Disease: Hexamitosis, infectious catarrhal enteritis.
Hosts: Turkey, peafowl, California valley quail, Gambel's quail, chukar partridge, ring-neck pheasant, golden pheasant. See Levine, Beamer and McNeil (1952) for references. H. meleagridis has been transmitted from the turkey to the chicken, quail and domestic duck, and from the ring-neck pheasant, quail and chukar partridge to the turkey.
Location: Duodenum and small intestine of younger birds; some occur in the cecum and bursa of Fabricius, especially in adults.
Geographic Distribution: United States, Canada, Great Britain, South America (Uruguay). The distribution of hexamitosis in California has been discussed by Hinshaw, McNeil and Kofoid (1938). It has been reported from Connecticut by Jungherr and Gifford (1944), from Indiana by Doyle, Cable and Moses (1947), from Virginia by Farr, Wehr and Jaquette (1948), from Alberta by Vance and Bigland (1956), from Scotland by Campbell (1945) and from England by Slavin and Wilson (1953). It also occurs in Illinois.
Prevalence: The published reports of outbreaks of hexamitosis are too few to give a true picture of its importance. It occurs in all major turkey producing areas in the United States and in other countries as well. It appears to be particularly important in California. The U. S. Dept, of Agriculture (1954) estimated that it causes an annual loss of $667,000 in turkeys in the United States.
Morphology: The body is 6 to 12 u long and 2 to 5 u wide, with a mean of 9 by 3 u. The two nuclei contain round endosomes 2/3 the diameter of the nucleus. Anterior to each nucleus is a large blephararoplast or group of blepharoplasts from which 2 anterior and 1 anterolateral flagella arise. Just behind this blepharoplast is another from which the caudal flagellum arises. The caudal flagella pass posteriorly in a granular line of cytoplasm to their points of emergence near the posterior end of the body. Hexamita moves rapidly without the spiralling characteristic of trichomonads.
Life Cycle: Multiplication is by longitudinal binary fission. Slavin and Wilson (1953) and Wilson and Slavin (1955) described what they believed to be schizogony and cyst formation, but Hoare (1955) considered their idea to be purely speculative and inacceptable.
Pathogenesis: Hexamitosis is a disease of young birds; adults are symptomless carriers. The mortality in a flock may be as high as 70 to 80%, but heavy losses seldom occur in poults over ten weeks old. Affected poults appear nervous at first, have a stilted gait, ruffled, unkempt feathers, and a foamy, watery diarrhea. They usually continue to eat, but chirp continually. They lose weight rapidly, become listless, weak and finally die. Birds often do not appear to be ill until shortly before death, but examination will reveal that they are thin and have lowered temperatures. Birds which recover grow poorly, and an outbreak may leave many stunted birds in its wake.
The incubation period is 4 to 7 days. Poults may die within a day after signs appear. In acute outbreaks, the mortality reaches a peak in the flock in 7 to 10 days after the first birds die; in other flocks, deaths may continue for 3 weeks.
The principal pathological changes are found in the small intestine. Catarrhal inflammation with marked lack of tone is present in the duodenum, jejunum and ileum. The intestinal contents are usually thin, watery and foamy, with localized bulbous swellings filled with watery fluid. The small intestine, especially the anterior part, is inflamed and edematous. The cecal contents are usually fluid, and the cecal tonsils are congested.
Epidemiology: Hexamita is transmitted thru contaminated feed and water. Carrier adult birds which have survived earlier attacks are the most important source of infection for turkey poults. Sometimes the disease does not appear in the earlier hatches but strikes the later ones after the adults have been sold. This may come about because the infections in the earlier hatches were very light or perhaps because the virulence of the strains was too low to cause noticeable disease. According to Hinshaw (1959) it may take several passages in poults of a strain from carrier turkeys before an acute outbreak occurs.
Wild quail, pheasants and chukar partridges sharing the range with turkeys may also be a source of infection. Hot weather and overcrowding may also contribute to the severity of an outbreak. In addition, the role of flies deserves study. Turkey poults are excellent fly-catchers, and these insects might carry the protozoa from one pen to another.
Diagnosis: Hexamitosis can be diagnosed by finding the protozoa in scrapings from the small intestine, and particularly from the jejunum and duodenum. The smears should be mixed with physiological salt solution and examined while fresh. Hexamita can be readily differentiated from Trichomonas, Giardia or Cochlosoma by its small size, absence of a sucker or undulating membrane, and characteristic motion. Impression smears can also be made of cross sections of fresh small intestine, dried rapidly and stained with Giemsa's stain; the protozoa are often found in groups in the crypts. Hexamita can also be found in the bursa of Fabricius and cecal tonsils in carrier birds.
Cultivation: Hexamita meleagridis has not been cultivated in artificial culture media, but Hughes and Zander (1954) cultured it axenically in the chorioallantoic fluid of chick embryos.
Treatment: No treatment has apparently been uniformly successful for hexamitosis. McNeil (1948) recommended replacing the drinking water for several days with a mixture of 3% dried whey in 1-2000 aqueous copper sulfate solution. It must be begun early in an outbreak to be effective, and Wilson and Slavin (1955) did not find it to be of value in their studies.
Almquist and Johnson (1951) found in preliminary tests that streptomycin was ineffective, but that penicillin, chlortetracycline and oxytetracycline were of some value. Enheptin also gave good results when fed as 0.1% of the mash for 14 days. Wilson and Slavin (1955) said that they tested every antiprotozoal drug available commercially in England (including antimalarials, trypanocides, amoebicides and antiluetics) without success. Enheptin was only about 50% effective in experimentally infected poults. The most promising drug was di-n-butyl tin dilaurate, which appeared to control mild field outbreaks and to lower the death rate in more severe ones.
Mangrum et al. (1955) reported that furazolidone reduced mortality in experimentally infected turkey poults. McNeil (1956) mentioned that nithiazide had been used successfully by Merck, Sharp & Dohme Research Laboratories in a combined outbreak of histomonosis and hexamitosis.
Prevention and Control: Hexamitosis can be prevented by proper management and sanitation. Poults should be separated from adults, and separate caretakers should be used for the two groups. If feasible, breeding birds should be sold 2 weeks before any poults are hatched. Separate equipment should be used for different groups of birds. Attendants should keep out of the pens, and the feeders and waterers should be placed where they can be reached from the outside. Feeders and waterers should be placed on wire platforms. Young birds should be kept on wire. Ranges frequented by pheasants, quail and chukar partridges should be avoided. General sanitation and fly control should be practiced.