Rickettsia rickettsii

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Rickettsia rickettsii
Rickettsia rickettsii.jpg
Scientific classification
Domain: Bacteria
Phylum: Proteobacteria
Class: Alphaproteobacteria
Order: Rickettsiales
Family: Rickettsiaceae
Genus: Rickettsia
Species: R. rickettsii
Binomial name
Rickettsia rickettsii
Brumpt, 1922

Rickettsia rickettsii (abbreviated as R. rickettsii) is a gram negative, intracellular, coccobacillus bacteria, that is around 0.8 to 2.0 micrometers long[1]. R. rickettsii is most known as the causative agent of Rocky Mountain spotted fever.[1] R. rickettsii is one of the most pathogenic Rickettsia strains known to humans and affects a large majority of the Western Hemisphere and small portions of the Eastern Hemisphere.[1]


Rocky Mountain spotted fever first emerged in the Idaho Valley in 1896. At that time, not much information was known about the disease; it was originally called Black Measles because patients had a characteristic spotted rash appearance throughout their body. The first clinical description of Rocky Mountain Spotted Fever was reported in 1899 by Edward E. Maxey.

Howard Ricketts (1871–1910) was an associate professor of pathology at the University of Chicago in 1902. He was the first to identify and study Rickettsia rickettsii. At the time, the trademark rash now began to slowly emerge in this influential western Montana area, killing at a 80-90% mortality rate. His research entailed interviewing victims of the disease and collecting and studying infected animals. He was also known to inject himself with pathogens to measure its effects. Unfortunately, his research was cut short after his likely death from an insect bite.

S. Burt Wolbach is credited for the first detailed description of the pathogenic agent that causes R. rickettsii in 1919. He clearly recognized it as an intracellular bacterium which was seen most frequently in endothelial cells.

Pathogen life cycle[edit]

The most common host for the R. rickettsii bacteria are ticks.[2] Ticks that carry the R. rickettsia bacteria fall into the family of Ixodidae ticks, also known as "hard bodied" ticks.[3] There are currently three known tick specifics that commonly carry the R. rickettsii bacteria in the eastern and western hemispheres.[3] Ticks are considered to be vectors, reservoirs and amplifiers of this disease.[2]

Transmission in ticks[edit]

The ticks known to carry the R. rickettsii disease are as follows: American dog tick (Dermacentor variabilis), the Rocky Mountain Wood Tick (Dermacentor andersoni), and the Brown dog tick (Rhipicephalus sanguine). [3]

Ticks can contract R. rickettsii bacteria by many means. First, an uninfected tick can become infected when feeding on the blood of an infected vertebrate host in the larval or nymph stages, a mode of transmission called transstadial transmission.[4] Once a tick becomes infected with this pathogen, they are infected for life.[4] Both the American dog tick and the Rocky Mountain wood tick serve as long-term reservoirs for Rickettsia rickettsii, in which the organism resides in the tick posterior diverticulae of the midgut, the small intestine and the ovaries.[4] In addition, an infected male tick can transmit the organism to an uninfected female during mating.[4] Once infected, the female tick can transmit the infection to her offspring, in a process known as transovarial transmission.[4]

Transmission in mammals[edit]

Due to its confinement in the midgut and small intestine, Rickettsia rickettsii can be transmitted to mammals, including humans. Transmission to mammals can occur in multiple ways. One way of contraction is through the contact of infected host feces to an uninfected host.[4] If infected host feces comes into contact with a wound or open skin, it is possible for the disease to be transmitted.[4] Additionally, an uninfected host can become infected with R. rickettsii when eating food that contains the feces of the infected tick.[4]

Another; more well know, way of contraction is by the bite of an infected tick.[4] After getting bitten by an infected tick, R. rickettsiae is transmitted to the bloodstream by tick salivary secretions or, as mentioned previously, through contamination of broken skin by infected vector feces.[4]

Rickettsia have been found to distort the sex ratio of their hosts by eradicating males and undergoing pathogenesis- they do so primarily via horizontal gene transfer.By eradicating male hosts, female host can pass the R. rickettsii gene to her offspring giving the R. rickettsii bacteria yet another way to infect hosts.

By having multiple modes of transmission this ensures the persistence of the R. rickettsii bacteria in a population. Also, by having multiple modes of transmission this helps the disease adapt better to new environments and prevents it from becoming eradicated. R. rickettsii have evolved a number of strategical mechanisms or virulence factors that allow them to evade the host immune system and successfully infect the host.


R. rickettsii invades the endothelial cells that line the blood vessels. Endothelial cells are not phagocytic in nature; however, after attachment to the host cell surface, the pathogen causes changes in the host cell cytoskeleton that induces phagocytosis. Since the bacteria can now induce phagocytosis the R. rickettsii gene can be replicated and further invade other cells in the hosts body.

Around the World[edit]

R. rickettsii is found on every continent excluding Antartica. The disease was first discovered in North America and since then has been identified in almost every corner of the earth. The spread of R. rickettsii is likely due to the migration of humans and animals around the globe. However, R. rickettsii tends to thrive in warm damp places and this can be seen by contraction rates around the world.[5] Environments are constantly changing so the fluctuation of the disease is never constant in a population and this correlates to the evolution of the R. rickettsii bacteria.

Clinical manifestations[edit]

Early-stage lesions of RMSF

The Centers for Disease Control and Prevention states that the diagnosis of RMSF must be made based on the clinical signs and symptoms of the patient and later confirmed using specialized laboratory tests. However, the diagnosis of RMSF is often missed due to its non-specific onset. The clinical signs and symptoms that a patient may experience could appear and may be misdiagnosed as other diseases even by the most experienced physician. If not treated the illness may become serious, leading to hospitalization and fatality.

Initial signs and symptoms[edit]

During the initial stages of the disease, the patient will experience fever, nausea, vomiting, loss of appetite, and conjunctival infection (red eyes).


The classic RMSF rash occurs in about 90% of patients and develops 2 to 5 days after the onset of fever. The characteristic rash appear as small, flat pink macules that develop peripherally on the patient's body, such as the wrists, forearms, ankles, and feet. During the course of the disease, the rash will take on a more darkened red to purple spotted appearance and a more generalized distribution.

Late signs and symptoms[edit]

Diarrhea, abdominal and joint pain, and pinpoint reddish lesions (petechiae) are observed during the late stages of the disease.

Long-term implications[edit]

Patients with severe infections may require hospitalization. They may become thrombocytopenic, hyponatremic, experience elevated liver enzymes, and other more pronounced symptoms. It is not uncommon for severe cases to involve the respiratory system, central nervous system, gastrointestinal system or the renal system. This disease is worst for elderly patients, males, African-Americans, alcoholics, and patients with G6PD deficiency.

Diagnosis and treatment[edit]

Physician diagnosis[edit]

A proper physician's diagnosis is crucial during the early stages of RMSF. However, due to the fact that the signs and symptoms are very non-specific at onset, RMSF can often be misdiagnosed. For this reason, it is vital for a physician to treat the patient based on suspicion alone.

Laboratory confirmation[edit]

Rocky Mountain Spotted Fever is often diagnosed using an indirect immunofluorescence assay (IFA), which is considered the reference standard by the Centers for Disease Control and Prevention (CDC). The IFA will detect an increase in IgG or IgM antibodies.

A more specific lab test used in diagnosing RMSF is polymerase chain reaction or PCR which can detect the presence of rickettiae DNA.

Immunohistochemical (IHC) staining is another diagnostic approach where a skin biopsy is taken of the spotted rash; however, sensitivity is only 70%.


Doxycycline and Chloramphenicol are the most common drugs of choice for reducing the symptoms associated with RMSF. When it is suspected that a patient may have RMSF, it is crucial that antibiotic therapy be administered promptly. Failure to receive antibiotic therapy, especially during the initial stages of the disease, may lead to end-organ failure (heart, kidney, lungs, meningitis, brain damage, shock, and even death.

Preventative Measures

The main preventive measures are taken by containing and eliminating the carrier of the pathogen. Wearing long sleeve shirts and pants when in grassy areas, clearing the yard from leaf piles, and placing piles of wood in the sun to eliminate the chance for ticks to residing in them. Also according to the CDC, using insect repellent and checking pets for ticks after being out in wooded or grassy areas can decrease the chances of being bitten by a tick carrying the pathogen.


  1. ^ a b c Perlman, Steve J.; Hunter, Martha S.; Zchori-Fein, Einat (2006-09-07). "The emerging diversity of Rickettsia". Proceedings of the Royal Society of London B: Biological Sciences 273 (1598): 2097–2106. doi:10.1098/rspb.2006.3541. ISSN 0962-8452. PMC 1635513. PMID 16901827. 
  2. ^ a b Parola, Philippe; Paddock, Christopher D.; Raoult, Didier (2005-10-01). "Tick-Borne Rickettsioses around the World: Emerging Diseases Challenging Old Concepts". Clinical Microbiology Reviews 18 (4): 719–756. doi:10.1128/CMR.18.4.719-756.2005. ISSN 0893-8512. PMC 1265907. PMID 16223955. 
  3. ^ a b c Parola, Philippe; Davoust, Bernard; Raoult, Didier (2005-06-01). "Tick- and flea-borne rickettsial emerging zoonoses". Veterinary Research 36 (3): 469–492. doi:10.1051/vetres:2005004. ISSN 0928-4249. PMID 15845235. 
  4. ^ a b c d e f g h i j Radolf, Justin D.; Caimano, Melissa J.; Stevenson, Brian; Hu, Linden T. (2012-02-01). "Of ticks, mice and men: understanding the dual-host lifestyle of Lyme disease spirochaetes". Nature Reviews Microbiology 10 (2): 87–99. doi:10.1038/nrmicro2714. ISSN 1740-1526. PMC 3313462. PMID 22230951. 
  5. ^ Openshaw, John J.; Swerdlow, David L.; Krebs, John W.; Holman, Robert C.; Mandel, Eric; Harvey, Alexis; Haberling, Dana; Massung, Robert F.; McQuiston, Jennifer H. (2010-07-01). "Rocky Mountain Spotted Fever in the United States, 2000–2007: Interpreting Contemporary Increases in Incidence". The American Journal of Tropical Medicine and Hygiene 83 (1): 174–182. doi:10.4269/ajtmh.2010.09-0752. ISSN 0002-9637. PMC 2912596. PMID 20595498. 

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