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Bloody mucus and death

post #1 of 3
Thread Starter 
Yesterday evening, i noticed my layer huddled in the corner of the coop. She didnt scamper off when we collected eggs, and really barely moved. I looked and saw she was a bloody, mucus mess in her vent area. Shes just under a year old, andhasnt laid in about a month. Shes never been a frequent layer, so i thought maybe a soft egg. Today, shes dead. Her name was henrietta. We are sad. What could have caused this? I didnt see anything necessarily sticking out, like anything had prolapsed.
post #2 of 3
Sometimes they can have a prolapse that will attract pecking when red tissue sticks out of the vent. It could be vent pecking which may lead to cannibalism once the chickens see blood. Have you noticed any agressive behavior in any hens or rooster? Some causes of cannibalism are too little room in the coop, not enough protein in the diet, not getting out to free range every day. Having things to keep occupied while in the coop can help. Limit extra light in the coop to 12 hours daily. Are they getting a balanced layer feed? Sometimes boosting protein to 20% can help if they are pecking feathers. Watching their behaviour while sitting with them can sometimes identify a bully, which can then be separated for a week or so to cool off. Sorry for your loss.
post #3 of 3
 

Overview of Histomoniasis in Poultry

(Blackhead, Infectious enterohepatitis)

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Histomoniasis is caused by a protozoan that infects the ceca, and later the liver, of turkeys, chickens, and occasionally other galliform birds. In turkeys, most infections are fatal, whereas in other galliforms susceptibility varies between species and breeds.

Etiology

The causative agent of histomoniasis is the anaerobic, single cell protozoan parasite Histomonas meleagridis that can exist in flagellated (8–15 μm in diameter) and amoeboid (8–30 μm in diameter) forms. Histomonas is most often transmitted in embryonated eggs of the cecal nematode Heterakis gallinarum. A large percentage of chickens and other gallinaceous birds harbor this worm, which serves as a reservoir. Three species of earthworms can act as vectors for H gallinarum larvae containing H meleagridis, which are infective to both chickens and turkeys. H meleagridis survives for long periods within Heterakis eggs, which are resistant and may remain viable in the soil for years. Histomonads are released from Heterakis larvae in the ceca a few days after entry of the nematode and replicate rapidly in the ceca. The parasites migrate into the submucosa and muscularis mucosae and cause extensive and severe necrosis. Histomonads reach the liver either by the vascular system or via the peritoneal cavity, and rounded necrotic lesions quickly appear on the liver surface. Histomonads interact with other gut organisms, such as bacteria and coccidia, and depend on these for full virulence. In turkeys, transmission is by direct cloacal contact with infected birds or via fresh droppings, resulting in histomoniasis quickly spreading throughout the flock. Infection has not been shown to spread in this manner in chickens.

Traditionally, histomoniasis has been thought of as affecting turkeys, while doing little damage to chickens. However, outbreaks in chickens may cause high morbidity, moderate mortality, and extensive culling. Liver lesions tend to be less severe in chickens but often involve secondary bacterial infections. Morbidity can be especially high in young layer or breeder pullets. Layer flocks recover but lack uniformity. Experimental infections with Histomonas of 16-wk-old layers have demonstrated reduced egg production during infection. Tissue responses to infection may resolve in 4 wk, but birds may be carriers for another 6 wk.

Clinical Findings

Signs of histomoniasis are apparent in turkeys 7–12 days after infection and include listlessness, reduced appetite, drooping wings, unkempt feathers, and yellow droppings in the later stages of the disease. The origin of the name “blackhead” is obscure and misleading, with only a few birds displaying a cyanotic head. Young birds have a more acute disease and die within a few days after signs appear. Older birds may be sick for some time and become emaciated before death.

Lesions:

The primary lesions of histomoniasis are in the ceca, which exhibit marked inflammatory changes and ulcerations, causing a thickening of the cecal wall. Occasionally, these ulcers erode the cecal wall, leading to peritonitis and involvement of other organs. The ceca contain a yellowish green, caseous exudate or, in later stages, a dry, cheesy core. Liver lesions are highly variable in appearance; in turkeys, they may be up to 4 cm in diameter and involve the entire organ. In some cases, the liver will appear green or tan. The liver and cecal lesions together are pathognomonic. However, the liver lesions must be differentiated from those of tuberculosis, leukosis, avian trichomonosis, and mycosis. Lesions are also seen in other organs, such as the kidneys, bursa of Fabricius, spleen, and pancreas. Studies by PCR show that Histomonas DNA can be found in the blood and in the tissues of most organs, whether lesions are present or not. Histopathologic examination is helpful for differentiation of diseases.

Histomonads are intercellular, although they may be so closely packed as to appear intracellular. The nuclei are much smaller than those of the host cells, and the cytoplasm less vacuolated. Scrapings from the liver lesions or ceca may be placed in isotonic saline solution for direct microscopic examination; Histomonas spp must be differentiated from other cecal flagellates. Molecular diagnosis is possible with published PCR primers.

Prevention and Treatment

Because healthy chickens and gamebirds often carry the cecal worm vector, any contact between turkeys and other galliforms should be avoided and care should be taken to reduce the worm population. Worm eggs, from contaminated soil, can be tracked inside by workers, causing infection. Arthropods such as flies may also serve as mechanical vectors. Because H gallinarum ova can survive in soil for many months or years, turkeys should not be put on ground contaminated by chickens. Once established in a turkey flock, infection spreads rapidly without a vector through direct contact. Dividing a facility into subunits using barriers can contain the outbreaks to specific units. Histomonads that are shed directly into the environment die quickly. Thus, in a turkey facility, where Heterakis is unable to complete its life cycle, decontamination is not required.

Immunization has only been partially successful in controlling histomoniasis, and reports differ on its effectiveness. The immune response of turkeys to live attenuated Histomonas requires 4 wk to develop. Vaccination of 18-wk-old pullets 5 wk before experimental infection has been shown to prevent a drop in egg production. Most workers have concluded that immunization of birds against this disease using live cultures is not practical. Killed organisms stimulate some immunity when given SC or IP but do not offer protection.

No drugs are currently approved for use as treatments for histomoniasis. Nitarsone is available for prophylaxis by feed medication. Nitarsone is mixed with the feed at 0.01875% and fed continuously. A 5-day withdrawal period is required for animals slaughtered for human consumption. Under most conditions, nitarsone is effective, although some outbreaks in turkeys on medication have been reported. Historically, nitroimidazoles such as ronidazole, ipronidazole, and dimetridazole were used for prevention and treatment and were highly effective. Some of these products can be used by veterinary prescription in non-food-producing birds. Frequent worming of chickens with benzimidazole anthelmintics helps reduce exposure to heterakid worms that carry the infection.

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