After 27 years with no detected cases, an outbreak of anthrax occurred in a beef cattle herd in the south of Sweden. The outbreak was unusual as it occurred in winter, in animals not exposed to meat-and-bone meal, in a non-endemic country.The affected herd consisted of 90 animals, including calves and young stock. The animals were kept in a barn on deep straw bedding and fed only roughage. Seven animals died during 10 days, with no typical previous clinical signs except fever. The carcasses were reportedly normal in appearance, particularly as regards rigor mortis, bleeding and coagulation of the blood. Subsequently, three more animals died and anthrax was suspected at necropsy and confirmed by culture and PCR on blood samples.The isolated strain was susceptible to tetracycline, ciprofloxacin and ampicillin. Subtyping by MLVA showed the strain to cluster with isolates in the A lineage of Bacillus anthracis.Environmental samples from the holding were all negative except for two soil samples taken from a spot where infected carcasses had been kept until they were picked up for transport.The most likely source of the infection was concluded to be contaminated roughage, although this could not be substantiated by laboratory analysis. The suspected feed was mixed with soil and dust and originated from fields where flooding occurred the previous year, followed by a dry summer with a very low water level in the river allowing for the harvesting on soil usually not exposed. In the early 1900s, animal carcasses are said to have been dumped in this river during anthrax outbreaks and it is most likely that some anthrax spores could remain in the area.The case indicates that untypical cases in non-endemic areas may be missed to a larger extent than previously thought. Field tests allowing a preliminary risk assessment of animal carcasses would be helpful for increased sensitivity of detection and prevention of further exposure to the causative agent.
Faecal samples from 54 dogs with diarrhoea and 54 control dogs were cultured for Campylobacter, Salmonella and Yersinia species and controlled for enteric viruses. The campylobacter were identified as either C jejuni/coli or C upsaliensis. In the diarrhoeic group 16 dogs (29.6 per cent) were positive for campylobacter, 10 C upsaliensis and six C jejuni/coli. Concomitant infection with parvovirus was evident in six of the dogs with diarrhoea and campylobacter-positive faecal cultures. In the control group 13 dogs (24.1 per cent) were positive for campylobacter; three of the isolates were C upsaliensis and six C jejuni/coli. Four isolates could not be identified. The most prominent clinical findings in naturally occurring cases were an acute onset of vomiting (12 of 16), diarrhoea (16 of 16) which was often haemorrhagic (nine of 16) and a raised rectal temperature. Dogs were infected experimentally with both C jejuni (three dogs) and C upsaliensis (three dogs). The challenge strains could be identified in faecal samples from all the dogs, but clinical signs of diarrhoea were seen in only one dog infected with C jejuni. Soft faeces was passed by one dog infected with C upsaliensis. It is concluded that C jejuni/coli or C upsaliensis are either primary pathogens or, after predisposing factors such as virus infections, act as secondary pathogens. It also seems probable that Campylobacter species are present in the intestinal flora of the normal dog.
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