Histopathology of experimental myiasis in mice as a result of infestation and experimental implantation of Dermatobia hominis larvae.

A laboratory model of myiasis as a result of Dermatobia hominis (L.) larvae was developed using mice as hosts. Mice in three groups were each infested with one newly hatched larva and skin biopsies processed for histopathology at 4, 12, and 20 d postinfestation (dpi). Mice in three other groups were each subjected to implantation of one larva collected from an infested (donor) mouse at 4, 12, and 20 dpi. Skin lesions of these receptor mice were then assessed at 10, 14, and 6 d postimplantation (dpimp), respectively. The inflammatory process in infested mice at 4 dpi was discrete, consisting of a thin necrotic layer around the larva, edema, many neutrophils, few eosinophils, mast cells, and proliferation of fibroblasts. At 12 dpi, there was a thicker necrotic layer, edema, many neutrophils and eosinophils, few mast cells, neoformation of capillaries, proliferation of the endothelium and fibroblasts, and early stages of fibrosis. These histopathological characteristics together with fibrosis were observed over a large area of the lesion at 20 dpi. Mice submitted to larval implantations demonstrated similar skin histopathology to that seen in the infested rodents, 10 dpimp corresponding to 12 dpi and 6 or 14 dpimp to 20 dpi. In all mice, the progressive acute inflammatory process followed a sequence linked to factors such as size of larvae and presence of secretory-excretory products. Both infested mice and those implanted experimentally with D. hominis larvae were shown to be suitable models for the study of the parasite-host relationship in this important zoonotic myiasis.

Implantation of human bot fly larvae in host skin.

Adult males of Mus musculus each infested with four first-instar (L1) larvae of Dermatobia hominis (Linneaus, Jr.) were used as donors of larvae to other mice (recipients). Larvae at four (L1), six (early L2), 12 (L2), or 20 (L3) days postinfestation (dpi), were implanted into the skin of each recipient. Only two of 38 mice (5.3%) were refractory to implants and three died after implantation. Developmental times (pre- plus postimplantation) of implanted larvae were of similar duration to those in larvae that completed their development in the original mice. The L3 that emerged from implanted hosts developed to pupae and fertile adult specimens, whose L1 descendants were used to maintain the D. hominis life cycle in our laboratory. The model described here has several potential applications, including studies of the host relationship with specific instars and the development of management and control measures to combat this Neotropical myiasis.