Development of Animal Viruses and Rickettsiae in Ticks and Mites

Recent investigations on arboviruses and rickettsiae in relation to their vectors have centered upon the isolation of new agents from arthropods and the possible role of arthropods as vectors or reservoirs of microorganisms. There are relatively few papers which analyze in detail the relationships between viruses, rickettsiae, and their vectors. These relationships, character­ ized by benign infections of acarines and vertebrates, were established in the evolutionary development of viruses and rickettsiae, their vectors, host, and the external environment. In the opinion of many authors, as reviewed by Philip (78), these microorganisms were originally symbiotes of acarines and became secondarily pathogenic for vertebrates through the parasitic habits of their arthropod hosts. The presence of intracellular rickettsia-like organisms in ticks supports this hypothesis (103). The transmission of microorganisms by vectors can be classified in differ­ ent ways (62); in this paper, the commonly known classification used by Chamberlain & Sudia (30), distinguishing the biological and mechanical mode of transmission, will be employed. The question of whether arthropods can also be regarded as reservoirs was discussed by Philip (78). In a number of cases, acarines can be considered as reservoirs of viruses and rickettsiae since these microbial agents often persist for several years in their bodies, and may be transmitted through several generations. The majority of these agents, pathogenic for verte­ brates, does not cause any detectable harm to the arthropod vectors; this fact also supports the hypothesis mentioned above. The presence of an infectious agent in a vector depends not only on the arthropod alone, but on all factors determining its ecology (15, 16, 115). In this paper it is intended to make a more or less complete survey of the recent knowledge of the mechanisms of growth and development of viruses and rickettsiae in ticks and hematophagous mites. We shall try to demon­ strate briefly this process from the reception of the infection by the vector to its transmission to the vertehrate host.2