Ectoparasite Burden, Clinical Disease, and Immune Responses throughout Fur Mite (Myocoptes musculinus) Infestation in C57BL/6 and Rag1(-/-) Mice.
Immunocompetent weanling mice infested with Myocoptes musculinus harbor high mite loads, yet burdens decrease with age. The development of immunity to the parasite may explain this observation. In this study, we followed M. musculinus burdens in Rag1(-/-) mice and immunocompetent C57BL/6 controls from 4 to 36 wk of age and compared the clinical signs and body weights of noninfested and infested mice of both strains over time. In addition, histopathology of skin lesions and expression of cytokines and transcription factors associated with Th1- and Th2-type immune responses were assessed. Myocoptes burdens decreased and remained low in B6 mice over time, whereas Rag1(-/-) mice showed an initial decrease in burdens after 4 wk of age followed by an increase from 24 to 36 wk. In addition, Rag1(-/-) mice had higher burdens than B6 mice over time. Both strains of infested mice exhibited clinical signs of fur mite infestation-including alopecia, poor weight gain, mite-associated debris, and pruritus-and clinical signs positively correlated with the severity of the Myocoptes burden. Histopathology of skin from both strains of infested mice showed decreased lesion severity with age, likely a result of declining mite populations. Finally, compared with noninfested controls, infested B6 mice had increased expression of markers associated with the Th2-type immune response, which increased in magnitude with increasing age and duration of infestation. These results suggest that development of adaptive immunity plays a role in control of fur mite populations and that heavier infestations may result in more severe clinical signs and skin lesions.
Research Animal Resources, Johns Hopkins School of Medicine, Baltimore, Maryland, USA; Department of Molecular and Comparative Pathobiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA. cmoats1@jhmi.edu.
Cassandra R
CR
Moats
Department of Molecular and Comparative Pathobiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA; Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.
Victoria K
VK
Baxter
Department of Molecular and Comparative Pathobiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Nathan M
NM
Pate
Research Animal Resources, Johns Hopkins School of Medicine, Baltimore, Maryland, USA; Department of Molecular and Comparative Pathobiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Julie
J
Watson
D000818:Animals; D001835:Body Weight; D016207:Cytokines / Q000378:metabolism; D018398:Homeodomain Proteins / Q000235:genetics*; D008810:Mice, Inbred C57BL; D008924:Mite Infestations / Q000276:immunology / Q000473:pathology / Q000662:veterinary*; D008925:Mites / Q000276:immunology*; D059208:Parasite Load; D012376:Rodent Diseases / Q000276:immunology / Q000469:parasitology* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology
D016207:Cytokines; D018398:Homeodomain Proteins; C064658:RAG-1 protein