Conventionally raised Chinese Meishan and European Large White pigs were intragastrically challenge exposed with 2. 1 X 10(10) enterotoxigenic Escherichia coli strains bearing colonization factor K88, 987P, F41, or F41 plus K99. In response to challenge exposure with the K88-positive (K88+) organisms, 96% of Large White pigs died within 48 hours, whereas none of the Meishan pigs died. Both breeds of pigs had similar susceptibility to strains bearing 987P or F41. Lastly, Meishan pigs were found to be more susceptible than Large White pigs to a strain expressing K99 and F41. In pigs with diarrhea, challenge-exposure strains intensively colonized the jejunum (10(8) to 10(10) bacteria/g of tissue) and, to less extent, the duodenum (except K88+ strain, which comprised 10(8)/g). In most cases, jejunal concentrations of the challenge-exposure strains were substantially lower in pigs that did not have diarrhea. Half the resistant Meishan pigs eliminated the K88+ strain from the intestines. Colostral antibody titer that agglutinated challenge-exposure strains did not differ between Meishan and Large White gilts. Results indicate that resistance of pigs to the K88+ strain did not extend to enterotoxigenic strains bearing other well-known factors. They indicate, in addition, that genetic resistance to K88+ strains described in pigs in Europe may exist in pigs in China.

Tissues from cattle that died of experimentally induced mucosal disease (n = 3), naturally acquired mucosal disease (n = 6), or naturally acquired chronic bovine viral diarrhea (n = 4) were examined. Consistent findings were lymphocytic depletion of lymphoid tissues, degeneration of myenteric ganglion cells, and mild adrenalitis. Intracytoplasmic viral antigen was detected in myenteric ganglia and in endocrine glandular cells. Noncytopathic virus was isolated from all cattle, and cytopathic virus was isolated from 12 of 13 cattle.

Ten colostrum-deprived calves were assigned to 1 of 2 treatment groups (5 calves/group), and fed colostrum that had either low (naturally infected cows) or high (immunized cows) antibody titers to bovine coronavirus (BCV). All calves were inoculated orally and intranasally with virulent BCV when they were 24 to 48 hours old and challenge exposed 21 days later. Blood, feces, nasal secretions, tears, saliva, and bronchoalveolar lavage (BAL) fluids were collected weekly from each calf for 5 weeks after inoculation. The titers to whole BCV or the relative amounts of isotype-specific antibodies to BCV structural proteins were evaluated in these samples by ELISA or immunoblotting, respectively. Both pools of colostrum contained primarily IgG1, IgG2, and IgA antibodies to the E2 and E3 BCV proteins. Calves fed the high-titer colostrum had correspondingly higher amounts of passive IgG1 and IgA antibodies to whole BCV and to the E2 and E3 BCV proteins in serum, feces, and BAL fluid at postinoculation week 1 than those calves fed low-titer colostrum. Active IgG1, IgA and IgM antibody responses in serum and active IgA and IgM antibody responses in most mucosal secretions to whole BCV and to the E2 and E3 proteins were lower or delayed in calves fed high-titer colostrum, compared with responses in calves fed low-titer colostrum. In contrast, increased responses to the BCV N protein were observed in all samples (except in serum and BAL fluid) in the calves fed high-titer colostrum, compared with calves fed low-titer colostrum. Upon challenge exposure, responses to E2 and E3 BCV proteins in serum and BAL fluid were lower in the group fed high-titer colostrum, compared with those in the group fed low-titer colostrum. Our findings indicate that the level of passive immunity in calves at the time of BCV inoculation can influence the development of active antibody responses in serum, feces, and mucosal secretions to whole BCV and to some BCV proteins individually.

In vitro adherence to intestinal epithelial cells by enterotoxigenic Escherichia coli strains bearing K88, K99, F41, or 987P adhesins and of their variants not bearing adhesins (K88-, K99-, or F41-) was investigated in European Large White and Chinese Meishan pigs. Possible relationship between adherence and virulence was also examined. The K88-positive (K88+) strain strongly adhered to intestinal epithelial cells from 26 of 28 Large White pigs. This strain had previously been found to be highly virulent for Large White pigs. The only surviving pig was of nonadherent phenotype, and cells from 4 dehydrated moribund pigs had strong adherence. By contrast, the same K88+ strain found previously to have little pathogenicity for Meishan pigs adhered with variable intensity to cells from 17 of 23 Meishan pigs; correlation was not evident between adherence and virulence. The K99+F41+ strain of porcine origin and the F41+ strain generally adhered strongly to cells from 24 and 23 Meishan pigs, respectively, and to cells from 25 of 26 Large White pigs. Correlation was not found between adherence and virulence for the 2 strains. A K99+F41+ strain of bovine origin adhered to cells from 20 of 22 Meishan and 22 of 23 Large White pigs, and a K99-F41+ variant adhered to cells from 19 of 23 Meishan and 23 of 24 Large White pigs. The adhesin-negative variants never adhered to intestinal epithelial cells. Strain 987 known not to readily produce 987P adhesin after in vitro growth never adhered to cells during the test. Results indicated that K88, K99, and F41 adhesins were responsible for in vitro adherence and, except for the K88+ strain in Large White pigs, adherent phenotype was not a sufficient condition to make a pig susceptible to enterotoxigenic E coli. The contribution of physiologic factors and their genetic origin to the degree of resistance of the individual is not yet completely understood for every enterotoxigenic E coli strain and breed of pig.

Two federally licensed attenuated live transmissible gastroenteritis (TGE) virus vaccines (an IM vaccine and an oral-IM vaccine) and 1 nonlicensed nonattenuated live TGE virus vaccine were evaluated and compared in sows free of TGE virus-neutralizing antibodies. Litters from the sows were challenge exposed at 3 and 5 days of age, and results were combined according to the vaccine administered to the sows. The survivability of pigs suckling sows vaccinated with the nonattentuated vaccine was significantly (P less than 0.01) greater than that of pigs suckling sows vaccinated with the IM attenuated vaccine, significantly (P less than 0.05) greater than that of pigs suckling sows vaccinated with the oral-IM attenuated vaccine, and significantly (P less than 0.05) greater than that of pigs suckling sows that had not been vaccinated. The differences, however, between survivability of litters from sows vaccinated with the IM attentuated vaccine or the oral-IM attenuated vaccine and that of litters from the sows not vaccinated were not significant (P greater than 0.10). The nonattenuated TGE vaccine, although giving a higher level of protection than the attenuated vaccine was eventually overwhelmed. Dexamethasone did not increase the incidence of diarrhea, and levamisole did not potentiate the lactogenic immunity in sows after given their first dose of the nonattenuated vaccine. Survivability in litters suckling sows that developed diarrhea after given their first dose of the nonattenuated vaccine was not greater than that in litters suckling sows that did not develop diarrhea. The best results were obtained when 3-day-old suckling pigs were challenge exposed with virulent TGE virus.

In 1985, 22 pony foals reared in a helminth-free environment were tested daily for oocysts of Cryptosporidium sp by use of fecal flotation. Oocysts were found in all foals. Oocysts were first observed in feces collected from foals 9 to 28 days after birth. The mean period of oocyst shedding was 10 days and ranged from 2 to 18 days in individual foals. Diarrhea was observed in 14 of 22 (64%) foals and began before the period of oocyst shedding. Fecal samples also wre examined for other infective agents. Salmonella poona was isolated from 1 foal that did not have diarrhea, and coronavirus particles were observed in the feces of 2 foals with diarrhea. Cryptosporidium sp oocytes also were observed in feces of 2 of 17 Thoroughbred foals, 3 of 14 Quarter Horse foals, and 3 of 26 pony foals reared on pastures with their dams. Samples from pasture-reared foals were collected at irregular intervals. Of the 11 Crytosporidium-positive fecal samples collected from pastured foals, 2 were from foals with diarrhea. A similar survey was conducted during the 1986 foaling season, using the same procedures. Examination of 300 samples from 58 Quarter Horse, Arabian, and pony foals did not detect oocysts. Daily examination of feces from 10 pony foals reared under helminth-free conditions for 30 days also failed to detect Cryptosporidium oocysts.

Eighteen strains of Escherichia coli serogroup O115:K"V165" isolated from 1- to 8-week-old pigs with diarrhea were tested for toxigenicity, pathogenicity in pigs and mice, serum resistance, mannose-resistant hemagglutination (MRHA), F165 and other surface antigens, colicin V (Col V), aerobactin, and biotype. Twelve strains were positive for heat-stable enterotoxin (STb), MRHA-negative, and F165-negative; 5 strains were enterotoxin-negative, MRHA-positive, and F165-positive; and 1 strain was MRHA-positive, but F165- and enterotoxin-negative. Six of the 12 STb-positive strains moderately colonized the ileum of newborn colostrum-deprived pigs within 24 hours after inoculation. Two of the colonizing strains were able to induce watery diarrhea. All 12 STb-positive strains were nonpathogenic for adult mice and were serum-sensitive; 11 of 12 were Col V-negative, 9 of 12 did not produce aerobactin, and 10 of 12 belonged to biotypes other than 1 or 2. All 6 enterotoxin-negative strains colonized the small and large intestines, associated with peritoneal serosal surfaces, and induced septicemia and polyserositis in newborn colostrum-deprived pigs 1 to 2 days after inoculation. In contrast, 3 STb-positive strains poorly colonized the intestines and did not induce septicemia in pigs at 3 days after inoculation. All 6 enterotoxin-negative strains were Col V-positive, produced aerobactin, and belonged to biotype 1 or 2. Of the 5 enterotoxin-negative, F165-positive strains, only 4 were pathogenic for intraperitoneally inoculated adult mice and were serum-resistant. The enterotoxin-negative, F165-negative strain was neither serum-resistant nor mouse-pathogenic. O-agglutinable mutants of the mouse-pathogenic strains were, for the most part, no longer pathogenic for adult mice, although these strains remained unchanged for biotype and production of MRHA, F165, and Col V, and 3 of 4 mutant strains were serum-resistant. Thus, E coli strains of the same serogroup isolated from diarrheic pigs may cause either intestinal or extraintestinal disease upon reinoculation of pigs, depending on the virulence attributes produced by the strains.

A double-antibody ELISA for the detection of coronaviruses in intestinal contents from turkey poults with diarrhea was developed. Antibodies were raised in rabbits and guinea pigs against a Minnesota isolate of turkey enteric coronavirus (TCV) propagated in embryonating turkey eggs and were purified by density-gradient centrifugation. The specificity of antisera was confirmed by hemagglutination-inhibition and immunoelectron microscopy. Absorption of anti-TCV hyperimmune sera with egg extracts or egg ovalbumin and the use of different dilution and blocking buffers influenced the sensitivity and specificity of the ELISA. Reciprocal cross-reactivity was detected among turkey, chicken, bovine, and murine coronaviruses. Antisera to the transmissible gastroenteritis virus of swine, the rabbit enteric coronavirus, or the human coronavirus strain 299E failed to react with TCV. The TCV cross-related only moderately with the avian infectious bronchitis virus and the hemagglutinating encephalomyelitis virus of swine. Investigations with samples from 47 commercial turkey flocks in Quebec with episodes of transmissible enteritis revealed that the ELISA was more sensitive than was electron microscopy for dectection of TCV.

Thirty-four preweaning pigs with induced enteropathogenic Escherichia coli diarrhea were treated with electroacupuncture, traditional acupuncture, or neomycin. In the group treated with electroacupuncture, points GV-1, bilateral ST-36, and Bai-hui were stimulated electrically. In the group treated with traditional acupuncture, points GV-1, bilateral ST-36, BL-20, bulb points, bilateral ear tip, and Shan-gen were used. Acupuncture points CV-12 and bilateral ST-25 also were treated with moxibustion (applying heat generated by a burning herb, Artemisia argyi). Hemoacumpuncture also was applied to Shan-gen, bilateral ear tip, and bulb points. Pigs in the third group were given neomycin orally. Five pigs were inoculated with E coli, but were not treated and served as nontreated controls. At postinoculation day 5, 60% of control pigs and greater than 80% of pigs in treated groups recovered from diarrhea. However, at postinoculation day 3, recovery rates for pigs in the control and group treated with electroacupuncture were only 20 and 27.3%, respectively; whereas pigs treated with acupuncture or neomycin attained 81.8 and 71.4% of recovery rates, respectively. Seemingly, traditional acupuncture, but not electroacupuncture, was effective in controlling induced E coli diarrhea in pigs at its early stage.

Eimeria spp., calves (exper.) treated with lasalocid (Bovatec) or decoquinate (Deccox) and premunized did not develop diarrhea, calves premunized but not treated were no more resistant to challenge than nonpremunized calves, premunization alone cannot be expected to prevent coccidiosis when animals are exposed to large numbers of oocysts