History
An 8-week-old female backyard Polish Frizzle chicken with a history of ill thrift was euthanized at the owner's request and submitted for necropsy. The chicken never fully developed after hatching and had a poor body condition, compared with that of other chickens hatched at the same time.
Clinical and Gross Findings
On external examination, blood was exiting the cloaca. The ceca were bilaterally enlarged and dark red and internally contained abundant dark red material in the lumen (Figure 1). A nodular, soft protuberance was palpated on the dorsal surface of the cranium. Longitudinal sections of the skull revealed a craniodorsal out-pocketing of the brain and meninges through a cleft in the cranium. No other notable gross changes were observed.
Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page→
Photographs of the ceca (A and B) and skull (C and D) of an 8-week-old backyard chicken with a history of ill thrift that was euthanized and necropsied. In panels A and B, both ceca are enlarged and dark red, and contain luminal hemorrhagic and necrotic cores. In panels C and D, the entire and longitudinally sectioned skull is shown. There is a craniodorsal out-pocketing of the brain and meninges (meningoencephalocele) through a cleft (cranioschisis) in the cranium.
Citation: Journal of the American Veterinary Medical Association 251, 11; 10.2460/javma.251.11.1253
Photographs of the ceca (A and B) and skull (C and D) of an 8-week-old backyard chicken with a history of ill thrift that was euthanized and necropsied. In panels A and B, both ceca are enlarged and dark red, and contain luminal hemorrhagic and necrotic cores. In panels C and D, the entire and longitudinally sectioned skull is shown. There is a craniodorsal out-pocketing of the brain and meninges (meningoencephalocele) through a cleft (cranioschisis) in the cranium.
Citation: Journal of the American Veterinary Medical Association 251, 11; 10.2460/javma.251.11.1253
Photographs of the ceca (A and B) and skull (C and D) of an 8-week-old backyard chicken with a history of ill thrift that was euthanized and necropsied. In panels A and B, both ceca are enlarged and dark red, and contain luminal hemorrhagic and necrotic cores. In panels C and D, the entire and longitudinally sectioned skull is shown. There is a craniodorsal out-pocketing of the brain and meninges (meningoencephalocele) through a cleft (cranioschisis) in the cranium.
Citation: Journal of the American Veterinary Medical Association 251, 11; 10.2460/javma.251.11.1253
Histopathologic Findings
Histologically, the cecal mucosa had extensive areas of necrosis and hemorrhage, which occasionally affected the submucosa and muscle layers (Figure 2). Enterocytes were often expanded by intracellular protozoal organisms morphologically consistent with Eimeria spp. Characteristic intracellular protozoal stages included macrogamonts, microgamonts, schizonts containing numerous merozoites, and oocysts that also filled the cecal lumen and were admixed with a necrotic and hemorrhagic core composed of heterophils, fibrin, hemorrhage, and clusters of cocci and bacilli. Expanding the lamina propria and submucosa and multifocally extending into the muscular and serosal layers were moderate numbers of lymphocytes and plasma cells with fewer heterophils and macrophages admixed with hemorrhage and edema. The duodenum, jejunum, and ileum contained variable amounts of necrotic debris and heterophils along with scant numbers of protozoal gamonts on the superficial mucosa. In these areas, the lamina propria contained small numbers of lymphocytes and plasma cells. The prolapsed area of the brain near the cranioschisis had small foci of neuronal necrosis and scattered foamy macrophages (gitter cells). The superficial bursal epithelium and interlobular areas were expanded with heterophils and macrophages. The apical surface of the superficial bursal epithelium contained multiple, 3- to 5-μm-diameter, round, basophilic, Giemsa-staining organisms, which were morphologically consistent with Cryptosporidium spp. Bursal lymphoid follicles were not depleted. No other major histologic changes were observed.
Photomicrograph of a section of cecum in the chicken in Figure 1. Multifocal areas of crypt necrosis and inflammation are present (asterisk). There are multiple protozoal schizonts (arrow) and macrogametes (arrowheads). H&E stain; bar = 100 μm. Inset—A mature oocyst is illustrated (center). H&E stain; bar = 50 μm.
Citation: Journal of the American Veterinary Medical Association 251, 11; 10.2460/javma.251.11.1253
Photomicrograph of a section of cecum in the chicken in Figure 1. Multifocal areas of crypt necrosis and inflammation are present (asterisk). There are multiple protozoal schizonts (arrow) and macrogametes (arrowheads). H&E stain; bar = 100 μm. Inset—A mature oocyst is illustrated (center). H&E stain; bar = 50 μm.
Citation: Journal of the American Veterinary Medical Association 251, 11; 10.2460/javma.251.11.1253
Photomicrograph of a section of cecum in the chicken in Figure 1. Multifocal areas of crypt necrosis and inflammation are present (asterisk). There are multiple protozoal schizonts (arrow) and macrogametes (arrowheads). H&E stain; bar = 100 μm. Inset—A mature oocyst is illustrated (center). H&E stain; bar = 50 μm.
Citation: Journal of the American Veterinary Medical Association 251, 11; 10.2460/javma.251.11.1253
Morphologic Diagnosis and Case Summary
Morphologic diagnosis: severe, bilateral, trans-mural necrohemorrhagic typhlitis with intralesional coccidian organisms; cranioschisis with meningoencephalocele and neuronal necrosis; and heterophilic and histiocytic bursitis with intralesional Cryptosporidium spp.
Case summary: cecal coccidiosis with cranioschisis, meningoencephalocele, and bursal cryptosporidiosis in a chicken.
Comments
Coccidiosis in poultry is caused by multiple species of Eimeria, an Apicomplexan protozoal parasite.1 In the United States, Eimeria tenella, Eimeria acervulina, and Eimeria maxima are the most common species causing coccidiosis in chickens.2 Clinical signs are mainly the result of destruction of intestinal epithelium during replication of the organisms. The lifecycle of Eimeria organisms begins when sporulated oocysts in the environment or feces of infected chickens are ingested by susceptible individuals. After ingestion, infective sporozoites are released during digestion of oocysts in the ventriculus (gizzard) and invade the intestinal epithelium.1 Within the crypt epithelium, sporozoites become trophozoites and undergo multiple rounds of asexual reproduction, invading adjacent epithelial cells. Sexual reproduction occurs when intracellular macrogametes and microgametes form zygotes and mature to oocysts. These environmentally resistant oocysts exit the cells and are shed in the feces to restart the infective cycle. The prepatent period of species of Eimeria is approximately 4 to 7 days.2
Coccidiosis is diagnosed on the basis of the clinical signs and the typical pathological changes in the intestinal mucosa. Eimeria spp have a predilection for specific sites in the gastrointestinal tract; given the cecal lesions observed in the chicken of the present report, E tenella was considered the most likely infective species because it has a propensity to invade the cecal epithelium.3 Eimeria tenella is the most pathogenic coccidian organism for chickens, and its reproduction causes extensive cell destruction, hemorrhagic diarrhea, reduced feed intake and weight gain, and death.3 Consistent with the postmortem findings in this chicken, gross lesions of E tenella infection include a thickened cecal wall, hemorrhagic cecal contents, cecal distention, and mucosal necrosis. Recombinant DNA techniques can be used to differentiate among different species and strains of Eimeria as well as to determine possible links between strains and drug resistance.4 These tests were not done in the case described in the present report.
Avian coccidiosis causes an annual economic loss of approximately $2.4 billion worldwide.3 The main factors contributing to economic loss are decreased weight gain, subsequent increased feed-to-conversion ratio, costs of prevention and treatment, and high mortality rates in affected poultry.5 Poultry coccidiosis has been traditionally controlled with administration of ionophores and synthetic compounds such as nicarbazin,3 but drug resistance and concerns about anticoccidial drug residues have created a movement toward switching these control measures with use of vaccines containing live attenuated or nonattenuated organisms.6 Although attenuated vaccines contain less virulent strains of Eimeria that produce fewer oocysts, nonattenuated vaccines consist of nonmodified Eimeria spp.5 Therefore, the occurrence of clinical coccidiosis is a concern, and the use of nonattenuated vaccines and dosing with that type of vaccine must be carefully controlled.5 Free-range and backyard chickens are often not protected by a strict prophylactic program and are more susceptible to develop parasitic infections.7 The chicken of the present report was in a backyard flock.
The cranioschisis and meningoencephalocele in this young chicken were likely congenital defects. Cranioschisis is one of the most common skeletal malformations in chickens and causes considerable losses in the poultry industry.8 The breed standards of tall, prominent feather crests, such as those for Araucana and Silkie breeds, favor the development of cranial malformations and meningoencephalocele or exencephaly.9 Skeletal disorders such as cranioschisis have many different causes including genetic and nutritional disorders.8 Embryonic hypoxia can also cause defects such as cranioschisis.10 The presence of neuronal necrosis at the herniated area may suggest that the chicken of the present report had unnoticed clinical signs associated with the cranial malformation.
Infection by Cryptosporidium spp in several avian species has been described.11 These are also Apicomplexan protozoal parasites that infect the mucosal epithelium of many organs. These organisms are extracytoplasmic but intracellular and typically appear to be located at the surface of infected cells. Infection occurs through ingestion or aspiration of oocysts in the environment, and similar to what was suspected in the case described in the present report, cryptosporidiosis is considered a secondary pathogen in immunosuppressed birds in most instances.11
Acknowledgments
At the time of the investigation, Allison Watson was a visiting (externship) student at the Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, Ga.
References
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