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Diseases / List of Parasitic Diseases / Disease description:

Toxoplasmosis

Histopathology toxoplasmosis wallaby heart. Click here for full-page view with caption. Histopathology toxoplasmosis wallaby lung. Click here for full-page view with caption. Immuohistochemistry Toxoplasma gondii issue cyst wallaby heart. Click here for full-page view with caption. Immunohistochemistry Toxoplasma gondii wallaby lung. Click here for full-page view with caption. Toxoplasma gondii issue cyst liver, wallaby - Romanovwsky stained impression smear. Click here for full-page view with caption. Toxoplasma gondii tachyzoites, wallaby heart impression smear. Click here for full-page view with caption. Toxoplasma gondii tissue cyst, wallaby heart impression smear. Click here for full-page view with caption.

INDEX - INFORMATION AVAILABLE

GENERAL INFORMATION

SUSCEPTIBILITY, DISEASE CHARACTERISTICS & DIAGNOSIS

TREATMENT & CONTROL

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THE FOLLOWING INFORMATION IS HELD ON THE INFECTIOUS AGENT INFORMATION PAGE
Toxoplasma gondii (Protozoa- Apicomplexa)

  • Parasite Structure and Identification
  • Associated Host Species of Parasite (Animal Types Affected) and Hazard / Risk
  • Parasite Life Cycle, Transmission and Effects of Chemicals
  • Transmission and Biogeographical / Climatic Range for Parasite

CLICK THIS LINK FOR Toxoplasma gondii (Protozoa- Apicomplexa)

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General and References

Disease Summary

Protozoal disease, particularly important as a cause of abortion in sheep and as a congenital infection in humans.

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Alternative Names (Synonyms)

Toxoplasma gondii infection.

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Disease Type

 Parasitic

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Infectious/Non-Infectious Agent (directly associated with the Disease)

Toxoplasma gondii, a tissue-dwelling protozoan first described from the north-American rodent Ctenodactylus gundii (the gundi or gondi) in 1908. (J591.147.w1, J591.148.w2)
  • Interest in the protozoan as a parasite of man grew in the late 1930's, as its role in congenital eye problems and encephalomyelitis was recognised. By the beginning of the 1960's, Toxoplasma gondii had become known as an important cause of abortion in sheep, but at this time the natural life cycle of this protozoan was still very unclear and the definitive host unknown. Transmission of Toxoplasma gondii from the faeces of cats, leading to the acknowledgement of cats as the definitive host of this parasite, was only described in 1965. (J9.206.w1)

Species/Taxa

Chemical

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Physical

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References

Disease Author

Dr Debra Bourne MA VetMB PhD MRCVS (V.w5)

Referee

Prof. Elizabeth Innes (V.w171)

References

Detailed references are provided attached to specific sections.

ORGANISATIONS-

  • --

ELECTRONIC LIBRARY
(Further Reading)
Click image for full contents list of ELECTRONIC LIBRARY

 

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Epidemiology and Host Susceptibility Factors

Incubation Period, Time Course and Persistence of Disease

General Editorial Description
1) INCUBATION PERIOD
  • In humans, 5-18 days from presumed time of exposure. (J4.196.w3)
  • In experimental infection in Lepus timidus- Mountain hare, clinical signs were seen in one hare seven days after oral inoculation. (J42.117.w1)
  • In a Pan troglodytes - Chimpanzee experimentally infected orally with about 2.5 million oocyts divided over two days, less than a week. (J258.2-5758.w1)
2) DISEASE DURATION (TO RECOVERY) IN INDIVIDUAL ANIMALS
  • In humans with acute toxoplasmosis, hospitalisation due to clinical disease lasted 7-20 days. (J4.196.w3)
  • In pigs, usually less than three weeks to recovery. (J32.164.w2)
  • In experimentally inoculated guinea pigs, 7-12 days from onset of clinical signs to death. (J100.72.w1)
3) TIME COURSE / PERSISTENCE OF DISEASE IN A SUSCEPTIBLE POPULATION
  • The presence of Toxoplasma gondii in the environment may be maintained over long periods. (B217.13.w13)

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Mortality / Morbidity / Susceptibility / Life stage affected

General Editorial Description The manifestation of clinical toxoplasmosis after infection with Toxoplasma gondii depends on a number of factors, including the strain of the parasite, the dose size, route and form of the infecting parasite, the species, age and immune status of the host. (B650.w1, B599.1.w1, J4.203.w6)
1) NUMBER OF DEATHS
  • Most infections with Toxoplasma gondii are not associated with mortality (or any clinical signs), although some hosts will die of acute toxoplasmosis. (B599.1.w1)
  • In pigs, in day-old piglets mortality may be high, but by 8-10 days old there is only a minor reaction.  (B211.25.w25)
  • Mortality as high as 50% has been reported in pigs. (J32.19.w1)
  • In untreated congenital toxoplasmosis with clinical signs, mortality may reach 12%. (J4.196.w3)
  • Fatal disease occurs occasionally in Oryctolagus cuniculus domesticus - Domestic European rabbit. (J495.42.w3)
    • Occurs in outbreaks with many deaths, particularly in young rabbits. (J63.8.w1)
    • High mortality with acute toxoplasmosis (50% mortality in two weeks in one outbreak in 600 young rabbits). (J63.8.w1)
  • In Lepus europaeus - Brown hare:
    • A high incidence of acute fatal toxoplasmosis has been reported in these hares in Scandinavia. (B208.17.w17d, J1.30.w8)
    • In experimentally infected Lepus europaeus - Brown hare, all individuals given 10 oocysts or more died. (J32.93.w2)
  • In experimentally inoculated guinea pigs, usually fatal. (J100.72.w1)
2) NUMBER OF ANIMALS AFFECTED
  • It is probable that all mammals and birds can become infected with Toxoplasma gondii however species vary greatly in their susceptibility to the development of clinical disease. Cattle and horses are relatively resistant, sheep often abort if infected during pregnancy, Australian marsupials are quite susceptible and small New World primates (Callitrichidae - Marmosets and Tamarins (Family)) and lemurs (e.g. Lemuridae - Large lemurs (Family)) are very susceptible. (Th3, J4.205.w1)
  • Infection may be common, but clinical disease is rare in waterfowl (J4.205.w1, B15).
  • In bears, infection is relatively common (seroprevalence rates as high as 80% detected in Pennsylvania black bears Ursus americanus - American black bear) (J1.29.w14), but clinical disease is rare: one, fatal case reported. (P5.31.w2)
  • Clinical signs in infected ferrets are uncommon, but may be seen in immunosuppressed individuals. (J10.34.w1)
  • In Oryctolagus cuniculus domesticus - Domestic European rabbit:
    • Exposure to this infection is reported as widely prevalent in the domestic rabbit. However, infection is usually subclinical and latent; clinical disease is rare. (B601.11.w11, B603.4.w4, J15.28.w1)
    • Toxoplasmosis occurs in outbreaks with many deaths, particularly in young rabbits. (J63.8.w1)
  • In Pan troglodytes - Chimpanzees experimentally infected orally with about 2.5 million oocyts divided over two days, no clinical signs in an individual already seropositive, and mild clinical illness in an individual previously seronegative. (J258.2-5758.w1)
  • In humans, as in other species, clinical signs normally occur only on initial infection; however reinfection, with clinical signs and rising antibody titres suggesting acute toxoplasmosis on two distinct occasions, has been recorded (J100.146.w2).
3) EFFECTS OF AGE, SEX AND REPRODUCTIVE STATUS
  • In a variety of species, the percentage of individuals seropositive for Toxoplasma gondii increases with increasing age. This has been shown e.g. in humans (J19.108.w1), cats (J32.33.w1), sheep (J11.75.w1), goats (J32.40.w2), pigs (J32.42.w1), raptors (J11.79.w2) and Perameles gunnii - Bandicoots () (P1.1993.w10). A survey of dingoes in south eastern New South Wales, Australia, found 6/62 to be seropositive; those which had IgM to Toxoplasma gondii, indicating recent infection, were all 2-3 years old. It was postulated that these dingoes usually encounter Toxoplasma gondii at 1-2 years old and that those encountering the protozoan as pups were less likely to survive. (J1.26.w19)
  • In humans, lymphadenopathy associated with infection was more common in males than in females under 15 years of age, but more common in females than in males among individuals over 25 years. (B599.1.w1)
  • In pigs, higher mortality has been seen in piglets and growing pigs than in adults. (J32.19.w1)
  • In rabbits, acute disease is primarily found in young rabbits. (B614.10.w10)
  • Adult rats are resistant to clinical disease but juveniles may die due to infection. (B208.17,w17d)
  • Adult dogs are resistant to clinical disease, but puppies are susceptible. (B208.17,w17d)
  • "Stress" including lactation and pregnancy may increase susceptibility. (B208.17,w17d)
  • It has been suggested that there may be a breed predisposition to congenital toxoplasmosis in Abyssinian cats. (J4.203.w6)
  • In humans
    • Transplacental infection is most frequent when Toxoplasma gondii is encountered during the third trimester, but neonatal illness is more common in those infected in the first and second trimesters. (B636.w1)
    • Transmission does not usually occur in subsequent pregnancies but has been noted occasionally in the later stages of pregnancy from chronically infected mothers, in whom decreased immunocompetence may allow recurrent parasitaemia. (J133.64.w1, B636.w1)
    • Immunocompetent adult humans infected with Toxoplasma gondii usually show either no clinical signs or only mild, non-specific signs.(J4.196.w3, J694.47.w1)
    • Clinical disease is commoner when the protozoan is first encountered by the old or the very young. (J96.51.w1, J694.47.w1)
4) EFFECTS OF BODY CONDITION AND OTHER DISEASES
  • Susceptibility to clinical disease is increased in the very old, very young, fetuses, and individuals which are immunocompromised. (Th3, J4.205.w1)
  • "Stress" may increase susceptibility. (B208.17,w17d)
  • Susceptibility to clinical disease may be increased by the presence of concurrent disease (e.g. in carnivores, infection concurrent with distemper (Canine Distemper). (Th3, J4.205.w1)
    • Concurrent distemper and toxoplasmosis have been noted in a variety of carnivora, such as dogs, skunk, Cape hunting dogs, mink, racoons and foxes. (B282.3.w3, J1.14.w16, J4.200.w4, J521.25.w1)
    • In humans, toxoplasmosis is a well-known and important complication of acquired immunodeficiency syndrome (AIDS) (B599, J4.205.1, J694.47.w1), and can be seen in patients with malignant diseases of the lymphoid system, e.g. Hodgkin's Disease. (J98.1984ii.w1)
    • Penguins dying of toxoplasmosis at Philadelphia zoo were also infected with avian herpesvirus. (J45.27.w1)
    • A manatee found with Toxoplasma encephalitis also had Proteus pneumonia and abscesses. (J4.183.w7)
    • Superinfection with Isospora felis may lead to reshedding of oocysts by cats. (J9.262.w1)
  • Clinical toxoplasmosis is much more likely to occur if the immune capabilities of the host are diminished (B650.w1, J4.205.w1, J694.47.w1).
    • In humans, both recrudescence and, less commonly, acute primary toxoplasmosis are important complications of people undergoing immunosuppressive therapy. (J4.196.w3, J694.47.w1; J595.9.w1).
    • In hamsters recrudescence of infection may be produced by prolonged cortisone administration (J133.64.w2)
    • In cats, high-dose corticosteroid therapy has led to reshedding of oocysts and to development of clinical disease. (J26.11.w)
    • Experimental infections with Toxoplasma gondii have shown an increase in susceptibility to this protozoan in pregnant mice, compared to non-pregnant controls. (J494.92.w1)
  • Both the elderly and the very young are more susceptible to toxoplasmosis. (J3.99.w4, J4.196.w8)
    • Neonates have, to a greater or lesser degree, depending on species, a reduced immune competence, compared with older animals of the same species, and are generally more susceptible to toxoplasmosis. (J31.19.w3, J4.196.w3, J4.205.w1).
    • The fetus is particularly susceptible to toxoplasmosis because fetuses have incomplete immunocompetance and also because, the fetus is encountering the organism directly in the bloodstream, effectively an intravenous rather than an oral infection (J595.4.w1, J595.9.w1). Inoculation of mice of various ages produced higher levels of infection in old mice, compared with younger animals. (J216.120.w1)

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Clinical & Pathological Characteristics, and Diagnosis

Clinical Signs (by physiological system)

Overall Clinical Presentation
  • Infection may be inapparent or cause severe disease with non-specific signs, neurological signs, abortion and/or other signs, depending on the species affected. (Th3, J4.205.w1)
  • In most cases, infection caused by Toxoplasma gondii is subclinical (B650.w1, B208.17.w17d), with the individual seroconverting and in most species harbouring tissue cysts for years if not for the lifetime of the host. (J4.196.w2).
  • Clinical signs are variable; different tissues may be most affected. (B22.32.w15)
  • Disease when it occurs is often mild, with non-specific signs such as lethargy, mild pyrexia and lymphadenopathy. (J96.51.w1). More serious manifestations of toxoplasmosis frequently involve respiratory signs, neurological signs and death. In some species toxoplasmosis results in abortion, with few or no other clinical signs in the dam. The commonest time for clinical disease to occur is at the time of the initial infection, but recrudescence may occur due to immunosuppression of the host, including that produced by stress, drugs or interaction with infection by other organisms (B599, B650.w1). Local reactions may be seen following rupture of a tissue cyst, especially in the retina. (J4.196.w3)
  • Encephalitis, pneumonia, neonatal mortality. In sheep, abortions and stillbirths. (B211.25.w25)

Humans

  • The most common results of congenital infections are chorioretinitis, hearing impairment and mental retardation. Mental retardation may be mild, moderate or severe. Ophthalmic and aural problems may not be apparent at birth but be manifest later (J694.47.w1, B636.w1).
  • Symptoms, when present, usually include lymphadenopathy, headache and a sore throat. (J96.51.w1, J694.47.w1)
  • Fever, lymphadenopathy (particularly noted in the caudal cervical chain of lymph nodes), headache, malaise, often muscle pain (e.g. 60%), stiff neck in about 50%, anorexia in about 50% and maculopapular rash in about 33%. Confusion has been noted also. (J4.196.w3)
  • Rare manifestations include chronic illness with splenomegal, hepatitis, pneumonia and haemolytic anaemia. (J4.196.w3)
  • In fatal cases, commonly pneumonia, hepatitis. myocarditis and encephalitis detected. (J4.196.w3)
  • Congenital infection usually does not produce clinical signs, but infection can result in premature birth, intrauterine growth retardation, retinochoroiditis (seen in abut 75% of individuals) and generalised disease. (J4.196.w3)
    • Generalised neonatal illness can involve jaundice, splenomegaly, fever, anaemia, hepatomegaly, lymphadenopathy, pneumonia and rash, also neurological abnormalities: retinochoroiditis, convulsions, nystagmus, internal hydrocephalus, micrencephaly and intracerebral calcifications. Late sequelae can develop including convulsions, mental retardation, palsies, spasticity, severe visual impairment, slight auditory impairment and precocious puberty. (J4.196.w3)
  • In the immunosuppressed, severe generalised and fatal disease may develop from primary infection. In chronically infected individuals, immunosuppression can allow recrudescence which usually manifests as encephalitis involving one or multiple focal lesions. (J4.196.w3)
  • The commonest form of toxoplasmosis seen in AIDS patients is a non-suppurative encephalitis due to recrudescence of latent infection and it appears that approximately 30% of AIDS patients seropositive for Toxoplasma will develop encephalitis due to the parasite; the incidence in AIDS patients therefore varies depending on the infection rate in the population (J416.252.w1, J270.15.w1)

In a Pan troglodytes - Chimpanzee experimentally infected orally with about 2.5 million oocyts divided over two days: (J258.2-5758.w1)
  • Listlessness and anorexia for about a week. (J258.2-5758.w1)
  • Superficial lymph nodes enlarged for about six weeks. (J258.2-5758.w1)
  • No clinical signs in a similarly-infected chimpanzee which was already seropositive. (J258.2-5758.w1)

Felis catus - Domestic cat

  • Persistent pyrexia, unresponsive to antibiotics, may indicate toxoplasmosis, but fever is not always present. (J196.81.w1, J4.203.w7)
  • With the enteroepithelial infection cycle, usually no clinical signs, but occasionally vomiting and diarrhoea may be seen. (B583.w2)
    • In kittens with concurrent illness such as acute viral respiratory infection just after weaning, severe signs of enteric disease may be seen.
  • General signs: fever, anorexia, weight loss, malaise, jaundice. (B583.w2)
  • Lameness; on palpation, discomfort of both muscles and joints may be noted. (B583.w2)
  • Enlarged tonsils, lymphadenopathy, splenomegaly. (B583.w2)
  • With respiratory tract involvement, dyspnoea, coughing. (B583.w2)
    • Radiography may detect diffuse interstitial to alveolar patterns and sometimes pleural effusion. (B583.w2)
  • With CNS involvement (encephalitis), there may be ataxia, seizures or focal signs. (B583.w2)
  • With ocular involvement, anterior uveitis and/or retinochoroiditis. Also non-specific inflammatory signs such as vitreal opacity, vitreal haemorrhage, retinal detachment, hypaema, cataracts, lens luxation, glaucoma, keratic precipitates. (B583.w2)
  • Abdominal radiography may reveal diffuse increased density due to peritoneal effusion, or more discrete increases in density associated with hepatomegaly or lymphadenopathy, or reduced right cranial quadrant contrast associated with pancreatitis. (B583.w2)
  • Note: often, clinical signs are low-grade and chronic. (B583.w2)

Ovis aries - Domestic sheep

  • Abortion. (J112.20.w1)
  • Typically stillborn and/or weak lambs, sometimes also mummified fetuses, due to infection of the ewe in mid-gestation. (B217.13.w13)
    • On the placenta, cotyledons bright red and speckled with pale spots. (B217.13.w13)

Bos taurus - Domestic cattle

  • In adult cattle, generally no clinical signs. (B211.25.w25)
  • Fever, dyspnoea, nervous signs such as ataxia and hyperexcitability, later lethargy. (B211.25.w25)
  • Transient fever, anorexia, sometimes diarrhoea, sometimes respiratory distress. (J112.20.w1)
  • Calves may be born weak, or stillborn, but abortion is not generally noted. (B211.25.w25)
  • In calves, mild fever and lymphadenopathy to fever, depression, weakness, diarrhoea, anorexia, poor weight gain and dyspnoea may occur. (B211.25.w25)
    • In three-month-old calves following oral administration of oocysts and tissue cycts, fever, respiratory distress, nasal discharge, conjunctival hyperaemia. (J11.62.w2)

Sus domesticus - Domestic pig

  • In adults: J32.19.w1
    • Often no clinical signs. (B211.25.w25, J32.19.w1)
    • Debility, weakness and incoordination, tremor, cough and diarrhoea may be seen. (B211.25.w25, J32.19.w1)
    • Abortion, premature or stillborn piglets; piglets may also survive then develop clinical signs and die. (B211.25.w25, J32.19.w1)
  • In weaned pigs, generally fever, anorexia and weight loss but recovery within three weeks. (J32.164.w2)
  • In piglets, fever 40-42 C (104-107 F) and diarrhoea; piglets may die after several weeks of illness. (B211.25.w25)
  • In piglets 2-4 weeks of age, fever and diarrhoea, also dyspnoea and cough, neurological signs particularly ataxia, and wasting. (B211.25.w25)
  • In piglets: some born dead. Others developed clinical signs at less than three months of age, particularly dyspnoea, also fever, anorexia, weakness, nasal discharge, ear cyanosis, diarrhoea, ataxia, visual defects. (J32.19.w1)
  • Fever, convulsions and deaths were seen in 17-day-old piglets on a farm in Thailand.

Equus caballus - Domestic horse

  • Clinical disease is not normally seen. (B211.25.w25)

Rangifer tarandus - Reindeer

Lagomorphs

  • Acute, chronic and latent forms of toxoplasmosis have been described in Oryctolagus cuniculus domesticus - Domestic rabbit. (J63.8.w1)
  • Toxoplasma gondii infection in rabbits is usually subclinical and latent (B601.11.w11, J15.28.w1) or causes only mild signs (transient fever). (J42.117.w1); acute disease may be seen e.g. in young rabbits. (B614.10.w10)
  • Toxoplasmosis is often an acute, fatal disease in Lepus europaeus - Brown hare and Lepus timidus - Mountain hare. (J1.30.w8)
  • Clinical findings may include:
    • Anorexia, central nervous system signs, raised temperature, death within 2 - 8 days. (J63.8.w1, J495.42.w3)
    • Sudden anorexia (B603.4.w4, B614.10.w10)
    • Fever (>104 F) (B601.11.w11, B603.4.w4, B614.10.w10, J15.28.w1)
    • Lethargy (B601.11.w11, B614.10.w10, B603.4.w4)
    • Hepatosplenomegaly may occur; the spleen can become ten times its normal size (B603.4.w4)
    • Increased respiratory rate (tachypnoea) (B614.10.w10, J42.117.w1)
    • Serous or seropurulent nasal and ocular discharge (B614.10.w10, J42.117.w1, J63.8.w1)
    • Head tremors (B601.11.w11, B602.20.w20, B609.2.w2, B614.10.w10, J15.28.w1)
    • Head tilt (B600.12.w12, B606.13.w13, B609.2.w2)
      • Note: toxoplasmosis is a rare cause of head tilt. (B603.1.w1)
    • Ataxia (B601.11.w11, B602.20.w20, B603.3.w3, B606.13.w13, B609.2.w2, B614.10.w10, J15.28.w1)
    • Dysuria (B603.1.w1)
    • Muscle tremors (B603.4.w4, B606.13.w13)
    • Convulsions may occur within a few days of the onset of the clinical signs. (B603.4.w4, B609.2.w2, B614.10.w10, J63.8.w1)
    • Posterior paresis (B602.20.w20, B603.3.w3, B609.2.w2, J15.28.w1)
    • Paralysis in some cases, particularly in the hindquarters. (B601.11.w11, B602.20.w20, B603.4.w4, B606.13.w13, B609.2.w2, B614.10.w10, J63.8.w1)
    • Tetraplegia (B602.20.w20, B603.1.w1, B609.2.w2)
    • Death usually after two to eight days of illness. (B603.4.w4, B614.10.w10, J15.28.w1, J63.8.w1)
  • In three pet French lop rabbits: (J495.42.w3)
    • Anorexia, dehydration, tetraplegia and temperature 41.6 C (J495.42.w3)
    • Anorexia, ataxia, developing to muscle tremors, posterior paresis, temperature 41.1 C (J495.42.w3)
    • Sudden death. (J495.42.w3)
  • In experimentally infected Lepus europaeus - Brown hare. (J32.93.w2)
    • Lassitude, sitting in a corner, loss of shyness, ruffled fur and reduced food consumption. (J32.93.w2)
    • No behavioural changes in some hares before death. (J32.93.w2)
  • Chronic toxoplasmosis may be seen in older rabbits: the course of the disease is protracted and the rabbit becomes anorexic and emaciated. This commonly results in anaemia. Central nervous signs may occur as the disease progresses, usually as posterior paralysis. Sudden death may occur but many animals recover. (B614.10.w10, J63.8.w1)
Mustela putorius furo - Ferret
  • Systemic signs include anorexia, lethargy, depression, dehydration; pyrexia; individuals are known to reach 105.3F; clinical jaundice associated with hepatitis; respiratory distress, dyspnoea and orthopnoea (difficulty breathing when lying down); diarrhoea; tachycardia. (B626, J10.34.w1)
  • Neuromuscular signs of posterior weakness and ataxia. (B626, J10.34.w1)
  • Ocular and neurological signs including corneal oedema and ataxia, blindness, and lesions such as retinitis or iritis. (B626)
  • In congenitally infected ferret kits, some died without obvious clinical signs, while survivors showed stunted growth. (J10.34.w1)

Cavia porcellus - Domestic guinea pig

  • In experimentally inoculated guinea pigs, fever 39.8 - 40.5 C, sometimes higher; for 3 - 5 days, also ruffled coat, hunched body position, wasted flanks and flaccid abdomen. (J100.72.w1)
  • Vulval bleeding and fetal death associated with toxoplasmosis has been reported in a guinea pig. (J3.129.w7)

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Clinical Pathology (Testing Samples incl. Serology)

Overall Clinical Pathology findings

Cats

  • Haematological and biochemical findings are very variable, none are pathognomonic, and changes may include nonregenerative anaemia, neutrophilic leucocytosis, lymphocytosis, monocytosis, neutropaenia, eosinophilia, raised serum proteins, raised creatine kinase, raised bilirubin, raised alaninie aminotransferase, raised alkaline phosphatase and raised lipase. Gammaglobulinaemia, when it occurs, combined with fever and CNS and ocular manifestations may lead to an erroneous diagnosis of FIP. Tachyzoites may be detected in blood. (B583.w2)
  • Antibodies against Toxoplasma gondii, Toxoplasma gondii antigens and antigen-containing immune complexes may be detected in serum. (B583.w2)
    • ELISA, IFA or agglutination tests are used most commonly. (B583.w2)
    • In sublinically infected cats, IgM may be detected by ELISA within 2-4 weeks in 90% of cats; titres >1:256 being detected only in the first 20 weeks post infection in experimentally infected cats..
    • In cats with clinical toxoplasmosis, IgM was detected in serum in 93.3% and IgG in 60% and IgM may be detected for longer periods than 12 weeks. (B583.w2)
    • IgM may increase again temporarily after glucocorticoid administration or repeat infection with Toxoplasma gondii. (B583.w2)
    • IgG is usually detectable within three weeks following experimental infection, in cats without clinical signs, and generally remains positive for years, sometimes at high titres (higher than 1:16,384 has been documented). (B583.w2)
    • Rising IgG indicates recent infection/active disease, but often the initial rise, which occurs within 2-3 weeks after IgG is first detectable, has occurred prior to the first sample being taken. (B583.w2)
    • Antigens may be detected by ELISA within four weeks of infection in subclinically infected cats and in some cases may be detectable intermittently for months to years. (B583.w2)
    • Antigen-antibody complexes may be detected by ELISA. (B583.w2)
      • Cats with ocular toxoplasmosis are more likely to have circulating Toxoplasma-containing immune complexes. (B583.w2)
    • The dam of a stillborn calf Rangifer tarandus - Reindeer, had an antibody titre against Toxoplasma gondii of 1: 12,800 using the modified agglutination test. (J32.110.w1)
    • Following experimentaloral  infection with oocyts,
  • Urinalysis is unremarkable. (B583.w2)
  • CSF analysis is generally normal in cats with subclinical infection. In cats with suspected toxoplasmosis affecting the CNS, protein levels were sometimes raised (normal to 149 mg/dL), nucleated cell counts reached up to 28 cells/mL, particularly lymphocytes. Tachyzoites may be detected. IgG and IgM antibodies may be detected. (B583.w2)
  • Tachyzoites may be detected in pleural or peritoneal effusions and in tracheal washes. (B583.w2)
  • In aqueous humour, IgM, IgG and Toxoplasma-containing immune complexes may be detected; titres of complexes in aqueous humour may be higher than in serum. (B583.w2)

Lagomorphs:

  • Haematology, biochemistry and urinalysis are usually normal unless the Toxoplasma organisms have affected non-neural tissue. (B609.2.w2)

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Pathological Findings (by anatomical system)

Overview

Histopathology toxoplasmosis wallaby heart. Click here for full-page view with caption. Histopathology toxoplasmosis wallaby lung. Click here for full-page view with caption. Immuohistochemistry Toxoplasma gondii issue cyst wallaby heart. Click here for full-page view with caption. Immunohistochemistry Toxoplasma gondii wallaby lung. Click here for full-page view with caption. Toxoplasma gondii issue cyst liver, wallaby - Romanovwsky stained impression smear. Click here for full-page view with caption. Toxoplasma gondii tachyzoites, wallaby heart impression smear. Click here for full-page view with caption. Toxoplasma gondii tissue cyst, wallaby heart impression smear. Click here for full-page view with caption.

  • Lesions found in toxoplasmosis are predominantly caused by destruction of cells in which tachyzoites multiply and the accompanying inflammatory reaction, but delayed-type hypersensitivity also plays a role (J133.64.w2, J595.4.w1). Infection by the oral route is likely to produce lesions initially in the epithelium of the intestine, followed by the intestinal and mesenteric lymph nodes and then the liver, after which, if neither death nor immunity has prevailed, infection becomes widely disseminated and lesions may develop in many organs. (B650.w1)
  • The pathological effects of Toxoplasma gondii are affected by the regenerative capacities of the organs involved and the speed of the immune response. Where destruction of cells by multiplying tachyzoites is matched by normal cell turn-over, as in the intestinal epithelium of adult cats, pathological changes may be minimal. Conversely, parasite multiplication and cell destruction may continue in immunologically-privileged sites, such as the central nervous system and the eye, after the immune response has controlled infection in other areas of the body. (B650.w1)
  • Delayed-type hypersensitivity is involved in the response to the rupture of tissue cysts and release of bradyzoites, and plays a role in the development of the resultant lesions. (J595.4.w1, J133.64.w2)
GROSS PATHOLOGY
  • Multiple necrotic foci in affected organs: CNS, myocardium, lungs. Less commonly in the liver, spleen and kidneys. Other lesions with visceral involvement include pneumonitis, hydrothorax, ascites, intestinal ulceration and lymphadenitis. (B211.25.w25)
  • Sheep:
    • Placentary cotyledons dark red, speckled with pale foci of necrosis; intercotyledonary areas normal. (B217.13.w13, J3.88.w4)
    • Mummified fetus - miniature, chocolate brown in colour, with a grey-brown placenta. (B217.13.w13)
    • Decomposed fetuses (having died later in gestation), often with clear/bloody subcutaneous oedema, variable clear/blood-stained fluid in body cavities. (B217.13.w13)
  • Pigs:
    • Pneumonia, hydrothorax, ascites, focal hepatic necrosis, enteritis, lymphadenitis. (J32.19.w1)
    • In piglets, particularly pneumonia. (J32.19.w1)
  • A Rangifer tarandus - Reindeer, the placenta associated with a stillborn calf showed haemorrhagic cotyledons containing white, friable flecks.. (J32.110.w1)
  • Waterfowl miliary white, necrotic foci in the liver, congestion of the lungs, splenomegaly with areas of necrosis, clear to sanguineous exudate in body cavity. Crescent-shaped Toxoplasma gondii organisms visible on Giemsa-stained smears of liver and peritoneal fluid. (J5.6.w1)
  • A six-day-old Ursus maritimus - Polar bear with generalised infection, lesions were most severe in the liver, skeletal muscles and brain. There was necrosis of the liver and pancreas. (B22.32.w15, P5.31.w2)
    • Liver: Pinpoint necrotic foci, petechial haemorrhages. (P5.31.w2)
    • GIT: Mucosal haemorrhage. (P5.31.w2)
    • Skeletal muscles: Very pale and marbled. (P5.31.w2)
    • Lungs: Acute oedema. (P5.31.w2)
    • Cardiac: Right ventricle dilated. (P5.31.w2)
  • Lagomorphs:
    • Generalised lesions are seen characterised by extensive necrosis of heart, lungs, liver, spleen and lymph nodes - swollen organs with multiple, necrotic foci.. (B614.10.w10)
  • Ferrets
    • Pulmonary: Multiple white foci (necrotic areas) in lung tissue. (B626, B627.16.w16,J10.34.w1)
    • Cardiac: multiple necrotic areas may be present. (B626, B627.16.w16)
    • Hepatic: multiple necrotic areas may be present. B626, B627.16.w16)
  • Guinea pigs
    • In experimentally inoculated guinea pigs, in the peritoneal and sometimes also the pleural cavity, clear mucinous exudate. Usually splenomegaly (variable degree) and sometimes pale liver. Usually the lungs showed patchy consolidation. (J100.72.w1)
HISTOPATHOLOGY
  • In acute toxoplasmosis, typically in organs such as the small intestine, mesenteric lymph nodes, liver, adrenal cortex, heart, and skeletal muscle there is focal to locally extensive areas of necrosis . Severe pulmonary congestion and oedema is also a frequent finding, often accompanied by interstitial pneumonia. Where the central nervous system is involved, toxoplasmosis results in a non-suppurative meningo-encephalitis. (J351.33.w1)
  • In chronically-infected asymptomatic individuals, cysts with little or no tissue reaction may be found in a variety of organs such as the liver, heart, skeletal muscles and brain. Recrudescence due to immunosuppression in a chronically infected individual may lead to extensive necrotic lesions with little inflammatory reaction. (B650.w1)
  • Retinochoroiditis is the commonest manifestation of ocular toxoplasmosis in humans, but iridocyclochoroiditis is the most frequent finding in cats with ocular toxoplasmosis. (J4.203.w7)
  • Pigs:
    • Lungs, liver, spleen, lymph nodes and adrenales, foci of necrosis and granulomatous inflammation. (J32.19.w1)
    • In piglets, pneumonia with oedema, fibrino-necrotic alveolitis and mononuclear cell infiltration. Also acute enteritis, mesenteric lymphadenitis, granulomatous nephritis, hepatitis, non-supppurative encephalitis, chorioretinitis. (J32.19.w1)
    • Toxoplasma gondii organisms have been found associated with lesions, and confirmed by mouse inoculation. (J32.19.w1)
  • In a stillborn calf Rangifer tarandus - Reindeer, the cerebellum and cerebrum showed multiple scattered foci of necrosis and loss of the parenchyma with associated peripheral infiltration by microglia. In the heart, a group ofToxoplasma gondii organisms was seen without any associated host tissue changes. The placentary cotyledons contained foci of necrotic villi and associated degenerating tachyzoites. Immunohistochemical staining confirmed that parasites in the brain, heart and placenta were Toxoplasma gondii. (J32.110.w1)
  • In a six-day-old Ursus maritimus - Polar bear (P5.31.w2)
    • Liver: localised areas of necrotising inflammation; at the margins of such lesions, Toxoplasma tachyzoites and in cells, pseudocysts containing Toxoplasma.
    • Pancreas: Necrotising inflammation.
    • Lung: Slight interstitial inflammatory reaction.
    • Heart: Slight cellular proliferation.
    • Skeletal muscles and diaphragm: Significant necrosis, with pseudocycts in the area around the necrotic lesions. 
    • Thymus: Significant necrosis, with pseudocycts in the area around the necrotic lesions.
    • Retina: Slight accumulation of lymphoblastic cells in foci in the retina, with Toxoplasma cysts present. 
    • CNS: Purulent meningitis, mainly per-ventricular lesions, with oedema and Toxoplasma cysts. (P5.31.w2)
  • In four- to seven-month old Kodiak bears (Ursus arctos - Brown bear) at Rostock Zoo. (P5.29.w5)
    • CNS: Encephalitis, toxoplasma cysts present. (P5.29.w5)
    • Pulmonary: Interstitial pneumonia with Toxoplasma present. (P5.29.w5)
    • Cardiac: Myocarditis. (P5.29.w5)
  • In lagomorphs
    • The vascular connective tissue and the reticuloendothelial elements are most often affected. There is pronounced cellular necrosis with or without inflammatory cell infiltration. (B614.10.w10)
    • Toxoplasma gondii trophozoites may be seen intra- and extracellularly. (B614.10.w10)
    • In experimentally infected Oryctolagus cuniculus domesticus - Domestic rabbit killed at eight days post inoculation, lesions were minor, mainly focal mononuclear cell accumulations in the liver, (J42.117.w1)
    • CNS: 
      • Focal necrotic areas in the brain. (B609.2.w2)
      • Non-suppurative meningoencephalitis. (B609.2.w2)
    • Hepatic:
      • Focal interstitial granulomatous hepatitis. (B603.3.w3)
      • In Lepus timidus - Mountain hare, areas of necrotic hepatocytes, small amount of macrophage infiltration, Toxoplasma gondii organisms found in groups or singly in association with lesions. (J42.117.w1)
      • In three French Lop rabbits, multifocal necrosis and granulomatous reaction, with both tachyzoites and tissue cysts. (J495.42.w3)
      • In experimentally infected Lepus europaeus - Brown hare, irregular foci of coagulative necrosis. (J32.93.w2)
    • Lymph nodes:
    • Splenic:
      • In Lepus timidus - Mountain hare, focal necrosis. (J42.117.w1)
      • In three French Lop rabbits, multifocal necrosis and granulomatous reaction, with both tachyzoites and tissue cysts. (J495.42.w3)
      • In experimentally infected Lepus europaeus - Brown hare, irregular foci of coagulative necrosis, slight peripheral inflammatory reaction, and slight follicular lymphocyte depletion. (J32.93.w2)
    • Pulmonary:
      • In Lepus timidus - Mountain hare, focal necrosis. (J42.117.w1)
      • In three French Lop rabbits, multifocal necrosis and granulomatous reaction, with both tachyzoites and tissue cysts. (J495.42.w3)
    • Bone marrow:
    • Cardiac:
    • GIT:
      • In Lepus timidus - Mountain hare, foci of necrosis in the mucosa. (J42.117.w1)
      • In experimentally infected Lepus europaeus - Brown hare, in the small intestines, epithelial cell necrosis and desquamation, in the lamina propria hyperaemia and haemorrhages, and in the submucosa a mixed inflamatory exutdate. Toxoplasma gondii tachyzoites were present in the epithelial lining. (J32.93.w2)
    • Skeletal muscles:
    • Diaphragm:
    • In chronic toxoplasmosis in rabbits, marked reticuloendothelial hyperplasia especially in the lymph nodes, liver, spleen, and central nervous system. Toxoplasma gondii organisms are more difficult to isolate than in the acute disease. (B614.10.w10, J63.8.w1)
    • In latent infection in rabbits: primarily CNS lesions in the form of cysts with or without reaction. Gliosis and granulomatous encephalitis with perivascular cuffing and nonsuppurative meningitis may be found. These lesions may be confused with Encephalitozoonosis. (B614.10.w10)
    • Immunohistochemistry: 
      • In Lepus timidus - Mountain hare, Toxoplasma gondii demonstrable in multiple organs, particularly liver, mesenteric (and popliteal) lymph nodes, small intestine, spleen, lung and bone marrow. (J42.117.w1)
      • In Oryctolagus cuniculus domesticus - Domestic rabbit, organisms rarely detected at eight days post-inoculation. (J42.117.w1)
      • In three French Lop rabbits, positive reaction to anti-Toxoplasma gondii serum but not to anti-Neospora caninum serum. (J495.42.w3)
  • Ferrets
    • Hepatic: Multiple foci of coagulated necrosis, lightly infiltrated by macrophages. (J10.34.w1)
    • Myocardium: Multiple foci of coagulated necrosis were present, with diffuse interstitial infiltration with moderate numbers of lymphocytes. A small number of protozoa were found and intrascarcoplasmic Toxoplasma-like colonies. (J10.34.w1)
    • Lung: Diffuse pneumonia with macrophages within the alveoli. Also foci of coagulative necrosis and protozoal colonies within the macrophages. (J10.34.w1)
    • CNS: 
      • Cysts have been found in the brains of ferrets that are serologically positive for Toxoplasma gondii. (J10.34.w1)
      • Mengingoencephalitis or meningoencephalomyelitis has been found in ferrets that showed posterior weakness and ataxia. (B626)
    • Immunohistochemistry: Immunohistochemistry confirmed that the protozoan detected associated with lesions in various organs in ferret kits in New Zealand was Toxoplasma gondii. (J10.38.w1)
  • Rats
    • In naturally infected rats, in the brain, round to oval cysts 10-80 um diameter, containing tightly packed organisms. Sometimes nodular accumulations of microglial cells, and small granulomas of polyhedral or fusiform cells. Occasionally also a few degenerating cells. Sometimes slight to moderate perivascular infiltration (lymphocytes, large mononuclear cells); occasionally small clumps of foamy macrophages. (J100.72.w1)

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Diagnostic Criteria

General Indicative Signs

Clinical signs are non-specific. (B208.17.w17d, J133.64.w3, J596.28.w1) Lethargy and anorexia, respiratory signs or neurological signs, of varying severity and duration, have been described in a variety of species.

  • The wide variety of presentations means that toxoplasmosis has a place on a large number of differential diagnosis lists. (J4.163.w7)
  • Clinical signs in a single animal are not usually sufficient, by themselves, for diagnosis, although a late abortion/neonatal mortality syndrome in sheep is very suggestive (B693.26.w26), as are the classical signs of retinochoroiditis, hydrocephalus or microcephaly and intercranial calcification in human neonates, and Toxoplasma gondii is responsible for at least 35% of cases of chorioretinitis in humans (J96.51.w1, J416.150.w1, J694.47.w1). Clinical signs may be more useful for presumptive diagnosis where a toxoplasmosis problem is known to occur.

Suggestive signs include:

In humans

  • The commonest presenting sign is peripheral lymphadenopathy, sometimes accompanied by a headache or sore throat. (J96.51.w1, J694.47.w1)

In cats

  • Persistent pyrexia, unresponsive to antibiotics, may indicate toxoplasmosis, but fever is not always present. (J4.203.w7, J196.81.w1)
  • Clinical signs which can be attributed to toxoplasmosis, in combination with serological evidence of infection, exclusion of other common causes of the clinical signs, and response to treatment, allow a tentative diagnosis of toxoplasmosis. (B583.w2)

In Australian marsupials

  •  Toxoplasmosis should be considered in animals with neurological signs, respiratory signs or sudden death. (B336.34.w34, B637.w1, J2.22.w4, J24.70.w2)

In sheep

  • Abortion, weak/stillborn lambs, and typical placental lesions: cotyledons dark red, speckled with pale foci of necrosis; intercotyledonary areas normal. (B217.13.w13, J3.88.w4)
    • Inspection of the placenta for the typical pale foci of necrosis in the cotyledons may be of more diagnostic use than gross examination of the fetus for lesions (J3.88.w4, B693.26.w26).
  • Typical visible changes in lambs include: (B217.13.w13)
    • Mummified fetus - miniature, chocolate brown in colour, with a grey-brown placenta. (B217.13.w13)
    • Decomposed fetuses (having died later in gestation), often with clear/bloody subcutaneous oedema, variable clear/blood-stained fluid in body cavities. (B217.13.w13)
    • Note: these changes indicate probable intrauterine infection but are not specific for toxoplasmosis. (B217.13.w13)

Guinea pigs

  • In experimentally inoculated guinea pigs, typical tachyzoites could be found (cresentic forms) on a smear of peritoneal exudate, pleural exudate, or organs. (J100.72.w1)
Definitive Diagnosis

Histopathology toxoplasmosis wallaby heart. Click here for full-page view with caption. Histopathology toxoplasmosis wallaby lung. Click here for full-page view with caption. Immuohistochemistry Toxoplasma gondii issue cyst wallaby heart. Click here for full-page view with caption. Immunohistochemistry Toxoplasma gondii wallaby lung. Click here for full-page view with caption. Toxoplasma gondii issue cyst liver, wallaby - Romanovwsky stained impression smear. Click here for full-page view with caption. Toxoplasma gondii tachyzoites, wallaby heart impression smear. Click here for full-page view with caption.  Toxoplasma gondii tissue cyst, wallaby heart impression smear. Click here for full-page view with caption.

  • Finding of tachyzoites from acute clinical cases (e.g. in urine, pulmonary aspirates, CSF, pleural effusion, peritoneal effusion) confirms active infection. However, such tachyzoites are rarely found. (B583.w2)
  • Finding of tissue cysts e.g. on histological examination, or by immunoperoxidase staining, or by bioassay, confirms the presence of Toxoplasma gondii but does not differentiate between subclinical infection and clinical disease. (B583.w2)
    • Both Toxoplasma gondii tissue cysts and tachyzoites (free or intracellular) can be seen on normal haematoxylin and eosin stained histology sections and also visualised on impression smears stained with Romanowski stains. Because Toxoplasma gondii tissue cysts may persist in the host, it must be remembered that the finding of such cysts is evidence only of exposure to the organism at some time in the past, and in the absence of lesions attributable to toxoplasmosis should be regarded as an incidental finding. Immunohistochemical staining may be used to detect small quantities of Toxoplasma gondii in sections, which may be missed by conventional staining techniques, and to differentiate Toxoplasma gondii from other organisms such as Neospora caninum with similar histological morphology. (B634, J13.50.w5, J133.177.w1)
  • In ovine abortion:
    • Presence of antibodies against Toxoplasma gondii in fetal fluids or in lamb serum from a blood sample taken before the lamb has suckled, since antibodies do not cross the placenta. (B217.13.w13, J4.196.w12)
    • IgM in a post-suckling sample (IgG could represent maternal antibodies). (B217.13.w13)
    • Rising titre in the ewe: this is unlikely as the infection will probably have occurred some weeks earlier. (B217.13.w13)
  • Immunohistochemical demonstration of the organism, e.g. using the ABC indirect immunoperoxidase method or the peroxidase anti-peroxidase (PAP) method. (B217.13.w13)
  • PCR detection, in placenta, or in fetal brain, liver or lung, of viable or nonviable Toxoplasma gondii organisms, targeting the B1 gene or sometimes the P30 gene. (B217.13.w13)
  • In a stillborn calf Rangifer tarandus - Reindeer, diagnosis was made on the basis of lesions and parasite morphology, immunohistochemical staining and serology of the dam (MAT titre 1:12,800). (J32.110.w1)
  • For further information on different serological tests and virus identification see: Toxoplasma gondii - Detection and Identification Techniques

Similar Diseases
  • Neosporosis (Neospora caninum infection) as a cause of abortion. Immunohistochemical staining may be used to differentiate between Toxoplasma gondii and Neospora caninum, since they have similar histological morphology. (J13.50.w5)
  • Other causes of abortion in sheep: enzootic abortion (chlamydial infection), Campylobacter infection, listeriosis, border disease, salmonellosis. (B217.13.w13)
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Treatment and Control

Specific Medical Treatment (Antiserum, Antidote, Anti-parasitic etc.)

Specific Medical Treatment
  • Use of sulphonamides, usually with pyrimethamine for a synergistic effect. (B599)
    • Sulphonamides block the metabolic mathway involving p-aminobenzoid acid. Pyrimethamine blocks the folic-folinic acid cycle. (B599.1.w1)
    • Thrombocytopaenia or leucopaenia may occur; folinic acid and yeast can be given to counteract this without interfering with the effect on Toxoplasma gondii, since the host cells can use presynthesised folinic acid, while the parasite cannot. (B599)
    • In humans, 500 mg of sulphadiazine, sulphamethadine, sulphamerazine (or any other sulphonamide which diffuses across the host cell membranes) is given four times a day, while a loading dose of pyrimethamine is given for the first three days (975 mg) followed by 25 mg/day thereafter, with 2 - 10 mg of folinic acid or 5 - 10 g baker's yeast. Treatment may continue for several weeks to months. (B599)
      • Not all sulphonamides are effective. Sulfadiazine, sulfamerazine, sulfamethazine, trisulfapyrimidine, sulfapyrazine, sulfalene, sulfadoxine and sulfamethoxazole may be used, at 100 mg/kg body weight, up to 4g, per day in divided doses. Sulphonamides which are NOT effective include sulfisoxazole, sulfacetamide, sulfasalazine, sulfasuxidine and sulfathaladine. (J4.196.w3)
      • Pyrimethamine is given orally at 1 mg/kg for each of the first three days, then 0.3 mg/kg orally once daily. (J4.196.w3)
      • In individuals with serious ocular lesions, corticosteroids may be used alongside these drugs to reduce inflammation due to delayed hypersensitivity reactions. (J4.196.w3)
    • Spiramycin and clindamycin have also been used. Spiramycin is less effective than pyrimethamine-sulphadiazine. Clindamycin is effective but may cause ulcerative colitis. Trimethoprim-sulphonamide does not produce the same synergistic effect as pyrimethamine-sulphonamide. (B599)
  • In cats:
    • Clindamycin hydrochloride, 25 mg/kg per day divided in two or three doses per day. (B583.w2)
      • Clinical signs not associated with the eyes or CNS may start to resolve within 2-3 days of the onset of therapy. (B583.w2)
      • Recurrence of clinical signs is more likely if therapy is stopped after less than four weeks. (B583.w2)
      • This drug does cross the cat's blood-brain barrier and has been used successfully in cats with CNS toxoplasmosis. (B583.w2)
      • For ocular lesions: clindamycin hydrochloride systemically plus corticosteroids given topically, orally or parentrally, particularly for anterior uveitis, to avoid additional damage due to inflammation. With retinochoroiditis, clindamycin alone may be effective. (B583.w2)
    • Trimethoprime-sulphonamide, 15 mg/kg orally twice daily. (B583.w2)
      • This had been effective in some cats with CNS signs. (B583.w2)
    • Sulphonamide-pyrimethamine combination treatment can be used  but often results in toxicity. (B583.w2)
  • In sheep:
    • Pyrimethamine plus sulfadimidine. (B217.13.w13)
      • Pyrimethamine (suspended at 10 mg/mL in 1% methyl cellulose and given intraperitoneally at 2 mg/kg on the first day, 1 mg/kg on each of the following two days), plus sulphamezathine (Sulphonamides) 1g per 3 mL solution, given at 5 mL/10 kg bodyweight on the first day, 2.5 mL/10 kg body weight on each of the following two days, subcutaneously), for each of three treatment periods at days 100, 115 and 130 of gestation. This was effective in reducing losses in experimentally infected sheep from (expected) 30% to 0%. (J3.132.w9)
    • Baquiloprim plus sulfadimidine has been used and gave "promising results". (B217.13.w13)
  • In pigs:
    • Pyrimethamine at 2.5 mg/kg body weight plus sulfamonomethoxine (Sulphonamides) at 60 mg/kg body weight was effective in preventing clinical toxoplasmosis in experimentally infected pigs. (J32.19.w1)
    • Pyrimethamine  at 500 ppm in feed plus sulfamonomethoxine (Sulphonamides) at 25 ppm in feed, starting seven days before massive (1,700,000) oral oocyst inoculation and continuing to 58 days post administration was effective; traeted pigs showed only mild clinical signs and survived, while untreated pigs died within 15 days. (J32.19.w1)
    • Treatment with 2-sulfamoyl-4,4 diaminodiphenyl sulfone (SDDS) starting seven dayys before infection resulted in milder clinical signs than in untreated pigs. In an outbreak, treatment with SDDS, 10 mg/kg per day for four days resulted in recovery of most of the treated pigs within 10 days. (J32.19.w1)
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  • No specific techniques described

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General Nursing and Surgical Techniques

Nursing and Supportive Care

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Surgical Treatment
  • Not applicable for this disease.

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Vaccination & Prophylactic Treatment

Vaccination
  • Vaccines using dead Toxoplasma gondii do not produce sufficient protection. (B217.13.w13)
  • A live vaccine using the S48 incomplete strain of Toxoplasma gondii has been used in sheep and shown to induce good, long-lasting immunity. (B217.13.w13)
    • Experimentally, sheep vaccinated, mated 77 days later, and challeneged with virulent Toxoplasma godii at 89-90 days gestation showed an earlier, shorter, less severe fever, compared with unvaccinated ewes, and produced more and larger lambs (72.3 - 80.8% viable lambs versus 17.8% in control challenged ewes). (J3.129.w7)
    • Sheep challenged at 18 months post vaccination were still protected. (J3.133.w4)
    • S48 is available as a commercially produced vaccine. It was first licensed in New Zealand in 1988 then in the UK and Eire in 1992 (J595.9.w3) and is still available, as Ovilis Toxovax. (J484.41.w2)
  • Another mutant strain of Toxoplasma gondii has been assessed for potential use as a live vaccine in sheep. MIC1-3KO is a mutant of the RH strain of Toxoplasma gondii in which the mic1 and mic3 genes have been disrupted. Experimentally, MIC1-3KO was shown to have similar efficacy to S48 in enabling sheep to produce live, viable lambs after challenge with virulent Toxoplasma gondii. A dose of 1 x 105 tachyzoites was sufficient to produce this effect, with no further increase in efficacy after using 2 x 106 tachyzoites per sheep. (J484.41.w2)
Prophylactic Treatment
Antiprotozoal drugs:
  • In sheep, feed containing Decoquinate given during pregnancy to provide 2 mg/kg bodyweight per day from about mid-pregnancy onwards can significantly reduce perinatal mortality in lambs due to toxoplasmosis. (B217.13.w13)
    • Decoquinate does not prevent infection of the ewe, therefore the sheep will become persistently infected and immune to future challenge, as usual. (B217.13.w13)
    • Experimentally, decoquinate at 2 mg/kg daily  in feed from 10 days before oral challenge with Toxoplasma gondii resulted in a delayed and reduced-severity febrile response, delayed antibody production, reduced placental damage, lengthened mean gestation period and increased number and weight of live lambs, compared to sheep similarly infected but not given any prophylatic treatment. (J3.138.w7)
    • Monensin (15 mg per sheep per day) has been used previously and proved effective, but the toxic:therapeutic ratio is low, therefore this drug is no longer approved for use in sheep. (B217.13.w13)
  • In immunocompromised humans, continuous prophylactic treatment may be required: either pyrimethamine at 25 mg per day or sulfadiazine at 4.0-6.0 g/day. (J4.196.w3)
    • Folic acid, 3-10 mg/day orally, or fresh yeast, 5-10 g/day orally, prevents the side effects of folinic acid deficiency. (J4.196.w3)
Passive immunisation:

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Personal protective measures:

For humans:

  • Wear gloves for gardening or other contact with soil. (B583.w2, B599)
  • Wear gloves when handling raw meat, including when field dressing a carcass during hunting, or cleans hands thoroughly after handling raw meat. (B583.w2, J4.196.w3)
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Environmental and Population Control Measures

General Environment Changes, Cleaning and Disinfection
  • Prevent infection in humans:
    • Wash with soap and water all cutting boards, knives etc. coming into contact with uncooked meat. (B599.1.w1)
    • Cook meat to 70 C (centre of the meat) before eating or feeding. (B599.1.w1)
      • To at least 65.5 C for 20 minutes. (B583.w2)
      • If the meat has changed colour, then it should have been heated to 60 C and tissue cysts should have been destroyed. (J4.196.w3)
    • Avoid tasting meat during cooking. (B599.1.w1)
    • Wash vegetables thoroughly before they are eaten, due to the risk of contamination with oocysts. (B599.1.w1)
    • Pregnant women should avoid contact with soil and raw meat, and preferably should not be the person to empty the cat litter tray (which should be emptied daily).
    • Wash litter trays with scalding water. (B583.w2)
    • Keep children's sandboxes covered when not in use. (B583.w2)
    • Note:
      • Generally, oocyst shedding occurs only after initial infection. Cats which are seropositive an are not presently shedding oocysts are unlikely to do so in the future. (B583.w2)
      • Oocysts are not infective immediately after being passed in the cat's faeces, and cats, being fastidious, generally do not allow faeces to remain on the fur/skin, therefore sporulated oocysts are unlikely to be found on the surface of a cat. (B583.w2)
    • Reduce viability of tissue cysts by freezing meat to -20 C for several days. (B583.w2)
  • Preventing infection of cats:
    • Feed cats only dry, canned or cooked food, not raw meat or raw liver. (B599.1.w1)
    • Cover rubbish bins to prevent cats from scavenging. (B599.1.w1)
    • Keep cats away from pregnant sheep and goats. (B599.1.w1)
    • Prevent cats from hunting. (B583.w2)
  • Promptly remove carcasses of pigs to prevent both cannibalism and consumption by cats. (B599.1.w1)
  • Bury or incinerate fetal membranes and dead fetuses following ovine abortion. (B599.1.w1)
  • Cover grain storage containers to prevent contamination with cat faeces. (B599.1.w1)
  • In zoos:
    • Feed cats cooked meat if possible, otherwise frozen meat, preferably beef as this is least likely to contain infective tissue cysts. (B599.1.w1)
    • Remove cat faeces daily, before sporulation of oocysts occurs. (B599.1.w1)
    • Heating of brooms, shovels etc. used in cleaning felid cages to 70 C for at least 10 minutes will eliminate infectivity. (B599.1.w1)
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Population Control Measures
  • On farms, maintaining a population of healthy adult cats, just sufficient for rodent pest control, and controlling breeding (and therefore production of kittens, which will become infected and shed oocysts at this time) is suggested. (B217.13.w13)
CLICK THE LINKS FOR Technique Descriptions, if available
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Isolation and Quarantine
  • Avoid housing cats near susceptible species such as New World monkeys and Australasian marsupials. (B599.1.w1)
CLICK THE LINKS FOR Technique Descriptions, if available
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CLICK THE LINKS FOR OVERVIEWS of management techniques available
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Authors & Referees

Authors Debra Bourne MA VetMB PhD MRCVS (V.w5)
Referee Prof. Elizabeth Innes (V.w171)

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