Cases reported "Rodent Diseases"

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1/3. trichophyton mentagrophytes var. quinckeanum as a cause of zoophilic dermatomycosis in a human family.

    trichophyton mentagrophytes var. quinckeanum is a zoophilic form of T. mentagrophytes. It induces murine favus in the form of coarse yellow scutules bigger than 1 cm in diameter. In March, 2002, a 52-year-old male patient was examined at the dermatology Clinic of the Medical faculty in Kosice with a 1-week anamnesis of a solitary, oval, annular focus, 3 cm in diameter, on the right side of his face, located subauricularly. When providing the history, he has mentioned that his 12-year-old son has a ,,similar skin disease". Clinical examination of the son showed similar annular oval lesion, size about 2 x 3 cm, located in the right chest region. Since January 2002 the family has kept a guinea pig. They have obtained it through a mediator from the Kosice ZOO. The material for mycological examination was taken from peripheral parts of the foci or desquamating lesions from the father, son, and the guinea pig. Scales were examined microscopically in 20 % KOH solution with Parker's blue-black ink. The findings proved the presence of septal hyphae and formation of arthrospores. Thus, dermatomycosis was confirmed in the father and son, caused by T. mentagrophytes var. quinckeanum, the source of which was a pet guinea pig (Fig. 3, Ref. 17).
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2/3. Evidence for exclusion of a mutation in NRAMP as the cause of familial disseminated atypical mycobacterial infection in a Maltese kindred.

    In mice, susceptibility to intracellular infections in inbred strains is controlled by a single locus, Lsh/Ity/Bcg, and the gene responsible has been cloned and designated Nramp (Natural resistance associated macrophage protein). We have identified a group of related children who appear to have a single gene defect, inherited recessively, which results in increased susceptibility to myocabacterial infection. The immunological defect observed in the affected children resembles that in mice homozygous for the Lsh/Ity/Bcg susceptible allele. To test the hypothesis that a mutation in NRAMP is responsible for the immunodeficiency observed in the affected children, we have typed eight markers in the region of human 2q34-q37 where NRAMP, the human homologue of Nramp, maps. We have shown discordance with the defect in one family and the chromosomes in the three affected children have different haplotypes making it unlikely that inheritance of an ancestral mutation in the NRAMP gene is the cause of increased mycobacterial susceptibility in this group of children.
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3/3. Human babesiosis in taiwan: asymptomatic infection with a babesia microti-like organism in a Taiwanese woman.

    An asymptomatic Babesia infection was confirmed by laboratory diagnoses. The intraerythrocytic protozoan (designed TW1) isolated from a 51-year-old Taiwanese woman appeared to be morphologically consistent with small-form piroplasm, and measurements indicated that it had a body size of 1.5 to 2.5 microm in diameter. The typical features of ring, binary, and tetrad forms were observed in Giemsa-stained thin blood smears. A persistent and low-grade parasitemia was established after hamster inoculation. Indirect immunofluorescent-antibody reactivities indicate that this strain (TW1) of Babesia was serologically related to, but not identical to, the Babesia species (B. microti) that infects rodents. Antibody titers in the patient's sera combined with the clinical symptoms suggested that the present case was a chronic and subclinical babesial infection. A neighborhood human serologic survey indicated that the infection may have been acquired accidentally from an infected rodent and localized within the same family. Indeed, rodents from areas around the neighborhood were trapped, and a high prevalence (83%) of babesial infection was observed. The possible vector responsible for the transmission remains to be identified.
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