Infección inducida en el roedor selvático Dasyprocta leporina (Rodentia: Dasyproctidae), con huevos larvados de Lagochilascaris minor (Nematoda: Ascarididae) Induced infection in the wild rodent Dasyprocta leporina (Rodentia: Dasyproctidae) with larval eggs of Lagochilascaris minor (Nematoda: Ascarididae)

Ejemplares de Dasyprocta leporina Linnaeus, 1758 fueron criados alejados de su ambiente natural. A los 3 ó 4 meses de edad, se los inoculó por vía oral con huevos de Lagochilascaris minor Leiper, 1909 obtenidos de una paciente nativa. Los huevos se los incubó por más de 80 dias, para que de ellos fuese posible obtener por compresión mecánica, larvas que se mantuviesen vivas en medio acuoso por 48 horas o más. Sacrificados los animales a los 14 ó 46 dias posteriores a la infección, se hallaron en los músculos esqueléticos larvas ovilladas dentro de nódulos inflamatorios, los cuales no presentaban reacción a cuerpo extraño, abscedación o calcificación. El desarollo de los nódulos no parecía afectar la normalidad de los hospedadores. Las larvas obtenidas eran similares a las descritas por SPRENT como de tercer estadio para estos helmintos. Ratones blancos infectados con material similar, no presentaron nódulos en sus músculos ni se pudo recuperar de sus tejidos larva alguna. Por los hallazgos obtenidos con la infección de estos animales, se postula que el helminto no posee ciclo pulmonar y que su desarrollo requiere de un hospedador intermediario.<br>Specimens of Dasyprocta leporina (Linnaeus, 1758) were raised out their natural environment. At three to four months of age they were orally inoculated with Lagochilascaris minor (Leiper, 1909) eggs obtained from a native patient. The eggs were incubated for more than 80 days so that it was possible to obtain, by mechanical compression, larvae that could be maintained alive in liquid medium for 48 hours or more. The animals were sacrificed 14-46 days after infection and tangled larva in inflammatory nodules were found in skeletal muscle without foreign body reaction, abscess formation or calcification. The development of the nodules did not seem to affect the hosts. The larvae obtained were similar to those described by SPRENT as the third stage of these helminths. When white mice were inoculated with similar material it was not possible to recuperate larva from their tissues nor were nodules found. Based on these results it is postulated that the helminth does not present a pulmonary cycle and that its development requires an intermediary host

Experimental life cycle of Lagochilascaris minor Leiper, 1909 Ciclo evolutivo experimental de Lagochilascaris minor, Leiper 1909

The life cycle of Lagochilascaris minor was studied using material collected from human lesion and applying the experimental model: rodents (mice, hamsters), and carnivorae (cats, dogs). In mice given infective eggs, orally, hatch of the third stage larvae was noted in the gut wall, with migration to liver, lungs, skeletal musculature and subcutaneous tissue becoming, soon after, encysted. In cats infected with skinned carcasses of mice (60 to 235 days of infection) it was observed: hatch of third stage larvae from the nodules (cysts) in the stomach, migration through the oesophagus, pharynx, trachea, related tissues (rhino-oropharynx), and cervical lymphonodes developing to the mature stage in any of these sites on days 9-20 post inoculation (P.I.). There was no parasite development up to the mature stage in cats inoculated orally with infective eggs, which indicates that the life cycle of this parasite includes an obligatory intermediate host. In one of the cats (fed carcass of infected mice) necropsied on day 43 P.I., it was observed the occurence of the self-infective cycle of L. minor in the lung tissues and in the cervical region which was characterized by the finding of eggs in different stages of development, third stage larvae and mature worms. It's believed that some component of the carnivorae gastrointestinal tracts may preclude the development of third stage larvae from L. minor eggs what explains the interruption of the life cycle in animals fed infective eggs. It's also pointed out the role of the intermediate host in the first stages of the life cycle of this helminth.<br>A partir de material colhido de lesões humanas estudou-se o ciclo evolutivo de Lagochilascaris minor empregando-se o modelo experimental: roedores (camundongos, hamster) e carnívoros (gatos, cão). Em camundongos inoculados com ovos infectantes, por via oral, observou-se eclosão de larvas de 3º estágio na parede do intestino, migração das mesmas para o fígado, pulmão, musculatura esquelética e tecido subcutâneo tornando-se em seguida encistadas. Em gatos alimentados com carcaças de camundongos infectados (60-235 dias de infecção) observou-se: eclosão de larvas de 3º estágio do interior dos nódulos (cistos) no estômago, migração através do esôfago, faringe, traquéia, e tecidos vizinhos (rino-orofaringe), linfonodos cervicais alcançando a fase adulta, em qualquer uma destas localizações, 9-20 dias pós inoculação. Não houve evolução do parasito até a fase adulta em gatos inoculados com ovos infectantes, por via oral, dado que reforça a necessidade do hospedeiro intermediário neste ciclo evolutivo. Em um dos gatos (alimentados com carcaças de camundongos infectados) necropsiado 43 dias pós inoculação, observou-se a ocorrência do ciclo auto-infectante de L. minor o que foi caracterizado pelo encontro de ovos em várias fases de evolução, larvas de 3º estágio e vermes adultos em tecidos do pulmão e região cervical. Acredita-se que algum componente do trato digestivo de carnívoros possa inviabilizar larvas de 3º estágio do interior de ovos L. minor, justificando a interrupção do ciclo evolutivo quando tais animais são inoculados com ovos infectantes. Ressalta-se o papel do hospedeiro intermediário nas primeiras fases do ciclo evolutivo deste helminto

Human pulmonary dirofilariasis: a review

The authors presented a detailed summary of the geographical distribution, clinical and pathological aspects of human pulmonary dirofilariasis. Although benign, this zoonosis, of which Dirofilaria immitis is the major etiological agent, represents a medical problem since it produces symptoms which may be confused with neoplasia and thus may subject patients to unnecessary thoracic surgery. Of 229 cases cited in the literature, only 17 were reported in Brazil, despite the existence of highly favorable conditions for the transmission of this infection in man. Thus it may well be that this parasitic infection remains underdiagnosed. Finally, the importance of a differential diagnosis between dirofilariasis and pulmonary neoplasia is emphasized in cases where there is a solitary subpleural nodule ("coin lesion") present. In addition, the development and improvement of modern immunological diagnostic techniques are essential to distinguish this benign disease from other pathological conditions and thus avoid unneccessary surgery. These techniques may reveal the true prevalence of this parasitic infection in our environment