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EQUINE VETERINARY EDUCATION
Equine vet. Educ. (2019) 31 (8) 398-402 doi: 10.1111/eve.12874
Case Report
Actinobacillus capsulatus peritonitis and chyloabdomen in a Warmblood gelding
A. M. Cullimore* , G. D. Lester and N. Stephens School of Veterinary and Life Sciences, Murdoch University, Murdoch, Western Australia, Australia. *Corresponding author email:
acullimore@hotmail.com Dr A. M. Cullimore’s Present address: Ascot Equine Veterinarians, Ascot, Western Australia, Australia
Keywords: horse; abdomen; Actinobacillus; chyle; peritonitis; chyloperitoneum
Summary Primary peritonitis in horses attributable to Actinobacillus equuli has been reported in Australia, New Zealand and North America. Published reports describe a rapid response to treatment with appropriate antimicrobial and supportive treatment and an excellent prognosis for survival. To our knowledge, this is the first reported case of Actinobacillus capsulatus in the horse. The case was complicated by the development of an idiopathic chylous abdominal effusion. The report highlights the importance of molecular methods in the correct identification of bacterial species. Prognosis for horses diagnosed with Actinobacillus peritonitis may be guarded given the atypical response to appropriate antimicrobial treatment in this case.
Introduction
Peritonitis, or inflammation of the peritoneum, in horses results from a number of infectious and noninfectious causes (Hall 2015). Most cases occur secondary to gastrointestinal disease (Elce 2006) or following urogenital trauma (Hall 2015). Primary peritonitis is uncommon in the adult horse (Gay and Lording 1980; Davis 2003; Tennent-Brown et al. 2010; Hall 2015) but is usually caused by
Streptococcus zooepidemicus,
Streptococcus equi subspecies equi, Corynebacterium pseudotuberculosis or Actinobacillus equlli (Stewart 2006). Primary peritonitis in horses attributable to Actinobacillus
equuli has been reported in Australia (Gay and Lording 1980; Golland et al. 1994; Matthews et al. 2001), New Zealand (Mogg and Dykgraaf 2006) and North America (Patterson- Kane et al. 2001; Stewart 2006; Tennent-Brown et al. 2010). Cases typically present with an acute onset of mild to moderate signs of abdominal pain, tachycardia, tachypnoea, fever, lethargy and inappetence (Gay and Lording 1980; Golland et al. 1994; Matthews et al. 2001, 2002; Mogg and Dykgraaf 2006; Watts et al. 2011). Published reports of primary Actinobacillus peritonitis
cases describe a rapid response to treatment with appropriate antimicrobial and supportive treatment (Gay and Lording 1980; Golland et al. 1994; Matthews et al. 2001; Mogg and Dykgraaf 2006; Watts et al. 2011) and an excellent prognosis for survival (Gay and Lording 1980; Golland et al. 1994; Matthews et al. 2001, 2002; Mogg and Dykgraaf 2006; Stewart 2006). This case describes the diagnosis, treatment and atypical
outcome of a 13-year-old Warmblood gelding that was referred to The Animal Hospital at Murdoch University for further investigation of peritonitis.
© 2017 EVJ Ltd Clinical features
History A 13-year-old Warmblood gelding presented to the referring veterinarian with acute onset of mild colic, lethargy and inappetence of less than 12 h duration. Abdominal
ultrasound demonstrated a mild increase in free peritoneal fluid. Peritoneal fluid was a strawberry colour, with a total nucleated cell count (TNCC) of 19,400 cells/lL (predominately nondegenerate neutrophils [79%]) and a total protein (TP) of 26 g/L, consistent with a diagnosis of peritonitis. The gelding was referred for further investigation and treatment.
Initial clinical findings On presentation, the gelding was tachycardic (heart rate: 80 beats/min), tachypnoeic (64 breaths/min) and febrile (rectal temperature: 39.4°C). Gingival mucous membranes were pink but tacky, with a normal capillary refill time. Intestinal sounds were present but reduced on auscultation. Abdominal ultrasound (Fig 1) and peritoneal fluid character (Fig 2) and cytology were consistent with that already reported. In addition, peritoneal fluid lactate was increased (7.3 mmol/L), glucose was 3.1 mmol/L, and pH of 7.203 and extracellular bacterial rods were observed. No abnormalities were detected on rectal palpation of the abdomen and no nasogastric reflux was present. Bloodwork performed demonstrated a leucopenia (WBC: 2.0 9 109 cells/L) and increased haematocrit (0.48 L/L). Venous lactate was within normal limits (1.7 mmol/L). A diagnosis of peritonitis was thus confirmed and peritoneal fluid was submitted for aerobic and anaerobic culture and sensitivity.
Treatment As the gelding appeared relatively stable and was not actively colicking, medical treatment with broad-spectrum antimicrobials [benzyl penicillin (22,000 IU/kg bwt, i.v. q. 6 h), gentamicin (6.6 mg/kg bwt, i.v., s.i.d.) and metronidazole (25 mg/kg bwt, per os, b.i.d.)], anti-inflammatories (flunixin 1.1 mg/kg bwt i.v.) and intravenous fluid therapy (Hartmann’s solution, approximately 100 mL/kg bwt/day) were instituted. Over the course of the next 24 h, the gelding remained tachycardic, although respiratory rate and temperature normalised. On repeat abdominal ultrasound the next day, there was no apparent change in the appearance or volume of free peritoneal fluid. Repeat rectal palpation was again considered within normal limits. Blood work confirmed that the gelding’s hydration status was corrected and medical management was continued, although intravenous
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