Bacteria Genomes - RICKETTSIA TYPHI

Rickettsial infections have played a significant role in the history of Western civilization. Epidemic typhus has been known since the 16th century and it has long been associated with famine and war. The outcome of several wars was influenced by epidemic typhus. Typhus killed or caused debilitated over 100,000 people in the two World Wars. In spite of its long history, it was not until the early part of the 20th century that the causative agent was determined. Howard Ricketts described the causative agent of Rocky Mountain spotted fever and was able to culture it in laboratory animals. Others then realised that the causative agent of epidemic typhus was related to the organism that Ricketts described. After the discovery of the importance of arthropod vector in the spread of typhus, vector control measures were instituted to try to control the disease.

Rickettsia typhi is a small (0.3 by 1 (m), obligately intracellular bacterium which was once thought to be part of the same family as Ehrlichia and Coxiella . Now, however, they are considered to be distinct unrelated bacteria. Like Chlamydia these bacteria were once thought to be viruses because of their small size and intracellular life cycle. However, they are true bacteria, small Gram - coccobacilli that are normally stained with Giemsa since they stain poorly by the Gram stain. Its cell wall morphology is that of a Gram-negative bacillus. Phylogenetically a member of the alpha subgroup of Proteobacteria, R. typhi is along with R. prowazekii considered to be a typhus group rickettsia.

In general rickettsiae have evolved numerous characteristics that take advantage of their intracytosolic niche to acquire ATP, amino acids, cytoplasmic forms of sugars, and other metabolic products of the host cell.

Rickettsia typhi evolved in close association with its arthropod vectors, various species of fleas. In its best known zoonotic cycle, R. typhi is acquired from the blood meal taken from a bacteremic Rattus species host. The rickettsiae invade and grow within the midgut epithelial cells of the flea from which they are shed into the flea faeces. The flea faeces are infective for rats and human, presumably via intracutaneous inoculation by scratching the pruritic skin, inhalation of aerosolised flea faeces, or introduction by the fingers into the mucous membranes such as the conjunctiva. Rats are rickettsemic without signs of illness, and rat fleas (Xenopsyble cheopis) remain infected for the rest of their lifespan, which is not affected by the infection. R. typhi do not spread effectively to other cells until their intracellular growth by binary fission results in accumulation of such large quantities of cytoplasmic bacteria that the infected host cell bursts, releasing large quantities of rickettsiae.

Rickettsia typhi are highly infectious. The organisms spread hematogenously throughout the human body and infect mainly endothelial cells. The subsequent pathologic effects include meningoencephalitis, maculopapular rash, interstitial pneumonia leading to adult respiratory distress syndrome in some patients, disseminated vascular lesions, and death in approximately 1% of cases. Pathogenesis is primarily due to destruction of the cells by the replicating bacteria. Destruction of the endothelial cells results in leakage of blood and subsequent organ and tissue damage due to loss of blood into the tissue spaces.

References:

J. Bacteriol. 186, 5842-5855 (2004)
http://www.hgsc.bcm.tmc.edu/projects/microbial/Rtyphi/
http://www.cdc.gov/ncidod/eid/vol8no6/01-0350.htm
http://www.med.sc.edu:85/mayer/ricketsia.htm