Does Salmonella co-infection worsen Histomonas meleagridis infection in turkeys?

Abstract

Histomoniasis, caused by Histomonas meleagridis (HM), leads to severe cecal and hepatic damage in turkeys. Although Salmonella Typhimurium (ST) commonly colonizes in the cecum, its influence on the progression of Histomoniasis remains unclear. This study was conducted to evaluate whether ST co-infection alters clinical outcomes, intestinal integrity, or performance in HM-challenged turkey poults. A total of 336 one-day-old male poults were allocated into four treatments in a 2 &#xd7; 2 factorial design with 6 replicates/treatment. Negative control (NC), HM challenge (T1), ST challenge (T2), and HM+ST challenge (T3). Birds were inoculated at d 18 and monitored for performance, mortality, lesions, gut permeability, Salmonella colonization, intestinal morphology, and hepatic apoptosis-related gene expression. HM challenge significantly reduced body weight, body weight gain, and feed intake while increasing FCR, mortality, and cecal and hepatic lesion scores (P < 0.01). ST challenge alone caused strong cecal colonization but remained subclinical, with no effect on performance, gut permeability (d28), clinical score, or lesion development. No HM &#xd7; ST interaction effects were detected for performance, mortality, gut integrity, or lesion severity. ST colonization levels were unaffected by HM co-infection. Histologically, HM reduced duodenal villus height and markedly increased cecal muscularis thickness, whereas ST caused only mild changes, with limited interaction effects that did not translate to worsened disease symptoms. Liver apoptosis-related gene expression analyses showed reduced mRNA expression of BAX and Caspase-3 in all challenged groups compared with the NC, while BCL-2 mRNA expression was elevated only in co-infected poults; however, these transcriptional changes were not accompanied by corresponding differences in pathological outcomes. In conclusion, HM was the primary driver of the disease, impairing growth and inducing severe lesions, whereas ST behaved as a subclinical colonizer that did not intensify Histomoniasis. These findings indicate that ST does not worsen HM-induced performance loss, lesions, or mortality under the current challenge model, reinforcing that ST remains a food-safety concern rather than a major contributor to Histomoniasis severity.