Final Toxoplasmosis

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Toxoplasmosis

Toxoplasmosis is a zoonotic infection of animals caused by the protozoan

parasite Toxoplasma gondii The disease runs a subclinical course and seldom causes

overt clinical diseases. The two-host coccidian , Toxoplasma gondii is an obligate

intracellular parasite, ubiquitous in nature that can infect virtually all warm-blooded

animals including humans. it is a blood and tissue dwelling protozoan (subphylum

Apicomplexa) and can take up residence in several different tissue types.

It was first discovered by Nicolle & Manceaux, in 1908 from the African

rodent Ctenodactylus gundi, then in 1909 differentiated the disease from Leishmania and

named itToxoplasma gondii. The Companion Animal Parasite Council states:

"Toxoplasmosis is one of the most important zoonotic parasites dealt with in veterinary

medicine.”It affects reproductive system,nervous system,skeletal muscles and eye.

Etiology

Structure of toxoplasma gondii

The disease is caused by Toxoplasma gondii which is the intestinal coccidian of cats and

is single species.Toxoplasma gondii occurs in several forms:

1. Pseudocysts (intracellular collection of trophozoites in cells in the acute stage of

http://en.wikipedia.org/wiki/Gundi

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http://en.wikipedia.org/wiki/Leishmania

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http://en.wikipedia.org/wiki/Gundi

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infection).

2. Trophozoites (intracellular parasites, about 6 X 2 micrometer crescent shaped with

central nucleus and multiply by binary fission forming pseudocysts)

3. Cysts (collection of trophozoites enclosed in a true tissue cyst, in the chronic stage or

latent infection);

4. Oocysts (oval, 10 X 12 micrometer, containes two sporocysts each containing four

sporozoites, and found in stool of infected cats).

T. gondii ultrastructure: two intracellular tachyzoites in a host cell.

T. gondii cyst



Predominant genotypes of T. gondii

Type I is highly virulent in mice and, perhaps, in human.

Type II predominates in infections of immunocompromised patients; relatively avirulent

in mouse. Type II strains are most often associated with human toxoplasmosis,especially in Europe.

Type III is not highly virulent in mouse, and causes chronic infections in humans.

Vectors and reservoirs

Members of the species Felidae, however, are the only known definitive hosts for the

sexual stages of T. gondii and, thus, serve as the primary reservoir for the parasite.

Numerous other species (notably rodents,sheep,goats,pigs,cows) are paratenic hosts andserve as intermediate hosts required for completion of the parasite’s life cycle .

In final host it occurs in small intestine and in intermediate host it occurs in muscle.liver

lungs and brain.

Classification

FAO List C disease

Epidemiology

Toxoplasmosis is found all throughout world. Cats become infected when they eat

infected rodents or other infected meat or when exposed to contaminated faeces of other cats, and infection involves gastrointestinal tract Human can be infected when they eat

undercooked, contaminated meat or when they accidentally eat mature eggs incontaminated soil or food. Infection in human and mammals, other than cat involves any

tissue. Congenital cases occur as a result of primary infection during early pregnancy

(often asymptomatic for mothers).Infection in human is common.

Infection is often highest in areas of the world that have hot, humid climates and lower altitudes. The seroprevalence of toxoplasmosis was estimated to vary from <2% up to

70% in the Southeast Asian population. An estimated 30-50% of the human population is

currently infected with Toxoplasma in the asymptomatic cyst form. In

immunocompromised patients, the cyst form may potentially lead to seriousdisease .Among domestic animals the prevalence of infection is highest in cats, sheep

,goats and swine and low in cattle .Antibodies has been found in 25-50% of the catsworldwide.

The parasite is readily destroyed by heating, drying ,freezing and thawing , and dies

quickly in carcasses of affected animals



In places where raw meat consumption is usual ,population shows high prevalence of

toxoplasmosis.

Children from 0-4 years don’t usually eat raw meat .If children are found infected

contamination from cat is suspected to be the source of infection.

Incubation period

The incubation period for Toxoplasmosis is usually from 5-20 days when associated with

cats;one outbreak from eating undercooked meat was associated with incubation period

of 10-23 days.

Mode of transmission

Toxoplasme has been reported to be transmitted by the following ways in man and

animals;



Transmission between animals

Cats are the only domestic species that shed infectious oocysts in feces. Cats may becomeinfected through ingestion of oocysts or ingestion of infected intermediate hosts such asrodents. Transmission to kittens through mother's milk is also possible. Most cats become

infected in the first year of life, and oocyst shedding is usually highest at the time

SOME CURIOSITIES ON

ANIMAL TOXOPLASMOSIS(I)

In acute infection phase, infected hens can transmit the Protozoa to their eggs. Hen’s

eggs can contain infective stages of Toxoplasma

Transmission to humans

Human typically become infected by three principal routes of transmission.

• Foodborne• Animal-to-human (zoonotic)

• Mother-to-child (congenital)

• Rare instances

Foodborne transmission

The tissue form of the parasite (a microscopic cyst consisting of bradyzoites) can betransmitted to humans by food. People become infected by:

• Eating undercooked, contaminated meat (especially pork, lamb, and venison)

• Accidental ingestion of undercooked, contaminated meat after handling it and notwashing hands thoroughly (Toxoplasma cannot be absorbed through intact skin)

• Eating food that was contaminated by knives, utensils, cutting boards, or other

foods that had contact with raw, contaminated meat.

http://www.cdc.gov/toxoplasmosis/epi.html#food%23food

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http://www.cdc.gov/toxoplasmosis/epi.html#rare%23rare



Human infection with the toxoplasma gondii

Animal-to-human (zoonotic) transmission

Cats play an important role in the spread of toxoplasmosis. They become infected byeating infected rodents, birds, or other small animals. The parasite is then passed in the

cat's feces in an oocyst form, which is microscopic.

People can be infected by:

•

Accidental ingestion of oocysts after cleaning a cat's litter box when the cat hasshed Toxoplasma in its feces

• Accidental ingestion of oocysts after touching or ingesting anything that has come

into contact with a cat's feces that contain Toxoplasma

• Accidental ingestion of oocysts in contaminated soil (e.g., not washing hands after gardening or eating unwashed fruits or vegetables from a garden)

• Drinking water contaminated with the Toxoplasma parasite

Mother-to-child (congenital) transmission

A woman who is newly infected with Toxoplasma during pregnancy can pass theinfection to her unborn child (congenital infection). The woman may not have symptoms,

but there can be severe consequences for the unborn child, such as diseases of thenervous system and eyes.

Rare instances of transmission

Organ transplant recipients can become infected by receiving an organ froma Toxoplasma-positive donor. Rarely, people can also become infected by receiving

infected blood via transfusion. Laboratory workers who handle infected blood can also



acquire infection through accidental inoculation.Infection has been traced to be

transmitted through infected semen(Dubey and Sharma ,1980).

Life Cycle:

The life cycle of T. gondii has asexual and sexual components. The asexual phase takes place in the intermediate host, which consists of most, if not all, warm-blooded animals.

The sexual phase occurs in enteroepithelial cells of the feline definitive host and results in

the production of oocysts.

Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only

shed for 1-2 weeks, large numbers may be shed. Oocysts take 1-5 days to sporulate in

the environment and become infective. Intermediate hosts in nature (including birds androdents) become infected after ingesting soil, water or plant material contaminated with

oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites

localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may

also become infected directly by ingestion of sporulated oocysts. Animals bred for

human consumption and wild game may also become infected with tissue cysts after

ingestion of sporulated oocysts in the environment .



Humans can become infected by any of several routes:

• eating undercooked meat of animals harboring tissue cysts .

•

consuming food or water contaminated with cat feces or by contaminatedenvironmental samples (such as fecal-contaminated soil or changing the litter box

of a pet cat) .

• blood transfusion or organ transplantation .

• transplacentally from mother to fetus .

In the human host, the parasites form tissue cysts, most commonly in skeletal muscle,

myocardium, brain, and eyes; these cysts may remain throughout the life of the host.

Diagnosis is usually achieved by serology, although tissue cysts may be observed instained biopsy specimens . Diagnosis of congenital infections can be achieved by

detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR .

Clinical signs

Cattle

Recent observations showed that toxoplasmosis is uncommon in cattle. Calves are more

susceptible than adults and the clinical signs of orally affected calves include diarrhea,

anorexia, poor weight gain, depression, weakness, dyspnea and fever. In some casejust a

lymphadenopathy. Congenitally affected calves show fever, dyspnoea, coughing,sneezing and neurological signs.

If the disease occurs in adults, symptoms include fever, dyspnoea, and nervous signs,

followed by lethargy. Stillborn calves and neonatal deaths may be seen.

Pigs

Pigs less than 3 weeks old are the more susceptible. Clinical signs include debility,weakness, incoordination, fever, wasting, dyspnoea and cough. In adults cough and

tremors predominate. In pregnant sows abortion, stillborn and premature are common.

Sheep

Lambs affected after birth show fever and dyspnoea. In pregnant ewes, abortions andstillbirths are common, abortions tend to occur in the last 3-4 weeks of

pregnancy. Symptoms in adults are uncommon and include fever, dyspnoea, and tremor.

Horses

The clinical disease appears to be rare in horses, however symptoms include progressiveneurological signs, including ataxia, circling, paresis and apparent blindness.



Cats

Cats are the definitive host, with infection common but clinical illness rare. Symptoms

may include:

• Loss of weight,

• Pneumonia,

• Encephalitis,

• Fever

In young cats dyspnoea associated with bronchopneumonia may be seen. Infection may

be fatal in young kittens.Other clinica manifestations

include,bilirubinemia,lymphadenitis,anaemia,iritis and intestinal obstruction.Acutedisease is characterized by anorexia,lethargy,pyrexia,dyspnoea and death.

Fine needle aspirate from cat lung. A ruptured large mononuclear cell with

multipleToxoplasma tachyzoites. Wrights stain, 100X

Birds

In Poultry symptoms can be sudden death or anorexia, emaciation, pallor, diarrhoa and

blindness.

Dog

Mostly occurs in asymptomatic form.Lesions involve lungs and central nervoussystem.Concurrent toxoplasmosis and distemper is common(Farrow and

Love,1975).Abortion and neonatal mortality may ensue.



.Dog muscle. Myonecrosis and myositis with intralesional T. gondii tissue cysts (arrows)

containing developing bradyzoites. H&E stain, 40X.

• Humans

The infection is very common in humans, but clinical disease is of low incidence

and occurs only sporadically. Postnatal infection is less severe disease andcommonly presents as a generalised lymphadenopathy that may resolve without

treatment in a few weeks. Toxoplasmosis is typically classified as follows:

o Congenital toxoplasmosis

The classic clinical triad of retinochoroiditis, cerebral calcifications, and

convulsions defines congenital toxoplasmosis. Other findings include

hydrocephalus, microcephaly, organomegaly, jaundice, rash, fever, and psychomotor retardation. It accounts for relatively few cases; however, they

tend to account for most acute and fatal infections.

o Acquired toxoplasmosis

The acquired infection is usually subclinical and asymptomatic. In 10-20% of cases that become symptomatic, the patient develops a flulike illness

characterized by fever, lymphadenopathy, malaise, myalgias, and a

maculopapular skin rash that spares the palms and the soles. 16 In individualswho are immunocompetent, the disease is benign and self-limited

o Toxoplasmosis in the immunocompromised host

Host immune function plays an important role in the pathogenicity of

toxoplasmosis. Patients who are immunocompromised often develop life-threatening pneumonitis; myocarditis; encephalitis; and an atypical, sight-

threatening, severe necrotizing retinochoroiditis.



o Ocular toxoplasmosis

The hallmark of the disease is a necrotizing retinochoroiditis, which may be

primary or recurrent. The retina is the primary site for the multiplying parasites, while the choroid and the sclera may be the sites of contiguous

inflammation.

Inactive chorioretinal scar secondary to toxoplasmosis

Diagnosis

Clinical signs are non-specific and the organism is difficult to demonstrate

.therefore,diagnosis in man and animals is accomplished by serological tests.

Isolation of Toxoplasma gondii

Parasite can be demonstrated from lymoh fluid,placenta ,cotyledons and muscles.It

requires mouse inoculation.Methylene blue dye test

DNA testing

Serological tests

Complement fixation test

Indirect haemagglutination test

Direct agglutination test

Latex agglutination test

Flourescent antibody test

Enzyme Linked Immuno-Sorbent assay(ELISA)

Immunoflourscene



T. gondii tachyzoites, stained with fluorescent antibodies

Treatment

There is no satisfactory treatment.Drugs like pyremethamine and sulfonamides have been

used with success. The various drugs are;

Pyrimethmine @ 1 mg/kd b.wt orally for the first 3 days followed by 0.4 mg/kg b,wt.

(Cat, Dog,Man,Pig).

Sulphonamides @ 100 mg/kg b,wt. orally once.

Trimethoprim and Sulphame-thoxazole @ 80 mg of Trimothoprim and 400 mg of

sulphamethoxazole(Man)

Spiramycin @ 2-3 gm/day in divided doses (Man)

Azithromycin@ 2-4 gm/day (Man)

Clindamycin @ 150-300mg/adult at 6 hr interval( Man)

Monensin @ 5 mg/kg b.wt. (Sheep)

S.D.D.S(Diaminodiphenyl Sulfone) @ 5 mg/kg b.wt. (Cat).

Control

1)Epidemiological control

a)By preventing exposure to cats

Cat population control in endemic areas.

Cat should not be allowed to feed raw or uncooked meat.

Proper faeces disposal of cat for e.g. by burning.



Drug medication to young cats to suppress shedding of oocyst.

Control rodent populations and other potential intermediate hosts.

b) By preventing exposure to man

Do not eat raw or undercooked meat. Meat should be cooked to a temperature of at least

160°F for 20 minutes in order to destroy tissue cysts.13.

• Do not drink unpasteurized milk.

• Do not eat unwashed fruits and vegetables.

• Wash hands and food preparation surfaces with warm soapy water after handling

raw meat.• Wear gloves when gardening. Wash hands after gardening.

• Wash hands before eating (especially for children).

• Keep children's sandboxes covered.

•

Do not drink water from the environment unless it is boiled.• Do not feed raw meat or undercooked meat to cats. Also, do not give them

unpasteurized milk.

• Do not allow cats to hunt or roam.

• Do not allow cats to use a garden or children's play area as their litter box.

• Remove feces from the litter box daily and clean with boiling or scalding water.

Pregnant women, and persons with suppressed immune systems, should not clean thelitter box.

2) Chemotherapeutic control

Drugs may be fed as a prophylactive measure at periodicl interval to arrest development

of oocyst and their shedding through faeces.

3)Immunization

No fruitful vaccination available. Both kille d and live vaccine have been used in ewes

with variable results.

Final Toxoplasmosis

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