EQUINE VETERINARY EDUCATION Equine vet. Educ. (2018) 30 (4) 197-199 doi: 10.1111/eve.12839


Clinical Commentary


Mycobacterial infections in equids: Clinical characteristics and diagnostic techniques


D. G. M. Sutton†* and A. L. Michel‡ †Weipers Centre Equine Hospital, School of Veterinary Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK; and ‡Bovine Tuberculosis and Brucellosis Research Programme, Department of Veterinary Tropical Disease, Faculty of Veterinary Science, University of Pretoria, Pretoria, South Africa. *Corresponding author email: david.sutton@glasgow.ac.uk


Summary Mycobacterial infections in equids are relatively rare but the case report (Charlesworth 2018) detailed in this issue highlights that Mycobacterium bovis infections may still result in clinical signs in this incidental host and have zoonotic potential. Most reported cases of M. bovis in horses have a protracted disease course, with features including pyrexia, weight loss and oedema with a nonspecificinflammatory profile. As such, the clinical features of disease overlap with conditions such as neoplasia, peritonitis, protein-losing enteropathies and bacterial infections including Rhodococcus equi and Lawsonia intracellularis. In this clinical satellite article, mycobacterial infections in equids are considered in terms of incidence and mode of transmission, key clinical features and perhaps most importantly, in terms of the diagnostic techniques that can be used in order to reach a definitive (ante mortem) diagnosis. The major zoonotic risk to veterinary personnel is likely to occur at the time of post-mortemexamination of infected horses, and awareness of these potential risks remains of the utmost importance.


Mycobacterial infections rarely feature in lists of differential diagnoses in equine medicine, but in this issue, a case of multisystemic bovine tuberculosis in a pony residing in the UK is reported (Charlesworth 2018). Historically, prior to improved control measures for Mycobacterium bovis, the reported incidence of granulomatous tubercles in the viscera of equine specimens was as high as 2% in one Czech abattoir survey (Krejci 1958), with equine infection rates linked to stocking densities of co-grazing infected cattle. The widespread implementation of the intradermal tuberculin test for cattle with culling of positive reactors is likely to account for the drop off in confirmed cases of bovine tuberculosis (bTB) in horses, such that mycobacteria in the avian complex (MAC) have become relatively more important in this species (Pavlik et al. 2004, 2008; Kriz et al. 2010; M€


onki et al. 2016). The case reported here highlights the fact that horses


may still contract and harbour M. bovis for prolonged periods of time during which the infection may be activated and result in clinical manifestation. Due vigilance is required by equine veterinarians due to the zoonotic nature of M. bovis infection. The main route of infection for bTB in horses is thought to be ingestion (Sarradell et al. 2015) with the primary disease complex developing in the intestine and mesenteric lymph nodes (Monreal et al. 2001) then leading to faecal shedding of organisms. The pulmonary form of the disease in


equids is more likely to occur via aerosol transmission from infected cattle (Keck et al. 2010; Hlokwe et al. 2016) and may present a greater zoonotic risk to personnel in close contact than the intestinal form. Horses and other perissodactyls have been considered to


be relatively resistant to M. bovis infection compared with other domestic and wild animal species (O’Reilly and Daborn 1995; Michel et al. 2017). In the case reported here, the affected pony had concurrent pars pituitary intermedia dysfunction (PPID), which has been linked anecdotally to higher incidence of secondary infections (McFarlane 2011) and increased severity of fungal (Randleff-Rasmussen et al. 2017) and parasitic disease (McFarlane et al. 2010; Raftery et al. 2015). Horses with PPID have been demonstrated to have less effective neutrophil activity due to reduced oxidative burst and impaired chemotaxis (McFarlane et al. 2015). A familial immunodeficiency was also suspected to be present in two sibling Fjord horses, both of which developed enteric infection with Mycobacterium avium subsp. hominissuis (Kriz et al. 2010). Clinical disease in humans infected with Mycobacterium tuberculosis is much higher among HIV- positive individuals (WHO 2009). Characterisation of the immune response to different pathogens is required in equine PPID, but it would be reasonable to expect that this defined population may be at increased risk of developing clinical signs of mycobacterial disease in the face of sufficient challenge. The effect of pergolide treatment on cell mediated immunity in PPID ponies has still to be proven.


Clinical signs


The clinical signs of M. bovis infection in horses are variable depending on the primary organ affected and whether or not there is generalised infection. Alimentary infections cause granulomatous enterocolitis resulting in chronic weight loss, oedema, lethargy, diarrhoea and intermittent pyrexia with insidious progression (Sarradell et al. 2015; M€


onki et al. 2016).


Mesenteric lymph nodes are likely to be enlarged on palpation per rectum and there may be a nodular profile to the spleen. The disease course may last several months with progressive wasting and ventral oedema. Key differential diagnoses are likely to include neoplasia, peritonitis, protein-losing enteropathies and Lawsonia intracellularis infections in younger horses. Pulmonary infections may cause coughing, pyrexia and epistaxis if there is a single tuberculous granuloma (Hlokwe et al. 2016), whereas secondary miliary pulmonary infiltration results in chronic weight loss, sternal oedema, dyspnoea, nasal


© 2017 EVJ Ltd


197

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