Fatal disseminated toxoplasmosis in an immunocompetent cat.

A 10-year-old domestic short hair cat was referred for investigation of anorexia and polydipsia of 3 days' duration. Clinically the cat was obese, pyrexic (39.8 °C), had acute abdominal pain and severe bilirubinuria. Haematology and serum biochemistry revealed severe panleukopenia, thrombocytopenia, markedly elevated alanine aminotransferase (ALT) and five-fold increased pre-prandial bile acids. Ultrasonographic evaluation of the abdomen did not identify any abnormalities. Serum tests for feline immunodeficiency virus (FIV) and feline leukaemia virus (FeLV) were negative. Broad-spectrum antibiotic treatment for infectious hepatitis was to no avail; the cat deteriorated and died 72 h after admission. Necropsy revealed mild icterus and anaemia, severe multifocal hepatic necrosis, serofibrinous hydrothorax, pulmonary oedema and interstitial pneumonia. Histopathology confirmed the macroscopic findings and revealed multifocal microgranulomata in the brain and myocardium, as well as areas of necrosis in lymph nodes and multifocally in splenic red pulp. Long bone shaft marrow was hyperplastic with a predominance of leukocyte precursors and megakaryocytes and splenic red pulp showed mild extramedullary haemopoiesis. Immunohistochemical staining for Toxoplasma gondii was strongly positive, with scattered cysts and tachyzoites in the liver, lymph nodes, spleen, lungs, brain, salivary glands and intracellularly in round cells in occasional blood vessels. Immunohistochemical staining for corona virus on the same tissues was negative, ruling out feline infectious peritonitis (FIP). Polymerase chain reaction (PCR) on formalin-fixed paraffin-wax embedded tissues was positive for Toxoplasma sp., but attempts at sequencing were unsuccessful. This was the first case report of fulminant disseminated toxoplasmosis in South Africa, in which detailed histopathology in an apparently immunocompetent cat was described.

Capillary and venous Babesia canis rossi parasitaemias and their association with outcome of infection and circulatory compromise.

This observational study of 100 dogs naturally infected with Babesia canis rossi determined whether severity of parasitaemia was associated with outcome of infection and documented the relative distribution of parasitised red blood cells (pRBC) in capillary and venous circulation. The association between increased parasitaemias and outcome with a clinically compromised circulation was also investigated. Outcome was defined as either hospitalisation with death, or hospitalisation with eventual recovery or treatment as an outpatient. Dogs were enrolled if large babesias were found on stained thin capillary blood smears made from an ear prick. Thin venous smears were prepared from jugular or cephalic blood. Parasitaemias were manually counted and expressed as the percent pRBC. Ten dogs died, 50 recovered after hospitalisation and 40 were treated as outpatients. Venous sampling site did not affect venous parasitaemia (P=0.6). Both capillary and venous parasitaemias of dogs that died were significantly higher than those of dogs that recovered after hospitalisation (P=0.002) and dogs that were treated as outpatients (P<0.0001). When assessing the whole group, capillary parasitaemia (median 0.61%, range <0.05-71.6%, interquartile range (IQR) 0.22-3.75%) was significantly higher than venous parasitaemia (median 0.14%, range 0-30.6%, IQR 0.046-0.52%) with P<0.0001. The 21 dogs with a clinically compromised circulation were more likely to die (P<0.0001) and had significantly higher capillary (median 5.98%, range 0.09-71.6%, IQR 2.44-19.41%) and venous (median 2.81%, range <0.05-30.6%, IQR 0.17-9.03%) parasitaemias than the 79 dogs with a clinically normal circulation (capillary median parasitaemia 0.38%, range <0.05-12.87%, IQR 0.16-1.42%; venous median parasitaemia 0.096%, range 0-6.13%, IQR <0.05-0.33%; P<0.0001). This study shows that high parasitaemia is significantly associated with death in B c rossi infected dogs. The previous clinical suspicion that capillary parasitaemias are usually higher than venous parasitaemias is confirmed. Thus capillary samples are the most appropriate diagnostic samples. Prior observations that a clinically compromised circulation is associated with death are confirmed. Despite the highly significant association between compromised circulation and higher parasitaemia, it is thought unlikely that parasite burden is the sole trigger for circulatory collapse.