Demodex folliculorum and Demodex brevis are obligatory parasites in the hair follicles and in the pilosebaceous glands. Although most people are infested with these mites, only a small number develop the clinical symptoms of demodicosis.
a. Cellular and humoral immunity
We investigate the immune response to the infestation of the human skin by Demodex mites. The presence of mites was determined by microscopic inspection of secretion from sebum glands. The immune response was evaluated in the peripheral blood by identifying membrane markers of different immune cells using monoclonal antibodies, while the concentration of IgA, IgM, and IgG was calculated by simple radial immunodiffusion using anti-IgA, IgM, and IgG. The level of circulating immune complexes and total haemolytic complement, as well as the preparatory and digestive function of neutrophils, and the functional activity of leukocytes were also studied.
The absolute numbers of CD95+ was higher in patients with demodicosis. The absolute number of CD3+, CD4+, CD8+, and CD16+ cells, the ratio of CD3+/CD20+, and the functional activity of leukocytes were significantly lower in individuals infested with Demodex mites. No significant differences were found in the percentage and absolute number of CD20+ cells, the ratio of CD4+/CD8+ T cell subpopulations, circulating immune complexes, CH50, activity and index of phagocytosis and the level of IgM, IgG and IgA antibodies between individuals infested with Demodex mites and the control group (A 87).
b. Association between HLA specificity and demodicosis
Twenty-five patients with human demodicosis and 150 controls were typed for HLA-A, B, Bw, and Cw using the microlymphocytotoxicity method. The immune response was evaluated by identifying membrane markers of different immune cells using monoclonal antibodies. An association between the frequency of HLA Cw2 and Cw4 haplotypes and human demodicosis was established. The risk of developing clinical symptoms of this disease is 5.0 times higher for people with the Cw2 phenotype and 3.1 times higher for those with the Cw4 haplotype. Individuals who have the HLA A2 phenotype are 2.9 times more resistant to demodicosis. A positive correlation between demodicosis and the haplotypes A3-Cw4, A3-Cw2, A3-B17, A3-B35 and B35-Cw4 was found. In addition, an association between Cw2 and Cw4 alleles in the phenotype of patients with demodicosis and a decrease in the number of NK cells was found (A 82).
Twenty-five patients with demodicosis and thirteen age-and-sex-matched healthy subjects participated in the study. The presence of mites was determined by microscopic inspection of sebum gland secretions. The immune response was evaluated by identifying membrane markers of different immune cells using monoclonal antibodies (anti-CD3+, CD4+, CD8+, CD16+, CD20+, and CD95+) while the concentration of IgA, IgM, and IgG was measured by simple radial immunodiffusion. The level of circulating immune complexes and total haemolytic complement, as well as the preparatory and digestive function of neutrophils and the functional activity of leukocytes were also studied. Patients were typed for HLA-A, B, Bw and Cw using the microlymphocytotoxicity method. The comparison between patients with and without the A2 phenotype showed that the later have lower numbers of CD8+, lower functional activity of leukocytes, higher concentrations of IgA, larger affected skin areas and are more often affected by deep papulous and papulo-pustulous forms of demodicosis than those with the A2 phenotype, showing that this allel has a protective role in demodicosis. Patients exhibiting the Cw2 phenotypes were rather susceptible to demodicosis. They showed decreased numbers of CD3+, increased levels of phagocytic activity, higher mite density and more severe skin damages as compared to patients lacking Cw2. Conclusions: HLA A2 and Cw2 phenotypes have an important diagnostic, prognostic and pathogenetic significance and could have a possible role in resistance or susceptibility to demodicosis by regulating the end phase of the immune response (A 91).
c. Demodicosis classification
Although there are several clinical variants of this disease, a clear classification is missing. We attempted to characterize the clinical features and course of the different forms of demodicosis. For this purpose a prospective study of 87 patients with clinical symptoms of demodicosis and positive acarological findings was conducted. Each patient was examined an average of six times during the treatment period. We suggest that demodicosis be divided into both primary and secondary types. The usual etiological agent of primary demodicosis is D. folliculorum, which causes an erythemato-squamous eruption in the facial T-zone. The rash starts on unaltered skin and covers 8 - 15% of the face. Pruritus accompanies the onset of the rash, while erythema is first apparent after papulo-pustules are seen and disappears after treatment. Half the patients show seasonal exacerbations. Secondary demodicosis is usually caused by D. brevis and characterized by a symmetrical malar papulo-pustular eruption. It develops on diseased skin and covers 30 - 40% of the face. Pruritus starts after the lesion exacerbation, but erythema, precedes the papulo-pustular phase and persists after treatment. Most patients flare during the summer. Conclusions: The facial distribution, seasonality and pathogenesis, as well as the species of mite involved, must be taken into consideration in separating the various forms of demodicosis (A 94).
Additional publications on this subject: A 23, A 25, C 29 and C 41