Abstract
Clostridium perfringens is an important food-borne zoonotic pathogen and a member of the commensal gut microbiome of many mammals. Predisposing factors such as coinfection with other pathogens or diet change can, however, cause overgrowth and subsequent disease development. Here we investigated the occurrence of C. perfringens in a free-ranging badger population with up to 100% prevalence of herpesvirus infection. Herpesvirus reactivation is known to be associated with increased susceptibility bacterial infections. PCR screening of rectal swabs from 69 free-ranging badgers revealed 15.9% (11/69, 95% CI = 9.1–26.3%) prevalence of detectable C. perfringens (Type A) DNA in the digestive tracts of assymptomatic animals. The results of Fisher’s exact test revealed C. perfringens detection was not biased by age, sex and seasons. However, badgers with genital tract gammaherpesvirus (MusGHV-1) reactivation (p = 0.007) and infection with a specific MusGHV-1 genotype (p = 0.019) were more prone to of C. perfringens proliferation, indicating coinfection biased dynamics of intestinal C. perfringens. An inclusion pattern analysis further indicated that, causally, MusGHV-1 reactivation potentiated C. perfringens detection. Whether or not specific MusGHV-1 genotype infection or reactivation plays a role in C. perfringens overgrowth or disease development in badgers will require further investigation. Nevertheless, a postmortem examination of a single badger that died of fatal disease, likely associated with C. perfringens, revealed MusGHV-1 detection in the small intestine.
Highlights
Infections generally remain sub-patent, clinically severe disease can occur when host immunity is compromised due to senescence, stress responses, coinfections or neoplastic disease conditions (Sehrawat et al 2018). One such comorbidity factor is the proliferation of Clostridium perfringens, as reported in Asian elephant calves (Elephas maximus) diagnosed with fatal Elephant endotheliotropic herpesvirus (EEHV) infection (Boonsri et al 2018), and dairy cows (Frazier et al 2002) and other captive artiodactyls (Flach et al 2002) with Bovine herpesvirus 4 (BHV-4) infection
We found no overall association between rectal swab MusGHV-1 and C. perfringens detection rate (Fisher’s exact test: p = 1), nor any effect of season, sex, or age (Table 2)
We identified an imbalance of observations in the opposite diagonal of the inclusion correlation matrix (Fig. 1 provides a 2 9 2 matrix of MusGHV-1 DNA detected in genital swabs (x) and C. perfringens DNA detected in rectal swabs (y), collected concurrently from the same individual, where a = 9, b = 23, c = 2, d = 34, Fig. 1b)
Summary
A 3-year study by Vierheilig et al (2013) revealed higher prevalence and abundance of C. perfringens in the feces of Carnivora than of ruminant wildlife species; another study by Cox et al (2005) reported similar findings These results suggest diet plays an important role in the epidemiology of C. perfringens (Silva et al 2014), and second, that carnivores (such as feral dogs, cats, fish-eating avian species, foxes or badgers), omnivores (wild boar or domestic chickens) or scavengers (vultures) (Meng et al 2017) may be significant sources of environmental C. perfringens contamination. This would evidence that detection of either pathogen was not dependent and that one caused a predisposition to infection with the other; that is, when b is greater than c (or when c is greater than b), infection of pathogen x is highly likely to predispose infection with pathogen y (or y is highly likely to predispose for x) (Cavali-Sforza and Bodmer 1972)
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