400
EQUINE VETERINARY EDUCATION / AE / AUGUST 2019
6.81 9 1012 cells/L) and mild lymphopenia (1.33 9 109 cells/L). Treatment with firocoxib was continued.
Two months post initial presentation On repeat evaluation, 2 weeks later (approximately 2 months after initial presentation), the gelding appeared brighter and the volume of peritoneal fluid had decreased significantly although fluid cytology and triglyceride levels (5.6 mmol/L) remained consistent with a chylous effusion.
Three months post initial presentation Approximately 1 month later, the gelding presented with acute onset of tachycardia, tachypnoea and pyrexia. A substantial accumulation of cellular peritoneal fluid was present on abdominal ultrasound (Fig 3). A decision was
made for euthanasia due to a markedly increased peritoneal fluid TNCC (500 9 109 cells/L) containing 88% degenerate neutrophils and intra- and extracellular Gram-negative rods. Peritoneal fluid collected ante-mortem yielded a moderate pure growth of Actinobacillus
spp., identified as
Actinobacillus capsulatus by PCR.1 Searches for 16S rRNA sequences were performed with FASTA and BLAST.
Necropsy findings Post-mortem findings were consistent with severe, subacute to chronic, generalised fibrinosuppurative peritonitis with peritoneal effusion and multifocal subserosal intestinal petechial and ecchymotic haemorrhage (Fig 4). There was no evidence of abdominal adhesions, vascular compromise or perforation of the gastrointestinal tract, urinary tract perforation or an abscess/neoplasia compromising intestinal integrity. A definitive cause of the chyloabdomen could not be located. A thorough search for nodular disease and/or dilated lymphatics, particularly in the region of the cistern chyli and within the root of the mesentery, was undertaken to no avail. The medial iliac lymph nodes and the root of the mesentery and adjacent connective tissues in the region of
the cistern chyli were extremely oedematous. Histology of the root of the mesentery showed little change. Approximately 200 mL of turbid, pale orange fluid was also present in the pericardial sac, and this fluid also cultured Actinobacillus species, identified as Actinobacillus capsulatus by PCR.
Discussion
To our knowledge, this is the first clinical report of Actinobacillus capsulatus infection in the horse. Actinobacillus capsulatus is recognised as a primary pathogen of lagomorphs (Blackall et al. 1997; Meyerholz and Haynes 2005). The majority of previous reports of peritonitis due to Actinobacillus spp. have been accepted to have been due to Actinobacillus equilli, diagnosed either via positive culture (Gay and Lording 1980; Golland et al. 1994; Matthews et al. 2001, 2002; Tennent-Brown et al. 2010), or on the basis of characteristic clinical signs, abdominal fluid variables and response to treatment (Matthews et al. 2001, 2002). The initial presentation of this horse, with signs of mild
colic, lethargy, inappetence, tachycardia, tachypnoea and a fever, was consistent with the clinical presentation of horses in other reports of Actinobacillus peritonitis (Gay and Lording 1980; Golland et al. 1994; Matthews et al. 2001, 2002; Mogg and Dykgraaf 2006; Watts et al. 2011). The response to appropriate antimicrobials, however, was disappointing in this case, with persistence of clinical signs much longer than typically reported with primary Actinobacillus peritonitis (Golland et al. 1994; Matthews et al. 2001). Although prolonged treatment is sometimes required, reported survival from A. equuli peritonitis is excellent with appropriate antimicrobial treatment (Golland et al. 1994; Matthews et al. 2001; Watts et al. 2011), even in the case of an immunosuppressed filly (Tennent-Brown et al. 2010). A major clinical difference between acute peritonitis
associated with A. equuli compared to that secondary to intestinal catastrophes is the lack of clinical progression to
Fig 3: Transabdominal ultrasound image of left abdomen caudal to stomach at final presentation demonstrating a substantial accumulation of cellular peritoneal fluid.
© 2017 EVJ Ltd
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