HISTOMONAS 



77 



possible (Frank, 1953), but it is of minor 

 importance. 



Epidemiology: Histomonas is ex- 

 tremely common in Heterakis-irdecieA 

 chickens, and these birds constitute the 

 principal reservoir of infection for turkeys. 

 This accounts for the fact that it is almost 

 impossible to raise turkeys successfully 

 on the same farm with chickens. In addi- 

 tion, wild gallinaceous birds such as the 

 wild turkey, pheasant, quail and ruffed 

 grouse may be infected, but their role as 

 reservoirs of infection for domestic tur- 

 keys has not been properly assessed. 



Birds become infected most commonly 

 by ingesting infected Heterakis eggs. In- 

 fective eggs can survive for one to two 

 years or even longer in the soil. Farr 

 (1956) infected chickens and turkeys with 

 Hisfonioiias from eggs which had been in 

 the soil in Maryland for 66 weeks. 



Pathogenesis : Histomonosis can 

 affect turkeys of all ages; the course and 

 mortality of the disease vary with age. 

 Poults less than 3 weeks old are refrac- 

 tory according to Swales and Frank (1948), 

 but from this age to about 12 weeks, the 

 disease is acute and may cause losses 

 averaging 50% of the flock and ranging up 

 to 100%. The birds often die 2 or 3 days 

 after showing the first signs of disease. 

 In older birds, the disease is more chronic, 

 and recovery may take place. The mortal- 

 ity decreases with age, and losses in these 

 birds rarely exceed 25%. However, even 

 birds of breeding age may be affected. 



Chickens are much less susceptible 

 than turkeys. They ordinarily show no 

 signs of disease, but serious outbreaks 

 may occur in young birds. Histomonosis 

 occasionally occurs in the peafowl (Gray- 

 bill, 1925; Dickinson, 1930), guinea fowl 

 (Graybill, 1925) and quail (GraybiU, 1925). 

 Serious outbreaks may occur in captive 

 ruffed grouse (Tyzzer and Fabyan, 1920; 

 Graybill, 1925) and chukar partridges 

 (Honess, 1956). Altho the parasite occurs 

 in pheasants, it is apparently not very 

 pathogenic for them. 



When the histomonads are released 

 in the cecum, they enter the wall and 



multiply, causing characteristic lesions. 

 Later they pass by way of the blood stream 

 to the liver. 



The incubation period is 15 to 21 days. 

 The first sign of disease is droopiness. 

 The birds appear weak and drov/sy, and 

 stand with lowered head, ruffled feathers 

 and drooping wings and tail. There is a 

 sulfur-colored diarrhea. The head may 

 or may not become darkened. This sign, 

 which is responsible for the name black- 

 head, may also occur in other diseases, 

 so the term is a misnomer. 



The principal lesions of histomonosis 

 occur in the cecum and liver. One or both 

 ceca may be affected. Small, raised pin- 

 point ulcers containing the parasites are 

 formed first. These enlarge and may in- 

 volve the whole cecal mucosa. Sometimes 

 the ulcers perforate the cecal wall and 

 cause peritonitis or adhesions. The mu- 

 cosa becomes thickened and necrotic. It 

 may be covered with a characteristic, foul- 

 smelling, yellowish exudate which may 

 consolidate to form a dry, hard, cheesy 

 plug that fills the cecum and adheres 

 tightly to its wall. The ceca are markedly 

 inflamed and often enlarged. 



The liver lesions are pathognomonic o 

 They are circular, depressed, yellowish 

 to yellowish green areas of necrosis and 

 tissue degeneration. They are not encap- 

 sulated, but merge with the healthy tissue. 

 They vary in diameter up to a centimeter 

 or more and extend deeply into the liver. 

 In older birds the lesions are often con- 

 fluent. 



Other organs such as the kidney and 

 lung may occasionally be affected. P. P. 

 Levine (1947), for example, described 

 numerous white, round areas about 1 mm 

 in diameter in the kidneys of an affected 

 turkey. 



The parasites can be readily found on 

 histologic examination of the lesions. Hy- 

 peremia, hemorrhage, lymphocytic infil- 

 tration, and necrosis occur, and macro- 

 phages and giant cells are present. The 

 pathology of histomonosis in turkeys has 

 been described by Malewitz, Runnels and 

 Calhoun (1958) among others. 



