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1979) A preliminary report on the trombiculid mites from rodents in Kweichow province. Acta Entomologica Sinica, 22, 93 -97. Wang Dun-qing et al. (1965) Studies of two types of Trombicula deliense Walch (Trombiculidae, Acarina). Acta Entomologica Sinica, 14, 383-389. Wang Dun-qing (1981) Tentative regrouping of subgenus Leptotrombidium Nagayo et al., 1916 (Trombiculidae, Acarina). Acta Entomologica Sinica, 24, 459-464. Wang Dun-qing et al. (1981) Five new trombiculid mites of the genus Leptotrombidium (Acarina: Trombiculidae). Acta Zootaxonomica Sinica, 6 (l), 44-52. Wang Dun-qing & Liao, Hau-rong (1984) Type A of Leptotrombidium deliense is a new species, Leptotrombidium rubellum sp.nov. Wuyi Science Journal, 4, 231-234. Wang Dun-qing et al. (1985) Two new species of chigger mites in western Hunan, China (Acari: Trombiculidae). Acta Zootaxonomica Sinica, 10, 152-155. Wang Dun-qing (1985) Studies on the monstrosities of trombiculid larvae. Acta Entomologica Sinica, 28, 437-443. Wang Dun-qing (1988) Biosystematic problems in relation to the vectors of scrub typhus in China.

Upon entry into the cytoplasm of irradiated chicken embryo cells in slide chamber cultures infected over a 2-h period, yolk sac-grown virulent (Breinl strain) and attenuated (E strain) Rickettsia prowazeki underwent indistinguishable reproducible intracellular growth cycles. They promptly entered an exponential growth phase, without detectable lag and without microscopic evidence for any unusual early replicative phase. The generation time for both strains was 8.8 to 8.9 h at 34 C. During most of this period, the state of the organisms and growth were very similar from one cell to another. The exponential-growth phase continued for at least 36 to 48 h, when the rickettsiae became too numerous to count by microscopic examination. Between about 36 and 48 h, cells packed with rickettsiae began irregularly to break down and release organisms. These began to initiate new infection cycles in previously uninfected cells over many hours, as demonstrated by the rise in percentage of cells infected, yielding a highly disordered infected culture with different cells containing rickettsiae in diverse stages of growth. The organisms underwent regular minor changes in morphology, similar to those seen in bacterial cultures, in the first infection cycle. As the cells became packed with rickettsiae, the microorganisms regularly diminished in size to become minute coccobacillary to coccoid forms. However, the rickettsiae in the second and subsequent infection cycles in aging cultures often assumed filamentous or swollen bizarre forms. Only the first infection cycle conformed closely to the concept of a one-step growth cycle. A set of terms is proposed and defined for the infection cycle.

Unique features of the primary site of rickettsial replication in typhus fevers, i.e., within the endothelial cells of small blood vessels in tissues, suggest that effector mechanisms, other than those dependent on phagocytosis by activated macrophages with enhanced microbicidal properties, most likely are necessary to explain the cell-mediated immune control of intracellular rickettsial replication in these sites. Theoretically, such mechanisms might involve contact between infected endothelial cells and activated T lymphocyte subpopulations or macrophages or immunologically induced soluble factors or lymphokines. Support for the existence of at least one of these alternative effector mechanisms is presented here for Rickettsia prowazekii. Cultures of human blood leukocytes, upon immunologically specific stimulation with R. prowazekii antigen or nonspecific stimulation with the mitogen phytohemagglutinin, produce soluble factor(s) in the supernatant fluid which, in culture, have (a) an intracellular antirickettsial action on R. prowazekii-infected human endothelial cells, fibroblasts, and macrophages, and (b) a specific cytolytic action on R. prowazekii-infected, but not uninfected bystander, human fibroblasts. Neither action is demonstrable in R. prowazekii-infected chicken embryo fibroblasts. The factor(s) has no direct antimicrobial action on extracellular rickettsiae and is inactivated by heating at 56 degree C for 1 h or by acid treatment at pH 2. Expression of the antirickettsial action requires new host cell messenger transcription and protein synthesis, whereas the cytolytic action does not. The circumstances of production and action and the properties of the factor(s) responsible for the intracellular antirickettsial, and perhaps also the cytolytic action are consistent with those of immune interferon (IFN-gamma).

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Preincubation of Rickettsia mooseri with human typhus convalescent serum, which is not rickettsiacidal but which confers passive protection to animals, opsonizes the rickettsiae for enhanced phagocytosis by monocyte-derived human macrophages in cell culture and renders them susceptible to destruction within the macrophages. Nonspecific opsonization by preincubation of the rickettsia with methylated bovine serum albumin enhances phagocytosis, but the rickettsiae are not prepared for intracellular destruction. Instead, they grow within the macrophages and eventually destroy these cells. Thus, immune serum and macrophages, neither of which is capable of killing these rickettsiae alone, act in concert to destroy the virulent organisms. In this system, immune serum appears to exert two distinct, possibly dissociable, actions on the rickettsiae: enhancement of phagocytosis and preparation for intracellular destruction. Complement is not required for this action but, when present with immune serum, markedly enhances phagocytosis of the rickettsiae, often leading to rapid destruction of the macrophage.

To characterize IgM and IgG antibody responses in Rocky Mountain spotted fever (RMSF), a microtiter enzyme-linked immunosorbent assay (ELISA) using density gradient-purified Rickettsia rickettsii as antigen was developed. Sera of vaccinated individuals and patients with RMSF were tested by ELISA and by indirect fluorescent antibody (IFA) tests. Diagnostic agreement between ELISA and the IFA test was 76% and 52% for IgG and IgM antibody, respectively. Diagnostic agreement between the ELISA for IgG antibody and the IFA test for total immunoglobulins was 84%. The ELISAs for IgM and IgG antibody were as specific (100%) and as sensitive (100%) as the IFA test (83%-100%) in detecting antibody increases in paired sera from persons with RMSF and were superior to the IFA test in detecting seroconversions in vaccinees. The ELISA also detected antibodies in a single convalescent-phase serum with sensitivity and reliability. The ELISA for IgG antibody is appropriate for seroepidemiology and serodiagnosis since it permits measurement of antibody at a single dilution of serum up to a year after illness.

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