Feline Toxoplasmosis
World Small Animal Veterinary Association World Congress Proceedings, 2013
Vanessa Barrs, BVSc(hons), MVetClinStud, FANZCVSc (Feline Medicine)
Small Animal Medicine, Faculty of Veterinary Science, The University of Sydney, NSW, Australia

Aetiology and Seroprevalence

Toxoplasmosis is caused by the intracellular coccidian Toxoplasma gondii. Infection occurs after ingestion of bradyzoite cysts in the tissues of intermediate vertebrate hosts resulting in patent infections in 97% of naïve cats. Ingestion of sporulated oocysts in contaminated food or water results in patent infections in only 20% of cats. As the definitive host, cats are the only species with an enteroepithelial phase of infection, in which oocysts are shed transiently in faeces (for 1–2 weeks in most cats). Oocysts are not infective until sporulation 1 to 5 days after excretion in faeces. All species infected by T. gondii undergo an extraintestinal phase of infection, in which tachyzoites replicate widely in body tissues. However, infection is not eliminated and organisms persist for life as tissue-encysted bradyzoites (latent infection). Exposure to T. gondii is most common in the first year of a cat's life. Seroprevalence is not significantly different between cats from urban and rural environments. In the USA, seroprevalence of T. gondii IgG or IgM antibodies in 12, 628 clinically ill cats was 31.6%.1

clinical features

The enteroepithelial phase of infection is asymptomatic or there is transient small-bowel diarrhoea. The extraintestinal phase of infection is usually clinically silent since most cats mount an immune response that contains infection. Clinical disease occurs in a small proportion of cats during primary infection and in reactivated latent infections where immunosuppression induces cyst rupture, tachyzoite replication and tissue damage. Risk factors for clinical disease include FIV, FeLV or FIP, neoplasia and chronic administration of certain immunosuppressive drugs, especially cyclosporin.3 Disease can be acute or chronic and focal or systemic. Systemic signs reflect organ involvement. Hepatic, pulmonary, CNS and pancreatic involvement is common. Clinical signs in acute systemic infection can include lethargy, anorexia, pyrexia or hypothermia, dyspnoea (pulmonary, pleural space or cardiac involvement), jaundice, abdominal distension (peritoneal effusion) and diffuse or multifocal CNS signs. Acute infections are often fatal, especially in kittens born to queens infected during pregnancy. Focal infections include uveitis, chorioretinitis and focal CNS infection.4

Diagnosis

Clinical examination should include fundoscopy to look for evidence of chorioretinitis. Haematological findings are nonspecific but can include nonregenerative anaemia, neutrophilic leukocytosis, lymphocytosis, monocytosis and eosinophilia. In severe acute infections there may be neutropenia with a degenerative left shift, lymphocytopenia and monocytopenia. Abnormalities in serum biochemistry and urinalysis depend on severity of organ involvement (e.g., pancreatitis, hepatitis/cholangitis, myositis) and can include proteinuria, bilirubinuria, azotaemia, hyperbilirubinaemia, and elevations in serum protein, liver enzymes and creatine kinase. In acute illness, total plasma protein may be decreased. Thoracic radiographic findings can include a diffuse bronchointerstitial pattern, patchy alveolar infiltrates and/or pleural effusion. Advanced imaging (ultrasound, CT, MRI) can assist in detection of effusion and specific organ involvement.

Serology to detect IgG and IgM anti-T. gondii antibodies must be interpreted together with clinical findings (Tables 1 & 2).2 Using ELISA tests, positive IgM titres develop in 80% of cats 1 to 4 weeks postinfection and are usually negative by 16 weeks after infection. Positive IgG titres develop 3 to 4 weeks postinfection and peak 2 to 4 weeks after initial detection. In recrudescent infections, there may be no rising IgG titre and IgM titres may remain negative. IgG can be detected in CSF and aqueous humor of both normal and clinically ills cats, but IgM has only been detected in clinically ill cats.

Table 1 Interpreting T. gondii ELISA serology IgG results

Test result

Interpretation

A ≥ 4-fold increase in titre in paired serum samples taken 2–4 weeks apart

- Recent or active infection (true positive)

A < 4-fold increase in titre in paired serum samples taken 2–4 weeks apart

- No recent or active infection (true negative)
- Maximal IgG titre occurred before sampling period or rising titre did not occur, e.g., recrudescent infection (false negative).

A single high positive result (e.g., 1: 1000)

- Reflects only the presence of T. gondii within tissues. High titres can persist for many years due to latent infection (bradyzoite tissue cysts)

Table 2 Interpreting T. gondii ELISA serology IgM results

Test result

Interpretation

Titre > 1:64

- Recent or active infection (true positive)
- Persistent high titre beyond the period of active or recent infection (false positive), e.g., some healthy cats, FIV-infected cats, glucocorticoid treatment.

Titre < 1:64

- No recent or active infection (true negative)
- Did not mount an IgM response (false negative), e.g., 20% healthy cats, recrudescent infection

Definitive diagnosis requires cytological or histological detection of T. gondii tachyzoites in effusions, BAL fluid, CSF, aqueous humour or tissues. Sensitivity is low and increased by use of immunofluorescent/immunohistological methods, and specificity is high. In a study of 100 cases of toxoplasmosis confirmed histologically at autopsy, definitive antemortem diagnosis was made in 4% of cases only.5 Since T. gondii DNA can be amplified from blood, aqueous humour and CSF of healthy cats with latent infections, PCR assays are more useful to confirm the identity of tachyzoites/tissue cysts detected in clinical specimens. Oocyst shedding in cats can be detected by centrifugal faecal flotation using Sheather's sugar solution or zinc sulfate. Alternatively, T. gondii DNA can be detected in faeces by PCR.

Treatment

Clindamycin 12.5 mg/kg PO or IV q 12 h, or trimethoprim sulphonamide 15 mg/kg PO q 12 h, or azithromycin 10 mg/kg PO q 24 h for a minimum of 4 weeks. Pyrimethamine 0.25–0.5 mg/kg PO q 12 h is synergistic when combined with sulphonamides. A 5 mL water swallow should be administered after giving clindamycin since oesophagitis and esophageal strictures can occur. Common supportive treatments include IV fluid therapy, intranasal oxygen (dyspnoea) and enteral feeding (naso-esophageal or oesophagostomy tube feeding). Cats with acute toxoplasmosis should be monitored for body-cavity effusions, pneumonia, hepatic failure, pancreatitis, encephalomyelitis and myocarditis. Additional supportive therapy may be required, e.g., anticonvulsants in seizuring patients, diuretics, ACE inhibitors for congestive heart failure, analgesia for pancreatitis. A CBC should be performed every 2 weeks for detection of myelosuppression in cats treated with sulfonamides or pyrimethamine.

Client Education

The USA Centers for Disease Control does not recommend testing healthy cats for T. gondii antibodies. Seronegative pet cats present a greater infection risk to owners than IgG seropositive cats, because in the latter the period of oocyst shedding has already passed and the risk of re-shedding is low. IgM seropositive cats could be shedding oocysts. Measures to reduce the risk of seronegative pet cats acquiring infection include indoor housing, feeding canned/dry food only and prevention of exposure to intermediate-hosts (e.g., rodents, birds) and vectors (e.g., cockroaches). Raw meat diets should be avoided. Although seropositive cats are generally immune to recurrent primary infection, gut immunity to T. gondii can wane in some cats, six-years post infection. Therefore, similar recommendations to minimise the risk of recurrent infection could be made for seropositive cats.

Clients are at risk of infection from contact with pet cats only during the transient period of oocyst shedding. Other sources of infection include ingestion of tissue cysts in undercooked meat or from contaminated food preparation areas; ingestion of oocysts from unwashed vegetables, sandpits, gardening and litter trays. Measures to minimise human infection risk include freezing meat to kill tissue cysts, avoiding undercooked or microwaved meat and unpasteurised dairy products, washing vegetables and wearing gardening gloves. Litter trays should be cleaned daily with boiling water while wearing gloves.

References

1.  Vollaire MR, et al. J Vet Intern Med. 2003; 17: 425.

2.  Barrs VR. Toxoplasmosis titres. In: Five Minute Veterinary Consult: Diagnostic Procedures and Laboratory Tests. S Vaden, J Knoll, LP Tilley & FW Smith (eds.), Blackwell Publishing 2009:501–503.

3.  Barrs VR, et al. Aust Vet J. 2006;84:30.

4.  Lindsay SA, et al. J Feline Med Surg. 2010;12:818.

5.  Dubey JP, et al. J Am Vet Med Assoc. 1993;203:1556.

  

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Vanessa Barrs, BVSc(hons), MVetClinStud, FANZCVSc (Feline Medicine)
Faculty of Veterinary Science
The University of Sydney
Sydney, NSW, Australia


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