTESTINUM
Viral shedding  FAECES & ORAL
Transmision  aerosol  dropplet
• Host  multiple species
INFLUENZA VIRUS
• RNA virus  8 SEGMEN GENOME
• VIRUS ENVELOPE has SURFACE
PROTEIN  HEMAGLUTININ &
NEURAMINIDASE
• 3 TYPE  A, B, C
• TYPE A  ANTIGENIC SCHIFT &
ANTIGENIC DRIFT
• TYPE B  ANTIGENIC DRIFT
• TYPE C  RELATIVELY STABLE
Courtesy of Linda Stannard, University of Cape Town, S.A.
CHARACTERISTIC of INFLUENZA VIRUS
Main Antigen is a surface

glycoprotein permukaan 
Hemaglutinin & Neuraminidase
• Hemagglutinin (HA) 
attach to the host cell
protective antibody
• Neuraminidase (NA) 
Remove neuraminic acid from
mucin & release from cell
Also 8 segmented code gene of
10 protein
18 HEMAGLUTININ H1- H18

11 NEURAMINIDASE  N1- N11
 H1-H16& N1-N9
M2 all in aquatic birds
 H17N10 in Bats found in
Guatemala
 H18N11 in Bats in Peru
M1NS1
PB1 PB2 PA HA NP NA M2NS2 NOMENCLATURE
A/Chicken/HK/5/98 (H5N1)
A/NY/7708/04 (HxNx)
Slide courtesy of Dr. David Wentworth
80-120 nm
H17N10 isolated from little yellow-shouldered bats, found in
Guatemala
1. Tong S, et al. (2012) A distinct lineage of influenza A virus

from bats. Proc Natl Acad Sci USA 109(11):4269–4274.
2. Li Q, et al. (2012) Structural and functional characterization
of neuraminidase-like molecule N10 derived
from bat influenza A virus. Proc Natl Acad Sci USA
109:18897–18902.
3. Zhu X, et al. (2012) Crystal structures of two subtype
N10 neuraminidase-like proteins from bat influenza A
viruses reveal a diverged putative active site. Proc Natl
Acad Sci USA 109:18903–18908.
H18N11 isolated from bats, found in Peru (Zhu et al. 2012)
It has been identified an influenza A virus from little yellow-
shouldered bats captured at two locations in Guatemala. It is
significantly divergent from known influenza A viruses.
The HA of the bat virus was estimated to have

diverged at roughly the same time as the known subtypes of
HA and was designated as H17.
The neuraminidase (NA) gene is highly

divergent from all known influenza NAs, and the internal genes
from the bat virus diverged from those of known influenza A
viruses before the estimated divergence of the known
influenza A internal gene lineages.
Attempts to propagate this virus in cell cultures and
chicken embryos were unsuccessful, suggesting
distinct requirements compared with known
influenza viruses.
Despite its divergence from known influenza A viruses

 the bat virus is compatible for genetic exchange
with human influenza viruses in human cells,
suggesting the potential capability for reassortment &
contributions to new pandemic or panzootic influenza
A viruses.
Classification (View hierarchy)
Viruses (Virus) → ssRNA viruses → ssRNA
negative-strand viruses →
Orthomyxoviridae → Influenzavirus A
(Influenza A virus) → Influenza A virus →
H17N10 subtype
Primary Descendants (View list)
bat/Guatemala/164/2009(H17N10))
http://www.oie.int/animal-health-in-the-world/update-on-avian-
influenza/2015/
UPDATE ON HIGHLY PATHOGENIC AVIAN INFLUENZA IN ANIMALS

(TYPE H5 and H7)
This page has been set up at the start of the epizootic of Highly
Pathogenic Avian Influenza due to H5N1 in South East Asia in late
2003, before its expansion later to other continents. It groups in a
single place for stakeholders interested by this important zoonotic
disease, all immediate notifications and follow-ups reports notified
by OIE Member Countries on Highly Pathogenic Avian Influenza due
to serotype H5N1 and other serotypes.
The graph gives the total number of outbreaks of Highly
Pathogenic Avian Influenza (subtype H5N1) in poultry since 2003. It
is kept up-to-date as soon as new outbreaks are notified to the OIE.
Last report received on 6 March 2015
VIRUS INFLUENZA A
• ANTIGENIC SCHIFT & ANTIGENIC

DRIFT PROTEIN HA & NA
• ANTIGENIC SCHIFT HA 
PANDEMI
• ANTIGENIC DRIFT HA & NA 
EPIDEMI
• BIASANYA  GEJALA FLU RINGAN
• KEMATIAN  karena KOMPLIKASI
PNEUMONIA

A. ANTIGENIC DRIFT
B. REASSORTMENT
or ANTIGENIC SCHIFT
C. RECOMBINATION
Source : Webster RG and Hulse DJ. 2004. Microbial adaptation and change : avian
influenza. Rev. sci.tech.Off. int. Epiz. 2004, 23 (2) : 453 - 465

A. ANTIGENIC DRIFT  errors during the replication of

influenza v. which are unable to be repaired 
accumulate amino acid changes within the viral
genome  the existing strains being replaced by a
new antigenic variant  EPIDEMI
B. REASSORTMENT or ANTIGENIC SCHIFT  the
exchange of ribonucleic acid (RNA) segments
between 2 genotypically different influenza viruses
infecting a single cell  The generation of a novel
strain &/ subtype  PANDEMI
C. RECOMBINATION  2 different source of RNA
contribute to asingle influenza RNA segment
ANTIGENIC DRIFT  errors during the replication of influenza v. which are

unable to be repaired  accumulate amino acid changes within the viral
genome  the existing strains being replaced by a new antigenic variant
REASSORTMENT or ANTIGENIC SCHIFT  the exchange of ribonucleic acid

(RNA) segments between 2 genotypically different influenza viruses infecting
a single cell  The generation of a novel strain & subtype
RECOMBINATION  2 different source of RNA contribute to a single

influenza RNA segment
The genesis of a SINGLE GENOTYPE
AI Virus A/H5N1 in 2004
Li, K.S., Y. Guan, J. Wang, G.J.D. Smith, K.M. Xu, L.

Duan, A.P. Rahardjo, P. Puthavathana, C. Buranathai,
T.D. Nguyen, A.T.S. Estoepangestie, A. Chaisingh, P.
Auewarakul, H.T. Long, N.T.H. Hanh, R.J. Webby,
L.L.M. Poon, H. Chen, K.F. Shortridge, K.Y. Yuen, R.G.
Webster and J.S.M. Peiris. 2004.
Genesis of a highly pathogenic and potentially pandemic
H5N1 influenza virus in eastern Asia.
Nature, 430 : 209 – 213.
The genesis of a single H5N1 genotype in 2004
Gs/Gd/96-like viruses reassorted w/ viruses
from wild aquatic birds (genotype C) 
multiple genotypes appearing in 2001
Some 2001 H5N1 viruses transmitted from
domestic poultry back to wild aquatic birds 
a new set genotypes for 2002
In 2002  HA gene of H5N1 strain showed
significant antigenic drift  pronounced in the
genotype Z & Z+ viruses isolatd in late 2002 &
from human in early 2003
In 2004  these circulating viruses have
evolved to include only genotype Z
The colour coding of the schematically shown

virus particles  the virus lineages
A gap in the neuraminidase or non-structural
protein gene segments  a deletion
“ANTIGENIC DRIFT” Virus Influenza A
Aso called as “point mutation” of gene HA causing a “minor HA

changes”
• a continually process
• Immunity limited to 1 strain only
• Vaccine must test annually
• 6 – 8 months process (USA : 85 billion trivalent dose)
• Target  high risk people (inactive) & healthy people
(LAIV)
• Causing the seasonal flu epidemics
PHYLOGENETIC ANALYSIS of HPAI VIRUS
• Nucleoprotein v AI 5 host specific : classical
equine (15 years ago), recent equine, gulls, swine
& human
• Nucleoprotein & gene lineages v AI different
between virus isolate Eurasia & America 
Latitudinal Migrating Birds doesn’t contribute to
the virus distribution
• Longitudinal Migrating Birds  plays an important
role on the continuity of evolution of AI virus
• AI Virus  low speed of evolution rate, around
60 years the AI virus in the aquatic birds was
static
• Antigenic drift (NA) & antigenic shift (HA)
• Causes a mild infection in POULTRY
• Can mutates  HIGHLY PATHOGENIC VIRUSES
• Had been recognised  AI-OUTBREAK in the world

• HIGH MORTALITY in POULTRY
• HPAI determination  according to molecular & pathogencity
characteristics
Susceptible Animals to Avian Influenza Virus
No. Susceptible Animals SUBTYPES
& Human HEMAGGLUTININ NEURAMINIDASE
1. Aquatic Birds H1 – 15 N1 – 9
2. Ducks H1 -12 N1 – 9
3. Turkeys H1 -10 N1 – 9
4. Chickens H4, 5, 6, 7, 9, 10 N1, 2, 4, 7
5. Sea Birds H1 – 7, 9 - 16 N1 – 9
6. Pigs H1, 3,5 N1- 2
H1N1, H1N2, H3N2, H5N1
7. Horses H3,7 N7-8
H7N7, H3N8
8. Seawolf H10 N4
9. Harbour seals H3, 4, 7 N3, 5, 7
H7N7, H4N5, H3N3
10. Whale H3, 13 N2, 9
H3N2, H13N9
11. Fam. Felidae : Leopard, Tiger, H5 N1
Cats H5N1
12. Dogs H5 N1
H5N1
13. HUMAN H1-3, 5, 7 N1,2,7,8
H1N1, H2N2, H3N2, H5N1, H7N7
14. Yellow shouldered Bats H17, H18 N10, N11
H5,H7, H9
9-13,15-16
H17
H5
H5
• Causes Infection of Respiratory Tract & GI Tract of Birds
Usually doesn’t cause a disease in Wild Birds
Frequently genetic re-assortment
Morbidity & mortality in POULTRY
• Virus shedding through RESPIRATORY TRACT & FAECES

• By low temperature & low humidity  several days to week
• Survive in water
• Survie on the surface
• Should be desinfected to prevent its spread
VIRUS AVIAN INFLUENZA A
• TDK menyebabkan sakit pd UNGGAS LIAR
• Ada hubungannya dg INF RINGAN pd UNGGAS PIARAAN
• DPT BERUBAH  HIGHLY PATHOGENIC VIRUSES
• Ada hubungannya WABAH PENY FLU BURUNG di DUNIA

• TDK menyebabkan penyakit pd UNGGAS LIAR
• MORTALITAS TINGGI pd UNGGAS PIARAAN
• Determinasi HPAI berdasarkan kriteria secara molekuler &
pathogenitas
IMPACT of INFLUENZA
• Seasonal Epidmics in the 4 temperate regions
USA, Canada, Eropa, Rusia, Cina, Jepang, Australia, Brasil,
Argentina
• Year round in tropical area
In equator  Africa & Southeast Asia
IMPACT of INFLUENZA PANDEMI
INFLUENZA PANDEMI in 20th Century 
1. 1918 – 1919 “SPANISH FLU” A (H1N1)
Highst Fatality caused by INFLUENZA
> 500.000 in the USA & 50 million in the world
Most dead in several days of infection,otherwise died later
accompanied by complications
Almost a half of the deaths were healthy young & old people
H1N1 is still circulating until now since the outbreak in 1970
2. 1957 -1958 “ASIAN FLU” A (H2N2)
Started in China in late February 1957 & spread to the USA in
June 1957
3. 1968 – 1969 “HONG KONG FLU” A (H3N2)
Started in Hong Kong in the early 1968 & spread to the USA
at the end of the year
H3N2 is still circulating until now
THE CAUSATIVE AGENT OF INFLUENZA PANDEMI
1918 - 1919 “SPANISH FLU” Not yet know the
A (H1N1) virus origin  avian ??
STILL CIRCULATE TODAY
Virus has gene combination

1957 - 1958 “ASIAN FLU” of human influenza virus &
A (H2N2) avian virus influenza
HA, NA, PB1 = Avian
1968 - 1969 “HONG KONG FLU”

A (H3N2)
HA, PB1 = Avian
RECENTLY PANDEMI FLU
 H1N1  emerged in Mexico April 2009
 Structure of the virus is different from 1918-

1919 & the circulating H1N1 virus  this incl. 4
genes from European swine, Mexican Swine,
Human & Birds  Swine Flu
 WHOSince June 2009

 CFR  H1N1 MEXICO < H5N1
3/24/2022 AI-Zoonosis_S1_Soelih_2021
AI-Zoonosis_S1_Soelih_2011 31
Avian Antigenic “shift”
reassortant Pandemic
virus
Avian virus Quail/HK/G1/97 (H9N2)
Goose/Guangdong/1/96 (H5N1)
Teal/HK/W312/97 (H6N1)
Reassortment in humans
Avian virus Human virus
Model of the
emergence of a
pandemic
influenza virus Reassortment in swine Avian-Human
3/24/2022 AI-Zoonosis_S1_Soelih_2021 pandemic 32
reassortant virus
Reservoir of The New Influenza Virus A Subtype in
Human  Aquatic Birds (Ducks)
AVIAN INFLUENZA A HUMAN INFLUENZA A

H1 – H16 H1, H2, H3, H5, H7, H9
N1 – N9 N1,N2, N7, N8
HPAI INFECTION in HUMAN
The First Confirmed of HPAI Cases in Human following the
outbreak in Poultry
• H5N1 (Severe Respiratory Disease):
• 1997 HK  6 deaths / 18 cases
• 2003 HK  1 death / 2 cases
• 2003 – 2005 Vietnam, Thailand, Cambodia 
56 deaths /111 cases
• 2005  Indonesia 3 deaths / 4 cases
• 2003 Holland  1 death / 89 cases
The victims were mainly poultry farm workers
• 2004 Canada (2 cases, no death)
PANDEMIC PHASE (WHO)
PUBLIC HEALTH ASPECTS of HPAI VIRUS
Characteristic of the H5N1 virus  INAKTIVE by

• 56 0 C / 3 h & 60 0 C / 3 min
• pH acid  pH 4
• Chemicals: oxidator, sod dodecyl sulphate,
lipid solvents, -propiolactone
• Disinfektansia : formalin & Iodine
Survive in the animal tissues, faeces & water
• Mutate frequently
– Antigenic drift
• Point mutations accumulated during
virus replication
– Antigenic shift
• Hybrid virus emerges when cell infected
with two different influenza viruses
– Human, avian, swine, equine
• Transfer of influenza virus to a
different species
AI Virus is type A Influenza virus  genetic

reassortment to novel mammalia virus
Sea Wolf–AI virus isolate, caused death due to
pneumonia  has the same HA & NA with a
turkey-isolate of several decades ago.
H5  poultry has an important role in the
epidemiology of influenza in human  2003 – 2007
167 deaths/277 cases (WHO 1 March 2007)
H7  1 death in 2003 (Holland)
THE EPIDEMIOLOGY OF HPAI
Highly contagious
Hosts  at the start only in chicken, turkey, but than
in almost all birds species
Source of infection  Faeces & Secretory of Respiratory
Tract.
Survive in faeces, tissues & water
Transmision 
Direct contact w/ sick birds  faeces
Contamination of feed, waterm equipments &
clothes
Broken eggs in the incubator
Reservoir  aquatic birds & sea birds
Air <<
• Import restrictions
• Surveillance
• Appropriate biosecurity
– Control human traffic
– Introduction of new birds into flock
– Avoid open range rearing in waterfowl
prevalent areas
• Education of the poultry industry
• Prompt response to MP AI outbreaks
• Program Pengendalian Influenza pd Manusia

a) deteksi & identifikasi adanya varian virus influenza
baru pd saat yg tepat
b) menyeleksi strain virus yg cocok u/ vaksin
• Pengendalian Influenza pd Hewan
a) menunjang Program Pengendalian Influenza pd
manusia
b) Mengetehui ekologi v influenza yg berperan pd
kesehatan manusia & hewan
c) Determinasi secara molekuler adanya penularan pd
host lama & host baru
THERAPY  Amantadin, Oseltamivir

BIO SECURITY  eradicated & localised the virus
Hygienic & Sanitation precautions
1. Protecting the farm  avoiding contact to wild birds,
especially aquatic birds infected farm
2. Preventing the farm from unknown infected birds
3. Controlling any traffic  vehicle,human,equipment etc.
4. Washing & desifecting Procedure
5. “All in – all out”
Exotic  Biosecurity in an outbreak

• Stamping out totally
• Waste of cadaver & all poultry products
• Decontamination
• At least 21 days
• Central of the outbreak (5 km), buffer area (5 – 10
km) & free area >10 km
Endemic  Biosecurity  DEPOPULATION
Any question ???
Hantavirus Pulmonary Syndrome
(HPS)
MK ZOONOSIS – KHD 302

DEP. KESEHATAN MASYARAKAT VETERINER
FAKULTAS KEDOKTERAN HEWAN
UNIVERSITAR AIRLANGGA
3/24/2022 Zoo- Hanta V D_Soelih_Genap 1

2016
Hantaviruses
 suatu group virus yg terdapat pada
rodensia
 Beberapa strain Hantavirus , walaupun

jarang tp dapat menyebabkan kematian pd
manusia 
 Hantavirus pulmonary syndrome (HPS)
 Hemorrhagic Fever with Renal Syndrome
(HFRS)
2016
 Hantaviruses  RNA virus beruntai tunggal ,
memp amplop, single-stranded,
enveloped, negatif,
 Fam. Bunyaviridae
 Nama Hantavirus 
sejarah awal kejadian wabah di tepi Sungai
Hantaan – Korea Selatan
Virus ini diisolasi pd akhir 1970 oleh  Karl M.

Johnson & Ho-Wang Lee menyebabkan
wabah Korean hemorrhagic fever pd tentara
Amerika & Korea pd saat Perang Korea th 1950–
1953  yg kmd diketahui penyebabnya adalah
infeksi hantavirus

2016
2016
Beberapa tikus & tikus besar dpt membawa
penyakit yg serius seperti  HPS, HFRS,
Leptospirosis, lymphocytic choriomeningitis,
plague, and typhus.

2016
Hantavirus pulmonary syndrome
(HPS)
Penyebaran geografis HPS
 Di Benua Amerika

2016
2016
Sumber & Cara Penularan HPS
 Cara Penularan
 Per oral
 Per inhalasi
 Kontak langsung  menyentuh permukaan yg
terkontaminasi urine, kotoran, sarang tikus yg
terkontaminasi virus  & kmd tanpa mencuci
tangan meraba mata, hidung &
 gigitan tikus (mouse & rat)
 Penularan human-to-human transmission
pernah dilaporkan di Amerika Selatan 
penyebabnya strain virus Andes
 Sumber  urine & kotoran rodensia yg

mengandung hantavirus yg kmd mencemari
lingkungan
3/24/2022 & udara
Zoo- Hanta V D_Soelih_Genap 8
2016

2016

2016

2016
Inf. Hantavirus dapat menyepakan HPS pd manusia
 pembawanya adalah tikus (mice & rats)
Di Amerika Utara  deer mouse, white-footed

mouse, rice rat, the cotton rat
Namun, tidak semua deer mouse, white-footed
mouse, rice rat, or cotton rat membawa hantavirus

2016
 Rodensia lainnya  house mice, roof rats, &
Norway  hingga saat ini belum pernah diketahui
sebagai pembawa HPS bagi manusia
 Karena sulitnya memperkirakan apakah tikus

disekitar kita membawa hantavirus maka yg
terbaik adalah menghindari tikus liar, & utk
amannya harus selalu rajin membersihkan bekas
urine, kotoran, & sarang tikus di tempat tinggal
kita.
 Anjing & kucing  dilaporkan tidak menularkan

inf. hantavirus pd manusia

2016
Source & Route of Transmission
Beberapa kegiatan manusia yg beresiko dapat

tertular HPS 
- Membersihkan bekas urine, kotoran & sarang
tikus tidak sempurna
- Membersihkan ruangan / gudang yg sduah lama

tertutup
- Bekerja di area dihabitatnya tikus
Di USA belum pernah dilaporkan kasus

human to human transmission

2016
Symptomes of HPS
Masa inkubasi HPS pd manusia  1 – 5 minggu
1. S/ awal demam, nyeri otot & letih

2. Beberapa hr kmd  kesulitan bernafas
3. Kadang2 diikiuti dg  sakit kepala,
mengantuk, menggigil, mual, muntah,
diarrhea, & sakit perut
4. Biasanya  tidak terdapat discharge nasal,
gangguan tenggorokan, kemerahan kulit

2016
Hemorrhagic Fever with Renal Syndrome
(HFRS)
 suatu group penyakit dg GK mirip, disebabkan

oleh hantaviruses dr Familia Bunyaviridae
C/  berbagai strain virus Hantaan, Dobrava,

Saaremaa, Seoul, & Puumala
Termasuk HFRS 
 Korean hemorrhagic fever
 Epidemic hemorrhagic fever
 Nephropathis epidemica.

2016
Distribusi geografis HFRS
Diseluruh dunia
 Haantan virus  di Asia Timur, terutama di

China, Russia, & Korea
Puumala virus  di Skandinavia, Europe Barat,
& Russia Barat
 Dobrava virus  utamanya didaerah Balkan
 Seoul virus  di seluruh dunia
 Saaremaa virus  di Europe Tengah &
Skandinavia

2016
Sumber & Cara Penularan HFRS
Cara Penularan 
 Per inhalasi
 kontak langsung  luka kulit, membrana mucosa mata,
hidung & mulut
 Gigitan rodensia
 Human to human transmission  sangat jarang
Sumber Hantavirus
urine, kotoran, & saliva rodensia yg terinfeksi, yg juga
kmd mengkontaminasi sarangnya shg debu juga
mengandung hantaviruses

2016
Pencegahan Hanta Virus Disease (HVD)
Penularan dpt dicegah dg mencegah kontak dg
rodensia & udara yg terkontaminasi hantavirus
1. Tutup lubang masuknya tikus kedalam rumah /
gedung
2. Tutup rapat makanan & pakan hewan, air & sampah
water & garbage dlm kontainer
3. Perhatikan adanya kotoran hewan/tikus & sarangnya
ketika membersihkan rumah / gedung
4. Pd saat membersihkan area yg terkontaminasi
kotoran tikus, hindari jangan sampai dari menghirup
udara yg terkontaminasi, & hindari kontak langsung
5. Ketika akan membersihkan ruangan yg tertutup
lama  keluarkan udaranya terlebih dahulu dg
membuka pintu-jendela minimal 30 menit

2016
Prevention of Hanta Virus Disease
6. Bersihkan dg pel basah & kenakan sarung

tangan karet
7. Kenakan goggles & masker pd saat
membersihkan area yg terkontaminasi kotoran
tikus
8. Basahi area yg terkontaminasi kotoran tikus
dg larutan bleach disinfectant, & bersihkan dg
kain pel basah
9. Hindari membersihkan dg metode “kering” 
membersihkan debu, menyapu, vacuuming or
air-hosing.
10. U/ Public awareness  Buat Buku Petunjuk
Cara Pencegahan Infeksi Hantavirus di tempat
kerja & tempat umum
2016
Tip Cara Membersihkan  Jangan menggunakan

sapu atau penghisap debu u/ membersihkan urine,
kotoran, & sarang tikus  akan menyebabkan
partikel virus terangkat ke udara shg dpt terhirup
Sarang Tikus
Dapat terbuat dr berbagai jenis bahan  kertas,
tissues, insulation, & bahan isi furniture

2016
Untuk membersihkan area yg terkontaminasi

kotoran tikus sebaiknya menggunakan 
 Larutan disinfektan yg umum digunakan sehari-

hari  Pastikan tertulis di labelnya “disinfectant”
 Larutan Pemutih & Air  Campurkan 1 ½

cangkir cairan pemutih (bleach) dg 1 gallon air
Jumlah sedikit dg perbandingan 

Cairan pemutih : Air = 1 : 9

2016
Cara Membersihkan Area yg Terkontaminasi Tikus
1. Kenakan sarung tangan karet / plastik

2. Basahi dg disinfektansia atau larutan pemutih-air
 urine & kotoran tikus  Pastikan betul2 basah &
biarkan minimal 5 menit
3. Gunakan kertas pembersih u/ membersihkan urine
& kotoran tikus, kmd masukkan kantung plastik
buang di tempat sampah
4. Semprot dg disinfektansia
5. Bersihkan area tsb dg kain pel atau spons yg
dibasahi disinfektansia atau larutan pemutih-air
6. Membersihkan sarung tangan karet/plastik
setelah digunakan  Cuci dg sabun & air
mengalir, atau sebelum dibuka disemprot dg
disinfektansia atau larutan pemutih  kmd cuci
tangan dg sabun & air hangat
2016
Cara membersihkan ruangan, gudang, halaman
atau area diluar gedung
1. Buka dahulu pintu & jendela 30 menit sebelum mulai
dibersihkan
2. kenakan kaos tangan karet / plastik
3. Bersihkan urine, kotoran , sarang tikus, & bangkai
tikus dg disinfektansia atau larutan pemutih
4. Mop floors or spray dirt floors with a disinfectant or
mixture of bleach & water
5. Bersihkan lemari, laci & dg disinfektan atau lar.
Pemutih
6. Membersihkan furnitur  gunakan kain basahi dg
sampo, atau semprot dg deterjen, desinfektan, atau
larutan pemutih
7. Cuci semua perlengkapan tidur & pakaian
menggunakan deterjen dg air panas, setiap
terkontaminasi kencing atau kotoran tikus

2016
2016
2016
2016
Originally Posted by 01Aladdin
Silly Canadian... Over here in Australia (and a great deal of the rest of the
world) water isn't frozen solid everywhere. The bucket under the
peanutbutter mouse wheel is full of water (not ice) and so the hapless
mice will drown. Of course, in Canada this might be impossibly since the
only water there is frozen solid
http://board.jokeroo.com/funny-picture-memes/157921-perfect-mouse-
trap-2.html
2016
Pertanyaan ?????

2016
EBOLA
Zoonosis – KHD 302
Airlangga University
Zoo-Ebola_S1_Soelih_03.2021 1
EBOLA VIRUS
Definition
Ebola virus disease (formerly known as
Ebola hemorrhagic fever) is:
– A disease caused by the Ebola virus
– Is severe- fatality rate 90%
– Affects human and non human Primates
•Highest fatality Rate is found in the Zaire sub-
species.
•The only reported cases in the U.S., Italy and
England were all part of the Reston sub-species.
Family and Order
-Family: Filoviridae
-Order: Mononegavirales
-5 distinct sub-species
-Cote d’Ivorie(Ivory Coast) ebolavirus
-Reston ebolavirus
-Sudan ebolavirus
-Zaire ebloavirus
-Bundibugyo ebolavirus
- Characteristics of Filoviruses:
- Filamentous form with a uniform diameter

of approximately 80 nm but display great
variation in length.
- Nonsegmented negative-stranded RNA

genome containing 7 structural and
regulatory genes.
• Highest fatality Rate is found in the
Zaire sub-species.
• The only reported cases in the U.S.,
Italy & England were all part of the
Reston sub-species.
Category A Bio-agents:
Can be easily disseminated or
transmitted from person to person
− Result in high mortality rates and

have the potential for major public
health impact.
− Might cause public panic and social

disruption.
− Require special action for public

health preparedness (CDC)
category
• Ease of transmission
• Severity of morbidity and

mortality
• Likelihood of use (CDC)
History of Ebola virus
• Ebola first appeared in 1976 in two
simultaneous outbreaks.

Near the Ebola River in the
Democratic Republic of Congo
A remote area of Sudan.
Epidemiology
• 1975 cases
• 1069 deaths
• From Guinea, Liberia, Nigeria, and

Sierra Leone ( WHO 2014/8/14)
Countries with Widespread Transmission
(CDC 2.03.2015)
Total Cases
(Suspected, Laboratory-
Probable, & Confirmed
Country Confirmed) Cases Total Deaths
Guinea 3205 2808 2127
Liberia 9265 3153 4057
Sierra Leone 11443 8353 3530
Total 23913 14314 9714
Countries with an Initial Case or Cases
and/or Localized Transmission (CDC 2.03.2015)
Total Cases
Probable, & Confirmed
United 1 1 0
Kingdom
Total 1 1 0
Previously Affected Countries* (CDC 2.03.2015)
Total Cases
Probable, and Confirmed
Nigeria 20 19 8
Senegal 1 1 0
Spain 1 1 0
United States 4 4 1
Mali 8 7 6
Total 34 32 15
*There are currently no cases of Ebola virus disease (EVD) in Senegal, Nigeria,
Spain, the United States, and Mali. A country is considered to be free of Ebola virus
transmission when 42 days (double the 21-day incubation period of the Ebola virus)
has elapsed since the last patient in isolation became laboratory negative for EVD.
Source & Mode of Transmission
Source & Mode of Transmission
Signs & symptoms
• Fever & no response to treatment
for usual causes of fever in the area.
• Muscle pain
• Abdominal pain
• Rash
• Sore throat
• General body weakness
• Vomiting
• Bleeding
Management &Treatment
• NO CURE YET  a vaccine &
hyperimmune sera are still being
researched
• TOTAL ISOLATION/QUARANTINE
• INTENSIVE CARE TREATMENT
• SURVEILLANCE
PREVENTION
• AVOID AFFECTED AREAS/PEOPLE
• HANDWASHING
• PPE
Health specialists prepare for work in an isolation ward for patients at the Medecins Sans Frontieres
facility in southern Guinea
A Liberian street vendor wears protective gloves as a precaution to prevent infection with the
deadly Ebola virus while transacting business with customers in downtown Monrovia, Liberia
A Liberian nurse is being sprayed with
disinfectant after preparing several bodies of
victims of Ebola for burial on August 1, 2014.
Anak-anak di Liberia dg tertib antri cuci tangan dg
desinfektansia sebelum memasuki gereja u/ mengikuti do’a
agar Ebola dapat segera dibasmi di Providence Baptist Church
Zoo-Ebola_S1_Soelih_03.2021
Monrovia, Liberia, pd 3.08.2014 30
A nurse from Liberia sprays preventives to disinfect the waiting area for visitors at the ELWA
Hospital where a US doctor Kent Bradley is being quarantined in the hospitals isolation unit
having contracted the Ebola virus, Monrovia, Liberia
A nurse from Liberia disinfects the waiting area for visitors at the ELWA Hospital in
Monrovia, Liberia, July 28, 2014, where US doctor Kent Bradley was quarantined after
contracting the Ebola virus. Zoo-Ebola_S1_Soelih_03.2021 32
The Liberian daughter of a woman that died of Ebola is in tears as her mother is taken for
burial from the isolation unit in Foya, Lofa County, Liberia July 2, 2014.
Body of evidence: health workers transport a casket of a nun whose death resulted from an
Ebola infection in Zaire in 1995
Pekerja Kesehatan di Liberia sedang disemprot dg
larutan desifektansia setelah meanangani jenazah
pasien Ebola untuk dimakamkan 1.08.2014
Doctors in protective gear work inside the Medecins Sans Frontieres isolation ward as
Guinea faced the worst ever outbreak of the Ebola virus
Protective gear including boots, gloves, masks and suits, drying after being used in a
treatment room in the ELWA hospital in the Liberian capital Monrovia on July 24, 2014.
A boy walks through an empty class room on July 31, 2014 in Monrovia. Liberia announced
on July 30 it was shutting all schools and placing "non-essential" government workers on 30
days' leave in a bid to halt the spread of the deadly Ebola epidemic raging in West Africa.
39
Zoo-Ebola_S1_Soelih_03.2021
Liberian Deputy Health Minister Tolbert Nyensuah talks with protesters on the importance
of burying Ebola victims in Johnsonville outside Monrovia, Liberia August 2, 2014. The
military police were called in to control youths from the Johnsonville community who
staged a protest against the government's decision to bury Ebola victims in Johnsonville.
Liberian Christians hold holy communion in gloves to avoid contact with the deadly Ebola
virus during a service at the Providence Baptist Church in Monrovia, Liberia August 3, 2014.
Nigeria health officials wait to screen passengers at the arrival hall of Murtala Muhammed
International Airport in Lagos, Nigeria, Monday, Aug. 4, 2014. Nigerian authorities on
Monday confirmed a second case of Ebola in Africa's most populous country, an alarming
setback as officials across the region battle to stop the spread of a disease.
View of an isolation center for people infected with Ebola at Donka Hospital in Conakry.
Any questions ???
Ebola virus disease
Key facts
•Ebola virus disease (EVD), formerly known as Ebola haemorrhagic fever,

is a severe, often fatal illness in humans.
•EVD outbreaks have a case fatality rate of up to 90%.
•EVD outbreaks occur primarily in remote villages in Central and West

Africa, near tropical rainforests.
•The virus is transmitted to people from wild animals and spreads in the
human population through human-to-human transmission.
•Fruit bats of the Pteropodidae family are considered to be the natural

host of the Ebola virus.
•Severely ill patients require intensive supportive care. No licensed

specific treatment or vaccine is available for use in people or animals.
Ebola first appeared in 1976 in 2 simultaneous outbreaks, in
Nzara, Sudan, and in Yambuku, Democratic Republic of Congo.
The latter was in a village situated near the Ebola River, from
which the disease takes its name.
Genus Ebolavirus is 1 of 3 members of the Filoviridae family

(filovirus), along with genus Marburgvirus and genus Cuevavirus.
Genus Ebolavirus comprises 5 distinct species:
•Bundibugyo ebolavirus (BDBV)

•Zaire ebolavirus (EBOV)
•Reston ebolavirus (RESTV)
•Sudan ebolavirus (SUDV)
•Taï Forest ebolavirus (TAFV).
BDBV, EBOV, and SUDV have been associated with large EVD
outbreaks in Africa, whereas RESTV and TAFV have not. The
RESTV species, found in Philippines and the People’s Republic of
China, can infect humans, but no illness or death in humans from
this species has been reported to date.
Transmission
Ebola is introduced into the human population through close contact with
the blood, secretions, organs or other bodily fluids of infected animals. In
Africa, infection has been documented through the handling of infected
chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines
found ill or dead or in the rainforest.
Ebola then spreads in the community through human-to-human

transmission, with infection resulting from direct contact (through broken
skin or mucous membranes) with the blood, secretions, organs or other
bodily fluids of infected people, and indirect contact with environments
contaminated with such fluids. Burial ceremonies in which mourners have
direct contact with the body of the deceased person can also play a role in
the transmission of Ebola. Men who have recovered from the disease can
still transmit the virus through their semen for up to 7 weeks after recovery
from illness.
Health-care workers have frequently been infected while treating patients

with suspected or confirmed EVD. This has occurred through close contact
with patients when infection control precautions are not strictly practiced.
Signs & symptoms
EVD is a severe acute viral illness often characterized
by the sudden onset of fever, intense weakness,
muscle pain, headache and sore throat. This is
followed by vomiting, diarrhoea, rash, impaired kidney
and liver function, and in some cases, both internal and
external bleeding. Laboratory findings include low
white blood cell and platelet counts and elevated liver
enzymes.
People are infectious as long as their blood and

secretions contain the virus. Ebola virus was isolated
from semen 61 days after onset of illness in a man who
was infected in a laboratory.
The incubation period, that is, the time interval from

infection with the virus to onset of symptoms, is 2 to
21 days.
Diagnosis
Other diseases that should be ruled out before a diagnosis of EVD can
be made include: malaria, typhoid fever, shigellosis, cholera,
leptospirosis, plague, rickettsiosis, relapsing fever, meningitis, hepatitis
and other viral haemorrhagic fevers.
Ebola virus infections can be diagnosed definitively in a laboratory

through several types of tests:
•antibody-capture enzyme-linked immunosorbent assay (ELISA)

•antigen detection tests
•serum neutralization test
•reverse transcriptase polymerase chain reaction (RT-PCR) assay
•electron microscopy
•virus isolation by cell culture.
•Samples from patients are an extreme biohazard risk; testing should be
conducted under maximum biological containment conditions.
Vaccine and treatment
No licensed vaccine for EVD is available. Several vaccines are

being tested, but none are available for clinical use.
Severely ill patients require intensive supportive care. Patients are

frequently dehydrated and require oral rehydration with solutions
containing electrolytes or intravenous fluids.
No specific treatment is available. New drug therapies are being

evaluated.
Natural host of Ebola virus
In Africa, fruit bats, particularly species of the genera Hypsignathus

monstrosus, Epomops franqueti and Myonycteris torquata, are considered
possible natural hosts for Ebola virus. As a result, the geographic
distribution of Ebolaviruses may overlap with the range of the fruit bats.
Ebola virus in animals
Although non-human primates have been a source of infection for humans,

they are not thought to be the reservoir but rather an accidental host like
human beings. Since 1994, Ebola outbreaks from the EBOV and TAFV
species have been observed in chimpanzees and gorillas.
RESTV has caused severe EVD outbreaks in macaque monkeys (Macaca

fascicularis) farmed in Philippines and detected in monkeys imported into
the USA in 1989, 1990 and 1996, and in monkeys imported to Italy from
Philippines in 1992.
Since 2008, RESTV viruses have been detected during several outbreaks
of a deadly disease in pigs in People’s Republic of China and Philippines.
Asymptomatic infection in pigs has been reported and experimental
inoculations have shown that RESTV cannot cause disease in pigs.
Prevention and control
Controlling Reston ebolavirus in domestic animals

No animal vaccine against RESTV is available. Routine cleaning and
disinfection of pig or monkey farms (with sodium hypochlorite or other
detergents) should be effective in inactivating the virus.
If an outbreak is suspected, the premises should be quarantined

immediately. Culling of infected animals, with close supervision of burial
or incineration of carcasses, may be necessary to reduce the risk of
animal-to-human transmission. Restricting or banning the movement of
animals from infected farms to other areas can reduce the spread of the
disease.
As RESTV outbreaks in pigs and monkeys have preceded human

infections, the establishment of an active animal health surveillance
system to detect new cases is essential in providing early warning for
veterinary and human public health authorities.
Reducing the risk of Ebola infection in people
In the absence of effective treatment and a human vaccine, raising awareness

of the risk factors for Ebola infection and the protective measures individuals
can take is the only way to reduce human infection and death.
Pig farms in Africa can play a role in the amplification of infection because of
the presence of fruit bats on these farms. Appropriate biosecurity measures
should be in place to limit transmission. For RESTV, educational public health
messages should focus on reducing the risk of pig-to-human transmission as a
result of unsafe animal husbandry and slaughtering practices, and unsafe
consumption of fresh blood, raw milk or animal tissue. Gloves and other
appropriate protective clothing should be worn when handling sick animals or
their tissues and when slaughtering animals. In regions where RESTV has
been reported in pigs, all animal products (blood, meat and milk) should be
thoroughly cooked before eating.
Controlling infection in health-care settings
Human-to-human transmission of the Ebola virus is primarily associated with direct or

indirect contact with blood and body fluids. Transmission to health-care workers has
been reported when appropriate infection control measures have not been observed.
It is not always possible to identify patients with EBV early because initial symptoms
may be non-specific. For this reason, it is important that health-care workers apply
standard precautions consistently with all patients – regardless of their diagnosis – in
all work practices at all times. These include basic hand hygiene, respiratory hygiene,
the use of personal protective equipment (according to the risk of splashes or other
contact with infected materials), safe injection practices and safe burial practices.
Health-care workers caring for patients with suspected or confirmed Ebola virus
should apply, in addition to standard precautions, other infection control measures to
avoid any exposure to the patient’s blood and body fluids and direct unprotected
contact with the possibly contaminated environment. When in close contact (within 1
metre) of patients with EBV, health-care workers should wear face protection (a face
shield or a medical mask and goggles), a clean, non-sterile long-sleeved gown, and
gloves (sterile gloves for some procedures).
Laboratory workers are also at risk. Samples taken from suspected human and
animal Ebola cases for diagnosis should be handled by trained staff and processed
Zoo-Ebola_S1_Soelih_03.2021 57 in
suitably equipped laboratories.
The Ebola virus and it’s close relative the Marburg virus are members of the
Filoviridae family. These viruses are the causative agents of severe
hemorrhagic fever, a disease with a fatality rate of up to 90%. The Ebola virus
infects mainly the capillary endothelium and several types of immune cells. The
symptoms of Ebola infection include maculopapular rash, petechiae, purpura,
ecchymoses, dehydration and hematomas.
Since Ebola was first described in 1976, there have been several epidemics of
this disease. Hundreds of people have died because of Ebola infections, mainly
in Zaire, Sudan, Congo and Uganda. In addition, several fatalities have
occurred because of accidents in laboratories working with the virus. Currently,
a number of scientists claim that terrorists may use Ebola as a biological
weapon.
In the 3D model presented in this study, Ebola-encoded structures are shown in

maroon, and structures from human cells are shown in grey. The Ebola model is
based on X-ray analysis, NMR spectroscopy, and general virology data
published in the last two decades.
Nipah Virus Outbreak
• 1998-1999, Malaysia
– Respiratory and neurologic
syndrome in swine
– Encephalitis in humans
• More than 250 cases
• More than 100 deaths
– Initially mistaken for
Japanese encephalitis
– Discovered new Paramyxovirus
Nipah Virus
• Virus isolated in March 1999
• Quick national response with international
assistance
• 1.1 million pigs culled (out of 2.4 million
total)
• No new cases in Malaysia since 1999
Reservoir
• Flying foxes (fruit bats)
– Carry the virus
– Are not affected
– Virus found in
• Urine
• Partially eaten fruit
– Migratory
Photo courtesy of James Roth, Iowa State University
Nipah Field Investigations- Malaysia
Nipah Virus in Bangladesh
• Outbreaks of respiratory disease, high
fever, unconsciousness, vomiting,
headache
• 2002 to present
• Confirmed to be Nipah virus infection by
CDC
• Believed to be oral transmission from
contaminated fruit
Hendra virus
Emerged in Australia, 1994-1995
Killed 15 horses and 2 people
Horses
Peracute respiratory disease
Humans
Influenza-like disease
Severe respiratory distress
Meningoencephalitis
Picasso: Cat Catching a bird. http://www.people.hofstra.edu
Rabies Virus
• member of the Lyassavirus of the Rhabdoviridae.

• ssRNA enveloped virus, characteristic bullet-shaped appearance
with 6-7 nm spike projections.
• virion 130-240nm * 80nm
• -ve stranded RNA codes for 5 proteins; G, M, N, L, S
• Exceedingly wide range of hosts.
• There are 5 other members of Lyassavirus : Mokola, Lagosbat,
Duvenhage, EBL-1, and EBL-2.
• Duvenhage and EBL-2 have been associated with human rabies.
Rabies Virus
Structure of rabies virus (Source: CDC)
Rabies virus particles

Epidemiology
Rabies is a zoonosis which is prevalent in wildlife. The main

animals involved differs from continent to continent.
Europe fox, bats
Middle East wolf, dog
Asia dog
Africa dog, mongoose, antelope
N America foxes, skunks, raccoons,
insectivorous bats
S America dog, vampire bats
Pathogenesis
• The commonest mode of transmission in man is by the bite of a

rabid animal, usually a dog. Rabies is an acute infection of the CNS
which is almost invariably fatal.
• Following inoculation, the virus replicates in the striated or
connective tissue at the site of inoculation and enters the peripheral
nerves through the neuromuscular junction.
• It then spreads to the CNS in the endoneurium of the Schwann cells.
• Terminally, there is widespread CNS involvement but few neurons
infected with the virus show structural abnormalities. The nature of
the profound disorder is still not understood.
Laboratory Diagnosis
• Histopathology - Negri bodies are pathognomonic of rabies. However,
Negri bodies are only present in 71% of cases.
• Rapid virus antigen detection - in recent years, virus antigen detection
by IF had become widely used. Corneal impressions or neck skin
biopsy are taken. The Direct Fluorescent Antibody test (DFA) is
commonly used.
• Virus cultivation - The most definitive means of diagnosis is by virus
cultivation from saliva and infected tissue. Cell cultures may be used
or more commonly, the specimen is inoculated intracerebrally into
infant mice. Because of the difficulties involved, this is rarely offered
by diagnostic laboratories.
• Serology - circulating antibodies appear slowly in the course of
infection but they are usually present by the time of onset of clinical
symptoms.
Diagnosis of Rabies
Negri Body in neuron cell Positive DFA test (Source: CDC)

(source: CDC)
Management and Prevention
• Pre-exposure prophylaxis - Inactivated rabies vaccine may be

administered to persons at increased risk of being exposed to rabies e.g.
vets, animal handlers, laboratory workers etc.
• Post-exposure prophylaxis - In cases of animal bites, dogs and cats in a
rabies endemic area should be held for 10 days for observation. If signs
develop, they should be killed and their tissue.
• Wild animals are not observed but if captured, the animal should be
killed and examined. The essential components of postexposure
prophylaxis are the local treatment of wounds and active and passive
immunization.
• Once rabies is established, there is nothing much that could be done
except intensive supportive care. To date, only 2 persons with proven
rabies have survived.
Postexposure Prophylaxis
• Wound treatment - surgical debridement should be carried out.

Experimentally, the incidence of rabies in animals can be reduced by
local treatment alone.
• Passive immunization - human rabies immunoglobulin around the area
of the wound; to be supplemented with an i.m. dose to confer short
term protection.
• Active immunization - the human diploid cell vaccine is the best
preparation available. The vaccine is usually administered into the
deltoid region, and 5 doses are usually given.
• There is convincing evidence that combined treatment with rabies
immunoglobulin and active immunization is much more effective than
active immunization alone. Equine rabies immunoglobulin (ERIG) is
available in many countries and is considerably cheaper than HRIG.
Rabies Vaccines
The vaccines which are available for humans are present are inactivated whole
virus vaccines.
– Nervous Tissue Preparation e.g. Semple Vaccine - associated with the rare
complication of demyelinating allergic encephalitis.
– Duck Embryo Vaccine - this vaccine strain is grown in embryonated duck
eggs This vaccine has a lower risk of allergic encephalitis but is considerably
less immunogenic.
– Human Diploid Cell Vaccine (HDCV) - this is currently the best vaccine
available with an efficacy rate of nearly 100% and rarely any severe reactions.
However it is very expensive.
– Other Cell culture Vaccines - because of the expense of HDCV, other cell
culture vaccines are being developed for developing countries. However
recent data suggests that a much reduced dose of HDCV given intradermally
may be just be effective.
Control of Rabies
• Urban - canine rabies accounts for more than 99% of all human
rabies. Control measures against canine rabies include;
– stray dog control.
– Vaccination of dogs
– quarantine of imported animals
• Wildlife - this is much more difficult to control than canine
rabies. However, there are on-going trials in Europe where bait
containing rabies vaccine is given to foxes. Success had been
reported in Switzerland.
West Nile Virus Disease
MK ZOONOSIS – KHD 302

DEP. KESEHATAN MASYARAKAT VETERINER
FAKULTAS KEDOKTERAN HEWAN
UNIVERSITAR AIRLANGGA
4/14/2022 Zoo- WNV disease_Soelih_Genap 1

2016
West Nile Virus (WNV)
synonim 
 West Nile fever (WNF)

 West Nile encephalitis (WNE).

2016
West Nile Virus (WNV)
WNV  termasuk Fam. Flaviviridae, ditularkan oleh

nyamuk & caplak, & umumnya ditemukan di Afrika,
Asia Barat, & Timur Tengah
Vektor  Nyamuk Culex pipiens
 Sangat erat berhubungan dg virus penyebab St.

Louis encephalitis yg ditemukan di USA
Dpt menginfeksi manusia, burung, nyamuk, kuda

& beberapa mammalia lainnya

2016
 Inf WNV dapat
menimbulkan penyakit
yg serious
 WNV  wabah
musiman di Amerika
Utara yg terjadi mulai
musim panas & berlanjut
pd musim gugur

2016
Epidemiology WNV

2016
2016
Kejadian WNV
 >> Resiko infeksi WNV
tertinggi terjadi saat jumlah
vektor nyamuk tinggi & tidak
akan turun hingga aktifitas
nyamuk hilang ketika timbuylnya
suhu beku
 Di daerah dg 4 musim 
kasus inf. WNV terjadi
utamanya pd AKHIR MUSIM
PANAS ATAU AWAL MUSIM
GUGUR.
 Di belahan bumi selatan dg

iklim tropis  infeksi WNV
dapat terjadi sepanjang tahun
2016
Sumber & Cara Penularan WNV
Cara penularan yg utama 
melalui gigitan nyamuk yg
terinfeksi WNV
 Nyamuk terinfeksi apabila
menghisap darah burung yg
terinfeksi WNV  virus
bersirkulasi dalam darah
nyamuk hingga beberapa
hari
 WNV selanjutnya menuju
ke kelj. Saliva dari nyamuk
 Pada saat menghisap

darah  WNV akan
diinjeksikan pd manusia &
hewan, kmd berkembang
biak & dpt menimbulkan
penyakit
2016

2016

2016
Dalam jumlah kasus yg sangat sedikit, WNV

juga dpt ditularkan melalui 
 transfusi darah
 transplantasi organ
 menyusui
 kehamilan dari ibu kpd bayinya

2016
Bagaimana nyamuk dapat terinfeksi WNV? 

Nyamuk yg makan/menghisap darah burung yg terinfeksi WNV.
Burung yg terinfeksi dapat menjadai sakit maupun tidak.
Burung merupakan vektor, atau intermediate carriers WNVyg
penting u/ siklus hidup WNV & siklus penularan selanjutnya
2016
Resiko infeksi WNV pd saat kehamilan

Berdasarkan publikasi yg terbatas jumlahnya
hingga kini, belum dapat dideterminasi seberapa
besar persentase kejadian penularan WNV dari
ibu ke bayinya, maupun masalah pd kelahiran
bayi.
Karena ada kemungkinan terjadi penularan inf.
WNV pd ibu yg sedang hamil yg berdampak pd
kondisi kesehatan ibu, mk dianjurkan ibu kpd
hamil u/ menghindari gigitan nyamuk  gunakan
pakaian yg sesuai, oleskan mosquito repellents
containing DEET , karena DEET aman u/ ibu
hamil

2016
Penting u/ diingat bahwa WNV tidak
kontagius  tidak dapat ditularkan anatar
manusia
Seseorang tidak dapat tertular WNV

karena misalnya bersentuhan atau
berciuman dg penderita, atau dari
seorang perwat yg sedang merawat
penderita infeksi WNV
Manusia disebut sbg "dead-end" host u/

WNV  host yg dapat terinfeksi, yg
sistem imunnya dapat mencegah virus
bereplikasi shg jumlahnya tidak cukup u/
ditularkan kembali ke nyamuk & kmd kpd
host lainnya
2016
 Belum pernah dilaporkan, bahwa orang dapat

tertular setelah menangani unggas yg terinfeksi,
baik yg hidup maupun yg mati  akan tetapi,
sangat dianjurkan u/ menghindari kontak
langsung dg kulit ketika menangani
hewan/burung mati. Gunakan gloves atau double
plastic bags pd saat memindahkan & membuang
karkas unggas
 Belum pernah dilaporkan bahwa virus WNV dpt
ditularkan kpd manusia karena mengkonsumsi
unggas / hewan yg terinfeksi 
akan tetapi karena alasan praktik dlm bidang
kesehatan masyarakat & resiko tertular food-
borne pathogens  orang sebaiknya selalu
mengikuti prosedur dlm memasak daging secara
sempurna, baik daging unggas maupun mamalia
2016
Manusia yg beresiko tinggi tertular WNV
 Orang yg berada di daerah tertular / kasus aktif

WNV
 Orang berusia 50 tahun atau lebih beresiko

menderita infeksi WNV yg parah
 The American Academy of Pediatrics

menyatakan  anak-anak mempunyai resiko
rendah tertular infeksi WNV  walaupun pernah
dilaporkan usia termuda (5 th) menderita infeksi
WNV parah di New York

2016
Gejala Klinis WNV pd Manusia
1. Asymptomatis
2. Infeksi WNV Ringan
3. Infeksi WNV Parah

 Kebanyakan dr orang yg terinfeksi WNV  80%
(4 dari 5 orang) menunjukkan gejala yg paling
ringan atau asymptomatis
 Diperkirakan  20% org yg terinfeksi demam

WNV dg GK ringan, seperti demam, sakit kepala, &
nyeri sekujur tubuh, kadang disertai kemerahan
kulit didaerah badan & kebengkakan Lgl.

2016
 Masa inkubasi infeksi WNV pd manusia 

biasanya 2 – 15 hari
 GK/ umumnya berlangsung selama beberapa

hari, namun kadang pd beberapa orang bisa
sampai beberapa minggu
 GK WNV parah dg encephalitis atau

meningitis, dpt berlangsung hingga beberapa
minggu, namun kelainan neurologisnya tetap /
permanen

2016
1. Asymptomatis
 Tanpa GK pd kebanyakan penderita
 Kira-kira 80 % dr penderita demam

WNV tidak menunjukkan GK, & sulit
diketahui apakah nantinya akan timbul
GK atau tidak

2016
2. Infeksi WNV Ringan
GK ringan dpt ditemui pd beberpa penderita
 > 20 %
1. Demam
2. Sakit kepala
3. Nyeri di sekulur tubuh
4. Mual
5. Muntah
6. Kadang terdpt kebengkakan Lgl.,
kemerahan kulit di dada, perut &
punggung
GK dpt berlangsung terpendek selama

beberapa hari & trpanjang hingga
beberapa minggu
2016
3. Infeksi WNV Parah

 bisa terjadi pd beberapa pendserita  kir-kira 1 dr
150 penderita infeksi WNV menunjukkan GK parah
1. Demam tinggi 7. Tremor
2. Sakit kepala 8. Tidak sadar
3. Tengkuk kaku 9. Kelemahan otot
4. mengorok 10. Hilangnya penglihatan
5. Disorientasi 11. Mati rasa
6. Koma 12. Kelumpuhan
GK dpt berlangsung hingga beberapa minggu,

namun kelainan neurologis tetap permanent.

2016
Terjadinya GK parah & kematian pd orang yg
terinfeksi WNV
 setelah tergigit nyamuk

yg terinfeksi WNV, virus
bermultiplikasi pd sistem
vaskuler & kmd
menembus barier sirkulasi
darah di otak hingga
mencapai otak
 WNV akan menyebabkan

gangguan funsi CNS &
menyebabkan
keradanangan jaringan
otak
2016
Diagnosis WNV
Sample u/ konfirmasi diagnosis adanya infeksi

WNV  darah & cairan serebrospinal
D/  deteksi specific IgM antibody pd serum,

selain itu jg perlu pengujian serum pd fase
penyembuhan karena seringkali antibody belum
terbentuk pd saat GK timbul  IgM antibody-
capture enzyme-linked immunosorbent assay
(MAC-ELISA)

2016
Pengobatan WNV
 Belum ada T/ spesifik u/ infeksi WNV
 Infeksi WNV Ringan tidak membutuhkan pengobatan

khusus, hanya obat u/ mengurangi demam & sakit
 T/ supportive yg intensif  perlu u/ komplikasi adanya

infeksi di CNS (meningitis-encephalitis)
 Anti-inflammasi, infuse i.v., & intensive medical

monitoring perlu diberikan u/ kondisi yg parah
 Tidak ada antibiotika spesifik atau viral antidote yg cocok

u/ infeksi WNV
 Belum ditemukan vaksin u/ pencegahan WNV  masih

dalam penelitian ini, mungkin baru dlm beberapa tahun
kedepan
2016
Virus lain yg mirip dg WNV
WNV sangat dekat dg  the Japanese encephalitis virus &
the St. Louis encephalitis virus  di Tenggara & Barat bagian
Tengah dari AS
Juga mosquito-borne viral diseases & siklus hidup juga mirip

 siklus hidup burung - nyamuk, & yg kadang menyerang
manusia
Perbedaan utama 
The St. Louis encephalitis 
 "silent" pd burung  asymptomatis
 umumnya tidak menyebabkan kematian pd populasi burung
Shg tidak ada tanda2 bagi manusia sebelum terjadi kasis pd
manusia
WNV  strain Amerika pd burung utamanya burung gagak 

sakit & mati, & oki dpt menjadi early warning system bagi
manusia !!!
2016
Pencegahan WNV
Termudah & terbaik  menghindari gigitan nyamuk
1. Diluar rumah  mosquito repellents berisi  DEET, picaridin,
IR3535, minyak kayu putih, paramenthane-diol  Sesuai
anjuran yg tertera pd kemasan
2. INGAT Umumnya nyamuk aktif pd saat senja hingga fajar 
gunakan insect repellent & kenakan baju-celana panjang,
atau masuk kedalam rumah
3. Pasanglah Kasa anti nyamuk pd jendela & pintu
4. Basmi semua tempat nyamuk berkembang biak  jangan
biarkan air tergenang  pot tanaman, ember, tong & kaleng
bekas 
 Ganti air minum hewan piaraan & ganti tempat berendam
burung piaraan sekurang-kurangnya seminggu sekali
 Jangan biarkan ban bekas menjadi tempat penampungan
air hujan
 Kolam mainan anak-anak yg tidak digunakan
dikosongkan
2016
Batasi tempat habitat nyamuk &
tempat berkembang biaknya , u/
mengurangi penularan pd manusia 
 air tergenang  kaleng bekas,
plastic containers, ban bekas, atau
berbagai tempat dimana air
menggenang
 Minimal 1 -2 x seminggu
kosongkan/ganti air pd pot penyiram
tanaman , makan-minuman hewan
piaraan, birdbaths, penutup kolam
renang, ember, tong & kaleng
 Buang air dari penutup kolam

renang
 Check for clogged rain gutters &

clean them out.

2016
Mengurangi Resiko Terinfeksi WNV
 Insect repellent gosokkan di kulit  Yg efektif

20%-30% DEET (N,N-diethyl-meta-toluamide).
 Semprotkan obat nyamuk pd pakaian & tempat
persembunyian nyamuk  Permethrin atau preparat
anti nyamuk EPA lainnya  tidak utk digosokkan pd
kulit. Nyamuk kadang jg bisa menembus kain baju yg
tipis atau rajutan besar
 Berpakaian sesuai dg musim  pakai baju berlengan
& celana panjang terutama bila ada diluar ruangan
 Selambu pelindung u/ bayi  keranjang bayi waktu
dibawa keluar rumah & tempat tidur bayi
 Tetap didalam rumah pd saat  pagi buta, sebelum
fajar & senja hari yg merupakan waktu nyamuk sangat
aktif.
 Kasa nyamuk pd pintu & jendela
2016
Beberapa hal yg dapat dilakukan u/ mengurangi
resiko tertular WNV
1. Monitoring populasi burung 
surveillance unggas sakit &
mati di alam
2. Hindari genangan air, terutama
bila mengandung nutrisi tinggi
u/ Culex sp.
3. Pengendalian populasi nyamuk
 penyemprotan & pemberian
larvasida
Walaupun bila sudah dilakukan

pengawasan ketat ,
penyemprotan & pemberian
larvasida, WN Virus mungkin
masih tetap dpt menginfeksi
orang
2016
“Larvasid” & “Adulticides”
Larviasid
 Membunuh nyamuk yg belum dewasa / larva
 Produk Biologik & kimia  al. regulator
pertumbuhan serangga, film permukaan , atau
organofosfat .
 Diaplikasikan langsung di sumber air tempat

telur & larva nyamuk
 Bila penggunann benar larvisid dapat

membantu penurunan populasi nyamuk dg
menekan jumlah nyamuk baru

2016
“Larvicides” & “Adulticides”
Adulticides
 membunuh nyamuk dewasa.
 Cara penggunaan  handheld sprayers,

truck-mounted sprayers, or using airplanes.
 Bila dilakukan dg benar  berdampak

cepat dalam menekan jumlah nyamuk
dewasa di area tsb.  jumlah nyamuk yg
aktif menggigit yg mungkin pembawa WNV
menurun

2016
Contoh aplikasi “Larvasid” & “Adulticides”

2016
Therapy WNV
Tidak ada T/ spesifik u/ infeksi WNV
Pd WNV ringan menurut pengalaman, orang yg

menunjukkan tanda2 seperti panas tubuh
meningkat & nyeri tubuh, penyakit dpt
berlangsung selama mingguan – bulanan
Pd WNV parah  perlu penanganan lebih serius

di RS  supportive treatment  infuse, bantuan
respirasi & perawatan

2016
Apa yg harus dilakukan bila terinfeksi WNV?
WNV ringan  sembuh sedniri, tidak butuh
perwatan dokter -RS
Bila menjadi parah  misal sakit kepala hebat &

tidak sadar, segera bawa ke RS
Yg parah biasanya membutuhkan perawatan RS
Wanita hamil & menyusui  segera ke dokter

apanila terdeteksi ada GK/ terinfeksi WNV

2016
Imunitas terhadap WNV bisa seumur hidup, namun ada
kemungkinan menurun dlm beberap tahunkemudian

2016
FAKTA TENTANG WNV
Pd 2012 kejadian WNV di USA terus meningkat  yg terbaik adalah
mencegah digigit nyamuk. Mencegah terkena gigitan nyamuk
mengurangi risiko terkena infeksi WNV & penyakit lain yg mungkin
dibawa oleh vektor nyamuk
2016
Sumber bacaan
http://www.medicinenet.com/west_nile_virus_pict
ures_slideshow/article.htm
www.who.int
www.oie.int
dsb.

2016
Pertanyaan ?????

2016
Coronavirus Diseases
Zoonosis Lecture – KHD 302
Department of Veterinary Public Health

Veterinary Medicine Faculty
Airlangga University
MERSCoV-Zoonosis_S1_Soelih 1
Severe Acute Respiratory Syndrome
(SARS – CoV)
Middle East Respiratory Syndrome

Coronavirus
(MERS ‐ CoV)
COVID – 19
(SARS-CoV2)
What is Coronavirus
• Coronaviruses are a large family of viruses, some cause
illness in humans, & others cause illness in animals,
such as bats, camels, and civets.
• Human coronaviruses cause mild illness, such as the
common cold
• Severe acute respiratory syndrome (SARS) is a viral
respiratory illness caused by a coronavirus, called
SARS-associated coronavirus (SARS-CoV)
• Previous Coronaviruses have included SARS- CoV and
MERS-CoV. Since the end of 20199 there is a new
Coronavirus identified in Human in Wuhan China which
called as SARS-CoV-2 (previously 2019-nCoV), that has
not been previously identified in humans.
COVID-19_TSE_2021 4
Human Coronavirus Origins
• The most likely ecological
reservoirs for
coronaviruses are bats, but
it is believed that the virus
jumped the species barrier
to humans from another
intermediate animal host.
• This intermediate animal
host could be a domestic
food animal, a wild animal,
or a domesticated wild
animal which has not yet
been identified.
COVID-19_TSE_2021 5
Coronaviruses
• Coronaviruses belong to the
Coronaviridae family in the
Nidovirales order
• Corona represents crown-like
spikes on the outer surface of
the virus; thus, it was named
as a coronavirus
• Coronaviruses are enveloped
viruses, minute in size (65–
125 nm in diameter) and
contain a single-stranded RNA
as a nucleic material, size
ranging from 26 to 32kbs in
length
COVID-19_TSE_2021 6
• Coronaviruses (CoV) are a large family of
viruses that cause illness ranging from the
common cold to more severe diseases such as
Middle East Respiratory Syndrome (MERS-CoV)
& Severe Acute Respiratory Syndrome (SARS-
CoV)
• A novel coronavirus (nCoV) is a new strain that
has not been previously identified in humans.
• Coronaviruses are zoonotic
• Common signs of infection include:
– Respiratory symptoms
– Fever
– Cough
– Shortness of breath & breathing difficulties
– In more severe cases, infection can cause
pneumonia, severe acute respiratory syndrome, renal
failure & even death.
Coronaviruses (CoVs)
 RNA virus with envelope + strands
Human Corona Virus (HCoVs) was first isolated in

1960
7 CoVs (HCoVs) were identified 

1. HCoV-229E
2. HCoV-OC43
3. HCoV-NL63
4. HCoV-HKU1
5. SARS-CoV
6. Middle East Respiratory Syndrome Coronavirus
(MERS-CoV)
7. SARS-CoV2 ( previously 2019-nCoV)
Coronavirus Classification
1. Alpha
a. Human  HCoV-229E, HCoV-NL63
b. Animal  Pig-, Dog- & Cat-CoVs
2. Beta
a. Human HCoV-OC43, HCoV-HKU1,
b. Animal  MHV-, rat-, pig- & cow -CoVs
c. SARS-CoV (HCoV-SARS)
d. MERS-CoV
e. SARS-CoV2
3. Gamma
Chicken- & turkey- CoVs
4. Delta
Bird-CoVs
HCoVs : 229E, NL-63, OC-43, HKU1
Epidemiology
 Worldwide
 Seasonality: Winter and spring in temperate

climates
 Exposure common in early childhood
 Transmission likely to be droplet, contact, and

indirect contact
 Symptoms and viral loads high first few days of

illness
 Incubation period 2-5 days

HCoVs : 229E, NL-63, OC-43, HKU1
Clinical Spectrum of Illnes

1. Most often associated with upper respiratory
tract infections in children
2. Pneumonia & lower respiratory tract infections

in immunocompromised individuals & the
elderly
3. May play a role in exacerbations of underlying

respiratory diseases
Coronavirus infections
Coronaviruses are a large family of

viruses that cause a range of illnesses in
humans, from the common cold to the
Severe Acute Respiratory Syndrome
(SARS), MERS-CoV, & the SARS-CoV2.
Viruses in this family also cause a number
of animal diseases.
SARS
Epidemiology
 First recognized Nov., 2002 as sporadic
cases in Guangdong province, China
 Outbreak period 2002-2003
 Hong Kong hotel contributed to spread of

virus to several countries
 8,098 probable SARS cases  774 deaths
SARS
 Incubation period is 2-10d* (median 4d)
 Route of Transmission 
 through droplets  Aerosol spread?
 Fomites?
 Fecal- respiratory transmission
 Transmission most likely during 2nd week of

illness
SARS
 First emerge Nov. 2002 sporadically in Prov.

Guandong - China
 Outbreak in 2002-2003  in a Hotel in HK 

play a role on the transmission of SARS virus to
several countries
 774 death out of 8.098 probable SARS cases
 Incubation period  2 – 10 d (ca. 4 d)
 Super spreading events in the world
Clinical Spectrum of Illness SARS
1. Fever, myalgia, headache, chills 1-2d, followed by a

nonproductive cough and shortness of breath 5-7d
after onset
2. Most identified illnesses recognized in adults
3. ~25 % diarrhea
4. 20-30% management in ICUs
5. Acute Respiratory Distress Syndrome (ARDS),

mechanical ventilation
6. 10-15 % mortality rate, higher in adults >60y
Middle East respiratory syndrome coronavirus
(MERS-CoV)
MERS-CoV 
is a strain of coronavirus that causes MERS
was first identified in 2012 in Saudi Arabia.
The understanding of the virus and the disease it
causes is continuing to evolve.
Since April 2012, 206 laboratory confirmed
cases of human infection with Middle East
respiratory
syndrome coronavirus (MERS‐CoV) have been
reported to WHO, including 86 deaths
Clinical Spectrum of Illness: HCoVs: 229E, NL-
63, OC-43, HKU1
•Most often associated with upper respiratory
tract infections in children
•Pneumonia and lower tract infections in
immunocompromised individuals and the
elderly
•May play a role in exacerbations of
underlying respiratory diseases
MERS-CoV Case
First Reported
• 60 year old Saudi man
• Presented on June 13th with 7d h/o fever &
cough; recent shortness of breath
• Increasing blood urea nitrogen (BUN) &
creatinine, starting day 3 of admission
• White cell count normal on admission (but 92.5%
neutrophils) &increased to a peak of 23,800 cells
per cubic millimeter on day 10 with neutrophilia,
lymphopenia, & progressive thrombocytopenia
(Zaki et al. N Engl J Med 2012 367:1814-20 )
MERS‐CoV Human Cases  Sejak April 2012 , 86 kematian
dari 206 kasus + telah dilaporkan kepada WHO
Laboratory confirmed cases of MERS‐CoV infection by approximate time of

onset, March 2012 through March 2014.
First MERS-CoV Human case
• Severity  acute respiratory distress
syndrome (ARDS) & multiorgan disfunction
syndrome
• Death on 24 Juni 2012
• No comorbidity & no severe illness in other
close contact persons
124 healthcare
workers remained
healthy as of Jan.,
2013
Source:
Memish ZA et al.
NEJM epub May
29, 2013
Middle East Respiratory Syndrome Coronavirus (MERS-CoV)
(de Groot et al. J Virol. May, 2013; Epub ahead of print )
The Emerging of a new Corona virus 
MERS-CoV
Symptomes in Animals
Flu like syndrome in Camels
MERS-CoV cases (n=55)
with the history travelling from Uni Emirate Arab
Geographic distribution of laboratory‐confirmed cases
by country of presumed exposure since 20 January 2014
COUNTRY CASES DEATH

Jordan 1 1
Kuwait 1 1
Oman 2 1
Egypt 22 7
Uni Arab Emirate 2 0
TOTAL 28 10
CFR in Human is almost 50 %
Middle East Respiratory Syndrome Coronavirus (MERS-CoV)
(de Groot et al. J Virol. May, 2013; Epub ahead of print )
Recent MERS‐CoV animal studies
Egypt,  RT‐PCR detected MERS‐CoV in 3.6% (4 of 110)
apparently healthy dromedary camels in a slaughterhouse.
Genetic sequence of the viruses demonstrated small
differences from a reference strain previously taken from a
human case.
Serological study  Sera of 52 camels and from 179

slaughterhouse workers  MERS‐CoV reactive antibodies
were detected in 92% of camels but none of the workers.
The camels that tested positive were all imported from either
Sudan or Ethiopia.
Reference: Chu DKW, et al. MERS Coronaviruses in Dromedary Camels, Egypt.

Emerg Infect Dis, 2014 Jun, Vol 20, 6. Available at:
http://dx.doi.org/10.3201/eid2006.140299.
A recent publication in Emerging Infectious Diseases
reported the results of an investigation of a human case of
MERS‐CoV infection with exposure to an infected camel in
Saudi Arabia.
The humanderived virus and a partly sequenced virus from
the camels shared single nucleotide change that occurred in
no other known MERS‐CoV sequences.
The close relationship between the human and
camel‐derived viruses is consistent with a transmission
event occurring between the two.
Reference: Memish ZA, et al. Human Infection with MERS Coronavirus

after Exposure to Infected Camels, Saudi Arabia, 2013. Emerg Infect Dis,
2014 Jun (Early online release). Available at
http://dx.doi.org/10.3201/eid2006.140402.
COVID - 19
COVID-19_TSE_2021 36
COVID-19
• The virus that causes COVID-19 is known as SARS-
CoV-2
It appears to have first emerged in Wuhan, China, in
late 2019.
• The outbreak has since spread across China to other
countries around the world. By the end of January,
the new coronavirus had been declared a public
health emergency of international concern by the
WHO.
• The most commonly reported symptoms include a
fever, dry cough and tiredness, and in mild cases
people may get just a runny nose or a sore throat.
• In the most severe cases, people with the virus can
develop difficulty breathing, and may ultimately
experience organ failure. Some cases are fatal.
“COVID – 19” the name
Causative agent  SARS-CoV2  ICTV on

11.02.2020
WHO  Tuesday, 11.02.2020  officially

announced as “Covid-19" for the new CoV that 1st
identified in Wuhan-China on 31.12. 2019.
 Tedros Adhanom Ghebreyesus (WHO _
Dir.General) in Jenewa, Swiss.
Viruses are named based on their genetic structure to
facilitate the development of diagnostic tests, vaccines
&medicines. Virologists & the wider scientific community
do this work, so viruses are named by the International
Committee on Taxonomy of Viruses (ICTV).
ICTV announced “severe acute respiratory syndrome

coronavirus 2 (SARS-CoV-2)” as the name of the new virus
on 11 February 2020. This name was chosen because the
virus is genetically related to the coronavirus responsible
for the SARS outbreak of 2003. While related, the two
viruses are different.
Diseases are named to enable discussion on disease

prevention, spread, transmissibility, severity and treatment.
Human disease preparedness and response is WHO’s role, so
diseases are officially named by WHO in the International
Classification of Diseases (ICD)
The World Health Organization (WHO) on 11.03.2020
has declared the novel coronavirus (COVID-19)
outbreak a global pandemic
At a news briefing , WHO Director-General, Dr.
Tedros Adhanom Ghebreyesus, noted that over the
past 2 weeks, the number of cases outside China
increased 13-fold and the number of countries with
cases increased threefold. Further increases are
expected. He said that the WHO is "deeply
concerned both by the alarming levels of spread
and severity and by the alarming levels of inaction,"
and he called on countries to take action now to
contain the virus. "We should double down," he
said. "We should be more aggressive.”
COVID-19 Time Line up to April 2020
Covid-19 Update on 16 March 2021 in
Indonesia
Total as of 16.03.2021 23.02.2021

+ Recovery Death + Recovery Death
1.430.458 1.257.663 38.573 63 56 2
Covid-19 Update on 17 March 2021 in Gavi
Countries
GAVI, officially Gavi, the Vaccine Alliance (previously the GAVI
Alliance, and before that the Global Alliance for Vaccines and
Immunization) is a public–private global health partnership with the
goal of increasing access to immunisation in poor countries
Total as of 17.03.2021
+ confirmed Death
cases
17,393,814 285,453
42,489 497
new cases new deaths
*71 of 73 Gavi countries with confirmed cases
Update Covid 19 Situation in Indonesia & East Java
Province as of Wednesday, 17.03.2021
No. Confirmed East Java Indonesia

1. Cases 135464 +321 1437283 +6825
2. Recover 123726 +341 1266673 +9010
3. Death 9549 +26 38915 +162
http://infocovid19.jatimprov.go.id/
Update Covid 19 Situation in Surabaya
as of Wednesday, 17.03.2021
Total as of 22.02.2021 17.03.2021

+ Recover Death + Recover Death
21154 19593 1320 22,192 20,656 1338
0.19% 0.2% 0.075%
increase increase increase
* 198 Confirmation in Hospitalization
No change from last day
Numbers at a glance (WHO)
Countries/
No. Date & Time Confirmed Confirmed Areas/
Cases Death Territories
1. 22.02.2021 111 102 016 2 462 911 223
08.15 pm
GMT+7
2. 23.02.2021 111 419 939 2 470 772 223
08:48 pm
GMT+7
3. 17.03.2021 121,291,579 2,682,559 219
07:13 pm  Recovered
GMT+7 97,823,863
COVID-19 CORONAVIRUS PANDEMIC

Last updated: March 17, 2021, 07:13 GMT
COVID-19 Vaccines
• As of 18 February 2021 at least 7 different vaccines
across three platforms have been rolled out in countries.
Vulnerable populations in all countries are the highest
priority for vaccination.
• At the same time  > 200 additional vaccine candidates

are in development, of which more than 60 are in clinical
development.
• COVAX is part of the ACT Accelerator, which WHO
launched with partners in 2020.
aims to end the acute phase of the COVID-19 pandemic by

 speeding up the development of safe & effective
vaccines against COVID-19;
 supporting the building of manufacturing capabilities;
 working with governments & manufacturers to ensure
fair & equitable allocation of the vaccines for all countries
– the only global initiative to do so.
Safe and effective vaccines will be a
gamechanger: but for the foreseeable future we
must continue wearing masks, physically
distancing and avoiding crowds. Being
vaccinated does not mean that we can throw
caution to the wind and put ourselves and others
at risk, particularly because it is still not clear
the degree to which the vaccines can protect not
only against disease but also against infection
and transmission.
Bibliography
• WHO Summary and literature update – as of 27 March 201 Gerber, SI.
2013.
•Emergence of a novel Coronavirus in the Arabian Peninsula, Middle

East Respiratory Syndrome Coronavirus (MERS-CoV). Presented on the
Workshop “Middle East Respiratory Syndrome Coronavirus (MERS-
CoV): Information and Guidance for Clinicians”. Clinician Outreach and
Communication Activity (COCA) Conference Call June 13, 2013
• de Groot de Groot et al. J Virol. May, 2013; Epub ahead of print
• Memish ZA et al. NEJM epub May 29, 2013
• www.cdc.org/eid
• www.who.int
• www.oie.int
• www.fao.org
Any questions ???
SARS
COVID - 19
ANTHRAX
KHI 323-MK ZOONOSIS

Departemen of Veterinary Public Health
VETERINARY MEDICINE FACULTY
of AIRLANGGA UNIVERSITY
4/5/2010 Anthrax_Zoo_Soelih_2010 genap 1

SC
SYNONIMS
Malignant Carbuncle,Charbon,
Malignant Pustulae, Malignant Edema,
Woolsorter’s disease, Radang Limpa
ANTHRAX Æ is a disease, caused by

Bacillus anthracis , acute & often fatal,
could be occur in human & all warm blood
animals
GEOGRAHICAL DISTRIBUTION Æ all over

the world w/ enzootic & sporadic areas

SC
ETIOLOGY
Vegetative stage in the tissues of human &
animals, showed as big rod 3 – 5 µm, forming a
short bamboos chain in vivo & a long chains in
vitro
Gram negative, with capsule & could form spore in
the center
SPORE Æ in the presence of oxygene.
Resistance to heat, chemicalia.
Will be damaged/dead by heating of 100 ºC /1 hr
In blood agar mediumÆ the colony forms acaput
medusa, w/ diameter of 0,3 – 0,5 cm, white-gray,
non haemolysis, rough & turbid

SC
GEOGRAPHICAL DISTRIBUTION
ALL OVER THE WORLD Æ Africa, Asia,

North & South of America, East & West
Europe, Australia
INDONESIA Æ 10 ENDEMIC AREAS

West Sumatera (Siberit Island), Jambi,
West Java, Middle of Java, NTB, NTT,
South Celebes, Central Celebes, South-
East Celebes, Irian Jaya

SC
MAP OF THE GEOGRAPHICAL DISTRIBUTION OF
ANTHRAX

SC
Occurance in human
• Link to the outbreak in dometic animals
• In the Developing Country, especially in the
enzootic areas Æ in human with the occupation
hence to the animals such as in framers, wool
sorters, fur processing, p.o. infection caused by
eating bushmeat of dead animals w/ anthrax
• The incidence rate in developing country is
unknown while the victims do not visit the
doctor, the dcotor doesn’t report the case, & it
was only a clinical diagnostic
• Biological weapons, an Epidemic of Anthrax in

Sverdlovsk ,Uni Soviet (1979) : Dead ca 40
people due to gastrointestinal anthrax ,
controversion to the USA hundreds-thousands of
deaths due to pulmonary anthrax in several
weeks
SC
. Epidemic in Human Æ after handling sick
animals
Endemic areas Æ Haiti, America, South
Islands of Les Cayes
. Sporadic cases in Enzootic areas Æ per
oral infection after consuming meat of
slaughtered sick animals or even from a
dead body of sick animals.
Examples :
In Republic of Mali (1978) Æ 19 dead / 84
cases
Senegal Æ 237 dead / 254 cases.
High Mortality by anthrax intestinalis.
SC
OCCURANCE IN ANIMALS
Epidemics of
ANTHRAX are
common in
Enzootic areas
without a good
control program

SC
SUSCEPTIBLE ANIMALS
With variations of susceptibility
1. HERBIVORA Æ most susceptible animals

Includes Ruminantia Æ cattle, buffalo, goat &
sheep
Horse & pigs
2. MAMALIA Æ include Humans,
Carnivores Æ dogs & cats
3. BIRDS Æ Ostrich (Struthio camelus)
water fowls & chickens

SC
SOURCE & TRANSMISSION OF
ANTHRAX
1. Direct contact through skin

2. Per inhalation Æ Spora
3. Per oral

SC
SYMPTOMES IN ANIMALS
1.PERACUTE/APOPLECTIC Æ Ruminantia.
SUDDEN DEATH WITH OR WITHOUT BLEEDING
from mouth, nose, urogenital organs, ears. Blood
could not easily to clott. Sometimes Æ the body
temperature could arise 42 0C, terminal
convulsion, collapse, DEATH
2. Acute Æ Ruminantia & Horse.
1-2 days, SOMETIMES recovery within a week.
Symptomes within 48 h before death Æ
depression, anorexia, dyspneu, chills, oedema,
DEATH
3. Chronic Æ Pig, dog & cat
Acute gastroenteritis, odema pharynx, asphexia,
DEATH
SC
The dead body of a cattle caused by Anthrax, bleeding from the
nose, mouth, eyes, anal, & vulva
(Dokumentation : BPPH Yogyakarta)

SC
SC
Canine chronic anthrax

SC
SYMPTOMES IN HUMAN
INCUBATION PERIOD Æ
2 – 5 days
3 kinds of type :
I. Cutaneous Form
II. Pulmonary or
Respiratory Form
III. Gastrointestinal
Could followed with
meningoencephalitis

SC
I. Cutaneous Form:
. The most oneÆ direct contact
w/ sick animals or animla products
such as carcass, skin, wool
or fur.
In the part of the skin Æ very itchy,
Æ papulae Æ vesiculae Æ
“black eschar”.
. The victims feel OK, without or
just a mild symptomes, so
that they didn’t go to the
doctor.
Then the disease become more
serious Æ septichaemia &
Death w/ case fatality rate 5 - 20%

SC
II. Pulmonary or Respiratory Form
• Due to the inhalation of spores. It begins w/ mild
symptomes such as common mild respiratoric
disease, within 3 – 5 days become more serious
& acute w/ high temperature, shock & DEATH.
CFR 20 – 50 %
III. Gastrointestinal Form

• Due to the consumption of meat or other animal
products contaminated w/ B. anthracis.
• Mild gastroenteritis than become more serious ,
vomites & diarrhae haemorhagis & DEATH w/
CFR 25 -75 %.

SC
Cutaneous Anthrax—Vesicle Development
Day 6 Notice the edema

and typical lesions
SC
Cutaneous Anthrax—Vesicle Development
Eschar formation
Ulcer and Ulcer and

vesicle ring vesicle ring
SC
Virulence Factor & Pathogenesis
of B. anthracis
Activity of Factors I (EF), II (PA), and III (LF)
Factor(s) Edema Lethal Immunity
I - - -
II - - ++
III - - -
I+II + - ++
I+III - - +
II+III - ++ ++
I+II+III +++ +++ +
SC
DIAGNOSA
1. Symptomes
2. Laboratory examinations Æ
isolation & identification
3. Serological examinations

SC
Laboratory Examinations for ANTHRAX
1. Microscopic Æ Staining : methylen blue

polichromatic, Gram, Wright
2. Bacteriological cultures Æ Blood agar
media, protein broth
3. Identification of B.anthracis Æ biochemical
4. Ascoli test & biological test (lab animals)
5. PCR dan ELISA

SC
Polychrome methylene
blue stain of Bacillus
anthracis. Image courtesy
of Anthrax Vaccine
Immunization Program
Agency, Office of the Army
Surgeon General, United
States
Spleen swab
SC
PREVENTION & CONTROL
T/ DURING EPIDEMIC Æ 1. Injection of antiserum
2. Injection of Antibiotica : penicillin,
oxytetrasiclin, sulfonamid derivate
3. Chemoterapy
Therapy w/ antibiotica after sampling of the specimen
Isolation suspected animals
NO PERMISSON FOR SLAUGHTERING Æ TOTALLY STAMPING
OUT Æ BURNED & BURIED !!!
CONTROL OF ANIMAL TRANSPORTATION
Insecticide might be useful during a high epidemic
COOPERATIVE BETWEEN INSTITUTIONS is the most important
thing Æ Health care institutions, Live Stock Srvices of National
& District level, & Local Government
SC
PREVENTION OF ANTHRAX INFECTION
1. Do not entry the endemis areas of anthrax
Æ living & agrobusiness
2. Buying & consuming only “ASUH” meat Æ
save, healthy, wholesome & hallal
3. In epidemic area Æ consuming only a
weldone cooked of ASUH-meat
4. Animal Slaughtering only in abattoir & under
the supervission of an on duty Meat
Inspector
5. Government Legislation !!!

SC
SC
BRUCELLOSIS
Synonyms :
Malta Fever, Undulant Fever, Rock
of Gibraltar Fever, Bang’s Disease
MK ZOONOSIS - KHI 323
4/5/2010 Brucellosis_Z00_Soelih_2010 1
genapSC
It is a contagious, costly disease of ruminant
animals that also affects humans.
Although brucellosis can attack other animals, its
main threat is to cattle, bison, and swine.
The disease is also known as contagious abortion

or Bang's disease.
In humans, it's known as undulant fever because of
the severe intermittent fever accompanying human
infection or Malta fever because it was first
recognized as a human disease on the island of
Malta.
4/5/2010 Brucellosis_Z00_Soelih_2010
ZOO-Brucellosis/Soelih-2008 2
genapSC
A. DESCRIPTION OF THE ORGANISM
BRUCELLA IS A FASTIDIOUS, AEROBIC,

SMALL, GRAM NEGATIVE & COCCOBACILLUS
GRAM Staining BAP 48 h
Source : American Society for Microbiology – 15 October 2004

genapSC
B. HISTORY - 1
BRUCELLOSIS is a ZOONOTIC INFECTION w/ 4
species being recognized as causing infection
in HUMANs:
1. B. abortus Æ in Cattle
2. B. melitensis Æ in goats, sheep & camels
3. B. suia Æ in pigs
4. B. canis Æ in dogs
Named after DAVID BRUCE, M.D. Æ a British
Army Medical Doctor, who isolated B. melitensis
from the spleen of dead British Soldier on the
Island of Malta in 1887
genapSC
B. HISTORY - 2
Following the instruction of measures to prohibit
the consumption of goat milk, the number of cases
of brucellosis declined
ALICE EVANS - an American Scientist who did
landmark work on pathogenic bacteria in dairy
products, was central in gaining acceptance of the
pasteurization process to prevent brucellosis
1954 Æ B. suis became the first biological agent to
be weaponized by the US in the days of its offensive
biological warfare program. Its Inf Dose is very low
if acquired per inhalation route Æ potentially
effective bioterrorism agent & also make them a
hazard in the clinical microbiology laboratory
genapSC
C. GEOGRAPHIC DISTRIBUTION
In the US Æ 50 – 100 cases of Human Brucellosis yearly
Inf are seen in essentially two patient populations :
1. persons who work w/ unvaccinated animals Æ
farmers, Vets & abattoir workers
C/ B. abostus & B.suis by direct contact & per
inhalation
2. persons who ingest unpasteurized dairy products
contaminated w/ B. melitensis, mostly are persons
who travel to or migrate from endemic areas in dairy
animals such as rural areas of Latin American & the
Middle East
genapSC
D. SYMPTOMS IN ANIMALS
It is one of the most serious diseases of livestock
Considering the damage done by the infection in

animals-decreased milk production, weight loss in
animals, loss of young, infertility, and lameness
The rapidity with which it spreads and the fact that it

is transmissible to humans makes it all the more
serious
genapSC
D. SYMPTOMS IN HUMAN - 1
ACUTE & CHRONIC INFECTIONS

NON SPECIFIC & SYSTEMIC W/:
Fever, sweats, headache, anorexia, back pain, &
weight loss being frequent
CHRONIC Æ mimic miliary TBC w/suppurative
lesions in th liver, spleen & bone
MORTALITY Æ 5% in untreated individuals

Fortunately, the combination of pasteurization of
milk and progress in the eradication of the disease
in livestock has resulted in substantially fewer
human cases than in the past
genapSC
1. In the acute form (<8 weeks from illness onset),
nonspecific and "flu-like" symptoms including fever,
sweats, malaise, anorexia, headache, myalgia, & back
pain
2. In the undulant form (<1 year from illness onset),

symptoms include undulant fevers, arthritis, &
epididymo-orchitis in males
3. Neurologic symptoms may occur acutely in up to 5%

of cases
4. In the chronic form (>1 year from onset), symptoms

may include chronic fatigue syndrome, depression, &
arthritis
genapSC
4.People infected with the brucellosis organism usually
develop symptoms similar to a severe influenza, but this
disease, called undulant fever, persists for several weeks
or months and may get progressively worse.
5. Farmers, ranchers, veterinarians, and packing plant

workers are infected most frequently because they come
into direct contact with infected animals.
6. The initial symptoms are fatigue and headaches,

followed by high fever, chills, drenching sweats, joint
pains, backache, and loss of weight and appetite.
!! Undulant fever does not often kill its victims, but the
disease is too serious to be dealt with lightly.
genapSC
E. SOURCE & MODE OF TRANSMISSION
Brucella are shed in Æ

• milk
• or via the aborted fetus, afterbirth,
• or other reproductive tract discharges
• Commonly transmitted through abrasions of

the skin from handling infected mammals.
• In the United States, occurs more frequently
by ingesting unpasteurized milk or dairy
products.
• Highly infectious in the laboratory via
aerosolization; handling cultures warrants
biosafety level-3 precautions
genapSC
SOURCE & MODE OF TRANSMISSION IN HUMAN
In years past, prior to pasteurization, raw milk was considered the
prime source of brucellosis in humans.
Today, most humans contract the disease by coming in direct
contact with aborted fetuses, afterbirth, and uterine discharges of
diseased animals or with infected carcasses at slaughter.
However, one 1994 study suggests that human brucellosis in
California is most likely to be a food-borne illness (unpasteurized
milk or cheese products) acquired in Mexico or from Mexican
products consumed in California.
Rarely, if ever, does a human contract the disease from another
human
The disease may be transmitted to humans when slaughtering
infected animals or when processing contaminated organs from
freshly killed animals.
There is no danger from eating cooked meat products because the

disease-causing bacteria are not normally found in muscle tissue
and they are killed by normal cooking temperatures.
genapSC
HUMAN TO HUMAN TRANSMISSION ?
Direct person-to-person spread of brucellosis is extremely

rare.
1. Mothers who are breast-feeding may transmit the

infection to their infants.
2. Sexual transmission has also been reported.
3. For both sexual and breast-feeding transmission, if the

infant or person at risk is treated for brucellosis, their
risk of becoming infected will probably be eliminated
within 3 days.
4. Although uncommon, transmission may also occur via

contaminated tissue transplantation
genapSC
SOURCE & MODE OF TRANSMISSION IN ANIMALS
Brucellosis is commonly transmitted to susceptible animals by Æ
1. direct contact with infected animals or with an environment
that has been contaminated with discharges from infected
animals. Aborted fetuses, placental membranes or fluids, and
other vaginal discharges present after an infected animal has
aborted or calved are all highly contaminated with infectious
Brucella organisms.
2. Per oral Æ Cows may lick those materials or the genital area
of other cows or ingest the disease-causing organisms with
contaminated food or water.
3. Despite occasional exceptions, the general rule is that
brucellosis is carried from one herd to another by an infected
or exposed animal. This mode of transmission occurs when a
herd owner buys replacement cattle or bison that are infected
or have been exposed to infection prior to purchase. The
disease may also be spread when wild animals or animals
from an affected herd mingle with brucellosis-free herds.
genapSC
F. DIAGNOSIS
ANIMALS Æ
Screening test using to find a reactor in the stahl
1.Rose - Bengal Test (RBT)
2.CFT
IN HUMAN Æ
Brucellosis is diagnosed in a laboratory by finding Brucella
organisms in samples of blood or bone marrow.
Serologis also, can be done to detect antibodies against the

bacteria in blood Æ 2 blood samples should be collected 2
weeks apart.
genapSC
G. PREVENTION
1. Ranchers, farmers, or animal managers should clean
and disinfect calving areas and other places likely to
become contaminated with infective material
2. All individuals should wear sturdy rubber or plastic

gloves when assisting calving or aborting animals,
and scrub well with soap and water afterward
3. Precautions against drinking raw milk or eating

unpasteurized milk byproducts are also important
4. Ultimately, the best prevention is to eliminate

brucellosis from all animals in the area
genapSC
H. TREATMENT & PREVENTION IN HUMAN
There is no vaccine available for humans

Treatment can be difficult.
Æ Combination of doxycycline and rifampin are used for
6 weeks to prevent reoccuring infection
Æ Depending on the timing of treatment and severity of

illness, recovery may take a few weeks to several
months.
Æ Mortality is low (<2%), and is usually associated with

endocarditis
genapSC
H. TREATMENT & PREVENTION IN ANIMALS
Vaccination for Cows, sheep & goats Æ

1. Vaccine RB-51 or strain 19 Æ live attenuated
2. Vaccine REV-1
TREATMENT of animals is very costly
genapSC
• Food poisoning yg disebabkan oleh C.perfringens
terjadi jika makanan seperti daging sapi, kuah daging
dan daging ayam tidak didinginkan dan/atau dipanaskan
kembali.
Selanjutnya sejumlah besar sel vegetatifnya termakan.
Produksi toksin dalam saluran pencernakan disamakan
dengan sporulasi.
• C.perfringens merupakan penyebab utama dari luka

infeksi, memproduksi beberapa jenis toksin dan
menyebabkan reaksi lokal ataupun sistemik.
Jika toksin dihasilkan, alpha toksin  membran sel
rusak dan dapat menyebabkan gas gangren.
Kejadian pada manusia
Food poisoning yg disebabkan type A  terjadi

diseluruh dunia, terutama di negara berkembang.
Di United Kingdom  food poisoning merupakan
penyakit yg harus dilaporkan  30% dari semua
kasus  37 orang per outbreak.
Di USA  pada tahun 1976 – 1980, 62 outbreak
terpapar sebanyak 6093 orang dengan distribusi
regional.
Di Indonesia  belum ada laporan sampai saat ini.
Gejala pada manusia
• Penyakit terjadi lewat makanan  terutama daging merah,
unggas dimana C.perfringens type A berkembang biak 
a. strain thermoresisten (100oC / > 1 jam)
b. strain thermolabil & hemolitik (100oC / >10 min)
• Periode inkubasi  6-24 jam setelah makan.
Pada beberapa kasus dilaporkan hanya 2 jam 
dalam makanan terdapat preformed toxin
• S/ terjadi tiba-tiba 
1. kram perut dan diare, kadang2 tidak disertai muntah atau
demam.
2. Bertahan satu hari atau kurang dan berjalan ringan kecuali
pada orang yg lemah dapat berakibat fatal.
Food poisoning yg disebabkan C. perfringens type A biasanya tidak

membutuhkan pengobatan.
Gejala pada manusia
• Penyakit yg disebabkan oleh kolonisasi
C.perfringens type A dalam usus dan terjadi
produksi enterotoksin  gambaran klinis berbeda
dari Clostridial food poisoning yg lain, tetapi lebih
mirip dengan infeksi yg disebabkan Salmonella atau
Campylobacter  diare sampai 11 hari tetapi pada
2/3 kasus kejadiannya lebih pendek. Pada beberapa
kasus disertai faeses berdarah.
• Food poisoning yg disebabkan C.perfringens type C

 NECROTIC ENTERITIS, gangren lokal pada usus
kecil terutama jejunum
Gejala pada manusia
• Necrotic Enteritis oleh C.perfringens type A jarang terjadi

Sekarang ini, Necrotic Enteritis jarang terjadi
didunia belahan barat, walaupun dilaporkan
beberapa kasus terjadi pada remaja.
• Gastroenteritis pada manusia yg disebabkan oleh

C.perfringens type D jarang terjadi
Kejadian pada hewan
• Enterotoksemia oleh type B, C, D dan E  ruminansia
domestik
• Enterotoksemia oleh beberapa jenis C.perfringens 
disebabkan oleh absorpsi toksin yg diproduksi dalam
usus oleh beberapa type C.perfringens kedalam aliran
darah.
• Di negara berkembang  banyak kasus yg tidak
dilaporkan  gejala ringan dan berakhir kurang dari 24
jam.
• Diagnosa laboratoris tidak dapat dilakukan  tergantung
sampel makanan dan penderita, seringkali tidak
mencukupi.
Gejala pada hewan
• C.perfringens type A merupakan flora normal usus yg kadang2
memproduksi alpha toksin.
• Sapi  haya beberapa kasus.
• Yellow Lamb Disease  pada anak kambing yg menyusu 
terjadi di California dan Oregon (USA) selama musim semi
dimana banyak anak2 kambing yg sedang menyusu.
• S/ anak kambing depresi, anemia, jaundice dan
hemoglobinuria, dan mati 6-12 jam setelah terlihat gejala klinis.
C.Perfringens type B  Lamb dysentry

Di Britania Raya, Timur Tengan dan Afrika Selatan.
Menyerang Lamb berumur kurang dari 2 mgg, Calves dan Colts
S/ hemoragik enteritis dan luka pada mukosa
Gejala pada hewan
• C.perfringens type C 
1. menyebabkan “STRUCK”  hemorhagic
enterotoksemia pada domba dewasa di Great Britain.
2. NE pada calves, lamb, suckling pig dan unggas
pada beberapa bagian dunia.
• C. perfringens type D agen penyebab entrotoksemia
pada domba semua umur, diseluruh dunia.
Berhubungan dengan konsumsi makanan
berlebihan milk, pasture dan biji2an. Juga
menyerang kambing dan jarang terjadi pada sapi.
• C.perfringens type E  menyebabkan disentri atau
enterotoksemia pada Calves, Lamb di USA, Inggris
dan Australia
Sumber infeksi dan Cara penularan
• Reservoar alam dari C.perfringens type A adalah tanah
dan usus manusia dan hewan.
• Manusia merupakan sumber infeksi dengan jumlah

C.perfringens yg tinggi, daripada unggas dan sapi dan
keluar dalam ekskretanya  manusia merupakan
reservoar penting pada clostridial food poisoning.
• Jumlah C.perfringens type A dalam usus bervariasi

tergantung dari spesies hewan dan lokasinya 
Jumlah besar dalam usus kecil babi
Jumlah kecil pada usus domba, kambing dan sapi
Tidak dijumpai pada kuda
• C.perfringens type A – Enterotoksemia  terutama disebabkan
oleh ALPHA TOXIN yg dibentuk dalam usus dan dilepaskan
ketika sporulasi, usus kecil merupakan lingkungan yg baik.
• Sumber keracunan pada manusia  Kontaminasi makanan

oleh spora yg bertahan hidup waktu pemasakan  panas/
shock panas mengaktifkan spora untuk germinasi.
Bentuk vegetatif berkembang cepat jika makanan siap saji
dibiarkan pada suhu kamar dan toksin diproduksi dengan
konsentrasi tinggi jika temperatur tinggi dengan waktu yg
cukup  masuk kedalam usus ketika sporulasi dan
memproduksi toksin.
• Makanan yg merupakan sumber pencemaran adalah daging

merah dan unggas karena mengandung asam amino dan
vitamin yg dibutuhkan oleh C.perfringens.
• Sumber infeksi C.perfringens type A :
1. Terutama  daging merah dan unggas
2. Jarang  kacang2an, kentang, keju, seafood, salad
kentang dan mie.
3. Kaldu daging atau masak dalam jumlah banyak 
menyebabkan kondisi anaerob yg menyebabkan
bakteri berkembang biak ketika didinginkan atau
disimpan.
4. Makanan yg berpotensi menyebabkan keracunan
diproduksi dalam jumlah banyak di restoran dan
disajikan sehari kemudian.
• Spora C.perfringens dapat dimatikan dengan
pemasakan cukup, tetapi ada spora yg tahan panas 
memanaskan kembali sebelum disajikan dapat
menstimulasi perkembang biakan bakteri jika temperatur
tidak cukup panas.
• Bentuk vegetatif C. perfringens dengan konsentrasi
tinggi dalam makanan tidak dapat dimatikan oleh asam
lambung  masuk kedalam usus.
• Enterotoksin disintesa dalam usus jika sporulasi bakteri
tahan terhadap enzym usus  Cytotoxic effect dari
epitel usus mengakibatkan sistem transport elektrolit 
diare.
• Tidak semua strain C.perfringens toksigenik
• Disentri pada anak domba disebabkan C.perfringens
type B  terinfeksi mulai hari pertama kelahiran  dari
induk dan lingkungan. Anak domba yg menyusu akan
menjadi sakit. Bakteri berkembang biak dan
memproduksi Beta toksin ketika sporulasi.
• Hemorhagic enteritis pada domba dewasa disebabkan
C.perfringens type C (di tanah)  beta toksin.
• C.perfringens type D  ditanah dan usus domba sehat
 epsilon toksin.
• C.perfringens type B, C, D, E  memproduksi
enterotoksin pada hewan, berkembang biak cepat dalam
usus dan memproduksi toksin ketika di padang gembala
dan makan banyak rumput atau banyak mengkonsumsi
susu.
Peranan hewan dalam epidemiologi penyakit
• Food poisoning pada manusia yg disebabkan oleh makanan

terkontaminasi C.perfringens type A  sumber daging merah
dan unggas. Hewannya sendiri tidak berperanan langsung
secara epidemiologi  terdapat di tanah dan debu.
• Makanan yg berasal dari hewan merupakan substrat penting
untuk pertumbuhan bakteri sebagai sumber penyakit.
• Tanah dan usus manusia dan hewan merupakan reservoar dari
agen penyebab.
• C.perfringens type A terdapat pada otot dan organ hewan
beberapa jam setelah penyembelihan jika tidak secepatnya
didinginkan.
• Strain C.perfringens yg tahan panas mungkin dijumpai di lgl
mesenterika dari hewan setelah penyembelihan
Diagnosis
• Periode inkubasi dan gambaran klinis tanpa demam  berbeda
dengan Salmonelosis, Shigelosis dan Colibacilosis yg disertai
demam. Pada Clostridiosis jarang disertai muntah tetapi
Staphylococosis disertai muntah.
• Diagnosis laboratoris berdasarkan jumlah C.perfringens dari

makanan penyebab atau peralatannya ( 48 jam setelah timbul
penyakit  105 sel/g makanan atau 106 sel/g peralatan).
Diagnosis laboratoris untuk enterotoksemia pada hewan
 inokulasi pada tikus untuk identifikasi toksin spesifik 
inokulasi dengan isi usus dan yg lain dengan isi usus dan
antitoksin.
 Deteksi toksin secara langsung  latex agglutination,
enzyme immunoessay, kultur Vero sel dengan neutralizing
ab untuk menghambat cytopathic effect.
Kontrol
• Pada manusia :
 makanan yg mengandung daging harus disajikan panas dan
secepatnya setelah dimasak.
Jika tidak segera dimakan  simpan dingin.
 Jika mungkin, potong daging dengan irisan kecil ketika
masak.
 Kaldu sebaiknya dipisahkan dari daging.
 Pressure cooker  sangat baik untuk pencegahan.
 Bila perlu makanan dipanasi ulang dengan temperatur cukup
untuk membunuh sel vegetatif.
 Memberi penjelasan pada orang yg menyiapkan makanan 
dirumah, restoran, katering untuk mencegah pencemaran
C.perfringens pada daging dan unggas mentah.
Kontrol
• Pada hewan :
 managemen peternakan yg baik.
 pengawasan pada padang penggembalaan.
 Imunisasi aktif dengan toksoid spesifik  2 dosis
diikuti booster setelah 6 bulan (type D) atau setahun
(type C).
• Pencegahan pada anak domba :
 EWES divaksin dengan2 dosis dan dosis kedua diberikan 2
mgg sebelum partus.
 dysentri anak domba (type B)  EWES divaksinasi dengan
toksoid spesifik atau anak domba diimunisasi pasif dengan
antiserum ketika lahir.
 Pada C.perfringens type B dan C  beta toksin  toksoid
atau antiserum dari satu type memberikan imunisasi silang.
CAMPYLOBACTERIOSIS
MK ZOONOSIS – KHI 323
S1 FKH UNAIR
Campylobacteriosis_Zoo_Soelih_2011
6/9/2022 Genap 1
Campylobacter jejuni
Gram-negatif, batang bengkok,

Berbentuk seperti spiral
Merupakan bakteri enterik
Relatif rentan  mudah mati krn

suhu dingin atau panas
Campylobacteriosis  merupakan salah satu

bakteri yg dikenal sbg penyebab diare di USA
6/9/2022 Genap 2
SUMBER & CARA PENULARAN CAMPYLOBACTERIOSIS
Penanganan daging unggas yg

kurang benar
& daging unggas kurang matang
Hewan karier adl

PERORAL
Unggas krn suhu
tubuhnya sesuai utk
pertumbuhan kuman
Ditemukan di GI Tract MNS & HEWAN, kmd diangkut
ke rongga mulut & saluran urogenital. Menyebabkan
gastroenteritis, utamanya pd bayi baru lahir
6/9/2022 Genap 3
CAMPYLOBACTERIOSIS
S1 FKH UNAIR
4/25/22 Genap 1
Gram-negatif, batang bengkok,

Berbentuk seperti spiral
Merupakan bakteri enterik
Relatif rentan  mudah mati krn

suhu dingin atau panas
Campylobacteriosis  merupakan salah satu

bakteri yg dikenal sbg penyebab diare di USA
4/25/22 Genap 2
Campylobacter
 Survives in moist environments
 Weeks to months
 Some strains tolerate cold (-20C)
 Remains viable in:
 Feces (9 days)
 Milk (3 days)
 Water (2 to 5 days)
 Vaginal discharges
 Poultry litter (Both C. Jejuni and C. Coli can remain
infective in moist poultry litter for prolonged period.
C. fetus can survive in liquid manure for 24 hours
and soil for up to 20 days)
3
History of Campylobacter
First Isolation as Vibrio fetus in 1909 from
spontaneous abortions in livestock
Campylobacter enteritis was not recognized
until the mid-1970s when selective isolation
media were developed for culturing
Campylobacters from human feces
Most common form of acute infectious diarrhea
in developed countries: Higher incidence than
Salmonella and Shigella combined
4
Bacteria commonly found in animal feces. It
is one of the most common causes of human
gastroenteritis in the world. Food poisoning
caused by Campylobacter species can be
severely debilitating, but is rarely life-
threatening. It has been linked with
subsequent development of Guillain Barre
Syndrome (GBS), which usually develops
two to three weeks after the initial illness
5
SUMBER & CARA PENULARAN CAMPYLOBACTERIOSIS
Penanganan daging unggas yg

kurang benar
& daging unggas kurang matang
Hewan karier adl

PERORAL
Unggas krn suhu
tubuhnya sesuai utk
pertumbuhan kuman
Ditemukan di GI Tract MNS & HEWAN, kmd diangkut
ke rongga mulut & saluran urogenital. Menyebabkan
gastroenteritis, utamanya pd bayi baru lahir
4/25/22 Genap 6
Campylobacter causes Important Zoonotic Infections
7
Transmission: C. jejuni
Fecal-oral
Direct contact
Fomites
Bacteria found in/on:
 Vaginal discharges, abortion products
 Undercooked meat, raw milk
Mechanical vector
 Common housefly
8
Transmission:
C. fetus subsp. fetus
Ingestion
Contact with
 Feces, vaginal discharges, aborted
fetuses, fetal membranes
Venereal (cattle)
Fomites
 Semen, instruments, bedding
Cattle may become carriers
9
Disease in Humans
Nearly all cases due to C. jejuni
Enteritis
 Mild to fulminant or relapsing colitis
 Diarrhea (may contain blood)
 Fever, nausea, vomiting
 Abdominal pain
Complications uncommon
 Guillain-Barré syndrome
10
Disease in Humans
 C. fetus
 Opportunistic human pathogen
 Causes systemic infections
Immunocompromised persons at risk
11
Diagnosis
Presumptive diagnosis
 Microscopy
Characteristic darting motility
Curved or spiral rods
Definitive diagnosis
 Fecal or (rarely) blood cultures
Organism may be difficult to isolate
 Biochemical, antigen testing
 PCR, ELISA
12
Treatment
Supportive care
 Fluid and electrolyte therapy
 Antibiotics
 Efficacy not proven for mild
infections
 May reduce shedding
Complications
 Guillain-Barré syndrome
Requires intensive care
13
Species Affected
 Cattle (C. Fetus subs. Venerealis, C. Jejuni and C. Coli), sheep (C.
Jejuni, C. Fetus subs. Fetus and C. Coli)
 Chickens, Turkeys, Dogs, cats, Mink, ferrets, Pigs, Non-human
,
primates (C. Jejuni and C. Coli)
14
Disease in Animals
Enteritis
 Many species affected
 Young animals
 Diseased or stressed adults
Usually resolves in 3 to 7 days
 Intermittent diarrhea may persist
Newly hatched chicks and poults
 Acute disease and death
15
Disease in Animals
Reproductive disease
 Bovine genital campylobacteriosis
 Infertility
 Early embryonic death
 Abortion uncommon
Campylobacteriosis in sheep
 Late term abortion
 Weak lambs
 Metritis
 Death
16
Disease in Animals
Other Campylobacter spp. may cause
disease in animals
Species
 C. lari
 C. hyointestinalis
 C. upsaliensis
Disease
 Proliferative ileitis of hamsters
 Porcine proliferative enteritis
 Proliferative colitis of ferrets
17
Post Mortem Lesions
Congested and edematous
colon
Hemorrhagic colitis
Edematous lymph nodes
Placentitis (mild)
Autolyzed fetus
18
Diagnosis
Culture (fresh feces)
–Biochemical and antigen testing
Microscopy
 Characteristic darting motility
 Curved or spiral rods
PCR
ELISA
Serology (paired titers)
19
Diagnosis
Bovine genital campylobacteriosis
 Detection of IgA in cervical mucus
 Vaginal mucus agglutination test
 ELISA
 Culture
o Sheath washings
o Vaginal cultures
20
Morbidity and Mortality: Humans
Common cause of bacterial diarrhea

in the U.S.
 20 cases/100,000 people annually
Causes 5 to 14% of diarrhea
worldwide
Populations at risk
 Young children
 People in developing countries
 Immunosuppressed
21
Morbidity and Mortality: Humans
 C. jejuni, C. coli and C. fetus infections are found worldwide.
 Infections are particularly common in very young children in developing

countries, and in children and young adults in developed countries.
 Most cases are sporadic, but outbreaks, associated with sources such as raw
milk, are also seen.
 C. jejuni or C. coli diarrhea is usually self-limiting and generally resolves after 7

to 10 days; relapses can occur in approximately 10-25% of cases.
 Immunosuppressed individuals are at a high risk for severe or recurrent

infections or for septicemia.
 Deaths are rare in C. jejuni infections and are seen mainly in patients with
cancer or other debilitating diseases. The estimated case/fatality ratio for C.
jejuni infections is one in 1,000. Guillain-Barré syndrome is seen after
approximately 1 in 1000 diagnosed infections; up to 5% of these patients may
die and 30% or more may have residual weakness or other neurologic
22
Morbidity and Mortality: Animals
Asymptomatic carriage more common
than enteric disease
 Up to 45% of cats, 75% of dogs
 Higher in animal shelters, pet shops,
strays, rural animals exposed to
livestock
High incidence in poultry
Abortion in sheep
 10 to 20% abortion rate
Mortality low for all causes
23
Morbidity and Mortality: Animals
 Among livestock, Campylobacter jejuni has been isolated from the feces of 25-100%
of asymptomatic cattle and, in one study, the gallbladder of 11% of healthy sheep.
 Various studies have noted a particularly high incidence of infection in poultry, with
Campylobacter in 100% of the ceca of turkeys, 83% of chicken droppings and 88% of
duck droppings.
 C. jejuni contamination has also been seen in approximately 30% of chicken meat and
5% of red meat samples. Campylobacter species have also been isolated from 50% of
urban pigeons, 35% of migratory birds and 20-70% of seagulls.
 Gastrointestinal campylobacteriosis is usually self-limiting in mammals; however, up to

32% mortality may be seen with highly pathogenic isolates in chicks. Mortality is also
low in adult sheep and cattle affected by abortions and infertility.
 In sheep, the typical abortion rate is 10-20%, with 5% mortality in the ewes that
abort, due to metritis. Under some circumstances, (e.g. an outbreak in a naïve flock)
abortion rates can reach 70-90%.
24
Treatment
Antibiotics
 Limited information on efficacy
 May prevent exposed sheep from
aborting during outbreak
Bovine genital
campylobacteriosis
 Bulls may be treated
 Cows usually not treated
25
Prevention in Humans
Avoid unsafe foods
 Raw dairy products
 Undercooked meat
Separate raw foods
Good hygiene
Avoid sick animals
No human vaccine
26
Prevention in Animals
Vaccination available for:
 Abortion in sheep
 Bovine genital campylobacteriosis
Poultry facilities
 Sanitation
 Exclude pests
 All-in, all-out
 Closed flock
27
Disinfection
Campylobacter spp. susceptible
to:
 1% sodium hypochlorite
 70% ethanol
 2% glutaraldehyde
 Iodine-based disinfectants
 Phenolic disinfectants
 Formaldehyde
 Moist or dry heat
 Gamma irradiation and UV radiation
28
Additional Resources
Center for Food Security and Public Health
www.cfsph.iastate.edu
CDC: Campylobacter–
http://www.cdc.gov/nczved/divisions/dfbm
d/diseases/campylobacter/
CDC: Campylobacter Infection in Animals
http://www.cdc.gov/healthypets/diseases/campyl
obacteriosis.htm
29
TERIMA KASIH
30
LISTERIOSIS

S1 FKH UNAIR
Listeriosis_Zoo_Soelih-AML_2011
6/9/2022 genap_IND 1
Listeriosis
Sinonim : leukocytosis, mononucleosis,
listerial infection, listerellosis, listeriasis,
circling disease (pd hewan).
Etiologi : L. monocytogenes, motil, gram +

fakultatif aerob, parasit intraseluler pd sistem
retikulo endotelial.
Ada 7 serotipe  2 pathogen 
L. monocytogenes & L. bulgarica.
Figure 2. The four bacterial species in question. Clockwise
from top left: Salmonella enterica, Campylobacter jejuni,
Escherichia coli, Listeria monocytogenes.
Distribusi :  di seluruh dunia,
 pd tanaman, tanah, usus manusia & hewan.
Kejadian pd manusia
Paling riskan anak-2  hampir 50%, 1 – 18 th
Org dewasa tua  > 50 th
Abortus pd wanita hamil pd trisemester
kedua,
GK/ menggigil, demam, sakit kepala &
pusing. Setelah abortus, gejala bisa hilang,
tetapi L. monocytogenes dpt diisolasi dari
vagina, cervix, urine sampai beberapa
minggu 
Bayi lahir mati atau segera setelah
dilahirkan 
necrosis hati, meningitis & hydrocephalus
Pada dewasa  meningitis
 Listerial Meningitis dpt merupakan
komplikasi bagi penderita sakit berat
 kanker, long-term treatment
corticosteroid, diabetic & alkoholik.
Jika tidak ada pengobatan antibiotika 
CFR 70%
Kejadian pd hewan
Paling peka  DOMBA, KAMBING & SAPI  > 3 th
GK/
Encephalitis, kematiasn neonatal & septicemia.
Depresi, demam, inkoordinasi, tortikolis, kontraksi
spasmodic & paralysis otot wajah & tenggorokan,
salivasi profus, strabismus & conjunctivitis,
Berusaha berdiri tegak, jika mampu berjalan selalu
bergerak memutar (circles).
Fase akhir  hewan akan berbaring dgn
karakteristik gerakan mengunyah walaupun tidak
mau makan.
Septicemia hewan muda & dewasa.
Abortus pada bulan terakhir kebuntingan

tanpa gejala klinis. Jika terjadi infeksi uterus
biasanya pada bulan ketujuh kebuntingan,
fetus mati tertahan di uterus dan maserasi.
Mastitis subklinis, akut & kronis.

 adanya Listeria pada susu, dg pasteurisasi
tidak menjaminan keamanannya apalagi jika
TPCnya tinggi sebelum dilakukan pasteurisasi.
 tanaman, lumpur, pasture, air limbah, feses
- Bisa ditemukan pada 
manusia sehat,
20-30% feses & sal genital wanita hamil. 
sbg reservoir bagi foetus & bayi baru lahir.
 per oral (susu, olahan susu & peralatannya)

airborne,
fecal route
kontak sexual
trans uterine/placental kpd foetus
 Journal terbaru jg menyebutkan  pd daging & telur

Diagnosa : pemeriksaan darah, sekresi
vagina, feses.
Kontrol :
- T/ Antibiotika.
- Pada akhir kehamilan terkena flu-like
disease hati2 !
- Pasteurisasi susu,
- Kontrol rodent,
- Hygiene personal & lingkungan
- Cairan aborsi segera dimusnahkan.
6/9/2022 genap_IND 10
6/9/2022 genap_IND 11
Hamburger
6/9/2022 genap_IND 12
COLIBACILLOSIS

S1 FKH UNAIR
COLIBACILLOSIS_Zoo_Soelih-
6/9/2022 AML_2011 genap 1
Synonim
Colibacteriosis, Colitoxemia,
White scours, Gut edema of swine
Agent
E. coli, Gram negatif, aerobe, facultatif
anaerobe, bentuk batang sedang
Kejadian
seluruh dunia,
Daerah endemis di negara berkembang
6/9/2022 AML_2011 genap 2
SUMBER & CARA PENULARAN
Ada beberapa merupakan species

specific.
Susu, produk olahan susu, & produk

olahan daging  sumber E. coli pathogen.
Makanan asal hewan, kontak dg anjing &

kucing  sumber infeksi bagi anak-anak
6/9/2022 AML_2011 genap 3
KEJADIAN PADA HEWAN
DIARRHAE pd ANAK SAPI (white scours)

 akut pd anak sapi umur < 10 hari
 diare putih, cepat mengalami dehidrasi
Mastitis  karena E. coli pd Sapi dewasa

disertai gagngguan pada saluran air susu.
6/9/2022 AML_2011 genap 4
KEJADIAN PADA HEWAN - 2
Edema pd anak babi yg masih menyusu

 umur 6 – 14 minggu
 edema kelopak mata, abdomen &
bagian tubuh lainnya
Coligranuloma (Hjarre’s disease) pd

unggas dewasa  lesi granulomatous di
liver, caecum, limpa, sumsum tulang &
paru-paru
6/9/2022 AML_2011 genap 5
KEJADIAN PADA MANUSIA
ETEC: Enterotoxigenic E. coli

EIEC : Enteroinvasive E. coli
EHEC:Enterohaemorrhagic E. coli
EPEC :Enteropathogenic E. coli
6/9/2022 AML_2011 genap 6
Diagnosis
Kultur feses
Immunoassay  u/ mendeteksi enterotoxin
Therapi
• Ciprofloxacin
• Trimethoprim sulfa
6/9/2022 AML_2011 genap 7
PENCEGAHAN / KONTROL
1. Kebersihan individu
2. Menjaga hygiene
3. Pengawasan limbah
4. Proteksi produk olahan pangan
5. Vaksinasi  sudah dikembangkan
untuk babi & sapi
6/9/2022 AML_2011 genap 8
SALMONELLOSIS

S1 FKH UNAIR
Salmonellosis_Zoo_Soelih-AML_2010
6/9/2022 genap 1
Agen Penyebab
Sinonim: Salmonella food poisoning, Enteric

paratyphosis.
Hingga sekarang, ada > 1800 serotype

Salmonella penyebab keracunan makanan
food poisoning serotypes of.
S. dublin pd sapi, S. pullorum pd ayam.
6/9/2022 genap 2
RESERVOIR
SUMBER UTAMA bagi MANUSIA
 Unggas, sapi, domba & babi

Penularan terjadi di dapur 
- karkas ayam,
- daging sapi,
- susu unpasteurized,
- cara memasak yg salah
- kontaminasi silang,
- cara penyimpanan makan yg salah
6/9/2022 genap 3
RESERVOIR - 2
Penularan antar manusia  di rumah sakit
Tikus  mempunyai peranan penting dlm

kejadian salmonellosis pd manusia & hewan
Hewan lain 
Anjing (10%),
Kucing (0,6-27%),
Kera (20%),
Reptil (94%),
Burung
Kura-kura
6/9/2022 genap 4
RESERVOIR - 3
FDA (USA) MELARANG 
- penjualan ilegal telur kura-kura
- Kura-kura hidup dg panjang carapace <
10 cm
Pengecualian  u/ kebutuhan pendidikan

& penelitian , serta marine turtles yg
hingga kini diketahui bukan reservoir
Salmonella
6/9/2022 genap 5
PENULARAN
Per oral 
- kontaminasi via makanan & air,
- kontaminasi limbah
- kontak langsung
- pakan hewan  yg mengandung hasil
samping dr pemotongan hewan yg
masih mentah & tdk dimproses menjadi
pellet
6/9/2022 genap 6
GEJALA KLINIS PADA MANUSIA
Masa inkubasi  12-72 jam
GK/
Tergantung pd DOSIS INFEKSI  diare
encer selama 10 hr, dehidrasi, nyeri
abdominal, suhu tubuh meningkat
intermitten
6/9/2022 genap 7
GEJALA KLINIS PADA HEWAN
Masa inkubasi  1-5 hari
GK/
- Sub klinis
- intermittent or persistent carriers,
- fever,
- diarrhea,
- abortius
- Anak sapi  mortalitas tinggi
6/9/2022 genap 8
PERUBAHAN PA/
MANUSIA  enteritis, abses
HEWAN 
ileitis, inflamasi lgl mesenterica,
septicemia, pneumonia, dehidrasi,
Penurunan BB krn stimulasi dr eksresi
chlorid & inhibisi absorbsi sodium.
Abortus  krn proliferasi salmonella di
placenta yg menyebabkan necrosis
placenta
6/9/2022 genap 9
DIAGNOSA
MANUSIA  serotyping, phage typing.
HEWAN  Kultur feses, jaringan

postmortem & makanan aasal hewan
6/9/2022 genap 10
PENCEGAHAN PADA MANUSIA
1. Hygiene & sanitasi dapur

2. Penanganan daging yg dimasak dg benar
3. Makanan sisa jangan lupa disinpan di
lemari es
4. Cegah kontaminasi silang
6/9/2022 genap 11
PENCEGAHAN PADA HEWAN
1. Pengawasan kandang tertutup
2. Pemeliharaan dlm grup kecil
3. Hindari pencampuran hewan yg berbeda
asalnya
4. Sterilisasi pakan ternak
5. Pengawasan air minum
6. Cegah unggas liar & rodent masuk
7. Jaga kebersihan & lakukan desinfeksi
kandang
8. Unggas  Buang kotoran, desinfeksi telur
tetas, fumigasi inkubator
6/9/2022 genap 12
THERAPI
Manusia 
Trimethoprim- Sulfamethoxazole,
ampicillin, ciprofloxacin
Hewan  antibiotika & sulfonamides

segera bila terjadi diarrhea & panas dpt
menurunkan angka mortalitas
Tetapi kontraindikasi  pd hewan karier
krn akan memperpanjang masa kariernya
6/9/2022 genap 13
VAKSINASI
Pada Manusia  tidak ada
HEWan 
Anak Sapi  Vaksinasi terhadap S.
dublin & S. typhimurium
“ live vaccine” dg S. dublin 
memberikan proteksi bagus pd anak sapi
terhadap S. dublin & S. typhimurium.
6/9/2022 genap 14
STAPHILOCOCCAL FOOD POISONING
• Suatu kondisi yang disebabkan oleh adanya
ENTEROTOKSIN yg dihasilkan oleh S. aureus.
• Terdapat pada makanan yg terkontaminasi
• Bentuk kokus Gram positif.

• Bakteri S. aureus menyerap warna ungu dari
pewarnaan GRAM, kokus berpasangan dengan rantai
pendek atau bergerombol seperti buah anggur.
• Toksin dapat menyebabkan sakit pada manusia.
• Toksin
• Spesifik, dapat dikarakterisasi, bahan kimia beracun,
merupakan protein yg spesifik, mempunyai kekebalan,
diproduksi oleh mikroba, tanaman dan hewan.
• ENTEROTOKSIN
• Substansi toksik yg dihasilkan oleh saluran pencernakan
dan dapat menyebabkan muntah, diare dll.
• Biasanya enterotoksin dihasilkan oleh bakteri.
Bentuk penyakit secara alamiah
• Munculnya gejala biasanya cepat, dan pada beberapa
kasus akut  tergantung pada :
- Kepekaan individu terhadap toksin.
- Banyaknya konsumsi makanan yg terkontaminasi.
- Banyaknya toksin yg termakan.
- Kondisi kesehatan penderita.
• Gejala umum  mual, muntah, retching, kram perut dan
kelemahan.
Pada beberapa individu terjadi gejala subklinis.
• Pada kasus yg lebih parah  sakit kepala, kram otot,
perubahan tekanan darah dan denyut nadi.
• Pada umumnya kesembuhan terjadi 2 hari  pada
kasus yg lebih parah kesembuhannya lebih lama.
• Makanan penyebab food poisoning :
1. Daging dan produk olahannya.
2. Ayam dan produk olahan telur.
3. Salads  telur, tuna, ayam, kentang dll.
4. Produk Bakery  cream filled pastries,
cream pies dan chocolate eclairs.
5. Sandwich filling, susu dan produk olahannya.
• Makanan  selama persiapan makanan dan
jika diletakkan pada temperatur optimal
setelah persiapan makanan.
• Staphylococcus  terdapat di udara, air,

debu, sampah, susu, makanan dan peralatan makan,
lingkungan, manusia dan hewan.
• Intoksikasi pada manusia  disebabkan
termakannya toksin dalam makanan yg
diproduksi oleh S. aureus  biasanya
disebabkan makanan tidak dalam kondisi :
o o
cukup panas (> 60 C atau 140 F).
o o
cukup dingin (< 7,2 C atau 45 F).
• Manusia dan hewan merupakan reservoar
primer.
S.aureus terdapat di hidung, tenggorokan, rambut dan
kulit dari > 50% individu sehat.
Keadaan tsb semakin tinggi jika ada kontak dengan
individu sakit dan lingkungan rumah sakit.
• Food handlers  merupakan sumber utama penularan
melalui makanan.
Outbreak kasus keracunan makanan  peralatan
dan lingkungan dapat menjadi sumber kontaminasi
S. aureus.
Tingkat kesakitan
• Belum diketahui kejadian yg sebenarnya dari

Staphylococcal food poisoning  disebabkan:
1. Kecilnya respon penderita ketika diwawancara
dengan petugas kesehatan.
2. Diagnosa penyakit tidak jelas, disebabkan gejala yg
hampir sama dengan keracunan makanan yg lain
(mis. muntah yg disebabkan toksin Bacillus cereus).
3. Tidak cukupnya sampel untuk analisis laboratoris.
4. Pengujian laboratoris yg tidak tepat.
Tuberculosis
• Bovine tuberculosis (bTB) is a chronic
bacterial disease of animals caused
by Mycobacterium tuberculosis complex
primarily by M. bovis, M. caprae and to a
lesser extent M. tuberculosis.
• It is a major infectious disease among
cattle, and also affects other
domesticated animals and certain wildlife
populations, causing a general state of
illness, pneumonia, weight loss, and
eventual death.
• AGENT : Mycobacterium spp. (M.africanum,
M. avium, M. bovis, M. tuberculosis).
• Syndrome:
• Human: Pulmonary: Productive cough, fever,
weight loss, fatigue, night sweats, chest pain,
hemoptysis.
• Extrapulmonary: Cervical lymphadenitis
(scrofula), meningitis, osteomyelitis,
pericarditis; also associated with infection of
most other organs.
• Typically, encapsulated inflammatory
nodules (tubercles) with epithelioid and
giant cells surrounding caseous or
liquefied center.
• M. avian typically produces tubercle
lesions in birds only; in mammals, lesions
• usually slight (regional lymphadenitis) or
absent (stimulates tuberculin reactivity).
• Cattle: pulmonary (M bovis)-cough,
weight loss, decreased milk production.
• Swine: extrapulmonary (M. avium)-
pharyngeal, mesenteric lymphadenitis.
• Incubation period 4-12 weeks for
observable lesion (e.g., lung nodule) or
significant tuberculin reaction.
• The greatest risk is within 1-2 years, it
may be decades before progressive
disease evident.
• Case fatality rate: Severe outcome more
likely with primary infection in young or
immunodeficient (e.g., AIDS).
• Confirmatory tests: Direct microscopic

examination (presumptive) and aerobic
culture of lesion material (pus, sputum).
• Occurrence: Worldwide. Crowding and
any condition decreasing resistance
(particularly lung damage, AIDS)
• Prevalence increases with age. <100
human cases M. avium infection
confirmed, associated with bovine
mastitis.
• M. africunum, related to M bovis,
causes disease in people; nonhuman
host distribution still uncertain (cases
reported in zoo primates).
• Transmission: Primarily inhalation of
infectious droplets or droplet nuclei from
pulmonary lesion. Also ingestion,
particularly raw milk from cow with
mammary lesion.
• People are reservoir and main source for
M. tuberculosis; cattle for M. bovis.
• Wide range of mammalian species
infected from mammalian reservoirs,
but parrot only bird known to be
infected.
• Dogs and primates infected
particularly from exposure to human
infections.
CONTROL AND PREVENTION
• Individual / herd: Prolonged therapy
(several months) with isoniazid,
dihydrostreptomycin, ethambutol,
rifampicin, pyrazinamide.
• Prognosis good with proper therapy in
people and cattle (M bovis highly
sensitive).
• M. uvium infection is the exception,
highly resistant to antibiotics; surgical
excision of affected lymph nodes may
be needed.
• Local / community:
• Pasteurize milk.
• Immunize high-risk groups with BCG.
• Find cases with use of tuberculin test
(cattle, people, primates).
• Slaughter tuberculin reactor cattle.
Depopulate tuberculous poultry flocks.
• Screen radiographically tuberculin-
positive people.
• The tuberculin skin test is the standard
method of TB diagnosis in live domestic
animals.
• It consists of injecting bovine tuberculin (a
purified protein extract derived from M.
bovis) intradermally and then measuring
skin thickness at the site of injection 72
hours later to detect any subsequent
swelling at the injection site (sign of
delayed hypersensitivity associated with
infection).
Tuberculins Test
Antimicrobial Resistance
(AMR)
ZOONOSIS - KHD 302

DEPARTMENT OF VPH
6/9/2022 AMR-Zoo_TSE_2020 1
Key facts
 AMR threatens the effective prevention & treatment of
an ever-increasing range of infections caused by
bacteria, parasites, viruses & fungi
 AMR is an increasingly serious threat to global public

health that requires action across all government
sectors and society.
 Without effective antibiotics, the success of major

surgery & cancer chemotherapy would be compromised
 The cost of health care for patients with resistant

infections is higher than care for patients with non-
resistant infections  due to longer duration of illness,
additional tests & use of more expensive drugs.
 In 2016, 490 000 people developed multi-drug resistant

TB globally, & drug resistance is starting to complicate
the fight against HIV & malaria, as well.
6/9/2022 AMR-Zoo_TSE_2020 2
INTRODUCTION
WHO
 AMR threatens the effective prevention &
treatment of an ever-increasing range of
infections caused by microorganisms such as
bacteria, parasites, viruses & fungi.
 AMR happens when m.o. change when they

are exposed to antimicrobial drugs (such as
antibiotics, antifungals, antivirals, antimalarials,
& anthelmintics)
6/9/2022 AMR-Zoo_TSE_2020 3
 Microorganisms that develop antimicrobial
resistance are sometimes referred to as
“superbugs”  as a result, the medicines become
ineffective & infections persist in the body,
increasing the risk of spread to others.
 The WHO defines AMR as a

microorganism's resistance to an antimicrobial
drug that was once able to treat an infection by
that microorganism.
 A person or animal cannot become resistant to

antibiotics  Resistance is a property of the
microbe, not a person or other organism infected
by a microbe
6/9/2022 AMR-Zoo_TSE_2020 4
Antimicrobial resistance (AMR) 
is the ability of a microbe to resist the effects of
medication that once could successfully treat
the microbe
Antibiotic resistance (AR) 

is a subset of AMR, as it applies only
to bacteria becoming resistant to antibiotics
6/9/2022 AMR-Zoo_TSE_2020 5
What is the Cause
 Overuse of antimicrobials
 Natural oocurance
 Self medication
Overuse of antimicrobials  This leads to
microbes either developing a defense against
drugs used to treat them, or certain strains of
microbes that have a natural resistance to
antimicrobials becoming much more prevalent
than the ones that are easily defeated with
medication.
Antimicrobial resistance does occur naturally over
time, the use of antimicrobial agents in a variety
of settings both within the healthcare industry
and outside of has led to antimicrobial resistance
becoming increasingly more prevalent
6/9/2022 AMR-Zoo_TSE_2020 6
6/9/2022 AMR-Zoo_TSE_2020 7
 Overuse of antimicrobials
 This leads to microbes either developing
a defense against drugs used to treat them
certain strains of microbes that have a

natural resistance to antimicrobials
becoming much more prevalent than the
ones that are easily defeated with
medication.
 While antimicrobial resistance does occur

naturally over time, the use of antimicrobial
agents in a variety of settings both within
the healthcare industry & outside of has led
to antimicrobial resistance becoming
increasingly more
6/9/2022 prevalent
AMR-Zoo_TSE_2020 8
Antimicrobial resistance is mainly caused by
the overuse of antimicrobials. This leads to
microbes either developing a defense against
drugs used to treat them, or certain strains of
microbes that have a natural resistance to
antimicrobials becoming much more prevalent
than the ones that are easily defeated with
medication.[27] While antimicrobial resistance
does occur naturally over time, the use of
antimicrobial agents in a variety of settings
both within the healthcare industry and
outside of has led to antimicrobial resistance
becoming increasingly more prevalent
6/9/2022 AMR-Zoo_TSE_2020 9
Self medication by consumers 
 is defined as “the taking of medicines
on one's own initiative or on another
person's suggestion, who is not a
certified medical professional”
it has been identified as one of the

primary reasons for the development of
antimicrobial resistance
6/9/2022 AMR-Zoo_TSE_2020 10
Present situation
 ABR is present in every country.
 Patients with infections caused by

drug-resistant bacteria are at
increased risk of worse clinical
outcomes & death, & consume more
health-care resources
6/9/2022 AMR-Zoo_TSE_2020 11
6/9/2022 AMR-Zoo_TSE_2020 12
AMR Microorgnism
Resistance in bacteria
 Klebsiella pneumonia  ESBL*
 E. coli  ESBL
 Neisseria gonorrhoeae
 M. tuberculose
 S. aureus  MRSA*
Resistance in virus
 Virus Influenza
Resistance in Protozoa
 Plasmodium sp. Malaria
6/9/2022 AMR-Zoo_TSE_2020 13
 Resistance in Klebsiella pneumoniae –
common intestinal bacteria that can cause life-
threatening infections 
 carbapenem antibiotics, has spread to all
regions of the world
 K. pneumoniae is a major cause of hospital-

acquired infections such as pneumonia,
bloodstream infections, & infections in newborns
and intensive-care unit patients
 In some countries, because of resistance,

carbapenem antibiotics do not work in more than
half of people treated for K.
pneumoniae infections.
6/9/2022 AMR-Zoo_TSE_2020 14
 Resistance in E. coli 
 to one of the most widely used
medicines for the treatment of urinary
tract infections fluoroquinolone
antibiotics is very widespread.
 There are countries in many parts of

the world where this treatment is now
ineffective in more than half of patients.
6/9/2022 AMR-Zoo_TSE_2020 15
 Nisseria goenorrhoe
 Treatment failure to the last resort of medicine for
gonorrhoea  3rd generation cephalosporin antibiotics has
been confirmed in at least 10 countries  Australia, Austria,
Canada, France, Japan, Norway, Slovenia, South Africa,
Sweden and the United Kingdom of Great Britain and
Northern Ireland
 WHO recently updated the treatment guidelines for

gonorrhoea to address emerging resistance  The new WHO
guidelines do not recommend quinolones due to widespread
high levels of resistance
Treatment guidelines for chlamydial infections & syphilis

were also updated
6/9/2022 AMR-Zoo_TSE_2020 16
 S. aureus
 People with MRSA  are estimated to be 64%
more likely to die than people with a non-
resistant form of the infection.
 Enterobacteriaceae
 Colistin is the last resort treatment for
life-threatening infections caused by
Enterobacteriaceae which are resistant to
carbapenems  Resistance to colistin has
recently been detected in several countries
&regions, making infections caused by such
bacteria untreatable.
6/9/2022 AMR-Zoo_TSE_2020 17
 Resistance in tuberculosis (TB)
 In 2014  there were about 480,000 new

cases of multidrug-resistant tuberculosis (MDR-
TB) a form of tuberculosis that is resistant to
the 2 most powerful anti-TB drugs. Only about a
quarter of these (123 000 cases) were detected
and reported
MDR-TB requires treatment courses that are

much longer and less effective than those for
non-resistant TB
 Globally  only half of MDR-TB patients were

successfully treated in 2014
6/9/2022 AMR-Zoo_TSE_2020 18
 Resistance in tuberculosis (TB) .....
Among new TB cases in 2014, an estimated

3.3% were multidrug-resistant The proportion
is higher among people previously treated for
TB, at 20%
 Extensively drug-resistant tuberculosis (XDR-

TB), a form of tuberculosis that is resistant to at
least 4 of the core anti-TB drugs, has been
identified in 105 countries  An estimated 9.7%
of people with MDR-TB have XDR-TB.
6/9/2022 AMR-Zoo_TSE_2020 19
 Resistance in tuberculosis (TB) .....
(1) MDR-TB Resistance of Mycobacterium

tuberculosis against at least isoniazid &
rifampicin, the cornerstone medicines for
treatment of TB. Rifampicin-resistant disease
on its own requires similar clinical
management as MDR-TB
(2) XDR-TB  Resistance of Mycobacterium

tuberculosis to any fluoroquinolone & to at
least one of three second-line injectable drugs
 capreomycin, kanamycin & amikacin), in
addition to multidrug resistance.
6/9/2022 AMR-Zoo_TSE_2020 20
 Plasmodium falciparum
As of July 2016  resistance to the first-line
treatment for P. falciparum malaria artemisinin-
based combination therapies (ACTs  has been
confirmed in 5 countries of the Greater Mekong
subregion 
 Cambodia
 the Lao People’s Democratic Republic
 Myanmar
 Thailand
 Viet Nam
A "WHO Strategy for Malaria Elimination in the

Greater Mekong subregion (2015-2030)" was
endorsed by all 5 countries, as well as China
6/9/2022 AMR-Zoo_TSE_2020 21
 Resistance in HIV
 In 2010  an estimated 7% of people starting
antiretroviral therapy (ART) in developing
countries had drug-resistant HIV
 In developed countries, the same figure was
10–20%
 Some countries have recently reported levels
at or above 15% amongst those starting HIV
treatment, and up to 40% among people re-
starting treatment.
6/9/2022 AMR-Zoo_TSE_2020 22
 Resistance in influenza
 virtually all influenza A viruses circulating

in humans were resistant to one category of
antiviral drugs – M2 Inhibitors  amantadine
and rimantadine
 However, the frequency of resistance to the

neuraminidase inhibitor oseltamivir remains
low (1-2%)
Antiviral susceptibility is constantly

monitored through the WHO Global Influenza
Surveillance & Response System
6/9/2022 AMR-Zoo_TSE_2020 23
Prevention & control
 Antibiotic resistance is accelerated by the

misuse & overuse of antibiotics, as well as
poor infection prevention & control
 Steps can be taken at all levels of society to

reduce the impact & limit the spread of
resistance 
 Individuals
 Policy makers
 Health Proffesional
 Healthcare Industry
 Agriculture Sector
6/9/2022 AMR-Zoo_TSE_2020 24
 Agriculture Sector
 Only give antibiotics to animals under veterinary
supervision.
 Not use antibiotics for growth promotion or to
prevent diseases in healthy animals.
 Vaccinate animals to reduce the need for
antibiotics and use alternatives to antibiotics
when available.
 Promote and apply good practices at all steps
of production & processing of foods from animal
& plant sources.
 Improve biosecurity on farms & prevent
infections through improved hygiene & animal
welfare.
6/9/2022 AMR-Zoo_TSE_2020 25
 The “Global action plan on
antimicrobial resistance” has 5
strategic objectives 
 To improve awareness & understanding of
 To strengthen surveillance & research
To reduce the incidence of infection
To optimize the use of antimicrobial medicines
To ensure sustainable investment in countering

6/9/2022 AMR-Zoo_TSE_2020 26
6/9/2022 AMR-Zoo_TSE_2020 27
Any question ???
6/9/2022 AMR-Zoo_TSE_2020 28
Cysticercosis & Taeniasis
KHI 323 - ZOONOSIS

Cysticercosis-Taeniasis_Soelih_09-2010
6/9/2022 1
genap_SC
INTRODUCTION
Cysticercosis is a systemic illness caused by

dissemination of the larval form of the pork
tapeworm, Taenia solium.
Cause : cysticercus (larval cysts of tapeworm).
Adult tapeworm inside human intestine

Taenia soleum  cyst. cellulosae
Taenia saginata  cyst.bovis/ innermis
6/9/2022 2
genap_SC
• Encystment of larvae can occur in almost any
tissue. Involvement of the central nervous
system (CNS), known as neurocysticercosis
(NCC), is the most clinically important
manifestation of the disease and may present
with dramatic findings.
• Incidence of cysticercosis is increasing within
developed countries.
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SOURCE & TRANSMISSION
By accidentally swallowing pork tapeworm eggs.
Tapeworm eggs are passed in the bowel movement
of a person who is infected.
These tapeworm eggs are spread through food,

water, or surfaces contaminated with feces. This
can happen by drinking contaminated water or
food, or by putting contaminated fingers to your
mouth.
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• A person who has a tapeworm infection can
reinfect themselves (autoinfection).
• Once inside the stomach, the tapeworm egg

hatches, penetrates the intestine, travels
through the bloodstream and may develop
into cysticerci in the muscles, brain, or eyes.
Siklus hidup :
PATHOPHYSIOLOGY
Humans are the definitive hosts of T solium & can carry
an intestinal adult tapeworm (taeniasis), often without
symptoms. Intermittent fecal shedding of egg-containing
proglottids or free T solium eggs ensues, with the
intention that the intermediate host (normally pigs) will
ingest the excreted eggs in contaminated food or water.
T solium embryos penetrate the GI mucosa of the pig
and are hematogenously disseminated to peripheral
tissues with resultant formation of larval cysts
(cysticerci). When undercooked pork is consumed, an
intestinal tapeworm will again be formed, completing
the life cycle of the worm.
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Human cysticercosis occurs when T solium eggs
are ingested via fecal-oral transmission from a
tapeworm host.
The human then becomes an accidental
intermediate host, with development of
cysticerci within organs.
Cysticerci may be found in almost any tissue.

The most frequently reported locations are skin,
skeletal muscle, heart, eye, and most
importantly, the CNS (NCC).
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Symptomatology of NCC  is largely dependent
on the presence of pericystic inflammation,
the absence of which will usually manifest as
asymptomatic disease.
Host inflammatory response to cysticerci

depends on the parasite's ability to evade host
immunity; therefore, inflammation is
restricted to currently degenerating cysts
whose ability to evade host defenses is
faltering.
Lack of inflammation occurs with both healthy cysticerci
and those that have involuted, termed active and inactive
disease, respectively. Upon involution, cysts undergo
granulomatous change and exhibit calcification.
Cysts in various stages of viability can be seen
simultaneously in one host.
In patients with advanced HIV disease &

compromised cell-mediated immunity, NCC may exist
without significant host response & is likely to be
asymptomatic.
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For this reason, in symptomatic patients with CD4
counts under 200 cells/mm3 alternative diagnoses
should be considered more likely.
Clinical manifestations of NCC depend primarily on the
number and location of CNS cysticerci and the host's
immune response to infection.
Serious pathologic findings of NCC  seizures,

obstructive hydrocephalus, meningoencephalitis, and
vascular accidents.
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Involvement of brain parenchyma is common & leads
to the most frequent presentation of seizure or
headache.
Extraparenchymal ventricular & subarachnoid cysts
also are found.
These carry a worse prognosis and often lead to

obstructing hydrocephalus requiring surgical
intervention.
Cysticerci within the basilar cisterns or Sylvian
fissures may become quite large. Those within the
cisterns may also cause serious vasculitis and stroke.
Spinal NCC is rare.
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DISTRIBUTION OF CYSTICERCOSIS
Cysticercosis is found worldwide.
Infection is found most often in rural, developing
countries with poor hygiene where pigs are
allowed to roam freely and eat human feces.
This allows the tapeworm infection to be
completed and the cycle to continue.
Infection can occur, though rarely, if you have
never traveled outside of the United States.
Taeniasis and cysticercosis are very rare in Muslim
countries where eating pork is forbidden.
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l WHO: neurocysticercosis is "the most important
neurological disease of parasitic origin in humans."
l Responsible for rates of epilepsy that are 3 - 6X higher in
endemic countries.
l Affects ~50 million globally.
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Survey of neurologic patients for
cysticercosis (EITB)
Hospital % positive Tot. survey
location
Beijing, PRC (seizure) 44 198
Beijing, PRC (all neurol. adm.) 8 500
Bombay, India (seizure + ?) 32 107
Rwanda 21 34
(epileptic) 271
Mexico 11
(epileptic)
Peru 19 578
(epileptic)
Pork tapeworm
Pork from an infected pig treated (left) & untreated

(right) with a single dose (30 mg/kg) of Oxfendazole
Source: CDC
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Cysticercus pada otot jantung
Cysticercus pada otot daging

SYMPTOMS - 1
Signs and symptoms will depend on the location and
number of cysticerci in your body.
Cysticerci in the muscles:
Cysticerci in the muscles generally do not cause
symptoms. However, you may be able to feel lumps
under your skin.
Cysticerci in the eyes:
Although rare, cysticerci may float in the eye and cause
blurry or disturbed vision. Infection in the eyes may
cause swelling or detachment of the retina.
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SYMPTOMS - 2
Neurocysticercosis (cysticerci in the brain, spinal cord):
Symptoms of neurocysticercosis depend upon where &
how many cysticerci (often called lesions) are found in the
brain.
Seizures, & headaches are the most common symptoms.
However, confusion, lack of attention to people &
surroundings, difficulty with balance, swelling of the brain
(called hydrocephalus) may also occur.
Death can occur suddenly with heavy infections.
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PREVENTION & THERAPY
• Improved living conditions

• Control of livestocks slaughtering
• Health education
• Mass taeniacidal therapy for humans &
animals ie. Oxvendazole for pigs
• Vaccination  pigs
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HYDATIDOSIS & ECHINOCOCCOSIS
KHI 323 - ZOONOSIS

ZOO_Hydatidosis_Soelih_09- 1
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Synonyms :
Echinococcosis, Echinococciasis, Hydatid
disease, Hydatid Cyst
Hydatidosis or larval echinococcosis is the

cystic stage of Echinococcus granulosus, a
very small tapeworm of dogs and other canids.
This parasite has a cosmopolitan distribution

and is very common in parts of Africa, Latin
America and some countries of Southeast Asia.
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Hydatid disease in cattle is caused by the larval
stages of the 2-7 mm long tape worm Echinococcus
granulosus, which lives in the intestines of dogs and
other carnivores.
Several strains of E. granulosus exist, the cattle/dog

strain is primarily responsible for hydatid disease in
cattle.
In Africa hydatid disease is reported more

commonly in cattle that are communally owned or
are raised on free range, and which associate more
intimately with the domestic dogs.
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Hydatidosis in domestic ruminants inflicts
enormous economic damage due to the
condemnation of affected organs and
lowering of the meat, milk and wool
production.
Causative agents :
Echinococcus granulosus
Echinococcus multilocularis
Others  E. vogeli
E. oligarthrus
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Echinococcus granulosus  kista hydatida
(dog, wolf) (human,sheep)
Echinococcus multilocularis  hydatida

(dog,cat,wolf) alveolaris
(human,sheep)
GEOGRAPHICAL DISTRIBUTION:
Endemic areas 
Africa, Australia, South America, Asia,
Canada, Alaska & Some Area in Europe
The most important Endemic Areas 

Northern tundra of Europe & Asia, & its
American extension, Siberia & the Central
Asian Republic of The Russia
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Hydatid cyst pada hati sapi
Hydatid cysts in bovine

heart. Note the detached
germinal layer
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DEFINITIVE HOSTs :
- DOGs
- Wild CANIDs
- FELIDAEs
DOMESTICS CATs  seldom
INTERMEDIATE HOSTs :
Ruminants, Pigs, Horses, Rodents,
Human etc.
ZOO_Hydatidosis_Soelih_09-
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Echinococcus multilocularis
E. multilocularis which normally follows a fox-
rodent cycle in northern Siberia and North
America, is occasionally conveyed to human fur
trappers via fox pelts.
In humans it causes a frequently fatal form of

echinococcosis. The appearance and life cycle of
this cestode closely resemble those of E
granulosus, except for the restricted range and
small number of hosts.
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• The cyst, however, is extremely dangerous as it
lacks the laminated membrane that confines the
cyst of E. granulosus, and develops an invasive,
uncontrolled series of connected chambers
(hence the designation "multiloculate" and the
alternative name alveolar hydatid).
• It therefore resembles a malignant growth,

capable of budding off to cause metastatic
spread.
• The primary cyst usually forms in the liver.

• The disease is usually diagnosed late, when it is
inoperable, and ends fatally.
THE OCCURANCE IN MAN - 1
Hydatid disease (HD) is a world wide zoonosis produced by
larval stage of Echinococcus. There is paucity of literature on
specific findings related to various complications and unusual
anatomic locations.
Peritoneal echinococcosis is almost always secondary to

hepatic disease, although occasional cases of primary
peritoneal hydatid disease have also been reported
Peritoneal echinococcosis usually goes undetected until cysts
are large enough to produce symptoms
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CT scan is modality of choice in detecting
this disease. The unusual clinical
presentation of a case of primary
peritoneal hydatid disease compelled
authors to bring it to the literature to
enhance clinical experience of those
dealing such problem.
THE OCCURANCE IN MAN - 2
Infection caused by the ingestion of the echinococcus eggs 
food contamination & hands
The cysts of E. granulosus may take many years to produce

clinical symptoms. Many cysts are asymptomatic throughout
the infected individual’s life & are only discovered at autopsy,
during surgery, or in radiographs taken for other reasons.
The rupture of a hydatid cyst may induce sudden

anaphylactic shock in a previously asymptomatic individual.
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SOURCE OF INFECTIONS
& ROUTE OF TRANSMISSION :
Per oral  Contamination of food & hands

by Eggs of Echinococcus
1. E. granulosus Domestic transmssion cycle  the dog-
sheep-dog cycle
2. E. granulosus Wild transmission cycle & connection to
the domestic cycle
3. E. multilocularis Transmission cycle
4. E. vogeli Probable transmission cycle
5. E. oligarthrus Transmission Cycle
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LIFE CYCLE OF E. granulosus - 1
There are several types of life cycle of E. granulosus

involving different mammalian species
1. Cycle involves domesticated ruminants and dogs;

2. Cycle involves wildlife species, for example the warthog-
lion cycle in Africa.
3. Cycles involve domesticated animals and wildlife, such as
the dromedary camel-jackal cycle in some regions of sub-
Saharan Africa.
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LIFE CYCLE OF E. granulosus - 2
The infective eggs containing the oncosphere

passed in the faeces are accidentally ingested by
cattle, sheep, pigs, other animals or humans which
act as a intermediate hosts  the oncospheres in
the eggs penetrate the intestine & reach the liver,
lungs and other organs including the brain and
muscles to develop into hydatid cysts at the end of
about 5 months  These cysts measure commonly
5 - 10 cm and contain fluid. Some may reach up to
50 cm in diameter.
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LIFE CYCLE OF E. granulosus
Source : A. Permin and J.W. Hansen - Associate Professional Officer and Animal Health Officer,
respectively, Animal Health Service, Animal Production and Health Division, FAO, Rome.
FAO - Review of echinococcosishydatidosis a zoonotic parasitic disease.htm
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This page - http://www.dpiw.tas.gov.au/inter.nsf/WebPages/CART-6SA36R?open - was last
published on 16 June 2007 by the Department of Primary Industries and Water.
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A. Final host: dog (and other canids)
1.a. Echinococcus granulosus (beside it, the
worm is reproduced approximately half its
natural size)
b. Embryophore, the so-called egg with its six-
hooked larva (oncosphere)
B. Intermediate host: sheep (for E granulosus);

field mouse (for E granulosus): mouse (for E
multilocularis)
2a. Liver with Echinococcus cyst (hydatid stage)
b. Diagram of an Echinococcus hydatid with
daughter cysts and scoleces (compare with III)
c. Humans as the accidental intermediate host
(echinococcosis); the organs most often infected
are the liver and the brain
3-4. Isolated scoleces: invaginated (3), and
evaginated (4) on which the crown of hooklets
and the suckers can be seen
I. Echinococcus multiocularis, sexually mature
worm
II. Human liver infected by the hydatid of E
multilocularis
III. Hydatid cyst of E granulosus opened up;
daughter cysts visible.
Source : Donald Heyneman Medmicro Chapter 89.htm
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Others may produce daughters cysts
The life cycle is completed when a fertile

hydatid cyst is eaten by a definitive host,
the dog or the appropriate carnivore
Cattle and majority of intermediate hosts

show no clinical evidence of infection
However, in humans hydatid cysts can
cause serious disease
The diagnostic features of a
hydatid cysts
concentrically laminated thick outer layer within

which is a germinal layer
The Fertile hydatids  the germinal layer is

granular & has brood capsules each containing
protoscoleces. When brood capsules become
detached and float free in the cysts fluid they are
referred to as hydatid sand.
In some animals a fair proportion of hydatid may be
sterile.
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• Early radiologic imaging by US, CT, or MR
is essential.
• Serological tests, particularly with purified
E. multilocularis antigens, are sensitive
and highly specific.
• Treatment with mebendazole, albendazole
or praziquantel, and surgery should follow.
POST MORTEM FINDINGS IN CATTLE
Hydatid cysts as described are found in :

1. Liver, heart, lungs, spleen, kidneys
2. Muscle and brain
3. Any tissue including bone
JUDGMENT
• Carcass showing emaciation, edema and muscular
involvement is condemned and destroyed
• Otherwise the carcass is approved
• Affected viscera and any other tissue are also
condemned and destroyed
• Burying of carcass is not sufficient, since dogs may
retrieve the affected organs
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Peritoneal Hydatidosis
At laparotomy the subhepatic cyst was identified as huge ovarian cyst arising from right ovary
with one and a half turn around its pedicle
Source: Fazal Q. Parray, Mushtaq A. Gagloo, Asif Hamid Bhat, Nisar A. Chowdri, M. Muzamil Noor:
Peritoneal Hydatidosis. The Internet Journal of Surgery. 2007. Volume 9 Number 2.
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PERITONEAL HYDATIDOSIS
suggested possible diagnosis of
carcinoma ovary.
1 2 3
A 48 yrs old female presented with gradually increasing abdominal distention of two years duration.
Anorexia and weight loss were associated complaints. There were no jaundice, bowel or bladder
complaints. On clinical examination the distended abdomen was soft, non tender, no shifting dullness
and multiple small, firm nodular swellings in abdominal cavity with restricted mobility and minimal
movement with respiration (1).
Serologic work up was negative for E. granulosus and serum CA-125 was within normal limit.
Abdominal exploration revealed multiple cystic swellings with daughter cysts involving every
intraabdominal organ except intestine (2). Debulking surgery (3) followed by chemotherapy with
praziquantel and albendazole made uneventful but prolonged recovery. Patient is asymptomatic at eight
months follow up.
Source: Rajesh Godara, Ashish Dhingra, Vivek Ahuja, Pradeep Garg & Jyotesna Sen: Primary Peritoneal
Hydatidosis: Clinically Mimicking Carcinoma Of Ovary: The Internet Journal of Gynecology and
Obstetrics. 2007; Volume 7, Number 2
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Left kidney showing open hydatid cyst (black arrows); fragments of germinal membranes
with daughter cysts are also visible (white arrow).
Source: MILAD CHRIEKI, Echinococcosis--An Emerging Parasite in the Immigrant Population -

September 1, 2002 - American Family Physician.htm
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Alveolar hydatid cysts are
formed in the livers of rodents.
Brood capsules with
protoscoleces are seen in
some small cysts, while many
minute cysts contain no
protoscoleces
(PAS-haematoxylin stain)
Source: Yuzaburo OKU1, Junichi Watanabe2, Chihiro SUGIMOTO3, Nariaki NONAKA1, Jun MASTUMOTO1, Hiroyuki
WAKAGURI4, Yutaka SUZUKI4, Sumio SUGANO4, Atsushi TOYODA5, Yoshiyuki SAKAKI5, and Masao KAMIYA6
(1Graduate School of Veterinary Medicine, Hokkaido University, 2Institute of Medical science, The University of
Tokyo, 3Research Center for Zoonosis Control, Hokkaido University 4Graduate School of Frontier Science, The
University of Tokyo 5RIKEN Genomic Sciences Center, RIKEN 6OIE Reference Laboratory, Department of
Biosphere and Environmental Sciences, Faculty of Environment Systems, Rakuno Gakuen University ) . About this
Database : Echinococcus Full-Length cDNA project. Last updated July 10, 2006.
Echinococcosis Full-Length cDNA ProjectZOO_Hydatidosis_Soelih_09-
(Echinococcus multilocularis).htm 28
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Flies and possibly other insects may mechanically transport
eggs over considerable distances, having been contaminated
during feeding or egg-laying activities in or on the dung
(Lawson and Gemmell, 1985).
The survival of the infective egg is influenced by

environmental factors, such as humidity and temperature.
Eggs may survive for several months under moist conditions
and moderate temperatures, desiccation is detrimental and
they will only survive a short time when exposed to direct
sunlight and dry conditions.
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• The number of infective eggs ingested by
the intermediate host is therefore
determined by the level of contamination
and the infectivity of the eggs.
• Furthermore, the number of eggs that

develop into hydatid cysts is controlled by
the immune system of the host (Thompson
and Allsopp, 1988).
TREATMENT
A number of anthelmintic drugs have proved to be effective against

adult stages of E. granulosus in
DH  The best drug currently available is PRAZIQUANTEL  for all
juvenile and adult echinococci from dogs (Schantz, 1982; WHO 1992).
SURGERY is the treatment of choice at present
IH  BENZIMIDAZOLE COMPOUNDS have been shown to have
efficacy against the hydatid cyst in the intermediate host
Long-term treatment w/ ALBENDAZOLE  has a particularly marked

effect on the cysts (Morris et al., 1990; McManus and Smyth, 1986)
Long-term treatment w/ PRAZIQUANTEL  only has a limited effect

with few changes in the germinal layer of the cyst
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KHI 323 - ZOONOSIS
Departemen KESMAVET
FKH – UNAIR 1
Sejarah
●Toxoplasmosis adalah penyakit protozoa sistemis
yang menyerang semua hewan berdarah panas
● Disebabkan oleh Toxoplasma gondii
● Ditemukan pertama kali oleh Nicole dan
Manceaux th. 1909
● Sebagai penyakit zoonosa ditemukan oleh
Dr. Joseph Janku  kista pada retina pada anak
terserang hidrosefalus
● Th. 1937 Wolft dan Cowen menemukan
ensefalitis granulomatosa konginental
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HOST GEOGRAPHIC
• Definitive host : famili kucing.
• Intermediat host : mammalia berdarah
panas atau burung.
• Di seluruh dunia.
• Jarang terjadi pada hewan dengan
ekstrem temperatur
Parasit ini ada 3 bentuk :
1.tachyzoite bentuk proliferatif, dikenal sbg

tropozoit
● akan dihancurkan oleh cairan pencernaan
dlm bbrp menit
● berbentuk bulan sabit, pj 5-8 mikron, lebar 2-
5 mikron
● memperbanyak dg cara membelah diri
● berubah menjadi kista pd fase kronis
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2. Bradyzoit
● dibentuk dlm jaringan pd fase kronis
● lebih tahan dibanding tropozoit
● dlm daging tahan selama 68 hr pd suhu -4
C, mati pd suh 50 C slm 30 mnt
● Bentuk lonjong ukuran 10-100 mikron
3. Oosyst
● hanya terbentuk di usus halus kucing
● berbentuk oval, ukuran 10-12 mikron,
diploid dilindungi dinding yg kuat
● terjadi sporulasi
● penting untuk penularan, keluar lewat feses
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Siklus hidup ada 2 cara :
1. Reproduksi seksual
● terjadi pada selaput lendir usus kucing
● reproduksi terjadi secara pembuahan
2. Reproduksi aseksual
● terjd pd semua binatang induk semang
perantara termasuk manusia
● reproduksi secara membelah diri
● hasil pembelahan masuk kesemua sel
otot dan syaraf
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Life Cycle
Two Phases
Sexual
Asexual
SIKLUS HIDUP SEKSUAL
• Kucing terinfeksi karena makan oocyst atau makan
intermediate host.
• Bradyzoits atau sporozoits masuk kedalam sel usus
kecil.
• Parasit menjadi aseksual seperti pada reproduksi
seksual (Reproduksi seksual hanya pada kucing)
• Oocyst dihasilkan dari reproduksi seksual.
• Kucing mengeluarkan oocyst pada fesesnya.
• Oocyst menjadi infektif setelah 24 jam (sporulasi)
• Oocyst dapat termakan oleh intermediate host.
SIKLUS HIDUP ASEKSUAL
• Bradyzoit atau oocyst termakan oleh intermediate
host dan menginfeksi makrofag dari mukosa usus
halus.
• Didalam makrofag, tropozoit berkembang.
• Tachyzoit didistribusikan ke seluruh tubuh hewan.
• Setelah beberapa minggu parasit membelah
secara perlahan dan memproduksi zoitocyst
dalam bradyzoit (fase inaktif yg terbentuk setelah
terjadinya respon immun)
• Intermediate yg terinfeksi dapat termakan oleh
definitive host atau intermediate host yg lain.
SUMBER INFEKSI
• Tidak sengaja termakan feses kucing terinfeksi.

• Makanan atau peralatan yg tercemar daging
mentah.
• Air minum yang tercemar.
• Penerima tranplantasi organ yang terinfeksi
atau transfusi darah (jarang)
Sumber infeksi
• Sumber oocyst :
- domestik (kucing, anjing), kucing liar.
- rodensia : tikus.
• Lingkungan (tanah) jika lembab :
- reservoar dari oocyst yg infektif.
• Intermediate host :
- Reservoar dari cyst infektif dalam jaringan
(sapi, domba, kelinci)
• Siklus pada manusia :
- Infeksi :
- termakan oocyst yg infektif (feses kucing yg > 4 hari)
- termakan bradyzoit dan tacchyzoit pada daging setengah
matang
- darah atau jaringan yg mengandung “zoites”
- kongenital dengan transplasental trachyzoit
- Stadium proliferatif pada manusia :
- Tachyzoit hasil dari semua tahapan.
- Bradyzoit sumber dari pseudocyst sebagai IgG.
Kucing induk semang definitif dari T. gondii.
Kucing terinfeksi toxoplasma :
1. Oocyst infektif yang ada di alam
2. Cyst yang ada pada jaringan organ
3. Tachyzoite ada dicairan rongga perut
Kucing akan menghasilkan oocyst yang

dikeluarkan dlm tinja dalam 20 hr atau lebih bila
yang termakan oocyst, 3 – 10 hr kmd bila yang
termakan cyst jaringan, dan 19 hr bila yang
termakan tachyzoite
Oocyst tahan 184 hr terbuka kena sinar matahari

334 hr terbuka dlam perlindungan
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Kucing
• Kucing merupakan spesies hewan yang
menyebarkan stadium infeksius dalam
feses.
• Semua hewan dapat menularkan
Toxoplasmosis jika makan daging yang
terinfeksi.
• Kucing tertular karena makan rodent,
daging mentah, kecoak, serangga atau
karena kontak kucing terinfeksi, terinfeksi
feses kucing dan tanah yg terinfeksi.
Cara penularan
1. Acquired infection
• Makan daging mentah
• Sayuran yang mengandung ooccyst
• Peneliti
• Tranfusi darah
• Transplantasi organ
2. Congenital infection
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Gejala pada manusia
• Symptoma Toxoplasma jarang terjadi pada individu
normal normal.
• Kejadiannya serius pada wanita hamil dan manusia
dengan immunodeficient.
• Infeksi Kongenital  terjadi pada 1-5 per 1000
kehamilan, dimana 
– 5-10% mengakibatkan miscarriage,
– 10-13% bayi kesulitan penglihatan.
– Walaupun 58-70% wanita yg terinfeksi dapat
melahirkan normal, ttp sebagian bayi yg
dilahirkan menderita retino-chorditis atau mental
retardation pada anak2 atau remaja.
Symptoms in MAN - 2
• Ketika mereka dewasa  flu-like

symptoms, kadang2 bersamaan
dengan lymphadenopathy.
• Pada immunocompromised individuals
 infeksi secara umum menyebabkan
parasitemia pada otak, hati, paru2 dan
organ2 lain, seringkali menyebabkan
kematian.
Symptoms in ANIMALS
T. Gondii dapat menyebabkan penyakit pada kucing dan anjing 
lebih sering pada kucing.
S/ in pets 
• Demam, kehilangan nafsu makan dan depresi
• Gejala yg terjadi tergantung pada infeksi akut atau khronis dan
predileksi kista pada 
- Keradangan mata
– Pneumonia
– Arythmia cordis
– GI Tract muntah, diarrhea, sakit perut & jaundice
– Pada CNS  seizures, paralysis & hilangnya fungsi syaraf
– Pada otot  langkah kaku & lemas
– Anak kucing mungkin lahir dalam keadaan mati atau sakit.
Pada domba  Toxoplasmosis dapat menyebabkan ABORSI
Symptoms in ANIMALS - 2
Seperti pada manusia  pada hewan toxoplasmosis

terjadi pada hewan dengan supresed immune
sytems
Kucing w/ toxoplasmosis dapat terinfeksi juga dengan
beberapa virus seperti 
– Feline leukemia virus (FELV);
– Feline Immnunodfficiency Virus (FIV)
– Feline Infectious Peritonitis (FIP)
Anjing w/ DISTEMPER  dapat menderita
immunodefficiency & infeksi T. gondii
Patogenesis/Symptoma klinis
• Semua kasus asimptomatis
• Gejala menyerupai flu, pembengkakan
limfoglandula dan rasa sakit pada otot.
• Hepatitis, pneumonia, kebutaan dan
kelainan syaraf (infeksi akut)
- terutama pada individu dengan
compromised immune systems (AIDS)
Perjlnan klinis toxoplamosis ada 3 fase
1. Fase pertama
● Parasit beredar dlm ibu hamil, mperbnyk
diri dan merusak sel induk semang
● membentuk antibodi
2. Fase ke dua
● peningkatan antibodi
● parasit berkembang pd jar yg antibodi
rendah
3. Fase ke tiga
● infeksi kronis, terbentuk kista pada jar
otot dan syaraf
2010 genap
Kesehatan Masyarakat
• Resiko bagi ibu hamil dan bayi :
- Jika ibu terinfeksi lebih dulu sebelum hamil,
maka tidak ada resiko fetal transmission.
- Jika ibu terinfeksi selama hamil, fetus
beresiko (kongenital toxoplasmosis).
- Infeksi foetus dapat mengakibatkan aborsi
secara spontan.
- 70% bayi yang lahir kongenital toxoplasmosis
menunjukkan asymptomatis, tetapi 8%
menunjukkan kelemahan CNS.
Derajad kefatalan toxo pada ibu hamil
1. Infeksi trimester I (16 minggu)
14 % terkena : retino chorioditis, Pengapuran
otak, hidrocephalus dan retardasi mental
2. Infeksi trimester II (>16 sd 28 mgg)

29 % terkena :
Jaringan parut pada retina mata
Pengapuran pada kepala
Tidak ada gangguan mental
3. Infeksi trimester III (> 28 mgg)

Memberikan kelaianan ringan
2010 genap
Diagnosis Toxoplasma pd MANUSIA
• Morphologic test of T. gondii
• Culture or animal inoculation  rare
Isolasi parasit dari darah atau cairan tubuh,
dengan inokulasi intraperitoneal pada mice
atau tissue culture.
• 6 – 10 hari post inoculasi  diuji keberadaan
Toxoplasma dalam cairan peritoneal  jika
tidak dijumpai organismenya, dilakukan uji
serologis, 4 - 6 weeks setelah inokulasi.
• Serologic (terpenting)
• PCR  Deteksi material genetik dari parasit,
terutama mendeteksi infeksi kongenital pada
uterus.
Diagnosis/Pengobatan
• Diagnosis pada manusia berdasarkan tes
laboratorium.
- Biopsi
- ELISA
• Pyrimethamine dan Sulfonamide diberikan
bersama.
Pencegahan Toxoplasmosis pada
HEWAN
• Jangan memberi makan hewan  daging atau tulang
mentah  jangan mebuang kedalam sampah
• Jangan memberi pets  susu mentah.
• Jangan membiarkan pets berkeliaran untuk mencegah
terinfeksi oleh tikus atau burung.
• Bersihkan feses dari litter box setiap hari &  bakar atau
semprot
• Bersihkan litter boxes berkala dengan air panas
• Jangan biarkan anjing berhubungan dengan litter boxes
Pencegahan
1. Masaklah daging secara sempurna atau simpan
suhu beku pada -14 °C jika akan dimasak
setengah matang
2. Cucilah sayur2an
3. Biasakan mencuci tangan sblm makan
4. Kurangi jumlah kucing liar
5. Bersihkan alas kandang setiap hari
6. Khusus ibu hamil periksa secara rutin
2010 genap
DEPARTEMEN KESEHATAN MASYARAKAT VETERINER
FAKULTAS KEDOKTERAN HEWAN - UNAIR
FASCIOLIASIS
 Synonym : Hepatic Distomiasis,

Fasciolosis
 Ettiology : Fasciola hepatica dan

Fasciola gigantica
Ciri-ciri
 Suatu trematoda yang hidup di dalam
saluran empedu dari hewan herbivora
peliharaan maupun yang liar dan
kadang-kadang ditemukan pada
manusia. Bentuk F. Hepatica pipih
seperti daun salam, dengan ukuran
panjang 2,5 – 3 cm dan lebar 1,3 cm
berwarna kecoklatan
Siklus hidup
 Telur dari cacving dewasa terbawa oleh
empedu ke dalam saluran usus dan
dikeluarkan dari tubuh hewan melalui feses.
 Perkembangan telur tergantung pada
keadaan kondisi kelembaban dan suhu.
 Pada musim panas masa inkubasi telur
singkat yaitu dalam beberapa minggu timbul
miracidium (larva) dari telurnya sedangkan
pada suasana dingin baru muncul setelah
beberapa bulan.
 Daya tahan Telur cacing ini di alam
sangat tinggi yaitu dapat tetap bertahan
hidup di dalam feses selama 1 tahun.
 Daya tahan miracidium sangat lemah

dan harus menemukan host baru dalam
kurun waktu 8 jam. Host perantara
berupa siput dari familia Lymnaeidae
 Setelah Miracidium masuk ke dalam siput
berubah menjadi Sporocyst dan 3 minggu
kemudian menghasilkan Redia atau dapat
langsung berubah menjadi Cercaria.
 Bila keadaan lingkungan mendukung maka

cercaria dalam 6 minggu keluar dari siput,
tetapi bila suhu lingkungan di bawah 10 oC
maka stadium larva di dalam siput dapat
diperpanjang hingga 100.
 Setelah meninggalkan siput, cercaria
berenang di dalam air dan membentuk
cyste pada tanaman.
 Di dalam cyste berkembang menjadi

metacercariae dan dapat bertahan lama
disana bila keadaan lingkungannya
basah namun bila keadaan kering tidak
dapat bertahan lama.
 Matacercaria masuk ke dalam tubuh host
definitif karena termakan tanaman atau air
yang mengandung metacercaria.
 Di dalam duodenum larva membebaskan

diri dari amplop cyste, kemudian
menembus dinding usus masuk ke dalam
rongga perut dan parenchym hati menuju
saluran empedu dan menjadi dewasa
disana.
 Periode prepatent (dari infeksi hingga
pertama kali ditemukan telur di dalam
feses) memakan waktu 2 bulan.
 F. hepatica dapat hidup di dalam saluran

empedu untuk beberapa tahun.
LIFE CYCLE of F. hepatica - 4
6/9/2022 Fascioliasis_Zoo_Soelih_2011 10
LIFE CYCLE of F. hepatica - 4
Life Cycle of Fasciola hepatica has minimum duration 4-5 months

Prepatent period 10-12 weeks
6-8 weeks development in snail

Source : Mark Crawshaw & George Mitchell, SAC Veterinary Services, Ayr
Kejadian pada manusia
 Fasciola pada manusia terjadi secara

sporadis atau pernah terjadi kasus
wabah di beberapa negara di Amerika,
Eropa, Afrika dan Asia. Infeksi pada
manusia biasanya bersifat subklinis atau
dengan tanda klinis yang sangat ringan.
Kejadian pada hewan
● Fascioliasis merupakan penyakit umum pada
domba, kambing dan sapi di banyak tempat di
dunia.
● Pada daerah yang endemik kejadian penyakit
ini dapat mencapai 50 %.
● Kerugian produksi sapi menurun hingga 8 %
sedangkan pada keadaan infeksi berat dapat
mencapai 20 %.
● Penurunan produksi wool domba berkisar
antara 20 – 39 %
Penyakit pada manusia
 Parahnya penyakit ini tergantung jumlah
infeksi Faciola dan lamanya infeksi.
 Akibat migrasi Faciola muda di dalam
parenchym hati menyebabkan nekrosis.
 Di dalam saluran empedu Fasciola dewasa
menimbulkan keradangan, adenomatosa
dan fibrosis.
Egg of F. hepatica in stool
Infected liver w/ F. hepatica Adult F. hepatica
 Bila jumlah fasciola di dalam saluran
empedu sangat banyak dapat
menimbulkan penyumbatan saluran
empedu (billiary stasis), atrofi hati dan
cirrhosis periportal. Bila kasusnya sudah
kronis maka terjadi Cholecystitis dan
Cholelithiasis.
 Fase permulaan infeksi tanda klinisnya adalah
demam, kelesuan, pembesaran hati, nyeri
pada daerah rusuk kanan, eosinophilia dan
perubahan fungsi hati (pada uji patologi klinik).
 Pada fase kronis ditandai dengan manifestasi
hepatobiliary, demam, anemia dan eosinofilia.
Juga kadang-kadang terjadi nyeri lambung,
dyspepsia, berat badan berkurang, diare dan
demam terdapat juga jaundice (warna
kekuning-kuningan).
Penyakit pada hewan
 Bentuk akut
- Metacercaria yang menginvasi dan migrasi
di dalam parenchym hati.
- Akibat migrasi ini menyebabkan
hemorrhagia, hematoma dan robeknya hati,
keradangan hati dan saluran empedu dan
rusaknya jaringan hati.
- Domba yang terkena ini dapat mati dalam
1 – 2 hari
 Bentuk kronis
- berkembang pelan dan ditandai dengan
turunnya berat badan, kekurusan
(emaciation), oedema submaxillar,
anemia, kelemahan (debility) diare dan
asites.
- Sapi lebih tahan terhadap fasciola
daripada domba kecuali pedet muda.
- Infeksi pada angsa bersifat
asymptomatik demikian pula pada kuda.
Sumber infeksi dan cara penularan
 Tergantung pada siklus hidup siput yang
bertindak sebagai intermediate host.
 Sifat-sifat komposisi tanah dan faktor iklim.
 Fasciola dpt ditemukan ketinggian di atas 3700
meter.
 Lymnaea dapat dibagi menjadi 2 type yaitu
1. terfokus (reservoir) pada daerah basah
seperti sungai kecil, danau, rawa tempat
dimana siput berkembang biak. Biasanya
populasi lymnaea di daerah ini adalah uniform
dan dalam jumlah yang sedikit.
2. tersebar luas di daerah-daerah karena
konsentrasi lymnaea disuatu daerah
tinggi dan terbawa air/banjir/hujan.
 Manusia dapat terkena penyakit ini

karena suatu peristiwa tertelannya
metacercaria
Pengendalian
 Tidak mengkonsumsi sayur yang daerah

asalnya tidak diketahui atau berasal dari
pinggiran sungai (tanaman liar).
 Bahan kimia untuk membunuh Fasciola seperti
hexachlorethane, carbon tetrachloride,
hexachlorphene bithionol (untuk manusia),
oxyclozanide, nitroxynil, triclabendazole (untuk
hewan).
 Pemusnahan siput menggunakan bahan kimia
dan biologis.
 Pengeringan tanah (area)
TRICHINOSIS
KHI 323 - ZOONOSIS

Departemen KESMAVET
FKH – UNAIR
09/06/2022 Trichinosis_Zoo_Soelih-2011 1
Synonims :
TRICHINELLOSIS, TRICHINIASIS
 is a parasitic disease caused by

eating raw or undercooked pork or wild
game infected w/ the larvae of
roundworm T. spiralis, commonly called
the trichina worm.
Causative Agent
There are 8 Trichinella species  5 species are
encapsulated & 3 are non-encapsulated.
• Previously there are 3Trichinella species are known

to cause trichinosis  T. spiralis, T. nativa, & T. britovi
•The few cases in the US are mostly the result of

eating undercooked game, bear meat, or home-reared
pigs.
•It is common in developing countries where meat fed
to pigs is raw or undercooked
•Many cases also come from developed countries in
Europe and North America  raw or undercooked
pork and wild game may be consumed as delicacies.
Recently ………
• T. spiralis  intestinal nematode of many wild
and domestic carnivores & omnivores
• T. nativa  Arctic bears
• T. pseudospiralis  mammals & birds
• T. nelsoni  African predators & scavengers
• T. britovi  carnivores in Europe & Western
Asia
Occurance in the World
– worldwide, most common in

Europe & US
– incidence rate: ≤ 2%
Life cycle
– larva released from ingested cyst
– invade mucosa of small intestine where
they develop into adults
– after 4 weeks (life span in intestine),
females release larva that migrate to
striated muscle
– encystment complete in 4-5 weeks
• note: T. pseudospiralis does not encyst
– may remain viable for several years
Life cycle - 2
Source & Route of Transmission
• Reservoir 
– swine, dogs, cats, rodents, many wild
animals, especially bears, boars,
marine mammals, and large felids
• Transmission 
ingestion of raw or undercooked meat
• pork & pork products
• bear meat
• marine mammal meat
• hamburger adulterated with pork
A number of infections have been traced to contaminated bear meat.
SYMPTOMS IN MAN
• Incubation period:
– generally 8-14 days; up to 45 days
• Symptoms:
– from inapparent to highly fatal
– Initial symptoms include nausea, diarrhea, vomiting,
fatigue, fever, & abdominal discomfort.
– myalgia
– edema - periorbital and facial edema
– conjunctivitis
– fever
– eosinophilia
– gastrointestinal - diarrhea, pain, vomiting
SYMPTOMS IN MAN - 2
• Life threatening
symptoms 
– myocarditis
– CNS
involvement
– pneumonitis
SYMPTOMS IN MAN - 3
Image 140_09. Trichinellosis (Trichinella spiralis) Here the parasitic disease Trichinosis is manifested by
splinter hemorrhages under the finger nails. Trichinosis, or trichinellosis, is caused by eating raw or
undercooked pork infected with the larvae of a species of worm called Trichinella. Initial symptoms
include nausea, diarrhea, vomiting, fatigue, fever, and abdominal discomfort.
Red Book Online Visual Library, 2009. Image 140_09. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
SYMPTOMS IN MAN - 4
Image 140_05. Trichinellosis (Trichinella spiralis) Trichinella spiralis organisms on cross section of muscle
biopsy of the patient in images 140_03 and 140_04.
SYMPTOMS IN MAN - 5
Image 140_06. Trichinellosis (Trichinella spiralis) This patient with trichinosis had periorbital swelling,
muscle pain, diarrhea, and 28% (0.28) eosinophils.
DIAGNOSIS in MAN
• Serology
– EIA
• ES (excretory-secretory) products - TLS-1
surface antigens conserved in all species,
can be used for detection in animals or
humans
• Ab levels not present until 3-5 weeks post
infection - IgM, IgG, IgE; peak in 2-3 months
• IgG most sensitive
• used for routine screening
– Bentonite flocculation
• Muscle biopsy
• Microscopic examination
Larva from Alaskan bear Larva in cyst from muscle
DIAGNOSIS in MAN - 2
Diagnosis: detection of larvae in muscle
Trichinella spiralis larvae in muscle section.
A larva in a "teased muscle" preparation.
TREATMENT for MAN
• Anthelmintics
– mebendazole (Vermox®)
– only effective against intestinal stages,
not encysted stage
• Corticosteriods
– decrease severity of symptoms during
muscle invasion phase
PREVENTION for MAN
• Proper cooking of pork and pork products
and meat from wild animals
– internal temperature should reach 160ºF
(71ºC)
• Irradiation of food effective

– low level gamma - sterilization
– higher levels - effectively kills trichinae
• Freezing will inactivate larvae of T.

spiralis but not of T. nativa (arctic strains)
PREVENTION for MAN - 2
• Larvae may be inactivated by the heating, freezing (caution), or
irradiation of raw meat.
• Freezing may only be effective for T. spiralis, since some other
species, such as T. nativa, are freeze resistant & can survive long-term
freezing.
• Unsafe and unreliable cooking of meat includes the use of
microwave ovens, curing, drying, & smoking, as these methods are
difficult to standardize & control.
• Cooking meat products to an internal temperature of 165 °F (74 °C)
for a minimum of 15 seconds.
• Freezing pork < 6 inches thick for 20 days at 5 °F (−15 °C) or three
days at −4 °F (−20 °C) kills larval worms.
Cooking wild game meat thoroughly.
• Freezing wild game meats  unlike freezing pork products, even for
long periods of time, may not effectively kill all worms  the species
of trichinella that typically infects wild game is more resistant to
freezing than the species that infects pigs.
PREVENTION for MAN - 3
The CDC’s recommendation 

"Curing (salting), drying, smoking, or
microwaving meat does not consistently kill
infective worms.“
However, under controlled commercial food
processing conditions some of these methods
are considered effective by the USDA
PREVENTION for ANIMALS
• Hygienic pig farming
• Cooking all meat fed to pigs or other wild
animals.
• Keeping pigs in clean pens with floors that can
be washed (such as concrete).
• Not allowing hogs to eat uncooked carcasses of
other animals, including rats, which may be
infected with trichinosis.
• Cleaning meat grinders thoroughly when
preparing ground meats.
• Control & destruction of meat containing
TRICHINIAE, e.g., removal & proper disposal of
porcine diaphragms prior to public sale of meat.
Protozoan infections
KESMAVET
Malaria
• AGENT : Plasmodium spp. ( P.
cynomolgi, P. knowlesi, P. inui P.
schwetzh P. simium, P. bmzilhnum)
• Syndrome:
• Human: cyclical febrile periods
accompanied by chills, sweating, and
headache.
• Animal: with the exception of P.
bradianum, which can be fatal,
• most infections of nonhuman primates
are mild versions of the human form.
• Incubation : 10-30 days, months.
• Case fatality rate: None. Recovery is
spontaneous.
• Confirmatory tests: Microscopic,
Giemsa-stained thick blood smear
• Occurrence: Africa, Asia, Latin
America.
• Transmission: anopheline mosquitoes.
• CONTROL AND PREVENTION
• Individual / herd: Treat with chloroquine
or amodiaquine. Use repellents.
• Local community: Mosquito control,
screening.
• National / internationaI: None.
Amebiasis [Entamoeba histolytica]
• Entamoeba histolytica is well recognized
as a pathogenic ameba, associated with
intestinal and extraintestinal infections.
• E. dispar, E. moshkovskii, and E.
bangladeshi, are generally not associated
with disease although investigations into
pathogenic potential are ongoing
• E. histolytica may be observed with ingested
red blood cells (erythrophagocytosis); E.
dispar may occasionally be seen with ingested
erythrocytes as well, although its capacity for
erythrophagocytosis is much less than that
of E. histolytica. Non-pathogenic
amebae (e.g. Endolimax nana, Iodamoeba
buetschlii, other Entamoeba species) are
important because they may be confused
with E. histolytica in diagnostic investigations.
• Geographic Distribution
• Pathogenic Entamoeba sp. occur
worldwide and are common in fresh water
contaminated with human feces. The
majority cases in developing countries.
• In industrialized countries, risk groups
include men who have sex with men,
travelers, recent immigrants,
immunocompromised persons, and
institutionalized populations.
• Clinical Presentation
• The majority of infections restricted to the
lumen of the intestine (“luminal amebiasis”) are
asymptomatic. Amebic colitis, or invasive
intestinal amebiasis, occurs when the mucosa is
invaded. Symptoms include severe dysentery
and associated complications. Severe chronic
infections may lead to further complications
such as peritonitis, perforations, and the
formation of amebic granulomas (ameboma).
• Amebic liver abscesses , Pleuropulmonary
abscess, brain abscess, and necrotic lesions on
the perianal skin and genitalia.
• Occurrence in Animals:
• relatively common in nonhuman primates., dogs
and rats, and on occasion from naturally infected
cats and swine, cattle
• Experimental infections have been in numerous
rodents (mice, rats, guinea pigs, hamsters, and
jerboas) and also in rabbits
• Confirmatory tests:
• Microscopic examination of fresh feces
from diarrheic patients for trophozoites or
cysts in feces of asymptomatic
individuals.
• Treatment with an amebicide is
diagnostic when clinical signs are
reduced.
• Radiology and/or test serum by
hemagglutination for evidence of
extraintestinal infection.
Balantidiasis
• AGENT : Balantidium coli
• Syndrome: Human: Colic, tenesmus,
nausea, vomiting, diarrhea. In severe
cases-anorexia, bloody dysentery, and
weakness.
• Infection is often asymptomatic.
• Animal: Usually subclinical.
• Incubation period: Probably 3-4 days.
• Occurrence: Worldwide. Swine, as well
as rats, dogs, and nonhuman primates
serve as major sources of infection for
humans.
• Transmission: Consumption of water or
vegetables contaminated with feces from
infected animals.
• Direct fecal-oral transmission of cysts
from asymptomatic humans.
• Contlrmatory tests: Microscopic
examination of fresh feces from
diarrheic patients for trophozoites or cysts
in feces of asymptomatic.
• Individual herd: Treat with
metronidazole.
• Personal hygiene should include
thorough cooking of food and boiling of
water possibly contaminated with pig
feces.
Cryptosporidiosis
• AGENT : Cryptosporidium spp. (C. parvum,
possibly others).
• Syndrome: Human: Abdominal pain, nausea,
watery diarrhea lasting 3-4 days.
• In immunodeficient or immunosuppressed people,
the disease is severe, with persistent diarrhea (6-
25 evacuations per day) and maladsorption of
nutrients.
• Animal: Normally a clinical disease only
among young.
• Gastroenteritis and diarrhea in ruminants.
• A respiratory syndrome among chicken
and turkey poults.
• Incubation period: 3-7 days.
• Case fatality rate: In normal persons the disease
is self-limiting.
• In immunocompromised individuals, disease is
severe and case fatality rate may be high.
• Confirmatory tests: Microscopic examination of
fresh feces for the identification of oocysts.
• Transmission: Oocysts are infective when
passed in feces. Not species specific (strain
from one animal can infect many other
species).
• Fecal-oral transmission from infected animals
or humans.
• Individualberd At present there is no effective
treatment.
• Good personal hygiene. Immunocompromised
individuals should avoid contact with diarrheic
animals or people.

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ZOONOSES

Over 200 ZOONOSES have been described since many

HOW IMPORTANT ? 1. Dangerous

3. Effect to the public

II. LIFE CYCLE OF THE CAUSATIVE AGENT  1. DIRECT ZOONOSES

III. CAUSATIVE AGENT  1. BACTERIOSES

CYCLO ZOONOSES VERTEBRATE-1 VERTEBRATE-2

An infection or infestation shared in nature by humans and other animals.

 anthropozoonosis , cyclozoonosis , metazoonosis , saprozoonosis ,

 Combination terms may be used

• In 1920 RINDERPEST occurred unexpectedly in

The United Nations, which replaced the League of

• 1952 Official agreement between the OIE and the

• On 30 January 1928, the first Conference met in

Recognizing that human health (including mental

Executive Summary JAVMA One Health Initiative Summary Report

Lagomorph diseases Bee diseases

Crustacean diseases Other diseases

Crustacean diseases Other List B diseases

ZOONOSIS - KHD 302

INFLUENZA  A Viral Non Food Borne Disease - ZOONOSIS

• Natural reservoir  AQUATIC BIRDS Virus Influenza A

Courtesy of Linda Stannard, University of Cape Town, S.A.

Main Antigen is a surface

18 HEMAGLUTININ H1- H18

Slide courtesy of Dr. David Wentworth

1. Tong S, et al. (2012) A distinct lineage of influenza A virus

The HA of the bat virus was estimated to have

The neuraminidase (NA) gene is highly

Despite its divergence from known influenza A viruses

UPDATE ON HIGHLY PATHOGENIC AVIAN INFLUENZA IN ANIMALS

Last report received on 6 March 2015

• ANTIGENIC SCHIFT & ANTIGENIC

The three mechanisms used by influenza

The three mechanisms used by influenza

A. ANTIGENIC DRIFT  errors during the replication of

ANTIGENIC DRIFT  errors during the replication of influenza v. which are

REASSORTMENT or ANTIGENIC SCHIFT  the exchange of ribonucleic acid

RECOMBINATION  2 different source of RNA contribute to a single

Li, K.S., Y. Guan, J. Wang, G.J.D. Smith, K.M. Xu, L.

The colour coding of the schematically shown

Aso called as “point mutation” of gene HA causing a “minor HA

Highly Pathogenic Avian Influenza Viruses (HPAI)

• Virus shedding through RESPIRATORY TRACT & FAECES

Highly Pathogenic Avian Influenza Viruses (HPAI)

STILL CIRCULATE TODAY

Virus has gene combination

1968 - 1969 “HONG KONG FLU”

 H1N1  emerged in Mexico April 2009

 Structure of the virus is different from 1918-

 WHOSince June 2009

Avian virus Quail/HK/G1/97 (H9N2)

AVIAN INFLUENZA A HUMAN INFLUENZA A

Characteristic of the H5N1 virus  INAKTIVE by

AI Virus is type A Influenza virus  genetic

• Program Pengendalian Influenza pd Manusia

THERAPY  Amantadin, Oseltamivir

Exotic  Biosecurity in an outbreak

Endemic  Biosecurity  DEPOPULATION

• The two major categories of