Prevalence of pathogenic bacteria in Ixodes ricinus ticks in Central Bohemia.

Bacteria associated with the tick Ixodes ricinus were assessed in specimens unattached or attached to the skin of cats, dogs and humans, collected in the Czech Republic. The bacteria were detected by PCR in 97 of 142 pooled samples including 204 ticks, i.e. 1-7 ticks per sample, collected at the same time from one host. A fragment of the bacterial 16S rRNA gene was amplified, cloned and sequenced from 32 randomly selected samples. The most frequent sequences were those related to Candidatus Midichloria midichlori (71% of cloned sequences), followed by Diplorickettsia (13%), Spiroplasma (3%), Rickettsia (3%), Pasteurella (3%), Morganella (3%), Pseudomonas (2%), Bacillus (1%), Methylobacterium (1%) and Phyllobacterium (1%). The phylogenetic analysis of Spiroplasma 16S rRNA gene sequences showed two groups related to Spiroplasma eriocheiris and Spiroplasma melliferum, respectively. Using group-specific primers, the following potentially pathogenic bacteria were detected: Borellia (in 20% of the 142 samples), Rickettsia (12%), Spiroplasma (5%), Diplorickettsia (5%) and Anaplasma (2%). In total, 68% of I. ricinus samples (97/142) contained detectable bacteria and 13% contained two or more putative pathogenic groups. The prevalence of tick-borne bacteria was similar to the observations in other European countries.

The toxic effect of chitosan/metal-impregnated textile to synanthropic mites.

BACKGROUND: Plasma treatment enables effective binding of chitosan film to textile fibres. Heavy metal ions such as Ag(+) adsorbed onto the chitosan coating are known to enhance toxicity to microorganisms. The acaricidal effect of chitosan and chitosan/metal adducts with Ag(+) , Zn(2+) and Cu(2+) was tested in laboratory experiments. Tested species Acarus siro, Dermatophagoides farinae, D. pteronyssinus and Tyrophagus putrescentiae are allergen producers and important pests in house dust, stored food and feed. The mortality was compared after 24 h of exposure of mites to plasma-treated textiles. RESULTS: Chitosan/Ag(+) textile caused at least 80% mortality of all species tested. Chitosan/Zn(2+) and chitosan/Cu(2+) textiles had a smaller effect on mite mortality than chitosan/Ag(+) . The conversion of chitosan/Ag(+) finishing to chitosan/Ag2 O did not influence the mortality of mites in biotests, except that of Tyrophagus putrescentiae, where the mortality decreased from 86 to 64%. CONCLUSION: The results support a great potential of chitosan/Ag(+) fibres in acaricidal materials and/or mite protective food packages.

Overexpression of IL-4 alters the homeostasis in the skin.

IL-4 has been implicated to play an important role in the pathogenesis of many inflammatory diseases including skin diseases such as atopic dermatitis. Because it is not clear which pathologic features of atopic dermatitis are dependent on IL-4, we assessed the consequences of IL-4 overexpression in the skin, using transgenic mice overexpressing IL-4 ubiquitously. Although transgenic mice display no clinical signs of skin inflammation, IL-4 induced a wide spectrum of pathologies including an increased number of mast cells and Langerhans cells in dermis and epidermis, respectively, focal deposition of collagen and a considerably reduced adipocyte layer in the dermis as well as an increased mitotic activity of keratinocytes, reflected in acanthosis and hyperkeratosis. The increase in Langerhans cell number may be explained in part by the substantially reduced Langerhans cell emigration from the epidermis in transgenic mice. The molecular mechanism behind this phenomenon remains to be clarified. Under in vitro culture conditions, Langerhans cells from transgenic mice undergo a maturation process similar to that of Langerhans cells from control mice, and their immunostimulatory capacity is also comparable. In contrast, transgenic Langerhans cells are superior to control Langerhans cells in their antigen-processing capacity. We conclude that the overexpression of IL-4 in the skin is, by itself, not sufficient for the induction of a full-blown atopic dermatitis phenotype, but several changes seen in the skin of transgenic mice mirror the cardinal pathologic manifestations of this disease.