Detection and heterogeneity of herpesviruses causing Pacheco's disease in parrots.

Pacheco's disease (PD) is a common, often fatal, disease of parrots. We cloned a virus isolate from a parrot that had characteristic lesions of PD. Three viral clones were partially sequenced, demonstrating that this virus was an alphaherpesvirus most closely related to the gallid herpesvirus 1. Five primer sets were developed from these sequences. The primer sets were used with PCR to screen tissues or tissue culture media suspected to contain viruses from 54 outbreaks of PD. The primer sets amplified DNA from all but one sample. Ten amplification patterns were detected, indicating that PD is caused by a genetically heterogeneous population of viruses. A single genetic variant (psittacid herpesvirus variant 1) amplified with all primer sets and was the most common virus variant (62.7%). A single primer set (23F) amplified DNA from all of the positive samples, suggesting that PCR could be used as a rapid postmortem assay for these viruses. PCR was found to be significantly more sensitive than tissue culture for the detection of psittacid herpesviruses.

Staphylococcus aureus pneumonia in turkey poults with gross lesions resembling aspergillosis.

The present report describes a case of Staphylococcus (Staph.) aureus pneumonia in turkey poults. Initially, 3-day-old poults with a history of increased mortality were submitted for necropsy. The poults had severe bilateral consolidation of the lungs with miliary caseous nodules. The gross lesions in the lungs were highly suggestive of aspergillosis. The next day, postmortem examinations were performed on 60 dead poults at the farm, and all 60 had similar lung lesions. Histopathologic examination of affected lungs revealed severe subacute multifocal bronchopneumonia with intralesional bacteria. Tissue Gram stain of lung sections demonstrated gram-positive bacterial cocci. Gomori methenamine silver stain of the lungs failed to demonstrate fungal agents. The histologic distribution of the lesions suggested an aerogenous route of infection. Staphylococcus aureus was isolated in pure culture from affected lungs. Hatchery contamination was suspected because of the severity and early onset of the lesions. Bacterial monitoring at the hatchery demonstrated marked Staph. aureus contamination in two setters, a hatcher's air duct, and the poult room. Improved hatchery cleaning and disinfection prevented a reoccurrence of the problem.

Respiratory diseases of gallinaceous birds.

Respiratory conditions constitute many of the diseases affecting all avian species, including gallinaceous birds. Clinical signs and gross lesions of different respiratory diseases are often similar, and establishing a definitive diagnosis may require ancillary laboratory testing. Determination of a specific diagnosis allows practitioners to select the most effective therapies and to prescribe a management program that prevents recurrence.

Reticuloendotheliosis in captive greater and Attwater's prairie chickens.

Reticuloendotheliosis in captive greater (Tympanuchus cupido pinnatus) and Attwater's (T. cupido attwateri) prairie chickens is reported for the first time. Between September 1993 and August 1994, two adult female wild-caught greater prairie chickens housed at Texas A&M University (College Station, Texas, USA) were observed with multiple subcutaneous nodules. Both birds were euthanatized. Complete necropsy examinations revealed lesions limited to the skin of each bird. Histopathologic examination of lesions revealed pleomorphic lymphoreticular cells suggestive of reticuloendotheliosis and reticuloendotheliosis virus (REV) was demonstrated in tumor tissue by polymerase chain reaction and virus isolation. Between September 1994 and June 1995, five additional greater prairie chickens and two Attwater's prairie chickens were euthanatized or found dead with evidence of lymphoreticular neoplasia in multiple organ systems. Initial testing of the captive flock in December 1994 for evidence of viremia and antibody to reticuloendotheliosis virus revealed over 50% of the tested birds were viremic, but none developed antibodies. Subsequent testing between January 1995 and January 1996 indicated that once infected with reticuloendotheliosis virus, Attwater's prairie chickens tended to remain outwardly healthy despite persistent viremia compared to infected greater prairie chickens which had higher morbidity and mortality rates within 60 to 90 days after initial detection of viremia and did not usually develop persistent viremia. Antibodies to REV were detected in only three captive greater prairie chickens and only in 1995. Six of the nine birds that were euthanatized or found dead due to reticuloendotheliosis developed viremia prior to death; three birds were not tested prior to death. Testing of free-ranging greater and Attwater's prairie chickens for reticuloendotheliosis is recommended prior to translocation or release.

Infectious bursal disease virus variant from commercial Leghorn pullets.

An infectious bursal disease virus (IBDV) was isolated from 39-to-43-day-old commercial leghorn pullets suspected of having infectious bursal disease (IBD). These chickens had been vaccinated with a commercial live IBDV vaccine at 28 and 35 days of age. An isolate designated IN was recovered using specific-pathogen-free (SPF) chickens and the BGM-70 established cell line. Experimental studies using SPF chickens vaccinated with either inactivated vaccines made from the vaccine strain used in the problem flock or a standard-type vaccine indicated no protection against the IN isolate. However, two variants and another standard-type vaccine induced protection against the IN isolate. Cross-neutralization tests indicated that the IN isolate differed antigenically from commercial vaccine strains and was related to the variant IBDV strains recently isolated from broilers. To our knowledge, this is the first report of a variant IBDV recovered from commercial layer chickens in the United States.

Furazolidone-associated cardiomyopathy in two Indiana flocks of ducklings.

Furazolidone (FZ)-induced congestive cardiomyopathy was diagnosed as the cause of high mortality and unthriftiness in two flocks of white pekin ducklings. Cumulative mortality at 7 weeks of age was 10.0-14.4%. Samples of FZ-supplemented feeds fed to flocks 1 and 2 from day 1 to day 14 had 140 and 150 mg FZ/kg, respectively. Both flocks had various degrees of water restriction. Clinically, the ducklings had dyspnea, incoordination, and abdominal distention. Necropsy findings included pulmonary edema and congestion, ascites, atrophic congested livers covered with sheets of fibrin, and cardiac enlargement with biventricular dilatation. Cardiac alterations were minimal by light microscopy. Ultrastructurally, scattered myocytes had myofibrillar lysis. These outbreaks occurred following intake of FZ at therapeutic dosages and emphasize the high susceptibility of young ducklings to FZ cardiotoxicity.