6i2 COMMUNICABLE DISEASES OF LABORATORY ANIMALS 



passer." Repeated tests by the writer have failed to substantiate this view. In fact 

 careful postmortem examinations accompanied by cultural studies indicate that the 

 paratyphoid bacilli select in all probability the intestinal tract as the portal of entry; 

 they penetrate the digestive tube early in the course of an experimental infection 

 per OS and localize in the regional lymph nodes and in the spleen. Unquestionably, 

 various accessory factors, the nature of which is as yet unknown, are required to 

 produce an active disease. The susceptibility of the animals and the dosage of the 

 bacilli are probably subordinate to certain predisposing nutritional, seasonal, or en- 

 vironmental conditions (sudden temperature changes, Freund).' Since the para- 

 typhoid infections in guinea pigs behave slightly different from those studied by 

 Topley,^ Amoss,-' Webster,'' and others on mice, detailed investigations of spon- 

 taneous epidemics are urgently needed. Such a study has recently been reported by 

 Smith and Nelson.^ Their interesting data show that the intestinal carrier state in 

 guinea pig paratyphoid associated with a localization of the organism in the spleen 

 was of relatively short duration. This is of interest since in mice the fecal excretion 

 of bacilli persists over considerable periods of time (Topley and Ayrton). During the 

 epidemic period the individuals of low natural resistance were killed ofif, and the in- 

 fective agent maintained itself in the female pigs which acted as chief focus of dis- 

 semination to their susceptible young and to the population at large. The majority 

 of the sows excreted the bacilli either by way of the digestive tract, the uterus, or the 

 mammary gland — even in one case intra-uterine transmission was noted. No evidence 

 could be produced that the virulence of the causative organism had decreased. Since 

 the factor or factors which caused the transition from the epidemic to endemic phase 

 in the presence of younger generations could not be established. Smith and Nelson ad- 

 vanced the very acceptable hypothesis that the transition from epidemic to endemic 

 phase was due to a combination of the weeding out of individuals of low natural 

 resistance with a gradual adjustment of the invading organism to the population on a 

 lowered level of virulence. It is a well-known fact that paratyphoid may exist latent 

 in a stock of guinea pigs and may be recognized only during the breeding season on 

 account of the high mortality of pregnant females or when the resistance of the ani- 

 mals is lowered through various experimental procedures. In a number of instances 

 the writer has observed that these occurrences were followed by a series of active and 

 fatal cases of the disease in the same and in the adjacent cages. Although the factors 

 or agencies for these deaths among adult guinea pigs, which had been in contact for 

 many months with the carrier animals, could not be determined, it appears not un- 

 likely that in the light of Lockhart's'^' observations fluctuations in the virulence of the 

 paratyphoid bacilli must be considered. 



The clinical manifestations of paratyphoid are not very characteristic, and various 

 symptoms have been ascribed by the different authors. As a rule, the sick animals show a 



' Freund, R.: loc. cit. 



2 Topley. W. W. C: Lancet, i, 477, 531, 645. London, 1926. 



^Amoss, H.: /. Exper. Med., 36, 25, 45. 1922. 



* Webster, L. T.: A. J . Ilyg-, 4, 134. 1924. 



5 Smith, T., and Nelson, J. B.: op. cit., 45, 365. 1927. 



^Lockhart, L. P.: J. Hyg., 25, 50. 1926. 



