Disease surveillance of Ontario small flocks – update

Leonardo Susta, Nancy Brochu, Michele Guerin, Csaba Varga, Brandon Lillie, Marina Brash

The prospective pathogen surveillance study carried out by the AHL and Pathobiology regarding small flocks (non-quota / non-commercial) has come to an end. The study ran from October 1st 2015 until September 29th 2017, and sought to determine the baseline prevalence of relevant infectious agents and diseases in postmortem submissions from Ontario small flocks. For a substantially discounted fee of $25.00 per submission, owners were encouraged to submit sick or dead birds (through their veterinarian) to the AHL locations in Guelph or Kemptville for postmortem examination and a pre-set array of microbiologic tests (conducted on all birds, regardless of lesions).

We received 160 submissions, for a total of 245 individual birds. Most submission derived from southwestern and eastern Ontario. Eighty-four percent of submissions were chickens, followed by turkeys (10 submissions), game birds (8 submissions), and ducks (8 submissions). As reported by the owners in the submission history, affected flocks ranged from 1-299 birds.

No federally reportable diseases were detected. A vaccine strain of avian avulavirus-1 (AAvV-1, formerly known as Newcastle disease virus), and a low pathogenic (H10N8) avian influenza A virus (AIV) isolate were detected in one chicken and one turkey submission (out of 160 tested), respectively. No lesions were associated with these viruses. Infectious laryngotracheitis virus (ILTV) was detected in 22 submissions (34 birds), and concurrent disease (e.g., presence of syncytia, intranuclear inclusion bodies, and tracheitis) was observed in 21 chickens. Salmonella spp. was detected in the cloacal swabs of 3 chickens (S. Anatum, S. Indiana, S. Ouakam), one turkey (S. Uganda), and one duck submission (S. Montevideo); no lesions consistent with salmonellosis were identified (subclinical infection).

The most frequently identified bacterial agents were Brachyspira spp. (37%, cloacal swabs, all species), Mycoplasma synoviae (MS, 36%, tracheal swabs, all species), Campylobacter spp. (35%, cloacal swabs, all species), Mycoplasma gallisepticum (MG, 23%, tracheal swabs, all species) (Fig. 1). No Mycoplasma iowae or meleagridis were identified.

The most frequently identified viral agents were infectious bronchitis virus (IBV, 39%, tracheal and cloacal swabs, chickens and gamefowl), fowl adenovirus (FadV, 35%, cloacal swabs, chickens), ILTV (15%, tracheal swabs, chicken and gamefowl), avian reovirus (4%, cloacal swabs, chickens and turkeys), and infectious bursal disease virus (IBDV, 1%, cloacal swabs, chickens) (Fig. 2). No avian bornavirus was detected. No gross or microscopic lesions consistent with infection with Brachyspira spp., Campylobacter spp., FAdV, reovirus, or IBDV were identified (subclinical infection).

Multiple respiratory pathogens were often detected in the same submission; 44 chicken submissions were positive for >1 respiratory pathogen. The most commonly detected pathogen combinations included MG, MS, and IBV (9%); MS and IBV (8%); MG and MS (4%); and MG, MS, and ILTV (3%). When considering single birds, infection caused by mixed respiratory infections was the most common cause of mortality (21% of tested birds). At the discretion of the pathologist assigned to the case, birds diagnosed with mixed respiratory infection were also tested for bacterial isolation; the most commonly isolated bacteria were Avibacterium spp., E. coli, and Gallibacterium spp.

The single most common viral cause of death was Marek’s disease (26 chickens), which was identified by pathognomonic lymphoid infiltrate of nervous tissue, especially peripheral nerves. The most common neoplastic diseases included ovarian adenocarcinoma with celomic spread (20 birds).

Although tested flocks did not appear to be a reservoir of federally reportable diseases, mixed respiratory pathogens were commonly detected in these flocks and were considered to be the leading cause of clinical signs / poor-doing. Frequent detection of ILTV and IBV underscores the importance of implementing adequate biosecurity practices by small flock owners. Detection of mycoplasma and Marek’s disease stresses the importance of purchasing chicks or ready-to-lay pullets from reputable sources (e.g., from hatcheries or co-ops), in order to obtain replacement chicks that are free of vertically transmissible pathogens, and that are properly vaccinated (at least for Marek’s disease).

Our study provides useful baseline information on the prevalence of pathogens and diseases in small flocks in Ontario for future prevalence studies. These data will contribute to producing knowledge translation publications for specialized training regarding poultry medicine aimed at Ontario veterinarians with an interest in small poultry flock medicine, as well as developing educational tools for small flock producers aimed at prevention and control of relevant diseases.   AHL

Prevalence (%) of bacterial pathogens in tested submissions.

Figure 1. Prevalence (%) of bacterial pathogens in tested submissions.

Prevalence (%) of viral pathogens in tested submissions.

Figure 2. Prevalence (%) of viral pathogens in tested submissions.

OAHN small flock poultry online veterinary course:  (FREE!) Veterinarians may access this course and associated resources by logging in to www.oahn.ca (obtaining an account is free and easy). Then click this link to access the recorded lectures from this 1-day course. http://oahn.ca/resources/poultry/small-poultry-flock-workshop-for-veterinarians-presentations-live-video-and-resources/

Campylobacter hepaticus hepatitis (spotty liver disease) recently reported in American conventionally housed layers  

Marina Brash, Durda Slavic


Spotty liver disease (SLD) was initially reported in laying hens raised in free-range and floor housing systems in Great Britain and Australia in the late 1990s and early 2000s. Reported clinical signs included enteritis, mortality, drop in egg production, and characteristic multifocal hepatitis (Fig. 1). Recently, SLD was reported in a large cage-raised layer complex in the United States, although there were earlier verbal communications of caged layers as well as broiler breeders and broilers, being very occasionally affected. This condition has never been confirmed in Ontario to our knowledge, but with the egg and meat bird industries undergoing dramatic housing and management changes, we need to continue to monitor mortality in our flocks for the presence of this newly emerging pathogen.

We want to remind the Ontario practitioners that the isolation of this novel Campylobacter sp. from affected tissues requires special enrichment and culture media as well as longer incubation times and these protocols were implemented a few years ago at the AHL. Based on recent information, bile is considered to be the best sample to submit for bacterial culture for Campylobacter hepaticus.

If white spotted livers are identified in any type of chicken and you wish to test for the presence of C. hepaticus, we request that you submit a fresh sample of liver that includes the intact gallbladder containing bile (Fig. 2). Routine bacterial culture will be conducted on the liver sample and only bile will be tested for the presence of this novel Campylobacter sp., if specifically requested under special instructions on the AHL submission form. In addition, please provide postmortem findings including the identification of white spotty livers and ensure the commodity class is correctly selected on the AHL submission form because only chicken bile will be tested for C. hepaticus. Regular bacterial culture charges will apply.  

Characteristic gross liver lesions of spotty liver disease. Photos courtesy of Dr. Kelli H. Jones, CEVA.

Figure 1: Characteristic gross liver lesions of spotty liver disease. Photos courtesy of Dr. Kelli H. Jones, CEVA.

Liver, including intact gallbladder containing bile, is the preferred sample for C. hepaticus culture.

Figure 2. Liver, including intact gallbladder containing bile, is the preferred sample for C. hepaticus culture.

Gastric neuroendocrine carcinoma in a 2-year-old bearded dragon

Emily Martin, Diana Gibbs

A 2-y-old male bearded dragon presented to the AHL for postmortem examination. There was a history of a mild decline in appetite starting early August progressing to anorexia by August 15. After 7-10 days, daily oral water therapy was started and the UVB lamp was changed (previous lamp installed January 2018). Fresh greens and vegetables or fruit were offered daily (mostly lettuce or spinach, peppers, plums, etc.). Mealworms and crickets were fed every third day (crickets gut loaded with vegetable and dusted with calcium). At 14 days, SQ fluids were administered and lab tests were run including a fecal float and radiographs. The radiographs were unremarkable and the fecal flotation revealed multiple parasites (a few Oxyurid eggs, occasional Entamoeba hartmanni-like cysts, a few trichomonad trophozoites, a few Chilomastix sp. cysts). Metronidazole treatment was started and began spoon-feeding Repashy Grub Pie daily. Over the clinical course, there was a weight loss of 33 g. On the evening of September 18, he was found unresponsive in his tank. He was brought to the AHL the next day for postmortem examination.

The most striking finding was the markedly enlarged liver with rounded borders and multifocal-to-coalescing tan nodules throughout the parenchyma, from pinpoint to 2 x 2 x 3 cm (Fig. 1). On cut section, the nodules were tan-yellow with firm consistency throughout or occasionally pale-pink with soft centers (Fig. 2). The remaining hepatic parenchyma was tan-green and the gallbladder was markedly distended. There was also a 1 cm x 3 mm firm cream mass within the stomach wall.

On histopathology of the liver, small-to-large, multifocal-to-coalescing masses expanded and replaced the normal architecture of the liver. Within these masses were neoplastic cells variably arranged in packets, acini, and trabecular cords separated by fine fibrous vascular stroma (Fig. 3). The cells had round euchromatic nuclei and scant cytoplasm. Within the masses, the neoplastic cells ranged from monomorphic populations at the margins to anaplastic populations with marked nuclear polymorphism in the center. The stomach metastatic gastric mass extended through the gastric mucosa and submucosa (Fig. 4). There was also evidence of vascular invasion.

The morphology of the mass was consistent with gastric neuroendocrine carcinoma. This is a neoplasm that has been described in young bearded dragons as highly malignant and readily able to metastasize. This tumor should be considered as a rule-out in cases of young bearded dragons (< 3-y-old) with clinical signs of anorexia, weight loss, weakness, or vomiting.   AHL


Lyons JA. A gastric neuroendocrine carcinoma expressing somatostatin in a bearded dragon (Pogona vitticeps). J Vet Diagn Invest 2010;22:316–320.

Ritter JM, et al. Gastric neuroendocrine carcinomas in bearded dragons (Pogona vitticeps). Vet Pathol 2009;46:1109–1116.

Figures 1-4. Neuroendocrine carcinoma in a bearded dragon. Figure 1, 2. Ventral surface and cut surface of liver. Figures 3, 4. Hepatic nodule. Gastric mass. H&E. 20X.

Figures 1-4. Neuroendocrine carcinoma in a bearded dragon. Figure 1, 2. Ventral surface and cut surface of liver. Figures 3, 4. Hepatic nodule. Gastric mass. H&E. 20X.