BACKGROUND: Rotavirus Group A is one of the most important causes of gastroenteritis as it is isolated from 30 to 50% of infant diarrhea from humans and other animals. G genotype of the virus is determined by gene sequence of a surface protein of the virus (VP7), one of the most important factors in inducing immunity against the virus which acts very specific to each genotype. OBJECTIVES: In the present study the presence of common bovine rotavirus genotypes A was examined in human rotavirus population. METHODS: A total of 100 stool samples from children under 2 years of age in Tehran and Varamin were collected and to track the presence of rotavirus A, were evaluated using ELISA method. Positive samples were isolated and cultured on the MA-104 cell line after several passages. The positive samples (49 samples) were determined to be the G type using semi-nested RT-PCR and primers specific for bovine common genotype. RESULTS: From 100 samples, 49 were positive in ELISA. Eight samples in the first semi nested RT-PCR showed the desired rotavirus bands and in the second round, the results were positive for the presence of bovine VP7 in two samples taken from Varamin, in one sample, G6, and in another sample, two genotypes of VP7, G6 and G8 were detected, indicating infection with at least two strains of human rotavirus reassortant. Six of the ELISA selected positive samples that were taken to the cell line MA104, showed effects of cell damage (CPE) after 4-5 consecutive passages, demonstrating proliferation of the rotaviruses of this study and so, their viability was confirmed. CONCLUSIONS: The results of this study indicate reassortment between bovine and human rotaviruses and show that in case of occurrence of bovine and human rotavirus infection and the emergence of new human type, due to reassortment strain differences in protein immunogen it is possible to overcome due to lack of maternal immunity in the human population and low efficiency of current vaccines and, ultimately, epidemic and considerable losses may occur. Hence, more research is warranted.

Virulence-associated genes have been recognised and detected in Campylobacter species. The majority of them have been proven to be associated with pathogenicity. This study aimed to detect the presence of virulence genes associated with pathogenicity and responsible for invasion, expression of adherence, colonisation and production of the cytolethal distending toxin (cdt) in Campylobacter jejuni and Campylobacter coli. Commercial chicken faecal samples were randomly sampled from chicken farms within the Durban metropolitan area in South Africa. Furthermore, human clinical Campylobacter spp. isolates were randomly sampled from a private pathology laboratory in South Africa. Out of a total of 100 chicken faecal samples, 78% (n = 78) were positive for Campylobacter growth on modified charcoal cefoperazone deoxycholate and from the random laboratory collection of 100 human clinical isolates, 83% (n = 83) demonstrated positive Campylobacter spp. growth following culturing methods. These samples were screened for the presence of the following virulence genes: cadF, hipO, asp, ciaB, dnaJ, pldA, cdtA, cdtB and cdtC. As expected, the cadF gene was present in 100% of poultry (n = 78) and human clinical isolates (n = 83). Campylobacter jejuni was the main species detected in both poultry and human clinical isolates, whilst C. coli were detected at a significantly lower percentage (p < 0.05). Eight per cent of the C. jejuni from human clinical isolates had all virulence genes that were investigated. Only one C. coli isolate demonstrated the presence of all the virulence genes investigated; however, the pldA virulence gene was detected in 100% of the C. coli isolates in poultry and a high percentage (71%) in human clinical C. coli isolates as well. The detection of cdt genes was found at higher frequency in poultry than human clinical isolates. The high prevalence rates of virulence genes detected in poultry and human clinical isolates demonstrate their significance in the pathogenicity of Campylobacter species.

Rotaviruses, causing acute gastroenteritis, that infect humans and animals around the world. There are many assays had been developed for the detection of rotavirus or the viral antigens. The present study was done on 79 samples of stool collected from pediatric patients with acute watery diarrhea aged from one months to 5 years admitted to Basrah Maternity and children hospital in Basrah province, during the period from October 2014 to February 2015. Ninety diarrheic fecal bovine samples were included in this study. All samples were used for the investigation and detection of rotavirus antigen by Enzyme-Linked Immunosorbent assay (ELISA).According to ELISA results, 10 out of 79(12.7%) pediatric stool samples rotavirus antigens were detected in children. Percentage (20.7%) of positive rotavirus antigen were detected in the patients at second age group (>6 months). Followed by 8% of patients at first age group (0.05). The percentage of rotavirus antigen was higher in males patients (16.7%) compared to females (P>0.05) and also the differences were not significant differences (P>0.05). These results of rotavirus antigen detection in 90 diarrheic bovine fecal samples showed that this antigen was excreted by 56.7%of diarrheic calves. Additionally the higher non-significant (P>0.05) excretion percentage according to age was observed in 63.4 % of calves > 1 year old and the lower percentage(51.1%) was observed in the first age group( < 1year) calves old. The differences in sex were not significant (P>0.05) in the percentage of rotavirus antigen detection were also detected as 63.5% of male fecal samples show positive rotavirus antigen excretion whereas only 47.4% of female fecal samples were positive.

Passive protection provided by sows inoculated with the virulent Miller strain of transmissible gastroenteritis virus (TGEV), or the ISU-1 strain of porcine respiratory coronavirus (PRCV), or both was evaluated in nursing pigs challenge exposed with virulent TGEV. Four sows (group B) were inoculated with PRCV oronasally twice at 4 and 2 weeks before parturition; 1 sow (group C) was inoculated similarly, but in 2 subsequent pregnancies; and 2 sows (group D) were oronasally primed with PRCV at 4 weeks before parturition, and 2 weeks later were administered a booster inoculation of virulent TGEV. Two additional sows (group E) remained uninoculated and served as seronegative controls, and 1 sow (group A) that had been naturally infected with TGEV served as a seropositive control. The degree of passive immunity transferred by these sows to their litters was assessed by challenge exposing the pigs of sows in groups BE (only the second litter of group C) with virulent TGEV at 3 to 5 days of age. After challenge exposure, clinical signs of infection and mortality were noted and fecal and nasal shedding of virus was assessed by ELISA. The IgA, IgG, and IgM antibody titers to TGEV were quantified in colostrum and milk of the sows by use of an isotype-specific monoclonal antibody-capture ELISA, using biotinylated monoclonal antibodies against each porcine isotype as detecting reagents. A plaque-reduction assay was used to quantify neutralizing antibody titers in serum, colostrum, milk, and fractionated whey (IgG and IgA/IgM). In the sow naturally infected with TGEV (group A), there was a pronounced decrease in IgG antibody titers to TGEV in the transition from colostrum to milk, and IgA TGEV antibodies became predominant, with high titers maintained throughout lactation. The 4 group-B sows partially protected their pigs after TGEV challenge exposure; mean mortality was 67%, compared with 100% in pigs suckling the 2 TGEV seronegative control sows (group-E litters). Although IgA TGEV antibodies were detected in colostrum and milk of group-B sows, IgG TGEV antibodies were the most abundant. The sow of group C had a marked increase in IgA TGEV antibody titers in colostrum and milk after reinoculation with PRCV during the second pregnancy, before TGEV challenge exposure of the litter. Its pigs were passively protected to a high degree after TGEV challenge exposure (27% litter mortality). The sows in group D, primed with PRCV and boosted with TGEV, provided the best passive protection after TGEV challenge exposure of their pigs. Not only litter mortality (27%) but also morbidity was reduced, compared with those factors for the other challenge exposed litters, and the sows did not become ill. In these swine, the high degree of passive protection observed could not be associated with the presence of only IgA TGEV antibodies in the milk, but high IgM TGEV antibody titers also were detected in colostrum and milk. Results of this study suggest that PRCV-inoculated sows are able to partially protect their pigs from TGEV challenge exposure and, on the basis of preliminary data, the degree of protection may increase after multiple PRCV exposures or after secondary exposure to TGEV during pregnancy. Also, an IgA respiratory tract-mammary gland link may exist as evident by the low titer of IgA TGEV antibodies in the milk of PRCV-inoculated sows, but may not be as efficient in inducing lactogenic IgA immunity as is the gastrointestinal tract-mammary gland link.

Pigs were inoculated with various strains of transmissible gastroenteritis virus (TGEV) or with porcine respiratory coronavirus (PRCV), and antigenic site-specific antibody responses were compared. A blocking-ELSIA was used to study to what extent antibodies in convalescent sera interfered with the binding of monoclonal antibodies (MAB) 57.16 or 57.110 to the attenuated TGEV/Purdue virus. Monoclonal antibody 57.16 is directed against the A site on the peplomer, neutralizes virus, and recognizes TGEV and PRCV. Monoclonal antibody 57.110 is directed against the X site on the peplomer, but does not neutralize virus, and recognizes only TGEV. Antibodies directed against TGEV and PRCV could be detected in a blocking ELISA, using MAB 57.16 as a conjugate. Antibodies directed against both viruses were detectable as early as 1 week after inoculation. Antibody titers correlated well with those in a virus-neutralization test. Antibodies against TGEV could be detected in a blocking ELISA, using MAB 57.110 as a conjugate. Such antibodies were not induced by a PRCV infection. In the blocking ELISA, using MAB 57.110 as a conjugate, antibodies were detectable as early as 2 weeks after inoculation. There was a significant difference between antibody titers reached after infection with various TGEV strains, however. This difference is ascribed to a variation of the antigenic site defined by MAB 57.110 in TGEV strains. Conditions for a differential test for TGE serodiagnosis, and for serologic discrimination between TGEV- and PRCV-infected pigs, are discussed. It is concluded that by using a blocking ELISA with MAB 57.110, no definite distinction can be made between antibodies directed against TGEV and PRCV, because low antibody titers develop after infection with some TGEV strains, and because antibodies directed against antigenic sites that PRCV has in common with TGEV may interfere with the binding of MAB 57.110 to TGEV.