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Cryptococcus neoformans is a yeast-like organism associated with pulmonary, meningoencephalitic, or systemic disease. This case report documents 2 cases of cryptococcosis with central nervous system involvement in captive cheetah (Acinonyx jubatus). In both cases the predominant post mortal lesions were pulmonary cryptococcomas and extensive meningoencephalomyelitis. Both cheetahs tested negative for feline immunodeficiency virus and feline leukaemia virus. The organism isolated in Case 2 was classified as Cryptococcus neoformans var. gattii, which is mainly associated with disease in immunocompetent hosts.

The thoracic radiographic changes of Pneumocystis carinii in 7 miniature Dachshunds were reviewed. The dogs were 7-12 months old and presented with polypnea, exercise intolerance and clinical signs suggestive of immune-incompetence. P. carinii pneumonia was diagnosed in all the dogs using transtracheal aspirate cytology and confirmed at postmortem in 3 dogs that died. Radiographically, diffuse pulmonary changes were present and varied from a mild interstitial and bronchial pattern to an alveolar pattern. Radiographic evidence of cor pulmonale was present in 1 dog. The most severe radiographic changes were seen in 2 of the dogs that died.

South African canine babesiosis is caused by the virulent Babesia canis rossi. In recent years, this common disease has been detected in 12% of dogs presented at the outpatients' division of the University of Pretoria's (Onderstepoort) Veterinary Academic Hospital, and 31% of the affected dogs have been hospitalized as seriously ill. Of these hospitalized cases, 50% had severe anaemia at presentation, 32% had moderate anaemia and 18% were non-anaemic (often polycythaemic), frequently with central-nervous-system signs or multiple organ failure. A retrospective survey of 662 hospitalized cases revealed that the haematology, clinical biochemistry and patient profile (signalment) of the severely anaemic dogs were distinct from those of the non-anaemic, indicating that the babesiosis in these two groups of dogs should be viewed as two different disease in terms of the postulated, underlying, 'pathomechanisms'. The severely anaemic dogs exhibited hypoxic hepatic disease and an increase in serum urea (without a concomitant increase in creatinine), seldom had profound electrolyte imbalances and tended to have a much more profound leucocytosis, consisting of a left-shifted inflammatory leucogram, with higher numbers of circulating metamyelocytes, lymphocytosis and monocytosis. In contrast, the non-anaemic dogs exhibited severe azotaemia (which could be of renal or pre-renal origin) and often showed a marked electrolyte disturbance (reflecting acid-base abnormalities) and a very mild leucocyte response; such dogs often presented as leucopenic, many being lymphocytopenic. These results indicate that the severely anaemic dogs had developed haemolytic disease (possibly immune-mediated), whereas the non-anaemic dogs had developed an acute and overwhelming inflammatory response. The mean age of the non-anaemic dogs (2.66 years) was less than the dogs in the 'severe anaemia group' (0.83 years). Dogs belonging to the traditional fighting breeds (bull terriers, pit bull terriers and Staffordshire bull terriers) were noticeably over-represented in the non-survivors of the acute inflammatory response, possibly indicating an underlying genetic basis for the different presentations. It is evident that the inflammatory-response disease presentation, which is similar to complicated falciparum malaria in humans, amy serve as an animal model for the disease.

A 14-month-old, male German shepherd dog was evaluated for chronic, recurrent Escherichia coli urinary tract infection. An initial diagnosis of emphysematous cystitis was made, which resolved with appropriate antibacterial therapy. The urinary tract infection, however, did not resolve and on further investigation a bladder trigone diverticulum was evident, thought to be congenital in origin. This report describes the apparent ultrasonographic and radiological changes, and surgical repair of the diverticulum, and reviews the literature with regard to both congenital bladder trigone diverticulum and emphysematous cystitis. The former has never been documented in the dog and the latter is an unusual finding in a non-diabetic dog.

A 9-year-old male German shepherd dog was evaluated for clinical and clinico-pathological changes that were suggestive of Addison's disease. On further investigation the basal plasma cortisol concentration was high, a normal cortisol response to ACTH stimulation occurred, plasma renin activity was elevated and low serum aldosterone concentration was present. A diagnosis of hyperreninaemic hypoaldosteronism was made. Replacement fludrocortisone resulted in complete normalisation of the electrolyte and fluid imbalances. Hyperreninaemic hypoaldosteronism has never been reported in the dog.

A 3-year-old male German shepherd dog was presented with severe generalised seizures. The dog was protein-intolerant and showed severe hyperammonaemia on ammonia stimulation. The hyperammonaemic state was present for at least 6 weeks and then spontaneously resolved. No obvious cause (liver disease, portocaval shunts, urea cycle enzyme deficiencies, drug therapy or urinary tract obstruction) could be identified. It is possible that this dog had a variation of transient hyperammonaemic syndrome, described in man and recently in a juvenile Irish wolfhound, that extended into adulthood.

A 2-year-old cat was presented with generalised muscle tremors and progressive fore- and hindlimb ataxia, 5 months after the initiation of chemotherapy for thymic lymphoma. The lymphoma was treated with combination chemotherapy (cyclophosphamide, vincristine and prednisolone), which resulted in remission. The neurological signs progressed to paralysis and the cat subsequently died. On autopsy, multiple meningiomas were diagnosed, which is an unusual finding. It is possible that the lymphoma chemotherapy resulted in the development of the multiple meningiomas as secondary malignancies.

Renal pathology associated with haemoglobinaemia resulting from Babesia canis infection is ascribed to haemoglobinuria, with or without a contribution from anaemic hypoxia. This study was undertaken to investigate the relative roles of haemoglobinaemia and hypoxia in renal function and pathology in the dog. Three groups of 6 dogs each were used over a 4-day period. The dogs in the 1st group were infused with homologous canine haemoglobin, anaemic hypoxia was induced in the 2nd group, and both treatments were applied in the 3rd group. Full urinalyses, serum urea and creatinine concentrations, fractional clearance of sodium and the activity of urine enzymes, were assessed daily. At the end of the trial period, the glomerular filtration rate (GFR) was determined and kidney specimens collected for light and electron microscopy. In the group with hypoxia only, the urine sediment contained more casts and a greater number of renal tubular epithelial (RTE) cells than in either of the other groups. Hypoxia resulted in greater enzymuria, suggestive of RTE cell pathology, whereas haemoglobinuria did not appear to have any effect on urine enzyme activity. Hypoxia resulted in a decreased GFR. Histological examination revealed a mild, single-cell tubular necrosis in the majority of the animals (all 3 groups), with granular casts in the hypoxic groups. There appeared to be a large individual variation in the ability of the kidney to handle infused haemoglobin. It was concluded that severe haemoglobinaemia did not induce a significant nephropathy, anaemic hypoxia appeared to cause a very mild nephropathy, and the combination of haemoglobinaemia and anaemic hypoxia did not exacerbate this change. These lesions were very different from those described in canine babesiosis.

A six-month-old Rhodesian ridgeback dog was presented for evaluation of facial swelling. Chronic renal failure was clinically diagnosed based on urinalysis, biochemical changes and ultrasonography. The facial swelling was due to fibrous osteodystrophy, which was evident on survey radiographs of the skull. On post mortem examination, chronic renal failure as a result of renal dysplasia was confirmed. This is the first reported case of renal dysplasia in this breed of dog.

This article reviews Pneumocystis carinii and presents four cases in the miniature dachshund. The cases presented with hyperpnoea, tachypnoea and exercise intolerance. There were also clinical signs suggestive of immune incompetence in all the dogs. P carinii pneumonia was diagnosed in all four cases on transtracheal aspirate cytology. Immunological studies showed low globulin levels on serum electrophoresis, decreased lymphoblast transformation response (in the two cases that were tested) and a deficiency of immunoglobulins A, G and M. Light and electron microscopy as well as anti-canine immunoglobulin G immunoperoxidase staining studies were performed on one case which had died because of the disease. From these four cases, it appears that P carinii pneumonia in the miniature dachshund may be the result of an immunodeficiency. It does not, however, appear to be a classic primary severe combined immunodeficiency syndrome as the dogs appeared to respond to treatment, did not show growth failure and did not manifest overwhelming commensurate bacterial infections.

Phaeohyphomycosis is a rare fungal disease of animals and man, generally thought to occur in compromised or debilitated hosts, although in man the majority of infections have occurred in otherwise healthy patients. To investigate the possible role of immune suppression in systemic phaeohyphomycosis, certain aspects of the immune system of 2 dogs with systemic Xylohypha bantiana infection were investigated. White cell and differential cell counts, serum protein electrophoresis and serum immunoglobulin fractions were determined. The only consistent finding was lymphopaenia. Although there is no specific evidence for it, a lymphopaenic state might predispose to systemic phaeohyphomycosis.

Rhabdomyolysis was diagnosed in two dogs with babesiosis. The first animal presented with muscle pain and caramel-coloured urine, and had markedly elevated serum myoglobin and muscle enzymes. Acute renal failure complicated the clinical picture. The second dog exhibited muscle pain and tremors, together with neurological signs and pulmonary oedema, and died soon after admission. Muscle necrosis and haemorrhage were found at necropsy. In human malaria, a disease clinically similar to canine babesiosis, rhabdomyolysis is unusual, but clinically silent muscle damage appears to be common. Likewise, biochemical evidence of muscle damage is readily found in experimental bovine babesiosis. Muscle enzymes were mildly elevated in three dogs with severe babesiosis and pigmenturia but there was no obvious muscle damage, indicating that this might also apply to canine babesiosis. The pathogenesis of infection-associated rhabdomyolysis and acute renal failure remains unclear, but inflammatory cytokines and nitric oxide could play an important role.

Higher levels of urinary met-haemoglobin were found in dogs with naturally occurring Babesia canis infection (n = 6) than in control subjects (n = 5). The urinary haemoglobin in the affected cases ranged from 1 to 4 g/l of which 28-95% was met-haemoglobin. This was a significant finding in that met-haemoglobin has been shown to be nephrotoxic in the dog, especially in the presence of aciduria. Acidic urine was also demonstrated in those dogs with B. canis infection, which may aggravate the nephrotoxic effect of the met-haemoglobinuria. Thus naturally infected B. canis cases showing haemoglobinuria may in fact have significant met-haemoglobinaemia, which may predispose them to renal disease.

This case report describes a young male German Shepherd dog that presented with bleeding from the lip 24 hours after being bitten by a boomslang (Dispholidus typus). Bites from this snake are infrequently encountered in dogs due to the shy habits of the snake. The boomslang venom is a potent procoagulant causing a consumption coagulopathy with resultant profuse haemorrhage. The only effective treatment is the administration of specific antiserum. Antiserum administration in this patient resulted in cessation of bleeding within one hour after administration. The article also discusses treatment options if antiserum is unavailable. This is the first recorded case of boomslang envenomation in the dog.

Uncomplicated canine babesiosis was diagnosed in 2 dogs based on the presence of trophozoites of Babesia canis in red blood cells on examination of a peripheral blood smear. The haemogram picture was that of a leukaemoid response with severe anaemia, high total white cell count and thrombocytopaenia. Treatment with babesiacidal drugs, together with blood transfusion, was successful in eliminating the Babesia parasites and reducing the leukaemoid response. The various leukograms of canine babesiosis and human malaria are compared and briefly discussed.

An adult male German Shepherd dog presented with a chronic non-painful, non-weight bearing lameness of the right hind limb. On clinical examination a contracted sarotorius muscle was palpable. Histopathology of the affected muscle confirmed replacement fibrosis and muscle contracture. Surgical excision of the muscle resulted in complete recovery.

A cat with primary intratracheal squamous cell carcinoma presented with severe dyspnoea and a dry cough. Radiographic changes included pulmonary hyperinflation and tracheal thickening at the thoracic inlet. On post mortem examination, proliferative, white, granular nodules in the trachea were confirmed to be an anaplastic squamous cell carcinoma.