Rickettsia honei

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Classification

Higher order taxa

Bacteria; Proteobacteria; Alphaproteobacteria; Rickettsiales; Rickettsiaceae

Species

NCBI: Taxonomy

Rickettsia honei

Description and significance

Rickettsia honei belong the the spotted fever group (SFG), and are etiological agents of typhus and spotted fever in humans. Rickettsiae are are transmitted by lice, fleas, tick, and mites. Rickettsia honei is named after the American pathologist Howard Taylor Ricketts. Despite the name, Rickettsia spp. do not cause rickets (Greek rhakis, "spine"), a disorder of bone development caused by vitamin deficiency. An AFG rickettsiosis-like ailment was identified in 1991 on Flinders Island of Australia and was named Fliners Island spotted fever (FISF). The causative agent of FISF was isolated from buffy coat preparations from the blood of two patients and named R. honei. Rickettsia are a genus of gram negative, rod shaped bacteria and they are short and often paired rods, 0.3-0.5 x 0.8-2.0 um. Rickettsiae retain basic fuchsin when stained by the method of Gimenez. The organisms are obligately intracellular and reside free in the cytoplasm of the eucaryotic host cell, where they divide by binary fission. Organisms of the genus Rickettsia are typically surrounded in the host cell by and electron-lucent zone that has been proposed to represent a slime layer, which is stabilized by the presence of antibodies. During the course of infection, rickettsial morphology can change: older cells can become smaller and more electron dense. SFG rickettsiae usually do not form cacuoles and crystalline structures.

Genome and genetics

Rickettsia honei is most closely related to Rickettsia slovaca and Rickettsia rickettsii. R. honei and the Thai tick typhus rickettsia (TT-118) are identical in DNA sequences of the gene encoding the 17 kDa protein, gltA, and ompA, and they have only 1 nucleotide difference in the 16S rRNA gene. Thus, R. honei and TT-118 are considered a single species. A rickettsia genetically identical to R. honei has been detected by PCR in Aponoma hydrosauri ticks from Flinders Island and Tasmania. The major antigens of Rickettsia are lipopolysaccharide, lipoprotein, outer membrane proteins, and heat shock proteins. The Weil-Felix reaction has been used as a presumptive diagnostic test for rickettsial diseases. It is based on the cross-reaction of antibodies to rickettsial antigens from primary rickettsial infections with the somatic antigens of three strains: Proteus vulgaris strains OX19, and OX2, and Proteus mirabilis strain OXK. The cross-reactive antigens between Rickettsia and Proteus are most likely present in the LPS. The O-polysaccharides of the LPS of typhus rickettsiae are composed of glucose, glucosamine, quinovosamine, and phosphrylated hexosamine. All rickettsiae have a 135-kDa outer membrane protein B (OmpB) that has been identified in all Rickettsia species examined. The sequence of the gene encoding the 17-kDa prtoein gene are conserved among rickettsial species, indicating the importance of itto the survival of the rickettsiae. The mol % G + C of the DNA is not determined. Type strain of Rickettsia honei is: RB, ATCC VR-1472. GenBank accession number (16SrRNA): U17645, AF060705.

Nutrition and metabolism

The nutritional requirements of the rickettsiae, as distinct from those of their host cells, are not known. Rickettsiae grow in heavily irradiated cells that have lost the ability to divide, and they grow in the presence of a low level of cycloheximide that inhibits host protein syntheses. Under these conditions, rickettsiae incorporate exogenous amino acids and adenine, but not thymidine. Thus, rickettsial growth occurs independently of host cell protein synthesis, host cell division, and DNA or RNA synthesis. Rickettsiae require a Co2 enriched atmosphere to grow in chicken embryo cells when an organic buffer is substituted for sodium bicarbonate. Macimal rickettsial growth occurs only in host cells with an intracellular proline pool of 1.0 mM or greater.

Ecology / Pathology

Ecology: A consistent characteristic of Rickettsia species is their residence in an arthropod host as at least a part of their ecological niche. Transovarian maintenance from one generation of tick, mite, or flea to the next via infected ova that hatch into infected larvae is a factor in the maintenance in nature of all SFG rickettsiae. Knowlege of rickettsial ecology is preponderantly based on investigations of medical epidemiology and hematophagous arthropods. The view of the diversity and evolutionary origin of Rickettsia is likely overly anthropocentric. Pathology: A number of Rickettsia species cause severe disease in humans. Before the advent of the broad-spectrum antibiotics, epidemic typhus and Rocky Mountain spoted fever had a very high case fatality rate. R.honei causes Flinders Island spotted fever, which is also deadly to humans. Rickettsiae are inoculated into the skin in the saliva during feeding by and infected tick, mite, or flea or by scrathing of rickettsia-laden feces deposited by an infected louse or flea. Rickettsiae are distributed throughout the body via the bloodstream where they enter their principal target, endothelial cells. In the interaction of rickettsiae with host cells, the entry process involves three steps: attachment, internalization, and escape from the phagosome. Rickettsiae adhere to the host cell by means of a rickettsial adhesin and a host cell receptor.

Current Research

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References

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Authored by Jessica Szuba, a student of CJ Funk at John Brown University