A widespread outbreak of tularemia in Sweden in 2000 was investigated in a case-control study in which 270 reported cases of tularemia were compared with 438 controls. The outbreak affected parts of Sweden where tularemia had hitherto been rare, and these “emergent” areas were compared with the disease-endemic areas. Multivariate regression analysis showed mosquito bites to be the main risk factor, with an odds ratio (OR) of 8.8. Other risk factors were owning a cat (OR 2.5) and farm work (OR 3.2). Farming was a risk factor only in the disease-endemic area. Swollen lymph nodes and wound infections were more common in the emergent area, while pneumonia was more common in the disease-endemic area. Mosquito bites appear to be important in transmission of tularemia. The association between cat ownership and disease merits further investigation.

No abstract

Transmission sites of specific Francisella tularensis genotypes were highly localized during natural outbreaks of human tularemia.

Tularemia, caused by the bacterium Francisella tularensis, where F. tularensis subspecies holarctica has long been the cause of endemic disease in parts of northern Sweden. Despite this, our understanding of the natural life-cycle of the organism is still limited. During three years, we collected surface water samples (n = 341) and sediment samples (n = 245) in two areas in Sweden with endemic tularemia. Real-time PCR screening demonstrated the presence of F. tularenis lpnA sequences in 108 (32%) and 48 (20%) of the samples, respectively. The 16S rRNA sequences from those samples all grouped to the species F. tularensis. Analysis of the FtM19InDel region of lpnA-positive samples from selected sampling points confirmed the presence of F. tularensis subspecies holarctica-specific sequences. These sequences were detected in water sampled during both outbreak and nonoutbreak years. Our results indicate that diverse F. tularensis-like organisms, including F. tularensis subsp. holarctica, persist in natural waters and sediments in the investigated areas with endemic tularemia.

A retrospective study of clinical tularaemia in an emergent area in Sweden is presented. 234 patients seen during the y 2000-2004 were studied, using case files and a questionnaire. There was a predominance of ulceroglandular tularaemia (89%), occurring in late summer and early autumn, reflecting the dominance of mosquito-borne transmission. The incubation period varied from a few hours to 11 d, with a median of 3 d. Cutaneous manifestations of tularaemia, apart from primary lesions, were noted in 43% of the cases. Coughing was common, even in patients with ulceroglandular tularaemia, supporting the view that haematogenous spread to the respiratory system occurs. Regular laboratory tests, such as WBC, ESR and C-reactive protein, were in general only moderately elevated. In the earlier y studied, the Doctor's Delay was substantial as was the misdiagnosis and prescription of inadequate antibiotics. In the later y, however, the delay and misdiagnosis were significantly lower, reflecting the increased recognition of the disease by the physicians in the area. A few relapses occurred, all in patients treated with doxycycline. No lethality was seen, reflecting the benign course of tularaemia type B infection.

Tularemia is a febrile disease caused by the highly contagious bacterium Francisella tularensis. We undertook an analysis of the transcriptional response in peripheral blood during the course of ulceroglandular tularemia by use of Affymetrix microarrays comprising 14 500 genes. Samples were obtained from seven individuals at five occasions during 2 weeks after the first hospital visit and convalescent samples 3 months later. In total, 265 genes were differentially expressed, 95 of which at more than one time point. The differential expression was verified with real-time quantitative polymerase chain reaction for 36 genes (R 2 ¼ 0.590). The most prominent changes were noted in samples drawn on days 2-3 and a considerable proportion of the upregulated genes appeared to represent an interferon-g-induced response and also a proapoptotic response. Genes involved in the generation of innate and acquired immune responses were found to be downregulated, presumably a pathogen-induced event. A logistic regression analysis revealed that seven genes were good predictors of the early phase of tularemia. This is the first description of the transcriptional host response to ulceroglandular tularemia and the study has identified gene subsets relevant to the pathogenesis of the disease and subsets that may serve as early diagnostic biomarkers.

We propose a nonlinear mitigation algorithm designed from an ASIC perspective, and analyze implementation aspects. Given 9 signal and 11 coefficient bits, reach is increased by 105% compared to linear compensation in single-channel 16-QAM transmission.

The capacity and reach of long-haul fiber optical communication systems is limited by in-line amplifier noise and fiber nonlinearities. Phase-sensitive amplifiers add 6 dB less noise than conventional phase-insensitive amplifiers, such as erbium-doped fiber amplifiers, and they can provide nonlinearity mitigation after each span. Realizing a long-haul transmission link with in-line phase-sensitive amplifiers providing simultaneous low-noise amplification and nonlinearity mitigation is challenging and to date no such transmission link has been demonstrated. Here, we demonstrate a multi-channel-compatible and modulation-format-independent long-haul transmission link with in-line phase-sensitive amplifiers. Compared to a link amplified by conventional erbium-doped fiber amplifiers, we demonstrate a reach improvement of 5.6 times at optimal launch powers with the phase-sensitively amplified link operating at a total accumulated nonlinear phase shift of 6.2 rad. The phase-sensitively amplified link transmits two data-carrying waves, thus occupying twice the bandwidth and propagating twice the total power compared to the phase-insensitively amplified link.