Rickettsia rickettsii: Difference between revisions
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'''''Rickettsia rickettsii''''' (abbreviated as ''R. rickettsii) is a gram negative intracellular bacteria, that is only around 0.8 to 2.0 micrometers long. R. rickettsii is most known to cause various strains of spotted fever. R. rickettsii is one of the most pathogenetic rickettsia strains known to human and effects a large majority of the western hemisphere and small portions of the eastern hemisphere.'' <ref>{{Cite journal|title = The emerging diversity of Rickettsia|url = http://rspb.royalsocietypublishing.org/content/273/1598/2097|journal = Proceedings of the Royal Society of London B: Biological Sciences|date = 2006-09-07|issn = 0962-8452|pmc = 1635513|pmid = 16901827|pages = 2097-2106|volume = 273|issue = 1598|doi = 10.1098/rspb.2006.3541|language = en|first = Steve J.|last = Perlman|first2 = Martha S.|last2 = Hunter|first3 = Einat|last3 = Zchori-Fein}}</ref> |
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'''''Rickettsia rickettsii''''' (abbreviated as ''R. rickettsii'') is a unicellular, Gram-negative coccobacillus (plural coccobacilli) that is native to the [[New World]]. It belongs to the spotted fever group (SFG) of ''Rickettsia'' and is most commonly known as the causative agent of [[Rocky Mountain spotted fever]] (RMSF). By nature, ''R. rickettsii'' is an [[obligate intracellular parasite]] that survive by an [[endosymbiotic]] relationship with other cells. |
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''R. rickettsii'' is a non-motile, non-spore forming aerobic organism. Cells are typically 0.3–0.5 × 0.8–2.0 μm in size. They lack a distinct nucleus and membrane bound organelles. Their outer membrane is composed mostly of [[lipopolysaccharides]]. |
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RMSF is transmitted by the bite of an infected [[tick]] while feeding on warm-blooded animals, including humans. Humans are considered to be accidental hosts in the ''Rickettsia''–tick life cycle and are not required to maintain the rickettsiae in nature. |
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==History== |
==History== |
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==Pathogen life cycle== |
==Pathogen life cycle== |
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The most common host for the R. rickettsii bacteria are ticks. Ticks that carry the R. rickettsia bacteria fall into the family of ''Ixodidae'' ticks, also known as "hard bodied" ticks. There are currently three known tick specifics that commonly carry the R. rickettsii bacteria in the eastern and western hemispheres. Ticks are considered to be vectors, reservoirs and amplifiers of this disease.<ref name=":0">{{Cite journal|title = Tick-Borne Rickettsioses around the World: Emerging Diseases Challenging Old Concepts|url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1265907/|journal = Clinical Microbiology Reviews|date = 2005-10-01|issn = 0893-8512|pmc = 1265907|pmid = 16223955|pages = 719-756|volume = 18|issue = 4|doi = 10.1128/CMR.18.4.719-756.2005|first = Philippe|last = Parola|first2 = Christopher D.|last2 = Paddock|first3 = Didier|last3 = Raoult}}</ref> |
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The life cycle of ''Rickettsia rickettsii'' is considered to be a complex one. Survival is dependent on both an invertebrate vector, (the hard tick- Family Ixodidae) and a vertebrate host (including mice, dogs, rabbits). Humans are considered to be accidental vectors and are not essential in the rickettsial cycle. In addition, a sequence of events occur between both hosts in the successful transmission of rickettsial disease. |
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''Rickettsia rickettsii'' mostly affects canines and humans. |
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===Transmission in arthropod vectors=== |
===Transmission in arthropod vectors=== |
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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).'' <ref>{{Cite journal|title = Tick- and flea-borne rickettsial emerging zoonoses|url = http://www.ncbi.nlm.nih.gov/pubmed/15845235|journal = Veterinary Research|date = 2005-06-01|issn = 0928-4249|pmid = 15845235|pages = 469-492|volume = 36|issue = 3|doi = 10.1051/vetres:2005004|first = Philippe|last = Parola|first2 = Bernard|last2 = Davoust|first3 = Didier|last3 = Raoult}}</ref> |
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First, an uninfected tick can become infected when feeding on the blood of an infected |
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]]''. Once a tick becomes infected with this pathogen, they are infected for life. 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.<ref name=":1">{{Cite journal|title = Of ticks, mice and men: understanding the dual-host lifestyle of Lyme disease spirochaetes|url = http://www.nature.com/nrmicro/journal/v10/n2/full/nrmicro2714.html|journal = Nature Reviews Microbiology|date = 2012-02-01|issn = 1740-1526|pmc = 3313462|pmid = 22230951|pages = 87-99|volume = 10|issue = 2|doi = 10.1038/nrmicro2714|language = en|first = Justin D.|last = Radolf|first2 = Melissa J.|last2 = Caimano|first3 = Brian|last3 = Stevenson|first4 = Linden T.|last4 = Hu}}</ref> |
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Due to its confinement in the midgut and small intestine, it is possible for mammals, including humans, to contract rickettsial disease from open skin/wound contact with the feces of the organism. In addition, an infected male tick can transmit the organism to an uninfected female during mating. Once infected, the female tick can transmit the infection to her offspring, in a process known as ''[[transovarial transmission]]''. |
Due to its confinement in the midgut and small intestine, it is possible for mammals, including humans, to contract rickettsial disease from open skin/wound contact with the feces of the organism. In addition, an infected male tick can transmit the organism to an uninfected female during mating. Once infected, the female tick can transmit the infection to her offspring, in a process known as ''[[transovarial transmission]]''.<ref name=":1" /> |
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===Transmission in mammals=== |
===Transmission in mammals=== |
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An uninfected mammal can become infected with ''Rickettsia rickettsii'' when eating food that contains the feces of the infected tick. They can also be infected through the bite of an infected tick. |
An uninfected mammal can become infected with ''Rickettsia rickettsii'' when eating food that contains the feces of the infected tick. They can also be infected through the bite of an infected tick.<ref name=":1" /> |
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Humans acquire ''Rickettsia rickettsii'' infection from infected vectors. After getting bitten by an infected tick, rickettsiae are transmitted to the bloodstream by tick salivary secretions or, as mentioned previously, through contamination of broken skin by infected vector feces. |
Humans acquire ''Rickettsia rickettsii'' infection from infected vectors. After getting bitten by an infected tick, rickettsiae are transmitted to the bloodstream by tick salivary secretions or, as mentioned previously, through contamination of broken skin by infected vector feces.<ref name=":1" /> |
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All these modes of transmission ensures the survival of ''Rickettsia'' in nature. |
All these modes of transmission ensures the survival of ''Rickettsia'' in nature. ''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. |
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''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. |
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==Virulence== |
==Virulence== |
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==In vivo versus in vitro studies== |
==In vivo versus in vitro studies== |
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''[[In vivo]]'' studies reveal that ''Rickettsia rickettsii'' invade endothelial lining of small to medium vessels in the human host, causing vascular permeability. When tested ''[[in vitro]]'', it is shown that the bacterium infects every kind of cell of the mammalian host. |
''[[In vivo]]'' studies reveal that ''Rickettsia rickettsii'' invade endothelial lining of small to medium vessels in the human host, causing vascular permeability. When tested ''[[in vitro]]'', it is shown that the bacterium infects every kind of cell of the mammalian host. |
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==Epidemiology== |
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The name [[Rocky Mountain spotted fever]] is somewhat of a misnomer. Cases of Rocky Mountain spotted fever have been reported in every continent except [[Antarctica]], and in every state in the U.S. except for [[Alaska]], and [[Hawaii]]. |
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Approximately 90% of all infections occur within the months of April to September, the time period in which adult and nymphal ticks are the highest. The areas of the U.S. with the greatest reported cases of RMSF are the mid to south Atlantic states, including DE, MD, DC, VA, WV, NC, SC. |
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It is estimated that approximately 1200 or more new cases of RMSF will present on a yearly basis. |
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==Clinical manifestations== |
==Clinical manifestations== |
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===Antibiotics=== |
===Antibiotics=== |
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[[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 (circulatory)|shock]], and even death. |
[[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 (circulatory)|shock]], and even death. |
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== Evolution == |
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The R. rickesttii bacteria was discovered in the 17th century and has since undergone many evolutionary changes. The first clinical description of Rocky Mountain Spotted Fever was reported in 1899 by Edward E. Maxey. By the 1900's R. rickettsii was the only known tick borne disease in the western hemisphere. Many more tick borne diseases have since been discovered, but the last article published on Rickettsioses was in 1977, since then much evolution has occurred within the species.<ref name=":0" /> Many studies have been conducted on the correlation with the prevalence of R. rickettsii and the increase in global temperature. A study looking at all patients who had contracted R. rickettsii disease in the United States from 2000-2007 showed a steady increase in the number of individuals effected. The same study also showed that more individuals contracted R. rickettsii disease in the warmer months of June- August. However, the incidence of contraction of R. rickettsii disease has fluctuated greatly over the years due to fluctuating global and local environmental changes. <ref>{{Cite journal|title = Rocky Mountain Spotted Fever in the United States, 2000–2007: Interpreting Contemporary Increases in Incidence|url = http://www.ajtmh.org/content/83/1/174|journal = The American Journal of Tropical Medicine and Hygiene|date = 2010-07-01|issn = 0002-9637|pmc = 2912596|pmid = 20595498|pages = 174-182|volume = 83|issue = 1|doi = 10.4269/ajtmh.2010.09-0752|language = en|first = John J.|last = Openshaw|first2 = David L.|last2 = Swerdlow|first3 = John W.|last3 = Krebs|first4 = Robert C.|last4 = Holman|first5 = Eric|last5 = Mandel|first6 = Alexis|last6 = Harvey|first7 = Dana|last7 = Haberling|first8 = Robert F.|last8 = Massung|first9 = Jennifer H.|last9 = McQuiston}}</ref> Another study conducted verified that an increase in environmental temperature increases the vitality of both infected and uninfected ticks.<ref>{{Cite journal|title = Natural Blood Feeding and Temperature Shift Modulate the Global Transcriptional Profile of Rickettsia rickettsii Infecting Its Tick Vector|url = http://dx.doi.org/10.1371/journal.pone.0077388|journal = PLoS ONE|date = 2013-10-14|pmc = 3796454|pmid = 24155949|pages = e77388|volume = 8|issue = 10|doi = 10.1371/journal.pone.0077388|first = Maria Fernanda B. M.|last = Galletti|first2 = André|last2 = Fujita|first3 = Milton Y.|last3 = Nishiyama Jr|first4 = Camila D.|last4 = Malossi|first5 = Adriano|last5 = Pinter|first6 = João F.|last6 = Soares|first7 = Sirlei|last7 = Daffre|first8 = Marcelo B.|last8 = Labruna|first9 = Andréa C.|last9 = Fogaça}}</ref> Given this information the fluctuation of the contraction of this disease over the years suggests that there has been an evolutionary impact on the R. rickettsii disease. |
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==References== |
==References== |
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Revision as of 15:42, 20 October 2015
| Rickettsia rickettsii | |
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| Species: | R. rickettsii
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| Binomial name | |
| Rickettsia rickettsii Brumpt, 1922
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Rickettsia rickettsii (abbreviated as R. rickettsii) is a gram negative intracellular bacteria, that is only around 0.8 to 2.0 micrometers long. R. rickettsii is most known to cause various strains of spotted fever. R. rickettsii is one of the most pathogenetic rickettsia strains known to human and effects a large majority of the western hemisphere and small portions of the eastern hemisphere. [1]
History
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.
Howard Ricketts (1871–1910) was an American pathologist and infectious disease researcher who was the first to identify and study the organism that causes Rocky Mountain spotted fever. He received his undergraduate degree in zoology from the University of Nebraska and his medical degree from Northwestern University School of Medicine. Ricketts completed his internship at Cook County Hospital in Chicago, IL, followed by a fellowship in pathology and cutaneous diseases at Rush Medical College.
In 1902, Ricketts became the associate professor of pathology at the University of Chicago. The trademark rash, which first appeared in the Idaho Valley, now began to slowly emerge in the Bitterroot Valley region, a highly influential area in western Montana and had an 80–90% mortality rate. During his tenure as associate professor, Ricketts was funded and recruited by the University of Chicago, the State of Montana, and the American Medical Association to conduct research on Rocky Mountain spotted fever.
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.
Ricketts was also known for his research on typhus, which was very similar to spotted fever. Ironically, days after isolating the organism that he believed to cause typhus, he died. It was speculated that his death was likely caused from an insect bite.
S. Burt Wolbach is credited for the first detailed description of the etiologic agent in 1919. He clearly recognized it as an intracellular bacterium which was seen most frequently in endothelial cells. He was struck by the fact that in the tick, and also in mammalian cells, the microorganism was intranuclear. The nucleus was often completely filled with minute particles and often was distended. Although Wolbach recognized its similarity to the agent of typhus and tsutsugamushi fever (scrub typhus), he did not regard the designation 'rickettsia' as appropriate. He proposed the name Dermacentroxenus rickettsi. Dr. Emile Brumpt felt that the etiologic agent of RMSF, despite some uncertainty about its properties, belonged in the genus Rickettsia and in 1922 proposed the name Rickettsia rickettsii.
Pathogen life cycle
The most common host for the R. rickettsii bacteria are ticks. Ticks that carry the R. rickettsia bacteria fall into the family of Ixodidae ticks, also known as "hard bodied" ticks. There are currently three known tick specifics that commonly carry the R. rickettsii bacteria in the eastern and western hemispheres. Ticks are considered to be vectors, reservoirs and amplifiers of this disease.[2]
Transmission in arthropod vectors
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. Once a tick becomes infected with this pathogen, they are infected for life. 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]
Due to its confinement in the midgut and small intestine, it is possible for mammals, including humans, to contract rickettsial disease from open skin/wound contact with the feces of the organism. In addition, an infected male tick can transmit the organism to an uninfected female during mating. Once infected, the female tick can transmit the infection to her offspring, in a process known as transovarial transmission.[4]
Transmission in mammals
An uninfected mammal can become infected with Rickettsia rickettsii when eating food that contains the feces of the infected tick. They can also be infected through the bite of an infected tick.[4]
Humans acquire Rickettsia rickettsii infection from infected vectors. After getting bitten by an infected tick, rickettsiae are transmitted to the bloodstream by tick salivary secretions or, as mentioned previously, through contamination of broken skin by infected vector feces.[4]
All these modes of transmission ensures the survival of Rickettsia in nature. 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.
Virulence
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. They are able to avoid lysosomal fusion and oxidative burst by escaping from the phagosome into the cytoplasm where they multiply and spread.
Over the years, different virulence factors have been identified in R. rickettsii.
OmpA and OmpB
OmpA (rOmp) and Omp B (rOmp) have been identified as rickettsial outer surface proteins and are implicated in adherence of the bacterium to the host cell. The genes that encode these two surface proteins are designated as ompA and ompB, respectively.
rOmp B is the predominant surface membrane protein in R. rickettsii; Policastro et al., identified the rOmpA to rOmpB ratio to be 1:9 (1994).[5] While the surface proteins of the bacterium have been identified, the host cell protein receptor(s) have not.
T4SS
Entry into the host cell is mediated by a Type 4 secretion system' (T4SS) which is found in all Rickettsiae. The organization of the T4SS apparatus is a rather elaborate one; it is a tunnel-shaped structure that is embedded in the bacterial inner membrane and extends to the outer membrane. At least 12 or more proteins help form the tunnel-like apparatus. Once adherence to the host cell is established, the T4SS of Rickettsiae recruits substrates to the bottom of the apparatus, activating the complex via an ATP-dependent process that results in the direct transfer of the bacterium's DNA and other proteins into the host cell.
Phospholipase A2
Invasion of the host endothelial cell immediately triggers phagocytosis, where the rickettsiae escape from the phagosome and into the cytosol where replication takes place. Although the escape from the phagosome is not well understood, it is thought to be mediated by phospholipase A2 activity.
Actin polymerization
In the cytosol, the virulence factor Sca2 (Surface Cell Antigen 2) and the protein RickA form an actin tail that provides motility. RickA is thought to be responsible for directing the actin-based motility in R. rickettsii. RickA has been shown to activate the Arp2/3 complex in vitro, but "R. raoulti" expresses RickA and does not have acting-based motility.[6] The Sca2 virulence factor has been shown to be essential for actin tail formation in "R.rickettsii" Listeria. Comparisons of actin motility mechanisms appears to be independently evolved in Listeria, Shigella, and Rickettsia.
The actin tail in R. rickettsii is both longer and provides a straighter trajectory due the production of linear actin filaments.[7] The actin-based motility of R. rickettsii allows swift, unidirectional movement[citation needed] across the cytoplasm into adjacent cells, promoting cell to cell spread Endothelial cell damage caused by R. rickettsii can lead to end organ failure, DIC, and even death.
In vivo versus in vitro studies
In vivo studies reveal that Rickettsia rickettsii invade endothelial lining of small to medium vessels in the human host, causing vascular permeability. When tested in vitro, it is shown that the bacterium infects every kind of cell of the mammalian host.
Clinical manifestations
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.
Initial signs and symptoms
During the initial stages of the disease, the patient will experience fever, nausea, vomiting, and loss of appetite.
Rash
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
Diarrhea, abdominal and joint pain, and pinpoint reddish lesions (petechiae) are observed during the late stages of the disease.
Long-term implications
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
Physician diagnosis
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
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%.
Antibiotics
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.
Evolution
The R. rickesttii bacteria was discovered in the 17th century and has since undergone many evolutionary changes. The first clinical description of Rocky Mountain Spotted Fever was reported in 1899 by Edward E. Maxey. By the 1900's R. rickettsii was the only known tick borne disease in the western hemisphere. Many more tick borne diseases have since been discovered, but the last article published on Rickettsioses was in 1977, since then much evolution has occurred within the species.[2] Many studies have been conducted on the correlation with the prevalence of R. rickettsii and the increase in global temperature. A study looking at all patients who had contracted R. rickettsii disease in the United States from 2000-2007 showed a steady increase in the number of individuals effected. The same study also showed that more individuals contracted R. rickettsii disease in the warmer months of June- August. However, the incidence of contraction of R. rickettsii disease has fluctuated greatly over the years due to fluctuating global and local environmental changes. [8] Another study conducted verified that an increase in environmental temperature increases the vitality of both infected and uninfected ticks.[9] Given this information the fluctuation of the contraction of this disease over the years suggests that there has been an evolutionary impact on the R. rickettsii disease.
References
- ^ 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.
- ^ 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.
- ^ 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.
- ^ a b c d 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.
- ^ Policastro PF, Hackstadt T (November 1994). "Differential activity of Rickettsia rickettsii opmA and ompB promoter regions in a heterologous reporter gene system" (PDF). Microbiology (Reading, Engl.). 140 (11): 2941–9. doi:10.1099/13500872-140-11-2941. PMID 7812435.
- ^ Kleba, Betsy; Tina R. Clark; Erika I. Lutter; Damon W. Ellison; Ted Hackstadt (March 1, 2010). "Disruption of the Rickettsia rickettsii Sca2 Autotransporter Inhibits Actin-Based Motility". Infection and Immunity. 78 (5): 2240–7. doi:10.1128/IAI.00100-10. PMC 2863521. PMID 20194597. Retrieved March 9, 2014.
- ^ Goldberg, Marcia (December 2001). "Actin-Based Motility of Intracellular Microbial Pathogens". MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS. 65 (4): 31. doi:10.1128/MMBR.65.4.595-626.2001. PMC 99042. PMID 11729265. Retrieved March 9, 2014.
- ^ 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.
- ^ Galletti, Maria Fernanda B. M.; Fujita, André; Nishiyama Jr, Milton Y.; Malossi, Camila D.; Pinter, Adriano; Soares, João F.; Daffre, Sirlei; Labruna, Marcelo B.; Fogaça, Andréa C. (2013-10-14). "Natural Blood Feeding and Temperature Shift Modulate the Global Transcriptional Profile of Rickettsia rickettsii Infecting Its Tick Vector". PLoS ONE. 8 (10): e77388. doi:10.1371/journal.pone.0077388. PMC 3796454. PMID 24155949.
{{cite journal}}: CS1 maint: unflagged free DOI (link)
- Garrity, George; Brenner, Don J.; Staley, James T.; Krieg, Noel R.; Boone, David R.; Vos, Paul De; Goodfellow, Michael; Rainey, Fred A.; Schleifer, Karl-Heinz (2006). "Order II. Rickettsiales Gieszczkiewicz 1939..". Bergey's Manual® of Systematic Bacteriology: Volume Two: The Proteobacteria (Part C). Springer. pp. 96–. ISBN 978-0-387-29298-4.
{{cite book}}: External link in|chapterurl=|chapterurl=ignored (|chapter-url=suggested) (help) - Weiss, K. (1988). "The Role of Rickettsioses in History". In Walker, David H. (ed.). Biology of Rickettsial Diseases. CRC Press. pp. 2–14. ISBN 978-0-8493-4382-7.
- Weiss, E. (1988). "History of Rickettsiology". Biology of Rickettsial Diseases. pp. 15–32.
- Wilson, Brenda A.; Salyers, Abigail A.; Whitt, Dixie D.; Winkler, Malcolm E. (2011). Bacterial Pathogenesis: A Molecular Approach (3rd ed.). Amer Society for Microbiology. ISBN 978-1-55581-418-2.
External links
- "Rickettsia rickettsii genomes and related information". PATRIC Bioinformatics Resource Center. NIAID.
{{cite web}}: External link in|publisher=and|work= - "Rickettsia rickettsii: The Cause of Rocky Mountain Spotted Fever". Multiple Organisms: Organismal Biology. University of Wisconsin-La Crosse. 2007.
- Todar, Kenneth (2008–2012). "Rickettsial Diseases, including Typhus and Rocky Mountain Spotted Fever". Todar's Online Textbook of Bacteriology.
- "Rocky Mountain Spotted Fever (RMSF)". Centers for Disease Control and Prevention. 21 November 2013.