Leo Kartman

New knowledge on the ecology of sylvatic plague.

The history of plague is an eloqueiit example of changing concepts, of investigation in which numerous hypotheses have been advanced, their limitations described, their positive values extracted, and their remaining skeletons buried in favor of new ideas. Known in classical antiquity, in the illiddle Ages, and in the pandemia of the latter Nineteenth and early Twentieth centuries, plague has been studied primarily as an epidemic disease causing widespread mortality in human populations. Until romparatively recently, plague was thought to be fundamentally a disease of domestic rats in which rat fleas were the major vectors. Ry 1928 it was clear that sylvatic or wild-rodent plague represented an independent epizootiologic entity, and since that time it has been recognized that sylvatic plague may transfer to domestic rodents under certain conditions (Pollitzer, 1954). Detailed historical and ecologic views and reviews of plague in the western United States have been written by Meyer (1942a and 1942b), while the works 01 Pollitzer (1954) and Macchiavello (1954) document the vast world literature. The world distribution of sylvatic plague has been summarized by Garnham (1949). Sylvatic plague is now known to be established in wild rodents and their fleas in the western region of the United States and in western Canada. Recently the presence of wild rodent plague was shown in Mexico with the isolation of the organism from prairie dogs in the northern state of Coahuila (Varela and Vasquez, 1954). FIGURE 1 shows the distribution of plague in animals as a result of extensive surveys, especially from 1936 to 1950, conducted by the TJnited States Public Health Service and by certain states. The predominance of wild-rodent over rat-borne plague is shown in FIGURE 2. Wildrodent plague foci have been found in 131 counties of 15 western states in surveyc from the Pacific Coast to the 100th meridian, an area comprising about 40 per cent of Ihe continental United Stales. The evidence shows that the disease in wild rodents forms a vast enzootic reservoir as a potential threat to humans. Pollitzer (1954) lists 91 plague cases and 57 deaths in 7 wcstern states during the period 1908 to 1951 as having been contracted from wildrodent sources. In June 1956 a fatal human case occurred in Ventura County, Calif.; this was apparently contracted from ground squirrel fleas. FICURE 3 s h o w the distribution of human plague cases resulting from conlaci wiih wild rodeiits, with the exception of the case shown in Michigan, which is a laboratory infection.

Skin Reactivity in Guinea Pigs Sensitized to Flea Bites The Sequence of Reactions

Summary Experimental evidence is presented which demonstrates the occurrence of a definite sequence of events in the skin reactions of guinea pigs following repeated exposure to flea bites. The sequence was: I—induction of sensitivity; II—predominately delayed skin reactivity; III—delayed and immediate responses; IV—predominately immediate reactivity; V—non-reactivity.

Allergy to Flea Bites. I. Experimental Induction of Flea-Bite Sensitivity in Guinea Pigs.

Abstract Sensitization of guinea pigs to flea bites, by exposure to the bites of Pulex irritans, P. simulans and Ctenocephalides felis felis, resulted in a delayed 12 to 24-hour reaction. The development of hypersensitivity and resulting lesions very closely duplicated the early phases of sensitivity in human beings subjected to intradermally injected foreign proteins or to the bites of insects such as mosquitoes or blackflies. The present results differed sharply from the reported results of experimental sensitization of rabbits to the bites of various mosquitoes. Guinea pigs sensitized to one species of flea as a rule reacted to all flea species used in the experimental work reported here. This would seem to indicate the presence of a common antigenic factor present in P. irritans, P. simulans, and C. f. felis.

Allergy to flea bites. III. The experimental induction of flea bite sensitivity in guinea pigs by exposure to flea bites and by antigen prepared from whole flea extracts of Ctenocephalides felis felis

Abstract Guinea pigs were sensitized to flea bites by previous exposure to Ctenocephalides felis felis. Delayed reactions appeared at from 5–7 days following daily exposures. Two to 5 days following the appearance of delayed reactions, the animals showed both delayed and immediate types of reactivity. The induction of sensitivity by flea bites was independent of the number of fleas biting. Sensitivity to flea bites induced either by intradermal injection of whole flea extract in saline or by flea bites was systemic and appeared to be an allergic phenomenon. Sensitivity of guinea pigs to flea bites was induced by intradermal injections of whole flea extracts in saline. Guinea pigs injected intradermally with whole flea extract reacted to flea bites. Conversely, when sensitized by flea bites, they reacted to challenge with the extract. While sensitivity to flea bites induced by flea bites required a latent period of 5–7 days, sensitivity to flea bites induced by whole flea extract required 10–14 days.

Notes on the fate of avirulent Pasteurella pestis in fleas.

Abstract By the use of in vitro feeding techniques, fleas ( Xenopsylla cheopis ) were fed upon six avirulent strains of Pasteurella pestis in suspensions of rat blood. Three of the strains (A1122, “14,” and B741-10-9) showed a capacity to multiply in the fleas and eventually to cause blockage of the proventricular valve. The other strains apparently did not survive in the fleas. Plate counts of the number of bacilli of each strain in fleas, processed at intervals after the infectious blood meal, confirmed the findings with regard to blocking rates. In another experiment, seven different concentrations of avirulent P. pestis strain A1122 were fed to X. cheopis . The results showed a direct relation between the number of bacilli in the infectious blood meal and the blocking rates in the fleas. Thus the vector efficiency of fleas may be limited by a “threshold” of the degree of bacteraemia in wild rodents infected with P. pestis

The physiological and biochemical role of the host's skin in the induction of flea-bite hypersensitivity. I. Preliminary studies with guinea pig skin following exposure to bites of cat fleas☆

Abstract Activity related to flea-bite hypersensitivity could be recovered from skin fractions of guinea pigs following flea bites. The activity resided in nonsaline-extractable as well as in saline-extractable portions. The former could induce flea-bite hypersensitivity; the latter could induce sensitivity only with adjuvants. The adsorption of materials secreted by the flea to elements of the hosts skin, and the role of the hosts skin in the induction of flea-bite hypersensitivity is demonstrated.