VIOLIN: Vaccine Investigation and Online Information Network

Pathogen Page

Rickettsia spp

I. General Information

1. NCBI Taxonomy ID:

2. Disease:

Spotted Fever, Typhus

3. Introduction

Rickettsia is a genus of non-motile, Gram-negative, non-sporeforming, highly pleomorphic bacteria that can present as cocci (0.1 μm in diameter), rods (1–4 μm long) or thread-like (10 μm long). Obligate intracellular parasites, the Rickettsia survival depends on entry, growth, and replication within the cytoplasm of eukaryotic host cells (typically endothelial cells). Because of this, Rickettsia cannot live in artificial nutrient environments and are grown either in tissue or embryo cultures (typically, chicken embryos are used). In the past they were positioned somewhere between viruses and true bacteria. The majority of Rickettsia bacteria are susceptible to antibiotics of the tetracycline group. Rickettsia species are carried by many ticks, fleas, and lice, and cause diseases in humans such as typhus, rickettsialpox, Boutonneuse fever, African tick bite fever, Rocky Mountain spotted fever, Australian Tick Typhus, Flinders Island Spotted Fever and Queensland tick typhus. They have also been associated with a range of plant diseases. Like viruses, they only grow inside living cells. The name rickettsia is often used for any member of the Rickettsiales. They are thought to be the closest living relatives to bacteria that were the origin of the mitochondria organelle that exists inside most eukaryotic cells (Wiki: Rickettsia). Rickettsial diseases vary in clinical severity according to the virulence of the Rickettsia and host factors, such as age, male gender, alcoholism, and other underlying diseases. The most virulent rickettsiae are R. rickettsii and R. prowazekii, which kill a significant portion of infected persons, unless the diseases are treated sufficiently early in the course of infection with an effective antimicrobial agent, usually doxycycline (Textbook of Bacteriology).

4. Microbial Pathogenesis

All rickettsial infections begin with introduction of the organisms into the skin, either through a tick bite or cutaneous abrasions contaminated by flea or louse feces. Rickettsiae enter dermal cells including endothelium and proliferate locally intracellularly with endothelial cell-to-cell spread for most SFG rickettsioses resulting in an eschar or tache noire, a zone of dermal and epidermal necrosis approximately 1 cm in diameter with a surrounding zone of erythema. Eschars do not occur in epidemic and murine typhus and are rarely observed in Rocky Mountain spotted fever (Textbook of Bacteriology).

5. Host Ranges and Animal Models

Rickettsia are generally carried by ticks and fleas and can be transmitted to humans and other warm-blooded mammals (Wiki: Rickettsia).

6. Host Protective Immunity

Rickettsial infection stimulates an early innate immune response with activation of natural killer cells and production of gamma interferon (gamma IFN), which act in concert to dampen rickettsial growth. Acquired immunity develops with clonal expansion of CD4 and CD8 T lymphocytes as well as antibody-producing B cells. Clearance of intraendothelial rickettsiae is achieved by rickettsicidal effects due to cytokine activation of the infected endothelial cells themselves. Cell mediated immunity (CMI) plays an important role as expected in infection by an intracellular parasite, but antibodies (including those directed at epitopes of OmpA and OmpB) also play a role in protective immunity (Textbook of Bacteriology).

Loading Pathogen Genes...

Loading Host Genes...

Loading Vaccines...

Loading References...

Table of Contents