James F. Davis

Experimental reproduction of severe hypoglycemia and spiking mortality syndrome using field-derived and embryo-passaged preparations.

The clinical signs, enteritis, weight depression, and hypoglycemia of spiking mortality syndrome were experimentally reproduced in broiler breeders and broiler chicks. Inocula included 1) virus-like particles from intestines of chicks with spiking mortality syndrome that had been banded in a discontinuous Renograffin gradient, 2) homogenized darkling beetles collected from litter of farms where spiking mortality syndrome had occurred repeatedly, and 3) homogenized embryos which had been inoculated with the Renograffin-banded material. Arkansas variant infectious bronchitis virus and arenavirus-like particles were identified in the inocula. Serology on samples from surviving chicks suggested the presence of an avian encephalomyelitis virus in one of the inocula. One-day-old (n = 172) and 2.5-day-old (n = 30) chicks were inoculated orally, and some were also injected intraperitoneally or subcutaneously, with 0.5 ml of the inocula. Twelve to fourteen days postinoculation, chicks were fasted for 4-6 hours, then briefly stressed with a cool water spray. Within 1.5 hours, inoculated chicks began dying with severe hypoglycemia and clinical signs of spiking mortality syndrome. Body weights were significantly depressed. Uninoculated controls (n = 130) from the same hatches, also fasted and stressed, were unaffected clinically and were not hypoglycemic. One group (n = 52) of inoculated chicks exposed to a controlled lighting program was unaffected clinically, had significantly higher mean plasma glucose levels, and had significantly less body weight depression than chicks exposed to continuous lighting. We concluded that exposure to controlled amounts of light/darkness can ameliorate much of the hypoglycemia, mortality, and runting-stunting associated with spiking mortality syndrome of chickens. The significance of the viruses and virus-like particles detected in the inocula is currently under investigation.

Markedly Reduced Pancreatic Glucagon Levels in Broiler Chickens with Spiking Mortality Syndrome

Pancreata from 19 hypoglycemic field broilers with spiking mortality syndrome and 19 clinically normal field broilers with normal blood glucose levels were collected and quick-frozen in liquid nitrogen immediately after the chicks were bled and killed. All chicks were 16 days old and were of the same genetic cross. Pancreata were weighed, and acid-alcohol extractions were made on each specimen. Radioimmunoassays for glucagon levels were made on each extract. Mean pancreatic glucagon content of the hypoglycemic chicks was depressed 14-fold (93.1%) compared with that of the non-hypoglycemic group. There was a close correlation between plasma glucose levels and pancreatic glucagon levels (P = 0.0001).

Adenovirus Particles and Inclusion Body Hepatitis in Pigeons

Adenovirus should be added to the list ofdifferential diagnoses of liver disease in pigeons when intranuclear inclusion bodies are present. This report describes adenovirus particles in the nuclei of hepatocytes, hepatitis, necrosis and death in pigeons from two premises. Although a cause-and-effect relationship between adenovirus, liverlesions and death ofthesepigeons is logical, otherfactors such as excessive administration of medication may have exacerbated virus infection and clinical signs.

Myocarditis in 9- and 11-Day-Old Broiler Breeder Chicks Associated with a Reovirus Infection

SUMMARY. Nine- and 11-day-old male broiler breeder chicks from a flock with excessively high mortality were found to have ascites, fibrotic and necrotic livers, and round, thin-walled hearts. Virus isolation on liver homogenates and sequencing of PCR products of the isolate identified a reovirus whose sequence varied from sequences of other published reoviruses. Histopathology supported a diagnosis of reovirus-associated myocarditis and myocardial necrosis. This virus was possibly transmitted vertically from the primary breeder flock. RESUMEN. Reporte de Caso—Miocarditis en pollitos reproductores pesados de 9 y 11 días de edad asociada con una infección por reovirus. Pollitos reproductores pesados de nueve y 11 días de edad, procedentes de una parvada con mortalidad excesivamente alta, mostraron ascitis, hígado fibrótico y necrótico, y corazones redondos, con paredes delgadas. Mediante el aislamiento viral de homogeneizados de hígado y la secuenciación de los productos PCR se identificó un reovirus cuya secuencia varía de las secuencias de otros reovirus publicados. La histopatología confirmó el diagnóstico de miocarditis y necrosis del miocardio asociada con reovirus. Este virus posiblemente se transmitió verticalmente, de la parvada de reproductores.

Reovirus Infections in Young Broiler Chickens

SUMMARY Selected 10-to-21-day-old broiler chickens from flocks undergoing runting-stunting syndrome were found to have significant pancreatic damage, grossly and histologically. Six reoviruses, with sequences that varied, both from each other and from S1133 reovirus, were isolated from these pancreases and from pancreases of specific-pathogen-free leghorn sentinels placed on two of the broiler farms for 7 days. RESUMEN Reporte de Caso—Infecciones por reovirus en pollos de engorde jóvenes. Se encontró daño pancreático significativo macroscópico y microscópicamente en pollos de engorde de 10 a 21 de edad seleccionados por bajo crecimiento en parvadas con síndrome de mala absorción. Se aislaron seis reovirus, con secuencias que variaron tanto unos de otros como con respecto a la de cepa S1133, a partir del páncreas de las aves afectadas y del páncreas de aves Leghorn libres de patógenos específicos que fueron alojadas como centinelas en dos granjas de pollos de engorde por siete días.

Diagnoses of Infections by the So-Called Chick Anemia Agent: Anemia and Direct Transmission Electron Microscopic Detection of Virus

Blood from 48 chicks was examined for anemia (packed cell volume), and plasma was examined for virus particles by direct transmission electron microscopy (DTEM). There was agreement between the occurrence of anemia and the presence of CAA virus particles in plasma from anemic chicks (Kappa = 0.2425, Z = 2.096, P = 0.036). Although DTEM is a method that can be used to diagnose CAA in chicks, more sensitive, economical and less laborious diagnostic assays are needed.

Transmissible Viral Proventriculitis Identified in Broiler Breeder and Layer Hens

SUMMARY. Transmissible viral proventriculitis (TVP) is a recognized cause of production losses in broiler chickens, but previously it has not been reported in broiler breeder and commercial layer hens. In this study, TVP was identified in broiler breeder and commercial layer hens, 9–20 wk of age, based on histopathologic detection of characteristic microscopic lesions. Microscopic lesions in proventriculi of affected hens consisted of glandular epithelial necrosis, ductal epithelial hyperplasia, replacement of glandular epithelium with ductal epithelium, and diffuse interstitial lymphoid infiltration. Additionally, chicken proventricular necrosis virus (CPNV), a virus previously identified as the etiology of TVP in broiler chickens, was detected in proventriculi of TVP-affected hens using a reverse transcriptase–polymerase chain reaction procedure. The findings identify TVP as a potential cause of production losses in broiler breeder and commercial layer hens and provide additional evidence for etiologic involvement in TVP by CPNV.

Acute Monensin Toxicosis in Broiler Breeder Chickens

SUMMARY. Peracute onset of disease was reported in a 42-wk-old broiler breeder flock that was presented by error with feed containing monensin at approximately seven times the approved level for broiler chickens. Morbidity and mortality were extremely high, and the affected chickens displayed feed refusal, decreased water consumption, and severe paralysis that ranged from abnormal gait to a complete inability to move. During the first 10 days postingestion of the suspect feed, mortality in hens reached 13.7% and 70.9% in the roosters. Hen day production decreased from 67% to 3% in the same period of time. A total of 638 g/ton of monensin was detected in suspect feed samples by one laboratory and 740 g/ton in a second laboratory. Twenty-one days after removal of the suspect feed, the mortality rate returned to normal levels in both hens and roosters, albeit feed consumption and egg production remained extremely low, which prompted the company involved to eliminate the flock.

Incidence of anemia and polycythemia in clinically ill Georgia broilers.

The incidence of anemia and polycythemia was established in clinically ill Georgia broilers that were tested for packed cell volume (PCV) during 1988 and 1989. More than 66% (324/488 = 66.4%) of PCV-tested broiler chicks were anemic, and less than 2% (8/488 = 1.6%) of PCV-tested chicks were polycythemic. The incidence of anemia was significantly (P less than 0.001) higher than expected (2.5%) at age 7 days (56.9%), 14 days (83.9%), 21 days (74.7%), 28 days (58.7%), and 35 days (57.9%). The incidence of polycythemia was significantly (P less than 0.001) higher than expected (2.5%) in 35-day-old broilers (21.1%) but was not significantly different from the expected rate in broilers at age 7 days (0%), 14 days (1.8%), 21 days (0.3%), and 28 days (4.3%). The established rates for anemia were much higher than we would have hypothesized. This led us to believe that either 1) an etiology for anemia is present in epizootic proportions in Georgia broilers, or 2) the standard method for establishing reference intervals for anemia in animals does not apply to broiler chicks.

Comparisons of Packed Cell Volumes (PCVs) from So-Called Chicken Anemia Agent (CAA; a Virus)-Free Broilers to PCVs from CAA-Free Specific-Pathogen-Free Leghorns

Packed cell volumes (PCVs) from 3-, 7-, 14-, 21-, 28-, and 35-day-old clinically healthy chicken anemia agent (CAA)-free and specific-pathogen-free (SPF) leghorn chicks were compared with PCVs from age-matched clinically healthy CAA-free broiler chicks. The PCVs of the SPF chicks regressed significantly (F = 20.6, df = 2/3, P < 0.025) on age in a linear fashion. The PCVs of the broiler chicks regressed significantly (F = 9.56, df = 2/3, P < 0.05) on age in a cubic parabola. The mean PCVs of the broiler chicks were significantly (P < 0.05) higher than PCVs of SPF chicks at every tested time interval. Results indicate that PCV values are higher in broiler chicks than in SPF leghorn chicks, and that PCVs increase as chicks age. Clinicians, diagnosticians, and investigators who intend to work with chicken blood must be aware of these differences.