No abstract

Heat stress has been found to cause adverse effects on small intestinal microstructure, but little is known about its impact on chicken's cecum. In this research, the histopathological alterations of broiler chicken's cecum following chronic heat stress were evaluated. 20 broiler chickens were randomly divided into control group and treatment group containing 10 replicates, respectively. Both groups were reared under standard conditions until 21 days of age. From day 22 to day 42, the control group was kept at 24-28⁰C as well as relative humidity of 40-55%, while the treatment group was exposed to high temperature of 36-40⁰C and relative humidity of 45-65% for eight hours per day. At the end of the period, proximal part of each chicken's cecum was collected and made into histopathological slides with Hematoxylin and Eosin staining. Villus height, villus width, crypt depth, villus surface area, and villus height to crypt depth ratio were examined from 10 villi per replicate. Results analysis revealed that chronic heat stress profoundly (P<0.05) reduced the crypt depth. Insignificant (P>0.05) changes of the villus despite the longterm heat exposure might imply that the damage is at its early phase. In conclusion, chronic heat stress can produce morphological alterations in the ceca of broiler chickens, though requiring longer duration due to cecum's durability.

Infection with intestinal whipworms (Trichuris spp.) causes widespread morbidity and may alter responses to enteric and extraintestinal co-infections. Here, we show that Trichuris muris infection in mice increases co-infection with two evolutionary divergent enteric pathogens, the bacterium Citrobacter rodentium and the helminth Heligmosomoides polygyrus. Co-infection caused reduced weight gain and promoted type-1-biased inflammation. In contrast, T. muris-infected mice were more resistant to migrating Ascaris suum larvae in the lungs. Our results highlight the divergent nature of pathogen interactions, and suggest that whipworm infection is a risk-factor for co-infections with other pathogens within the gastrointestinal tract.