EQUINE VETERINARY EDUCATION / AE / MAY 2018


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During follow-up assessment 3 days post-presentation, a circular structure with a thickened double wall was evident on abdominal ultrasonography (total diameter 60 mm, wall thickness 15 mm) (Fig 5). Caecocaecal or caecocolic intussusception was suspected. A faecal nematode egg count identified <200 epg. Faecal flotation for cestodes was not performed. Faecal sedimentation was positive for G. aegyptiacus ova. Three faecal cultures obtained no growth of Salmonella spp. The horse was treated with a combined oxyclozanide/levamisole product (Tramizan10, oxyclozanide 7.5 mg/kg bwt per os, levamisole 5.6 mg/kg bwt per os). Despite mild intermittent colic signs, lethargy and occasional mild tachycardia, reintroduction of food was tolerated and medication discontinued. The horse was discharged with instructions to return if there was clinical deterioration, but otherwise in 2 weeks for repeat assessment. On follow-up assessment the owner described resolution of colic signs and a normal demeanour at home. Clinical examination was normal and abdominal ultrasonography did not detect the previously described circular structure. Faecal sedimentation was negative for G. aegyptiacus ova.


Discussion


Gastrodiscus aegyptiacus has been previously described in small numbers of equine colic cases (Azzie 1975; Applewhaite and Ruiz 1983). In the present case series, typhlocolitis as well as caecocaecal and caecocolic intussusceptions are reported in association with G. aegyptiacus infestation. Although G. aegyptiacus cannot definitively be determined as the cause of the disease reported here, the unusual and consistent presence of these parasites in cases of caecocaecal or caecocolic intussusception justifies further investigation into the possibility of an aetiopathological role. Demonstration of causation by any gastrointestinal


pathogen in a clinical context is challenging due to the likelihood of a mixed infection. Not only can the gastrointestinal tract be concurrently infected/infested with many pathogens, but compromise by one pathogen may lead to increased ease of colonisation by another. Horses can carry Salmonella spp. without bacterial shedding, yet may


subsequently shed under times of physiological stress (House et al. 1999; Kim et al. 2001; Ernst et al. 2004). Three cases in this series (43%) were identified as shedding Salmonella at some point during hospitalisation. This is higher than the overall prevalence of Salmonella shedding (11%) detected on routine faecal screening in the equine population at the OVAH. It is possible that Salmonella could have played a role in the clinical signs observed, or influenced the relative pathogenicity of G. aegyptiacus in the gut. However, it is also possible that Salmonella shedding developed secondary to physiological stress from factors such as transport, antimicrobial treatment or G. aegyptiacus infestation. Only one of the cases in this series (Case 2) had a


cestode faecal flotation technique performed (Rehbein et al. 2011); this was negative for A. perfoliata infestation. Immunodiagnostics for cestode infestation were not performed as this is not available in South Africa. During necropsy however, A. perfoliata was not seen in any case so it is unlikely that this parasite was involved in these cases. In all four of the cases previously reported with


cyathostominosis and caecal intussusception clinical signs of diarrhoea were described. Additionally, faecal cyathostomin larvae were present in all cases (Mair et al. 2000). Only one case of caecal intussusception reported in the current series had diarrhoea, and no cases demonstrated faecal cyathostomin larvae. Furthermore, no cases of caecal intussusception had a nematode egg count greater than 200 epg. In the current case series histological assessment of the intestine was only performed for Cases 1 and 4. No encysted cyathostomin larvae were observed upon histological assessment of these cases. Although it is acknowledged that these findings do not exclude a role for cyathostomins in these cases, it is considered by the authors to be unlikely in the present case series. If G. aegyptiacus is pathogenic, the factors determining


which animals are affected are yet to be determined. It is recognised for a number of parasitic species that amongst a population of animals, some individuals will develop heavier parasite burdens than others (Relf et al. 2013). Furthermore, some will develop clinical signs and some will not (Proudman and Edwards 1993). The specific host factors involved in defence against parasite infestation are minimally understood in the horse. Work in ruminants has demonstrated specific genetic elements associated with resistance to infestation (Stear et al. 1999). The extent of clinical signs seen with G. aegyptiacus


Fig 5: Ultrasonographic image of a suspected caecal intussusception (Case 7).


infestation may or may not be related to the level of parasite burden. An association between the severity of intestinal pathology and number of parasites present has been demonstrated for A. perfoliata and cyathostomin species (Murphy and Love 1997; Pavone et al. 2011). In this series, all cases subject to necropsy examination had heavy G. aegyptiacus burdens (individual parasite counts were not performed) as demonstrated in Fig 3. Furthermore, another horse from the same property as Case 2 developed caecal intussusception (caecocolic) and at necropsy was observed to have a severe G. aegyptiacus infection. This case was not included in our case series due to the absence of a number of important pieces of information. This supports the suggestion that heavy burdens may be more likely to be associated with severe disease. At necropsy the intussuscepted caeca all showed severe macroscopic circulatory changes due to the intussusception (variable


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