Tungiasis (sand flea disease): a parasitic disease with particular challenges for public health.

Tungiasis (sand flea disease) is caused by the penetration of females of Tunga penetrans into the skin of the feet. Within 2 weeks of penetration the burrowed flea increases its volume by a factor of 2,000. This is paralleled by intense inflammation of the surrounding tissue. Acute and chronic inflammation leads to the development of painful and debilitating clinical pathology. This results in impaired physical fitness and mobility. The social implications of tungiasis-associated morbidity are multifold. Children with tungiasis are teased and ridiculed, adults feel ashamed and stigmatized. There is anecdotal evidence that tungiasis negatively affects educational achievements. Impaired mobility and physical fitness will have a negative impact on household economics. Sand flea disease is common in resource-poor communities in South America and in sub-Saharan Africa with prevalence in the general population of up to 60%. In East Africa, it has re-emerged in epidemic dimensions in recent years. Hitherto, no effective drug treatment has been at hand. Traditional treatment, i.e., the manipulation of burrowed sand fleas with blunt and inappropriate instruments may facilitate the transmission of blood-derived pathogens. Prevention is feasible through regular application of a repellent based on coconut oil. Owing to its strong association with poverty, sand flea disease would be an excellent starting point for a community-based fight against rural poverty.

T cell responses in coinfection with Onchocerca volvulus and the human immunodeficiency virus type 1.

Onchocerca volvulus and the human immunodeficiency virus (HIV) are two immunocompromising infectious agents of major public health concern in Uganda. To examine the effect of coinfection with O. volvulus and HIV on cellular immune responses, lymphocyte proliferative responses and cytokine production of peripheral blood mononuclear cells (PBMC) from persons infected with O. volvulus with and without HIV type 1 infection were compared. Proliferation of PBMC to PHA and tuberculin (PPD) in coinfection was less (P = 0.08, P < 0.01) than in O. volvulus infection. O. volvulus extract stimulated lymphocyte proliferation in microfilaria-negative and HIV-negative O. volvulus infection while only an inconspicuous response was observed in microfilaria-negative coinfection. After stimulation of PBMC with PPD, the production of interferon-gamma (IFN-gamma), interleukin (IL)-4 and IL-5-demonstrated in O. volvulus infection-were reduced in coinfection with HIV (P < 0.01). While both groups failed to produce IFN-gamma in response to O. volvulus extract, only O. volvulus infected persons generated pronounced IL-5 and low IL-4 levels (0.01 > P = 0.02). The cellular immune responses in coinfection suggested an HIV-related lack of specific reactivity to O. volvulus antigen and impairment of IL-4 and IL-5 production in addition to the lack of IFN-gamma response on antigenic stimulation.