African horse sickness (AHS) is a fatal vector transmitted viral disease of horses caused by the African horse sickness virus (AHSV). This disease is characterised by circulatory and respiratory failure, resulting from vascular endothelial injury affecting many organs. The susceptibility of dogs to AHS has been demonstrated in the past following experimental infection through consumption of infected horse meat. Thirty three clinical cases of AHS in dogs (cAHS) have been documented, without a history of ingesting infected horse meat, over a period of 12 years. The clinical cases included in this study presented with a history of acute respiratory distress syndrome or sudden death. The macroscopic and histological changes were mostly characterised by acute interstitial pneumonia, serofibrinous pleuritis and mediastinal oedema. Confirmation of cAHS was obtained by AHS specific NS4 antibody immunohistochemistry and/or AHSV specific duplex real time RT-quantitative PCR. Here, we document the clinical and postmortem diagnostic features of confirmed cAHS cases with no history of ingestion of AHS infected horse meat.

Glioblastoma multiforme (GBM) represents the final endpoint of anaplastic progression in astrocytomas. GBM which arise without clinical evidence of a prior low-grade astrocytoma (LGA) have been designated de novo GBM, and are thought to develop rapidly from initial tumour formation. However, a purely clinical definition of de novo GBM does not exclude a long-standing, asymptomatic low-grade tumour. This study therefore sought to determine the genetic features of a unique group of cases in which GBMs were documented to have arisen radiographically in defined period of time (radiographically defined de novo GBM). Clinical and genetic features were examined in a group of 11 patients with a histological diagnosis of high-grade astrocytoma at first biopsy and radiographically defined de novo GBM. The mean age of the patients at tumour diagnosis was 62 years (range 32-87). Six of 11 tumours arose in the temporal lobes. Eight of 11 tumours had epidermal growth factor receptor (EGFR) overexpression, and EGFR gene amplification was found in five of the six analysed cases. Overexpression of p53 was observed in only one tumour, and a TP53 mutation was present in this case. p16 immunostaining was undetectable in 10 cases, and homozygous deletion of CDKN2A was observed in four of the six studied tumours. pRb expression was lost in four tumours. Mutations in the PTEN gene were detected in two of six cases. The results in this unique group of cases confirms the prior hypothesis that the profile of genetic alterations in de novo GBM is distinct from that of GBM arising from a known LGA, and that these specific genetic pathways promote the rapid development of GBM.

Meningiomas are the most common primary brain tumour in dogs and cats. However, whilst there are numerous reports of extracranial (spinal, orbital and sinonasal) meningiomas in the dog, there have only been a few case reports of spinal meningiomas, and no post-mortem confirmed orbital or sinonasal meningiomas in cats. In this report, a 20-year-old captive tiger (Panthera tigris altaica) with a history of chronic ocular inflammation resulting in enucleation, spontaneously developed tetanic convulsions (epileptic seizures) that over a 2-year period resulted in a gradually worsening condition and the animal was eventually euthanized. At autopsy, a focal, expansile, neoplastic mass was found in the caudal nasal cavity midline, abutting the cribriform plate and slightly compressing the calvarium. Histological analysis revealed nasal turbinates attached to a well-circumscribed expansile multi-lobular mass consisting of interlacing whorls and streams of neoplastic cells supported by a variably fibrous to microcystic collagenous matrix displaying rare psammoma bodies. The diagnosis was sinonasal transitional meningioma. This is the first report of a captive wild felid with an extracranial meningioma, specifically a tiger with a sinonasal transitional meningioma.

Pigmentation of the skin is a crucial component in the pathogenesis of melanocytic neoplasms and other skin-related tumors, as melanin is known to function in both the absorbance of ultraviolet radiation and as an antioxidant. Very limited information exists regarding the incidence and metastatic potential of neoplastic conditions of the skin in game animals, especially wildebeests, relative to domestic animals. Four cases of cutaneous melanoma in color-variant golden and king wildebeests ( Connochaetes taurinus) (from 2014 to 2015) in South Africa were investigated. Melanoma in these captive animals was characterized using histopathology, transmission electron microscopy, and an immunohistochemistry panel, which consisted of monoclonal antibodies against three melanocytic markers: Melan A, PNL2, and S100. Overall, 2/4 cases (50%) of the melanocytic neoplasms stained strongly positive for all the melanocytic markers, while 4/4 cases (100%) stained positively for at least one of the markers. Cutaneous melanocytic neoplasia has not been reported in wildebeests; the current study suggests that selection of wildebeests for coat color potentially predisposes to this condition.

Malignant melanomas tend to be locally destructive, aggressive tumours commonly associated with recurrence and/or metastasis. In this report, a 13-year-old captive white African lioness (Panthera leo), with a recent history of intermittent bouts of lethargy and inappetence, presented with a distended abdomen (due to ascites) and a small, round crusty lesion on the ear. An abdominal ultrasound showed the presence of masses on the liver and an exploratory laparotomy revealed multiple pale lesions on the liver and omentum. Histopathology revealed sheets of pleomorphic neoplastic cells compressing the non-neoplastic liver tissue. Similar neoplastic cells had multifocally expanded and effaced omentum adipose tissue, as well as formed a well-circumscribed mass in the ear sample, extending from close to the epidermis to the lateral and deep margins of the section. All three tissue samples had a high mitotic index (15 per 10 HPF), and critically, in the ear sample, there were rafts of neoplastic cells in the lymphatics, indicating lymphovascular invasion. Immunohistochemistry for the melanoma marker, PNL-2, showed strong positivity in all three tissue samples. Thus, the diagnosis was of malignant melanoma with metastasis to the liver and omentum. This is the first report of metastatic cutaneous melanoma in a lion.

Cutaneous squamous cell carcinoma (SCC) is a slow growing but locally invasive neoplasm, most commonly caused by prolonged exposure to ultraviolet (UV) radiation. Whilst SCC accounts for 15% of skin tumours in domesticated cats, cutaneous SCC in non-domesticated felids (apart from captive snow leopards) appears to be uncommon, with only three reports in the literature to date. In this report, a captive African lion (Panthera leo) presented with two ulcerative lesions on the nasal planum. Histopathology of the lesions revealed epidermal keratinocyte dysplasia and neoplastic basal- and supra-basal epithelial cells with dyskeratosis and evidence of basement membrane breaching and dermal invasion, consistent with a diagnosis of SCC. There was also evidence of laminar fibrosis and inflammation of the subjacent dermis suggesting that the SCC most likely resulted from UV-induced neoplastic transformation of the epidermal squamous epithelium following actinic keratosis. The lion was treated with hypofractionated radiation therapy and remained in remission until his death (euthanised 17 months later because of age-related chronic renal failure). This is the first report of cutaneous SCC in a lion with evidence of actinic damage and resolution after radiation therapy.

A 10-month-old, spayed, female beagle (case 1) and an unrelated two-year-old, intact, female labrador retriever (case 2), both living in Pretoria, South Africa, presented individually on separate occasions with acute onset dyspnoea and severe hypoxia. Thoracic radiographs demonstrated severe, diffuse interstitial to alveolar lung patterns with mild pleural and mediastinal effusion. Mixed airway inflammation was seen on transtracheal aspirate cytology in case 1. Both cases received supportive therapy, but only one dog survived (case 2). African horse sickness (AHS) was diagnosed at necropsy based on histopathology and immunohistochemistry in case 1 and was diagnosed antemortally using reverse transcriptase-PCR on whole blood in case 2. To the authors’ knowledge, this is the first report to detail the haematological, biochemical, thoracic radiological, arterial blood gas and transtracheal aspirate cytology findings of AHS in dogs. This report also describes the treatment of a dog surviving clinical AHS infection.

A 13-year-old intact male miniature schnauzer presented with lethargy, distended abdomen and pallor. Pancytopenia was identified on complete blood count with a severe thrombocytopenia. Cavitatory severe splenomegaly was identified on abdominal ultrasound. Two weeks of immunosuppressive therapy had no effect on the thrombocytopenia and a splenectomy was performed. The platelet count returned to normal within 24 hours of splenectomy. Isolated splenic haemangiomatosis was confirmed on histopathology and immunohistochemistry. The anaemia and severe thrombocytopenia in conjunction with the ultrasound findings and histopathology are characteristic of Kasabach-Merritt syndrome in people. This is the first case of Kasabach-Merritt-like syndrome described in the dog.