The 1997–2005 tularemia outbreak in Bulgaria affected 285 people. Ten strains were isolated from humans, a tick, a hare, and water. Amplified fragment length polymorphism typing of the present isolates and of the strain isolated in 1962 suggests that a new genetic variant caused the outbreak.

Some of the proposed laboratory diagnostic strategies (swab PCR) are not invasive and could represent a new approach for resolving rare and hard-to-diagnose cases of oculoglandular tularemia.

During a recent large tularemia outbreak in Bulgaria we found several cases that were remote from the main focus. One case had an unusual mode of transmission. A hunter acquired tularemia through a nail scratch from a buzzard (Buteo buteo) and consequently developed a typical ulceroglandular form of the disease. The diagnosis was confirmed by serological methods and successful cultivation. Comparative strain typing was performed by high-resolution multi-locus variable-number tandem repeat analysis (MLVA). The isolated strain was identical to one of the outbreak genotypes. We consider that this case represents a bird-to-human transmission of F. tularensis.

Introduction: Tularemia is an uncommon but potentially fatal zoonosis. А second outbreak of tularemia in Bulgaria, about 40 years after the first, occurred in 1997 in two western regions, near the Serbian border. In 2003 tularemia reemerged in the same foci. This retrospective study aimed to evaluate the clinical characteristics and the efficacy of antibiotic therapy in a tularemia resurgence in the Slivnitza region in [2003][2004]. Methodology: A total of 26 cases were evaluated. Using medical records, the following data were collected for all patients: symptoms, physical signs, and microbiology results of agglutination tests, cultures and PCR assays. Results: Twenty-four of 26 suspected tularemia patients were laboratory confirmed by agglutination test and/or culture. Fifteen (57.7%) patients had clinical presentation compatible with oropharyngeal, 8 (30.8%) with glandular, and 3 (11.5%) with oculoglandular tularemia. The most frequent symptoms were swollen neck (84.6%) and sore throat (76.9%). Lymphadenopathy (100%) was the most common finding. Francisella tularensis (F. tularensis) was detected by PCR, providing a definitive diagnosis in 82.3% of the cases. All the patients were treated with antibiotics considered effective against F. tularensis; however, therapeutic failure was observed in 23.1% of the cases, which was related to a delay in the initiation of antibiotics. Conclusion: The tularemia outbreak in west Bulgaria near the Serbian border was probably food-borne, associated with a surge in the rodent population. The oropharyngeal form was the most common. Although the disease runs a benign course, late initiation of antimicrobial therapy might delay complete recovery.

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Downstream regulatory element antagonist modulator (DREAM) protein is a 31 kDa Ca 2+-regulated transcriptional repressor. It functions as a silencer of the gene transcription. In low intracellular free Ca 2+ concentration DREAM tightly binds to the downstream regulatory element (DRE) of gene promoter and impedes the transcription. In higher Ca 2+ concentrations DREAM binds Ca 2+ and disconnects from DRE of the gene promoter enabling transcription. We report that DREAM is expressed in different human tissues including the pancreas, where it is located in the islets of Langerhans. Location of DREAM in RIN-F5 cells in cultures is restricted to the nucleus and membranes and changes after increased Ca 2+ -levels. The proteins dissociate from dimmers to monomers and translocate out of the nucleus. The expression of DREAM in β-cells in the islets of Langerhans regulates the promoter activity of the insulin gene by directly interacting with the sequence located between +52 bp and +81 bp downstream of the transcriptional start site of the promoter. Our results provide evidence for the existence of DRE sequence in the insulin gene promoter. It is suggested that DREAM is a repressor of insulin gene transcription, whose effect is mediated by direct binding to DRE sequence.

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