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PubMed2000

Neutralization epitopes on the antigenic domain II of the Orientia tsutsugamushi 56-kDa protein revealed by monoclonal antibodies.

Monoclonal antibodies (MoAbs) reactive with the authentic Orientia tsutsugamushi 56-kDa protein were generated. MoAb FS10 and FS15 showed in vitro, as well as, in vivo neutralizing activity upon O. tsutsugamushi infection. Deletion mutants of the gene for 56-kDa protein of O. tsutsugamushi Boryong were expressed to map the binding region. FS10 and FS15 are bound to amino acids (aa) located in an antigenic domain II, at residues 140-160 and 187-214, respectively. Computer modeling indicated that aa 146-153 were important for antigenicity against FS10. A sequence for aa 142-150 was highly homologous between oriential strains. These results suggest that the antigenic determinant for neutralizing MoAbs is an epitope within aa 140-160. Furthermore, this region may be important for the adhesion/invasion or intracellular survival of O. tsutsugamushi within host cells.

Amino Acid Sequence↗
PubMed1997

Characterization of Orientia tsutsugamushi isolated in Taiwan by immunofluorescence and restriction fragment length polymorphism analyses.

A total of 10 strains of Orientia tsutsugamushi were isolated from field rodents and chiggers in Taiwan, and characterized by immunofluorescence analysis with monoclonal antibodies and by restriction fragment length polymorphism analysis of the 56-kilodalton (kDa) protein gene. The isolates were divided into two groups consisting of 1 and 9 strains which showed some relation to Gilliam and Karp type strains, respectively. However, all these isolates possessed characteristics distinct not only from those of known prototype strains including Gilliam and Karp but also from all isolates from Japan. These findings suggest the existence of a large number of immunotypic and genotypic variants among the strains of O. tsutsugamushi, and the distribution of distinguishable strains in each area to which this species is endemic.

Animals↗
PubMed2001

Orientia tsutsugamushi infection: overview and immune responses.

Orientia tsutsugamushi, an obligate intracellular bacterium, was isolated for the first time in 1930. Infections by virulent strains are characterized by fever, rash, eschar, pneumonia, myocarditis, and disseminated intravascular coagulation. Here we review the general aspects of O. tsutsugamushi and immune responses in terms of inflammation, protective immune mechanisms, and immunogenic antigens.

Animals↗
PubMed1982

Serological analysis of Rickettsia tsutsugamushi isolates from North Queensland.

Fifty-two Rickettsia tsutsugamushi isolates from humans, rodents and chiggers in North Queensland were serologically characterized by the direct immunofluorescence test. A majority (71%) of the isolates was a mixture of two or more strains. The most frequently detected strains in the 52 isolates were TA716 (84%), TA763 (42%), TA686 (33%), and Karp (31%). The Gilliam strain was detected in only 4% of the isolates.

Animals↗
PubMed2004

[Tsutusgamushi fever after travel to Southeast Asia].

HISTORY AND CLINICAL FINDINGS: A 49-year-old travel guide fell ill during his return from a 6-week-stay in Vietnam, Myanmar and Thailand. He developed high fever and severe headache. On admission, the body temperature was at 39.5 degrees C with relative bradycardia. A black, crusted skin lesion of approximately 5 mm diameter was noted on the chest wall and was interpreted as an insect bite. INVESTIGATIONS: CRP and liver enzymes were elevated. Total leucocyte count was normal but the differential count showed a left shift and aneosinophilia. Imaging procedures revealed splenomegaly and small pleural effusions on both sides. TREATMENT AND COURSE: The patient was treated with a parenteral quinolone based on the initial suspicion of typhoid fever. Failure of this treatment and negative blood cultures raised concerns about the possibility of Tsutsugamushi fever, based on travel history and a re-evaluation of the skin lesion as an eschar. Tsutsugamushi fever was suspected on epidemiological and clinical grounds and was confirmed by the detection of specific IgM to Orienta tsutsugamushi and by seroconversion of IgG antibodies during follow-up. Even before immunodiagnostic confirmation was available, a course of doxycycline was started. This led to rapid improvement of the patient's condition. CONCLUSION: In febrile travellers returning from Southeast Asia, Tsutsugamushi fever has to be considered in the differential diagnosis. The causative agent, Orienta tsutsugamushi is transmitted by larvae of trombiculid mites (chiggers). Leading symptoms are fever continua, cephalgia, and a primary lesion (eschar) at the site of cutaneous inoculation. The Eschar is easily overlooked and has to be searched carefully. Diagnosis is confirmed by the detection of specific antibodies. However, serology may be negative in the beginning. Therefore, treatment with doxycycline should be initiated on clinical grounds.

Anti-Bacterial Agents↗
PubMed1998

[Tsutsugamushi fever. Rare rickettsiosis after a stay in the Philippines].

HISTORY AND CLINICAL FINDINGS: After returning to his native Germany from a holiday in the Philippines a 37-year-old man was admitted because of high fever, cervical lymphadenopathy, pharyngitis and conjunctivitis, transient skin rash, nausea and vomiting, leukocytosis with shift to the left, atypical lymphocytes, as well as increased transaminases, LDH and cholestasis-indicating enzymes. INVESTIGATIONS: Stool, sputum and urine cultures were negative. The chest radiogram showed bilateral mild interstitial infiltration. Antibody titres against Rickettsia tsutsugamushi were markedly raised (IgG 1:128, IgM 1:2048). DIAGNOSIS, TREATMENT AND COURSE: Empirical antibiotic treatment with ciprofloxacin (200 mg twice daily intravenously) had no effect. As the mild signs of interstitial pneumonia progressed, clarithromycin (500 mg twice daily orally) was substituted with rapid fall in fever and gradual improvement. Tsutsugamushi infection was diagnosed serologically and the antibiotic changed to doxycycline (100 mg twice daily orally), continued for 14 days. Full remission occurred. CONCLUSIONS: Tsutsugamushi fever should be included in the differential diagnosis if, in addition to a history of a visit to an endemic area, there is the clinical triad of skin necrosis at the site of a mite bite, regional lymphadenopathy and skin rash (in this case, no skin lesion). The infection can be lethal without adequate treatment. Tetracyclines and possibly also macrolide antibiotics are effective against the causative organism.

Adult↗
PubMed2000

Pericarditis due to Tsutsugamushi disease.

Tsutsugamushi Disease is an acute febrile illness caused by Rickettsia tsutsugamushi, which enters into the human bloodstream through the bite of leptotrombidium. It is characterized by eschar, fever and cutaneous rash. Pericardial effusion in Tsutsugamushi Disease is not a common manifestation, although a high rate of effusion was reported in autopsy in those who had died of the disease. Here, we report a case of Tsutsugamushi pericarditis documented by indirect immunofluorescent test of pericardial fluid, and give a brief review of the literature.

Aged↗
PubMed1979

Intracellular localization of Rickettsia tsutsugamushi in polymorphonuclear leukocytes.

Rickettsia tsutsugamushi (Gilliam strain) was serially propagated in BHK-21 cell cultures and incubated with guinea pig peritoneal polymorphonuclear leukocytes to study the ultrastructural features of rickettsial uptake and entry into the leukocytes. Significant numbers of rickettsiae were phagocytized selectively by these leukocytes within 30 min. About one-half of these rickettsiae remained sequestered in phagosomes but the other one-half were free from the phagosome and localized directly in the polymorphonuclear leukocyte cytoplasm. Various stages of rickettsial release from the phagosomes were observed. Once free within the polymorphonuclear leukocyte cytoplasm, the rickettsiae were preferentially localized in the glycogen-packed areas which are devoid of lysosomes and other cytoplasmic organelles. This study indicates that rickettsiae phagocytized by polymorphonuclear leukocytes can escape from the phagosome into the cytoplasm.

Animals↗
PubMed2005

Attenuation of HIV-1 infection by other microbial agents.

Although potentiation of human immunodeficiency virus (HIV) type 1 (HIV-1) infection has been known to occur in coinfection with a variety of pathogens and types of vaccination, there are emerging data on specific infectious agents that may attenuate HIV-1 infection. New literature suggests that certain pathogens are capable of inhibiting HIV-1 replication. These include GB virus C, measles virus, Orientia tsutsugamushi, and human T lymphotropic virus types 1 and 2. In addition, there are conflicting data on the effects of Mycobacterium tuberculosis on the replication of HIV-1, with some suggesting that this organism may inhibit HIV-1 replication. Also remaining controversial are the possible protective effects of HIV type 2 against HIV-1 infection. In this review, we summarize and critically discuss the body of emerging literature concerning infections that may have the ability to attenuate HIV-1 infection.

Disease Progression↗
PubMed1976

Clinical response of silvered leaf monkeys (Presbytis cristatus) to infection with strains of Rickettsia tsutsugamushi virulent and avirulent for mice.

Silvered leaf monkeys (Presbytis cristatus) inoculated with avirulent strains of Rickettsia tsutsugamushi showed little or no signs of disease, whereas those inoculated with moderately or fully virulent strains developed severe disease. Infection with the virulent strains produced early leukocytosis followed by leukopenia and significant decreases in packed-cell volumes. In animals infected with avirulent strains, these parameters were normal throughout the experimental period.

Animals↗
PubMed1977

Patterns of rickettsemia and antibody response in silvered leaf monkeys (Presbytis cristatus) after inoculation with virulent and avirulent strains of Rickettsia tsutsugamushi.

Most silvered leaf monkeys inoculated with selected strains of Rickettsia tsutsugamushi developed rickettsemia. The time of onset and the duration of rickettsemia were related to the infecting strains, but these parameters could not be correlated with the virulence of the strain. The rickettsemia was not terminated by the appearance of humoral antibody, as detected by the indirect fluorescent antibody test. The specificities of the antibody responses were related to the antigens present in the infecting strains.

Animals↗
PubMed1981

Clinical and immunologic responses of silvered leaf monkeys (Presbytis cristatus) to experimental reinfection with Rickettsia tsutsugamushi.

Silvered leaf monkeys (Presbytis cristatus) that had recovered from active Rickettsia tsutsugamushi infections 14 months previously became rickettsemic when inoculated with homologous, related, or unrelated strains of R. tsutsugamushi. In contrast to the results after the initial infection that produced disease, no signs were observed after the subsequent infections. Most animals responded with detectable titers of antibody to the Karp antigen regardless of the inoculated strains. Strains recovered during rickettsemia usually had antigens related only to the challenge strains, but in three silvered leaf monkeys, antigens characteristic of both the original and the challenge strains were detected.

Animals↗
PubMed1985

Development of antigen-specific cell-mediated immune responses after infection of cynomolgus monkeys (Macaca fascicularis) with Rickettsia tsutsugamushi.

Cynomolgus monkeys were evaluated for cellular immune responses after infection with the Karp strain of Rickettsia tsutsugamushi. Antibody and clinical signs of localized and systemic infection were also evaluated. Animals challenged with homologous or heterologous strains at various times after a primary infection were also followed up. Naive monkeys developed eschars, lymphadenopathy, rickettsemia, and elevated body temperatures. Antibody in these animals was IgM followed by IgG. Lymphocyte proliferation and production of gamma-interferon by peripheral blood mononuclear leukocytes also were demonstrated. If challenged six years after the initial infection, clinical signs and cellular responses were indistinguishable from naive animals but an anamnestic IgG antibody response was noted. If challenged eight months after the initial infection, complete resistance was noted, but if challenged at one year, a localized cutaneous lesion developed. The majority of animals infected previously had preexisting lymphocyte activity, a characteristic suggesting long-term immunologic memory that was not protective against rechallenge.

Animals↗