Transmission of murine typhus rickettsiae by Xenopsylla cheopis, with notes on experimental infection and effects of temperature.

In studies on experimental infection of Rickettsia mooseri (= R. typhi) in Xenopsylla cheopis and laboratory rats, it was found that 10 days after the infectious feeding, the fleas were voiding feces that were infective to rats upon inoculation. The feces remained infective for at least the duration of the experiment, and a quantity as small as 0.2 micrograms of feces would result in seroconversion of 67% of the rats upon inoculation. Fleas were capable of transmitting the infection to rats as early as seven days after feeding on rickettsemic rats, but the rate of transmission was much higher late in the course of rickettsial development in the flea, e.g., virtually 100% by day 17. Fleas transmitted R. mooseri infection even when they fed on the host for a maximum of 30 min and were removed from the rats at least 25 min before they could be expected to deposit any feces. These and other data suggest that R. mooseri may be transmitted by X. cheopis by the feeding process, and not merely through contact with infective feces or crushed fleas. The ambient temperature had a profound effect upon rickettsial growth in the fleas. At 18 degrees C, the rickettsial content of the fleas was below detectable levels for at least ten days and remained low throughout, whereas at 24 degrees C and 30 degrees C the rickettsial titer was consistently two or three times greater. However, if, after six days, the fleas were transferred from an environment of 18 degrees C to one at 24 degrees C or 30 degrees C, the rickettsial growth increased by two or three logs within one week.

Transovarial transmission of murine typhus rickettsiae in Xenopsylla cheopis fleas.

It has been generally accepted that infected fleas do not pass on Rickettsia mooseri, or indeed any other known pathogen, to their progeny. It is reported here that such transovarial transmission does occur in laboratory-infected Xenopsylla cheopis fleas. By means of the direct fluorescent antibody test, Rickettsia mooseri was observed in cells of the hemolymph of infected fleas. As many as 11 percent of the adults and 2.9 percent of the larvae of the generation reared therefrom, had demonstrable rickettsiae. Moreover, batches of the F1 fleas were capable of transmitting the infection to more than 18 percent of the rats they infested. The data support the contention that Xenopsylla cheopis fleas play an important role in the maintenance of murine typhus in rats in nature.

Experimental infection with Rickettsia mooseri and antibody response of adult and newborn laboratory rats.

Quantitative studies of selected features of peripherally induced Rickettsia mooseri (= R. typhi) infection in Rattus norvegicus-derived white laboratory rats revealed a unique association between microbe and amplifying vertebrate host which appears to be especially conducive to maintenance of the enzootic cycle. Both adult and newborn (1-3 days old) rats were highly susceptible to percutaneous infection (ID50 = approximately 1 organism), but neither showed signs of disease or died even when inoculated with 10(4)-10(5) plaque-forming units. Gain in body weight of infected newborn rats was indistinguishable from that of uninfected newborn rats over the first 3 weeks of life. The course of the systemic infection, as measured by the rise and fall of R. mooseri titers in blood, brain and kidney and the serum antibody response, was almost identical in adult and newborn rats. Thus, despite their immaturity in certain immunological processes, newborn rats controlled postnatal R. mooseri infection about as well as did adult rats. The rickettsemic period of about 10 days corresponds to the period of infectivity of inoculated rats for fleas. Rickettsiae were not isolated from blood, brain or kidneys by methods employed for more than 4-5 weeks after infection. Serum antirickettsial antibodies persisted for at least 60 weeks postinfection, i.e., longer than the usual life span of rats in nature and, hence, are a valid measure of the cumulative experience of rat populations with R. mooseri infection.

Rickettsia mooseri infection in the fleas Leptopsylla segnis and Xenopsylla cheopis.

Detailed observations on the acquisition and propagation of experimental Rickettsia mooseri infection in two species of fleas are presented. Rickettsia mooseri infection became detectable by means of the direct fluorescent antibody test about 2 days earlier in Leptopsylla segnis than in the putative vector, Xenopsylla cheopis. By the 6th day after the infective feeding, the entire lining and the lumen of the midgut in L. segnis contained masses of rickettsiae and the agent was being passed in the feces of the flea, whereas in X. cheopis these events did not occur until the 8th day. Basic behavioral differences in the two species of flea may explain these discrepancies and also influence their ability to serve as vectors of murine typhus. As a semisessile flea and sustained feeder, L. segnis only rarely attaches to a second individual and thus has an opportunity to acquire a heavy dose of rickettsiae, if feeding on a rickettsemic host. X. cheopis, in contrast, feeds rapidly and intermittently, even on man, and generally leaves its host soon thereafter, later returning to the same or another host to feed again. While L. segnis may not be as efficient a vector as X. cheopis regarding the intramurine cycle or transmission to man of murine typhus, the dense accumulation of infective feces on certain sites on the fur of the host raises the possibility of air-borne infection to man or rodent. Infection with R. mooseri had no effect on the survival of X. cheopis and L. segnis. Furthermore, no visible cytopathological effect was found in the paraffin-embedded sections of infected fleas.(ABSTRACT TRUNCATED AT 250 WORDS)

Capillaria hepatica in small mammals collected from Shoa Province, Ethiopia.

A total of 1,110 small mammals has been examined for Capillaria hepatica in Shoa Province, Ethiopa. Nineteen of 308 (6.2%) Rattus rattus and 1 of 212 (0.5%) Praomys albipes were infected. The data indicate that C. hepatica was essentially limited to commensal rats (R. rattus).

Ecology of Capillaria hepatica (Bancroft 1893) (Nematoda). II. Egg-releasing mechanisms and transmission.

The egg-releasing mechanism and transmission ecology of Capillaria hepatica among Norway rat populations of the Baltimore Zoo were studied from 1972 to 1974. Nearly all adult rats were infected, while 65% of juveniles had infections. The mean egg count per liver was calculated to be 457,783 (N = 39 livers) and ranged from 11,270 to 1,400,000 eggs per liver. Data from the present study suggest that cannibalism serves as a primary egg-releasing mechanism and is a source of infection within the burrows. Increased infection rates among juveniles in spring support the hypothesis of maintenance of C. hepatica infections within the burrow system through cannibalism. Predation was responsible for scattered foci of infection throughout the study area and considered as a secondary source of infection. Decomposition was an important egg-releasing mechanism in secondary foci and in the warmer season when insects were active. However, of 849 carrion-associated insects and soil invertebrates collected from around decomposing rats, eggs of C. hepatica were found in only two species of beetles. This suggests a minor role for insects and soil invertebrates as egg disseminators.

Leptospirosis in small mammals of Iran: II: isolation of Leptospira grippotyphosa from Mus msuculus.

The serotype of Leptospira grippotyphosa, which is most frequently encountered among sheep, cattle and man in Iran, was isolated from the kidney of a house mouse, Mus musculus, by direct culture and animal inoculation. This is the first time that a rodent reservoir of L. grippotyphosa in Iran has been investigated and reported.

Ecology of Capillaria hepatica (Bancroft 1893) (Nematoda). 1; Dynamics of infection among Norway rat populations of the Baltimore Zoo, Baltimore, Maryland.

Seventy-five per cent of 845 Norway rats examined in the Baltimore Zoo for Capillaria hepatica were infected. Nearly all adult rats and 65% of juveniles were infected. Only 8% of 299 infected rats were heavily infected. The prevalence and intensity of infection increased with the size of the host. There were no seasonal differences in infection rates among adults, but juveniles collected during spring had higher infection rates than those collected during winter. Prevalence of C. hepatica infection varied from one place to another. No correlation between infection rate, vegetative cover, soil type, monthly rainfall, mean daily temperature, or food habits of rats was found. The dynamics of rat populations are perhaps the most important factors in the maintenance and dynamics of C. hepatica infections. Rapid population turnover contributes to the rapid release of a great number of eggs into the environment and high recruitment rates provide sufficient numbers of susceptible hosts for the parasite to complete its cycle.

Trypanosomes of small mammals in Iran.

Trypanosomes in the subgenera Herpetosoma, Schizotrypanom and Megatrypanum were found in 31 small mammals representing nine species of the orders Rodentia, Insectivora and Chiroptera in Iran.

First detection of tularaemia in domestic and wild mammals in Iran.

During a study on the ecology of small-mammal-borne infections in Iran, over 4 600 wild mammals were collected at 47 localities. Attempts were made to isolate Francisella tularensis from the spleens of 3 548 of these animals. All were found to be negative. In addition, sera from 200 sheep and cattle and from 39 wild mammals were tested: 8 sheep, 3 oxen, and 1 hedgehog showed evidence of recent infection. This is the first report of tularaemia in Iran. The relationship of these findings to the potential distribution of natural foci in Iran and adjacent countries indicates that the infection in Asia may be more widespread than was previously thought.