Studies have been made in the field and in the laboratory on the lifecycle, maintenance and host-parasite relationships of Ackertia globulosa, a filarial parasite of African rodents. In natural habitats in Kenya the parasite was found in 4 species of rodents, with a high prevalence of infection in Lemniscomys striatus striatus (the striped mouse). The adult worms are highly site-specific to the pulmonary arteries and release microfilariae that travel via the blood to the skin where they concentrate principally in the ears. This is a good adaptation to the feeding habit of the tick Haemaphysalis leachii leachii, which was identified as a natural vector of A. globulosa in Kenya and attaches preferentially to the head region on striped mice. A histological examination of tick attachment sites revealed that the ingestion of microfilariae may be further enhanced by their accumulation beneath the mouthparts during the 3 day feeding period. In H. leachii the microfilariae of A. globulosa develop to infective stage larvae in 14-18 days. Studies made by dissection and histological techniques revealed that development is intracellular and occurs for the first 9 days in the epidermis and for the next 5 days in fat cells. Third-stage larvae then enter the haemocoel and are transmitted to rodents when the ticks next feed. A. globulosa was established in the laboratory and maintained in mongolian jirds (Meriones unguiculatus) and laboratory bred striped mice. In experimentally infected rodents the Microfilarial densities were low although 63% developed patent infections. The prepatent period is 74-88 days and the adult worms survive for up to 500 days. The development of A. qlobulosa was studied in experimentally infected jirds. Microfilariae and adult worms caused no serious pathology in the vertebrate host although a few microfilariae were found in the eyes of heavily infected striped mice. The treatment of experimentally infected rodents with diethylcarbamazine resulted in the destruction of 80-100% of the microfilariae in skin but appeared to be ineffective against the adult worms. Skin responses seen in animals after drug treatment suggest that a Mazzotti-type reaction may have been elicited. The potential of A. globulosa in rodents as a laboratory model infection and primary chemotherapeutic screen for human onchocerciasis and streptocerciasis is discussed. An investigation was also made of possible relationships between tick-bits hypersensitivity in Mongolian jirds and the tranmission of Dipetalonema viteae by its soft tick vector. Jirds sensitised to the bites of Ornithodoros moubata produced vigorous immediate and delayed hypersensitivity reactions but remained fully susceptible to all stages of the arthropod and to infection with filarial larvae transmitted by infected ticks. Although the uptake of microfilariae by ticks fed on hypersensitive animals was relatively greater than on normal hosts, the difference was not sufficient to identify hypersensitivity to tick bites as a significant influence on the transmission of D.viteae. The relevance of these findings to the epidemiology of human filarial infections is discussed.