Recent multilocus studies of congeneric birds have shown a pattern of elevated interspecific divergence on the Z chromosome compared to the autosomes. In contrast, intraspecifically, birds exhibit less polymorphism on the Z chromosome relative to the autosomes. We show that the four black-and-white Ficedula flycatcher species show greater genetic divergence on the Z chromosome than on the autosomes, and that the ratios of intraspecific polymorphism at Z-linked versus autosomal markers are below the neutral expectation of 75%. In all species pairs, we found more fixed substitutions and fewer shared polymorphisms on the Z chromosome than on the autosomes. Finally, using isolation with migration (IMa) models we estimated gene flow among the four closely related flycatcher species. The results suggest that different pattern of evolution of Z chromosomes and autosomes is best explained by the faster-Z hypothesis, since the estimated long-term gene flow parameters were close to zero in all comparisons.

BackgroundNigeria has a high tuberculosis incidence, and genotyping studies of Mycobacterium tuberculosis Complex (MTC) in the country are necessary in order to improve our understanding of the epidemic.MethodsIsolates of MTC were isolated from cases of pulmonary tuberculosis in Jos, North Central region of Nigeria during 2006-2008. Drug susceptibility test (DST) was performed on 77 of 111 isolates by proportion method on Lowenstein Jensen (LJ) slope while genotyping of mycobacterial DNA was performed by spoligotyping. The SpolDB4 database and the model-based program 'spotclust' were used to assign isolates to families, subfamilies and variants.ResultsA total of 111 pulmonary isolates from consecutive tuberculosis patients in the city of Jos, Plateau State, Nigeria were spoligotyped. A total of 84 (76%) of the isolates belonged to the Latin American Mediterranean (LAM) family. Of these, 78 isolates were assigned to the LAM10 lineage. Among these, 66 exhibited identical spoligopatterns. Drug susceptibility profiles obtained were not consistently associated with any spoligopattern.ConclusionsThe dominance of few M. tuberculosis lineages suggests either a high rate of transmission, frequent import of closely related strains, or a highly conserved genotype. It remains to be confirmed whether the predominance of identical LAM10 represent an outbreak.Spoligotyping was useful to gain an overall understanding of the local TB epidemic. This study demonstrated that the incidence of TB in Jos, Nigeria may be caused by a few successful M. tuberculosis families, dominated by the LAM10 family.

Shiga toxin-producing Escherichia coli (STEC) may cause haemolytic uraemic syndrome (HUS). Age ≤5 years and presence of stx2a and eae are risk factors for the development of HUS. In this study, we investigated STEC isolates for the presence of adhesins, toxins and molecular risk assessment (MRA) factors to identify virulence genes associated with HUS development. We included non-duplicate isolates from all STEC infections (n = 340, HUS = 32) reported to the Norwegian National Reference Laboratory (NRL) for Enteropathogenic Bacteria from 1992 to 2013. The most common STEC were O157:H7/H− (34%) and O103:H2 (14%). We retrospectively screened the isolates by three multiplex polymerase chain reactions (PCRs) for adhesins (n = 11), toxins (n = 5) and MRA (n = 15). We calculated odds ratios (ORs) and adjusted odds ratios (aORs) for associations with HUS development. On average, isolates were positive for 15 virulence genes (range: 1–24); two toxins (range: 0–4), five adhesins (range: 0–8) and eight MRA genes (range: 0–13). The gene combinations were clustered within serotypes. Isolates from HUS cases were positive for eae and IpfA O26, and negative for saa, eibG, astA, cnf, subA and pic. We identified 11 virulence genes with a significant association to HUS development. Multivariable analyses adjusted for age group and Shiga toxin identified nleH1–2 [aOR 8.4, 95% confidence interval (CI); 2.18–32.3] as an independent risk factor for the development of HUS from an STEC infection. This study demonstrated that the non-LEE effector protein nleH1–2 may be an important predictor for elevated risk of developing HUS from STEC infections. We recommend the NRL for Enteropathogenic Bacteria to consider including nleH1–2 screening as part of routine STEC surveillance.Electronic supplementary materialThe online version of this article (doi:10.1007/s10096-017-2974-z) contains supplementary material, which is available to authorized users.

BackgroundDuring the previous century Norway had a high incidence of tuberculosis, but no molecular epidemiological studies could be performed and these previously epidemic strains have been disappearing during the last decades. Currently, tuberculosis among native Norwegians is in the elimination phase, and it is still not known what type of M. tuberculosis was so efficiently controlled during the second half of the 20th century. However, many elderly Norwegian-born people still develop TB that cannot be clustered to imported or recently transmitted strains of M. tuberculosis. Thus, the majority of these cases are results of reactivation of disease that was transmitted many decades ago.Methodology/Principal FindingsA total of 213 strains of M. tuberculosis isolated during 1998–2005, from patients born in Norway before 1950 were genotyped in the current study. The findings demonstrated a highly homogenous M. tuberculosis population among the patients. A total of 40% belonged to the T-family, were 35% were assigned to T1 sub- family (T2 = 0, 93%, T3 = 1, 4% and T4 = 2, 3%). As many as 35% of the isolates belonged to the Haarlem family, were 15% were assigned to Haarlem1 and 19% to Haarlem3. The remaining 25% belonged to 15 different other families. The RFLP-patterns indicated that the isolates were not a result of recent transmission, but rather represented well established strains that apparently dominated in Norway many decades ago.Conclusions/SignificanceThe T 1, Haarlem 1, and Haarlem 3 families of M. tuberculosis were abundant among patients born in Norway before 1950. The M. tuberculosis cases represented reactivated disease that had been acquired before 1994 and were likely to have been latent for several decades. Thus, the current study indicated that the T 1, Haarlem 1, and Haarlem 3 families may have been common in Norway, when tuberculosis represented a serious public health threat during the first half of the 20th century.

We described the population structure of Bordetella pertussis (B. pertussis) in Norway from 1996 to 2019 and determined if there were evolutionary shifts and whether these correlated with changes in the childhood immunization program. We selected 180 B. pertussis isolates, 22 from the whole cell vaccine (WCV) era (1996–1997) and 158 from the acellular vaccine (ACV) era (1998–2019). We conducted whole genome sequencing and determined the distribution and frequency of allelic variants and temporal changes of ACV genes. Norwegian B. pertussis isolates were evenly distributed across a phylogenetic tree that included global strains. We identified seven different allelic profiles of ACV genes (A–F), in which profiles A1, A2, and B dominated (89%), all having pertussis toxin (ptxA) allele 1, pertussis toxin promoter (ptxP) allele 3, and pertactin (prn) allele 2 present. Isolates with ptxP1 and prn1 were not detected after 2007, whereas the prn2 allele likely emerged prior to 1972, and ptxP3 before the early 1980s. Allele conversions of ACV genes all occurred prior to the introduction of ACV. Sixteen percent of our isolates showed mutations within the prn gene. ACV and its booster doses (implemented for children in 2007 and adolescents in 2013) might have contributed to evolvement of a more uniform B. pertussis population, with recent circulating strains having ptxA1, ptxP3, and prn2 present, and an increasing number of prn mutations. These strains clearly deviate from ACV strains (ptxA1, ptxP1, prn1), and this could have implications for vaccine efficiency and, therefore, prevention and control of pertussis.