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Biomedical subjects

C E Kirkpatrick

Publications and source records attributed to C E Kirkpatrick.

46 records · Page 3Linked to original sources

Susceptibility of domestic cats to infections with Giardia lamblia cysts and trophozoites from human sources.

The object of this study was to determine the importance of domestic cats in the epidemiology of human giardiasis. Of six laboratory-reared cats inoculated with cultured Giardia lamblia trophozoites from humans, only one showed the presence of cysts in the feces, and cysts were found on only 1 of the 80 days of observation. In a second experiment, eight cats were inoculated with G. lamblia cysts isolated from a human being. Over an 8-week period of observation, two of eight cats were found to have passed cysts in their feces, one on only one day and the other on 2 days. Postmortem examination of all of the cats found to be passing G. lamblia cysts at some time during the experiments did not reveal any small-intestinal trophozoites. These results suggest that domestic cats are relatively insusceptible to G. lamblia from humans and, consequently, that cats probably are not significant reservoir hosts of Giardia spp. infective for human beings. Moreover, it appears that the Giardia spp. which parasitize cats are distinct from those of human beings.

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Hematozoa of raptors from southern New Jersey and adjacent areas.

Blood smears from 259 birds of 12 species, representing four families of raptors, from New Jersey, Pennsylvania, Delaware, and Virginia were examined for blood parasites. Infected birds constituted 59.1% of the total. Birds were infected with one or more of the following genera of protozoa: Leucocytozoon (43.2%); Haemoproteus (21.6%); Plasmodium (1.2%); and Trypanosoma (1.2%). Blood culture of 142 raptors of 11 species for Trypanosoma revealed a prevalence of 41.5%. Plasmodium circumflexum is reported for the first time in Accipiter striatus, and Trypanosoma sp. in Buteo jamaicensis.

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Splenic natural killer-cell activity in mice infected with Leishmania donovani.

Several strains of inbred mice were infected with the protozoan parasite Leishmania donovani, and, at several points during the infection, spleens of groups of these mice were tested for natural killer (NK)-cell activity vs lymphoma target cells in vitro and were evaluated for parasite burdens. Generally, elevated followed by normal (compared to uninfected control mice) or subnormal NK responses occurred as the result of infection. Elevated NK responses were not accompanied by high circulating levels of interferon, yet infected mice responded to an injection of an interferon inducer with interferon production as great as control mice. No consistent correlations among susceptibility phenotype to L. donovani infection, spontaneous NK activity phenotype, and infection-induced NK activation/depression patterns were detected among the various strains of mice.

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Mechanisms of depression of splenic natural killer cell function in C57BL/6 mice infected with Leishmania donovani.

C57BL/6 mice chronically infected with the protozoan parasite Leishmania donovani exhibit profoundly depressed splenic natural killer (NK) cell activity as measured by in vitro cytolysis of lymphoma target cells. Injection of infected mice with an interferon (IFN) inducer or in vitro treatment of infected splenocytes with IFN, a phorbol ester, or indomethacin failed to restore their NK activity to the degree shown by age-matched, uninfected mice. Fractionation of infected splenocytes by nylon wool, Sephadex G-10, or carbonyl iron and magnetism treatments was also unable to effect an increase in NK activity. Addition of infected splenocytes to uninfected ones in in vitro NK assays suppressed the NK activity of the latter, and the suppression could be partially or wholly abrogated by prior fractionation of infected splenocytes by the methods noted above. In vitro treatment of infected splenocytes with concanavalin A revealed the presence of NK activity in these cell populations. The results indicate that splenocytes in L. donovani-infected mice become insensitive to IFN stimulation; and the impairment of another, possibly IFN-independent pathway of NK-cell activation may also contribute to the observed L. donovani-induced depression in splenic NK activity in C57BL/6 mice.

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Leishmania chagasi and L. donovani: experimental infections in domestic cats.

The susceptibility of domestic cats to visceral leishmaniasis was examined by inoculating cats with amastigotes of Leishmania donovani and L. chagasi by the intravenous route, and with promastigotes of L. chagasi by the intradermal route. Parasites were recovered from intravenously inoculated cats as long as 16 weeks after inoculation, but parasites apparently did not locate in the viscera in cats inoculated intradermally. Parasites were not detected in intravenously inoculated cats killed at 24 weeks of infection. All cats developed significantly elevated serum antibody titers to Leishmania spp., but none developed the symptoms usually associated with visceral leishmaniasis in humans.

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Feline giardiasis: observations on natural and induced infections.

The excretion of Giardia sp cysts in the feces of naturally and artificially infected cats fluctuated sporadically, and cysts were undetectable several times during 7 weeks of observation. The mean prepatent period for Giardia infection in 7 cats was 9.6 days (range, 5 to 16 days). The amount of the cyst inoculum did not appear to affect the length of the prepatent period. Six of 11 cats had clinical signs consistent with those of giardiasis. Clinical signs and cyst excretion were eliminated after treatment with metronidazole or furazolidone. Moderate oral or parenteral doses of corticosteroids produced little, if any, alteration in the infection. Postmortem examination of 1 inoculated cat revealed Giardia trophozoites in the jejunum and upper portion of the ileum but not in the duodenum, lower portion of the ileum, cecum, or colon. Giardia cysts isolated from cat feces produced infection in Mongolian gerbils but not in C57BL/6J mice.

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Leishmaniasis in beige mice.

The courses of two protozoal diseases, cutaneous and visceral leishmaniasis, were examined in three groups of C57BL/6J mice. One group of mice was homozygous recessive for the beige gene (bg/bg). Beige mice are the genetic homologue of the human Chédiak-Higashi syndrome and, among other defects, are profoundly deficient in natural killer cell activity. Wild-type (+/+) mice, which respond to experimental cutaneous or visceral leishmaniasis by eventually eliminating their parasites, and heterozygous beige (bg/+) mice served as controls; both are phenotypically normal in natural killer cell activity, which is particularly high in the spleen. In bg/bg mice, the course of Leishmania tropica, a causative agent of cutaneous leishmaniasis, was similar to that in control mice after both primary and challenge inoculations. All groups of mice expressed similar humoral and cellular immune responses to L. tropica antigen. However, bg/bg mice failed to eliminate amastigotes of Leishmania donovani, a causative agent of visceral leishmaniasis, from their spleens over an observation period of 56 days, in contrast to bg/+ and +/+ controls. Similar levels of anti-leishmanial antibody were produced by all groups of mice, and all mice responded comparably to footpad injections of L. donovani antigen. The results of this study suggest a possible role for natural killer cells in recovery from L. donovani but not from L. tropica infection.

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Syngamiasis in juvenile American robins (Turdus migratorius), with a note on the prevalence of other fecal parasites.

Of 105 juvenile American robins (Turdus migratorius L.) examined for fecal parasites, 77.1% were infected with one or more species of endoparasite. Syngamus sp. was the most commonly encountered parasite, found in 57.1% of the birds. There was a significant association between the presence of Syngamus sp. eggs in feces and signs of respiratory-tract disease. A single oral dose of fenbendazole (100 mg/kg of body weight) eliminated Syngamus sp. infection from all of 18 birds treated, yet 10 of 16 untreated controls apparently were "self-cured" over the 12-day period of observation.

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