Outbreak of Yersinia pseudotuberculosis O:1 infection associated with raw milk consumption, Finland, 2014.

In March 2014, a Yersinia pseudotuberculosis (YP) outbreak was detected by a municipal authority in southern Finland. We conducted epidemiological, microbiological and traceback investigations to identify the source. We defined a case as a person with YP infection notified to the National Infectious Disease Registry between February and April 2014, or their household member, with abdominal pain and fever≥38 °C or erythema nodosum. Healthy household members were used as household-matched controls. We identified 43 cases and 50 controls. The illness was strongly associated with the consumption of raw milk from a single producer. The odds ratio of illness increased with the amount of raw milk consumed. Also previously healthy adults became infected by consuming raw milk. Identical YP strains were identified from cases' stool samples, raw milk sampled from a case's refrigerator and from the milk filter at the producer's farm. The producer fulfilled the legal requirements for raw milk production and voluntarily recalled the raw milk and stopped its production. We advised consumers to heat the raw milk to 72 °C for 15 s. Current legislation for raw milk producers should be reviewed and public awareness of health risks linked to raw milk consumption should be increased.

Cosegregation of MIDD and MODY in a pedigree: functional and clinical consequences.

The aim of this study was characterization of a family carrying two mutations known to cause monogenic forms of diabetes, the M626K mutation in the HNF1alpha gene (MODY3) and the A3243G in mtDNA. Beta-cell function and insulin sensitivity were assessed with the Botnia clamp. Heteroplasmy of the A3243G mutation and variants in type 2 diabetes susceptibility genes were determined, and transcriptional activity, DNA binding, and subcellular localization of mutated HNF1alpha were studied. Thirteen family members carried the mutation in mtDNA; 6 of them also had the M626K mutation, whereas none had only the M626K mutation. The protective Ala12 allele in peroxisome proliferator-activated receptor (PPAR)gamma was present in two nondiabetic individuals. Carriers of both mtDNA and HNF1alpha mutations showed an earlier age at onset of diabetes than carriers of only the mtDNA mutation (median 22 vs. 45 years) but no clear difference in beta-cell function or insulin sensitivity. In vitro, the M626K mutation caused a 53% decrease in transcriptional activity in HeLa cells. The mutated protein showed normal nuclear targeting but increased DNA binding. These data demonstrate that several genetic factors might contribute to diabetes risk, even in families with mtDNA and HNF1alpha mutations.