Field investigations by Ricketts in western Montana on Rocky Mountain spotted fever established the principal features responsible for the persistence of Rickettsia rickettsii in nature. Unfamiliar with the causative agent, Ricketts proved conclusively that the wood tick, bermacentor andersoni, is the vector. He further demonstrated that the etiologic agent acquired by immature ticks from a variety of small mammals, particularly rodents and lagomorphs, is maintained transstadially and may be transmitted via eggs to the progeny of infected female ticks.* Ricketts' observations on transovarial infection were based on infectivity of larval ticks derived from females that were infected as adults by feeding on guinea pigs sick with spotted fever. Because no more than half of the females transmitted rickettsiae via eggs, he concluded that under natural conditions, this phenomenon does not occur in more than 50% of infected tick females.He also pointed out that the brood of an infected female may include many uninfected larvae.Although these findings were confirmed by many workers, quantitative data that pertain to transovarial infection did not become available until 1954, when Price reported that transovarial transmission in the field occurs about 30% of the time and that, when it does occur, rickettsiae are not passed to all filial ticks. Unfortunately, experimental data were not given, although the results were based "on a great many studies carried out with several strains of R . rickettsii and several lots of D . andersoni." In a similar study with a low-virulence strain of R . rickettsii in D . variubilis, the same author found that 30-40% of female ticks that had been infected as larvae and as nymphs by feeding on rickettsemic meadow voles passed rickettsiae to their offspring. Filial infection rates, determined by injection of oviposited eggs and engorged larvae into chick embryos, varied. Fifty percent of the transmitting females laid eggs, of which one of every 10 was infected, 15% showed one of every two to four eggs infected, and 35% had one of every 20-40 eggs infected. Similar results were obtained with engorged filial larval ticks.In contrast to these findings, Burgdorfer reported almost 100% transovarial and filial infection rates for D . andersoni infected either experimentally or naturally with virulent strains of R . rickettsii. Applying direct immunofluorescence to the examination of eggs, larvae, nymphs, and adults, this author found that rickettsia1 infections were retained throughout all developmental stages of the first filial generation and were again passed to 100% of eggs and larvae of the second generation. Since publication of these observations,
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