78 



HISTOMONAS 



McGuire and Cavett (1952) studied the 

 effect of histomonosis on the blood picture 

 of experimentally infected turkeys. The 

 non-protein nitrogen, uric acid and hemo- 

 globin levels declined progressively, but 

 tended to recover just before death. The 

 blood sugar rose during the incubation 

 period but decreased during development 

 of the liver lesions; severe hypoglycemia 

 was present just before death. The total 

 leucocyte count rose as the result of pro- 

 liferation of heterophils, myelocytes and 

 monocytes. 



If the birds recover, the protozoa dis- 

 appear from the tissues, and repair takes 

 place. The exudate and necrotic tissue in 

 the ceca are incorporated into the cecal 

 plug, which becomes smaller and is finally 

 passed. U the lesions were not too severe, 

 the ceca may eventually appear entirely 

 normal, but in other cases there may be 

 so much scarring that the lumen is oblit- 

 erated. In the repair process, the lesions 

 are invaded by blood vessels, lymphoid 

 cells and connective tissue. The liver 

 lesions may be completely repaired or 

 there may be extensive scar tissue. 



Immunity : Birds which recover from 

 histomonosis are immune to reinfection. 

 In addition, as mentioned above, suscep- 

 tibility decreases with age. 



Lund (1959) found that infection of tur- 

 keys with a nonpathogenic strain of Histo- 

 monas did not protect the birds against 

 subsequent infection with a pathogenic 

 strain introduced by feeding Heterakis eggs, 

 altho it did afford some protection against 

 rectally introduced pathogenic histomonads. 



Diagnosis : Histomonosis can be di- 

 agnosed from its lesions. Those in the 

 liver are pathognomonic. In case of doubt 

 and in order to differentiate the liver le- 

 sions from those caused by tumors, tuber- 

 culosis or mycotic infections, histologic 

 examination is desirable. The cecal le- 

 sions can be distinguished from those 

 caused by coccidia by microscopic exam- 

 ination of scrapings from the mucosa. 



Cultivation : Histomonas was first 

 cultivated by Drbohlav (1924) in a diphasic 

 medium consisting of coagulated egg white 



slants overlaid with blood bouillon contain- 

 ing 1% peptone. It has since been culti- 

 vated in a number of other media, both di- 

 phasic and monophasic (Tyzzer, 1934; 

 De Volt and Davis, 1936; Bishop, 1938). 

 Delappe (1953, 1953a) found that addition 

 of penicillin or streptomycin or both to 

 Laidlaw's culture medium facilitated the 

 initial isolation of the protozoa, but he was 

 unable to obtain axenic cultures. When the 

 bacteria disappeared, the protozoa did 

 likewise. 



Treatment: Since histomonosis can 

 be prevented by proper management, drug 

 therapy should be regarded as a secondary 

 line of defense against the disease. The 

 chemotherapy of this disease has been re- 

 viewed by Wehr, Farr and McLoughlin 

 (1958). 



While a number of phenylarsonic acid 

 and quinoline derivatives have been used 

 with some success in the past, the only 

 one of them which is now used to any extent 

 is 4-nitrophenylarsonic acid. When fed as 

 0.0125 to 0.075% of the mash or 0.006 to 

 0. 04% of the drinking water for 3 days be- 

 fore and 21 days after experimental infec- 

 tion, this compound prevents death. How- 

 ever, there is a high relapse rate following 

 cessation of treatment. Hence, to be effec- 

 tive this compound must be fed continuously 

 until 5 days before slaughter. Mashes con- 

 taining 0.01 to 0.03% of this compound 

 stimulate growth, but 0.02% in the drinking 

 water decreases egg production of adults 

 and growth and livability of poults (Moreng 

 and Bryant, 1956). 



Thiazole derivatives are used most 

 commonly against histomonosis. Three of 

 these are enheptin, acetylenheptin, and 

 nithiazide (Hepzide). The first is 2-amino- 

 5-nitrothiazole, and the other two are de- 

 rivatives of it. Enheptin was introduced 

 by Waletzky, Clark and Marson (1950), 

 and its activity was confirmed by a number 

 of workers, including McGregor (1953), 

 Jungherr and Winn (1950), DeVolt, Tromba 

 and Hoist (1954), and Joyner and Kendall 

 (1955). Acetylenheptin (2-acetylamino-5- 

 nitrothiazole) was found by Grumbles, 

 Boney and Turk (1952, 1952a, 1952b) to be 

 just as effective as enheptin; it was also 

 studied by Brander and Wood (1955) and 



