Comparative Surfaceome Analysis of Clonal Strains with Different Pathogenicity Reveals Strain-Dependent Profiles.

a poultry-specific intestinal protozoan parasite, is histomonosis's etiological agent. Since treatment or prophylaxis options are no longer available in various countries, histomonosis can lead to significant production losses in chickens and mortality in turkeys. The surfaceome of microbial pathogens is a crucial component of host-pathogen interactions.

Experimental reproduction of histomonosis caused by Histomonas meleagridis genotype 2 in turkeys can be prevented by oral vaccination of day-old birds with a monoxenic genotype 1 vaccine candidate.

Histomonosis (syn. blackhead disease) is caused by the protozoan parasite Histomonas meleagridis and can result in high mortality in turkey flocks, a situation driven by the limitation of prophylactic and therapeutic interventions. Multi-locus sequence typing confirmed the existence of two genotypes, with the vast majority of reported histomonosis outbreaks being caused by genotype 1 in contrast to only a few detections of genotype 2.

Comparative investigation of IFN-γ-producing T cells in chickens and turkeys following vaccination and infection with the extracellular parasite Histomonas meleagridis.

The re-emerging disease histomonosis is caused by the protozoan parasite Histomonas meleagridis that affects chickens and turkeys. Previously, protection by vaccination with in vitro attenuated H. meleagridis has been demonstrated and an involvement of T cells, potentially by IFN-γ production, was hypothesized.

Co-infection of Chicken Layers With and Avian Pathogenic Is Associated With Dysbiosis, Cecal Colonization and Translocation of the Bacteria From the Gut Lumen.

Histomonosis in chickens often appears together with colibacillosis in the field. Thus, we have experimentally investigated consequences of the co-infection of birds with and avian pathogenic (APEC) on the pathology, host microbiota and bacterial translocation from the gut. Commercial chicken layers were infected via oral and cloacal routes with -tagged APEC with or without whereas negative controls were left uninfected.