Dissemination of Spotted Fever Rickettsia Agents in Europe by Migrating Birds

Migratory birds are known to play a role as long-distance vectors for many microorganisms. To investigate whether this is true of rickettsial agents as well, we characterized tick infestation and gathered ticks from 13,260 migratory passerine birds in Sweden. A total of 1127 Ixodes spp. ticks were removed from these birds and the extracted DNA from 957 of them was available for analyses. The DNA was assayed for detection of Rickettsia spp. using real-time PCR, followed by DNA sequencing for species identification. Rickettsia spp. organisms were detected in 108 (11.3%) of the ticks. Rickettsia helvetica, a spotted fever rickettsia associated with human infections, was predominant among the PCR-positive samples. In 9 (0.8%) of the ticks, the partial sequences of 17kDa and ompB genes showed the greatest similarity to Rickettsia monacensis, an etiologic agent of Mediterranean spotted fever-like illness, previously described in southern Europe as well as to the Rickettsia sp.IrITA3 strain. For 15 (1.4%) of the ticks, the 17kDa, ompB, gltA and ompA genes showed the greatest similarity to Rickettsia sp. strain Davousti, Rickettsia japonica and Rickettsia heilongjiangensis, all closely phylogenetically related, the former previously found in Amblyomma tholloni ticks in Africa and previously not detected in Ixodes spp. ticks. The infestation prevalence of ticks infected with rickettsial organisms was four times higher among ground foraging birds than among other bird species, but the two groups were equally competent in transmitting Rickettsia species. The birds did not seem to serve as reservoir hosts for Rickettsia spp., but in one case it seems likely that the bird was rickettsiemic and that the ticks had acquired the bacteria from the blood of the bird. In conclusion, migratory passerine birds host epidemiologically important vector ticks and Rickettsia species and contribute to the geographic distribution of spotted fever rickettsial agents and their diseases

Review on the validity of self-report to assess work-related diseases

Self-report is an efficient and accepted means of assessing population characteristics, risk factors, and diseases. Little is known on the validity of self-reported work-related illness as an indicator of the presence of a work-related disease. This study reviews the evidence on (1) the validity of workers' self-reported illness and (2) on the validity of workers' self-assessed work relatedness of an illness. A systematic literature search was conducted in four databases (Medline, Embase, PsycINFO and OSH-Update). Two reviewers independently performed the article selection and data extraction. The methodological quality of the studies was evaluated, levels of agreement and predictive values were rated against predefined criteria, and sources of heterogeneity were explored. In 32 studies, workers' self-reports of health conditions were compared with the "reference standard" of expert opinion. We found that agreement was mainly low to moderate. Self-assessed work relatedness of a health condition was examined in only four studies, showing low-to-moderate agreement with expert assessment. The health condition, type of questionnaire, and the case definitions for both self-report and reference standards influence the results of validation studies. Workers' self-reported illness may provide valuable information on the presence of disease, although the generalizability of the findings is limited primarily to musculoskeletal and skin disorders. For case finding in a population at risk, e.g., an active workers' health surveillance program, a sensitive symptom questionnaire with a follow-up by a medical examination may be the best choice. Evidence on the validity of self-assessed work relatedness of a health condition is scarce. Adding well-developed questions to a specific medical diagnosis exploring the relationship between symptoms and work may be a good strateg

Advanced paternal age effects in neurodevelopmental disorders?review of potential underlying mechanisms

Multiple epidemiological studies suggest a relationship between advanced paternal age (APA) at conception and adverse neurodevelopmental outcomes in offspring, particularly with regard to increased risk for autism and schizophrenia. Conclusive evidence about how age-related changes in paternal gametes, or age-independent behavioral traits affect neural development is still lacking. Recent evidence suggests that the origins of APA effects are likely to be multidimensional, involving both inherited predisposition and de novo events. Here we provide a review of the epidemiological and molecular findings to date. Focusing on the latter, we present the evidence for genetic and epigenetic mechanisms underpinning the association between late fatherhood and disorder in offspring. We also discuss the limitations of the APA literature. We propose that different hypotheses relating to the origins of the APA effects are not mutually exclusive. Instead, multiple mechanisms likely contribute, reflecting the etiological complexity of neurodevelopmental disorders