Two hundred ninety-six Eschericbia coli isolates from feces or intestines of calves with diarrhea were hybridized with 7 gene probes. One probe (the eae probe) was derived from the eae gene coding for a protein involved in the effacement of the enterocyte microvilli by the group of bacteria called attaching and effacing E coli (AEEC), and 2 probes were derived from genes coding for the Shiga-like toxins (SLT) 1 and 2 produced by the verocytotoxic E coli (VTEC). The other 4 probes were derived from DNA sequences associated with the adhesive properties of enteroadherent E coli (EAEC) to cultured cells (the EAF probe for the localized adherence pattern, probes F1845 and AIDA-1 for the diffuse adherence pattern, and the Agg probe for the aggregative adherence pattern). Hybridization results for the eae probe were in agreement, for all but 1 of the 8 isolates, with previously published phenotypic results of microvilli effacement. The latter was previously reported as effacing the microvilli of calf enterocytes, but was eae probe-negative. Two classes of isolates hybridized with the eae probe. Members of a first class (60 isolates) additionally produced a positive signal with 1 or both of the SLT probes (VTEC-AEEC isolates). Isolates hy- bridizing with the eae and the SLT1 probes were the most frequent: 56 isolates (ie, 93% of all VTEC-AEEC). Members of the second class (10 isolates) failed to hybridize with either SLT probe (non-VTEC-AEEC isolates). Most isolates of these 2 classes belong to only 4 serogroups: O5, O26, O111, and O118. In addition to these 2 AEEC classes, a VTEC class (20 isolates) was observed. Such isolates were positive with 1 or both SLT probes, but were negative with the eae probe. All but 1 isolate belonged to serogroups not found among the AEEC isolates. Only 7 of all AEEC and VTEC isolates were positive with the EAF, the F1845, or the AIDA-1 probe, and none were positive with the Agg probe. On the other hand, 32 non-VTEC, non-AEEC isolates were po.

Fifteen isolates of Escherichia coli obtained from the blood and tissues of septic foals had plasmid DNA of size ranging from 2.5 to 93 megadaltons. These isolates grew in normal equine serum (serum resistant), a trait previously documented to be expressed by isolates obtained from blood and tissues of septic foals, but not by isolates obtained from the feces of clinically normal horses. Of these isolates, 3 contained conjugal plasmids that encoded resistance to multiple antimicrobial agents linked to serum resistance and, in 1 isolate, to production of aerobactin as well. Serum resistance and production of aerobactin are related to virulence of septicemic E coli from non-equine sources.

Efficacy of albendazole for treating giardiasis in dogs was assessed in 3 experiments. In experiment 1, Giardia cysts were cleared from feces of 5 of 7 dogs (as determined by the zinc-sulfate concentration technique) after the dogs received a single dose of albendazole (25 mg/kg of body weight, PO), whereas feces of 3 of 7 dogs became clear of cysts without treatment. In experiment 2, feces of 5 of 5 dogs became clear of cysts after albendazole treatment (25 mg/kg, PO, q 12 h for 4 doses); feces of 1 of 5 untreated control dogs became clear. In experiment 3, feces of 18 of 20 dogs became clear of cysts after albendazole 25 mg/kg, PO, q 12 h for 4 doses) was given; none of the 20 control dogs had feces clear of cysts. Signs of toxicosis were not observed in any dog. These results indicate that a single dose of albendazole (25 mg/kg, PO) is not effective for treating giardiasis in dogs. However, 4 doses of albendazole (25 mg/kg, PO, q 12 h) are highly effective and nontoxic for treatment of giardiasis in dogs.

Cows and calves from a 1,600-cow drylot dairy were screened for IgG antibodies to Salmonella dublin lipopolysaccharide (LPS), using an indirect ELISA. The ELISA was performed on milk samples from lactating cows and on sera from nonlactating cows and calves. Fecal samples were collected from calves and nonlactating cows for culture of Salmonella spp. All seropositive cattle were retested by culture and ELISA 5 times at monthly intervals or until antibody concentration decreased. None of the cattle remained culture-positive and seronegative. Prior to and during the sample collection period, approximately 30% of calves < 8 weeks old died of S dublin infection. Vaccination of cows with a killed S dublin/S typhimurium vaccine at cessation of lactation was a routine management practice. The ELISA-determined Igg response to vaccination had decreased by 50 days after vaccination. Eight cows and 5 calves that maintained a high serologic response to S dublin were purchased and moved to a research facility for 6 months of intensive monitoring. Lactating cows were milked twice daily, and culture of milk and feces for Salmonella spp was performed 5 times/wk. Serum IgG antibodies to S dublin LPS were measured weekly, using ELISA. At the end of 6 months, all 13 cattle were necropsied and tissues were obtained for culture of Salmonella spp. All 8 cows and 5 calves maintained persistently high ELISA titer for the 6 months of testing, and shed S dublin in the milk and/or feces during the same period. On this basis, they were termed S dublin carriers. Salmonella dublin was isolated from mammary tissue of 2 calves at necropsy, indicating that bacteremia may be a mode of mammary infection by S dublin. Results of the study indicated serologic testing can be used successfully on a large dairy to identify S dublin carrier cattle. Using initial milk screening, 42 of 1,268 lactating cows were identified as suspect, requiring repeated serologic testing. One nonlactating cow, 7 of the 42 suspect lactating cows, and 5 of the 222 calves maintained an Igg response, and were found to be S dublin carriers. Carrier cows shed S dublin in 3.35% of fecal samples and 2.51% of milk samples, and carrier calves shed S dublin in 17.26% of fecal samples.

Rectal swab specimens were collected from 362 apparently healthy dogs of different origin, age, breed, and sex. Specimens were obtained in summer, autumn, and winter. Ninety-five thermophilic Campylobacter spp were isolated: C jejuni biotype I, n = 57, C jejuni biotype II, n = 1, C coli, n = 36, and C laridis, n = 1. Biotypes of C jejuni recovered were the same as those associated with Campylobacter-induced enteritis in human beings. Prevalence of C jejuni was significantly (P < 0.05) greater: in dogs < 6 months old than in adult dogs; in dogs living under high density and cohabitation housing conditions for long periods; and in autumn.

To evaluate the effect of ketoprofen on fecal output during secretory diarrhea, 16 calves were given approximately 200 micrograms of heat-stable Escherichia coli enterotoxin by suckling on 2 occasions. On one day, treatment was not administered. On the other day, either 3 mg of ketoprofen/kg of body weight (n = 8) or 6 mg of ketoprofen/kg (n = 8) was administered 1 hour before and 3 hours after administration of enterotoxin. Fecal output was no different after 8 or 24 hours from calves given 3 mg/kg, but fecal output was less at 8 hours and 24 hours for calves given 6 mg/kg (P = 0.0588), compared with the control day.

Fifteen isolates of Escherichia coli obtained from the blood and tissues of septic foals had plasmid DNA of size ranging from 2.5 to 93 megadaltons. These isolates grew in normal equine serum (serum resistant), a trait previously documented to be expressed by isolates obtained from blood and tissues of septic foals, but not by isolates obtained from the feces of clinically normal horses. Of these isolates, 3 contained conjugal plasmids that encoded resistance to multiple antimicrobial agents linked to serum resistance and, in 1 isolate, to production of aerobactin as well. Serum resistance and production of aerobactin are related to virulence of septicemic E coli from non-equine sources.

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 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.

Studies were undertaken to determine the efficacy of milbemycin oxime against the enteric adult stages of Trichinella spiralis and of albendazole against the muscle stage larvae in experimentally infected dogs and cats. Specific-pathogen-free Beagle pups (n = 6) and domestic shorthair kittens (n = 6) were inoculated with 7,500 first-stage larvae of Trichinella spiralis. Physical examination (including collection of blood and fecal samples) was performed weekly. During the first week after inoculation, all animals had mild gastrointestinal tract disturbances, but stages of T. spiralis were not observed in the feces. Beginning on postinoculation day (PID) 10, 3 pups and 3 kittens were treated with milbemycin oxime (1.25 mg/kg of body weight, PO, q 12 h) for 10 days. Muscle biopsy specimens were taken from dogs and cats on PID 26 and 29, respectively. Mean numbers of larvae per gram of muscle were 30.3 in the control and 37.7 in the treated dogs. Mean numbers of larvae per gram of muscle in the control and treated cats were 318.7 and 89.3, respectively. Two dogs and 2 cats were removed from the study at that time. The remaining animals, 2 each of the control and milbemycin oxime-treated animals, were given albendazole (50 mg/kg, PO, q 12 h) for 7 days starting at PID 31 and 34 in dogs and cats, respectively. Muscle biopsy specimens were again taken at PID 46 and 49, for dogs and cats, respectively; mean numbers of larvae recovered from muscle were 0.6 for dogs and 13.5 for cats.