Generalized weakness, lethargy, and anorexia in a hen

Bianca Santana de Cecco Louisiana Animal Diagnostic Disease Laboratory, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA

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 DVM, PhD
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Jeongha Lee Louisiana Animal Diagnostic Disease Laboratory, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA

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 DVM;Maria S. Mitchell, DVM, MS
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Fabio Del Piero Louisiana Animal Diagnostic Disease Laboratory, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA

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 DVM, PhD, DACVP

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History

A 1-year-old female chicken from a backyard flock of 33 chickens was presented for postmortem evaluation after being euthanized due to clinical worsening. In the previous few months, 13 of these 33 chickens died after presenting clinical signs of generalized weakness, lethargy, and anorexia. No signs of diarrhea or upper respiratory signs were noted. Another chicken had died 2 weeks earlier, and on gross examination, the veterinarian described a dilated oviduct with the presence of eggs with the consistency of boiled eggs of varying sizes. In addition, the veterinarian described lung consolidation and compression.

Clinical and Gross Findings

The coelomic cavity contained approximately 5 mL of yellow viscous material (yolk material), often adhered to the surface and serosa of organs (Figure 1). The oviduct was markedly distended with a thin wall, and the lumen contained 1 light-yellow caseous mass, measuring 6.2 X 4.0 X 3.6 cm, which at the cut surface presented concentric rings of different colors (yellow and white; Figure 2). The mucosa of the oviduct was dark red and mildly edematous, multifocally covered with egg yolk.

Figure 1
Figure 1

Photograph of the coelomic cavity of a 1-year-old hen that was euthanized after clinical worsening. The hen presented with abdominal distention, lethargy, and anorexia. Deposits of yellow viscous yolk material are evident in the surface and serosa of organs.

Citation: Journal of the American Veterinary Medical Association 261, 7; 10.2460/javma.22.10.0475

Figure 2
Figure 2

Photograph of the cut surface of the mass within the oviduct. The mass presents concentric layers of white and yellow material. The mucosa of the oviduct is mildly reddened and covered with opaque white material.

Citation: Journal of the American Veterinary Medical Association 261, 7; 10.2460/javma.22.10.0475

Histopathologic Findings

Samples of the oviduct, intestines, lung, liver, spleen, kidney, proventriculus and ventriculus, heart, and brain were fixed in neutral-buffered 10% formalin and processed for histologic examination. Microscopically, the oviduct mucosa presented multifocal to coalescing areas of mild necrosis with intense deposition of an eosinophilic amorphous material mixed with cellular debris, moderate aggregates of bacilli bacteria, and mild to moderate infiltration of heterophils, macrophages, and lymphocytes (Figure 3). The submucosa was moderately expanded by edema, congestion, and mild infiltration of lymphocytes. The serosa of the small and large intestines had mild to moderate deposition of eosinophilic amorphous material, a small number of heterophils, and bacilli bacterial aggregates. The spleen, liver, and lung parenchymas had multifocal areas with mild to moderate infiltration of heterophils characterizing mild splenitis, pneumonia, and hepatitis, respectively. No significant abnormalities were noted in the remaining organs.

Figure 3
Figure 3

Photomicrograph of the oviduct. The mucosa contains deposition of eosinophilic amorphous material associated with cellular debris, moderate aggregates of bacteria, and mild to moderate infiltration of heterophils. H&E stain; bar = 240 μm.

Citation: Journal of the American Veterinary Medical Association 261, 7; 10.2460/javma.22.10.0475

Microbiological Findings

Samples from the oviduct and caseous mass from the chicken were inoculated onto blood agar (Remel tryptic soy agar with 5% sheep blood; Thermo Fisher Scientific), and MacConkey agar plates (Remel; Thermo Fisher Scientific). Inoculated blood plates were aerobically incubated at 37 °C with 5% CO2 for the first 24 hours and without CO2 for the next 48 hours. Inoculated MacConkey agar plates were incubated at 37 °C for up to 72 hours. Moderate growth was present on both blood agar and MacConkey agar after 24 hours. Bacterial colonies were subsequently identified using a MALDI-TOF MS Biotyper compass (Bruker). The bacterial colonies were identified as nonhemolytic Escherichia coli.

Morphologic Diagnoses and Case Summary

Morphologic diagnosis: fibrinonecrotizing and heterophilic salpingitis, peritonitis, diffuse, moderate to severe with intralesional bacilli bacterial aggregates.

Case summary: salpingoperitonitis and sepsis associated with E coli.

Comments

Infections with avian pathogenic E coli, collectively termed colibacillosis, are the most common infectious bacterial disease in poultry and are responsible for significant economic losses to the poultry industry.1,2 Several entities have been associated with this bacterium including coligranuloma (Hjarre disease), air sac disease (chronic respiratory disease), swollen-head syndrome, venereal colibacillosis, colisepticemia, coliform cellulitis, yolk sac infections, salpingitis, osteomyelitis, orchitis, panophthalmitis, and peritonitis.2 Among commonly reported E coli extraintestinal infections are salpingoperitonitis syndrome (SPS) and E coli peritonitis syndrome.13 While SPS is a chronic condition commonly referred to as “egg peritonitis,” E coli peritonitis syndrome is related to acute mortality reaching up to 10% or more in combination with severe sepsis and fibrinous polyserositis.1,3 Outbreaks of salpingitis and peritonitis cause major economic losses due to mortality, reduced egg production, and culling of infected hens.1,2,4

Although the pathogenesis of SPS is not well established, the major hypothesis is that the oviduct infection in egg-laying chickens is caused by E coli or other bacterial species that are normally present on cloacal mucus membranes. Heavy egg production and associated estrogenic activity can predispose to salpingitis by relaxing the sphincter between the vagina and cloaca, leading to an ascending invasion of the bacteria from the cloaca.2

Clinical signs vary from inapparent to total unresponsiveness just prior to death depending on the specific lesion caused by E coli. Localized infections generally result in fewer and milder clinical signs than systemic diseases. Broilers with SPS can present with abdominal distension, apathy, anorexia, loss of egg-laying capacity, and eventually sudden death.2,4 A flock that appears clinically normal when examined during the day but has an excess number of dead birds the following morning is a common finding in mildly affected flocks. This type of pattern is classic for egg layer and breeder flocks experiencing coliform salpingitis and/or peritonitis.2 At postmortem examination, peritonitis appears as deposits of yellow viscous exudate with the appearance of coagulated yolk on serosal surfaces that may be localized or disseminated throughout the coelomic cavity.2 While in the oviduct the laminated appearance of the mass on the cut section identifies the oviductal origin, representing the alternating layers of exudate and secretions from continued ovulation.2,4

Microscopically, inflammatory cells are not a significant component of the exudate, and heterophils, although present, are not numerous and can be mainly observed migrating through the mucosal epithelium. The mucosa can be compressed by the expanding luminal mass, and the tubular secretory glands in the lamina propria are separated from each other by edema and fibrin deposition. The relatively mild microscopic changes in the oviduct are in sharp contrast to the massive gross lesions, but most of the material obstructing the oviduct has come from ovulations and secretions, not inflammation.2,5

The risk for colibacillosis increases with increasing infection pressure in the environment. Good housing hygiene and avoiding overcrowding are very important practices. Other principal risk factors are the duration of exposure, virulence of the strain, breed, and immune status of the animal.4 Therefore, biosecurity is essential to the control of colibacillosis. Reducing the numbers of E coli through water, feed, environmental sanitation, and good air quality and protecting the flock from factors, especially viral infections, that decrease host resistance will sharply reduce the likelihood of colibacillosis.2 Maintaining good air and litter quality is fundamental to reducing the risk of a flock developing colibacillosis.2

Acknowledgments

The authors declare that there were no conflict of interest.

We thank members of the Histology and Bacteriology sections at the Louisiana Animal Disease Diagnostic Laboratory, School of Veterinary Medicine, Louisiana State University, for their assistance.

References

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    Nolan LK, Barnes HJ, Vaillancourt J, Abdul-Aziz T, Logue CM. Colibacillosis. In: Diseases of Poultry. 13th ed. Wiley; 2013:751805.

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    Jordan FT, Williams NJ, Wattret A, Jones T. Observations on salpingitis, peritonitis and salpingoperitonitis in a layer breeder flock. Vet Rec. 2005;157(19):573577.

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    Lutful Kabir SM. Avian colibacillosis and salmonellosis: a closer look at epidemiology, pathogenesis, diagnosis, control and public health concerns. Int J Environ Res Public Health. 2010;7(1):89114.

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    Barnes HJ, Fletcher OJ, Abdul-Aziz T. Reproductive system. In: Avian Histopathology. 4th ed. American Association of Avian Pathologists; 2016:589590.

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