Histological evaluation of cardiac remodelling in equine athletes.

Approximately 1-2 per 100,000 young athletes die from sudden cardiac death (SCD) and extreme exercise may be associated with myocardial scar and arrhythmias. Racehorses have a high prevalence of atrial fibrillation (AF) and SCD but the presence of myocardial scar and inflammation has not been evaluated. Cardiac tissues from the left (LAA) and right (RAA) atrial appendages, left ventricular anterior (LVAPM) and posterior (LVPPM) papillary muscles, and right side of the interventricular septum (IVS-R) were harvested from racehorses with sudden cardiac death (SCD, n = 16) or other fatal injuries (OFI, n = 17), constituting the athletic group (ATH, n = 33), and compared to sedentary horses (SED, n = 10). Horses in the ATH group had myocyte hypertrophy at all sites; increased fibrosis at all sites other than the LAA; increased fibroblast infiltration but a reduction in the overall extracellular matrix (ECM) volume in the RAA, LVAPM, and IVS-R compared to SED horses. In this horse model, athletic conditioning was associated with myocyte hypertrophy and a reduction in ECM. There was an excess of fibrocyte infiltration and focal fibrosis that was not present in non-athletic horses, raising the possibility of an exercise-induced pro-fibrotic substrate.

Brain magnetic resonance imaging and histopathology findings in a dog with global brain ischaemia following cardiopulmonary arrest.

BACKGROUND: Global brain ischaemia following cardiopulmonary arrest is uncommonly reported in veterinary medicine yet neurologic injury after arrest is a known morbidity. CASE REPORT: An 18-week-old male entire Cavalier King Charles Spaniel-Poodle was referred following 3 days of neurologic abnormalities after cardiopulmonary arrest. After resuscitation, the animal had decerebrate rigidity, a stuporous mentation and intermittent episodes of vocalisation and apnoea. A brain magnetic resonance imaging (MRI) was undertaken 4 days after cardiopulmonary arrest, with standard sequences (T1-weighted, T2-weighted and fluid-attenuated inversion recovery) as well as diffusion-weighted imaging to better discern ischaemic injury and cytotoxic oedema for prognostic reasons. MRI findings were consistent with global brain ischaemia affecting the hippocampus, cerebellum and substantia nigra, the latter two not previously identified in canine cases of global brain ischaemia. The patient was euthanased on day eight post-cardiopulmonary arrest due to a lack of neurological improvement and developing sepsis as a complication. Ante-mortem identification of affected areas of the brain was confirmed on histological examination, with evidence of ischaemic injury seen in the cerebrum, hippocampus, cerebellum, basal nuclei and thalamus. CONCLUSION: This report describes ante-mortem MRI and postmortem findings in a dog with global brain ischaemia following cardiopulmonary arrest. A multimodal approach to neuroprognostication in patients recovering from cardiopulmonary arrest is recommended.

Radiographic and CT appearance of cavitary pulmonary lesions in a lamb.

BACKGROUND: Pulmonary abscesses may be cavitary lesions on thoracic radiographs and computed tomography (CT). CASE REPORT: A 26-day-old, cross-breed lamb presented for respiratory distress despite procaine penicillin treatment. Thoracic radiographs revealed several pulmonary ovoid thin-walled gas and soft tissue opacity structures. CT showed that these gas-filled structures enclosed mildly contrast enhancing soft tissue attenuating material and surrounded the lobar bronchus to the right middle and caudal lung lobes. Imaging revealed pulmonary cavitary lesions, and chronic pulmonary abscesses was confirmed with histopathology on samples obtained from a right caudal lung lobectomy. CONCLUSION: To the authors' knowledge, this is the first radiographic and CT report of cavitary pulmonary lesions in a lamb. The pulmonary abscesses in this case were suspected to be due aspiration pneumonia occurring during bottle feeding, along with the high possibility of failure of passive transfer from its orphan history.

Chlamydia psittaci: a suspected cause of reproductive loss in three Victorian horses.

Chlamydia psittaci was detected by PCR in the lung and equine foetal membranes of two aborted equine foetuses and one weak foal from two different studs in Victoria, Australia. The abortions occurred in September 2019 in two mares sharing a paddock northeast of Melbourne. The weak foal was born in October 2019 in a similar geographical region and died soon after birth despite receiving veterinary care. The detection of C. psittaci DNA in the lung and equine foetal membranes of the aborted or weak foals and the absence of any other factors that are commonly associated with abortion or neonatal death suggest that this pathogen may be the cause of the reproductive loss. The detection of C. psittaci in these cases is consistent with the recent detection of C. psittaci in association with equine abortion in New South Wales. These cases in Victoria show that C. psittaci, and the zoonotic risk it poses, should be considered in association with equine reproductive loss in other areas of Australia.

Histological survey for oxalate nephrosis in Victorian koalas (Phascolarctos cinereus).

The Mount Lofty Ranges koala (Phascolarctos cinereus) population in South Australia has a high prevalence of the renal disease oxalate nephrosis, for which an underlying genetic cause is suspected. South Australian koalas primarily originate from those in French Island, Victoria; however, oxalate nephrosis has not previously been reported in Victorian koalas. Examination of kidney tissue sections from 63 koalas across Victoria found that nine koalas were affected by oxalate nephrosis (14.3%). These included 2/5 koalas from French Island (40%), 4/14 koalas from the western regions (29%), 2/11 Raymond Island koalas (18%), and 1/13 Cape Otway koalas (8%). There were no cases of oxalate nephrosis identified in the Strzelecki koalas (n = 12). These findings suggest that oxalate nephrosis occurs in koalas from French Island and populations that have received significant influx of koalas from French Island, but not in the Strzelecki region, which has little to no French Island input. This lends support to the theory that an inherited abnormality of oxalate metabolism could underlie the high prevalence of oxalate nephrosis in the Mount Lofty Ranges koala population, and molecular investigations are currently underway to investigate a genetic cause.

Evidence for marsh mallow (Malva parviflora) toxicosis causing myocardial disease and myopathy in four horses.

REASON FOR PERFORMING THE STUDY: Investigation of toxicosis caused by Malva parviflora was required after 4 horses from the same farm developed severe muscle fasciculations, tachycardia, sweating and periods of recumbency leading to death or euthanasia after ingesting the plant. OBJECTIVES: To describe historical, clinical, clinicopathological and pathological findings of 4 horses with suspected M. parviflora toxicosis. The role of cyclopropene fatty acids (found in M. parviflora) and mechanism for toxicosis are proposed. STUDY DESIGN: Case series. METHODS: Historical, physical examination, clinicopathological and pathological findings are reported. Due to similarities with atypical myopathy or seasonal pasture myopathy acyl carnitine profiles were performed on sera from 2 cases and equine controls. Presence of cyclopropene fatty acids was also examined in sera of 2 cases. RESULTS: M. parviflora had been heavily grazed by the horses with little other feed available. Horse 1 deteriorated rapidly and was subjected to euthanasia. Horse 2 was referred to hospital where severe myocardial disease and generalised myopathy was determined; this horse was subjected to euthanasia 36 h after admission. Horse 3 died rapidly and Horse 4 was subjected to euthanasia at onset of clinical signs. Post-mortem examinations performed on 3 horses revealed acute, multifocal cardiac and skeletal myonecrosis. Myocyte glycogen accumulation was absent when examined in Horse 2. Acyl carnitine profiles revealed increased C14-C18 acyl carnitine concentrations in cases relative to controls. Cyclopropene fatty acids were detected in sera of cases but not controls. CONCLUSION: These findings suggest aetiology different to that of atypical myopathy or seasonal pasture myopathy. We hypothesise that cyclopropene fatty acids in M. parviflora interfere with fatty acid ß-oxidation in horses in negative energy balance, causing the clinical signs and abnormal acyl carnitine profiles. These equine cases suggest a pathophysiological course that closely mimics the human genetic condition very long chain acyl CoA dehydrogenase deficiency.

Osteopetrosis in a neonatal donkey.

Osteopetrosis is a rare disorder characterised by a defect in osteoclastic bone resorption. This report describes osteopetrosis in a neonatal donkey that suffered a displaced tibial fracture. Radiographic examination identified generalised reduction in medullary cavity size, thickened mid-diaphyseal cortices and conical metaphyseal bone extending toward the mid-diaphysis of long bones. Postmortem examination identified additional fractures and brittle bones. Histologically, osteoclasts were absent in multiple bone sections. Diaphyseal cortices consisted of concentric bone lamellae with marrow tissue infiltration. Large wedges of secondary spongiosa extended from the metaphyseal growth plate. Clinical and histopathological features were similar to an osteoclast-deficient, autosomal recessive form of osteopetrosis in humans.

Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5.

Chronic gastritis from Helicobacter pylori infection is a major factor in the development of gastric adenocarcinoma. Factors that regulate gastritis severity are important in determining which individuals are susceptible to H. pylori-associated disease. Although protease-activated receptor 1 (PAR1) has been identified as one such host factor, its mechanism of action is unknown. Using chimeric mice, we demonstrated that PAR1-mediated protection against H. pylori gastritis requires bone marrow-derived cells. Analyses of the gastric mucosa revealed that PAR1 suppresses cellular infiltration and both T helper type 1 (Th1) and T helper type 17 (Th17) responses to infection. Moreover, PAR1 expression was associated with reduced vaccine-mediated protection against H. pylori. Analyses of H. pylori-stimulated macrophages revealed that PAR1 activation suppressed secretion of interleukin (IL)-12 and IL-23, key drivers of Th1 and Th17 immunity, respectively. Furthermore, PAR1 suppressed interferon regulatory factor 5 (IRF5), an important transcription factor for IL-12 and IL-23, both in the infected mucosa and following bacterial stimulation. PAR1 suppression of IRF5 and IL-12/23 secretion by macrophages provides a novel mechanism by which the host suppresses the mucosal Th1 and Th17 response to H. pylori infection. Dysregulation of this process is likely an important factor in the susceptibility of some individuals to H. pylori-associated disease.