EQUINE VETERINARY EDUCATION / AE / AUGUST 2019
401
This case was also complicated by the development of Fig 4: Post-mortem image of the right side of the abdomen with
abdominal organs in situ demonstrating generalised fibrinosuppurative peritonitis.
SIRS and shock (Gay and Lording 1980). The cytological profile of peritoneal fluid of horses with Actinobacillus equilli peritonitis is characterised by the predominance of nondegenerate neutrophils (Gay and Lording 1980; Golland et al. 1994; Matthews et al. 2001; Mogg and Dykgraaf 2006; Stewart 2006; Tennent-Brown et al. 2010; Watts et al. 2011). This contrasts to the profile of peritoneal fluid in peritonitis cases due to an intestinal catastrophe, in which neutrophils demonstrate severe degenerative changes (Gay and Lording 1980), suggesting that A. equuli is of low toxicity. In our case, peritoneal fluid cytology at initial presentation was consistent with that of a classic A. equilli peritonitis, with a predominance of nondegenerate neutrophils. However, the peritoneal fluid findings of predominately degenerate neutrophils at final presentation were highly inconsistent to that of other reports of A. equilli peritonitis, despite yielding a pure growth of an Actinobacillus spp. The pertinent difference in our case was the identification of Actinobacillus capsulatus on PCR. Historically, the classification of Actinobacillus species has
been made on the basis of phenotypic or biochemical characteristics, which can be a difficult and unreliable task (Sternberg and Brandstrom 1999; MacInnes 2010). In an Australian study that re-examined previously diagnosed isolates of A. equuli using a more extensive range of phenotypic tests, 7 of 16 of the isolates were demonstrated to have been misclassified as A. equuli, one of which was re- classified as Actinobacillus capsulatus (Blackall et al. 1997). The family Pasteurellaceae and genus Actinobacillus have undergone a long series of taxonomic revisions (Naushad et al. 2015) and increasing emphasis has been directed to the division of bacteria into groups based on molecular methods (MacInnes 2010). Our case highlights the importance of such methods in the correct identification of species, as outlined by the identification of A. capsulatus in both peritoneal and pericardial fluid at post-mortem, as the prognosis of such cases in the future may be guarded. Unfortunately, we did not use molecular methods to further identify the species of Actinobacillus present at initial presentation and thus cannot definitively identify the initial species present.
chyloabdomen, an uncommon cause of abdominal effusion in the horse (May and Good 2007; Cesar et al. 2010; Fish et al. 2015). Chyloabdomen develops when lipid-rich fluid from a mesenteric lymphatic vessel leaks into the abdominal cavity due to vessel rupture or increased intralacteal pressure due to obstruction. Differentials that could cause this include trauma, tears induced by intra- abdominal adhesions, intra-abdominal lymphadenopathy, primary or secondary lymphangiectasia, thoracic duct disease, cardiac disease, fungal disease, neoplasia or congenital anomalies of lymphatics (Nelson 2001; May and Good 2007; Cesar et al. 2010; Fish et al. 2015). The assumption in our case was that the gelding developed a primary peritonitis that may have led to adhesion formation within the abdominal cavity, which at some point may have damaged a lymphatic duct and ruptured into the abdomen, causing ongoing but improving chyloabdomen. The aetiology of chylous effusion in many cases can be difficult to determine and thus remain termed idiopathic (Meadows and MacWilliams 1994). Despite a thorough post- mortem examination, the definitive cause of chyloabdomen could not be found in our case.
Conclusion
To our knowledge, this is the first reported case of Actinobacillus capsulatus in the horse. The case highlights the importance of molecular methods in the correct identification of bacterial species. Failure of horses diagnosed with Actinobacillus peritonitis to respond rapidly to appropriate antimicrobial treatment should prompt further investigation and could result in a guarded to poor prognosis.
Authors’ declaration of interests No conflicts of interest have been declared.
Ethical animal research
Ethical review not applicable for this retrospective case report.
Source of funding None.
Acknowledgements Special thanks to Drs Aswin Beck and Eleanor Crispe for their contribution to veterinary care in this case.
Authorship
A. Cullimore managed the clinical case and prepared the manuscript. N. Stephens performed the post-mortem and contributed to the description of necroscopy findings. G. Lester managed the clinical case and edited the manuscript. All authors approved the final manuscript.
Manufacturer's address 1Western Diagnostic Pathology, Myaree, Western Australia, Australia.
© 2017 EVJ Ltd
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80 |
Page 81 |
Page 82 |
Page 83 |
Page 84 |
Page 85 |
Page 86 |
Page 87 |
Page 88
