AIM: To conduct a country-wide prevalence study of bovine group A rotavirus, coronavirus, Cryptosporidium parvum, Salmonella spp. and enterotoxigenic K99⁺ Escherichia coli (K99) in calves on New Zealand dairy farms. METHODS: Faecal samples (n=1,283) were collected during the 2011 calving season from calves that were 1–5 and 9–21 days-old on 97 dairy farms, and were analysed for the presence of bovine group A rotavirus, coronavirus, Cryptosporidium and Salmonella spp., and K99. Farm-level prevalences were calculated and relationships between demographic variables and the presence of enteropathogens were examined using logistic regression models. RESULTS: Of the 97 farms, 93 (96%) had at least one sample infected with enteropathogens. The standardised farm prevalences of bovine group A rotavirus, bovine coronavirus and C. parvum were 46, 14 and 18%, respectively, in calves that were 1–5 days-old, and 57, 31 and 52%, respectively, in calves that were 9–21 days-old. The farm-level prevalence of K99 was 11% in calves that were 1–5 days-old. Salmonella spp. were found in three and four samples, from calves that were 1–5 and 9–21 days-old, respectively. No associations between explanatory variables and the presence of the enteropathogens were identified at the farm level. At the calf level, the odds of C. parvum shedding and of co-infection with any combination of pathogens were greater in calves that were 9–21 than 1–5 days-old. CONCLUSIONS AND CLINICAL RELEVANCE: This study provides epidemiological estimates of the prevalence of calves’ enteropathogens in New Zealand, which could be used for infection risk assessment or estimation of the environmental loads of pathogens shed in cattle faeces.

We performed a survey aimed at analyzing milk samples collected from cows with mastitis for the presence of extended-spectrum β-lactamase (ESBL)-producing Escherichia coli. Single-quarter mastitic milk samples obtained from 400 cows in 23 Greek dairy herds with a history of E. coli mastitis were processed for the selective isolation of ESBL-producing E. coli. The antimicrobial susceptibility of the ESBL-producing isolates was analyzed using agar disk diffusion, and minimum inhibitory concentrations of colistin were determined by broth microdilution. We used PCR followed by DNA sequencing to characterize the β-lactamases and mcr-1 (colistin resistance) genes, and for phylotyping and multilocus sequence typing. We found a total of 89/400 (22.25%) E. coli isolates from 12/23 (52%) farms. Six isolates originating from 6 cows on a single farm were ESBL producers and were resistant to cefquinome, amoxicillin-clavulanic acid, aztreonam, ampicillin, and colistin. Five of these isolates were resistant to trimethoprim-sulfamethoxazole, and 5 to streptomycin. The 6 ESBL producers were mcr-1-positive and carried blaTEM-1 genes; 3 also carried blaCTX-M genes, and 3 carried blaSHV genes. All of the ESBL producers belonged to phylogroup A, multilocus sequence type ST666 (n = 5), or a single locus variant of ST666 (n = 1). To our knowledge, this is the first report of endemic bovine mastitis caused by mcr-1-positive, ESBL-producing E. coli. These results highlight the value of active surveillance of antimicrobial resistance not commonly tested by diagnostic laboratories for the early detection of novel resistant strains.

Cryptosporidiumisolates from diarrheic foals in New Zealand (n= 9) were identified asC. parvum, subtyped at two polymorphic loci, and compared with human (n= 45) and bovine (n= 8) isolates. FoalC. parvumisolates were genetically diverse, markedly similar to human and bovine isolates, and carried GP60 IIaA18G3R1 alleles, indicating a zoonotic potential.

AIM: To assess the occurrence of Cryptosporidium oocysts in faecal specimens from foals, and investigate an outbreak of neonatal cryptosporidiosis in foals revealed in the course of the study. METHODS: Faecal specimens from foals received by a diagnostic veterinary laboratory in New Zealand between 2006 and 2007 were submitted to Massey University and tested microscopically for the presence of Cryptosporidium oocysts. The Cryptosporidium isolates in the oocyst-positive specimens were genetically identified to species level. In addition, specimen submission data from the participating laboratory for 2005–2007 were examined. In the course of the study, the identification of one Cryptosporidium-positive specimen triggered an on-farm investigation. RESULTS: Twelve faecal specimens submitted by the participating laboratory between 2006 and 2007 were tested further, and three were positive for C. parvum. Specimen submission records indicated a total of 67 faecal specimens were tested for Cryptosporidium by the participating laboratory between 2005 and 2007; 12 (18%) were positive. The on-farm investigation on a broodmare farm revealed a high incidence of neonatal diarrhoea in foals; C. parvum was the only enteropathogen found in the faeces of 4/4 affected foals examined. The diarrhoea in all those foals was self-limiting, manifesting during the second week of life, resembling foal heat diarrhoea, and accompanied by a short but intense period of shedding oocysts. CONCLUSIONS AND CLINICAL RELEVANCE: The fact that Cryptosporidium parasites were identified in 18% of faecal specimens from foals analysed for this agent in 2005–2007 by the participating laboratory indicated that infection with this agent in foals is not uncommon. Collectively, the results of this and previous studies performed in New Zealand indicate C. parvum is a cause of diarrhoea in newborn foals, potentially accounting for a proportion of cases empirically diagnosed as foal heat diarrhoea. It is therefore advisable to take precautions when handling diarrhoeic foals, until this potentially zoonotic agent is ruled out in the laboratory.