Francisella
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Francisella is a genus of pathogenic, Gram-negative bacteria.They are small coccobacillary or rod-shaped, non motile organisms, which are also facultative intracellular parasites of macrophages.[1] Strict aerobes, Francisella colonies bear a morphological resemblance to those of the genus Brucella.[2] The bacteria penetrate into the body through damaged skin and mucous membranes, or through inhalation. Humans are most often infected by tick bite or through handling an infected animal. Ingesting infected water, soil, or food can also cause infection. Tularemia can also be acquired by inhalation; hunters are at a higher risk for this disease because of the potential of inhaling the bacteria during the skinning process.
Francisella tularensis is an intracellular bacterium, meaning that it is able to live as a parasite within host cells. It primarily infects macrophages, a type of white blood cell. It is thus able to evade the immune system. The course of disease involves spread of the organism to multiple organ systems, including the lungs, liver, spleen, and lymphatic system.
Causes
Causative Agent
- The type species, F. tularensis, causes the disease tularemia or rabbit fever.[3] F. novicida and F. philomiragia (previously Yersinia philomiragia) are associated with septicemia and invasive systemic infections.
- It should be noted that the taxonomy of the genus is somewhat uncertain, especially in the case of F. novicida (may be a subspecies of F. tularensis).
- In general, identification of species is accomplished by biochemical profiling or 16S rRNA sequencing.
- F. tularensis is found in widely diverse animal hosts and habitats and can be recovered from contaminated water, soil, and vegetation.
- A variety of small mammals, including voles, mice, water rats, squirrels, rabbits, and hares are natural reservoirs of infection. [4]
- They acquire infection through tick, fly, and mosquito bites and by contact with contaminated environments. [5]
- Epizootics with sometimes extensive die-offs of animal hosts may herald outbreaks of tularemia in humans.
- Humans can become incidentally infected through diverse environmental exposures: bites by infected arthropods; handling infectious animal tissues or fluids; direct contact with or ingestion of contaminated food, water, or soil; and inhalation of infective aerosols.
- Humans can develop severe and sometimes fatal illness, but do not transmit the disease to others. [4]
Genomics
- Studies conducted on a strain of the Schu S4 genome report a genome size of less than 2 Mbp.
- F. tularensis is composed of a large majority of genes, unique to the species.
- Lesser amount of genes responsible for the encoding of transport and binding.
- There are few matches for genes responsible for gene regulation and energy metabolism between F. tularensis and other documented
Pathogenesis
Mechanism of infection
- Francisella tularensis is one of the most infectious bacteria known; fewer than ten organisms can cause disease leading to severe illness.
- The bacteria penetrate into the body through damaged skin and mucous membranes, or through inhalation.
- Humans are most often infected by tick bite or through handling an infected animal. Ingesting infected water, soil, or food can also cause infection.
- Tularemia can also be acquired by inhalation; hunters are at a higher risk for this disease because of the potential of inhaling the bacteria during the skinning process.
- Tularemia is not spread directly from person to person.
- Francisella tularensis is an intracellular bacterium, meaning that it is able to live as a parasite within host cells.
- It primarily infects macrophages, a type of white blood cell. It is thus able to evade the immune system.
- The course of disease involves spread of the organism to multiple organ systems, including the lungs, liver, spleen, and lymphatic system.
- The course of disease is similar regardless of the route of exposure. Mortality in untreated (pre-antibiotic-era) patients has been as high as 50% in the pneumonic and typhoidal forms of the disease, which however account for less than 10% of cases.[6]
- Overall mortality was 7% for untreated cases, and the disease responds well to antibiotics with a fatality rate of about 2%.
- The exact cause of death is unclear, but it is thought be a combination of multiple organ system failures.
References
- ↑ Allen LA (2003). "Mechanisms of pathogenesis: evasion of killing by polymorphonuclear leukocytes". Microbes Infect. 5 (14): 1329–35. PMID 14613776.
- ↑ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. pp. 488&ndash, 90. ISBN 0-8385-8529-9.
- ↑ Collins FM (1996). Pasteurella, Yersinia, and Francisella. In: Baron's Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1.
- ↑ 4.0 4.1 Tularemia. Ellis J, Oyston PC, Green M, Titball RW. Tularemia. Clin Microbiol Rev. 2002;15(4):631-46. http://www.ncbi.nlm.nih.gov/pubmed/12364373 Accessed March 28, 2016
- ↑ Francisella tularensis Bacteria Associated with Feline Tularemia in the United States. Larson MA, Fey PD, Hinrichs SH, Iwen PC. Francisella tularensis bacteria associated with feline tularemia in the United States. Emerging Infect Dis. 2014;20(12):2068-71. Accessed March 28, 2016
- ↑ Tularemia. CIDRAP. http://www.cidrap.umn.edu/cidrap/content/bt/tularemia/biofacts/tularemiafactsheet.html#_Overview_1 Accessed March 28, 2016