A case-control study of atypical guttural pouch empyema in Arabian foals.

BACKGROUND: Upper respiratory disease was reported over many seasons in Arabian foals on a single stud farm in the Middle East. Affected foals were noted to have mucopurulent nasal discharge, cough, fever and tachypnea. All affected foals had been empirically treated with a macrolide and rifampicin, by the referring veterinarian without improvement. On endoscopic examination, all affected foals had significant guttural pouch empyema (GPE). OBJECTIVES: (1) To document a previously unreported presentation of guttural pouch empyema (GPE) in a family of juvenile Arabian foals; (2) To document the cytological and microbial composition of the empyema; (3) To identify clinical signs significantly correlated with the presence of GPE, as predictors for the need for guttural pouch (GP) endoscopy; (4) To demonstrate successful resolution of the identified syndrome with mechanical GP lavage and evidence based antimicrobial use, improving antibiotic stewardship and the one-health approach to respiratory disease in this demographic of foals. METHODS: Evaluation and scoring of clinical signs, upper airway endoscopy and thoracic ultrasound were performed in 14 affected foals and 10 age-matched controls, followed by comparative tracheal and guttural pouch sputum culture and cytological evaluation. Therapeutic GP lavage was performed and response to therapy monitored. RESULTS: GPE, cranioventrally distributed ultrasonographic lesions and opportunistic pathogen infection suggested a primary lesion of GPE with aspiration of GP discharge into the lungs. GP lavage resolved the empyema and associated clinical signs in all cases. CONCLUSIONS: Cytological examination of tracheal and guttural pouch aspirates revealed a neutrophilic exudate with lipid-laden phagocytes, suggestive of engulfed milk. Bacteriology revealed a high prevalence of Streptococcus equi ssp. zooepidemicus admixed with other opportunistic pathogens. Streptococcus equi ssp. equi was not isolated in any case.

CD3+ T-Lymphocytic Coeliac-Mesenteric Ganglioneuritis Associated with Colonic Torsion and Inflammatory Bowel Disease in an Arabian Broodmare.

A 5-year-old Arabian broodmare with acute colic was diagnosed with lymphocytic ganglioneuritis of the coeliac-mesenteric ganglia and lymphocytic‒plasmacytic enterocolitis resembling inflammatory bowel disease. No significant pathogens were identified by aerobic culture or histopathological examination. The ganglia were multifocally infiltrated with small lymphocytes that were immunopositive for CD3 and negative for CD20 and CD79a antigens, indicating CD3+ T-lymphocyte-mediated coeliac-mesenteric ganglioneuritis. The findings suggest immune-mediated inflammatory bowel disease resulting in disturbance of the autonomic nervous system in the gastrointestinal tract, as in ulcerative colitis in humans. Histopathological features in this case differ from those of equine enteric dysautonomia and chronic intestinal pseudo-obstruction, which are characterized by neuronal degeneration and inflammation, respectively, and mostly affect the mural ganglion plexuses. To the best of our knowledge, this is the first report of CD3+ T-lymphocytic extramural enteric ganglioneuritis in equine inflammatory bowel disease.

Idiopathic multifocal myocardial atrophy with fibrosis and fatty infiltration involving Purkinje fibres in a 13-year-old Arabian broodmare: Histopathological features.

Myocardial atrophy with fibrosis and fatty infiltration involving the cardiac conduction system is relatively unusual in horses. We herein report of such a case in a 13-year-old Arabian broodmare that had spontaneously died on a paddock. An autopsy revealed multifocal myocardial atrophy with concomitant fibrosis and fatty infiltration in both the ventricles and interventricular septum. The Purkinje fibres in the ventricles and interventricular septum were surrounded by thick fibrous or adipose tissues adjacent to atrophic myocardial cells. Myocardial fibrosis and fatty infiltration were likely secondary to myocardial atrophy, occurring as a pathological response triggered by the repair of muscular wall injury. However, there were no major vascular pathologies (e.g. atherosclerosis and arteriosclerosis); hence, the pathogenesis of myocardial atrophy was unclear. There was no evidence of myocardial atrophy ̵ induced pathologies such as infarct, ischaemic lesions, myocardial degeneration, myocarditis and endocarditis. However, such an unusual histopathological pattern may be associated with rapid clinical deterioration and death.