Streptobacillus Moniliformis: Difference between revisions
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Typically, Streptobacillus moniliformis is spread through bites from rats, leading to the nickname of RBF (16). It is also possible to become infected due to rat handling (2) or intake of contaminated substances from rats, such as food, drinking water, or feces (17). Haverhill fever is a term used to describe RBF contracted by such indirect contact (3). The speed of infectivity is not entirely understood, making infection rate difficult to assess. Symptoms appear between 3-21 days after infection, yet most people start showing symptoms 3-10 days after being infected (4). | Typically, Streptobacillus moniliformis is spread through bites from rats, leading to the nickname of RBF (16). It is also possible to become infected due to rat handling (2) or intake of contaminated substances from rats, such as food, drinking water, or feces (17). Haverhill fever is a term used to describe RBF contracted by such indirect contact (3). The speed of infectivity is not entirely understood, making infection rate difficult to assess. Symptoms appear between 3-21 days after infection, yet most people start showing symptoms 3-10 days after being infected (4). | ||
= | =10. Pathology= | ||
The most common symptoms of RBF observed in humans consist of high fever, rashes, joint and muscle pain, nausea, vomiting, and headaches (2). Haverhill fever presents with more severe gastrointestinal symptoms (3). Infection may lead to bacterial endocarditis (inflammation of the inner lining of the heart), pericarditis (inflammation of the pericardium), bronchitis (inflammation of the lining of the bronchial tubes), and persistent arthritis (swelling/tenderness of the joint). Children and infants who have been infected commonly experience anemia, weight loss, and diarrhea (2). While other symptoms have been observed, such as signs of pneumonia (17), they seem to be on an individual basis and not found in most cases. If left untreated in infants or those with pre-existing heart disease, RBF is likely to prove fatal (2). | |||
=8. Current Research= | =8. Current Research= | ||
Include information about how this microbe (or related microbes) are currently being studied and for what purpose | Include information about how this microbe (or related microbes) are currently being studied and for what purpose |
Revision as of 14:48, 6 December 2021
1. Classification
a. Higher order taxa
The scientific classification for S. moniliformis is as followed, according to NCBI (1): Domain - Bacteria Phylum - Fusobacteria Class - Fusobacteriaceae Order - Leptotrichiaceae Genus - Streptobacillus Species - Moniliformis
2. Introduction
The bacterium Streptobacillus moniliformis is a Gram-negative bacterium known for causing RBF (Rat Bite Fever) in humans. RBF is a zoonotic disease typically caused by direct contact with an infected rodent, such as via a rat bite (2), but it can also be contracted by indirect contact with an infected rodent through consumption of contaminants (Haverhill fever) (3). When humans are infected with S. moniliformis, the distinguishable symptoms consist of high fevers, rashes, joint and muscle pain, nausea, vomiting, and headaches (2). Children are the main population that is affected by this disease, due to the increase in children owning pets such as mice, rats, guinea pigs, hamsters, etc. (4). RBF is not well known in the United States, so data on this disease is limited (4). With increased crowding in cities where wild rodents tend to thrive, coupled with the increase in children owning rodents, people may be more susceptible to S. moniliformis than they were in the past (5). Current research focuses on advancements in detection and identification methods (2).
3. History
S. moniliformis was first isolated from the blood of a patient who had previously been bitten by a rat in 1914. It was then given one of its first names, Streptothrix muris ratti (6). In 1925, the bacterium attained its current name, Streptobacillus moniliformis (7). S. moniliformis has also been known as “Haverhillia multiformis”, which was named after a 1926 outbreak in Haverhill, MA that caused Haverhill fever, which is a form of RBF (8).
4. Morphology
S. moniliformis are Gram-negative bacteria that are rod-shaped (bacillus), non-encapsulated, non-spore forming, and are susceptible to decolorization by acids during staining (9). Under the microscope, S. moniliformis are often described as “string of beads” or a necklace, as the cells can be arranged in chains (filamentous) or clumps (10). The bacteria have a highly variable appearance (pleomorphic) because they often vary in size and shape. For instance, they can be as small as 0.1 μm to 3.5 μm and have been observed to have a spindle-like shape (fusiform) or long strand that resembles hair (10). S. moniliformis grows best on supplemented anaerobic blood agar and serum supplemented thioglycolate broth, on which it forms small gray-white colonies with adjacent pinpoint colonies on the former and loose, fluffy colonies in the latter (11).
5. Genome structure
The genome of S. moniliformis consists of 1,673,280 base pairs and is arranged in a single circular chromosome with one plasmid. 93.04% of the genome is coding and 26.28% of the genome consists of G+C bases (12). A total of 1,566 genes have been identified, with 1,511 being protein-coding genes, but only 67.31% of the genes have been predicted to have functions like translation of ribosomal structure, carbohydrate transport and metabolism, and cell membrane biogenesis (12). There have only been 55 observed RNA genes (12). Additionally, there has been one CRISPR repeat observed (12). It is unclear whether there are reported genes involved in pathogenesis (12).
6. Metabolic processes
S. moniliformis is a chemoheterotroph, using carbohydrates as an energy source, and monosaccharides and starch as carbon sources (12). The bacterium does not produce catalase or oxidase enzymes, suggesting that the bacterium uses fermentation for metabolism. The bacterium produces acid from metabolism of glucose, fructose, maltose, and starch, but no gas (12). There is disagreement regarding the oxygen requirements of the bacterium: S. moniliformis has been classified as a facultative anaerobe (13) and a microaerophile (14), while S. moniliformis isolated from guinea pigs specifically has been shown to behave as an obligate anaerobe (15).
7. Ecology
S. moniliformis survives in mammalian hosts. Rats are the most common carriers of S. moniliformis and harbor the bacteria in their upper respiratory tract (13). S. moniliformis has low pathogenicity in rats (13). Mice often harbor the bacterium and experience infection symptoms, such as enlargement of the lymph nodes and formation of small abscesses (13, 14). S. moniliformis in guinea pigs caused similar clinical symptoms as those in mice, such as lymph node enlargement (13). There have also been cases of S. moniliformis colonization in gerbils, ferrets, cats, dogs, turkeys, nonhuman primates, and koalas (13, 14). Most S. moniliformis cases have been reported from the United States, yet the bacterium is found worldwide, including many European countries, Australia, Canada, Mexico, Brazil and Paraguay. Few cases have been reported from Africa and Asia (14). Furthermore, there have been conflicting findings regarding the oxygen requirements of the bacterium, as one study stating that the bacterium is a facultative anaerobe while another study stating that it is a microaerophile, necessitating further research (13, 14).
8. Host Range and Susceptibility
S. moniliformis is able to infect all humans, however, the highest number of RBF cases are reported in children and young adults (4). Children account for over 50% of RBF cases in the United States (14). Older adults (greater than or equal to the age of 60) who are suffering with RBF stay at hospitals for longer periods of time in comparison to children and young adults, although older adults have lower rates of hospitalization (4). RBF hospitalization also differs by race: White populations have similar rates of hospitalization, but the Black and Hispanic population vary in rates of hospitalization. 85% of people infected with RBF live in an urban setting (4).
9. Transmission
Typically, Streptobacillus moniliformis is spread through bites from rats, leading to the nickname of RBF (16). It is also possible to become infected due to rat handling (2) or intake of contaminated substances from rats, such as food, drinking water, or feces (17). Haverhill fever is a term used to describe RBF contracted by such indirect contact (3). The speed of infectivity is not entirely understood, making infection rate difficult to assess. Symptoms appear between 3-21 days after infection, yet most people start showing symptoms 3-10 days after being infected (4).
10. Pathology
The most common symptoms of RBF observed in humans consist of high fever, rashes, joint and muscle pain, nausea, vomiting, and headaches (2). Haverhill fever presents with more severe gastrointestinal symptoms (3). Infection may lead to bacterial endocarditis (inflammation of the inner lining of the heart), pericarditis (inflammation of the pericardium), bronchitis (inflammation of the lining of the bronchial tubes), and persistent arthritis (swelling/tenderness of the joint). Children and infants who have been infected commonly experience anemia, weight loss, and diarrhea (2). While other symptoms have been observed, such as signs of pneumonia (17), they seem to be on an individual basis and not found in most cases. If left untreated in infants or those with pre-existing heart disease, RBF is likely to prove fatal (2).
8. Current Research
Include information about how this microbe (or related microbes) are currently being studied and for what purpose
9. References
It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.