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PubMed1992

Murine typhus endocarditis.

We have described a 28-year-old male sheepfarmer who had fever, headache, chills, malaise, and aortic insufficiency. Echocardiography revealed a tricuspid aortic valve with a large vegetation on the right cusp, an enlarged left ventricle, and diastolic flutter of the mitral valve. Repeated blood cultures were negative. Seroconversion of IgG and IgM to Rickettsia typhi was found on the 13th day of hospitalization. The patient was treated with tetracycline for 1 year and remained afebrile and free of symptoms for 9 months, when he was lost to follow-up. IgM and IgG fluorescent antibodies to R typhi remained positive during 8 months of the follow-up period. We believe this to be the second reported case of endocarditis due to R typhi and the first not treated surgically.

Adult↗
PubMed1994

The role of tumor necrosis factor in host defense against scrub typhus rickettsiae. I. Inhibition of growth of Rickettsia tsutsugamushi, Karp strain, in cultured murine embryonic cells and macrophages by recombinant tumor necrosis factor-alpha.

Recombinant murine tumor necrosis factor-alpha (TNF-alpha) inhibited intracellular growth of Rickettsia tsutsugamushi, Karp strain, in the mouse embryo cell line C3H/10T1/2 clone 8 at doses of 100 to 10 U/ml. The growth inhibitory effect of TNF-alpha was also evident when peritoneal exudate macrophages or bone marrow-derived macrophages were used as the host cell for rickettsial growth. Interferon-gamma (IFN-gamma), at doses up to 1,000 U/ml, did not affect the growth of this strain of rickettsiae in the mouse embryo cell line but, as expected, profoundly inhibited rickettsial growth in peritoneal exudate macrophages and bone marrow-derived macrophages. The effect of TNF-alpha on rickettsial growth in the mouse embryo cell line was not reproducibly enhanced by IFN-gamma. Treatment of the cell line with TNF-alpha delayed rickettsial cytopathic effects, but the rickettsiae ultimately grew to high numbers in the cells and caused cell death. These findings show that, at least in our system, R. tsutsugamushi is resistant to IFN-gamma-mediated antirickettsial effects in cells other than macrophages. The results of this study support the suggestion that TNF-alpha may inhibit rickettsial growth in cells other than macrophages.

Animals↗
PubMed1994

The role of tumor necrosis factor in host defense against scrub typhus rickettsiae. II. Differential induction of tumor necrosis factor-alpha production by Rickettsia tsutsugamushi and Rickettsia conorii.

The present study was undertaken to investigate the ability of members of two different groups of Rickettsia to stimulate macrophages or immune lymphocytes to produce TNF. It was found that R. conorii, a spotted fever group rickettsia, readily induced murine peritoneal macrophages or the macrophage-like cell line P388D1 to produce relatively high levels of TNF. The interaction of macrophages with viable organisms or heat-killed organisms resulted in TNF production. In contrast, viable or killed R. tsutsugamushi did not stimulate the production of detectable TNF even though viable organisms grew to high numbers in both cell types. It was found that the appropriate immune spleen cells stimulated with heat-killed R. tsutsugamushi or R. conorii produced TNF, and TNF activity was found in the sera of immune mice after injection with rickettsial antigen. Infection of naive mice with viable R. tsutsugamushi resulted in high TNF levels in ascites, but TNF was not found in ascites obtained from infected athymic (nu/nu) mice. These data support the suggestion that spotted fever group rickettsiae, such as R. conorii, possess components perhaps on the surface that interact with macrophages to induce TNF production and this component is lacking in R. tsutsugamushi. Antigens of R. tsutsugamushi and R. conorii will stimulate immune cells to produce TNF activity. These data are compatible with the suggestion that the TH-1 subset of T cells is predominant in immunity to R. tsutsugamushi.

Animals↗
PubMed1989

Experimental transmission of murine typhus by Xenopsylla cheopis flea bites.

Transmission of Rickettsia typhi to rats by the bites of Xenopsylla cheopis (Rothschild) fleas was investigated. Procedures rigorously excluded the possibility of contamination of the host skin by flea faeces. Fleas with R. typhi infection (21-25 days post-infection) which fed through bolting cloth (45 min exposure to ten fleas) transmitted rickettsiae with a success rate of 20%. Infective fleas allowed free access to their host for 8 h (10-15 fleas/rat) gave transmission rates of 45-68%. They were also capable of inoculating R. typhi through a membrane of rat skin on a feeder. Only fleas which had been infected for 21 days or longer transmitted R. typhi orally. Oral transmission appeared to be the result of regurgitation of rickettsiae present in the foregut lumen rather than through salivary secretions.

Animals↗
PubMed1992

Tsutsugamushi disease (scrub typhus).

Two patients with Tsutsugamushi disease (fever) were successfully treated with tetracycline derivatives after typical eschars were found, although one of the patients was initially misdiagnosed as having a drug reaction eruption. Prompt diagnosis and treatment are important because this disease can be associated with considerable morbidity and simple effective treatment is easily available.

Adult↗