1. Coccidiosis:
• Coccidiosis affects most species of poultry, waterfowl, gamebirds, and pigeons. The information presented here will focus on the small chicken flock but the principles discussed are generally applicable to other species. The typical history of a flock with coccidiosis is that of increased mortality in a flock of young chickens (2 to 18 weeks of age). Affected birds will be depressed, have ruffled feathers, be reluctant to move, and often the feathers around the vent will be soiled with fecal material due to diarrhea. In severe cases bloody droppings may be observed.
• Lesions
• A postmortem examination of a bird that has succumbed to coccidiosis will reveal distinct pathology in one or more regions of the intestines. Coccidial species are both highly host specific and infect a specific region of the intestines. Nine species of coccidia infect chickens, three of these are most commonly associated with severe disease. Eimeria acervulina affects the duodenum and upper intestines, numerous small (0.5 to 1.0 mm) white foci can be seen on the mucosal surface of the intestines and the intestinal wall is thickened. E. necatrix affects primarily the middle portion of the small intestines; lesions include distinct white spots in the mucosa (schizonts), ballooning of the intestines, and mucoid blood tinged intestinal contents. E. tenella infects the ceca of the chicken and severe hemorrhage is seen in the cecal lumen with caseous cecal cores developing in more chronic cases. Birds that recover from coccidiosis develop short lived species specific immunity. With constant exposure to coccidial oocysts in the environment, previously infected chickens do not develop clinical disease. Different avian species have different, host specific, Eimeria spp. Or Isospora spp. Renal coccidiosis is seen in domesticated geese Eimeria truncata as well as in some wild avian species.
• Diagnosis
• A diagnosis of coccidiosis can be established by preparing a wet mount of a mucosal scraping from the intestines of an infected bird and examining it by light microscopy. The coccidial oocysts and schizonts can readily be identified at 100X magnification. A fecal flotation is also very effective in demonstrating coccidial oocysts. The specific species of coccidia involved in a disease outbreak can be established by tissue tropism and oocyst morphology but this is not necessary as all species respond well to the commonly used therapeutic agents.
• Treatment
• Coccidiosis is effectively treated with amprolium in both chickens and turkeys. Amprolium is available in a 9.6% solution which is administered in the drinking water at 0.024% for 3 to 5 days (1/3 oz. Of 9.6% amprolium per gallon of drinking water). Once the flock has responded to treatment with amprolium the dosage is lowered to 0.006% amprolium in the drinking water for an additional 1 to 2 weeks. An equally effective medication for the treatment of coccidiosis is sulfadimethoxine as per label instructions. Other sulfa drugs are also effective in the treatment of coccidiosis but care must be taken with all sulfa drugs to avoid toxicity and observe withdrawal times prior to slaughter.
• Prevention
• Once a farm has experienced an outbreak of coccidiosis it is extremely difficult to eliminate the highly resistant coccidial oocysts from the environment. All subsequent flocks must be kept on a coccidiosis prevention program. With layers and game birds, raising the birds on wire can prevent coccidiosis. If well managed this practice will break the coccidial life cycle. However, if birds are still able to reach their droppings when raised on wire coccidiosis may still occur. Broilers raised on the ground or litter are commonly fed coccidiostats (monensin, salinomycin, lasalocid, halofuginone, nicarbazin, and amprolium) in the feed until slaughter. Care must be taken to observe the appropriate feed withdrawal times. Layer pullets are often kept on a coccidiostat for the first 16 weeks of life and then treated for disease if necessary later in life. Turkeys are usually only kept on coccidiostats until 10 weeks of age as they are generally more resistant to coccidiosis.
2. Histomoniasis
• Definition
• Histomoniasis is a parasitic disease of gallinaceous birds characterized by sulfur colored diarrhea, depression, anorexia and death. Histomoniasis is also called blackhead in turkeys due to the cyanosis of the skin of the head, which occurs during the terminal stages of this disease.
• Occurrence
• Histomoniasis has been reported in the USA, Canada, and Mexico, wherever susceptible birds are present. Numerous gallinaceous birds are affected by histomoniasis with turkey, chukar partridge, and ruffed grouse being severely affected. Species which will become infected but may or may not develop severe disease include, chicken, peafowl, guinea fowl, bobwhite quail, and pheasant.
• Etiology
• The etiologic agent of histomoniasis is Histomonas meleagridis a protozoan which is sensitive to environmental conditions and all disinfectants. H. meleagridis exists in two phases: nonamoeboidal and ameboidal. The amoeboidal phase (8016 microns) is pleomorphic with numerous pseudopodia and is the "invasive" phase during an infection. The "vegetative" phase (12-21 microns) is found in the degenerating center of hepatic lesions and in the lumen of the intestines.
• The life cycle of H. meleagridis is intimately associated with the cecal nematode of chickens, Heterakis gallinarum and several species of earthworms found in the soil. The histomonads are able to persist in the environment inside the heterakis egg to be ingested later by a susceptible host. Likewise certain earthworms will ingest histomonad infected heterakis eggs and if eaten by a susceptible avian host will serve as a transport host.
• Transmission and clinical signs
• The transmission of histomoniasis occurs primarily via heterakis eggs and earthworms as described above but direct transmission by the ingestion of fresh droppings containing viable histomonads may also occur.
• The chicken, often serving as an inapparent host to both heterakis and histomonads, is considered the most important vector for histomoniasis. In commercial poultry operations where poultry species are not mixed this no longer presents a problem but in multi-species backyard flocks histomoniasis commonly occurs.
• The clinical signs of histomoniasis in turkeys include, sulfur-colored diarrhea, depression, anorexia, cyanosis, and death. Mortality in affected young turkeys in high (70-100%). In chickens sulfur-colored droppings are seldom seen but bloody droppings may be observed. Mortality in chickens varies most commonly from 0-30%.
• Pathology
• The lesions of histomoniasis develop on the liver and ceca. During the initial phase of infection a thickened hyperemic cecal wall with a serous/hemorrhagic exudate is found. Caseation of this cecal exudate then occurs and a cheesy cecal core is formed. Ulceration of the cecal wall often occurs in affected birds and this sometimes develops into a perforated ceca and a generalized peritonitis. The hepatic lesions of histomoniasis are large areas of hepatic necrosis (0.5-1.0 cm). These areas of hepatic necrosis have a depressed center surrounded by a raised ring. "Bulls eye" hepatic lesions in conjunction with caseous cecal cores are pathognomonic for histomoniasis.
• Histologically, a progressively more severe mixed inflammatory response is seen in an infected ceca. Numerous bacteria, juvenile heterakis, and histomonads are commonly seen. The cecal core is composed of sloughed epithelium, fibrin, erythrocytes, and leukocytes. Coagulative necrosis and histomonad invasion may extend well into the muscular tunic of the cecum. Large areas of hepatic necrosis/hepatitis are observed with many histomonads observed in the peripheral area of the lesion.
• Diagnosis
• Histomoniasis can be diagnosed based on characteristic gross lesions and/or histologic lesions.
• H. gallinarum can be isolated from tissues of freshly killed affected birds in special broth media.
• Control
• The exclusion of chickens from turkey farms has drastically decreased the incidence of this disease. In general turkey farms should be located on sites with dry, sandy, loose soil. This type of soil contains fewer earthworms.
• Susceptible birds may be fed a histomoniasis preventative in the feed. Currently the only available preventative is Histostat an arsenical which may cause slight growth depression. The very effective blackhead preventatives/treatments emtryl (dimetridazol) and Ipropan (ipronidazole) are no longer available in the United States. Metronidazole (Flagyl) can be used effectively in the treatment of pet birds not intended for human consumption (peacocks or the pet backyard turkey). An oral dose of 60 mg/kg body weight for 5 consecutive days is effective. Treated birds should be moved to noncontaminated premises to prevent reinfection.
3. Trichomoniasis
• Definition
• Trichomoniasis is a disease of the upper digestive tract, seen in pigeons, doves, raptors, turkeys, chickens as well as many other wild birds.
• Occurrence
• Trichomoniasis (Trich. For short) occurs frequently in pigeons and doves, as well as raptors which feed upon them. The disease is called canker in pigeons and frounce in falcons. With the current improved management practices in the poultry industry trichomoniasis is not common in turkeys and chickens. Outbreaks usually occur in warm climates or during warm weather.
• Etiology
• The etiological agent of trichomoniasis is Trichomonas gallinae (Tg). Tg is a pear-shaped flagellated protozoan with 4 anterior flagella and an undulating membrane to provide motility.
• The life cycle of Tg is very simple; it divides by longitudinal binary fission.
• Transmission
• Nearly all pigeons are carriers of Tg. The pathogenicity of the different strains of Tg is very variable. Adult pigeons transfer the organism to squabs via the "pigeon milk".
• Raptors often contract trichomoniasis by eating infected pigeons and doves.
• Turkeys and chickens contract the disease by drinking stagnant surface water containing T. gallinae . Pigeons are believed to be the most common vector by which the water supplies are contaminated.
• Clinical signs
• Affected birds may have difficulty closing their mouths and may drool and make repeated swallowing movements.
• Severely affected birds will stop eating, become depressed, ruffled in appearance, and emaciated before death.
• Lesions
• Lesions are seen in the mouth, sinuses, pharynx, esophagus, crop, and proventriculus.
• Typical lesions are white to yellow plaques or raised masses.
• Diagnosis
• Gross lesions are very suggestive of trichomoniasis but are not unlike those seen with visceral pox, candidiasis, and hypovitaminosis A.
• histopathology of the lesions will help distinguish trichomoniasis from the above diseases.
• The presence of large numbers of trichomonads in the oral fluids is usually considered confirmatory. A wet mount of fresh oral fluids will reveal the motile trichomonads when examined microscopically.
• Prevention
• Eliminate any carrier birds as they will contaminate the waterers with Tg.
• Provide clean fresh water and eliminate sources of stagnant water.
• Avoid contact between pigeons and doves and susceptible poultry.
• A low preventative level of protozoacide can be fed in the ration or in the drinking water. Agents that have been used are dimetridazole (Emtryl), nithiazide (Hepzide) and Enheptin.
• Treatment
• Several drugs have been used to treat trichomoniasis including Emtryl (dimetridazole), aminonitrothiazole, and Enheptin. These drugs are no longer available for use in the U.S.A.
• Back yard flocks or pigeons not used for food production may be effectively treated with dimetridazole by prescription of a veterinarian (1000 mg/L in drinking water for 5-7 days).
4. Other avian protozoal diseases seen in gallinaceous birds include Leucocytozoonosis, Cryptosporidiosis, and Hexamitiasis ( Hexamita meleagridis ).

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