Zoonoses by protozoans

ZOONOSES BY

PROTOZOANS

Dr. NEETHU K P

Dept. of Vet. Public Health

College of Veterinary and Animal Sciences, Mannuthy, Kerala

INTESTINAL PROTOZOAL

INFECTION SYSTEMIC PROTOZOAL

INFECTION

• Amoebiasis

• Giardiasis

• Cryptosporidiosis

• Balantidiasis

• Cyclosporidiosis

• Microsporidiosis

Toxoplasmosis

Leishmaniasis

African trypanosomiasis

(sleeping sickness)

American trypanosomiasis

(Chagas’ disease)

Malaria

Babesiosis

TOXOPLASMOSIS

Toxoplasma gondii

Subphylum Apicomplexa

Family Eimeriidae

Obligate intracellular parasite

Definitive host – cats

Intermediate hosts – sheep, goats, pigs, humans

All warm-blooded animals, including mammals and birds

Second commonest opportunistic infection in AIDS patients, with as high as 75 % mortality

Distribution

Dark red- >60% Yellow- 20-40% Green- <1% Red – 40-60% Blue- 10-20% White- Absence of data

In INDIA…

The prevalence of toxoplasmosis in India was as high as 77%

in women of reproductive age

IgG and IgM antibodies were found in 24.3% and 2% of the

samples, respectively

A higher prevalence of T. gondii infection has been recorded

in women belonging to low socio-economic groups

(Dumne et.al,2007)

Higher seroprevalence was observed in pigs (14.0%), sheep

(7.9%), goats (8.8%) and camels (7.5%)

The prevalence of T. gondii in cats (2.5%) is low when

compared with that in Western countries

The incubation period is uncertain but probably ranges from

5–23 days in humans

PATHOPHYSIOLOGY

There are three infective stages of T. gondii:

Rapidly dividing invasive tachyzoite

Slowly dividing bradyzoite in tissue cysts

Environmental stage, the sporozoite, protected inside an

oocyst

MODES OF TRANSMISSION

Contd….

Toxoplasmosis can be transmitted transplacentally if the mother

becomes infected during pregnancy or if immunosuppression

reactivates a prior infection.

Transmission of Toxoplasma to a fetus is extraordinarily rare in

immunocompetent mothers who have had toxoplasmosis earlier

in life.

Past infection confers resistance to reinfection.

DISEASE IN MAN

Acute toxoplasmosis

CNS toxoplasmosis

Congenital toxoplasmosis

Ocular toxoplasmosis

Disseminated or non-CNS disease in immunocompromised patients

ACUTE TOXOPLASMOSIS

Asymptomatic

10 to 20% of patients develop bilateral, nontender cervical

or axillary lymphadenopathy.

Mild flu-like syndrome of fever, malaise, myalgia,

hepatosplenomegaly

Self-limited.

CNS TOXOPLASMOSIS

Most patients with AIDS or other immunocompromised

patients with encephalitis

Headache, altered mental status, seizures, coma, fever

Focal neurologic deficits, such as motor or sensory loss,

cranial nerve palsies, visual abnormalities, focal seizures.

CONGENITAL TOXOPLASMOSIS:

Spontaneous abortion, stillbirth, birth defects

The percentage of surviving fetuses born with toxoplasmosis depends on when maternal infection is acquired

15% during the 1st trimester

30% during the 2nd

60% during the 3rd.

Most infants born to mothers infected during the 3rd trimester appear healthy at birth but are at high risk of seizures, intellectual disability, retinochoroiditis

Disease in neonates - severe, particularly if acquired early in

pregnancy; - jaundice, rash, hepatosplenomegaly

Characteristic tetrad of abnormalities: bilateral

retinochoroiditis, cerebral calcifications, hydrocephalus or

microcephaly and psychomotor retardation.

Prognosis is poor.

OCULAR TOXOPLASMOSIS

This type usually results from congenital infection that is

reactivated, often during the teens and 20s, but rarely, it

occurs with acquired infections.

Focal necrotizing retinitis

Secondary granulomatous inflammation of the choroid

Ocular pain, blurred vision, sometimes blindness.

DISSEMINATED INFECTION AND NON-

CNS INVOLVEMENT:

Less common

Primarily in severely immunocompromised patients.

Pneumonitis, myocarditis, polymyositis, diffuse

maculopapular rash, high fevers, chills, and prostration.

Untreated disseminated infections are usually fatal.

DISEASE IN CATS

Most postnatally acquired infections in cats are

ASYMPTOMATIC.

Prepatent period variable - 3 days to several weeks.

Shedding occurs for 1-2 weeks

DIAGNOSIS:

Sabin- Feldman Dye Test: most sensitive test, but rarely used.

IFA

Latex agglutination test

ELISA.

MRI

Brain biopsy

Tachyzoites in blood or body fluids confirms active infection.

SABIN-FELDMAN DYE TEST

Live tachyzoites stain blue with alkaline methylene blue dye.

Live tachyzoites are mixed with different dilutions of the

patient's serum

The mixtures are then incubated for an hour, stained with dye,

and examined with a microscope.

If antibodies to T gondii are present in the patient's serum, they

will damage the organisms.

The damaged organisms will not take up the dye and appear as

pale "ghosts" compared to undamaged organisms.

Test is very sensitive and specific and remains the reference

method.

TREATMENT IN MAN:

The treatment of choice is pyrimethamine plus either

trisulfapyrimidines or sulfadiazine.

Folinic acid is given to avoid the hematologic effects of

pyrimethamine-induced folate deficiency.

PREVENTION/CONTROL:

Freezing of meat to -20ºC (-4ºF) for 2 days or heating to

60ºC (140ºF) kills cysts.

Children's play areas should be protected from cat and dog

feces.

Daily cleaning of cat litter pans (since oocysts not infective

for 2 to 3 days)

Wear gloves

Wash hands before eating

Should only be fed dry, canned, or cooked meats

Pregnant women shouldn’t handle cats

AFRICAN TRYPANOSOMIASIS

African Sleeping Sickness

Gambian Trypanosomiasis

Rhodesian Trypanosomiasis

Cattle -Nagana.

Trypanosoma brucei gambiense and T brucei rhodesiense

T.b.brucei - rarely infects humans-T. brucei are lysed by a factor

in human serum, whereas T. rhodesiense and T. gambiense are

not.

Vector: tsetse fly (Glossina palpalis, G. tachinoides, or G. fuscipes).

Trypanosoma brucei gambiense is found in 24 countries in west

and central Africa.

Accounts for more than 98% of reported cases of sleeping

sickness

Causes a chronic infection.

Trypanosoma brucei rhodesiense - 13 countries eastern and

southern Africa.

2% of reported cases

Causes an acute infection

In 2009, the number of cases reported was 9878

2012 there were 7216 cases recorded. (who,2013)

RESERVOIRS

Many wild and domestic animals harbour infection

In Rhodesian trypanosomiasis - domestic cattle and pigs

In Gambian trypanosomiasis, humans are the main reservoir

However the precise epidemiological role of the animal

reservoir in the gambiense form of the disease is not yet well

known.

DISTRIBUTION

TRANSMISSION:

Transmission is by the tsetse fly bite.

Mother-to-child infection: the trypanosome can cross the

placenta and infect the fetus.

Mechanical transmission through other blood sucking insects

is possible.

Accidental infections have occurred in laboratories due to

pricks from contaminated needles.

DISEASE IN ANIMALS:

Occasionally mild disease occurs in domestic animals

DISEASE IN HUMANS:

1. The trypanosomal chancre:

Seen at site of the tsetse bite

Appears about 48 hours after and lasts 2-4 weeks.

Local pruritic, painful inflammatory reaction with regional

lymphadenopathy

2. The hemolymphatic stage:

Usually absent or unnoticed in T. b. gambiense infections.

Irregular fevers, headaches, joint pains,

malaise, pruritus, papular skin rash, edemas.

Myocarditis

Trypanosomes enter the lymphatics - lymphadenopathy - T. gambiense is the enlarged cervical lymph nodes, called Winterbottom’s sign

3. The meningoencephalitic stage:

Insomnia

Motor and sensory disorders

Abnormal reflexes

Somnolence to coma.

DIAGNOSIS:

Definitive diagnosis requires identifying the organism in the

bite lesion, blood, lymph node aspirate, or CSF.

Serologic tests become positive after 12 days.

TREATMENT: Hemolymphatic stage: Suramin, eflornithine or pentamidine.

Late disease: melarsoprol or eflornithine or tryparsamide

plus suramin.

PREVENTION/CONTROL:

Wear long sleeves and trousers in endemic areas

Use mosquito nets while sleeping.

Repellents do not work on tsetse flies.

Pentamidine is used as a chemoprophylaxis against the

Gambian type.

A new form of human Trypanosomiasis in

India

First human case of T evansi infection in humans was

reproted in the district of Chandrapur in Maharashtra

He had presented episodes of fever associated with

sensory disorders

The patient continued to present peaks of fever at 7–10-

day intervals, with systematically high blood parasite

levels

(WHO , FEBRUARY 2005)

AMERICAN TRYPANOSOMIASIS

Chagas's Disease

Chagas-Mazza Disease

South American Trypanosomiasis

Trypanosoma cruzi

Reduvid bugs

RESERVOIR AND INCIDENCE

Dogs, cats, and guinea pigs are the main reservoirs for human

infection.

T. cruzi occurs only in the Americas- Southern South America

to northern Mexico, Texas, and the south western U.S.

An estimated 12 million people are infected, mostly in rural

areas, resulting in about 60,000 deaths yearly.

TRANSMISSION: Humans are infected when the insect's feces become rubbed

into the wound caused by the bite of an infected bloodsucking insect (triatomid) or when the conjunctiva, mucous membranes or abrasions become contaminated.

Blood transfusions from infected persons

Congenital infection

Breast milk

Laboratory accidents

DISEASE IN HUMANS:

Acute illness usually occurs in children

If the primary site of infection is the eye there is unilateral

edema of eyelids and conjunctivitis - Romaña's sign –

PATHEGNOMONIC

Furuncles (chagoma) appear at the point of entry of the

infection.

Signs - fever, malaise, enlarged lymph nodes, liver and

spleen.

Rarely myocarditis and meningoencephalitis

The chronic phase

a) Asymptomatic (indeterminate form) - more frequent,

typically in the beginning of the chronic phase and lasting

all life in most of the patients

b) Cardiac form - 30% of the patients, with conduction

disorders, arrhythmia, cardiomyopathy, heart failure and

secondary thromboembolism

c) Digestive lesions -megaoesophagus and megacolon

DISEASE IN ANIMALS: Acute and in apparent infection - wild animals

The acute form- fever, enlarged liver, lymph nodes and heart irregularities

Lasts 10-30 days – no clinical signs usually - sometimes myocarditis occurs.

Chronic disease in dogs.

Lesions in dogs resemble those in humans.

DIAGNOSIS:

In the acute stage, trypanosomes should be looked for by

examination of anticoagulated fresh blood for motile organisms.

In the chronic stage, the parasite can only be detected by

culture or xenodiagnosis.

TREATMENT:

Therapy is unsatisfactory

PREVENTION/CONTROL:

Destroy the vector by insecticides. Use insect nets to prevent

bites. Screen blood donors

LEISHMANIASIS 1. Cutaneous leishmaniasis: most common

Chiclero ulcer, pianbols, uta and buba (in the Americas)

Oriental sore, Aleppo boil (in the Old World)

Baghdad boil, Delhi boil, Bauru ulcer (in the Middle East)

2. Visceral leishmaniasis: kala-azar -most serious

3. Mucocutaneous :espundia

Cutaneous leishmaniasis

Leishmania mexicana

L. brasiliensis

L. tropica

Visceral leishmaniasis - L. donovani, L. infantum, and L. chagasi.

300 000 Estimated cases of visceral leishmaniasis (VL) and

over 20 000 deaths annually

1 million Cases of cutaneous leishmaniasis (CL) reported in

the last 5 years.

310 million People at risk of infection in six countries

reporting over 90% VL cases worldwide

(WHO)

RESERVOIRS AND INCIDENCE Wild animals, dogs and humans serve as reservoirs.

Humans are the only known reservoir in India.

The geographic distribution of the cutaneous disease is Texas,

Mexico, Central and South America, India, Pakistan, the Middle

East, southern Russia, the Mediterranean coast and Africa.

The distribution of visceral leishmaniasis is poorly reported, but

foci probably occur in the Mediterranean basin, the Middle East,

India, China, Mexico, Central and South America, and Africa.

TRANSMISSION

Sandfly vectors

Congenital

Blood-borne transmission of visceral leishmaniasis are

possible

DISEASE IN HUMANS:

The primary lesion is a painful ulcer or nodule at the site of infection

with residual scarring skin and mucous membranes.

Infiltration by inflammatory cells at the inoculation site supports the growth of the parasite.

Large area of chronically inflamed granulation tissue.

The overlying skin undergoes hyperplasia and then necrosis with spreading ulceration.

The lesions may heal, become fibrosed or extend indefinitely to produce considerable disfigurement.

Chronic skin ulcerations with raised

edges at site of sand fly bite.

Cutaneous leishmaniosis

In the visceral disease

Intermittent irregular fever occurs with sweats, enlarged

spleen, weight loss and anemia leading to ascites, edema,

diarrhea and secondary infections.

Dark pigmentation of the skin may occur.

There is gross enlargement of liver and spleen.

Without treatment, the case fatality rate is 90%.

Mucocutaneous leishmaniasis

Leads to partial or total destruction of mucous membranes of

the nose, mouth and throat.

Post kala-azar dermal leishmaniasis

(PKDL)

PKDL is a sequel of visceral leishmaniasis

Appears as macular, papular or nodular rash usually on face, upper arms, trunks and other parts of the body.

It usually appears 6 months to 1 or more years after kala-azar has apparently been cured.

People with PKDL are considered to be a potential source of kala-azar infection

DISEASE IN ANIMALS:

L. mexicana causes ulcers of the skin in rodents and other wild animals- at the base of the tail.

L. braziliensis causes a systemic infection with few skin lesions in wild animals. No skin lesions have been found in dogs.

Dogs infected by L. tropica may suffer form cutaneous lesions similar to those found in humans.

L. donovani produces visceral lesions in dogs, with enlarged lymph nodes, liver and spleen.

DIAGNOSIS:

Definitive diagnosis is achieved by finding the parasite-either

the amastigote in stained smears or biopsies, or the motile

promastigote in culture.

Serologic and skin tests provide only indirect evidence of

infection.

TREATMENT:

Treatment remains inadequate because of drug toxicity, long

courses required, and frequent need for hospitalization. The

drug of choice is sodium antimony gluconate. Alternative

drugs for some forms of infection are amphotericin B and

pentamidine.

PREVENTION/CONTROL:

Use insecticides in house and buildings to control the vector.

Eliminate rubbish heaps which are breeding areas for

sandflies.

Avoid sandfly bites by protective clothing.

Keep dogs indoors after sundown and remove infected dogs.

Sarcocystosis

Intestinal sarcocystosis

Sarcocystis hominis

DH- Human

IH- Cattle

Muscular sarcocystosis

S. lindemanii

Man dead end host

S. suihominis

DH- Humans

IH- Pig

Epidemiology

Worldwide, the incidence of intestinal sarcocystosis is

estimated to be 6-10%

Approximately 20% of people in Malaysia are sero positive

Throughout Southeast Asia, 21% of autopsy specimens

contain the parasite

More than 60 cases have also been reported in the U.S often

as an incidental finding

Life cycle

Symptoms

Intestinal

sarcocystosis

IP- 3 to 6 hours

Often asymptomatic

Mild fever

Diarrhea

Chills

Vomiting

Respiratory problems

Muscular sarcocystosis

Muscle cyst

Myalgia

Muscle weakness

Transitory edema

PREVENTION Intestinal sarcocystosis

People should avoid eating raw or undercooked beef or pork

Sarcocysts in meat can be destroyed by

Cooking at 700C for 15 minutes

Freezing at –40C for 2 days or freezing at –200C for 1 day

Muscle sarcocystosis

Food contaminated by feces or dirt should be avoided

Good personal hygiene, such as hand washing, may also help to

prevent transmission

MALARIA Plasmodium knowlesy

Anopheles hackeri, Anopheles balabacensis

Parasite naturally occurring among several species of macaques in Southeast Asia

Long-tailed macaque (M. fascicularis)

Pig-tailed macaque (M. nemestrina)

Leaf monkeys (e.g.Presbytis melalophos)

Macaca cylopis

The parasite has not been found in M. mulatta (rhesus monkey) in the wild, probably because P. knowlesi in rhesus monkey produces a fulminant and almost invariably fatal infection

Asexual replication

• Fertilization and invasion of mosquito gut

• Infected cell releases sporozoites,

which migrate to the salivary glands.

Sexual replication

Exoerythrocytic

cycle

merozoites

released

"ring"

form trophozoite

ruptured

RBC releases

merozoites

schizont Male and

female

gametocytes

Sporozoites

released from

mosquito salivary

glands invade

hepatocytes

within 30 mins.

Erythrocytic

cycle

69 Cary Engleberg

Incubation period -11 to 12 days

Mild to very severe illness

Symptoms include fever, chills, sweats, and headache, and in

some instances, progress to serious illness including

jaundice, blood coagulation defects, shock, kidney or liver

failure, central nervous disorders and coma.

BABESIOSIS

Piroplasmosis

Babesia divergens and B. microti.

Ixodes tick

Babesiosis in humans is a rare intraerythrocytic infection

Natural hosts for B. microti are various wild and domestic

animals, particularly the white-footed mouse and white-

tailed deer.

TRANSMISSION:

Ixodes tick bites

Transmission from blood transfusion

Splenectomized, elderly, or immunosuppressed persons are

the most likely to have severe manifestations.

DISEASE IN ANIMALS:

Many animals show only mild fever and recover

spontaneously.

Hemolysis

Enlarged spleen, liver

Hemoglobinuric nephrosis.

DISEASE IN HUMANS:

B. microti infection lasts a few weeks to a month

Irregular fever, chills, headache, diaphoresis, myalgia, and

fatigue but is without malaria-like periodicity of symptoms.

Hemolytic anemia, hepatosplenomegaly.

The disease is self-limited and most patents recover without

sequelae.

Infection with B. divergens has only been reported in

splenectomized patients

Progresses rapidly with high fever, severe hemolytic anemia,

jaundice, hemoglobinuria, and renal failure; death usually

follows.

DIAGNOSIS:

ID of the intraerythrocytic parasite on Giemsa-stained blood smears or serology.

TREATMENT:

B. divergens: blood transfusions, renal dialysis, pentamidine plus trimethoprim-sulfa.

B. microti: Treat symptomatically since most case are self-limiting. In splenectomized patients, quinine plus clindamycin and transfusions.

CRYPTOSPORIDIOSIS

Cryptosporidium parvum- people and calves

In recent years, C. ubiquitum, has been emerging as another

major zoonotic species that infects persons

C hominis (formerly C parvum type I) is a specific human

pathogen


Rodents, birds (particularly turkeys and chickens), ruminants,

fish, reptiles, cats, dogs, rabbits, NHP's.

Children over 2 years of age, animal handlers, travelers, Cattle

farmers, Veterinarians who come in contact with farm animals

Infants and younger children in day-care centers

One of the three most common diarrheal-causing pathogens in

the world

10 billion oocysts per gram infected feces

Can be infected by just one oocyst

High burden of cryptosporidiosis among children in Indian slum

community (Rajiv Sarkar et al.,2013)

Prevalence in children with diarrhea has been found to range from

1.1% to 18.9% in India

Reported infection in bovines ranged from 11.32% to 69.32% in

India (Chhabra and pathak, 2012)

Cryptosporidium antibodies were detected in the serum of 20 of

23 cats (87%) suggesting that the exposure rate may be high.

TRANSMISSION

Transmission is usually fecal-oral

Often through water contaminated by livestock mammal

feces

Person to person transmission through feco-oral route

TRANSMISSION CYCLE

Oocysts passed in stool are fully sporulated and infectious

In humans and animals, the full life cycle occurs within a single host

Attach to the microvillus borders of enterocytes of the small bowel and also are found free in mucosal crypts

The host cell membrane deteriorates, leaving the parasitic membrane in direct contact with epithelial cell cytoplasm

Do not invade the tissues

Organisms attached

to an intestinal villus

Intestinal organisms

by scanning EM

39

Source Undetermined Source Undetermined

DISEASE IN MAN:

In immunocompetent persons- no symptoms to mild enteritis to marked watery without mucus or gross or microscopic blood.

Low-grade fever, malaise, nausea, vomiting, abdominal cramps, anorexia and weight loss

Self-limited and lasts a few days to about 2 weeks.

In immunologically deficient patients, the illness is characterized by profuse (up to 15L daily), cholera-like diarrhea and by fever, severe malabsorption, marked weight loss, and lymphadenopathy.

DISEASE IN ANIMALS

Severe watery diarrhoea in neonatal calves and lambs.

In turkeys and chickens, the parasites are reported to occur

in the sinuses, trachea, bronchi, cloaca, and bursa of

Fabricius.

The respiratory disease - coughing, gasping, and air sacculitis.

DIAGNOSIS

Diagnosis is by detection of oocysts in stool by a variety of

flotation or concentration methods

By mucosal biopsy, followed by special staining methods that use modifications of an acid-fast stain

Iodine staining

Acid fast staining

Fluorescein-labeled IgG monoclonal antibody

Iodine stain of stool Acid-fast stain of stool

42

Source Undetermined Source Undetermined

TREATMENT:

No successful treatment has been developed so far.

Supportive treatment

GIARDIASIS

Most common intestinal protozoan parasite of people in the

U.S.

The parasite occurs worldwide and is nearly universal in

children in developing countries.

Giardia lamblia

RESERVOIR AND INCIDENCE:

Humans are the reservoir for Giardia

Dogs and beavers have been implicated as a zoonotic source

of infection

In psittacines, the disease is commonly found in cockatiels

and budgerigars.

Giardiasis is a well-recognized problem in special groups

including travelers, campers, and persons with impaired

immune states.

However, Giardiasis does not appear to be an opportunistic

infection in AIDS.

TRANSMISSION

Only the cyst form is infectious by the oral route;

Trophozoites - destroyed by gastric acidity.

Most infections are sporadic

Fecal contamination of water or food

Person-to-person contact

After the cysts are ingested, trophozoites emerge in the

duodenum and jejunum. They can cause epithelial damage,

atrophy of villi, hypertrophic crypts, and extensive cellular

infiltration of the lamina propria by lymphocytes, plasma

cells, and neutrophils.

DISEASE IN MAN:

Most infections are asymptomatic.

Acute or chronic diarrhea, mild to severe, with bulky, greasy, frothy, malodorous stools, free of pus and blood

Upper abdominal discomfort, cramps, distention, excessive flatus

DISEASE IN ANIMALS:

Dogs and cats - Inapparent or produce weight loss and chronic diarrhea or steatorrhea, which can be continuous or intermittent, particularly in puppies and kittens.

Calves - Feces are usually soft, poorly formed, pale, and contain mucus. Gross intestinal lesions are seldom evident, although microscopic lesions, consisting of villous atrophy and cuboidal enterocytes, may be present.

DIAGNOSIS:

Diagnosis is by identifying cysts or trophozoites in feces or

duodenal fluid.

Unless they can be examined with an hour, specimens should

be preserved immediately in a fixative.

A stool ELISA test or IgM serology are available.

TREATMENT:

Tinidazole, Metronidazole (FLAGYL), quinacrine, or

furazolidone. Alternative drugs are Tinidazole or albendazole.

PREVENTION/CONTROL:

Hygiene, protective clothing, when handling animals.

Prevention requires safe water supplies, sanitary disposal of

human feces

Adequate cooking of foods to destroy cysts, protection of foods

from fly contamination, washing hands after defecation and

before preparing or eating foods

Endemic areas - avoidance of foods that cannot be cooked or

peeled.

AMEBIASIS

Amebic Dysentery, Amebiosis

Entamoeba histolytica.

RESERVOIR AND INCIDENCE:

The reservoir of E. histolytica is man.

Most prevalent and severe in tropical areas

It is estimated that there are about 50 million case of invasive

amebiasis and 40,000-100,000 deaths annually worldwide.

In the USA, seropositive rates up to 2-5% have been reported in

some populations.

Reported incidence of 0-31% in the feces of clinically normal

Rhesus monkeys, 2-67% in Chimps, and up to 30% in other

NHP.

TRANSMISSION

Transmission may be by ingestion of infective cysts,

contaminated water or food, by flies, or fomites.

Exists as resistant cysts or more fragile trophozoites

Cysts are the infectious form found in the stool of

asymptomatic carriers or patients with mild disease.

The cysts remain viable, if moist and cool for 12 days.

Remain viable for 30 days in water.

Laboratory animal personnel are usually infected from fecal

matter transferred to the skin or clothing.

DISEASE IN HUMANS Mild to moderate colitis: recurrent diarrhoea and abdominal

cramps, sometimes alternating with constipation; mucus may be present; blood is usually absent.

Severe colitis: semi formed to liquid stools streaked with blood and mucus, fever, colic, prostration.

In fulminant cases, ileus, perforation, peritonitis, and haemorrhage occur.

Hepatic amebiasis: fever, hepatomegaly, pain, localized tenderness.

DISEASE IN ANIMALS:

In dogs, infection by E. histolytica is generally asymptomatic

and frequently localized in the cecum.

Rhesus monkeys are generally resistant and usually

experience asymptomatic infection, but chronic, mild colitis

can occur.

In chimpanzees, the infection can persist for a long time, in

most cases subclinically, but sometimes it invades the tissues

causing ulcerative colitis and hepatic abscesses.

Trophozoites in Ulcer with Ingested Red Blood Cells

DIAGNOSIS:

Cysts or trophozoites in feacal sample

Indirect HI for hepatic amebiasis

Ultrasonography can locate the cyst and fine needle

aspiration is performed to find the organism.

Trophozoite in stool

Cyst in stool

TREATMENT:

May require the concurrent or sequential use of several drugs.

PREVENTION/CONTROL:

Strict sanitation and personal hygiene, protective clothing and

gloves.

Fecal screening of NHP.

Protect water supply from fecal contamination.

Usual chlorine levels don't destroy cysts. 10ppm chlorine

residual necessary to destroy cysts

Heat to 50ºC (122ºF) kills cysts.

Adequate cooking to destroy cysts.

Protect food from fly contamination.

BALANTIDIASIS

Balantidial dysentery

Large ciliated protozoan, Balantidium coli. Trophozoite 50-

70 microns by 40-50 microns.


Distributed worldwide especially in the tropics

Reservoir hosts – Swine, rats and NHP's.

Humans, great apes, and several monkey species

Incidence in NHP colonies - 0 to 63%

Usually asymptomatic, but may see diarrhoea.

TRANSMISSION:

Ingestion of cysts or trophozoites from infected animal or

human feces.

Cyst is the infectious form.

Contaminated water or food.

DISEASE IN ANIMALS AND MAN

Many infections are asymptomatic and probably need not be

treated.

Chronic

Recurrent diarrhea, alternating with constipation

Severe dysentery with bloody mucoid stools, tenesmus (the

constant feeling of the need to empty the bowel,

accompanied by pain, cramping, and involuntary straining

efforts), and colic may occur intermittently.

DIAGNOSIS:

Use fresh fecal samples to identify trophozoites or cysts.

Trophozoites in scrapings or biopsy of ulcers of the large

bowel.

TREATMENT:

Tetracycline or Iodoquinol

PREVENTION/CONTROL:

Good sanitation & personal hygiene practices in NHP and

swine colonies.

Protect water and food from fecal contamination.

Identify positive lab animals and treat.

REFERENCE

Dhumne M., Sengupta C., Kadival G., Rathinaswamy ,A.

And Velumani A. (2007). – National seroprevalence of

Toxoplasma gondii in India. J. Parasitol., 93: 1520-1521.

WHO ,Weekly epidemiological record, no. 7, 18 february

2005

www.who.int

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