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At least 865 records · Page 48Linked to original sources
PubMed1991

[Meningitis associated with tsutsugamushi disease--detection of intrathecal interferon-gamma synthesis and lymphocyte subsets in blood and CSF].

We report a case of meningitis associated with tsutsugamushi disease. The lymphocyte subpopulation study of peripheral blood revealed a reversed CD4/CD8 ratio (0.14), an increased number of activated T cells and an elevated cytotoxic T cell activity. In cerebrospinal fluid (CSF), the CD4/CD8 ratio was much higher (0.84) and activated T cells were less prevalent than in blood. These pictures of lymphocyte subsets were characteristic and different from that of viral meningitis. We also verified an elevation of interferon-gamma levels in CSF as well as in serum and intrathecal interferon-gamma synthesis while the specific antibody production in CSF compartment was not demonstrated. T cell-mediated immunity many play an important role not only systemically but also locally in the central nervous system in tsutsugamushi disease.

CD4-CD8 Ratio↗
PubMed1991

Rickettsial infection of the central nervous system: the role of prompt antimicrobial therapy.

Rickettsial diseases of man, which are prevalent in all the continents (except Antartica) continue to be a major health problem in tropical and temperate parts of the world. Rickettsioses must be considered in every traveller seeking medical attention soon after returning from endemic areas, since the disease can be associated with significant morbidity. When a definite diagnosis has been made by specific serological tests, prompt antimicrobial therapy is indicated. A tetracycline should be regarded as the drug of choice due to its high efficacy, low toxicity, superior in vitro activity and the possibility of relapse which can follow chloramphenicol therapy.

Anti-Bacterial Agents↗
PubMed1991

[Polymerase chain reaction for the diagnosis of tsutsugamushi disease].

A polymerase chain reaction (PCR) using specific oligonucleotide primers and Taq polymerase was developed for the detection of Rickettsia tsutsugamushi, the causative agent of tsutsugamushi disease. Oligonucleotide primers were synthesized on the basis of DNA sequences encoding 58 kD antigen of R. tsutsugamushi. Specific DNA amplification of 358 bp and 109 bp DNA fragments were demonstrated using patient's blood. This PCR method would enable to make a rapid and sensitive diagnosis of tsutsugamushi disease.

Antigens, Bacterial↗
PubMed1990

[The natural foci of the tsutsugamushi disease in the suburbs of Hang Zhou City].

In 1986, investigating tsutsugamushi disease in the suburbs of Hangzhou, We isolated Rickettsia tsutsugamushi from leptotrombidium gaohuense and its reservoir hosts, Rattus confucianus and Rattus fulvescens, which were collected in Yang Shan Wu village, Linan county. It proved there was a natural focus of tsutsugamushi disease in the suburbs of Hang zhou. Which is located at 30 degrees 35'. North latitude, and main forest of the East Tianmu Mountain, covered by wide and needle leaves, with more wide leaves than needle one. The vector is leptotrombidium gaohuense. The host are Rattus confucianus and fulvescens. Such focus belongs to inland-mountain type.

Adult↗
PubMed1990

Transmission of Rickettsia tsutsugamushi from Apodemus speciosus, a wild rodent, to larval trombiculid mites during the feeding process.

Transmission of Rickettsia tsutsugamushi (Rt) from a rodent to trombiculid mites was studied. Wild rodents, Apodemus speciosus, were subcutaneously inoculated with Karp strain of Rt, and larval trombiculid mites were released on the ear lobes for feeding, 10 and 20 days after infection. Isolation of Rt was performed from individual mites or pools of 2 to 7 mites by the mouse passage method. From Apodemus 10 days after Rt infection, possibly at the time of high rickettsiaemia, the infection rates among mites were 4/44 (9.1%) or higher in Leptotrombidium fuji, 1/20 (5%) in L. pallidum and 0/41 in L. deliense. From Apodemus 20 days after infection, no mite was infected in 50 L. fuji or 7 L. pallidum possibly due to reduced rickettsiaemia. Transmission of Rt from rodent to mite was proven to occur at low probability on appropriate conditions but not by the incidental chance.

Animals↗
PubMed1985

Rickettsiae and hosts.

Protective immunity to Rickettsia tsutsugamushi in a murine model is dependent upon the development of cell mediated immunity, as demonstrated by lymphocyte transfer, production of lymphokines and -interferon by thymus-derived lymphocytes, activation of macrophages by lymphokines and demonstration of delayed-type hypersensitivity response following exposure to these organisms. Infection of mice with small numbers of Rickettsia typhi inoculated by a peripheral route leads to a more complex pattern of immune development, with a distinction between resistance to local and systemic infection. Nevertheless, thymus-derived lymphocytes and activated macrophages play a major role in modulating pathogenesis of infection, and delayed-type hypersensitivity responses are evident. Spotted fever group rickettsiae also elicit a cell-mediated response in rodents, and protection against Rickettsia conorii infection has been achieved by adoptive transfer of thymus-derived lymphocytes from immune animals. Limited studies with Rickettsia akari suggest that activation of mouse macrophages is critical to host survival following infection with this organism.

Animals↗
PubMed1986

Mechanisms of immunity to rickettsial infection: characterization of a cytotoxic effector cell.

Rickettsiae, as other intracellular bacteria, are relatively sequestered from the effects of antibody and local antibody-independent responses. Considering the obligate intracellular nature of rickettsia, the exact mechanisms by which lymphocytes and macrophages encounter rickettsial antigens and eliminate the infection depends upon the appropriate presentation of antigen to the immune system. We demonstrate here that cells taken from the spleens of Rickettsia typhi- or R. tsutsugamushi-infected mice are able to lyse specifically tissue culture targets infected with the homologous organism. This effect was eliminated upon treatment of the spleen cells with anti-Thy-1.2 + complement. Furthermore such T cells exhibit H-2-restricted killing when tested on infected targets of different genetic backgrounds. We propose that a T cell-mediated cytotoxic immune mechanism exists that may play an important role in the elimination of rickettsial organisms during infection.

Animals↗
PubMed1986

Detection of surface antigen in Rickettsia tsutsugamushi infected mouse reticuloendothelial cells.

Antibody produced by immunizing CBA/CaJ mice with RE cells from C57B1/6J mice infected 14 days earlier with R. tsutsugamushi Gilliam strain bound readily to Gilliam strain non-cell associated rickettsiae and less readily to the periphery of infected RE cells. Conversely, antibody produced by immunizing with RE cells infected 21 days earlier did not bind to Gilliam rickettsiae but bound to the surface of RE cells from mice infected 21 days earlier. This binding was not related to alloantibodies because these were absorbed prior to testing. The demonstration of rickettsial antibody staining of infected cell associated antigen(s) in this assay system provides a new method for the detection of R. tsutsugamushi infection.

Animals↗