No abstract

An electron microscope study of infected human louse gut cells and feces was made to determine whether a valid correlation exists between the increased resistance of Rickettsia prowazeki (in the louse feces) to adverse environmental influences and changes in the organism which might be reflected in its ultrastructure. Upon fine structural examination of this intracellular parasite as it passed from the louse midgut cell to the feces, it was apparent that no such morphological changes had occurred.

Resistance to ticks, manifested as a reduction in the number of nymphs supported through engorgement, was developed in rabbits subjected to a series of nymphal tick infestations. Resistance appeared in rabbits receiving their initial exposure to nymphal ticks approximately 6 to 10 days after ticks were paced on them. It increased to become maximal between about 10 and 16 days, and then declined if a 2nd group of nymphs was not placed on the rabbits during this time. Although a single infestation of nymphs usually produced resistance, its detection by means of a 2nd infestation thus depended upon the time elapsed between the 2 feedings. The development of the immunity appeared to depend less on the number of ticks per infestation than on the frequency of infestation. A homocytotropic antibody was found in the sera of immune rabbits.

Evidence is presented to indicate that proteolytic and perhaps other enzymes of the louse midgut, essential to the nutrition of the louse, perform molecular dissection on the antirickettsial antibodies present in the blood of a typhus-immune host that selectively destroys, along with other functions, the portion of the antibody that determines the only known function by which antirickettsial antibodies may operate in host defense mechanisms, namely, opsonization of rickettsiae for enhanced ingestion by professional phagocytes and subsequent destruction. The epidemiologic significance of these findings is discussed in relation to the progressive destruction of cells that produce digestive enzymes of the louse midgut that occurs with progressive rickettsial infection, and the possibility of a negative feedback mechanism in transmission is introduced. Speculations that involve evolutionary concepts of both convergent and divergent varieties with respect to rickettsiae, potentially operational in a system that consists of an obligate blood-sucking arthropod vector and a vertebrate host capable of adaptive responses to both vector and rickettsial agent, are presented.