COMMUNICABLE DISEASES

CBD-1
 Introduction
• Majority of diseases in Africa are
communicable and remain a major health
problem
• Communicable diseases are of clinical and
public health importance because;
– They are common
– Some cause severe disease, disability
and death
– Some cause widespread outbreaks
– Most of them are preventable by simple
measures
– Many are particularly serious and
common in infants and children
 COURSE OBJECTIVES
• At the end of the course, students will
acquire knowledge on communicable
diseases, develop skills and attitudes to
assist the individual, family and community
manage and prevent the common
communicable diseases in the community.
 Supporting objectives
• Describe the basic concept of communicable
disease
• Describe the principles of control and prevention
of communicable diseases
• Discuss the levels of disease prevention, disease
surveillance and notification
• Describe common communicable diseases
Basic concepts of
communicable disease
 Definition of terms
• Communicable diseases;
– These are diseases which can be
spread from one living animal to
another, e.g. man to man, animal to
man, or animal to animal.
• Disease; disorder with specific cause
and recognizable signs and
symptoms
• Occurrence; frequency of a
disease without defining incidence
or prevalence.
• Reservoir; This is where the
disease-causing organisms
spreads from. It could be an
infected person, animal, place, or
object. The reservoir is the source
of infection.
• Infection; invasion of the body by harmful
organisms(pathogens) e.g. bacteria,
viruses
• Infectious agents; any agent that can be
transmitted from one person to another
• Incubation period; time between infection
and the appearance of symptoms and
signs of an illness. Usually expressed as a
range e.g. typhoid 10 – 20 days.
• Incidence; refers to new cases of a
disease or events occurring over any
specified period of time, e.g. number TB
cases diagnosed in one year.
• Prevalence; refers to the total number of
existing cases of a disease at a particular
point in time. The incidence increases the
prevalence of a disease
• Surveillance; is an epidemiological
practice by which the spread of disease is
monitored in order to establish patterns of
progression.
• Carrier; people with subclinical infection
who can spread their infection to other
people without their knowledge.
• Epidemic; occurs when new cases of a
certain disease, in a given human
population, and during a given period,
substantially exceed what is expected
based on recent experience.
Epidemiologists often consider the term
outbreak to be synonymous to epidemic
• Endemic; fairly constant number of new
cases, there is a balance between the
agent, environment and the host

• Pandemic; an epidemic of infectious

disease that has spread through human
populations across a large region; for
instance multiple continents, or even
worldwide.
• Morbidity; the state of being ill or
diseased
• Mortality; occurrence of a death in a
population.
• Case fatality rate ; is the proportion of
deaths within a designated population of
"cases“ over the course of the disease.
• Host; particular human or animal in which
an agent infects
• Agent; it’s a factor whose presence or
absence causes a disease.
• Environment; all that is external to the
agent and the human host
• Exposure; refers to coming into contact
with an organism, agent
• Prevention; inhibiting introduction of a
disease into and into an individual, group
of individuals or an area
• Control; steps taken to stop the spread or
reduce the severity of a disease that has
already occurred
 Pattern of communicable diseases
(epidemiological triad)
HOST
(MAN OR
ANIMAL)

DISEASE ENVIRONMENT
AGENT
• A delicate balance exists between the
agent, the host and the environment and it
can change in different ways
• The arrows show that each of the three
can have an effect on the other two
• Host (people) are affected by their
environment, but they can change it.
People can become ill and die because of
the agents, but pple can also control and
kill the agents.

• Agents; needs a suitable environment in

which to grow and multiply. If the
environment does not support the agent it
dies or transforms to a dormant state
 The Host and Infection
• An infection occurs when this micro-organism
begins to reproduce (multiply) and grow.
• When an organism infects a person, there are
three possible stages to consider.
• Incubation Period
• time between infection and the appearance of
symptoms and signs of an illness.
• Expressed as range (measles 10-14 days)
• The shorter the period the higher the
incidence
• Sub-clinical Infection
• At this stage, infection does not produce
clear signs and symptoms. The host's
immune system is trying to fight off the
agent.
• Clinical Infection
This is the period when the host develops
detectable symptoms and signs of an
illness..
 The Disease Transmission Cycle

• It illustrates the main stages by which an

organism grows, multiplies and spreads.
• Man may be the only host in which case
the infection spreads from man to man
e.g. measles
• Man may also be the final host from which
the organism has no chance to pass
further e.g. tetanus.
• The three parts of the transmission cycle
are
– Source
– Transmission
– Susceptible host
 Source
• It can be an infected person or animal or
the soil.
• People and animals may be clinical cases
or carriers
• An animal reservoir is also a source
• An agent may have more than one
reservoir e.g mycobacterium
 Susceptible host
• Refers to the host whose resistance is low
enough for him to get the disease
• Low resistance may be due to;
– Not having met the organism before and
therefore have no immunity e.g. measles
– Certain infections which give only a weak
immunity e.g. malaria
– Intercurrent illness e.g. TB
– Malnutrition, which can worsen infections
 Route of Transmission
• The way in which an organism leaves the
source/reservoir (the infected host) and
passes to a new susceptible host.
• Each agent has particular routes which
play a large part in how these organisms
spread in the community.
• The main routes of transmission are;
– Direct contact
• And indirect transmission;
– Vector aided
– Fecal Contamination of water and food
– Contact with animals or their products
– Transplacental
– Blood contact
– Airborne
 MAN MAN

MEASLES MALARIA

MAN MOSQUITO

ANIMALS

TETANUS
EXAMPLES OF
SOIL TRANSMISSION
CYLCES OF SOME
DISEASES
MAN
 PRINCIPLES OF MANAGEMENT OF
COMMUNICABLE DISEASES

• The aim of managing, preventing and

controlling, communicable diseases is to
first decrease life threatening disease and
mortality and then to decrease morbidity
• The control measures are continued
indefinitely
• The main methods of communicable
disease control is as shown on the table
below
Attacking the Interrupting the Protecting the
source route of susceptible
transmission host

•Treatment •Environmental •Immunization

•Immunization sanitation •Chemoproph
•Isolation •Immunization ylaxis
•Chemoprophy •Personal •Personal
laxis hygiene protection
•Reservoir •Behavior •Better
control change nutrition
•Notification •Vector control
•Disinfection
and sterilization
AGENT
The arrows show the
areas of intervention
of communicable
diseases

TRANSMISSION

RESERVOIR HOST
ATTACKING THE SOURCE
 Treatment of cases/contact tracing

• Treatment with chemotherapeutic agents

that are effective against the organism
• Treatment will stop spread
• Also called mass treatment where a high
percentage of the population known to
have the disease is treated
• Contact tracing is important to offer
testing, surveillance, prophylaxis
 Isolation of cases
• Means that the patient is not allowed to
come into contact with other people,
thereby controlling spread
• It can be difficult to achieve
 Surveillance of contacts
• Refers to keeping the exposed person
from other and watching him/her closely
for whole of the incubation period
• Also known as quarantine
 Reservoir control
• Used in those diseases that have their
main reservoir in animals
• Mass treatment, chemoprophylaxis or
immunization can be used
• E.g. trypanosomiasis, brucellosis
• Other ways include killing animals and so
destroying the reservoir e.g. rabies by
killing infected dogs
 Notification and reports
• Notification are essential in keeping watch
on the number of new cases and
monitoring effectiveness of control
programs
• It means that one immediately informs the
local health authorities
• Authorities take measures to confirm
suspicion and prevent the spread of the
disease
• Must be done using the fastest means
possible
• Notifiable diseases and epidemics are
reported to the ministry of health
• Some need international control
measures, they need to be reported to the
WHO; e.g. cholera, yellow fever, plague
• A good notification system provides early
warning of epidemics before they become
serious
• Notifiable diseases in Kenya include the
following
– Meningococcal
meningitis ,Rabies,Poliomyelitis
– Diphtheria,Tuberculosis, Anthrax
– Trypanasomiasis, Typhoid fever, Whooping
cough,
– Plague, Cholera, Measles
INTERRUPTING TRANSMISSION
 Environmental hygiene
• Food safety
• Water treatment and protection of water
sources
• Proper refuse and excreta disposal
• Adequate housing
 Personal hygiene
• Done to reduce contact diseases and
those through the faecal – oral route
• Hand washing
 Vector control
• Diseases that require vectors can be
controlled if the vectors are killed of
reduced
• This can be achieved by;
– Altering the env to be unfavorable to the
vector e.g. draining swamps, use of larvicides
• It can be expensive
 Disinfection and sterilization
• It aims at destroying the organism when it
is in the environment e.g sterilization of
surgical equipments; water treatment by
use of chlorine
 Population movements
• Achieved by stopping ppl moving around
or going on safari and even to forbid
gatherings like markets of festivals while
epidemic lastss
• This will reduce spread by carriers or
actual cases
 Protecting susceptible hosts
• Entails;
– Immunization
– Chemoprophylaxis
– Personal protection
– Better nutrition
– Reservoir control
 Immunization
• Done by use of vaccines
• Raises the immunity of the host; gives
primary protection
• Population coverage should high for
effective control in a community; e.g.
measles, over 80% of children must be
immunized
• Herd immunity; high proportion of the
population has been immunized
 Chemoprophylaxis
• Refers to administration of specific drugs
to protect the host e.g. malaria drugs
• They encourage drug resistance and must
be used only after careful analysis of cost,
benefit and toxicity
 Personal protection
• This means using barriers e.g. shoes
against hookworm, impregnated mosquito
nets and insect repellants against
mosquitoes
 Better nutrition
• Malnutrition increases the likelihood of
spread of infectious diseases e.g. measles
• Promotion of better nutrition helps control
the spread of communicable diseases
 Summary
• Communicable diseases are common and
preventable
• The pattern of communicable diseases has 3
components; agent, host, environment, each of
which affect the other two
• Principles of management of communicable
diseases are;
– Attacking the source
– Interrupting the transmission cycle
– Protecting the susceptible host
LEVELS OF DISEASE PREVENTION.

• Primary prevention aims to prevent

disease or injury before it ever occurs.
This is done by preventing exposures to
hazards that cause disease or injury,
altering unhealthy or unsafe behaviours
that can lead to disease or injury, and
increasing resistance to disease or injury
should exposure occur. Examples include:
 PRIMARY.
• legislation and enforcement to ban or
control the use of hazardous products
(e.g. asbestos) or to mandate safe and
healthy practices (e.g. use of seatbelts
and bike helmets)
• education about healthy and safe habits
(e.g. eating well, exercising regularly, not
smoking)
• immunization against infectious diseases.
 SECONDARY
• Secondary prevention aims to reduce the
impact of a disease or injury that has already
occurred. This is done by detecting and
treating disease or injury as soon as possible
to halt or slow its progress, encouraging
personal strategies to prevent reinjury or
recurrence, and implementing programs to
return people to their original health and
function to prevent long-term problems.
Examples include:
 SECONDARY
• regular exams and screening tests to
detect disease in its earliest stages (e.g.
mammograms to detect breast cancer)
• daily, low-dose aspirins and/or diet and
exercise programs to prevent further heart
attacks or strokes
• suitably modified work so injured or ill
workers can return safely to their jobs.
 Activities of Secondary Prevention

• ties of Secondary Prevention

• Screening tests to detect early the
pre symptomatic physiological and
anatomical indicators of disease, for
example pap smear, random blood
sugar test, etc.
• Case finding and case-tracing.
 Activities of secondary
• Screening surveys and examinations.
• Mass treatment and campaigns.
• Adequate treatment of disease.
• Follow-up of treated patients at
special
clinics and at their homes.
 TERTIARY
• Tertiary prevention aims to soften the
impact of an ongoing illness or injury that
has lasting effects. This is done by helping
people manage long-term, often-complex
health problems and injuries (e.g. chronic
diseases, permanent impairments) in
order to improve as much as possible their
ability to function, their quality of life and
their life expectancy. Examples include:
 TERTIARY
• cardiac or stroke rehabilitation programs,
chronic disease management programs
(e.g. for diabetes, arthritis, depression,
etc.)
• support groups that allow members to
share strategies for living well
• vocational rehabilitation programs to
retrain workers for new jobs when they
have recovered as much as possible.
Disease surveillance and
notification

CVBD 1
 Definition
• Disease surveillance
– It is an epidemiological practice by which the
spread of disease is monitored in order to
establish patterns of progression
– A key part of modern disease surveillance is
the practice of disease case reporting
 Function of monitoring
• communicable disease surveillance
system serves two key functions;
– early warning of potential threats to public
health and;
– programme monitoring functions which may
be disease specific or multi-disease in nature
 Core functions of surveillance systems

• They include
– case detection
– case registration,
– case confirmation,
– Reporting
– Data analysis and interpretation
– Public health response including reports and
feedback from the
systems to the data providers, stakeholders
and decision-makers.
 Case detection
• Case detection is the process of
identifying cases and outbreaks.
• Case detection can be through
the formal health system, private health
systems or community structures.
 Case registration
• Case registration is the process of
recording the cases identified.
• This requires a standardized register to
record minimal data elements on targeted
diseases and conditions.
 Case confirmation
• Case/outbreak confirmation refers to the
epidemiological and laboratory capacity for
confirmation.
• Capacity for case confirmation is enhanced
through improved referral systems, networking
and partnerships.
• This means having the capacity for appropriate
specimen collection, packaging and
transportation.
 Reporting
• Reporting refers to the process by which
surveillance data moves through the
surveillance system from the point of
generation.
• It also refers to the process of reporting
suspected and confirmed outbreaks.
Data analysis and interpretation
• Surveillance data should be analysed
routinely and the information interpreted
for use in public health actions.
 Epidemic preparedness
• Epidemic preparedness refers to the
existing level of preparedness for potential
epidemics and includes;
– availability of preparedness plans,
– stockpiling,
– designation of isolation facilities,
– setting aside of resources for outbreak
response, etc.
 Response and control

• Public health surveillance systems are

only useful if they provide data for
appropriate public health response and
control.
 Feedback
• Appropriate feedback can be maintained
through supervisory visits, newsletter and
bulletins.
 Support functions of surveillance
systems
The support functions are those that
facilitate implementation of the core
functions and include the following:
• standards and guidelines (case definitions,
laboratory guidelines, outbreak investigation
guidelines, etc);
• training for epidemiology and laboratory
personnel and/or community health agents;
 Support functions of surveillance
systems
• supervisory activities;
• communication facilities;
• resources (human, financial, logistical);
• monitoring and evaluation
• coordination.
 Notifiable disease
• A disease that, by statutory
requirements, must be reported to the
public health authority in the pertinent
jurisdiction when a diagnosis is made.
• A disease deemed of sufficient
importance to public health to require
that its occurrence be reported to
health authorities.
 Notifiable diseases
• Plague • Anthrax
• Cholera • Trypanasomiasis
• Measles • Typhoid fever
• Poliomyelitis • Whooping cough
• Diphtheria • Meningococcal
• Tuberculosis meningitis
• Rabies
 WHO
• Is the lead agency for coordinating global
response to major diseases
• It provides a central source of information
to member countries on health issues
 Scabies
• This is a parasitic infection of the
superficial layer of the skin characterized
by severe itching.
• It is caused by the female of an insect
called Sarcoptes scabiei (itch mite).
 epidemiology
• Common in rural Africa especially where
there is water shortage
• Infection and symptoms are more severe
in children than in adults
• Common in overcrowded environments
e.g. nursing homes, prisons,extended car
facilities
 Mode of transmission
• By direct close body contact e.g. sharing
bed, children playing, parent/children,
• Indirect bedclothes and clothing
• Poor living conditions and poor hygiene
promotes the spread of scabies.
 Pathophysiology
• The female mite burrows into the upper
layer skin (never below the stratum
corneum) and makes a small tunnel
• Within the tunnel, the insect deposits its
eggs and faeces
• The eggs hatch in four to five days and the
larvae leave the mother's tunnel and bury
themselves in the skin and in other places
 Signs and symptoms
intense itching, especially at night, and
eczema-like signs.
itchy rash has typical distribution especially
where the skin is curved (between fingers,
elbows, buttocks, etc)
 s/s contd
•the skin may be torn (excoriated) with
scratches and thus secondary infection
often follows.
•In people with reduced sensation e.g.
leprosy, infestation can be very extensive
and form thick crust
•Signs can also be extensive in cases of
immunosupression e.g. AIDS
 Diagnosis
• It is considered in patients with pruritus
and symmetric polymorphic skin lesions in
characteristic locations, especially when
there is history of contact with a case
– Anterior axillary locations
– Nipples, lower abdomen in women
– Belt line
– Front sides of wrist and elbows
 – External genitalia
– Thighs and buttocks
– Sides and webs of fingers
• Burrows should be sought
• Microscopic diagnosis of scrapings for
mite, eggs, faecal pellets
 Treatment
• Drug 10% benzyl benzoate emulsion
(BBE);
• Patient takes a warm bath, then applies
BBE on the whole body from neck down
• Repeat day 2, and day three bath and
apply again
• BBE has no effect on eggs, therefore
treatment should be repeated after 4 – 7
days to kill the larvae
 Management ctd
• If itching is severe treat it symptomatically
with calamine lotion.
• Trim the nails and teach on personal
hygiene
• Inform patients that the rash and pruritus
of scabies might persist for up to 2 weeks
• Treat secondary bacterial infections
• Treat the whole family
 Prevention of Scabies
•The best way of preventing and treating
scabies is good personal hygiene.
•Regular firm bathing, washing of clothes and
frequent use of soap will control scabies.
•Bedding and clothing should be washed in
hot water and aired for at least 72 hrs
• provision of adequate water supply
•The whole family should be treated to avoid
re-infection
Bacillary dysentery/Shigellosis
 Introduction
• it is an acute diarrheal disease xrized by
bloody stools, fever, vomiting, abdominal
cramps.
 Aetiology
• It is caused by a non-motile gram-negative
bacilli of the genus shigella spp.
• The organisms responsible for outbreaks are:
• Shigella sonnei
• Shigella dysenteriae
• Shigella flexneri
• Shigella boydii
• However, the first three organisms are the
most common causes of outbreaks.
 Epidemiology
• It is common especially in areas where
sanitation is low
• Epidemics occur in day care nurseries and
mental hospitals
• No carrier state
• Humans are the only known reservoir
Factors influencing occurrence
• Improper refuse disposal
• Inadequate water supply
• Large fly population
• Inadequate nutrition
• Contaminated water sources
• HIV infection
 Mode of Transmission

• Faecal-oral route. The 4Fs

• Indirect transmission may also occur
through dishes which are poorly washed.
• The shigella multiply in food which when
ingested causes dysentery.
 Pathophysiology
• Shigella are aerobic, non motile, glucose fermenting
gram negative rods, highly contagious causing
diarrhea after ingestion of a few ( 180 organisms)
• Causes damage in two ways
– Invasion of colonic epithelium – distal ilium
– Production of enterotoxin (shiga toxin)
• Local inflammation accompanied by ulceration
occurs, but organisms rarely penetrate the wall or
enter the blood stream.
• But the enterotoxin enhance virulence
 Clinical Features

• The disease has a short incubation period

of one to four days.
• Mild cases; non specific gastroenteritis
• Typical cases;
– Sudden of fever, headache, diarrhea with
streaks of blood, and colicky abdominal pains.
– Diarhoal stool is mixed with blood and mucus
 Clinical features cont’d
• Vomiting may also occur.
• Systemic;
– Toxaemia causes high fever and rapid pulse.
• Dehydration is also common and
dangerous as it may cause muscular
cramps, oliguria and shock.
• In infants, rectal prolapse may occur as
well as convulsions.
 Diagnosis

• Stool examination which shows the

presence of blood and mucus
• Stool microscopy which shows presence of
large numbers of white blood cells and
erythrocytes
• Stool culture for shigella spp.
• Sigmoidoscopy  reveal areas of
inflammed, enlarge mucosa with larger
areas of ulceration
 Management

• Mild bacillary dysentery is self-limiting and

all it requires is prevention or treatment of
dehydration.
• Severe infection:
• Fluid and electrolyte replacement;IV
ringers lactate to replace the lost
electrolytes or normal saline
• Antibiotics: oral ciprofloxacin 500mg
12 hourly for five to seven days OR
cotrimoxazole 960mg BD for 5 days
• Analgesics for colic such as codeine
phosphate and, paracetamol
• Belladonna used to treat abd pains
• Loperamide – anti diarrhoea
• Heath education on safe drinking water
(boiled/treated),safe food preparation, and
storage, washing hands with soap and
water, proper refuse disposal and proper
disposal of feacal matter.
• Advice on personal hygiene.
 Prevention and Control

• Safe water supply

• Improvement in personal hygiene
• Digging and use of pit latrines
• Practicing food hygiene
 Prevention and control
• Giving health education that emphasizes
environmental hygiene and breastfeeding
• Inspection of public eating places,
markets, boarding schools and camps
Amoebiasis
 Introduction
• This is a protozoal infection mainly of the
intestinal mucous membrane in humans
caused by entamoeba histolytica.
 Epidemiology
• The disease is found in all parts of the
world but more common where sanitary
conditions are poor.
• Prevalent among homosexual.
• Mortality from E.histolytica is estimated at
100 per year.
 Transmission
• Ingestion of cysts from fecally
contaminated food, or water
• Humans are the only hosts for E.histolytica
 Pathogenesis

• Once the cysts are ingested, the emerging

trophozoites take up residence in the
ascending colon where;
• they invade colonic epithelium and secrete
enzymes that cause localized necrosis;
• As the lesion reaches muscularis layer, a
typical ulcer forms that can undermine and
destroy large areas of the intestinal
epithelium
 Ct pathogenesis
• Progression into submucosa leads to
invasion of portal circulation (mesenteric
veins-vessels draining small intestines) by
the Trophozoites
• In the liver, it can lead to formation of liver
abscess.
 Clinical features
• Acute intestinal amoebiasis presents as dysentery
– Lower abd discomfort
– Flatulence
– Tenderness over sigmoid colon
– Tenesmus
• Chronic amebiasis
– Occasional diarrhea
– Wt. loss
– Fatigue
– Ameboma/scarring may form in recto sigmoid colon
• 90% of ppl are asymptomatic
• Liver abscess
– Right upper quadrant pain
– Wt loss
– Fever
– Tender and enlarged liver
• An amoebic liver abscess may perforate into
chest cavity; peritoneal cavity or through the
skin causing cutaneous amoebiasis
• Skin: ulcer is irregular and painful
• Pneumonia in the right lobe of the lung
 Diagnosis
• Stool microscopy for cysts of entamoeba
histolytica
• Chest xray – liver abscess
• Liver U/S
• Needle aspiration for microsocopy
 Management

• No treatment is necessary for asymptomatic patients as in

time they clear the infection.
• However, for invasive disease either one of the following
treatments is effective:
• Oral metronidazole 800mg eight hourly for five to seven
days
• Oral diloxanide furoate 500mg eight hourly for ten days
• In hepatic amoebiasis, oral metronidazole is very effective.

A three day course of 1.4g - 2.4g a day will treat the

disease.
• correct dehydration
 Extra-intestinal Amoebic Disease

• The most common site for extra-intestinal

amoebiasis is the liver where it forms a liver
abscess.
• Other secondary sites include lungs and
skin leading to:
• Amoebic infection of the skin
• Amoebic balanitis
• Amoebic lung abscess
• Amoebic brain abscess
 Prevention and Control

• Who is responsible for the spread of

amoebic dysentery?
• It is the cysts-passers who are usually asymptomatic.
Therefore in order to prevent and control this disease, you
need to do the following:
• Advise people to boil drinking water (chlorination does not kill
the cysts)
• Search for and treat carriers among
food handlers
• Commence a campaign for more latrines in an area with
endemic amoebiasis
• Conduct community campaigns about good personal hygiene
practices, such as regular hand washing
Cholera
 Introduction
• Cholera is an intestinal disease which is
characterized by sudden onset of profuse
watery stools and vomiting, leading to
severe dehydration, acidosis and
circulatory collapse.
 Etiology
• It is caused by a small comma-shaped
motile organism called vibrio cholerae.
• There are about four sub-strains of the
cholera vibrio, namely;
– El Tor
– Ogawa, Luaba and Hikojima. The El Tor sub-
strain causes cholera epidemics in
East Africa.
 Epidemiology of Cholera

• Cholera occurs in all parts of the world

where the living conditions are unsanitary.
• The human being is the reservoir and host.
• Animal reservoirs: shellfish, crabs and
shrimps, oyster; Vibrio's grow well in
brackish (salty water).
• Affects all sexes, ages equally
•
 Transmission
• Cholera is transmitted through the faecal-
oral route, mostly by water which has been
contaminated with faecal matter.
• The vibrios are very sensitive to the
gastric acid and so a large number of
organisms must be ingested for infection
to occur.
 Pathophysiology
• Bacteria adheres to cells of the brush border
of gut with help of bacterial enzyme mucinase
which dissolves glycoprotein coating
• Organsisms multiply and secrete an
enterotoxin called choleragen.
• Choleragen attaches to surface of
enterocytes, some are inserted into cytosol.
• There is overproduction of cyclic Amp which
enhances ion transport
 Pathophysiology
• This results in loss of water and ions from
the cell
• The watery efflux enters the lumen of the
gut resulting in massive watery diarrhea
that contains neither rbcs nor neutrophils
• Morbidity and death are due to
dehydration and electrolyte imbalance.
 Clinical Features

• Short incubation period; 2 hours -5 days

• Abt 75% of pple with infection don’t
develop signs and symptoms but can shed
organism into env for 7 – 14days
• 80% have mild s/s
• 20% acute disease and dehydration
 First Stage

• This stage lasts for 3 - 12 hours.

• During this stage profuse watery stool is passed by the
patient until faecal matter disappears.
• The stool becomes almost clear fluid with flakes of
mucus, giving it the classical rice-water stool appearance.
• Vomiting follows diarrhoea. Initially the patient vomits food
but soon after only clear fluid or rice-water is vomited.
• The patient develops severe cramps in the abdomen and
limbs due to electrolyte loss.
•
 Second Stage

• Signs of dehydration;
– the skin is cold, dry and inelastic
– Blood pressure drops severely, and it may not be
recordable.
– Weak and rapid pulse
– Oliguria or anuria
– urine production ceases
– patient collapses and may go into irreversible
shock.
•
 Third Stage

• This is the stage of recovery;

spontaneously or with treatment.
• The general condition rapidly improves,
diarrhoea becomes less profuse and the
patient is able to take oral fluids.
 Diagnosis

• Cholera should be suspected in any

outbreak of diarrhoeal diseases.
• The diagnosis is made on clinical grounds
and also through laboratory isolation of
vibrio cholerae from a rectal swab, stool or
vomitus specimen.
 Management

• Admit the patient

• Strict isolation not necessary
• Disinfect all hospital contact equipment
• Nurse pt in a cholera bed; stool passes to a collecting
bucket
• Rehydration;
– Oral – ORS (200 - 300ml per hour) with glucose
– IV fluids to treat shock or if pt is too weak to take
• Antibiotics treatment
– Doxycycline 100mg bd for 7 days OR
– Erythromycin 250mg qid for 5 days
– Children; erythromycin 30mg/kg/day tid for 3 days
 Management
Other mgt measures;
•The immediate notification of district medical officer.
Cholera is an internationally notifiable disease.
•Admission of patients in temporary treatment centres,
such as school or church
•Barrier nursing and patient isolation should be
practiced to prevent spread of
the disease.
•Disinfection of hospital equipment and proper disposal
of stool and vomitus into a pit latrine or septic tanks.
Cholera bed
 Prevention and Control

• As in fecal-oral diseases
• Provision of chemoprophylaxis to all
contacts of the patients including family,
friends and visitors using oral tetracycline.
• Administering cholera vaccine to health
care workers in contact with the patients
during the epidemics.
Enteric fevers

enteric fevers
 Introduction
• are produced mainly by S typhi (typhoid
fever) and, to a lesser degree, by S
paratyphi and S schottmuelleri, all of which
are strictly human pathogens
– are highly infective even with small numbers of bacteria (e.g., 200).

enteric fevers
 Transmission
• Both are mainly spread by the faecal-oral
route through contaminated food, water
and milk.
• Flies are also important in the
transmission of enteric fevers.

enteric fevers
TYPHOID FEVER

enteric fevers
 Epidemiology
• This is an infectious bacterial disease caused
by salmonella typhi.
• Typhoid fever is endemic in many regions of
East Africa, although epidemics can occur if
public water/food source has been
contaminated.
• Case fatality rate 3% with treatment and 10%
without adequate abx treatment.
• Human beings are the only known reservoir
and host.
enteric fevers
 Pathophysiology
• During an incubation period of 7-14 days, the
organisms multiply in the small intestine, enter
the intestinal lymphatics, and are
disseminated via the blood stream to multiple
organs.
• Multiplication takes place in the
reticuloendothelial system (esp liver, spleen
and bonemarrow)and lymphoid tissue of the
bowel, producing hyperplasia and necrosis of
the lymphoid Peyer's patches.
enteric fevers
 Pathophysiology
• Survival and growth of the organism within
phagocytic cells and predilection for invasion of
gallbladder is a feature of the disease
• Invasion of the gallbladder may lead to
development of carrier state and excretion of
bacteria in faeces for long periods
• A second and heavier invasion of the intestine
takes place through infected bile.
• This is responsible for the extensive lesions on
lymphoid tissue of small intestine.
enteric fevers
 Clinical Features
• The incubation period of typhoid fever is 7 - 21 days.
• The disease has a gradual onset which progresses
through the following four stages.
• prodrome
– Anorexia
– Lassitude
– Epistaxis
– Frontal headache
– Muscular pain
– Blurred tongue
– GIT discomfort
– Slight evening fever
enteric fevers
 First Week

• Body temperature rises day by day or in

steps to 39.5ºC or higher.
• Most patients cough because they develop
bronchitis and may also complain
of
• Constipation.
• relative bradycardia (pulse rate is slow than
expected)
• Tender splenomegaly
enteric fevers
 Second Week

• Temperatures is continuously high and

reaches a plateau
• ½ of pts may have “pea soup” diarrhea
• distended and tender abdomen due to
inflammation of lymphoid tissue in the
intestines
• The high temperature and toxaemia causes
mental confusion and disorientation in the
patient.
• Deafeness may occur
• Tongue dry ,sore and
entericred.
fevers
• Second week
• Pulse quickens and BP falls
• There is rash – Rose spots (picture)

enteric fevers
 Third Week

• Body temperature decreases step by step

and the patient improves slowly.
• If there is no improvement, the Peyer's
patches in the intestines perforate and
toxaemia increases.
• The patient becomes delirious and
incontinent of urine and stool, muscles
twitch and coma may precede death.

enteric fevers
 Fourth Week

• For the patients who do not suffer the

serious complications of the third week,
the fourth week is a period of
convalescence.
• The temperature drops back to normal and
the patient recovers gradually.

enteric fevers
 Diagnosis

• Blood culture- positive in the 1st week of illness

• Bone marrow cultures
• Stool and urine cultures – positive after 1 st week
• FBC – relative leukopenia in relation to fever
• Widal test – test becomes positive by end of 1 st
week – a 4 times rise in spared specimens obtained
2 weeks apart suggest S.typhi infection
• Stool to check for presence of occult blood

• Gold standard: isolation of bacilli cultures

enteric fevers
 Treatment

• The treatment of typhoid fever includes the following:

• Fluid replacement due to diarrhoea
• Oral norfloxacin 400mg 12 hourly for 10 - 14 days
• Oral ciproxacin 500mg bd. for 14 days
• Oral corticosteroids to prevent Jarisch-Herxheimer's
reaction
• Patient should be isolated in fly-proof room
• Contaminated articles should be disposed by incineration
• Stools and urine should be disposed of in a pit latrine or
septic tank
• Surgical treatment for perforated bowels
enteric fevers
 Complications
• Intestinal hemorrhage
• Chronic carrier state for s.typhi
• Intestinal perforation
– Peritonitis
– Sepsis

enteric fevers
 Prevention and Control

• Identification of the carriers especially

those who work as food handlers and treat
them promptly
• Administration of typhoid vaccine:
• Safe water supply
• Improvement in food hygiene
• Typhim VI vaccine; 0.5 ml IM (booster
every 3 years)

enteric fevers
PARATYPHOID FEVER

enteric fevers
 Paratyphoid Fever

• It is caused by bacteria known as

salmonella paratyphi types A, B and C.
• The disease runs a milder course than
typhoid fever and also has enlargement of
the spleen, bloodstained diarrhoea and
swelling of the Peyer's patches.

enteric fevers
 Symptoms
• Paratyphoid fever may present like typhoid
fever, but in most cases it presents as
gastroenteritis or transient diarrhoea.

enteric fevers
 Paratyphoid Fever

• Treatment
• The treatment of paratyphoid fever is as
follows:
• Intravenous fluid if diarrhoea is severe
• Oral rehydration if diarrhoea is mild
• Oral contrimoxazole two tablets bd. for five
to seven days

enteric fevers
 Paratyphoid Fever

• Prevention and Control

• The prevention and control measures are
similar to those that were covered under
typhoid fever.

enteric fevers
Bacterial food poisoning
 Introduction
• Illness caused by the consumption of food or
water contaminated with bacteria and/or their
toxins or with parasites, viruses, or chemicals.
• The most common pathogesn are
– E.coli
– Salmonella
– Clostridium perfringens
– Campylobacter
– Staph.aureus
 Causes
• The major causes of food poisoning
include intoxication with chemicals, toxins
produced by bacterial growth, and a
variety of organic substances such as
poisonous plants and mushrooms.
 Pathophysiology
• 2 broad categories;
– Noninflammatory
– Inflammatory
 Non inflammatory
• Caused by action of enterotoxins on the
secretory mechanisms of the mucosa of the
small intestines without invasion
• This leads to large volume of watery stools in
the absence of blood,pus or severe abd pain..
• Occasionally profound dehydration may result
• E.g. E.coli, Clostridium perfringens,
Stapphylococcus organisms, giardia lamblia,
rotavirus, adenovirus
 Inflammatory
• Caused by action of cytotoxins on the mucosa leading
to invasion and destruction.
• Colon or distal small bowel commonly involved
• Diarrhea is usually bloody, mucoid and leukocytes are
present
• Pts are usually febrile and appear toxic
• Smaller stool volume –dehydration unlikely
• Sometimes organism penetrate the mucosa and
proliferate in the local lymphatic tissue followed by
systemic dissemination Salmonella sp, Shigella
sp,Entamoeba histolytica
 Epidemiology
• Food poisoning occurs in small outbreaks
and mortality is usually low.
• Family members or institutions are usually
affected
• Some diagnosed cases of gastroenteritis
could be due to food poisoning.
 Types
• There are two common types of bacterial
food poisoning found in communities:
– Staphylococcal food poisoning
– Clostridium botulinum food poisoning
 Staphylococcal Food Poisoning

• This type of poisoning is caused by

contamination of food (for example, with pus
from a septic finger) by an infected person).
• The staphylococci in the pus multiply and
produce toxins when the food is allowed to
stand for several hours before being served.
• Although the bacteria itself is harmless if
ingested, the toxins it produces are very
poisonous
 Clinical picture;
• Following ingestion of the toxin-
contaminated food, there is sudden severe
abdominal cramping, nausea, vomiting,
diarrhea, headache and excessive
salivation.
• Vomiting is due to the toxin acting on the
central nervous system.
 Diagnosis
• This disease is usually recognized when
people who have shared food all fall sick
within a short time.
 Clostridium Botulinum Food Poisoning

• It occurs when food contaminated with

botulinum spores (from the soil) is kept warm
and in tightly covered containers for many
hours.
• The organisms multiply in warm anaerobic (low
oxygen) environments especially in protein-rich
foods.
• When such food is contaminated, clostridium
botulinum multiplies and starts producing
toxins.
 Clostridium food poisoning
• The contaminated food may appear
spoiled (greenish) and emit an offensive
odour.
• Once a person eats this food, they may
suffer a mild illness that requires no
medical treatment or a rapidly fatal illness
terminating in death within 24 hours.
 signs and symptoms:
• The symptoms of botulism begin to
manifest
12 - 36 hours after ingestion of toxin
contaminated food. The symptoms are due
ot inhibition of acetylcholine release in
nerve endings by the botulinum
• Nausea and vomiting
• Dizziness and tinnitus
• Seeing double images (diplopia)
 signs and symptoms:
• Inability to speak clearly (dysphasia)
• Difficulty swallowing (dysphagia)
• Difficulty breathing (dyspnoea)
• Muscle weakness (neck, limbs,
respiratory)
• Death may occur from sudden respiratory
paralysis and airway obstruction
 Diagnosis

• Diagnosis is difficult when only one person

is affected.
• However, diagnosis can be made when a
group of people who had consumed the
same food (especially tinned or canned
foods) suffers from the same neurological
symptoms without mental confusion or
loss of awareness.
 Management

• The main cause of death in botulism is

respiratory failure.

• The patient therefore must be managed in a

high-dependence unit.

• Cleansing enemas are administered to remove

unabsorbed toxin from the colon and botulinum
autotoxin serum is given and repeated after
two to four hours.
 Prevention and Control

• Health education to encourage people to serve

meals immediately they are prepared in order to
prevent growth of organisms, such as staphylococci
• Keeping food covered to keep off dust and rodents
• Thorough reheating of left over foods (to kill toxins
food must be heated to over 140°C)
• Excluding persons with skin infections from food
handling
• Refrigerating cooked food
• Keeping the kitchen and cooling areas clean
Brucellosis
 Brucellosis/malta fever
• A zoonotic infection caused by bacterial
genus Brucella
• Other names;
– Undulant fever
– Mediterrenean fever
– Gastric remittent fever
 Causes
• Brucellosis is a zoonotic disease
• They localize in the reproductive organs of host
animals causing abortions and sterility.
• They are shed in large numbers in in the animal’s
urine, milk, placental fluid and other fluids
• 4 species with significant human pathogenicity;
– Brucella melitensis (from sheep– highest pathogenicity)
– Brucella suis (from pigs, high pathogenicity)
– Brucella abortus (from cattle; moderate pathogenicity)
– Brucella canis (from dogs; moderate pathogenicity)
 Transmission
• Ingestion of infected dairy food products e.g.
unpasteurized milk or milk products such as
cheese.
• Direct contact with an infected animal or
inhalation of aerosols
• Humans are accidental hosts
• It can also be transmitted by contact with blood,
urine, tissues, through splashing of amniotic
fluid or milk on the conjunctiva and blood
transfusion.
 Epidemiology
• Found world wide predominantly in rural
areas among pastoral communities.
• It is also an occupational health hazard of
farmers, veterinarians, abattoir workers
and butchers.
• Case fatality rate < 2%
 Pathophysiology
• Organisms enter the body by various
routes, git, respiratory, conjunctivae,
mucous membranes
• Once within the blood stream, the
organisms quickly become intracellular
pathogens contained within macrophages
• After ingestion by phagocytes, about 15-
30% of brucellae survive,
 Pathophysiology cont’d
• Brucella that survive are transported into
lymphatic system and may replicate there
locally; or replicate in the kidney, liver,
spleen, breast tissue or joints causing both
localized and systemic infection; any
organ may be involved
• Development of cell mediated immunity is
the principal mechanism of recovery.
 Clinical Presentation

• The incubation period takes about two to

four weeks.
• Initially; non specific signs and symptoms;
– Headaches
– Fever
– Weakness
– Anorexia
– Rigors
 Clinical picture
• Undulating fever (rising and falling) in some ppl
• Night sweats
• Constipation
• Patients may also complain of pain in the large
joints like the hips and knees although any other
joint may be affected.
• Hepatomegally, splenomegally and
lymphadenopathy may also be present.
• If untreated, the disease can continue for many
months and the patients may become depressed.
 Diagnosis
• A serological diagnosis of brucellosis can be
made by doing an agglutination test in
dilutions. A level of 1:160 or above is
associated with the infection.
• Blood cultures rarely give positive results but a
bone marrow aspirate culture gives better
yields of up to 90%.
• Full haemogram - normochromic, normocytic
anaemia, neutropenia and lymphocytosis is
common.
 Treatment
• The treatment of brucellosis is doxycycline
100 mg BD or 200mg daily for 14 - 21
days and streptomycin 1gm IM OD for 3
weeks;
• In children below 8 yrs cotrimoxazole for 3
weeks
 Prevention
• Educate the community to boil or
pasteurize milk.
• Animal handlers and those at special risk
should be advised to take extra
precautions.
• Immunization of animals
Tetanus
 What is Tetanus?

 An infectious disease caused by

contamination of wounds from the
bacteria Clostridium tetani, or the
spores they produce that live in the
soil, and animal feces

 Greek words -“tetanosand teinein”,

meaning rigid and stretched, which
describe the condition of the muscles
affected by the toxin, tetanospasmin,
produced by Clostridium tetani
Sporulated Vegetative
 Causes
 Tetanus spores are found throughout the
environment, usually in soil, dust, and animal waste.

 Tetanus is acquired through contact with the

environment; it is not transmitted from person to
person.
 The usual locations for the bacteria to enter the body:
Causes
 Puncture wounds (such as
those caused by rusty
nails, splinters, or insect bites.)

 Burns, any break in the skin,

and IV drug access sites are
also potential entryways for the
bacteria.
 Route of Entry
• Apparently trivial injuries
• Animal bites/human bites
• Open fractures
• Burns
• Gangrene
• In neonates usually via infected
umbilical stumps
• Abscess
• Parenteral drug abuse
 epidemiology
Tetanus is an international health problem, as
spores are ubiquitous. The disease occurs
almost exclusively in persons who are
unvaccinated or inadequately immunized.
Tetanus occurs worldwide but is more common
in hot, damp climates with soil rich in organic
matter.
More common in developing and under
developing countries.
More prevalent in industrial establishment,
where agricultures workers are employed.
Tetanus neonatorum is common due to lack of
 Incubation Period
• Varies from 1 day to several months. It is
defined as the time from injury to the first
symptom.
 Period of onset
• It is the time from first symptoms to the
reflex spasm.

• An incubation period of 4 days or less

or
• A period of onset of less than 48 hr is
associated with the development of severe
tetanus.
pathogenesis
1. C. tetani enters body 2. Stays in sporulated form
until anaerobic conditions
from through wound.
are presented.

3. Germinates under 4. Tetnospasmin spreads using

anaerobic conditions and blood and lymphatic system,
begins to multiply and and binds to motor neurons.
produce tetnospasmin.

6. Binds to sites responsible for

5. Travels along the axons
inhibiting skeletal muscle
to the spinal cord. contraction.
•Initially binds to
peripheral nerve
terminals
•Transported within the
axon and across synaptic
junctions until it reaches
the central nervous
system.
•Becomes rapidly fixed
to gangliosides at the
presynaptic inhibitory
motor nerve endings,
then taken up into the
How the toxin acts?
Blocks the release of inhibitory
neurotransmitters (glycine and
gamma-amino butyric acid)
across the synaptic cleft, which
is required to check the nervous
impulse.
If nervous impulses cannot be
checked by normal inhibitory
mechanisms, it leads to
unopposed muscular contraction
and spasms that are
 Tetanus prone wound
• A wound sustained more than 6 hr before
surgical treatment.
• A wound sustained at any interval after
injury which is puncture type or shows
much devitalised tissue or is septic or is
contaminated with soil or manure.
 Clinical features
 Risus sardonicus: Contraction of the muscles at the angle
of mouth and frontalis
 Trismus (Lock Jaw): Spasm of Masseter muscles.
 Opisthotonus: Spasm of extensor of the neck, back and
legs to form a backward curvature.
 Muscle spasticity
 Prolonged muscular action causes sudden, powerful, and
painful contractions of muscle groups. This is called tetany.
These episodes can cause fractures and muscle tears.

 If respiratory muscle is involved – apnoea.

 Signs and Symptoms
Other symptoms include:
 Drooling
 Excessive sweating
 Fever
 Hand or foot spasms
 Irritability
 Swallowing difficulty
 Uncontrolled urination or defecation
 Diagnosis
 There are currently no blood tests that can be used
to diagnose tetanus. Diagnosis is done clinically.

Differential Diagnosis
 Masseter muscle spasm due to
dental abscess
 Dystonic reaction to phenothiazine
 Rabies
 Hysteria
 Principle of Treatment
• 1. Neutralization of unbound toxin with
Human tetanus immunoglobulin
• 2. Prevention of further toxin production by
-Wound debridement
-Antibiotics (Metronidazole)
 3. Control of spasm
- Nursing in quiet environment
- avoid unnecessary stimuli
- Protecting the airway
 4. Supportive care
- Adequate hydration
- Nutrition
- Treatment of secondary infection
- prevention of bed sores.
 Prevention

 Tetanus is completely preventable

by active tetanus immunization.

 Immunization is thought to provide

protection for 10 years.

 Begins in infancy with the DTP

series of shots. The DTP vaccine is
a "3-in-1" vaccine that protects
against diphtheria, pertussis, and
tetanus.
 Prevention
 Can be achieved by active immunization by tetanus
toxoid (5 doses – 0 day, 1 month, 6 month, 1 year, 1
year).
 Older teenagers and adults who have sustained
injuries, especially puncture-type wounds, should
receive booster immunization for tetanus if more than
10 years have passed since the last booster.

 Clinical tetanus does not produce immunity to further

attacks. Therefore, even after recovery patients must
receive a full course of tetanus toxoid.
RABIES
 Definition
• Rabies is a disease caused by infection
with the lassaviruses
 Transmission
• People are usually infected following a deep bite or scratch by
an infected animal.
• Dogs accounts for more than 90% of the cases in animals.
(WHO report 1992)
• They are the source of infection in all human rabies deaths
annually in Asia and Africa.
Bats are the source of most human rabies deaths in the
Americas.
• Bat rabies has also recently emerged as a public health
threat in
Australia and western Europe.
 Transmission
• direct contact by infected saliva with human mucosa
or fresh skin wounds.
• Human-to-human transmission by bite is
theoretically possible but has never been
confirmed.
• Rarely, rabies may be contracted by inhalation of
virus-containing aerosol or via
transplantation of an infected organ.
• Ingestion of raw meat or other tissues from animals
infected with rabies is not a source of human
infection.
 Epidemiology
• Rabies is present on all continents with the exception of
Antarctica,
• Once symptoms of the disease develop, rabies is nearly always
fatal.
• It occurs mainly in remote rural communities where measures to
prevent dog to human transmission have not been implemented.
• Approx 50,000 people die from rabies worldwide
• more than 10 million receive post exposure vaccination against
the disease.
• Children aged 5-15 years are at particular risk esp males
• More than 99% of human deaths from rabies occur in Africa, Asia
and South America (WHO 2002).
 Pathophysiology
• Virus multiplies at the bite site and infects
sensory neurons and move by axonal
transport to the CNS
• During transport, virus is sheltered; no immune
response occurs
• Virus multiplies in the CNS then travels down
the peripheral nerves to salivary glands and
other organs
• From the glands it enters the saliva – infection
by bite occurs
 Pathophysiology
• No viremic phase
• In the CNS encephalitis develops with
death of neurons and demyelination.
• Infected neurons contain inclusion bodies
in the cytoplasm called Negri bodies
(important for dx)
 Symptoms
• The incubation period for rabies is typically 1–3
months, but may vary from <1 week to >1 year.
• Incubation period varies with the site of bite;
shorter if around the head and neck
• Non specific
• fever pain or an unusual or unexplained tingling,
• pricking or
• burning sensation (paraesthesia) at the wound
site.
• Itching at the bite site
 Symptoms
• As the virus spreads through the CNS
progressive, fatal inflammation of the brain
and spinal cord develops.
• Two forms of the disease can follow;
• Furious rabies and paralytic rabies
 Furious rabies
• People with furious rabies exhibit signs of:
• Hyperactivity,
• Excited behaviour,
• Hydrophobia(due to spams of the muscles
of swallowing )
• Sometimes aerophobia.
• After a few days, death occurs by cardio-
respiratory arrest.
 Symptoms
• Paralytic rabies accounts for about 30% of
the total number of human cases.
• This form of rabies runs a less dramatic and
usually longer course than the furious form.
• The muscles gradually become paralyzed,
starting at the site of the bite or scratch.
• A coma slowly develops, and eventually
death occurs.
 Diagnosis
• Diagnosis is based on high index of suspicion;
history of stray animal bite, history of
hydrophobia
• Examination of Negri bodies in neurons of
animals
• In humans
– Antibody staining of biopsy specimen
– Isolation of virus from the saliva, CSF of rise of
antibody to the virus
– Autopsy: Negri bodies in corneal scrapings
 Treatment
• No antiviral treatment
• Supportive Rx is available
• Immediate care;
– Irrigate thoroughly with copious amounts
of saline solution
– Cleanse with soap solution(minimum of
15 minutes)
– Debride the wound
 Treatment cont’d
• Administer antibiotics
• Administer TT
• Infiltrate the wound with rabies
immunoglobulin; 20IU/kg body wt
infiltrated around the wound
• 20IU/kg given IM in gluteal region
 Prevention
• vaccination, either pre-exposure
vaccination or as part of post-exposure
treatment.
• Pre-exposure vaccination:
• May be recommended for anyone at
increased risk
• to rabies virus e.g Veterinarians and
veterinary laboratory staff etc.
• Pre-exposure prophylaxis - Primary
• Prophylaxis (using vero cell derived
vaccine) 0.5mls intramuscularly in the
deltoid muscle on days 0, 7 and 28 (3
doses) followed by a booster dose after 1
year
 Post-exposure vaccination:
• The indication for post exposure
vaccination, with or without rabies
immunoglobulin depends on the type of
the contact with rabid animal.
• There are three types:
• Category I Touching or feeding a
suspected animal, licks on the skin
• Category II Nibbling of the uncovered
skin, minor scratches or abrasions without
bleeding, licks on the broken skin
• Category III Single or multiple trans-
dermal bites or scratches; contamination
of mucous membrane with saliva from
licks.
 Prevention
• No treatment is needed for category 1 type of contact.
• Immediate vaccination is needed for category 2 and;
• vaccination and immunoglobulin administration is
recommended for category 3.
• For persons previously-immunized within the last 3
years - Give 2 booster doses on day 0 and 3
intramuscularly in the deltoid muscle
• Non-immunized persons –
• Give 5 doses of 0.5 ml each on days 0 3, 7, 14, 28 by
intramuscular injection into the deltoid muscle in adults
or the antero-lateral aspect of the thigh in children.
 Prevention
• If animal is captured, it should be
observed for 10 days and killed if
symptoms occur
• Immunization of dogs and CATs at 3
months, annually or every 3 years.
ANTHRAX

CVBD.
 DEFINITION.
• Anthrax is a disease with rapid
onset caused by the bacterium
Bacillus anthracis. Most forms of
the disease are lethal, and it
affects most animals. It can be
transmitted through contact with
infected meat.
 DEFINITION.
• Effective vaccines against anthrax are
available, and some forms of the
disease respond well to antibiotic
treatment. Anthrax can occur in three
forms: skin, inhalation, and intestinal.
 DEFINITION.
• Like many other members of the genus
Bacillus, B. anthracis can form dormant
spores that are able to survive in harsh
conditions for decades or even centuries.
Such spores can be found on all
continents, including Antarctica. When
inhaled, eaten, or come into contact with
an area of broken skin, they may become
reactivated and multiply rapidly.
 What causes anthrax?
• it was a German physician and
scientist, Dr. Robert Koch, who
proved that the anthrax bacterium
was the cause of a disease that
affected farm animals in his
community. Under the microscope,
the bacteria look like large rods.
 CAUSES.
• However, in the soil, where they live,
anthrax organisms exist in a dormant
form called spores. These spores are
very hardy and difficult to destroy. The
spores have been known to survive in
the soil for as long as 48 years.
 CAUSES.
• Eating is thought to be the most
common route by which herbivores
contract anthrax. Carnivores living in
the same environment may become
infected by eating infected animals.
Diseased animals can spread anthrax
to humans, either through direct
contact or by eating raw or
undercooked meat from infected
animals. B. anthracis bacterial spores
 Causes.
• Disturbed grave sites of infected
animals have been known to cause
infection over 70 years after the
animal's death.
 How is anthrax contracted?
• Anthrax can infect humans in three
ways. The most common is infection
through the skin, which causes an
ugly sore that usually goes away
without treatment. Humans and
animals can ingest anthrax from
carcasses of dead animals that have
been contaminated with anthrax.
 Contraction.
• Ingestion of anthrax can cause
serious, sometimes fatal disease. The
most deadly form is inhalation
anthrax. If the spores of anthrax are
inhaled, they migrate to lymph glands
in the chest where they proliferate,
spread, and produce toxins that often
cause death
 Signs and symptoms
• Lungs
• Respiratory infection in humans is
relatively rare and initially presents
with cold or flu-like symptoms for
several days, followed by pneumonia
and severe (and often fatal)
respiratory collapse.
 s/s
• Gastrointestinal
• Gastrointestinal (GI) infection in
humans is most often caused by
consuming anthrax-infected meat and
is characterized by serious GI
difficulty, vomiting of blood, severe
diarrhea, acute inflammation of the
intestinal tract, and loss of appetite.
 s/s
• After the bacterium invades the
gastrointestinal system, it spreads to
the bloodstream and throughout the
body, while continuing to make toxins.
GI infections can be treated, but
usually result in fatality rates of 25%
to 60%, depending upon how soon
treatment commences.
 s/s
• Skin
• Cutaneous anthrax, also known as
Hide porter's disease, is the
cutaneous (on the skin) manifestation
of anthrax infection in humans. It
presents as a boil-like skin lesion that
eventually forms an ulcer with a black
center (eschar).
 s/s
• In general, cutaneous infections
form within the site of spore
penetration between two and five
days after exposure. Unlike
bruises or most other lesions,
cutaneous anthrax infections
normally do not cause pain
 DIAGNOSIS.
• Various techniques are used for the
direct identification of B. anthracis in
clinical material. Firstly, specimens
may be Gram stained. Bacillus spp.
are quite large in size (3 to 4 μm
long), they grow in long chains, and
they stain Gram-positive.
 dx.
• To confirm the organism is B.
anthracis, rapid diagnostic techniques
such as polymerase chain reaction-
based assays and
immunofluorescence microscopy may
be used.
All Bacillus species grow well on 5%
sheep blood agar and other routine
culture media.
 TREATMENT.
• In most cases, early treatment can cure
anthrax. The cutaneous (skin) form of
anthrax can be treated with common
antibiotics such as penicillin, tetracycline,
erythromycin, and ciprofloxacin (Cipro).
The pulmonary form of anthrax is a
medical emergency. Early and continuous
intravenous therapy with antibiotics may
be lifesaving.
 Treatment.
• Of note, anthrax is a reportable
disease. That means that local or state
health agencies must be notified if a
case of anthrax is diagnosed. These
agencies can better characterize the
anthrax so that the affected individual
can receive the most effective
treatment for that particular organism.
 PREVENTION.
• Vaccines against anthrax for use in
livestock and humans.
• If a person is suspected as having
died from anthrax, every precaution
should be taken to avoid skin contact
with the potentially contaminated
body and fluids exuded through
natural body openings.
 Prevention.
• Anyone working with anthrax in a
suspected or confirmed victim should
wear respiratory equipment capable
of filtering this size of particle or
smaller.
• Dead victims who are opened and not
burned provide an ideal source of
anthrax spores.
• Health education on the source of
infection.
Gastroenteritis.

CVBD
 DEFINITIONS.
• Gastroenteritis, also known as
infectious diarrhea, is
inflammation of the
gastrointestinal tract that involves
the stomach and small intestine.
 S/S
• Signs and symptoms include some
combination of diarrhea, vomiting,
and abdominal pain. Fever, lack of
energy, and dehydration may also
occur. This typically lasts less than
two weeks. It is unrelated to influenza
though it has been called the stomach
flu.
 S/S
• Signs and symptoms usually begin
12–72 hours after contracting the
infectious agent. If due to a viral
agent, the condition usually resolves
within one week.
 S/S
• Some viral causes may also be
associated with fever, fatigue,
headache, and muscle pain. If the
stool is bloody, the cause is less likely
to be viral and more likely to be
bacterial. Some bacterial infections may
be associated with severe abdominal
pain and may persist for several weeks
CAUSES/PREDISPOSING FACTORS.

• Gastroenteritis can be due to

infections by viruses, bacteria,
parasites, and fungus. The most
common cause is viruses. In children
rotavirus is the most common cause
of severe disease. In adults, norovirus
and Campylobacter are common.
CAUSES/PREDISPOSING FACTORS

• Transmission may occur due to

eating improperly prepared foods,
drinking contaminated water, or
through close contact with an
individual who is infected. Testing to
confirm the diagnosis is typically not
needed.
 Pathophysiology.
• Gastroenteritis is defined as vomiting
or diarrhea due to infection of the
small or large bowel. The changes in
the small bowel are typically non
inflammatory, while the ones in the
large bowel are inflammatory. The
number of pathogens required to
cause an infection varies from as few
as one (for Cryptosporidium) to as
many as 108 (for Vibrio cholerae).
 Diagnosis.
• Gastroenteritis is typically diagnosed
clinically, based on a person's signs
and symptoms. Determining the exact
cause is usually not needed as it
does not alter management of the
condition
 DX.
• . However, stool cultures should be
performed in those with blood in the
stool, those who might have been
exposed to food poisoning, and those
who have recently traveled to the
developing world.
 DX.
• Diagnostic testing may also be done for
surveillance. As hypoglycemia occurs in
approximately 10% of infants and young
children, measuring serum glucose in
this population is recommended.
Electrolytes and kidney function should
also be checked when there is a
concern about severe dehydration.
 Differential diagnosis.
• Other potential causes of signs and
symptoms that mimic those seen in
gastroenteritis that need to be ruled
out include appendicitis, volvulus,
inflammatory bowel disease,
urinary tract infections, and
diabetes mellitus.
 DIFFERENTIAL DX.
• Pancreatic insufficiency,
short bowel syndrome,
Whipple's disease, coeliac disease,
and laxative abuse should also be
considered. The differential diagnosis
can be complicated somewhat if the
person exhibits only vomiting or
diarrhea (rather than both).
 DIFFERENTIAL DX.
• Appendicitis may present with
vomiting, abdominal pain, and a small
amount of diarrhea in up to 33% of
cases.[2] This is in contrast to the
large amount of diarrhea that is
typical of gastroenteritis.[2] Infections
of the lungs or urinary tract in children
may also cause vomiting or diarrhea.[
 DIFFERENTIAL DX.
• Classical diabetic ketoacidosis (DKA)
presents with abdominal pain,
nausea, and vomiting, but without
diarrhea. One study found that 17%
of children with DKA were initially
diagnosed as having gastroenteritis.
 MANAGEMENT.
• Gastroenteritis is usually an acute
and self-limiting disease that does not
require medication. The preferred
treatment in those with mild to
moderate dehydration is
oral rehydration therapy (ORT).
 MANAGEMENT.
• Antiemetic medications may be
helpful for treating vomiting.
• Metoclopramide might be helpful.
• Antibiotics are not usually used for
gastroenteritis, although they are
sometimes recommended if
symptoms are particularly severe[66] or
if a susceptible bacterial cause is
isolated or suspected.[67]
 MANAGEMENT.
• If antibiotics are to be employed, a
macrolide (such as azithromycin) is
preferred over a fluoroquinolone due
to higher rates of resistance to the
latter.
 PREVENTION.

• For infants prevent low birth weight and

prematurity by improving antenatal care.
• Oral rehydration therapy to reduce
diarrhea related deaths.
• Improvement of water and sanitation to
reduce transmission and number of
episodes of diarrhea
• Improve weaning practices and nutrition of
children
 PREVENTION.
• Investigation of diarrheal outbreaks.
• Immunization against measles.
• Sustained breast feeding.
• Continue breast feeding in the
second year.
• Antenatal care to reduce low birth
weight.