H. L. Thacker

Respiratory cryptosporidiosis in broiler chickens.

A flock of 7-week-old broiler chickens in northwestern Arkansas showed signs of respiratory distress. Gross pathologic alterations were excessive exudate in the tracheas and congestion of the nasal turbinates. An adenovirus was isolated from fresh trachea specimens. Microscopically, alterations in tracheal sections were thickened mucosa with inflammatory-cell lamina-proprial infiltrate and epithelial squamous metaplasia. Protozoan parasites present on the epithelial surface were identified by electron microscopy as Cryptosporidium spp. These organisms were attached to the tracheal mucosa epithelium and the luminal surface of mucous glands. The significance of the intercurrent adenovirus infection was not determined.

Verminous encephalitis in commercial chickens.

An outbreak of fatal encephalitis in four-week-old chickens is described. The causal agent was shown to be Baylisascaris procyonis, the common roundworm of raccoons.

Toxoplasmosis in mynahs.

Visceral toxoplasmosis was diagnosed in 23 mynahs (Acridotheres) imported from Mexico, which resulted in the death of all birds in the shipment. The affected birds were inappetent and depressed and had ruffled feathers before death. Gross alterations included mottled, enlarged livers with multiple diffuse subcapsular white foci, congested lungs, mottled spleens, and thickened air sacs. Microscopic alterations were multifocal granulomatous hepatitis, pneumonitis, diffuse splenitis, focal mononuclear myocarditis, and airsacculitis. Foamy macrophages in affected areas of the livers contained 8-10 protozoan organisms 1-3 nm in diameter. Similar organisms were present in affected spleens. The organisms were identified with special stains and electron microscopy as Toxoplasma gondii. Human infection was diagnosed in the caretaker by an attending physician. He was treated with pyrimethamine and apparently recovered.

Immune response of White Leghorn chicks from vaccination with different strains of infectious bursal disease virus and in the presence of maternal antibodies.

SUMMARY White Leghorn chicks 1 to 11 days old possessing maternal antibodies to infectious bursal disease (IBD) were vaccinated with the 2512-P48, 2512-P84, LKT, and BV strains of IBD virus by different routes. Their dams had been vaccinated against IBD at one day old and revaccinated at 14 weeks and every 90 days thereafter. The 2512-P48, 2512-P84, and LKT strains did not bestow satisfactory immunity on the progeny as measured by challenge and the agar-gel precipitin test. In contrast, the BV strain engendered good immunity when used as a vaccine at as early as 4 days old. Moderate lesions were found histologically in the cloacal bursa in the postvaccination period, although no clinical signs of IBD were noted. Significant immunosuppression did not occur when chicks were vaccinated with BV IBD virus at 4 days old, vaccinated against Newcastle disease 7 days later, and subsequently given Newcastle disease challenge virus. Primary vaccination of White Leghorn chicks to be placed in IBD-endemic areas in the field is discussed with reference to susceptibility to virus infection, vaccination status of the breeders, level of maternal antibodies (7), and the need for using IBD vaccine strains of differing degrees of virulence and immunogenicity to meet frequently varying field conditions.

Etiology and epidemiology of verminous encephalitis in an emu.

Verminous encephalitis was reported in 1978 in an emu (Dromaius novaehollandiae) from Indiana (8). The bird was the second of two emus that had developed severe ataxia followed by bilateral leg paralysis, which resulted in natural death of the first bird. The second emu was presented alive but unable to stand to the Purdue Animal Disease Diagnostic Laboratory. No gross lesions were found, but on histologic examination, focal malacic lesions and inflammatory changes were seen in the cerebellum, in association with an ascarid larva. No generic or specific identification of the parasite was made, nor was information presented concerning the possible source or mode of infection of the birds. Of the four other known outbreaks or cases of cerebrospinal nematodiasis in avian species (1,3,4,5), the two most extensive were positively linked to migrating larvae of Baylisascaris procyonis, the common roundworm of raccoons (3,4). In one of these, 622 chickens died following a single exposure to contaminated bedding (4), and in the other, all 85 quail died following exposure to a contaminated run (3). A third case involved central nervous system (CNS) disease in a chukar partridge; B. procyonis was suggested as the cause (5). In the fourth case, no identification was made of the ascarid species responsible for CNS disease in tumbler pigeons (1). The present report is based on a retrospective evaluation of a case of verminous encephalitis in an emu (8). New information is presented concerning the etiology and epidemiology of the parasite involved. Examination of sections of cerebellum revealed an ascarid larva within a focus of reactive malacia. The larva had prominent

Lesions Induced in the Respiratory Tract of Chickens by Serologically Different Adenoviruses

Ten strains of adenovirus representing 10 serotypes were administered intratracheally to two groups of 3-week-old specific-pathogen-free chickens. Birds in group 1 were given only adenovirus. Birds in group 2 were inoculated with a virulent infectious bursal disease virus (IBDV) by eye-drop at one day of age as well as with the adenovirus at 3 weeks. The chicks were examined daily. Respiratory rales were observed in some birds with the dual infection. Gross pathologic alterations were minimal and limited to multiple scattered, pale foci in the lungs of an occasional bird in various groups. Histopathologic changes in the lungs were those of multifocal interstitial and, occasionally, diffuse pneumonia. The pneumonic lesions were more severe in the chickens given IBDV. Tracheitis was seen with two of the serotypes.

Cerebrospinal nematodiasis in bobwhite quail.

Natural outbreaks of avian cerebrospinal nematodiasis have been reported in a chukar partridge (10), in pigeons (7), in an emu (16), and most recently as an extensive outbreak in commercial chickens (9). Migrating larvae of the common ascarid of raccoons, Baylisascaris procyonis, were the cause of the outbreak in commercial chickens (9) and were suggested to be the etiologic agent of encephalitis in the chukar partridge (10). This report describes an outbreak of verminous encephalitis in a flock of bobwhite quail, which resulted in a high death rate.

Erysipelas in domestic white Pekin ducks.

Two epornitics of erysipelas were diagnosed in domestic White Pekin ducks. The first was in 2,000 18-day-old ducklings with a 30% mortality. The other was in 2,400 breeder hens with losses of four or five birds a day. Gross pathologic lesions in birds necropsied from both instances were enlarged swollen livers with occasional subcapsular hemorrhages. Pure isolates of Erysipelothrix insidiosa only were cultured from the livers. Histologic examination revealed congestion and multifocal necrosis in the liver and spleen with associated reticuloendothelial cell proliferation. Special stains demonstrated numerous organisms within the reticuloendothelial cells.

Quaternary ammonium compound toxicity in chickens.

Two commercial White Leghorn flocks of 41,000 and 57,000 25-week-old hens experienced death losses of 676 and 1,089 birds in a week. Six birds from each flock were presented for necropsy to the Animal Disease Diagnostic Laboratory at Purdue University with a clinical history of excessive deaths, unsatisfactory production, and dehydration. Gross lesions were present on the tongue and on oral and pharyngeal mucosa as uniformly pale or white areas with interspersed multifocal sites of ulceration. Other changes were cyanotic, shriveled combs and wattles and ruptured ovarian follicles with concurrent egg yolk peritonitis. Microscopic examination revealed large areas of coagulative necrosis with multifocal epithelial ulceration of the oral and pharyngeal mucosae. There was an intense inflammatory, heterophilic response at the periphery of affected areas. Alterations in the abdominal viscera were limited to egg yolk peritonitis. The high death rate and oral lesions were attributed to accidental use of excessive levels of a quaternary ammonium disinfectant in the drinking water.

Fatal hepatic trematodiasis in cockatoos due to Platynosomum proxillicens.

Severe hepatic trematodiasis due to Platynosomum proxillicens was diagnosed as the cause of death in two sulfur-crested cockatoos (Cacatua sulfurea). Gross pathologic alterations included hepatomegaly in one bird and hepatic and generalized cyanosis in the other. Microscopic changes included multifocal hepatic necrosis, dilated fibrous bile ducts containing trematode, parasites, bile duct hyperplasia, and hepatic inflammation.