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At 4 days of age, 7 gnotobiotic pigs were orally inoculated with broth cultures of both Campylobacter sputorum subsp mucosalis (CSM) and Campylobacter hyointestinalis (CH). One pig was killed and evaluated each week for 7 weeks. Forty-eight hours after inoculation, CH and CSM were recovered from the feces of the pigs; thereafter, only CH was recovered. Organisms morphologically typical of Campylobacter sp were observed on the mucosal surface and on the crypt epithelial cells of the ileum, cecum, and colon from post-inoculation weeks (PIW) 2 through 7. Bacteria were clustered around the surface opening of goblet cells in pigs at PIW 6 and 7. Crypt epithelial cell proliferation and intracellular bacteria were not seen, except in 1 pig (killed at PIW 7) in which intracellular bacteria were seen only in the cecum. Therefore, CSM and CH did not induce porcine proliferative enteritis in gnotobiotic pigs.

One hundred and twenty female mice (CF1 strain) were divided into three groups of 40. The first group was injected intraperitoneally with broth cultures of Treponema hyodysenteriae. The second group was injected with a combination of T. hyodysenteriae and Bacteroides vulgatus. The third group was injected with Treponema innocens. Peritoneal wash from four mice of each group was collected at eight time intervals postinjection, then prepared for and examined by light and electron microscopy. Peritoneal wash from one mouse at each time interval was prepared for microbiological examination. Treponema hyodysenteriae produced peritoneal macrophage aggregation, transient neutrophilia and macrophage cytolysis. Cytolysis was characterized by rarefaction of the cytoplasm, vesiculation of the endoplasmic reticulum, mild swelling of the mitochondria and disruption of the nuclear and ctyoplasmic membranes. The combination of T. hyodysenteriae and B. vulgatus produced macrophage aggregation and marked neutrophil necrosis. Peritoneal macrophages phagocytized more T. hyodysenteriae than B. vulgatus during early postinjection intervals. Treponema innocens failed to produce cytotoxicity of peritoneal macrophages but did produce macrophage aggregation and transient neutrophilia. Treponema hyodysenteriae and T. innocens did not multiply in the mice peritoneal cavity and were reisolated up to 16 hours postinjection. Bacteroides vulgatus was reisolated up to 24 hours postinjection.

Twelve pigs were inoculated orally with pure cultures of Treponema hyodysenteriae. Pigs were necropsied at different time intervals postinoculation; colonic specimens were collected and prepared for light and electron microscopy. The earliest colonic lesion detected by electron microscopy consisted of superficial vascular congestion and dilatation, edema of the lamina propria and intercellular separation of the epithelial cells at the crypt shoulders. This lesion progressed to epithelial cell necrosis and extrusion into the lumen and extravasation of red cells. Large numbers of spirochetes were present and free, between, over and under necrotic epithelial cells whether in place or partially extruded. Spirochetal penetration of colonic enterocytes and intracytoplasmic multiplication were confirmed in this study. The spirochetes were found to invade the epithelial cells only from their lateral borders. The relationship between T. hyodysenteriae and the colonic anaerobes was not determined.

Infection with larvae of Baylisascaris procyonis, the raccoon ascarid, was the cause of neurologic disease affecting young pheasants on a commercial pheasant ranch in Wisconsin. The disease was chronic and insidious, affecting 1% to 2% of the birds over a period of 2 years. Histologic lesions in the brain consisted of multifocal areas of necrosis and inflammation associated with Baylisascaris larvae. Onset of the disease at the farm correlated with introduction of chopped straw as bedding for the young birds. The straw was from a neighbor's barn and was contaminated with raccoon feces that contained B procyonis eggs. Cessation of use of the contaminated straw resulted in cessation of CNS disease in pheasants on the ranch.

An outbreak of histomonad infection of an apparent atypical nature was diagnosed in a flock of about 850 Bobwhite quail. Mortality was 95% over a 3-week period. The most prominent gross pathologic lesions were in the livers: disseminated white foci of necrosis, 1 to 2 mm in diameter, and subcapsular multifocal splenic necrosis was seen occasionally; lower intestinal lesions were infrequent. Histologic examination of liver and spleen sections revealed focal necrosis associated with variable numbers of protozoal organisms identified as a Histomonad spp. Identification of the protoza was ascertained by electron microscopy. Histmonads were isolated from affected quail livers and propagated in specific-pathogen-free chicken embryos. Lesions produced in embryos were evaluated. Isolates of the organism were used to reproduce the disease in young Bobwhite quail.

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.

Cerebrospinal nematodiasis and visceral larva migrans were diagnosed in an Australian (Latham's) brush turkey (Alectura lathami) that died at the Indianapolis Zoo following a progressive neurologic disease. Histologically, multifocal areas of malacia, necrosis, and inflammation were seen in sections of cerebrum, cerebellum, and midbrain; lesions were most severe in the cerebellum. A large granuloma in a lung contained cross sections of a large ascarid larva identified as Baylisascaris. The CNS lesions were typical of larval migration, as documented in other avian species. An epizootiologic investigation indicated that Baylisascaris procyonis was the etiologic agent and that the bird had acquired the parasite through contact with fecal contamination from wild raccoons at the St Louis Zoo, where the bird had been raised.

Immunologic deficiency was suspected in an 18-month-old Standardbred horse with persistent fever, multifocal bacterial infection, and neutropenia with a large number of immature neutrophils. Serum protein electrophoresis revealed marked depression of the gamma-globulin fraction (0.2 g/100 ml). Immunologic testing and histologic examination of lymphoid tissues identified the immune deficit as agammaglobulinemia. Serum concentrations of immunoglobulin (Ig)G and IgG(T) were initially low and declined with time; IgM and IgA were not detectable. The horse failed to produce antibodies when inoculated with foreign antigens but had a positive cell-mediated skin reaction to intradermal phytolectin injection, and lymphocytes responded normally to in vitro stimulation by mitogens. Histologic examination of lymphoid tissues revealed absence of germinal centers and plasma cells.

Massachusetts-type infectious bronchitis viruses (IBV) designated H120, from three sources, have been evaluated as vaccines. Significant subtype variations were observed with the different vaccines based upon challenge virus infection and typical IB lesions induced where homologous and heterologous serotypes were used. In numerous cases, there was little agreement between challenge virus recovery from the respiratory tract and the presence or absence and severity of IB lesions. The study indicates that histopathological observations provide a sensitive, reliable indicator of the immune response to IB vaccination and augment the use of challenge virus isolation attempts. The data suggest that the use of the latter criterion alone was insufficient in evaluating IB immunity. The study also demonstrated that IB vaccine strains, although labeled similarly, varied in their immunogenic properties. Manipulation of infectious bronchitis virus (IBV) and other factors should be considered when obtaining and employing vaccine strains from different sources. Complete characterization of IBV vaccine strains used commercially should be stressed together with an appropriate labeling of each.

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.

Disseminated acute focal hepatic coagulation necrosis was present in 9 turkeys submitted from 5 outbreaks of hemorrhagic enteritis. The lesion was unaccompanied by inflammatory cell infiltrate, biliary hyperplasia, or pancreatic necrosis, all of which tentatively distinguish this lesion from that of turkey viral hepatitis. No inclusion bodies were found.

The 2512 infectious bursal disease virus (IBDV) strain maintained in the authors' laboratory was compared with apparent 2512 IBDV isolates designated I-2512, P-2512, and H-2512. The latter three viruses were obtained from different sources and, ostensibly, had their origin in the Purdue laboratory. Their effects on immunogenicity, transmissibility, pathogenicity, and cell cultures varied. One of these isolates was said to be only 2 embryo passages higher than the original seed virus in our laboratory. Included in the study, also for comparison, was a cell-cultured-adapted 2512-cloned attenuated virus. The findings emphasize changes that may occur in the identity of a virus from manipulation, mutation, storage, errors in labeling, or other factors. These characteristics should be identified if the virus is to be used as a vaccine, in research, or for other purposes. The need for well-characterized reference strains in repositories is discussed relative to their importance in potential vaccine research and development.

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.

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.

A young woodchuck (Marmota monax) with a history of CNS dysfunction and abnormal behavior was submitted frozen to the Animal Disease Diagnostic Laboratory, Purdue University, as a rabies suspect. The woodchuck was negative for rabies by the fluorescent antibody test. Histologically, multifocal areas of necrosis, malacia, and inflammation were seen in sections of cerebrum, midbrain, and cerebellum, accompanied by marked perivascular cuffing with eosinophils and lymphocytes. Sections of lung contained parasitic granulomas, one of which contained a large ascarid larva identified as Baylisascaris sp. The CNS lesions were typical of parasite migration, and resembled those commonly associated with infection with Baylisascaris larvae of raccoon or skunk origin. Cerebrospinal nematodiasis was diagnosed as the cause of the nervous disorder.

Eight strains of infectious bursal disease virus (IBDV) were characterized by the criteria of immunity and pathogenicity engendered in young chickens. Some strains have been used commercially, and the others are potential candidates for vaccines. They were administered by drinking water, eyedrop, vent drop, and subcutaneous and aerosol routes. The viruses varied widely in pathogenicity in terms of bursal damage, morbidity, and mortality. Immunity induced with different routes of administration also differed markedly when measured by challenge, virus serum-neutralizing antibody titers, and the agargel precipitin test. Maternally derived immunity interfered with stimulation of active immunity by some of the less pathogenic strains. The more virulent strains, however, were able to provide protection under similar circumstances, although bursal damage was frequently severe. Two strains proved relatively virulent by the criteria employed. Characteristics desirable for IBDV strains to be given as vaccines under field conditions to young chickens are discussed briefly.