History

In a flock of 23- to 24-week-old commercial broiler breeder chickens in northeast Georgia, an increasing number of birds developed swollen tibiometatarsal (hock) joints and became recumbent and unable to stand. On the farm, the flock was distributed between 2 housing facilities that contained 9,280 hens and 880 roosters. In general, the male birds were 1.1 kg (0.5 lb) underweight for their age. The mortality rate on the farm had consistently increased from 0.5% to 0.7% during the previous week; during that week, approximately 50 to 60 roosters and 8 to 12 hens either were found dead or had to be culled. Three affected chickens (both male and females) that were culled from the flock (representative of the 2 housing facilities) were submitted to the Poultry Diagnostic and Research Center at the University of Georgia.

The conditions in both housing facilities were inspected, and the litter in the scratch areas was damp throughout. Humidity and temperature within the housing facilities were high. The chickens were vaccinated against infectious bursal disease virus and reovirus infections with killed virus vaccines at 18 weeks of age, and the males had nose bones applied at that time. At 19 to 20 weeks of age, representative birds were tested for serum antibodies against avian influenza virus, Mycoplasma gallisepticum, Mycoplasma synoviae, and Salmonella pullorum; results were negative. Transportation of birds from the pullet house to the hen house occurred at 21 weeks of age. Egg production began at approximately 23.5 weeks of age.

Clinical and Gross Findings

The affected birds in the flock were underdeveloped and underweight and had severe signs of depression, closed eyes, lameness and reluctance to stand, and swollen tibiometatarsal joints and feet; they produced loose blood-tinged feces. The 3 birds submitted to the Poultry Diagnostic and Research Center were each necropsied, and findings were similar. On gross examination, the cecal wall was necrotic and the mucosa was thickened and had petechial hemorrhages. Cecal contents were brown, gritty, and blood tinged (Figure 1). Generalized hepatomegaly was present, and the liver had multiple dark slightly depressed areas surrounded by multifocal, white, pinpoint lesions. Other lesions included extensor tendonitis and pericarditis; a thick exudate was present in the tibiometatarsal joints suggestive of septic arthritis. The birds were emaciated with little to no body fat, and generalized muscle atrophy was present. The wattles contained abundant caseous material. The air sacs were moderately thickened with neovascularization.

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Photographs of the ceca (A) and liver (B) of a 23-week-old broiler breeder chicken that was culled from a commercial flock in which an increasing number of birds had developed swollen tibiometatarsal joints and became recumbent and unable to stand during the preceding week; mortality rate on the farm had consistently increased from 0.5% to 0.7% in that period. In panel A, the ceca have been incised to reveal a thickened mucosal wall with pseudomembranous exudate (cecum on right) and underlying mucosal reddening (cecum on left). On the surface of the 2 lobes of the liver in panel B, notice the multiple roughly circular areas that have a dark slightly depressed center surrounded by minute white foci.

Citation: Journal of the American Veterinary Medical Association 238, 8; 10.2460/javma.238.8.987

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Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page →

Histopathologic Findings

During necropsy, the major organs and several portions of the ceca and livers of the 3 broiler breeder chickens were promptly fixed in neutral-buffered 10% formalin, routinely processed, embedded in paraffin, sectioned, routinely stained, and examined via light microscopy.

In the ceca, most of the mucosa was eroded or ulcerated and covered by amorphous granular to compact fibrillar eosinophilic exudate with degenerate inflammatory cells, necrotic debris, hemorrhage, and bacteria. The lamina propria, submucosa, and, in some ceca, tunica muscularis contained a marked infiltrate of macrophages and lymphocytes with fewer multinucleated giant cells, heterophils, and plasma cells, accompanied by severe diffuse edema (Figure 2). Multiple areas in the lamina propria and submucosa contained abundant protozoal organisms in parasitic vacuoles. The protozoa were round and eosinophilic, consistent with histomonad trophozoites.

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Photomicrographs of a section of a cecum from another 23-week-old broiler breeder chicken that was culled from the affected flock. A—The cecal mucosa is severely ulcerated and covered with multifocal pseudomembranous exudate. The remaining lamina propria, submucosa, and tunica muscularis are infiltrated with lymphocytes, heterophils, plasma cells, and macrophages. H&E stain; bar = 500 μm. B—Numerous histomonad trophozoites (one of which is indicated by the arrow) are visible in areas of inflammation in the cecum. H&E stain; bar = 20 μm.

Citation: Journal of the American Veterinary Medical Association 238, 8; 10.2460/javma.238.8.987

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The livers had focal acute hepatocellular necrosis associated with a few heterophils. Multiple areas of mild lymphohistiocytic aggregates throughout the liver parenchyma were also observed. However, histomonad organisms were not detected in the liver sections.

Morphologic Diagnosis

Severe multifocal necrogranulomatous typhlitis with intralesional protozoal organisms consistent with histomonads and acute focal hepatocellular necrosis.

Comments

A diagnosis of histomoniasis in the flock of this report was made on the basis of the classic cecal and liver lesions along with histologic evidence of histomonad trophozoites in examined tissue sections. Histomoniasis (blackhead disease) is a protozoal disease caused by Histomonas meleagridis. The disease is characterized by necrotizing lesions in the liver and ceca in turkeys, chickens, and other gallinaceous birds. This disease is most common in turkeys not receiving prophylactic treatment with 4-nitrophenylarsonic acid,^a and morbidity and mortality rates in turkey flocks may reach 100%.¹ In chickens, the disease is less common and may resemble cecal coccidiosis or salmonellosis. Secondary bacterial infections (primarily infection with Escherichia coli, Clostridium perfringens, or Bacillus subtilis) are common in birds with histomoniasis. Without secondary infection, histomoniasis is typically not very severe.²

Histomonas meleagridis is a flagellate that is transmitted horizontally, especially through intermediate hosts such as the cecal nematode Heterakis gallinarum and earthworms.³ Transmission of the histomonads to birds occurs via ingestion of fresh feces, ingestion of embryonated cecal worm ova containing the protozoa, or ingestion of earthworms containing cecal worm larvae within their tissues.⁴ The histomonads invade the cecal walls and cause wall thickening with marked inflammation and ulceration of the ceca.⁵ Occasionally, these ulcers erode the cecal walls, leading to perforation and peritonitis. The ceca contain a yellowish-green caseous exudate or, in later stages, a dry caseous core. The characteristic lesion in the liver is a circular depressed area of necrosis up to 1 cm in diameter, which is circumscribed by a raised ring.⁵ Following infection, turkeys are more likely to develop these so-called target lesions in the liver than are chickens.⁶ In many instances, target lesions can be observed grossly in addition to being identifiable histologically in the livers of turkeys. In contrast, chickens will occasionally develop grossly visible liver lesions without microscopically identifiable trophozoites,⁷ as highlighted by the findings in the chickens from the flock of this report.

Histomoniasis may be prevented by including antihistomonal drugs in accurately measured amounts in poultry feed. Unfortunately, there is no such preventative medication approved for use in poultry available in the United States. The FDA withdrew registration for all nitroimidazoles on the basis that they were suspected carcinogens; thus, the poultry industry has no legal access to products for treatment of blackhead disease in turkeys or chickens.² Moreover, unless proper sanitation and husbandry measures (eg, temperature, ventilation, humidity, and litter treatment in housing facilities) are implemented, the cycle of disease can continue regardless of prophylaxis. Additional procedures can be taken to control this disease, such as housing chickens separate from turkeys and use of turkey ranges to house chickens only after a turkey-free interval of at least 4 years. Decreasing the amount of stress associated with crowding and other management issues (eg, nonoptimal ventilation, temperature, and litter conditions in housing facilities) can also contribute to limiting this disease.⁶

Chickens are the most suitable host for cecal worms and are the major reservoir of infection. Many years ago, it was proposed that blackhead disease could be prevented if turkeys were reared totally separately from chickens; when implemented, this practice is effective, even today. Poultry fanciers, producers of game birds (eg, quail and pheasants), and those who keep small flocks of free-ranging fowl often violate this rule of husbandry, with disastrous results.²

In the flock of this report, the chickens had recently been exposed to multiple stressors, including transportation to the broiler breeder facility as well as the placement of the birds in the 2 housing facilities. Prior to placement in the housing facilities, the hens were raised in a pullet house, the flooring of which was a compacted dirt pad that was covered with litter. The hens were adjusting to their new environment and just beginning egg production. The interval and quantity of feeding were altered to address the problem of underweight birds (primarily the males). The damp litter conditions and high housing humidity and temperature (results of abundant rainfall in the preceding weeks) were also not optimal. All these circumstances allowed for the adequate conditions for H meleagridis to become pathogenic.

Histomoniasis can have a major economic impact on the poultry industry. To prevent recurrent Histomonas infections at the farm described in this report, interventions were recommended to end the persistent life cycle of H gallinarum. Suggestions included treatment of the flock with levamisole, complete removal and replacement of litter between flock rotations, and improved biosecurity measures to prevent the reintroduction of cecal worms (cecal worms were not detected in this outbreak, but the hens had been raised on dirt flooring prior to moving to the breeder facility) and histomonads.