Pathogenesis of Histomonosis in Experimentally Infected Specific-Pathogen-Free (SPF) Layer-Type Chickens and SPF Meat-Type Chickens

Abstract

Several studies have shown differences in the course of histomonosis, the infection with the trichomonad parasite Histomonas meleagridis, in different chicken breeds. In the present study, 10 specific-pathogen-free (SPF) layer-type (LT) chickens and twelve SPF meat-type (MT) chickens were infected intracloacally with 200,000 H. meleagridis trophozoites. One and two weeks postinfection (p.i.), three birds of each group were euthanatized. The remaining birds were euthanatized 3 wk p.i. Infected birds showed severe gross lesions typical for histomonosis in ceca at the first and second week p.i., while livers showed necrotic foci at 2 and 3 wk p.i., but only very rarely at 1 wk p.i. Differences between groups in the severity of lesions were statistically insignificant. In histopathology, LT chickens showed a significantly more-severe necrosis and ablation of the cecal epithelium 1 wk p.i. Parasites without inflammation were also found in most investigated spleens and lungs but only in a few kidneys. Investigation of these organs for histomonal DNA by real-time PCR confirmed these results. In addition, the humoral immune response against histomonal actinin 1 and 3 was measured by an ELISA. The humoral immune response against actinin 1 started sooner and was significantly higher in LT chickens than in MT chickens. In conclusion, the results of the present study suggest that the genetic background of the birds influences the reaction to infection with H. meleagridis.

Histomonosis - an existing problem in chicken flocks in Poland

“…It is connected with the mechanism of early immune response activated in the intestinal mucosa, especially in caecal tonsils (Powell et al 2009 ; Windisch and Hess 2010 ). Lotfi et al ( 2014 ) suggested that, the genetic background of the chickens influences the reaction to infection with H. meleagridis .…”

“…It is considered that the type of poultry farming and hygienic conditions significantly influence the spread of the disease (Esquenet et al 2003 ; Grafl et al 2011 ). Renewed efforts in histomonosis investigations have led to new insights into the epidemiology and molecular characterization of H.meleagridis (Grabensteiner et al 2006 ; Hess et al 2006 ; Hu et al 2006 ; Bilic et al 2014 ; Lotfi et al 2014 ; Hess et al 2015 ). In order to improve control strategies, the research studies have boosted to develop of new treatment and prophylactic strategies including vaccination (Hu and McDougald 2002 ; Bleyen et al 2009 ; Hafez et al 2010 ; Van der Heijden et al 2011 ; Liebhart et al 2013 ; Hess et al 2015 ).…”

Excretion of Histomonas meleagridis following experimental co-infection of distinct chicken lines with Heterakis gallinarum and Ascaridia galli

“…Differences in the genetic resistance of layer chickens have been shown in nematode infections [ 13 , 14 ]. Infections with H. meleagridis without H. gallinarum suggested differences in the susceptibility between different chicken lines based on the immune response [ 15 , 16 ]. Contrarily, no significant difference in the occurrence of lesions was reported in four commercial layer strains of chickens after experimental infection with a clonal culture of H. meleagridis [ 17 ].…”

Histomonosis in Poultry: A Comprehensive Review

“…Histomonads have been observed in the bursa of Fabricius of 6-weekold commercial chickens diagnosed with histomonosis, further implicating the intracloacal route for natural infection (63). Although less common, H. meleagridis has also been shown to infect areas including the brain, pancreas, heart, lungs, kidneys, and spleen (64)(65)(66)(67)(68). Turkeys are especially vulnerable to histomonosis, and chickens (Figure 5) are less susceptible but function to serve as reservoirs and can develop the disease (17).…”