Studies on acquired resistance of the cotton rat against microfilariae ofLitomosoides carinii

Abstract

Cotton rats infected by infective third-stage larvae of Litomosoides carinii were treated at increasing time intervals by a threefold injection of living homologous microfilariae (mf) during the prepatent period. Starting with the first treatment 3, 4 or 5 weeks p.i. seven animals remained completely and two almost mf-negative (1 or 2 mf/mm3 each only once) until 16 weeks p.i. Starting 6, 7 or 8 weeks p.i. six animals developed a normal level of parasitaemia between 42 and 436 mf/mm3, two animals developed a continuous level of 1-2 mf/mm3. The number of fertile adult worms shedding great numbers of microfilariae in the pleural cavity was equal in all animals. However, in mf-negative animals the lung capillary blood showed, in the geometric mean, only 0.6% of the mf-concentration seen in mf-positive animals. The hypothesis is proposed that microfilariae accumulating primarily in the lung capillaries absorb all aggressive components specifically reacting with microfilarial antigens, i.e. neutralize the immune response against them to enable the development of the parasitaemia in the peripheral blood.

Differential tissular distribution ofLitomosoides sigmodontismicrofilariae between microfilaremic and amicrofilaremic mice following experimental infection

“…In humans, several cases of microfilariae detection in spleen, liver, bone marrow, lymph node, bronchial and kidney aspirates have been described (Vij et al , 2011; Vankalakunti et al , 2011; Varghese et al , 1996). The repartition of L. sigmodontis microfilariae in BALB/c mice is close to the one described previously for Sigmodon hispidus , the natural host of L. sigmodontis (Haas et al, 1981; Wenk, 1986; Wenk et al, 1979; Wenk et al, 1982). However, Wenk’s group reported almost no detection of microfilariae in the spleen of the jird, neither after intravenous inoculation nor during patency This difference can be due to technical approaches: in our study, microfilariae are detected by their DNA content, and thus dead or dying Mfs can be detected; furthermore, different susceptibilities of the hosts used for the experiment may influence detection.…”

Immunization with L. sigmodontis Microfilariae Reduces Peripheral Microfilaraemia after Challenge Infection by Inhibition of Filarial Embryogenesis

“…This is in contrast to Wenk and colleagues who found fully developed Mf in the uterus of female worms and in the pleural space of infected and Mf-immunized cotton rats [23]. The differences between both animal models in the mode of Mf reduction may be due to different susceptibilities of the hosts to L. sigmodontis .…”

Increased early local immune responses and altered worm development in high-dose infections of mice susceptible to the filaria Litomosoides sigmodontis

“…Amicrofilaraemia in a susceptible host can have several causes, among which the destruction of circulating microfilariae has been mostly documented [51,52]; specific antibodies targeted against microfilariae play an important role in this suppression [17,18,23,51]. More rarely, amicrofilaraemia may be due to the absence of microfilarial output by fecund female worms, as after ivermectin treatment, which is thought to momentarily block the laying of microfilariae [42,44].…”