Rickettsia rickettsii

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Rickettsia rickettsii
Rickettsia rickettsii.jpg
Scientific classification Red Pencil Icon.png
Domain: Bacteria
Phylum: Proteobacteria
Class: Alphaproteobacteria
Order: Rickettsiales
Family: Rickettsiaceae
Genus: Rickettsia
Species group: Spotted fever group
R. rickettsii
Binomial name
Rickettsia rickettsii
Brumpt, 1922

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

Rocky Mountain spotted fever human disease

Rocky Mountain spotted fever (RMSF) is a bacterial disease spread by ticks. It typically begins with a fever and headache, which is followed a few days later with the development of a rash. The rash is generally made up of small spots of bleeding and starts on the wrists and ankles. Other symptoms may include muscle pains and vomiting. Long-term complications following recovery may include hearing loss or loss of part of an arm or leg.

<i>Rickettsia</i> type of bacteria that causes typhus, among other diseases

Rickettsia is a genus of nonmotile, Gram-negative, nonspore-forming, highly pleomorphic bacteria that may occur in the forms of cocci 0.1 μm in diameter, rods 1–4 μm long, or threads of up to about 10 μm long. The term "rickettsia" has nothing to do with rickets, which is a deficiency disease resulting from lack of vitamin D; the bacterial genus Rickettsia was named after Howard Taylor Ricketts, in honour of his pioneering work on tick-borne spotted fever.



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);an associate professor of pathology at the University of Chicago in 1902, was the first to identify and study R. rickettsii. At this time, the trademark rash now began to slowly emerge in the western Montana area, with an 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 their effects. Unfortunately, his research was cut short after his death, likely 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

The most common hosts for the R. rickettsii bacteria are ticks. [2] Ticks that carry R. rickettsia fall into the family of Ixodidae ticks, also known as "hard bodied" ticks. [3] Ticks are vectors, reservoirs and amplifiers of this disease. [2]

Ixodidae family of arachnids

The Ixodidae are the family of hard ticks or scale ticks, one of the two big families of ticks, consisting of over 700 species. They are known as 'hard ticks' because they have a scutum or hard shield, which the other big family of ticks, the soft ticks (Argasidae), lack. They are ectoparasites of a wide range of host species, and some are vectors of disease.

There are currently three known tick specifics that commonly carry R. rickettsii. [3]

Ticks can contract R. rickettsii by many means. First, an uninfected tick can become infected when feeding on the blood of an infected vertebrate host; such as a rabbit, during the larval or nymph stages, this mode of transmission called transstadial transmission .[ citation needed ] Once a tick becomes infected with this pathogen, they are infected for life.[ citation needed ] 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.[ citation needed ] In addition, an infected male tick can transmit the organism to an uninfected female during mating.[ citation needed ] Once infected, the female tick can transmit the infection to her offspring, in a process known as transovarian passage . [4]

Transmission in mammals

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

Another way of contraction is by the bite of an infected tick.[ citation needed ] After getting bitten by an infected tick, R. rickettsiae is transmitted to the bloodstream by tick salivary secretions.[ citation needed ]

R. rickettsii has also been found to distort the sex ratio of their hosts. This is done by eradicating males and undergoing pathogenesis, this is done primarily via horizontal gene transfer. By eradicating male hosts, female host can pass the R. rickettsii gene to her offspring giving R. rickettsii bacteria yet another way to infect hosts. [ citation needed ]

By having multiple modes of transmission this ensures the persistence of R. rickettsii 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 has evolved a number of strategical mechanisms or virulence factors that allow them to invade the host immune system and successfully infect the host.


Since R. rickettsii needs a moving vector to contract the disease to a viable host it is more likely that this pathogen has moderately low virulence levels. This idea is supported by the tradeoff hypothesis which suggests that virulence of a pathogen will evolve until the level of virulence balances out with the level of transmission to maximize the spread of the pathogen. R. rickettsii invades the endothelial cells that line the blood vessels in the hosts body. Endothelial cells are not phagocytic in nature; however, after attachment to the 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

R. rickettsii is found on every continent excluding Antarctica. 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 R. rickettsii.

Clinical manifestations

The Centers for Disease Control and Prevention states that the diagnosis of Rocky Mountain Spotted Fever must be made based on the clinical signs and symptoms of the patient and then later confirmed using specialized laboratory tests. However, the diagnosis of Rocky Mountain Spotted Fever is often misdiagnosed due to its non-specific onset. If not treated properly the illness may become serious, leading to hospitalization and possible fatality.

Initial signs and symptoms

During the initial stages of the disease, the patient could experience:

Rocky Mountain Spotted Fever Rash Rocky Mountain spotted fever PHIL 1962 lores.jpg
Rocky Mountain Spotted Fever Rash


The classic Rocky Mountain Spotted Fever 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 become more evenly distributed.

Late signs and symptoms

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

Severe infections

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 complications. This disease is worst for elderly patients, males, African-Americans, alcoholics, and patients with G6PD deficiency. Deaths usually are caused by heart and kidney failure. [4]

Diagnosis and treatment

Laboratory confirmation

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 in the bloodstream.

A more specific lab test used in diagnosing Rocky Mountain Spotted Fever 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, accuracy 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 provides a barrier from possible tick bites. By clearing leaf piles from the yard this will lessen the likelihood of ticks being in close proximity. Also by placing piles of wood in the sun eliminate the chance for ticks to reside in them. 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 significantly.

Related Research Articles

Colorado tick fever (CTF) is a viral infection (Coltivirus) transmitted from the bite of an infected Rocky Mountain wood tick. It should not be confused with the bacterial tick-borne infection, Rocky Mountain spotted fever.

Boutonneuse fever Human disease

Boutonneuse fever is a fever as a result of a rickettsial infection caused by the bacterium Rickettsia conorii and transmitted by the dog tick Rhipicephalus sanguineus. Boutonneuse fever can be seen in many places around the world, although it is endemic in countries surrounding the Mediterranean Sea. This disease was first described in Tunisia in 1910 by Conor and Bruch and was named boutonneuse due to its papular skin rash characteristics.

Tick-borne diseases, which afflict humans and other animals, are caused by infectious agents transmitted by tick bites. Tick-borne illnesses are caused by infection with a variety of pathogens, including rickettsia and other types of bacteria, viruses, and protozoa. Because individual ticks can harbor more than one disease-causing agent, patients can be infected with more than one pathogen at the same time, compounding the difficulty in diagnosis and treatment. As of 2016, 16 tick-borne diseases of humans are known.

Murine typhus typhus transmitted by fleas (Xenopsylla cheopis), usually on rats

Murine typhus is a form of typhus transmitted by fleas, usually on rats. Murine typhus is an under-recognized entity, as it is often confused with viral illnesses. Most people who are infected do not realize that they have been bitten by fleas.

Meningoencephalitis central nervous system disease that involves encephalitis which occurs along with meningitis

Meningoencephalitis, also known as herpes meningoencephalitis, is a medical condition that simultaneously resembles both meningitis, which is an infection or inflammation of the meninges, and encephalitis, which is an infection or inflammation of the brain.

Howard Taylor Ricketts American pathologist

Howard Taylor Ricketts was an American pathologist after whom the Rickettsiaceae family and the Rickettsiales are named.

<i>Dermacentor variabilis</i> species of arachnid

Dermacentor variabilis, also known as the American dog tick or wood tick, is a species of tick that is known to carry bacteria responsible for several diseases in humans, including Rocky Mountain spotted fever and tularemia. It is one of the most well-known hard ticks. Diseases are spread when it sucks blood from the host, which could take several days for the host to experience some symptoms.

A canine vector-borne disease (CVBD) is one of "a group of globally distributed and rapidly spreading illnesses that are caused by a range of pathogens transmitted by arthropods including ticks, fleas, mosquitoes and phlebotomine sandflies." CVBDs are important in the fields of veterinary medicine, animal welfare, and public health. Some CVBDs are of zoonotic concern.

<i>Anaplasma phagocytophilum</i> species of prokaryote

Anaplasma phagocytophilum is a Gram-negative bacterium that is unusual in its tropism to neutrophils. It causes anaplasmosis in sheep and cattle, also known as tick-borne fever and pasture fever, and also causes the zoonotic disease human granulocytic anaplasmosis.

Anaplasmosis disease, mostly animal, caused by bacteria of the genus Anaplasma

Anaplasmosis is a disease caused by a rickettsial parasite of ruminants, Anaplasma spp. The microorganisms are Gram-negative, and infect red blood cells. They are transmitted by natural means through a number of haematophagous species of ticks. The Ixodes tick that commonly transmits Lyme disease also spreads anaplasmosis. Anaplasmosis can also be transmitted by the use of surgical, dehorning, castration, and tattoo instruments and hypodermic needles that are not disinfected between uses.

A rickettsiosis is a disease caused by intracellular bacteria.

Human granulocytic anaplasmosis human disease

Human granulocytic anaplasmosis (HGA) is a tick-borne, infectious disease caused by Anaplasma phagocytophilum, an obligate intracellular bacterium that is typically transmitted to humans by ticks of the Ixodes ricinus species complex, including Ixodes scapularis and Ixodes pacificus in North America. These ticks also transmit Lyme disease and other tick-borne diseases.

African tick bite fever spotted fever that has material basis in Rickettsia africae, which is transmitted by ticks

African tick bite fever (ATBF) is a bacterial infection spread by the bite of a tick. Symptoms may include fever, headache, muscles pains, and a rash. At the site of the bite there is typically a red skin sore with a dark center. Onset usually occur 4–10 days after the bite. Complications are rare, however may include joint inflammation. Some people do not develop symptoms.

Rickettsia helvetica, previously known as the Swiss Agent, is a bacterium found in Dermacentor reticulatus and other ticks which has been implicated as a suspected but unconfirmed human pathogen. First recognized in 1979 in Ixodes ricinus ticks in Switzerland as a new member of the spotted fever group of Rickettsia, the Rickettsia helvetica bacterium was eventually isolated in 1993. Although R. helvetica was initially thought to be harmless in humans and many animal species, some individual case reports suggest that it may be capable of causing a non-specific fever in humans. In 1997 a man living in eastern France seroconverted to Rickettsia 4 weeks after onset of an unexplained febrile illness. In 2010, a case report indicated that tick-borne R. helvetica can also cause meningitis in humans.

Rickettsia felis is a species of bacterium, the pathogen that causes cat-flea typhus in humans. In cats the disease is known as flea-borne spotted fever. Rickettsia felis also is regarded as the causative organism of many cases of illnesses generally classed as fevers of unknown origin in humans in Africa.

Rickettsia peacockii is a species of gram negative Alphaproteobacteria of the spotted fever group, identified from Rocky Mountain wood ticks. Its type strain is SkalkahoT. The organism is passed transstadially and transovarially, and infections are localized in ovarial tissues.

Haemaphysalis leporispalustris, the rabbit tick, is a species of tick that is widely distributed in the Americas, stretching from Alaska to Argentina. H. leporispalustris is known to have one of the largest distributions for a tick originating in the New World. It is a three-host tick and a member of the family Ixodidae, commonly called the "hard ticks," and the genus Haemaphysalis. Its common hosts are rabbits, hares, and sometimes ground-feeding birds. H. leporispalustris has a rigid scutum and a prominent capitulum projecting forward from its body and is often said to look like the "wood tick". It has a hemimetabolic life cycle. H. leporispalustris does not play a prominent role in disease transmission in humans but is a vector for disease in other animals.

Pacific Coast tick fever is an infection caused by Rickettsia philipii. The disease is spread by the Pacific coast ticks. Symptoms may include an eschar. It is within a group known as spotted fever rickettsiosis together with Rickettsia parkeri rickettsiosis, Rocky Mountain spotted fever, and rickettsialpox. These infections can be difficult to tell apart.


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