Toxoplasmosis is caused by the intracellular protozoan parasite Toxoplasma gondii. The parasite has a worldwide distribution and can infect all warm-blooded animals. It has a two-host life cycle (Figure 1), and domestic cats and other felids are the definitive hosts. All non-feline animals, including dogs and humans, are intermediate hosts. Invertebrates can serve as transport hosts through the mechanical carriage of T. gondii oocysts.
There are three stages in the protozoan’s life cycle. First, tachyzoites multiply actively in tissues, quickly spreading to almost all host organs and causing most of the toxoplasmosis pathology. Once they reach specific tissues in the central nervous system, muscle and viscera, they convert into bradyzoites. These remain latent in a cyst form, leading to a lifelong infection until a definitive host ingests the tissue. Then the bradyzoites are released, penetrating the small intestinal epithelial cells and giving rise to the schizonts that form gamonts and, finally, oocysts. Unsporulated oocysts are then excreted in faeces.
Sporozoites develop within the oocysts after one to five days of exposure to oxygen and the appropriate environmental temperature and humidity. This process is known as sporulation. Sporulated oocysts are the environmentally resistant and infectious stage. Hosts can become infected horizontally by ingesting tissues containing cysts, by consuming water or food contaminated with sporulated oocysts or by transfusion or transplantation with parasitised organs. Vertical transmission is the cause of a congenital toxoplasmosis infection (Calero-Bernal and Gennari, 2019; Lappin and Dubey, 2023).
Clinical signs of toxoplasmosis
Cats
Most cats infected with T. gondii never develop detectable clinical signs; in general, the feline enteroepithelial cycle rarely leads to clinical signs (Lappin and Dubey, 2023). Only 10 to 20 percent of experimentally inoculated cats develop self-limiting small bowel diarrhoea for one to two weeks following primary oral inoculation with T. gondii tissue cysts (Lappin and Dubey, 2023).
Most cats infected with T. gondii never develop detectable clinical signs; in general, the feline enteroepithelial cycle rarely leads to clinical signs
Fatal extraintestinal toxoplasmosis can develop in cats due to an overwhelming intracellular replication of tachyzoites following primary infection. Hepatic, pulmonary, central nervous system (CNS) and pancreatic tissues are commonly involved. Kittens infected by the transplacental or trans-mammary route develop the most severe signs of extraintestinal toxoplasmosis and generally die of pulmonary or hepatic disease.
Common clinical signs in cats with disseminated toxoplasmosis include lethargy, anorexia and respiratory distress. Disseminated toxoplasmosis has been described in cats diagnosed with feline immunodeficiency virus, feline leukaemia virus or feline infectious peritonitis or those treated with immunosuppressive medication, such as cyclosporine.
Chronic toxoplasmosis should be on the differential diagnosis list for cats with uveitis, chorioretinitis, cutaneous lesions, fever, myalgia, myocarditis with arrhythmias, weight loss, anorexia, seizures, ataxia, icterus, diarrhoea, respiratory distress, pyogranulomatous cystitis or pancreatitis (Calero-Bernal and Gennari, 2019; Lappin and Dubey, 2023).
Dogs
Toxoplasmosis is a rare primary disease in dogs; adult dogs with a normal immune system will unlikely be affected by toxoplasmosis. Puppies and adult dogs with a weakened immune system because of treatment with immunosuppressive medication or infection with canine distemper virus can be affected by toxoplasmosis. In dogs, the respiratory, gastrointestinal or neuromuscular system is most often affected by generalised toxoplasmosis (Calero-Bernal and Gennari, 2019; Lappin and Dubey, 2023).
Diagnosing toxoplasmosis
Detection of T. gondii antibodies in serum is used most frequently for the diagnosis of clinical toxoplasmosis in cats and dogs, but diagnosis should not be based on serology alone.
The measurement of two types of T. gondii antibodies in the blood, immunoglobulin G (IgG) and immunoglobulin M (IgM), can help diagnose toxoplasmosis. High levels of IgG antibodies in a healthy cat suggest that it has been previously infected, is most likely immune to the organism and is not excreting oocysts. These cats are no longer sources of infection for other hosts. In contrast, high IgM antibody levels suggest an active infection. The absence of T. gondii antibodies in a healthy cat suggests that the cat is susceptible to infection and would shed oocysts for up to two weeks following infection.
Detection of T. gondii antibodies in serum is used most frequently for the diagnosis of clinical toxoplasmosis in cats and dogs, but diagnosis should not be based on serology alone
Detection of oocysts in faeces is not a reliable method of diagnosis because they look like those of some other parasites. Additionally, cats shed oocysts for only a short period and are often not shedding oocysts when they show signs of the disease. Instead, a definitive diagnosis requires microscopic examination of tissue samples for the presence of tachyzoites and distinctive changes to the tissues.
A tentative ante-mortem diagnosis of clinical toxoplasmosis in dogs or cats can be based on the following combination of serology and clinical parameters (Lappin and Dubey, 2023):
- Demonstration of antibodies in serum that confirms exposure to T. gondii
- Demonstration of either an IgM titre higher than 1:64 or a fourfold or greater rise in IgG titre, which suggests recent or active infection
- Clinical signs of disease consistent with toxoplasmosis
- Exclusion of other common causes of the clinical signs
- Positive response to treatment
Treating toxoplasmosis
Clindamycin or sulphonamides, in combination with trimethoprim or pyrimethamine, are recommended for treating suspected or confirmed cases of toxoplasmosis. Most clinical signs caused by the disease should start to improve after one week of treatment, but treatment should be continued for four weeks where possible.
A suggested dosage recommendation for clindamycin is 10 to 12mg/kg PO every 8 to 12 hours. Trimethoprim-sulpha can be administered at 15mg/kg PO every 12 hours. You may also implement an oral combination of sulphonamide (30mg/kg every 12 hours for two weeks) and pyrimethamine (0.25 to 0.5mg/kg every 12 hours). Pyrimethamine is thought to be more effective than trimethoprim against a T. gondii infection.
However, cats may develop myelosuppression while receiving prolonged (more than two weeks) trimethoprim, sulfonamide and pyrimethamine therapy; thus, they may require folinic or folic acid replacement therapy (Schatzberg and Nghiem, 2012).
A T. gondii infection cannot be eliminated from tissues and can, therefore, result in disease relapse during periods of immunosuppression
A T. gondii infection cannot be eliminated from tissues and can, therefore, result in disease relapse during periods of immunosuppression. Most cats and dogs will be antibody positive for life, so there is little reason to repeat serum antibody titres after the clinical disease has resolved. There is also little reason to administer drugs to cats and dogs with T. gondii activity that are without clinical signs of toxoplasmosis.
Prognosis
The prognosis for toxoplasmosis is poor for cats or dogs with hepatic, CNS or pulmonary disease, particularly in those that are immunocompromised by anti-inflammatory drugs or viral infection. There is no evidence that any drug can eliminate a T. gondii infection; a relapse is always possible. Infected dogs and cats will remain seropositive. No vaccination is available for the prevention of clinical toxoplasmosis.
Public health aspects
The transmission of toxoplasmosis to people is an important public health issue. It is generally assumed that approximately 25 to 30 percent of the world’s human population is infected with Toxoplasma. Prevalence of T. gondii varies (from 10 to 80 percent) by geographical region due to differences in environmental conditions and cultural and food habits (Robert-Gangneux and Darde, 2012).
Toxoplasmosis is mainly a concern for people with a weakened immune system. In these individuals, the disease usually affects the central nervous system.Toxoplasmosis is also a concern for pregnant women because the parasite can migrate through the placenta and cause congenital toxoplasmosis. Potentially, this could result in stillbirth, blindness or intellectual disability of the infant.
Human infection may occur after eating undercooked meat or through the accidental consumption of sporulated oocysts from cat faeces. Touching cats is not likely to be a common way to acquire toxoplasmosis, but cat faeces should always be handled carefully.
