Infections of forest rat filaria, Breinlia booliati, in neonate and juvenile laboratory white rats.

The kinetics of Breinlia booliati infection in 3 inbred rat strains (Lewis, Wistar and Sprague Dawley) were investigated. One group of rats was infected as neonates (less than 24 hours of age) with third-stage larvae of B. booliati and the other group was infected as juveniles (4 weeks of age). The results showed that infection in the neonates were significantly different from the infection in the juveniles. The 60 rats infected as neonates, when necropsied between 8 to 10 months postinfection, yielded adult worms. The 2 neonatal infection groups of Lewis and Wistar strains showed highest susceptibility to the infections. The mean prepatent period was 85 days. Ninety to 95% of the infected rats were patent with microfilaraemia and a large percentage (33 to 47%) of them had high microfilaraemia counts exceeding 3000 mff/20 mm3 of blood and larger sizes (mean 157.11 mm for female adult worms and 61.88 mm for male adult worms. The adult worms were distributed equally in both the pleural (57%) and peritoneal cavity (43%). In most aspects, the neonatal infection group of the Sprague-Dawley strain was intermediate in susceptibility between the 2 neonatal infection groups of the Lewis and Wistar strains and the 3 juvenile infection groups. In contrast to neonatal infection groups, the 3 juvenile infection groups exhibited low infection rates (37%, 58% and 47% for the Lewis, Wistar and Sprague Dawley strains respectively), longer prepatent periods (mean 101 days), lower recovery rates (2 to 4%), lower adult worm loads (mean 0.4 to 0.8 female worms, and 0.2 to 0.8 male worms per rat), and smaller sizes (mean 141.24 mm for female adult worms and 53.75 mm for male adult worms). Forty-four to 57% of these infected rats harboured either single male or single female adult worms in the body cavity. Most (92%) of the adult worms recovered from the juvenile infection groups resided in the pleural cavity and the remaining 8% were recovered from the peritoneal cavity. Microfilaraemia could be detected in only 3/20 Lewis rats, 5/20 Wistar rats and 5/20 Sprague Dawley rats. The mean peak microfilaraemia of the 3 pooled juvenile infection groups was 632 mff/20 mm3 of blood, ranging from 7 mff/20 mm3 to 1856 mmf/20 mm3. Our results indicate that the susceptibility to B. booliati infection in white rats is both genetic and age-associated. The responses of the 2 distinct infection groups to B. booliati infections are discussed.