A series of studies has been conducted to expand knowledge of the pathogenicity, epidemiology, and treatment of histomoniasis in chickens and turkeys. The interaction of cecal coccidiosis with histomoniasis in chickens was investigated, using concurrent infections. Cecal lesions from H. meleagridis were severe in all inoculated control groups and did not appear to be affected by the introduction of Eimeria tenella infections. However, the severity of liver lesions and number of birds positive for liver lesions of H. meleagridis increased significantly with the presence of E. tenella. The positive relationship between infections of cecal coccidiosis and H. meleagridis in chickens suggests that, under field conditions, such dual exposure may contribute to increased clinical outbreaks of histomoniasis in chickens. The lateral transmission of H. meleagridis in turkeys was studied in floor pens in the absence of the carrier cecal worm Heterakis gallinarum. One group received no exposure. In other groups, either 10% (LE) or 25% (HE) of the birds were inoculated per cloaca with cultured H. meleagridis (200,000 cells/bird). Inoculated birds died at 10-18 days post-infection (DPI). Uninoculated-birds in the high exposure group (HE) died of histomoniasis beginning 16 DPI, and continued to 100% mortality by day 23 DPI. Uninoculated birds in low exposure group (LE) died beginning on day 19 DPI and continuing through day 31 DPI. All but one LE birds alive on day 31 DPI had severe liver and cecal lesions of histomoniasis at necropsy. There was no evidence of histomoniasis in unexposed birds at the end of experiment. These results suggested that lateral transmission of histomoniasis through a A series of studies has been conducted to expand knowledge of the pathogenicity, epidemiology, and treatment of histomoniasis in chickens and turkeys. The interaction of cecal coccidiosis with histomoniasis in chickens was investigated, using concurrent infections. Cecal lesions from H. meleagridis were severe in all inoculated control groups and did not appear to be affected by the introduction of Eimeria tenella infections. However, the severity of liver lesions and number of birds positive for liver lesions of H. meleagridis increased significantly with the presence of E. tenella. The positive relationship between infections of cecal coccidiosis and H. meleagridis in chickens suggests that, under field conditions, such dual exposure may contribute to increased clinical outbreaks of histomoniasis in chickens. The lateral transmission of H. meleagridis in turkeys was studied in floor pens in the absence of the carrier cecal worm Heterakis gallinarum. One group received no exposure. In other groups, either 10% (LE) or 25% (HE) of the birds were inoculated per cloaca with cultured H. meleagridis (200,000 cells/bird). Inoculated birds died at 10-18 days post-infection (DPI). Uninoculated-birds in the high exposure group (HE) died of histomoniasis beginning 16 DPI, and continued to 100% mortality by day 23 DPI. Uninoculated birds in low exposure group (LE) died beginning on day 19 DPI and continuing through day 31 DPI. All but one LE birds alive on day 31 DPI had severe liver and cecal lesions of histomoniasis at necropsy. There was no evidence of histomoniasis in unexposed birds at the end of experiment. These results suggested that lateral transmission of histomoniasis through a nylon wool column. Horse serum was added (15%), and filtrates were agitated gently in Petri plates, whereupon clusters of H. meleagridis formed. The aggregated suspensions were collected by centrifugation, loaded onto a 2-layer sucrose gradient and centrifuged at 2500 g for 10 min. A band of cells forming between the two layers was collected and washed 2 to 3 times with centrifugation. The resulting clumps of H. meleagridis were free of visible bacteria.