Embryonating eggs were inoculated with filtered porcine ileal mucosa containing intracellular curved rods (ICR) and incubated for 4 to 6 days. Three of 12 pigs given the eggs per os developed microscopic lesions of proliferative enteritis (PE). Nonchallenge-exposed control pigs did not develop lesions of PE. Four of six positive control pigs given ileal mucosa from pigs with PE also developed microscopic lesions of PE. All of the PE lesions were found in pigs necropsied 10 to 29 days after challenge exposure. None of the swine in the study had clinical signs or gross lesions of PE. Campylobacter spp were isolated from pigs with and without exposure to the ileal mucosa from pigs with PE. There was no relationship between Campylobacter spp isolation and development of lesions. Deoxyribonucleic acids extracted from embryonating chicken eggs injected with the equivalent of 0.5 mg of mucosal lesions and incubated for 4 days hybridized to a DNA probe specific for the ICR whereas DNA extracted from 1.5 mg of mucosal homogenates of the same proliferative tissue did not hybridize with the same probe. Results of these experiments indicated that ICR injected into eggs remained infective for pigs and suggest replication of ICR in the first-passage eggs.

The prevalence of mycoplasmal and ureaplasmal recovery from tracheobronchial lavage specimens and the prevalence of mycoplasmal recovery from pharyngeal swab specimens from dogs with (n = 38) or without (n = 26) pulmonary disease were determined. Similar mycoplasmal recovery rates were found for tracheobronchial lavage specimens from dogs > 1 year old with (21%) or without (25%) pulmonary disease. Prevalence of mycoplasmal recovery from tracheobronchial lavages was significantly associated with pulmonary disease among dogs < 1 year old (P = 0.04), and with dogs that had concurrent Bordetella (P = 0.006) and Streptococcus (P = 0.05) isolations. Among dogs with pulmonary disease, mycoplasmas were significantly (P = 0.02) more prevalent in dogs with septic inflammation than in dogs with nonseptic inflammation of the tracheobronchial tree. Ureaplasmas were only isolated from a tracheobronchial lavage specimen of 1 dog with pulmonary disease and from none of the dogs without pulmonary disease. Most dogs with (84%) and all dogs without pulmonary disease had mycoplasmas isolated from the pharynx. Seemingly, mycoplasmas are part of the normal pharyngeal flora of most dogs and normal inhabitants of the lower airway in about a fifth to a fourth of the canine population greater than or equal to 1 year old. Dogs < 1 year old with pulmonary disease and dogs with concurrent Bordetella or tracheobronchial streptococcal isolations may be more susceptible to mycoplasmal colonization of the lower airways. Seemingly, ureaplasmas are rarely associated with pulmonary disease, and are not normal inhabitants of the trachea and bronchi of dogs.

A method of extracting bacterial DNA from swine feces was developed and used in a molecular assay for the presence of ileal symbiont (IS) intracellularis, formerly known as the Campylobacter-like organism associated with swine with proliferative enteritis. Hybridization with a digoxigenin-labeled, IS intracellularis-specific probe detected the presence of IS intracellularis at a concentration of 10(7) organisms/g of feces. This method was sufficient to detect is intracellularis in the feces of swine with experimentally induced and naturally acquired infection. Results of the hybridization were in agreement with those from histologic postmortem examination.

In 6 anesthetized ponies, 3 segments of jejunum and 3 segments of small colon were isolated from the peritoneal cavity in plastic bags filled with Hanks' balanced salt solution. One jejunal and 1 small colon segment were subjected to venous strangulation obstruction for 3 hours (VSO-3), venous strangulation obstruction for 6 hours (VSO-6), or a 6-hour sham procedure to control for changes induced by isolation in a plastic bag. Additional segments of jejunum and colon that were not placed in bags served as controls for histologic examination and collagenase measurements. Samples of fluid surrounding the intestine were obtained for chemical analyses, nucleated cell count, aerobic and anaerobic bacteriologic culture, and measurement of collagenase activity. Full-thickness tissue samples were obtained for histologic examination and measurement of collagenase content. Bacteria did not cross the intestinal wall after 3 and 6 hours of VSO, despite severe mucosal lesions in these segments. At 6 hours, P(O2) was significantly less and P(CO2) was significantly (P < 0.05) greater in the fluid surrounding the VSO-6 jejunal segments, compared with the sham jejunal segments. The pH was significantly (P < 0.05) less in fluid surrounding VSO-6 small colon segments, compared with the sham colon segments at 6 hours. For jejunum and small colon, phosphate and lactate concentrations were significantly (P < 0.05) greater in VSO-6 fluid than in the corresponding sham fluids at 6 hours. Fibrin formed around all VSO segments, although fibrinogen was not detected in the surrounding fluid, indicating possible rapid conversion of fibrinogen to fibrin. Fluid collagenase activity increased significantly (P < 0.05) in all segments over 6 hours. The preparation used in this study was successful in measuring local changes on the serosal surface of intestine subjected to VSO and in isolating segments under study in a sterile environment.

In an abattoir-based case-control study, histologic, and macroscopic examination of porcine intestines at slaughter and 2 molecular assays were compared for use as diagnostic tests of proliferative enteritis (PE). Fecal samples and intestinal specimens were collected from pigs with grossly thick ileum and from clinically normal pigs at slaughter. Tissue specimens were fixed in neutral buffered 10% formalin, and sectioned. Sections stained with H&E were examined for proliferative lesions by a pathologist unaware of the group to which the pig had been assigned on the basis of results of gross examination. Adjacent tissue sections, stained with Warthin-Starry (silver) stain, were examined for presence of the intracellular bacterium of PE, ileal symbiont (IS)-intracellularis, in the enterocytes of the intestinal crypts by the senior author, who was unaware either of the group to which the pig had been assigned or diagnosis by the pathologist. Bacterial DNA was extracted from the fecal samples and assayed by dot-blot hybridization and polymerase chain reaction (PCR) for presence of IS-intracellularis DNA, without knowledge of results of the other examinations. The PCR assay for IS-intracellularis was a specific and sensitive diagnostic test for PE, and dot-blot hybridization was sensitive, but was less specific. Macroscopic examination of intestines at slaughter was a sensitive, but not specific, test. Association between IS-intracellularis and proliferative lesions was statistically examined in the same study. There was a highly significant (P = 0.0078) association between presence of naturally acquired proliferative lesions and intracellular infection induced by IS-intracellularis. The odds ratio of greater than or equal to 14 and estimated attributable fraction of greater than or equal to 92% indicate that IS-intracellularis may be a necessary cause of PE.

Undifferentiated distal respiratory tract disease (nasal discharge, cough, pneumonia) in foals (1 to 8 months old) is a burdensome economic problem on breeding farms yet, the infective agents associated with these episodes have not been well described. Possible causes of these episodes of illness were investigated by culturing specimens of proximal and distal airways of clinically diseased foals (n = 101), prior to any treatment, for aerobic and anaerobic bacteria and viruses (rhinoviruses, equine arteritis virus, equine herpesvirus subtype 1 [EHV-1], influenza virus, and adenovirus). Pairs of sera (n = 47) were examined for antibodies to influenza A virus, equine subtypes 1 and 2, EHV-1, and adenovirus antigens, and sera obtained from foals during acute infection were examined for antibodies (by agar gel immunodiffusion [AGID]) to equi factor antigens of Rhodococcus equi. Viruses were not isolated from the proximal (swab) or distal (bronchial lavage) airway specimens in foals, and only 2 of 47 randomly selected foals seroconverted to EHV-1. Serotiters to the other viruses were low and frequently decreasing between samples, which was compatible with maternally derived antibody. Streptococcus zooepidemicus was the predominant isolate from bronchial lavage specimens (88/101 cases), accompanied by alpha-hemolytic streptococci (8 cases), Bordetella bronchiseptica (13 cases), Staphylococcus epidermidis (9 cases), and other organisms in lesser frequency. Only Str zooepidemicus was recovered significantly (P < 0.05) more often in cases than in controls. The AGID test was found useful to detect 1/26 with presumed exposure to R equi, but positive tests results did not correspond well with bacterial culture results; positive AGID results were recorded in 34% of culture-negative foals. However, foals from which R equi was isolated were distinctive from the other foals on the basis of fever (> 39 C), lack of nasal discharge, blood neutrophilia and decreased percentage of neutrophils in bronchial lavage fluid samples. Isolation of Str zooepidemicus was significantly (P < 0.01) associated with increasing neutrophil percentage in bronchial lavage fluid. In conclusion, the pathogenic roles of Str zooepidemicus and R equi were established in this group of foals with distal respiratory tract infections by use of clinical, endoscopic, hematologic, and cytologic methods. There was no evidence of a viral cause for these infections, indicating that manifestations of distal respiratory tract infection are attributable to bacterial infection causing inflammation of the airways. Further studies are warranted to pursue more-sensitive methods for detection of viral antigen or antibody in undifferentiated distal respiratory tract disease episodes in foals.

Vaginal aerobic bacterial flora was studied in 5 healthy bitches before, during, and after a 10-day period of treatment with ampicillin and an equally long period of treatment with trimethoprim-sulfamethoxazole. Blood variables and antimicrobial drug susceptibility also were studied. Bacteria were isolated from all bitches before the first treatment period. Bitches from which only a sparse number of bacteria were isolated had flora that varied from day to day. In most instances when bitches were given an antibiotic to which their vaginal bacterial flora was susceptible, these bacteria were eradicated after only 1 day of treatment. This was true for pasteurellae, streptococci, and, in all but one case, Escherichia coli. Staphylococcus intermedius was more difficult to eradicate, and, although susceptible in vitro, it was unaffected by antibiotic treatment in 1 bitch and it took 7 days to eradicate in another. Eradication of aerobic bacteria in the vagina was total only in the bitch that had sparse flora from the beginning. Bacteria colonized within 0 (in 4/5 bitches) to 4 days after termination of treatment with ampicillin and within 0 (in 4/5 bitches) to 3 days for trimethoprim-sulfamethoxazole. Mycoplasmas emerged during and after both treatment periods, and E coli became apparent during treatment with trimethoprim-sulfamethoxazole. Because mycoplasmas may be genital pathogens in bitches and E coli is a common uropathogen, their appearance should be an argument against widespread use of antibiotics in healthy breeding bitches. Two bitches developed a vaginal discharge during treatment or shortly after. Blood variables did not change during the study, nor did antimicrobial drug resistance of the isolated bacteria.