Rickettsia rickettsii
Eric Evans

Rickettsia rickettsii is the bacterium that causes the disease known as Rocky Mountain spotted fever. The disease was originally characterized in 1896 in the Snake River Valley of Idaho and was originally called the black measles. It later became known as the Rocky Mountain spotted fever due to the area it was generally found, however it is now realized that the disease occurs throughout the continental United States, as well as southern Canada, Central America, Mexico, and parts of South America.

Rocky Mountain spotted fever spreads to humans though bite from Ixodes ticks. The disease generally becomes noticeable 2 – 14 days after the initial bite. The symptoms include severe headache, fever, muscle pain and eventually the development of a rash. The rash typically appears on the ankles and wrists as small, faint, pink spots.

The disease can be difficult to diagnose in the early stages, and without prompt and appropriate treatment it can be fatal. Nearly 40% of patients are unaware of the tick bite, and that the rash does not usually appear until 3-5 days later. Symptoms such as nausea, abdominal pain, vomiting, diarrhea and cough are often leads to misdiagnoses. Before the development of antibiotics 20-25% of those infected died, and even today 3-5% of cases are fatal generally due to misdiagnosis or improper treatment.

R. rickettsii are small, Gram-negative, aerobic, coccobacilli that live as obligate intracellular parasites on eukaryotic cells. After a tick bite they spread through the bloodstream and infect the endothelium of the host. After attaching to the cell membrane it is believed they somehow induce phagocytosis in the targeted cells because they enter cells that do not normally phagocytose. Once inside the host cell, they quickly escape from the phagosome membrane and enter the cytoplasm, though the mechanism is not well understood.

They live in either the cytoplasm or the nucleus of the infected cell and multiply through binary fission. They metabolize glutamate from the citric acid cycle of the host aerobically. It has been said that they have leaky membranes that leave them dependant on the osmolarity and nutritional environment in the host cell.

R. rickettsii rarely accumulate in large numbers and do not lyse the host cells even when they escape from the cell. The means by which they damage host cell membranes is uncertain, but there is evidence pointing towards the eventual accumulation of oxygen free radicals. The eventual death of the host endothelial cells due to this damage causes the blood vessels to become leaky giving rise to the rash as blood escapes the blood vessels.

*Disclaimer - This report was written by a student participaring in a microbiology course at the Missouri University of Science and Technology. The accuracy of the contents of this report is not guaranteed and it is recommended that you seek additional sources of information to verify the contents.


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