Abstract
No commercial immunodiagnostic tests for human scabies are currently available, and existing animal tests are not sufficiently sensitive. The recombinant Sarcoptes scabiei apolipoprotein antigen Sar s 14.3 is a promising immunodiagnostic, eliciting high levels of IgE and IgG in infected people. Limited data are available regarding the temporal development of antibodies to Sar s 14.3, an issue of relevance in terms of immunodiagnosis. We utilised a porcine model to prospectively compare specific antibody responses to a primary infestation by ELISA, to Sar s 14.3 and to S. scabiei whole mite antigen extract (WMA). Differences in the antibody profile between antigens were apparent, with Sar s 14.3 responses detected earlier, and declining significantly after peak infestation compared to WMA. Both antigens resulted in >90% diagnostic sensitivity from weeks 8–16 post infestation. These data provide important information on the temporal development of humoral immune responses in scabies and further supports the development of recombinant antigen based immunodiagnostic tests for recent scabies infestations.
Highlights
The ectoparasitic mite Sarcoptes scabiei causes a skin disease referred to as scabies in humans and as sarcoptic mange in other animal species
In wild animals measuring the extent of damaged skin may be useful proxy to evaluate mite burden [7]
Sar s 14.3 cDNA was polymerase chain reaction (PCR) amplified from S. scabiei var. suis using primers based on the S. scabiei var. hominis sequence
Summary
The ectoparasitic mite Sarcoptes scabiei causes a skin disease referred to as scabies in humans and as sarcoptic mange in other animal species. Sarcoptic mange is associated with adverse welfare and reproductive outcomes. In wild animals measuring the extent of damaged skin may be useful proxy to evaluate mite burden [7]. Crusted scabies can be associated with immunosuppressive conditions, such as HIV or HTLV-1 infection, following organ transplantation, or induced by immunosuppressive drugs including corticosteroids [8]. It is observed in a significant number of individuals with no overt immunosuppression or risk factor [9]. Host responses to S. scabiei are complex, with host species, previous exposure, mite immunomodulation, individual susceptibility and sex, all playing a likely role [11,12,13]
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