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This paper provides an overview of the development of typhus vaccines between the first and second world wars. It is shown that there was a shift in the classification of the causal Rickettsiae from being classed as bacteria to being conceptualised as a type of virus. This 'paradigm switch' stimulated interest in the possibility of producing an effective medicine.
On the basis of their earlier formula for modeling the possible development of the epidemic process of louse-borne exanthematous typhus the authors have calculated the probability of the development of such process for high indices (10 -- 12 % of convalescents with louse contamination rate among them reaching 20 -- 40 %) characterizing this process. The number of sources of this infection (primary patients), as well as the rate of increase and scale of louse contamination of the population, are of prime importance for the prognostication of the development of the epidemic.
A 21-year-old man presented with fever, rash, seizure, stiff neck and rapidly progressive bilateral pulmonary infiltrates. Cerebrospinal fluid (CSF) study revealed pleocytosis with predominant polymorphonuclear cells, and hypo-glycorrhachia. Status epilepticus occurred, followed by acute respiratory distress syndrome with respiratory failure. Blood and CSF cultures for bacteria were negative, but an indirect immunofluorescence assay revealed a fourfold rise in antibody to Rickettsia tsutsugamushi in paired serum and a 1:2560 (+) IgM antibody titer. Severe scrub typhus with meningoencephalitis and extensive pneumonitis was diagnosed. The patient survived after intravenous minocycline therapy and intensive care, including aggressive seizure control, supportive mechanical ventilation and avoidance of fluid overloading. He had a nearly complete recovery. Practicing physicians in Taiwan should be aware of this reportable disease and its potentially serious complications if not promptly diagnosed and treated.
Asymptomatic typhus infection was regularly modelled in guinea pigs with increased resistance to Rickettsia prowazeki; this infection was characterized by the presence of immunological shifts in the blood and immunity to reinfection, persistenc of rickettsia in the organs of animals in the absence of pyretic reaction and periorchites. Modelling in guinea pigs of asymptomatic infection is also possible against the background of passive immunity created by specific immune serum obtained during convalescence. Investigations demonstrated that rickettsiocidal activity (in experiments on chick embryos) and antiinfectious activity (in experiments on guinea pigs) of the sera was caused by 7S-antibodies.
Using immunoblots to analyze antigenic relationships among the pathogenic spotted fever and typhus group rickettsiae, I found that the rickettsial lipopolysaccharide (LPS) was a group-specific antigen. All the rickettsiae examined had 135-kDa and 58-kDa protein antigens. The spotted fever rickettsiae and Rickettsia canada had, in addition, 190-kDa protein antigens which were antigenic analogs of previously described protective antigens of R. conorii and R. rickettsii.
Morphological changes in the viscera of albino mice were studied over the course of North Asia typhus fever. In general, the microcirculatory bed in the studied organs (brain, liver, spleen, peritoneum, and testicle) corresponded to angioparalytical capillary and venular hyperemia. Macrophagic reaction (proliferation of stellate macrophages) transformed into granulomatous reaction in the course of the experiment. Macrophagic reaction of the spleen was characterized by blurred follicular pattern. In the testes a tendency to the loss of normal spermatogenesis was observed.
This article describes the clinical pattern and course of an ulcerating vulvovaginitis occurring within the overall clinical picture of a case of typhus abdominalis as a now rare complication of that severe infectious disease.
The identification of apparently fastidious microorganisms is often problematic. DNA from a rickettsia-like agent (called the ELB agent) present in cat fleas could be amplified by PCR with conserved primers derived from rickettsial 17-kDa common protein antigen and citrate synthase genes but not spotted fever group 190-kDa antigen gene. Alu I sites in both the 17-kDa and citrate synthase PCR products obtained with the rickettsia-like agent and Rickettsia typhi were different even though both agents reacted with monoclonal antibodies previously thought specific for R. typhi. The DNA sequence of a portion of the 17-kDa PCR product of the rickettsia-like agent differed significantly from all known rickettsial sequences and resembled the 17-kDa sequences of typhus more than spotted fever group rickettsiae. The rare stable transovarial maintenance of this rickettsia in cat fleas has important implications for the disease potential of cat fleas.
Monolayers of mouse resident peritoneal macrophages were incubated with typhus rickettsiae, and macrophage secretion of leukotriene B4 (LTB4) was assessed. Macrophages incubated with native rickettsiae, but not those incubated with hemolytically inactivated rickettsiae, secreted significantly more LTB4 than did sham-treated macrophages. Antirickettsial antiserum was opsonic and blocked hemolysis, and macrophages incubated with rickettsiae in the presence of antiserum did not secrete more LTB4 than those incubated with buffer alone. Native rickettsiae also stimulated alveolar macrophages to secrete LTB4 and prostaglandin E2 (PGE2), but inactivated rickettsiae had no effect. Finally, because trifluoperazine did not alter macrophage LTB4 secretion in the presence of rickettsiae, but inhibited PGE2 secretion, it was suggested that the mechanisms by which rickettsiae stimulated production of these autacoids may have differed.
Toxicities of three pyrethroids, d-phenothrin, decamethrin, and permethrin, were evaluated in the laboratory against Leptotrombidium fletcheri (Womersley & Heaslip). The susceptibilities between populations of the species infected and noninfected with scrub typhus were investigated. The three pesticides exhibited different toxicities to the chiggers. D- phenothrin was the most toxic, followed by decamethrin, then permethrin. There were no significant differences between susceptibilities of the infected and noninfected populations. Log-probit regression lines indicated that the species was most sensitive to increasing concentrations of d-phenothrin and least sensitive to permethrin. The results show that the three pesticides are potential candidates for chemical control of L. fletcheri. It may be possible in the future to conduct similar bioassays only with the noninfected population, thus reducing risk of infection to workers conducting the bioassays. Similarly, there may not be a need to separate field-collected chiggers into the two populations before performing the bioassays.
A dot-immunobinding assay (DIBA) was compared with a direct fluorescent antibody technique (DFAT) for the detection of Rickettsia tsutsugamushi infection in Leptotrombidium fletcheri (Womersley & Heaslip). Laboratory colonies of infected and noninfected chiggers were examined. The relative proportions of positive, negative, and indeterminate results were significantly different between DIBA and DFAT for infected but not for noninfected chiggers. DIBA was more sensitive and had a better negative predictive value and a lower false negative percentage than DFAT. It was concluded that DIBA is a suitable alternative to DFAT for detecting scrub typhus infection in chiggers.
Although frequently unrecognized, rickettsial infections may be an important cause for fever and exanthem in persons presenting to physicians in South India. Most often these patients are referred to dermatology departments with a diagnosis of "drug eruption." In the current study the authors analyzed 12 cases of rickettsial fever that were seen in the dermatology department of St. John's Medical College Hospital, Bangalore, between 1985 and 1989. The distinctive cutaneous eruption was found to be an important clue to an early clinical diagnosis. Specific serodiagnosis enabled us to confirm that Indian tick typhus, a member of the spotted fever group, was the most frequent cause for rickettsial fever presenting at our hospital.
Intranuclear development of Rickettsia canada, a typhus-group rickettsia, in cells of tick tissues is described and illustrated.
Rickettsia mooseri infection in skin at sites of intradermal inoculation was studied in nonimmune and immune guinea pigs with respect to dynamics of infection, localization of rickettsiae within tissues, and gross and microscopic pathology. Intradermal inoculation of R. mooseri into nonimmune guinea pigs resulted in gross lesions which, in magnitude, were directly related to the number of rickettsiae inoculated. The lesions progressively enlarged through 3 or 4 days and remained enlarged through at least 7 days. Histological examination revealed an early acute inflammation which progressed to a predominantly monocyte-macrophage inflammation and subsequently condensed into lymphocyte-containing granulomatous foci. Rickettsiae in the skin at sites of inoculation increased in numbers from 6 h through 3 days, in parallel with the increasing diffuse monocyte-macrophage inflammatory response, and then declined markedly on days 4 or 5 as ganulomatous foci appeared. Some rickettsiae, however, persisted through at least day 7. Fluorescent-antibody studies suggested that R. mooseri infected only a subset of cells available, i.e., cells associated with the microvascular system. Dissemination of infection was demonstrated by the presence of rickettsiae in the skin at sites distant from the point of inoculation. Immune guinea pigs, made immune by intradermal infection with R. mooseri 12 days before intradermal challenge, displayed an accelerated response. The lesions were maximal by 24 to 48 h and subsequently regressed. The inflammatory response of immune guinea pigs was a greater magnitude than the response of similarly challenged nonimmune guinea pigs, and the respose from acute inflammation through the formation of granulomatous lesions was accelerated. The number of rickettsiae in the skin of immune guinea pigs declined steadily from the time of inoculation, until no rickettsiae were recovered on or after day 3. Furthermore, dissemination of rickettsiae to sites in skin distant from the site of inoculation was not demonstrable. The results are discussed in terms of pathogenesis and of immunity to typhus.
Scrub typhus immunogens that received inadequate gamma radiation contained residual, viable rickettsiae. The presence of these organisms in the host was masked by the rapid immune response elicited by the large number of inactivated rickettsiae. Transfer of homogenized spleen cells from immunized mice to normal syngeneic recipients provided a sensitive technique for the detection of these viable, replicating organisms.
We examined the ability of monoclonal antibodies directed against lymphocyte surface antigens to block the lysis of typhus group rickettsia-infected cells by lymphokine-activated killer effectors. Lysis was significantly inhibited by OKT3 monoclonal antibody but not by OKT4 or OKT8 monoclonal antibody.
Lymphokine-activated killer cells caused significant lysis of target cells infected with typhus group rickettsiae (TGR) but not cells infected with Rickettsia tsutsugamushi. Monoclonal and polyclonal antibodies against TGR or TGR-infected cells failed to bind specifically to infected targets, as determined by flow cytometry or by immunoprecipitation of radiolabeled cell surface proteins. Major unaltered antigenic determinants of TGR therefore cannot be detected on the surface of infected targets.
A new assay is described for enumerating biologically active typhus rickettsiae (Madrid E strain), based on adsorption of rickettsiae to erythrocytes in the presence of NaF (which allows adsorption but not lysis) and lysis in the presence of anti-Rickettsia prowazeki immune serum (which allows only a single round of lysis). The number of lysed erythrocytes is then used to estimate the number of active rickettsiae.