Studies on Immunity in Rocky Mountain Spotted Fever. First Communication

Ricketts, Henry T.; Gomez, Liborio

doi:10.1093/infdis/5.2.221

Cited by 21 publications

(14 citation statements)

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“…The role of Dermacentor ticks in the transmission of the disease was documented in reports by King (156) and Ricketts (283) in 1906. Ricketts also isolated the causative organism in guinea pigs and demonstrated that it circulated between ticks and mammals in nature and that infected ticks could transmit the bacterium transovarially to their progeny (284,285). Ricketts, as well as another famous rickettsiologist, von Prowazek, died of typhus, and the agents of typhus and RMSF were subsequently named Rickettsia prowazekii and R. rickettsii, respectively, in their honor.…”

Section: Pathogens Described Prior To 1984mentioning

confidence: 99%

Tick-Borne Rickettsioses around the World: Emerging Diseases Challenging Old Concepts

2005

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SUMMARY During most of the 20th century, the epidemiology of tick-borne rickettsioses could be summarized as the occurrence of a single pathogenic rickettsia on each continent. An element of this paradigm suggested that the many other characterized and noncharacterized rickettsiae isolated from ticks were not pathogenic to humans. In this context, it was considered that relatively few tick-borne rickettsiae caused human disease. This concept was modified extensively from 1984 through 2005 by the identification of at least 11 additional rickettsial species or subspecies that cause tick-borne rickettsioses around the world. Of these agents, seven were initially isolated from ticks, often years or decades before a definitive association with human disease was established. We present here the tick-borne rickettsioses described through 2005 and focus on the epidemiological circumstances that have played a role in the emergence of the newly recognized diseases.

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Section: Pathogens Described Prior To 1984mentioning

confidence: 99%

Tick-Borne Rickettsioses around the World: Emerging Diseases Challenging Old Concepts

2005

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“…It is difficult to determine exactly when RMSF was first described, although the first clinical report of RMSF was made in 1899 by Maxey in Idaho: "A febrile disease, characterized clinically by a continuous moderately high fever, and a profuse or purpuric eruption in the skin, appearing first on ankles, wrists, and forehead, but rapidly spreading to all parts of body" (213,214). This disease has the reputation of being the most severe SFG rickettsiosis, since it can be lethal even in previously healthy and young patients (114,267,270).…”

Section: Previously Described Diseasesmentioning

confidence: 99%

Rickettsioses as paradigms of new or emerging infectious diseases

1997

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Rickettsioses are caused by species of Rickettsia, a genus comprising organisms characterized by their strictly intracellular location and their association with arthropods. Rickettsia species are difficult to cultivate in vitro and exhibit strong serological cross-reactions with each other. These technical difficulties long prohibited a detailed study of the rickettsiae, and it is only following the recent introduction of novel laboratory methods that progress in this field has been possible. In this review, we discuss the impact that these practical innovations have had on the study of rickettsiae. Prior to 1986, only eight rickettsioses were clinically recognized; however, in the last 10 years, an additional six have been discovered. We describe the different steps that resulted in the description of each new rickettsiosis and discuss the influence of factors as diverse as physicians' curiosity and the adoption of molecular biology-based identification in helping to recognize these new infections. We also assess the pathogenic potential of rickettsial strains that to date have been associated only with arthropods, and we discuss diseases of unknown etiology that may be rickettsioses.

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“…Although knowledge of a modest beneficial effect of antiserum treatment of experimental animals and human Rocky Mountain spotted fever dates from the early research of ricketts until the dawn of the antibiotic era, humoral immunity to rickettsiae was only recently established in contemporary immunologic terms (18,20,21). Passive transfer of polyclonal antibodies or particular monoclonal antibodies to outer membrane protein A (OmpA) or OmpB, but not Fab fragments of polyclonal antibodies or monoclonal antibody to lipopolysaccharide, protected C3H severe combined immune-deficient mice against 10 50% lethal doses of R. conorii (9).…”

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confidence: 99%

Effect of Antibody on the Rickettsia-Host Cell Interaction

et al. 2004

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A recent study demonstrated that polyclonal antibodies to Rickettsia conorii and monoclonal antibodies to outer membrane proteins A (OmpA) and B (OmpB) provided effective, Fc-dependent, passive immunity, even in severe combined immunodeficient mice with an established infection. In order to determine the mechanism of protection, mouse endothelial and macrophage-like cell lines were infected with R. conorii that had been exposed to polyclonal antibodies, monoclonal antibodies to OmpA or OmpB, Fab fragments of the polyclonal antibodies, or normal serum or that were left untreated. At 0 h, Fc-dependent antibody enhancement of R. conorii adherence to endothelial and macrophage-like cell lines was inhibited by the presence of normal serum, suggesting Fc receptor-mediated adherence of opsonized rickettsiae. At 3 h, the opsonized rickettsiae had been internalized. After 72 h, inhibited survival of rickettsiae exposed to polyclonal antibodies or monoclonal antibodies to OmpA or OmpB was evident compared with growth of untreated and normal serum-treated and polyclonal Fab antibody-treated R. conorii. Polyclonal antibodies and an anti-OmpB monoclonal antibody inhibited the escape of R. conorii from the phagosome, resulting in intraphagolysosomal rickettsial death. At 48 h of infection, rickettsicidal activity of macrophages by opsonized rickettsiae was inhibited by N G -monomethyl-L-arginine, superoxide dismutase, mannitol, or supplemental L-tryptophan, and endothelial rickettsicidal activity against opsonized rickettsiae was inhibited by N G -monomethyl-L-arginine, superoxide dismutase, catalase, or supplemental L-tryptophan. Thus, Fc-dependent antibodies protected against R. conorii infection of endothelium and macrophages by opsonization that inhibited phagosomal escape and resulted in phagolysosomal killing mediated by nitric oxide, reactive oxygen intermediates, and L-tryptophan starvation.

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Studies on Immunity in Rocky Mountain Spotted Fever. First Communication

Abstract: I The rabbit has recently been found to be susceptible to the strains now cultivated in laboratory animals.

Cited by 21 publications

References 0 publications

Tick-Borne Rickettsioses around the World: Emerging Diseases Challenging Old Concepts

Tick-Borne Rickettsioses around the World: Emerging Diseases Challenging Old Concepts

Rickettsioses as paradigms of new or emerging infectious diseases

Effect of Antibody on the Rickettsia-Host Cell Interaction

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