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Toxoplasmosis in the dog and cat

Last updated December 14, 2011

Toxoplasmosis is a protozoan disease with very varied clinical manifestations depending on the degree and spread (tissue or generalised) of the infection. The infection can potentially affect all warm-blooded animals, including humans.



Toxoplasma gondii is an obligate intracellular parasite (coccidium). It has a complex cycle in which the cat and a few other wild felidae (lynx, puma, ocelot, jaguar) serve as definitive hosts, i.e. they disseminate oocysts. Humans, mammals and birds are intermediate hosts. In cats, after the ingestion of oocysts, the intestinal phase occurs, during which Toxoplasma gondii invades the epithelial cells of the small intestine of the animal and multiplies. The parasite may also be disseminated in various extra-intestinal organs at the same time. The asexual phase (called schizogony), which involves the formation of mature schizonts, each containing from 4 to 30 merozoites, and the sexual phase, which leads to the formation of microgametocytes and macrogametocytes, take place in the intestine of cats. The resulting microgametes and macrogametes unite to form oocysts, which are then shed with the faeces into the environment. Shedding lasts for around 3 weeks, while the period that elapses between the ingestion of infectious material and the shedding of the oocysts with the faeces varies from 3 to 24 days. Oocysts have to sporulate in order to be infectious. Sporulation occurs in the external environment and, once mature, the oocysts contain two sporocysts. Only sporulated oocysts are infectious and remain so for at least 4 months in water or soil, and up to 1 year in the shade at 19°C. Trophozoites mark the acute phase of the disease both in cats and in the intermediate hosts. They appear as small, ovoid or semi-lunar bodies inside the cells of the reticuloendothelial system, leukocytes, monocytes and numerous other tissue cells where they multiply until forming a pseudocyst. When the invaded cell bursts, the protozoa are expelled and, once they have penetrated into other cells, they continue their proliferation cycle. The host’s immune defences allows the acute phase of the infection to be overcome and the transition to a subacute-chronic form, in which the parasite disappears from the blood and usually becomes localised in the muscles and central nervous system, where it multiplies until forming the terminal cyst. Cysts may persist in the tissues in a latent form for months or years.



There are various routes of transmission: ingestion of faeces or of infected meat and transplacental transmission.

Other routes of transmission: blood transfusion or transplantation of an infected organ (oocysts).



Cat: the signs and symptoms may be very severe in kittens infected transplacentally; in fact, kittens may be stillborn or die before weaning. The clinical signs are the expression of inflammatory processes in the liver, lung and central nervous system: abdominal enlargement, ascites, lethargy, depression, hypothermia, up to the occurrence of sudden death. Some kittens can develop chorioretinitis as the only sign, accompanied in some cases by a transient anterior uveitis. In adult cats the clinical signs can be the result of the spreading of tachyzoites, following acute exposure or the reactivation of a chronic infection (release of bradyzoites from oocysts) in conditions of severe immunosuppression. The most frequent clinical manifestations of post-natal toxoplasmosis are anorexia, lethargy, dyspnoea and ocular signs (uveitis, chorioretinitis). Other possible signs are continuous or intermittent fever, weight loss, jaundice, vomiting, diarrhoea, abdominal effusion, hyperaesthesia, stiff gait, intermittent lameness, neurological deficits, dermatitis and death. Experimental studies have shown that subjects co-infected with feline immunodeficiency virus (FIV) [evelop severe forms of pneumonia and hepatitis whereas ocular signs are more common in FIV-negative subjects. In addition, the neurological and ocular signs and symptoms appear to be attributable to the exacerbation of chronic forms more than to acute infections.

Dog:the clinical signs may be the result of infections localised in the respiratory, neuromuscular and gastrointestinal systems or of generalised infections. The neurological form can persist for many weeks without involving other systems, while severe liver or lung involvement can lead to the death of the subject in just a few days. Generalised forms of toxoplasmosis usually occur in dogs under 1 year of age and are characterized by fever, tonsillitis, jaundice, dyspnoea, diarrhoea and vomiting. In some dogs the predominant clinical signs are found in the myocardium (arrhythmias, heart failure). Very severe neurological and muscular forms can develop in adult dogs and are manifested as convulsions, cranial nerve deficits, tremors, ataxia, paresis and paralysis, gait abnormalities, muscular atrophy or stiffness. Ocular signs are very rare in dogs.



The tests to detect the main clinicopathological changes in dogs and cats with acute systemic toxoplasmosis include:

  • Complete blood count: non-regenerativeanaemia, neutrophilia, lymphocytosis, monocytosis, eosinophilia. Seriously ill cats may, however, have profound leukopenia [9],characterized by absolute lymphoctyopenia, neutropenia and reduced eosiniphil and monocyte counts.
  • Biochemical blood tests: hypoproteinaemia, hypoalbuminaemia and increases in alanine transaminase, aspartate  transaminase, alkaline phosphatase, creatine phosphokinase and bilirubin. In subjects who develop pancreatitis amylase and lipase levels may also be increased.
  • Urinalysis: in cats proteinuria and bilirubinuria may be present.



The diagnosis is based on an evaluation of the signs and additional information from several diagnostic tests.

Diagnostic tests

  • Serological tests can be used to detect the presence of anti-Toxoplasma gondii antibodies. The seroprevalence in cats is very high (30%). The use of serology is considerably limited because anti-toxoplasma antibodies can be present in both healthy and sick animals, and persist for months or years after infection. Generally, an increase in IgM occurs more commonly in clinically ill subjects or in FIV-positive cats than in healthy animals. IgM can be a more reliable disease marker than IgG or IgA, making it possible to distinguish active and recent infections.
  • Polymerase chain reaction analysis makes it possible to identify the presence of Toxoplasma gondii in various tissues, but it does not distinguish acute infections from chronic ones.
  • Tachyzoites can be detected during the acute phase of the infection through cytological examination of material obtained by fine needle aspiration from numerous tissues and body fluids, in particular peritoneal and thoracic effusions.
  • In spite of the high seroprevalence in cats, Toxoplasma gondii oocysts are difficult to isolate from the faeces of infected cats. In fact, cats shed oocysts for only 1 or 2 weeks after the initial exposure. Furthermore, during the phase in which they shed oocysts in the faeces, cats do not manifest clinical signs, let alone diarrhoea .





The drugs used in the treatment of toxoplasmosis suppress replication of the parasite but are not able to kill it. Clindamycin is the drug of choice in dogs and cats (3-13 mg/kg, per os, i.m., every 8 hours for 4 weeks). The clinical signs generally improve around 24-48 hours after beginning treatment. The use of clindamycin is limited by this drug’s gastrointestinal side effects and because it induces diarrhoea.

The combination of pyrimethamine and sulphonamide (respectively: 0.25-0.5 mg/kg, per os, b.i.d. for 4 weeks and 30 mg/kg, per os, b.i.d. for 4 weeks) may be used to treat systemic toxoplasmosis; also in this case the side effects can be severe, in particular due to the myelosuppressive action of these drugs.

In cases complicated by eye lesions, glucocorticoids can be used topically or systemically.

Anticonvulsants may be useful in subjects with severe neurological signs.



Prophylaxis consists of reducing the incidence of the infection in cats and, consequently, shedding of oocysts in the faeces. It is preferable to feed cats with commercial foods, or with meat that has been previously frozen or cooked in a gamma wave oven, in order to kill the cysts in the meat.

There is currently no vaccine capable of preventing the disease or shedding of oocysts in the faeces.



Humans can become infected by ingesting raw or undercooked meat containing cysts or oocysts shed in the faeces by recently infected cats. Infected cats shed oocysts for a very short time (less than 3 weeks) and are a risk for humans only during this period. It is very difficult to identify a cat in the oocyst shedding phase. To prevent environmental contamination, cat owners should always follow good basic rules of hygiene. During the oocyst shedding phase, cats do not have diarrhoea and they clean themselves regularly, so direct contamination is very difficult. Furthermore, the oocysts do not remain on the hair of cats that clean themselves during the brief oocyst shedding phase. It is also important to check mechanical carriers (earthworms, flies, snakes, cockroaches) that can contain or transport oocysts.

The best way to sterilise clothes is to immerse them in boiling water. Surfaces, even difficult to reach ones, can be easily decontaminated by steam cleaning.

Humans can become infected by inhaling or ingesting dust contaminated by oocysts. Oocysts can also contaminate gardening tools or clothing and be dispersed in the environment through wind, rain, animal paws, etc.

Toxoplasma gondiiinfection is especially dangerous during pregnancy. Transplacental infection occurs through the passage of tachyzoites to the foetus when a pregnant woman becomes infected for the first time. The foetus can become infected even when the mother has a chronic infection but is severely immunocompromised or positive for human immunodeficiency virus (HIV). Foetal infection is much more serious during the first half of pregnancy. The main sign of an intrauterine infection is retinochoroiditis. Antenatal diagnosis and prompt treatment of the mother considerably reduce the morbidity of the parasite in the unborn child.

Post-natal infection in humans is usually asymptomatic and self-limiting and lasts, on average, from 1 to 12 weeks. It is usually manifested only by lymphadenomegaly; it can become serious and even fatal only in severely immunocompromised subjects, in whom the infection becomes generalised. The most serious complication in HIV-positive subjects is toxoplasma encephalitis.


Suggested readings

  1. Green C.E. Toxoplasmosisi. In:  Toxoplasmosis and neosporosis. Infectious diseases  on the dog and cat. (2006), Third edition, Elsevier Saunders. 80, 754-768 
  2. Dubay J.P., Lappin M.R. Lindsay D.S. in: toxoplasmosis and other intestinal infections in cats and dogs. Veterinary Clinics of North America . Small animal Practice. Small Animal Parasites: biology and control. 2009, Elsevier Saunders. 32 (6), 1009-1027.

Vetpedia is translated by a team of expert scientific translators coordinated by Alberto Scalcerle (InterMed - Italian Association Medical Interpreters - coordinator) and Rachel Stenner (MA (Cantab) MB BS (Lon) - lead translator). 
For further information please contact: alberto.scalcerle@alice.it  www.scalcerle.net

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