Adult worm recoveries are shown in Table I. One male neonate mouse given 80 larvae developed a patent infection at 60 days and remained patent, although at low levels (2-5 microfilariae/100 ,l of blood), until killed at 140 days. All other mice failed to develop a microfilaremia. Six of the neonate mice infected with 40 larvae harbored adult worms. All mice infected as neonates with 80 larvae had adult worm burdens. None of the control mice infected at 8 wk of age harbored adults or microfilariae at necropsy. Approximately 77% of the adults were recovered from the peritoneal cavity. Worms were also found in the heart, lungs, reproductive organs, and thoracic cavity of some mice. There was a preponderance of female worms recovered (1 329, 676); the majority of these female worms, however, were recovered from the peritoneal cavities of only two mice. Male and female neonate mice appeared to be equally susceptible to infection. It is perhaps noteworthy that the only mouse that developed a patent infection had adult worms in the thoracic cavity. Although the evidence is based on only one animal, it is possible that the thoracic cavity may be a better site for worm development than the peritoneal cavity, lungs, heart, or reproductive organs. Most worms appeared viable, although a few partially calcified worms were found. The size of the adult worms recovered 140 days after infection was consistently smaller than those found in either cats (Schacher, 1962, J. Parasitol. 48: 693-706) or jirds (Ash and Riley, 1970, J. Parasitol. 56: 962-968); in the mice that were infected as neonates, female worms averaged 30.8 mm and male worms averaged 12.8 mm in length. The successful establishment of Brugia pahangi infection in neonate mice opens up the possibility of the ready availability of murine filarial infections. Experiments should be done to delineate the best protocol for infecting animals and the subsequent development of adult worms and microfilaremias. Mice harboring adult worms should be studied to detail the immunologic parameters that render neonate mice susceptible to infection. This work was supported by a research grant, No. AI-10250, from the United States-Japan Cooperative Medical Science Program. We are grateful to Virginia Hansen for editorial support.
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