Cerebral phaeohyphomycosis caused by Cladosporium spp. in two domestic shorthair cats

Two domestic shorthair cats presented for clinical signs related to multifocal central nervous system dysfunction. Both cats had signs of vestibular system involvement and anisocoria, and one had generalized seizure activity. Cerebrospinal fluid analysis revealed a neutrophilic pleocytosis with protein elevation in one cat and pyogranulomatous inflammation in the second. Electroencephalography and brain-stem auditory-evoked potentials in the first cat confirmed cerebral cortical and brain-stem involvement. Euthanasia was performed in both cats, and postmortem diagnoses of phaeohyphomycosis secondary to Cladosporium spp. were made based on histopathology and fungal culture in both cats.     

Invasive phaeohyphomycosis caused by Curvularia species in a dog

A 2-year-old female Boxer dog was presented with a history of skin lesions that started 1 month after being given oral glucocorticoids for a neurologic problem. Clinically, the animal had focal areas of alopecia with papules and nodules often with ulceration overlain by crusts. Lesions were most common on the dorsum and the lateral aspects of the trunk and extremities. Histologic evaluation revealed pigmented fungal organisms within the lumina of hair follicles and throughout the dermis and subcutis. These organisms were associated with a multinodular, pyogranulomatous luminal folliculitis/furunculosis, dermatitis, and panniculitis. Curvularia sp. was isolated from the cutaneous lesions. The histologic identification of dematiaceous fungal organisms in the hair follicles may explain how phaeohyphomycosis can occur without history of a penetrating injury.     

Subcutaneous phaeohyphomycosis caused by Moniliella suaveolens in two cats

Moniliella suaveolens was isolated in pure culture from histologically typical phaeohyphomycotic granulomas containing dematiaceous fungi in two cats. One cat had several slow-growing black lesions up to 2 cm in diameter in the abdominal subcutis. These lesions recurred after surgical excision was attempted. The second cat had a single black subcutaneous 0.5 X 1.5-cm lesion near one dewclaw. This lesion was successfully removed surgically without recurrence. M. suaveolens has not been isolated previously from lesions in animals including man.     

Equine proliferative enteropathy caused by Lawsonia intracellularis

Equine proliferative enteropathy (EPE) is a disease of foals caused by the obligate intracellular organism Lawsonia intracellularis. This emerging disease affects mainly weanling foals and causes fever, lethargy, peripheral oedema, diarrhoea, colic and weight loss. The diagnosis of EPE may be challenging and relies on the presence of hypoproteinaemia, thickening of segments of the small intestinal wall observed on abdominal ultrasonography, positive serology and molecular detection of L. intracellularis in faeces. Although the clinical entity, diagnostic work-up and treatment of EPE are well established and described, the epidemiology for this disease has remained largely unaddressed. This article reviews the aetiology, epidemiology, clinical signs, diagnosis, treatment and prevention of EPE.     

Equine diseases caused by known genetic mutations

The recent development of equine genome maps by the equine genome community and the complete sequencing of the horse genome performed at the Broad Institute have accelerated the pace of genetic discovery. This review focuses on genetic diseases in the horse for which a mutation is currently known, including hyperkalemic periodic paralysis, severe combined immunodeficiency, overo lethal white syndrome, junctional epidermolysis bullosa, glycogen branching enzyme deficiency, malignant hyperthermia, hereditary equine regional dermal asthenia, and polysaccharide storage myopathy. Emphasis is placed on the prevalence, clinical signs, etiology, diagnosis, treatment and prognosis for each disease.     

Fatal systemic phaeohyphomycosis caused by Ochroconis gallopavum in a dog (Canis familaris)

A 5-year-old Shetland Sheepdog was presented with a history of weakness, ataxia, anemia, thrombocytopenia, and occasional seizures. The dog had been treated for 6 months with prednisone for inflammatory bowel disease. A positive titer for Ehrlichia canis was detected 6 months before referral. The initial physical examination revealed a weak, laterally recumbent dog with pale mucous membranes. Neurologic examination revealed multiple neurologic deficits. A complete blood cell count (CBC) revealed normochromic, normocytic, nonregenerative anemia; lymphopenia; thrombocytopenia; and neutrophilic and monocytic leukocytosis. Urinalysis revealed proteinuria, with a specific gravity of 1.045. The dog was unresponsive to treatment and died. At necropsy, there was severe serofibrinous peritonitis and pleuritis, with randomly scattered dark brown necrotic foci present in multiple organs, including liver, spleen, kidney, and pancreatic lymph node. Histologically, there were extensive regions of parenchymal necrosis surrounded by neutrophils admixed with epithelioid macrophages, lymphocytes, and pigmented fungal organisms. Numerous brown, 2 to 6 microm in diameter, septate, branching hyphae, subsequently identified as Ochroconis gallopavum (formerly Dactylaria constricta var. gallopava), were observed.     

An experimental mycotoxicosis in sheep and goats caused by Drechslera campanulata, a fungal pathogen of green oats

Field outbreaks of a syndrome of unknown aetiology associated with the grazing of green oats (Avena sativa) in the south-western Cape Province were characterized by diarrhoea, photosensitivity and death in goats and by diarrhoea and a reduction in milk production in cows. A phytopathogenic fungus, Drechslera campanulata, was isolated from conspicuous reddish-brown leaf spots on oat plants collected from both outbreaks. Pure cultures on autoclaved maize of D. campanulata isolates from oat leaves implicated in both field outbreaks, as well as a Canadian isolate, proved to be highly toxic to ducklings, goats and sheep. Characteristic clinical signs of the fatal mycotoxicosis caused by D. campanulata culture material in goats and sheep were anorexia, apathy, diarrhoea and ruminal stasis. Photosensitivity, however, was not induced. Necrosis of the forestomach mucosa was the most characteristic gross pathological change. Histopathological findings included mild focal erosions to severe, diffuse, coagulative necrosis of the mucosa in the rumen, reticulum and omasum and congestion and haemorrhages in the abomasum. These results provide circumstantial evidence that green oat leaves infected by D. campanulata may cause outbreaks of a mycotoxicosis in grazing animals.     

Equine protozoal myeloencephalitis caused by Neospora hughesi in an adult horse in Saskatchewan

A protozoal parasite identified as Neospora hughesi was found in inflammatory lesions in the central nervous system of a Canadian-born adult horse presented with neurological signs. This is believed to be the first case of equine protozoal myeloencephalitis (EPM) caused by Neospora hughesi in a horse outside of the United States.     

Equine encephalomyelitis outbreak caused by a genetic lineage 2 West Nile virus in Hungary

Background: The spread of lineage 2 West Nile virus (WNV) from sub‐Saharan regions to Europe and the unpredictable change in pathogenicity indicate a potential public and veterinary health threat and requires scientific awareness. Objectives: To describe the results of clinical and virological investigations of the 1st outbreak of a genetic lineage 2 WNV encephalomyelitis in horses. Animals: Seventeen horses with neurologic signs. Methods: Information regarding signalment, clinical signs, and outcome was obtained for each animal. Serology was performed in 15 cases, clinicopathological examination in 7 cases, and cerebrospinal fluid was collected from 2 horses. Histopathology was carried out in 4 horses, 2 of which were assessed for the presence of WNV in their nervous system. Results: WNV neutralizing antibody titers were between 10 and 270 (median, 90) and the results of other serological assays were in agreement with those of the plaque reduction neutralization test. Common signs included ataxia, weakness, asymmetric gait, muscle tremors, hypersensitivity, cranial nerve deficits, and recumbency. Twelve animals survived. Amplicons derived from the infection‐positive specimens allowed molecular characterization of the viral strain. Conclusions and Clinical Importance: From our results, we conclude that this outbreak was caused by a lineage 2 WNV strain, even though such strains often are considered nonpathogenic. Neurological signs and survival rates were similar to those reported for lineage 1 virus infections. The disease occurrence was not geographically limited as had been the typical case during European outbreaks; this report describes a substantial northwestern spread of the pathogen.     

Equine uveitis.

Uveitis (inflammation of the iris, ciliary body, or choroid) is a potentially blinding condition with a significant economic impact on the horse industry. Variable symptoms are described, as well as a considerable range of structural and functional sequelae. Known causes of initial episodes include bacterial, viral, traumatic, and parasitic insults, with recurrence by immunologic mechanisms. Treatment strategies and management recommendations that may reduce the incidence or severity of episodes are discussed.     

Equine autoimmunity.

Although relatively little is known about autoimmunity and autoimmune mechanisms specifically in horses, the similarities between clinical syndromes with identifiable effector mechanisms in horses and other species suggest that comparable mechanisms may be applicable. Our understanding of equine autoimmunity undoubtedly will benefit from the extensive study of autoimmunity in other species.     

Equine anhidrosis.

The molecular basis of the pathophysiology of anhidrosis is still not well understood. Therefore, treatments are more often based on clinical impressions than on scientific fact. Treatment options for this condition will improve only when more is known about the molecular events that cause anhidrosis, especially as they relate to beta2-receptor dysfunction and stimulus-secretion coupling in the sweat glands of affected horses. Although this additional information is being attained, sound environmental management will continue to be a very important aspect of the treatment of horses affected with anhidrosis.     

Equine glaucoma.

Glaucoma is a diverse group of vision-impairing disorders that have as a common bond an elevation of intraocular pressure(IOP) to a level incompatible with the health of the eye. Glaucoma can be congenital, primary, or secondary. Congenital equine glaucoma is associated with developmental abnormalities of the iridocorneal angle or, in many cases, with the more severe anterior segment dysgenesis.