Pyothorax was diagnosed in 27 cats between 1983 and 2002. In 21 (78%) of the cases, pleural fluid culture and/or cytology was consistent with a mixed anaerobic bacterial infection of oropharyngeal origin. In six cases (22%), infection was caused by unusual pathogens or pathogens of non-oropharyngeal origin, including a Mycoplasma species, Cryptococcus gattii, Escherichia coli, Salmonella typhimurium and Staphylococcus aureus. The overall mortality rate was 22%. Treatment was successful in 18 of 19 cases (95%) where closed thoracostomy tubes were inserted. One case resolved only after thoracotomy. Actinomyces species were isolated in three cases and in contrast to dogs where thoracotomy is recommended, they were resolved with tube thoracostomy. Mechanical complications occurred in 58% of the cats with indwelling chest tubes. Probable mechanisms of pleural space infection were identified in 18 cats (67%) including haematogenous infection (n=1), direct inoculation of bacteria into the pleural space (n=1), intrathoracic oesophageal rupture (n=1) and parapneumonic extension of infection (n=15; 56%). Of the latter, perioperative aspiration was suspected in two cats, parasitic migration in two and antecedent upper respiratory tract infection was implicated in seven. Parapneumonic spread of infection after colonisation and invasion of lung tissue by oropharyngeal flora appears to be the most frequent cause of feline anaerobic polymicrobial pyothorax and contests the widespread belief that direct inoculation of pleural cavity by bite wounds is more common.

Given the rise in the incidence of invasive fungal infections (IFIs) and the expanding spectrum of fungal pathogens, early and accurate identification of the causative pathogen is essential. We developed a panfungal PCR assay that targets the internal transcribed spacer 1 (ITS1) region of the ribosomal DNA gene cluster to detect fungal DNA in fresh and formalin-fixed, paraffin-embedded (PE) tissue specimens from patients with culture-proven (n ‫؍‬ 38) or solely histologically proven (n ‫؍‬ 24) IFIs. PCR products were sequenced and compared with sequences in the GenBank database to identify the causal pathogen. The molecular identification was correlated with results from histological examination and culture. The assay successfully detected and identified the fungal pathogen in 93.6% and 64.3% of culture-proven and solely histologically proven cases of IFI, respectively. A diverse range of fungal genera were identified, including species of Candida, Cryptococcus, Trichosporon, Aspergillus, Fusarium, Scedosporium, Exophiala, Exserohilum, Apophysomyces, Actinomucor, and Rhizopus. For five specimens, molecular analysis identified a pathogen closely related to that identified by culture. All PCR-negative specimens (n ‫؍‬ 10) were PE tissues in which fungal hyphae were visualized. The results support the use of the panfungal PCR assay in combination with conventional laboratory tests for accurate identification of fungi in tissue specimens.

Angiostrongylus cantonensis is a metastrongyloid nematode found widely in the Asia-Pacific region, and the aetiological agent of angiostrongyliasis; a disease characterized by eosinophilic meningitis. Rattus rats are definitive hosts of A. cantonensis, while intermediate hosts include terrestrial and aquatic molluscs. Humans are dead-end hosts that usually become infected upon ingestion of infected molluscs. A presumptive diagnosis is often made based on clinical features, a history of mollusc consumption, eosinophilic pleocytosis in cerebral spinal fluid, and advanced imaging such as computed tomography. Serological tests are available for angiostrongyliasis, though many tests are still under development. While there is no treatment consensus, therapy often includes a combination of anthelmintics and corticosteroids. Angiostrongyliasis is relatively rare, but is often associated with morbidity and sometimes mortality. Recent reports suggest the parasites' range is increasing, leading to fatalities in regions previously considered Angiostrongylus-free, and sometimes, delayed diagnosis in newly invaded regions. Increased awareness of angiostrongyliasis would facilitate rapid diagnosis and improved clinical outcomes. This paper summarizes knowledge on the parasites' life cycle, clinical aspects and epidemiology. The molecular biology of Angiostrongylus spp. is also discussed. Attention is paid to the significance of angiostrongyliasis in Australia, given the recent severe cases reported from the Sydney region.

Systemic protothecosis was diagnosed in 17 Australian dogs between 1988 and 2005. There was a preponderance of young-adult (median 4 years), medium- to large-breed dogs. Females (12/17 cases) and Boxer dogs (7 cases, including 6 purebreds and one Boxer cross) were over-represented. Sixteen of 17 dogs died, with a median survival of four months. A disproportionate number of cases were from coastal Queensland. In most patients, first signs were referable to colitis (11/17 cases), which varied in severity, and was often present for many months before other symptoms developed. Subsequent to dissemination, signs were mostly ocular (12 cases) and/or neurologic (8 cases). Two dogs had signs due to bony lesions. Once dissemination was evident, death or euthanasia transpired quickly. Prototheca organisms had a tropism for the eye, central nervous system (CNS), bone, kidneys and myocardium, tissues with a good blood supply. Microscopic examination and culture of urine (5 cases), cerebrospinal fluid (CSF;1 case), rectal scrapings (4 cases), aspirates or biopsies of eyes (5 cases) and histology of colonic biopsies (6 cases) as well as skin and lymph nodes (2 cases) helped secure a diagnosis. Of the cases where culture was successful, P wickerhamii was isolated from two patients, while P zopfii was isolated from five. P zopfii infections had a more aggressive course. Treatment was not attempted in most cases. Combination therapy with amphotericin B and itraconazole proved effective in two cases, although in one of these treatment should have been for a longer duration. One surviving dog is currently still receiving itraconazole. Protothecosis should be considered in all dogs with refractory colitis, especially in female Boxers.

Compared with similar surveys overseas, our cats were older and male cats were over-represented. There was a notable subgroup of young cats with mediastinal involvement. Siamese/Oriental cats were over-represented in this subgroup as well as in the larger population of cats with lymphosarcoma. Compared with overseas surveys, renal involvement, mixed cases and atypical cases (including nasal lymphosarcoma) were more common. A new subcategory of nodal lymphosarcoma, with involvement restricted to node(s) of head and neck, was identified.

Eleven of 89 dogs (12 per cent) developed neurological signs within six days of surgical attenuation of a congenital extrahepatic portosystemic shunt. Neurological signs were not associated with hepatic encephalopathy or hypoglycaemia. Signs varied in severity from non-progressive ataxia (three dogs) to generalised motor seizures (four dogs), progressing to status epilepticus (three dogs). In a further four cases, ataxia and disorientation were treated vigorously with anticonvulsant medication, presumably preventing the development of seizures. Two dogs that developed status epilepticus died or were eventually euthanased. All other animals survived, although some had persistent neurological deficits. Postligation neurological complications were not prevented by gradual shunt attenuation. Prophylactic treatment with phenobarbitone (5 to 10 mg/kg preoperatively, followed by 3 to 5 mg/kg every 12 hours for three weeks) did not significantly reduce the incidence of neurological sequelae (2/31 [6 per cent] dogs with phenobarbitone vs 9/58 [16 per cent] without phenobarbitone; P = 0.2). However, no animal receiving phenobarbitone experienced generalised motor seizures or status epilepticus. In conclusion, these observations suggest that postligation neurological syndrome comprises a spectrum of neurological signs of variable severity. Perioperative treatment with phenobarbitone may not reduce the risk of neurological sequelae, but may reduce their severity.

A retrospective study of 155 cats and 40 dogs diagnosed with cryptococcosis between 1981 and 2001 was undertaken. Age, sex, breed, clinical findings, feline immunodeficiency virus and feline leukaemia virus status (in cats), species of Cryptococcus causing disease and region of domicile were recorded. Associations between variables were tested. Male and female cats were affected equally. Age ranged from 1 to 16 years, with a preponderance of cats aged between 2 and 3 years. Siamese, Himalayan and Ragdoll breeds were over-represented. Rural cats were more frequently infected with Cryptococcus gattii. Retroviral infection was not identified as a predisposing condition and was not correlated with either species of Cryptococcus or physical findings. Most cats had signs of nasal cavity infection, which was typically localised for a substantial period before invasion of adjacent structures or dissemination. Male and female dogs were affected equally. A marked preponderance of young, large breed dogs was noted. Border Collies, Boxers, Dalmatians, Dobermann Pinschers, Great Danes and German Shepherds were over-represented. Cryptococcus species involved was not affected by place of domicile. Although nasal cavity involvement was important, the canine cohort had a greater propensity to develop secondary central nervous system involvement and disseminated disease than feline cases. There were no clinical findings in either cats or dogs which could be reliably used to distinguish disease caused by Cryptococcus neoformans variety grubii from disease caused by Cryptococcus gattii. Both Cryptococcus species appear to be primary pathogens of cats and dogs, with the upper respiratory tract presumed to be the predominant primary site of inoculation in most but not all cases.

A retrospective study of cryptococcosis in domestic animals residing in Western Australia was conducted over an 11-year-period (from 1995 to 2006) by searching the data base of Murdoch University Veterinary Teaching hospital and the largest private clinical pathology laboratory in Perth. Cryptococcosis was identified in 155 animals: 72 cats, 57 dogs, 20 horses, three alpacas, two ferrets and a sheep. There was no seasonal trend apparent from the dates of diagnosis. Taking into account the commonness of accessions to Murdoch University, cats were five to six times more likely to develop this disease than dogs, and three times more likely than horses, while horses were almost twice as likely as dogs to become infected. Amongst the feline cohort, Ragdoll and Birman breeds were over-represented, while in dogs several pedigree breeds were similarly overrepresented. Dogs and horses tended to develop disease at an early age (one to five years), while cats were presented over a much wider range of ages. In cats and dogs the upper respiratory tract was the most common primary site of infection, while horses and alpacas tended to have lower respiratory involvement. The most striking finding of the study was the high frequency with which C. gattii was identified, with infections attributable to this species comprising 5/9 cats, 11/22 dogs, 9/9 horses and 1/1 alpaca, where appropriate testing was conducted. Preliminary molecular genotyping suggested that most of the C. gattii infections in domestic animals (9/9 cases) were of the VGII genotype. This contrasts the situation on the eastern seaboard of Australia, where disease attributable to C. gattii is less common and mainly due to the VGI genotype. C. gattii therefore appears to be an important cause of cryptococcosis in Western Australia.