BHU

Communicable Disease control

1 W
 Zoonotic disease
A zoonotic disease(Zoonosis) is a disease that can be passed
between animals and humans.
Zoonotic diseases can be caused by viruses, bacteria,
parasites, and fungi.
Scientists estimate that more than 6 out of every 10 infectious
diseases in humans are spread from animals.
Many people interact with animals in their daily lives.
We raise animals for food and keep them in our homes as pets.
We might come into close contact with animals at a county
fair or petting zoo or encounter wildlife when we clear
wooded land for new construction.
For most of these diseases, man is a dead-end of the
transmission cycle.
This means under normal conditions, man will not infect
other human beings.
These can include:
1) Coming into contact with the saliva, blood, urine, or feces
of an infected animal
2) Being bitten by a tick or mosquito (often called a “vector”)
3) Eating or drinking something unsafe (such as unpasteurized
milk, undercooked meat, or unwashed fruits and vegetables
that are contaminated with feces from an infected animal) 
 A) Food of Animals
1 . Taeniasis
Taeniasis is an intestinal infection with the adult stage of
large tapeworms.
Cysticercosis, taeniasis and hydatids are a subset of
‘cestode’ (tapeworm infection)
Cysticercosis refers to disease in the tissues caused by the
larval stage of one species of tapeworm – Taenia solium.
Infectious agent
Taenia saginata (beef tapeworm)

Taenia solium (pork tapeworm)

Epidemiology
 Worldwide; frequent where beef or pork is eaten raw or
insufficiently cooked and where sanitary conditions
permit pigs and cattle to have access to human feces.
Prevalent in Latin America, Africa, South East Asia and
Eastern Europe.
Reservoir
Humans are definitive hosts of both species of Taenia;
cattle are the intermediate hosts for Taenia saginata and
pigs for Taenia solium.
Mode of transmission and life cycle
 Eggs of Taenia saginata passed in the stool of an infected
person are infectious only to cattle in the flesh of which the
parasites develop into “cysticercus bovis”; the larva stage
of Taenia saginata.
In humans, infection follows after ingestion of raw or
under-cooked beef containing cysticerci; the adult worm
develops in the intestine.
Taenia Solium eggs to mouth of oneself or to another
person or ingestion of food or water infected with eggs-
embryos escape from the shells-penetrate the intestinal
wall lymphatics or blood vessels and are carried to the
various tissues where they develop to produce the human
disease of cysticercosis.
 Transmission
1. Cysticerci ingested in
undercooked meat. T. saginata
in beef T. solium in pork.

Human Host
2. Cysticerci attached to wall
Environment
of 6. Segments and eggs reach
small intestine. ground where animals feed.
3. Become mature Animal host:
tapeworms Cattle for T. saginata pig for
4. Eggs released when T. solium
7. Eggs ingested.
gravid
8. Embryos carried to
segments become detached. muscles. Develop into
5.
7
Eggs and gravid segments infective cysticerci.
Incubation period
 8-14 weeks, eggs appear in stool in both species.

Period of communicability-
 Larvae remain viable in animal tissues for years.

 Adult tapeworms may live in the human intestine and

shed eggs for up to 25 years, growing up to 8 metres in
length.
 T. saginata is not directly transmissible from person to
person, releasing eggs that are only infectious to cattle.
 T. solium is directly transmissible, having eggs that are
infectious both to humans and to pigs.

Susceptibility and resistance
 Susceptibility is general.

 No apparent resistance follows infection but more than

one tapeworm in a person has rarely been reported.
Clinical manifestation
 Symptoms of cysticercosis may appear after some days
and stay for 10 years after infection.
 Long motile proglottids can migrate out of the anus and
be seen on the perineum, on clothing or in the faeces.
 Minimal or mild abdominal/ Epigastric pain or
discomfort, nausea, change in appetite, nervousness,
anorexia, weakness and weight loss.
 Usually asymptomatic.
Diagnosis
 Identification of proglottidis (segments)

 Eggs in feces or anal swab

 Cysticercus – palpable subcutaneous cysticercus and

 microscopic examination of an excised cysticercus

confirms the diagnosis.
 Intracerebral and other tissues- CT scan, MRI or by x-
ray when the cysticerci are calcified.
Treatment
First line
Niclosamide, 2 g in a single dose P.O..
Alternatives
Albendazole, 400 mg in a single dose P.O.
OR
Praziquantel, 600 mg in a single dose P.O.
OR
Mebendazole, 200 mg P.O.BID for 3 days
Cysticercosis management
 Chemotherapy
 Surgery and supportive medical treatment
For symptomatic patients with neurocysticercosis,
admission is required.
Combination of Praziquantel and Albendazole can be
used.
Besides, high dose of glucocorticoids can be used to
decrease inflammation.
Prevention and control
1. Educate the public to:
 Prevent fecal contamination of soil, water, human &
animal foods
Cook beef and pork thoroughly.

Use latrines.

2. Identification and immediate treatment of cases.

3. Freezing of pork/beef below –5oc for more than 4 days
kills the cystraci effectively or cooking to a temperature
of 56oc for 5 minutes destroys cystcerci.
4. Deny swine access to latrines and human feces.
 2) Brucellosis
A systemic bacterial disease with acute or insidious onset
transmitted to humans from infected animals.
Infectious agent
 Brucella melitensis (most common worldwide), acquired
primarily from goats, sheep and camels.
B. abortus from cattle

B. suis from pigs

B. canis from dogs

These are small aerobic gram-negative bacilli, intracellular

parasites.
Epidemiology
 Worldwide.

 Predominantly an occupational disease of those working

with infected animals or their tissues especially farm
workers, veterinarians and abattoir workers
 Infections are usually seen in farmers,

 Outbreaks can occur among consumers of raw milk and

milk products, especially unpasteurized soft cheese from
cows, sheep and goats.
Reservoir-
Cattle, swine, goats and sheep, pet dogs.
Mode of transmission
By contact with tissues, blood, urine, vaginal discharges,
aborted fetuses and especially placentas (through breaks in
the skin).
Humans may be infected through contact with infective
material via cuts or abrasions in the skin, conjunctivae or
inhalation
Most commonly through ingestion of raw milk and dairy
products from infected animals (raw meat or bone
marrow).
Airborne infection occurs in humans in laboratories and
abattoirs.
Incubation period
 May last about 1-3 weeks but may be as long as several
months.
Period of communicability-
No evidence of communicability from person to person.

Susceptibility and resistance-

Severity and duration of clinical illness are subject to
wide variation.
Duration of acquired immunity is uncertain.
Clinical manifestation
 Abrupt onset of symptoms

Most common symptoms are:

Fever, chills, diaphoresis,

Headache, myalgia, fatigue,
Anorexia, joint and low back pain,
Weight loss, constipation,
Sore throat, and dry cough.
Physical examination reveals

 Often no abnormalities and patient looks well

 Some are acutely ill, with pallor, lymphadenopathy,

hepatosplenomegally, arthritis, spinal tenderness,
epididymoorchitis, skin rash, meningitis, cardiac
murmurs, or pneumonia
Reactive asymmetric polyartharitis (knees, hips,
shoulders, sacroiliac and sternoclavicular joints)
Diagnosis
 Exposure and consistent clinical features

 Serology- raised levels of B. agglutinin

 Blood or bone marrow culture

Treatment
Nondrug Treatment
Surgical intervention e.g. abscess drainage, joint
replacement will be needed for focal infections.
Drug Treatment
First Line:
 Doxycycline 100 mg PO bid + Rifampicin 600-
900mg/day for 6 weeks.
Alternative:
 Doxycycline 100 mg PO bid + Streptomycin (750mg-
1 gram/d IM for 2-3 weeks)
 (For children Trimethoprim-Sulfamethoxazole 8-
10mg/kg PO divided into 2 doses for 3 weeks +
Gentamicin 5-mg/kg/day IM or IV for 5-7 days.
Prevention and Control
1. Control depends on elimination of the disease among
domestic animals.
2. Educate people not to drink untreated milk or eat
products made from untreated milk.
3. Educate farmers and slaughterhouse workers and those
in meat processing plants and butcher shops as to the
nature of the disease and the risk in the handling of
carcasses and products of potentially infected animals.
4. Educate hunters to use barrier precaution (gloves and
clothing).
5. Eliminate infected animals.
6. Pasteurize milk; cook meat and bone well.
7. Proper disposal of placenta, discharges or fetus from
an aborted animal. Disinfect contaminated areas.
 3) Trichinellosis or Trichinosis
A disease caused by an intestinal round worm whose
larvae (trichinae) migrate to and become encapsulated in
the muscles.
Infectious agent
Trichinella spiralis, an intestinal nematode

Epidemiology
Worldwide, but variable incidence, depending in part on
practices of eating and preparing pork or wild animal meat.
Reservoir
Swine, dogs, cats, rats and many wild animals, including
fox, wolf, etc.
Mode of transmission
 By eating raw or insufficiently cooked flesh of animals
containing viable encysted larvae, chiefly pork and pork
products and "beef products”
It is a food-borne infection and not contagious from one
human to another unless infected human muscle is eaten.
Almost any carnivore (meat eater) or omnivore (eats
meat and plants for food) can both become infected and,
if eaten, can transmit the disease to other carnivores and
omnivores.
Life cycle

28
28
Incubation period
Systemic symptoms usually appear about 8 - 15 days
after ingestion of infected meat.
Susceptibility and resistance
Susceptibility is universal.
Infection results in partial immunity.
Clinical manifestation
 Symptoms result from invasion of the body by larvae
produced by the adult female worm in the intestine and
from their encystment in striated muscles.
 Infection ranges from symptomatic to mild febrile illness to a
severe progressive illness with multiple system involvement.
 Fever (low - high grade)

 Muscle pain mainly upon movement

Edema, and spasm (periorbital and facial)

Photophobia and conjunctivitis

 prostration

Dyspnea, coughing and hoarseness

Subconjuctival, retinal and nail splinter hemorrhage and

Rashes
Diarrhea, Abdominal cramps, Nausea and vomiting
Inflammatory reactions around larvae that reach tissues
other than muscles may result in:
􀂃 Meningitis
􀂃 Encephalitis
􀂃 Myocarditis
􀂃 Broncho-pneumonia
􀂃 Nephritis
􀂃 Peripheral and
cranial nerve disorders
Diagnosis
History of ingestion of raw or inadequately cooked pork
More specific tests (enzyme-linked immunosorbent
assays) are available that detect antibodies developed by
the infected person's immune response to the parasites =
Positive serologic test
The best test for trichinosis is a biopsy of muscle that
shows larvae in the muscle tissue.
Eosinophilia
Treatment
1. Hospitalization of the patient
2. Mebendazole or
3. Albendazole or
4. Thiabendazole
5. High doses of corticosteroids for 1-2 days followed by
lower doses for several days or weeks. But not for
intestinal stage.
Prevention and control
1. Educate the public on the need to cook all fresh pork
and pork products and meat from wild animals.
2. Freezing of pork and its products inactivates trichinae.
 4) Toxoplasmosis
Toxoplasmosis is a systemic protozoal disease that can be
either acute or chronic type with intracellular parasite.
Infectious agent
Toxoplasma gondii
Epidemiology
Worldwide in mammals and birds.
Infection in man is common.
About 47% of African , more than 50% adult population in
north America and west Europe shows antibodies to T. gondii
Only about 1% of persons showing antibody to T. gondii have
signs and symptoms of diseases
In Ethiopia : few studies indicated the disease found in
Ethiopia
Reservoir-
The definitive hosts are cats and other felines, which
acquire the infection mainly from eating infected
mammals (especially rodents) or birds and rarely from
feces of infected cats.
Only felines harbor the parasite in the intestinal tract
where the sexual stages of its life cycle takes place,
which result in the excretion of the oocyst in feces for
10-20 days or rarely longer.
The intermediate hosts of T. gondii include man, sheep,
goats, rodents, cattle, chicken and birds.
 The life cycle can be either hetroxenous (requiring two
hosts) or monoxenous (one host).
Both sexual and asexual reproduction occurs in man.
There are 4 or 5 main developmental forms in the life
cycle, but only trophozoites and cyst stages are found in
human.
All stages occur in the felines (cats).
Toxoplasma has two forms
1. Tachyzoites- occur in the early acute stage of infection.
2. Bradyzoites-occur in the chronic stage of infection,
develop slowly and multiply in the tissue to form a true
cyst.
 Mood of Transmission and lifecycle
1. Ingestion of cysts in raw or under-cooked meat
2. Ingestion of oocysts in food, drink or from hands
contaminated with feces of an infected cat.
3. Transplacental/congenital
4. Blood transfusion
5. Organ transplantation
39
Incubation period-
From 10-23 days.

 One common source outbreak from ingestion of under-

cooked meat is possible.
Period of communicability-
Not directly transmitted from person to person, except in
utero.
Oocysts shed by cats sporulate and become infective 1-5
days later and may remain infective in water or moist soil
for about a year.
Cysts in the flesh of an infected animal remain infective
as long as the meat is edible and uncooked.
Susceptibility and resistance
 Susceptibility to infection is general, but immunity is
readily acquired and most infections are asymptomatic.
 Duration and degree of immunity are unknown, but are
assumed to be long-lasting or permanent.
 Antibodies persist for a year, and probably for life.

 Patient undergoing cytotoxic or immuno-suppressive

therapy or patients with AIDS are at risk of developing
the disease.
 Clinical manifestation
Early infections
The acute form of this disease is characterized by
fatigue, lymphodenitis, chills, fever, headache and
myalgia.
Latent infections
Adults acquired infection are often asymptomatic , they
can cause the patient may develop maculopapular rash,
encephalomyelitis and hepatitis; retinochoriditis with
subsequent blindness has been known to occur on rare
occasions.
HIV associated toxoplasmosis
 Serious & often fatal opportunistic toxoplama
infections
 Infections are due to the reactivation of cysts
Cause encephalitis with fever , headache, mental
deterioration and seizures
Congenital Toxoplasmosis:
 The typical symptoms in an infected child include
hydrocephaly, microcephaly, choreoretinitis, convulsion
and psychomotor disturbance.
Most of these infections ultimately result in mental
retardation, severe visual impairment or blindness.
  Occur in about 1-5 per 1000 pregnancies of which 5-
10% result in miscarriage and 8-10% result in serious
brain and eye damage to the fetus
 10-13% of the babies will have visual handicaps

Diagnosis
Clinical sign and symptom

Serological test

Identifying toxoplasma in Giemsa stained histological

sections, aspirates of lymphnode, bone-marrow, CSF,
pleural fluid, peritoneal fluids and sputum
Cell culture
 Treatment
First line
Sulfadiazine, 1-2g P.O.QID for six weeks
PLUS
Pyrimethamine, 25-100mg, P.O. QID
PLUS
Folinic acid, 10-20 mg P.O. QID for six weeks
Followed by Maintenance
pyrimethamine, 25mg/day P.O. QID
Alternatives
 Sulfadoxin pyrimethamine, 1000 mg/50 mg, P.O. BID for
two days, then one tablet/day for 6 weeks.
PLUS
Folinic acid, 10-20mg ,P.O. QID for 6 weeks
OR
Clindamycin, initially 200-400mg I.V. QID followed by 300-
900 mg, P.O. TID PLUS
Pyrimethamine, 25-100 mg/day P.O
PLUS
Folinic acid, 10-20 mg/day P.O.
PLUS
Azitromycin, 900-1200mg P.O. QID
Followed by Maintenance pyrimethamine, 25mg/day P.O.QD
Prevention and control
1) The cause of primary infection with Toxoplasma can be
reduced by avoiding eating under-cooked or raw meat
and avoiding cyst-contaminated materials (i.e. cat’s litter
box).
2) Meat should be heated to 600c or frozen to kill cysts.
3) Hands should be washed thoroughly after work in the
garden and all fruits and vegetables should be washed.
4) Discourage cats from hunting.
5) Dispose cats’ feces daily.
6) Control stray cats and prevent them from gaining access
to sand boxes and sand piles.
7) Educate pregnant women.
To avoid cleaning litter pans or contact with cats.

Dietary meat; to heat to 60oc or freeze it.

To wear gloves during gardening.

8) Blood intended for transfusion into Toxoplasma

seronegative immuno-compromised individuals should
be screened for antibody to toxoplasma gondii.
9) Patients with HIV/AIDS who have severe symptomatic
toxoplasmosis should receive prophylactic treatment
(Prymethamine, sulfadizine, folinic acid) throughout
their life span.
 B) Animal Bite Diseases
1. Rabies

 Rabies ( From Latin: rabies, "madness") is a viral disease

that causes acute encephalitis in warm-blooded animals.
It is almost invariably fatal: acute vial encephalomyelitis
(attacking brain and meninges).
Infectious agent
Rabies virus
Epidemiology
Worldwide in wildlife particularly in developing countries.
Worldwide, roughly 97% of rabies cases come from dog
bites.
It is primarily a disease of animals (zoonotic).
It is primarily an infection of carnivores transmitted
through bite.
Reservoir
Dog is common in urban areas; in the wild, wild
carnivores and bats are reservoirs.
Mode of transmission-
Transmitted with saliva of rabid animal introduced by a
bite or scratch.
Transmission from man to man is dead-ended.
In Ethiopia the disease is transmitted to humans via dog,
and rarely, cat bites;
Incubation period-
Usually 3-8 weeks
Period of communicability
Usually 3-7 days before the onset of the disease and
throughout the course of the disease.
Susceptibility and resistance-
All mammals are susceptible to varying degrees.
Humans are more resistant to infection than several
animal species.
Clinical Manifestation
The clinical manifestation, which is the same in all species
including humans, has 3 phases:
1. Prodromal phase
2. Excitatory phase
3. Paralytic phase
A/Prodromal phase:
Non-specific symptoms,

Onset is heralded by a sense of apprehension, headache, fever

and nausea, abnormal sensations at the site of inoculation
(bite) is most significant, (i.e. paraesthesia, tingling sensations
at the bite site).
B/Excitatory phase or Aerophobia:
Slightest sound/wind excites the victim, irritability, restless,
nervousness, tendency to bite, are some of the symptoms.
C/Paralytic phase:
Spasm of swallowing muscles leads to drooling of saliva and
fear of water (hydrophobia).
Delirium and convulsions form and death is often due to
respiratory muscle paralysis.
Finally, the patient may experience periods of mania and
lethargy, eventually leading to coma.
The primary cause of death is usually respiratory
insufficiency.
Diagnosis
History of bite by known rabid animal and the bitten person
show typical symptoms leading to clinical diagnosis.
Treatment
Non-Drug Treatment
Wash the wound with soap and water thoroughly to
decrease the viral load.
Nurse patient in a quiet, darkened room.
Nutritional, respiratory and cardiovascular support when
required.
Never suture the wound as this will spread the virus
 Drug Treatment (post exposure prophylaxis)

1/ Human antirabies immunoglobulin, 20 IU/kg, should

be given immediately (half the dose should be infiltrated
around the site of the bite wound, and the other half be
given IM in the deltoid area).
Dosage forms: Injection, 150 IU ml in 2ml.

N.B. Store in refrigerator; do not freeze (discard if vaccine

has been frozen)
PLUS
2/ Human diploid cell strain vaccine (HDCV), 1 ml. IM,
given on days 0, 3, 7, 14 and 28
Prevention and control
1) Immunize all dogs and cats.
2) Detain and clinically observe for 10 days any healthy
appearing dog or cat known to have bitten a person.
3) Post exposure prophylaxis
Treatment of bite wounds

Specific immunologic protection

4) Keep dogs and cats at home.

5) Destroy stray animals where rabies is endemic.
 Animal Reservoir Diseases
A/ Leishmaniasis
A polymorphic protozoan disease of the skin and mucous
membrane or a chronic systemic disease caused by a
number of species of the genus leishmania.
Infectious agents
Leishmaniasis can easily classified clinically as

Visceral leishmaniasis
Cutaneous leishmaniasis
Mucocutaneous leishmaniasis
Diffuse cutaneous leishmaniasis
Cutaneous leishmaniasis(CL) is caused by
L. tropica
L. major
L. aethiopica
L. panamensis
L. guyanensis
L. peruviana
Visceral leishmaniasis(VL)
 Also called Kala azar, Dum- Dum fever, death fever ,
tropical spleenomegaly
 Caused by
L. donovani
L. infantum
 L. Chagasi
Mucocutaneous leishmaniasis(MCL) caused by

L. panamensis

L. guyanensis

L. bazilliensis

L. Aethiopica

In immunosuppressed persons, L.donovani, or L.

major or L.infantum.
Diffuse cutaneous leishmaniasis(DCL) caused by

L. amzonensis

L. aethiopica
Epidemiology
It occurs in sub-Saharan Africa, Sudan, the highlands of
Ethiopia, Kenya, Namibia and others
Urban populations including children may be at risk.
It is common where dog populations are high, generally
more common in rural than urban areas.
350 million people are at risk in 88 countries around the
world
72 of which are developing countries

An estimated 12 million cases world wide

1.5 to 2 million new cases occur every year

CL form representing 50 to 75% of all new cases

IN ETHIOPIA

Four species of Leishmania is found, namely,

L. aethiopica,

L.major

L. tropica

L. donovani
Visceral leishmaniasis (VL) >> L. donovani

Occurs mainly in arid and semiarid lowlands below

1,300 m altitude
Important endemic foci include
Gelana focus at lake abaya,
The segen valley (Aba- Roba focus) in Knoso Wereda
The Omo river plains and
The Metema and Humera plains in north western
Ethiopia
Cutaneous leishmaniasis

L. aethiopica, L.major, L. tropica

Endemic at altitudes 1400 - 2700m in most

administrative regions
Prevalence rates of 5.5 – 40% were reported from
villages in Shewa , Wello and G.Gofa with the highest
rate in Ocholo village in G. Gofa
Reservoirs
Locally variable; include human beings, wild carnivores
and domestic dogs.
Mode of transmission and lifecycle
Common mode of transmission.
Bite of infected female sand fly

Genera Phlebotomus in Old world

Lutzomyia in New world

Uncommon modes of transmission:

Congenital transmission,

Blood transfusion,

Sexual contact
Incubation period-
At least a week; up to many months.
Period of communicability-
Infectious to sand flies as long as parasites remain in
lesion, in untreated cases, usually a few months to 2
years.
 Eventual spontaneous healing occurs in most cases.
Clinical Manifestation
There are papules that further develop to ulcers.
The disease is characterized by fever,
hepatosplenomegally, lymphadenopathy, anemia,
leucopoenia, thrombocytopenea, and progressive
emaciation and weakness.
Old World CL
L. Tropica
Anthroponotic or
dog reservoir
dry ,urban ,chronic,
old world oriental
sore
'dry painless lesion’
L. Major

central Asia, middle

East, Africa
rural (rodent reservoir)
wet oriental sore
Early papules is
inflamed
Develop to large uneven
ulcer  Ulcers are moist or open
Self-healing (3-6mths) with seropurulent exudate
Diffuse Cutaneous Leishmaniasis

caused by L. aethiopica and L.

amazonensis

Skin lesion develop over large

areas of the body
Scaly, not ulcerated, nodules

Chronic and painless

Numerous parasites in lesions

Seldom heal despite treatment

Mucocutaneous Leishmaniasis
Known as espudia
Two stages
Simple skin lesion
2o mucosal involvement
Metastasis via blood or
lymphatic systems
Can occur after primary lesion
(up to 16 years)
Frequently in naso-pharyngeal
mucosae ,
Junction of skin and mucosa
Non-ulcerative type
Local edema (upper lip)
Ulcerative type
Rapid and extensive
mutilation
 Disfiguration is often extreme
with complete destruction of the
 Nasal septum,
 Perforation of the palate
 And damage of the tissues
of the lips and larynx
 Visceral leishmaniasis (VL)
Reticuloendothelial system affected
Spleen, liver, bone marrow, lymph nodes

The disease may be asymptomatic and self-resolving

but usually runs a chronic course and may be fatal
without treatment
 Untreated VL carries have progressive disease
75-95% mortality
Death generally within 2 years
Death usually occurs because of severe secondary
bacterial infections in advanced disease
•Pneumonia is the common complication
Fever, malaise, weakness

Wasting despite good appetite

Spleno- and hepatomegaly,

enlarged lymph nodes

Epistaxis (nose bleeding) and

bleeding of gums
Depressed hematopoiesis
Severe anemia
Leucopenia
Thrombopenia
A 12-year-old boy

suffering from visceral

leishmaniasis.
The boy exhibits

splenomegaly and
severe muscle
wasting (emaciation)

76
Diagnosis
 Demonstration of the parasite (blood or tissue)
Detecting amastigotes from scrapings, biopsy,
aspirates (gold standard)
By culture of the motile promastigote
Using serologic test

Treatment 
General:  
Supportive care includes treatment of concomitant
infections and blood transfusions
For VL
Specific:
First line
Sodium stibogluconate, 20 mg/Kg/day given IV OR IM
in a single dose for 28 consecutive days. Therapy should
be repeated using the same dose for another 40 to 60 days
in patients with relapse or incomplete response.
Alternatives
Amphotericin B, 0.25 to 1 mg/kg by slow infusion
QID, or three times a week for up to 8 weeks depending
on the response. OR
Pentamidine Isethionate, 3 to 4 mg/kg IM QID for up
to 15 doses.
For CL
Sodium stibogluconate, given intramuscularly IM OR
IV QID for 10 days.
Prevention and control
1. The avoidance of outdoor activities.
2. The use of mechanical barriers such as screens and bed
nets.
3. Wearing of protective clothing.
4. Application of insect repellent.
5. Treatment of cases.
6. Vector control and elimination of reservoir host (e.g.
 B/ African Trypanosomiasis
A systemic disease caused by protozoa characterized by
fever followed by general weakness and cerebral
involvement leading to death.
Infectious agent
The commonest agents are:
T. Brucei rhodesiense
Causes a rapidly progressing disease
Disease: East African or Rhodesian African sleeping
sickness
 T. Brucei gambiense
Causes a slowly developing disease

Disease: West African or Gambian African sleeping

sickness
Vectors for all species are tsetse flies of Genus Glossina.

Epidemiology
The trypanosomes that cause sleeping sickness are found
only in Africa.
 20,000 new cases are reported each year.

 In Ethiopia, the distribution of Trypanosomiasis is mostly

found in Jinca, Afar, Setitu Humera, Konso, Moyale, and
Dilla.
 T.b. rhodesiense is singled out as the species occurring

in Ethiopia
The Sleeping sickness foci are limited to Gambela
(the areas along Baro, Gilo and Akobo rivers), Gamo
Gofa (from Mursi-Bodi district), Kefa (from Maji),
and Welega ( from the settlement area in the Anger-
Didesa valley)
Reservoir
For T. brucie gambiense it is only humans.
For T. brucie rhodesiense the reservoir is dog, cattle, fox,
wolf and human beings.
Mode of transmission-
By the bite of infective Glossina Tsetse fly during blood
meal.
Congenital transmission
Blood transfusion
Laboratories: accidental infections,
Incubation period
T. brucei rhodensiense: 3 days to few weeks.
T. brucei gambiense: several months up to one year.
Period of communicability
As long as the parasite is present in the blood of
infected person or animal and infected Tsetse fly.
Susceptibility and resistance
All persons are equally susceptible for the disease.
Clinical Manifestation

Haemolymphatic
phase
Morphologically, the chancre is a localized inflammatory
site, with oedema, infiltrations of macrophages and
lymphocytes, and multiplying parasites, but without pus
as occurs in boils due to many other microbial infections.

The parasite spreads from the chancre into the lymphatics

and blood system.

Malaise

Headache, Weight loss

Hepatomegally and Tachycardia

 Stage II

Neurological phase

Abnormality in
CSF
 Day time
somnolence
Tremors
Parkinson’s
disease
Diagnosis
 C/M
 Thick blood smear
 Serological test
 CSF analysis
 Blood film
 Bone marrow biopsy
Treatment
For stage I (Normal CSF) – T.b. gambie treated
with
􀂃 Suramin or
􀂃 Eflornithine or
􀂃 Pentamidine
For stage II
Trypansamide
Prevention and control
1. Public education on personal measures to protect against
insect bite.
2. Eradication of vectors.
3. Drug treatment of infected humans.
4. Avoiding areas to be known by harboring infected
insects.
5. By wearing protective cloth and by using insect
repellents.
6. Reducing tsetse fly number by:-
Identifying and studying the breeding habits of local
vector
Selectively clearing the bush and wooden areas
especially around game reservoirs, water holes, bridges
and along rivers bank
Using and maintaining insecticide impregnated tsetse fly
traps.
7. Spraying vehicles with insecticide as they enter and
leave tsetse fly infested areas
8. Prohibit blood donation from those who have visited or
lived in endemic areas.
10Q