Rickettsia japonica

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1. Classification

a. Higher order taxa

  • Domain: Bacteria
  • Kingdom: Prokaryote
  • Phylum: Proteobacteria
  • Class: Alphaproteobacteria
  • Order: Rickettsiales
  • Family: Rickettsiaceae
  • Genus: Rickettsia
  • Species: R.japonica

Figure 1: This unrooted phylogeny tree of the Rickettsia genus shows that R.japonica is closely related to Rickettsia rickettsii due to their genetic coding. The majority of the spotted fever group need two hosts and share the same characteristics which correlate with the difference in their genetic code (1).

2. Description and significance

Rickettsia japonica belongs to the genus of Rickettsia, a small Gram-negative genus which are split into spotted fever and typhus groups (2). R.japonica, discovered in 1984, is different from other Rickettsia in that the species has distinct surface polypeptides and antibodies that only react tow R. japonica (3). This strain causes Japanese spotted fever, is highly pathogenic even fatal, and transferable through ticks, lice, and mites (4). R. japonica is an obligate intracellular pathogen with a small genome. As a result, the genomic diversity of this bacteria is low (4). Because of its genome size, many strains of R. japonica have been isolated and analyzed revealing few polymorphisms among the sequences.
R. japonica is pervasive in the Asian and Oceanic geographical regions (5). The bacteria is spread through animals traveling by air and ground specifically ones that are in higher abundance in warm and humid climates (2). Due to the rising influence of global climate change, it is possible that the transmission of this bacteria could continue to spread and evolve (6). There is also the possibility that household pets may become the most abundant victim. Fortunately, a treatment for early stages of Japanese spotted fever consisted of antibiotics, which proved successful and efficient (7).

3. Genome structure

R. japonica has a small genome, 1.1-1.6 MB, due to it being an obligate intracellular pathogen. Because genomic diversity is low, polymorphisms are not abundant across the other strains of Rickettsia (4). Mobile genetic elements like plasmids are present across the different strains of the species which is indicative of conjugation and horizontal gene transfer. The few amount of single nucleotide polymorphisms among the strains of R. japonica are representative of its low genomic diversity. R. japonica have one circular chromosome with a size of 1.3 MBP, one set of rRNA genes, and 1,186 regions that can express proteins (8). The guanine and cytosine content of the genome is roughly 32.7% and 31.8% (8). R. japonica has a specific open-reading frame , a 216 base pair specific set of genes, within the genome across the bacteria that assists with diagnosis of the disease through DNA sequencing. The nucleotide sequence within this open-reading frame was identical across all strains of R. japonica (6).

4. Cell structure

R. japonica is an obligate intracellular bacterium (4). It is a Gram-negative rod that has a periplasmic space between the inner and outer membrane with lipopolysaccharides concentrated in the outer membrane. It is non-motile, does not form spores, and is considered pleomorphic meaning it is able to change its shape and size in adapting to a certain environment (9).
This bacterium has an outer layer composed of a unknown slime substance, producing a three-layered cell wall and are 0.4-0.5 x 0.8-1.5 micrometers in diameter (3). The inner membrane is thick while the outer membrane is thin (10). R. japonica has a plaque morphology when allowed to grow or cultured in eukaryotic cells. The cell wall is composed of peptidoglycan and is often localized to the nucleus, the endothelial and smooth muscle cytosol. It is classified as a zoonese, a type of disease that comes from animals pathogens which are transmissible to humans through mechanical or biological vectors (11). Replication methods are currently unknown, but this bacterium has major outer membrane proteins; rOmpB and rOmpA, which are implicated for the adhesion and protective immunity. rOmpB is the most common outer membrane protein which has functions of the S layer as well(12). rOmpA is involved in actin activity within the cell allowing the bacterium to invade and multiply within a host cell (12).

5. Metabolic processes

R. japonica requires a eukaryotic host to proliferate. Its optimal growth range lies between 32°C - 35 °C (13). R. japonica requires the shortest time of Rickettsia strains to form plaques which begins the infection cycle OF 2-3 days. The bacterium will enter the host cell and lyse it to release progeny (13). Glutamic acid and glutamine are important organic molecules that assist in host cell penetration. Glutamate is oxidized in order to create ATP to assist in survival of the cell (13). Coupling energy creation with penetration allows the bacterial cell to integrate into the host cell (13). Pyruvates are also important organic molecules that enhance the pathogenicity of the cell. While the mechanism of this is unclear, it is known that pyruvate is essential for the respiration of the bacterium (13). In addition, incubating the cell with pyruvate is sufficient to restore the loss of biological activity (13). R. japonica multiply through transverse binary fission but low pH is unfavorable to cell survival(14). This bacterium is known to have transporter systems, which take host metabolites like NAD+ to power the TCA cycle and to acquire vitamins and cofactors (15).

6. Ecology

Habitat; symbiosis; contributions to the environment.

7. Pathology

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

8. Current Research

Include information about how this microbe (or related microbes) are currently being studied and for what purpose

9. References

It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.