tularemia

Definition

Tularemia is an illness caused by a bacterium. It results in fever, rash, and greatly enlarged lymph nodes.

Description

Tularemia infects a variety of wild animals, including rabbits, deer, squirrels, muskrat, and beaver. Humans can acquire the bacterium directly from contact with the blood or body fluids of these animals, from the bite of a tick or fly which has previously fed on the blood of an infected animal, or from contaminated food or water.

Tularemia occurs most often in the summer months. It is most likely to infect people who come into contact with infected animals, including hunters, furriers, butchers, laboratory workers, game wardens, and veterinarians. In the United States, the vast majority of cases of tularemia occur in the southeastern and Rocky Mountain states.

— Rosalyn Carson-DeWitt, MD

[New Latin, after Tulare, a county of south-central California.]

A worldwide disease caused by infection with the bacterium Francisella tularensis, which affects multiple animal species. Infection in humans occurs frequently from skinning infected animals bare-handed or from the bites of infected animals, ticks, deer flies. The mortality rate varies by species, but with treatment it is low. Ungulates are frequently infected but generally suffer low mortality.

Tularemia can be difficult to differentiate from other diseases because it can have multiple clinical manifestations. Nonspecific signs frequently include fever, lethargy, anorexia, and increased pulse and respiration rates. The disease can overlap geographically with plague, and both may lead to enlarged lymph nodes (buboes). However, with tularemia, the buboes are more likely to ulcerate. If tularemic infection results from inhalation of dust from contaminated soil, hay, or grain, either pneumonia or a typhoidal syndrome can occur. Rarely, the route of entry for the bacteria is the eyes, leading to the oculoglandular type of tularemia. If organisms are ingested, the oropharyngeal form can develop, characterized by abdominal pain, diarrhea, vomiting, and ulcers. See also Plague.

Tularemia is not transmitted directly from individual to individual. If the infected person or animal is untreated, blood remains infectious for 2 weeks and ulcerated lesions are infectious for a month. Deer flies (Chrysops discalis) are infective for 2 weeks, and ticks are infective throughout their lifetime (usually 2 years).

A number of antibacterial agents are effective against F. tularensis, the most effective being streptomycin. Penicillin and the sulfonamides have no therapeutic effect. See also Antibiotic.

Tularemia is a potentially severe and fatal bacterial zoonosis caused by a gram-negative coccobacillus, Francisella tularensis. Tularemia occurs only in the Northern Hemisphere, most commonly in the United States and Europe. In nature, infection occurs mostly in rodents, rabbits, and hares. Humans become infected by handling infectious animal carcasses; eating or drinking contaminated food or water; being bitten by infective ticks, flies, or mosquitoes; or by inhaling contaminated aerosols. The disease is not transmitted person-to-person. The more severe F. tularensis strain A occurs only in the United States and Canada, while the milder strain B occurs throughout the Northern Hemisphere.

Tularemia in humans is relatively rare, and it takes several forms, depending on the route of inoculation. The ulceroglandular form is the most common. It is characterized by an ulcer that develops where infection has penetrated the skin, accompanied by painful swelling of nearby lymph glands. Other forms include the glandular, oculoglandular, oropharyngeal, pneumonic, intestinal, and septic ("typhoidal") types. Following a usual incubation period of three to five days (sometimes longer), all forms have similar acute onsets of fever, headache, musculoskeletal pain, progressive weakness, and weight loss. Patients with tularemia pneumonia typically develop a cough with minimal or no sputum production, chest pain, and difficulty in breathing. Patients with the septic form sometimes develop complications of bleeding, respiratory failure, and shock. All forms can be cured by treatment with antibiotics such as streptomycin, gentamicin, or tetracyclines. The disease can be fatal if not treated early with appropriate antibiotics.

Tularemia is best prevented by avoiding sick or dead animals, protecting against tick and insect bites, and by sanitary practices that protect against contamination of food and water by infected animals.

(SEE ALSO: Vector-Borne Diseases; Zoonoses)

Bibliography

Beran, G. W. (1994). Handbook of Zoonoses, 2nd edition. Boca Raton, FL: CRC Press.

Dennis, D. T. (1998). "Tularemia." In Maxcy-Rosenau-Last Public Health and Preventive Medicine, 14th edition, ed. R. B. Wallace. Stamford, CT: Appleton & Lange.

— DAVID T. DENNIS

Tularemia is a plague-like disease caused by the bacterium Francisella tularensis. U.S. weapons stores of tularemia bacteria were reported destroyed in 1973. Until the demise of the Soviet Union, its biological weapons development program actively developed strains of the bacterium that were resistant to antibiotics and vaccines. As of March 2003, the whereabouts and disposition of some Soviet era tularemia stocks remains uncertain.

Tularemia is listed as potential bioterrorist weapon because it is easily obtained and potentially lethal.

World Health Organization (WHO) estimates hypothesize that if 50 kg of "weaponized" or highly virulent bacterium Francisella tularensis was dispersed in aerosol form over a large city, depending on weather and exposure patterns, there could be as many as 250,000 infections resulting in a projected 19,000 deaths.

Tularemia bacterium is transferred to humans from animals (i.e., a zoonosis) such as rodents, voles, mice, squirrels, and rabbits. Reflecting the natural origin of the disease, tularemia is also known as rabbit fever. Indeed, the rabbit is the most common source of the disease. Transfer of the bacterium via contaminated water and vegetation is possible as well.

The disease can easily spread from the environmental source to humans (although direct person-to-person contact has not been documented). This contagiousness and the high death rate among those who contract the disease made the bacterium an attractive bioweapon. Both the Japanese and Western armies experimented with Francisella tularensis during World War II. Experiments during and after that war established the devastating effect that aerial dispersion of the bacteria could exact on a population.

Tularemia naturally occurs over much of North America and Europe. In the United States, the disease is predominant in south-central and western states such as Missouri, Arkansas, Oklahoma, South Dakota, and Montana. The disease almost always occurs in rural regions. The animal reservoirs of the bacterium become infected typically by a bite from a blood-feeding tick, fly, or mosquito.

The causative bacterium, Francisella tularensis is a Gram-negative bacterium that, even though it does not form a spore, can survive for protracted periods of time in environments such as cold water, moist hay, soil, and decomposing carcasses.

The number of cases of tularemia in the world is not known, as accurate statistics have not been kept, and because illnesses attributable to the bacterium go unreported. In the United States, the number of cases used to be high. In the 1950s, thousands of people were infected each year. This number has dropped considerably, to less than 200 each year, and those who are infected now tend to be those who are exposed to the organism in its rural habitat (e.g., hunters, trappers, farmers, and butchers).

Humans can acquire the infection through breaks in the skin and mucous membranes, by ingesting contaminated water, or by inhaling the organism. An obligatory step in the establishment of an infection is the invasion of host cells. A prime target of invasion is the immune cell known as macrophages. Infections can initially become established in the lymph nodes, lungs, spleen, liver, and kidney. As these infections become more established, the microbe can spread to tissues throughout the body.

Symptoms of tularemia vary depending on the route of entry. Handling an infected animal or carcass can produce a slow-growing ulcer at the point of initial contact and swollen lymph nodes. When tularemia is inhaled, the symptoms include the sudden development of a headache with accompanying high fever, chills, body aches (particularly in the lower back) and fatigue. Ingestion of the organism produces a sore throat, abdominal pain, diarrhea, and vomiting. Other symptoms can include eye infection and the formation of skin ulcers. Some people also develop pneumonia-like chest pain. An especially severe pneumonia develops from the inhalation of one type of the organism, which is designated as Francisella tularensis biovar tularensis (type A). The pneumonia can progress to respiratory failure and death. The symptoms typically tend to appear three to five days after entry of the microbe into the body.

The infection responds to antibiotic treatment and recovery can be complete within a few weeks. Recovery produces a long-term immunity to re-infection. Some people experience a lingering impairment in the ability to perform physical tasks. If left untreated, tularemia can persist for weeks, even months, and can be fatal. The severe form of tularemia can kill up to 60% of those who are infected if treatment is not given.

A vaccine is available for tularemia. To date this vaccine has been administered only to those who are routinely exposed to the bacterium (e.g., researchers). The potential risks of the vaccine, which is a weakened form of the bacterium, have been viewed as being greater than the risk of acquiring the infection.

Further Reading

Books

Chin, J. "Tularemia." In Control of Communicable Diseases Manual. Washington, DC: American Public Health Association, 2000.

Dennis, D. T. "Tularemia." In: Wallace, R. B. ed. Maxcy-Rosenau-Last Public Health and Preventive Medicine, 14th edition. Stamford: Appleton & Lange, 1998.

A highly contagious disease of rodents caused by Francisella (Pasteurella) tularensis which may infect farm animals and humans. Biotype A, F. tularensis biovar tularensis, is prevalent in North America associated with tick-borne tularemia in rabbits and is more virulent than biotype B, F. tularensis biovar holarctica (palaearctica), which is found in Asia, Europe, and North America associated with mosquitoes and with water-borne disease in aquatic rodents and rarely causes disease in higher mammals. The clinical disease is very variable, depending on where the infection localizes.

A highly infections disease with symptoms that include a high fever, pneumonia, pleuritis. it can cause respiratory failure and death. Because it is highly infectious, it is a possible terrorist bacteriological agent.

Tularemia
Classification and external resources
A tularemia lesion on the dorsal skin of right hand.
ICD-10	A21.
ICD-9	021
DiseasesDB	13454
eMedicine	med/2326 emerg/591 ped/2327
MeSH	D014406

Tularemia (also known as "rabbit fever", "deer fly fever", "Ohara's fever" ^[1]:286) is a serious infectious disease caused by the bacterium Francisella tularensis.^[2] A gram-negative, non-motile coccobacillus, the bacterium has several subspecies with varying degrees of virulence. The most important of those is F. tularensis tularensis (Type A), which is found in lagomorphs in North America and is highly virulent for humans and domestic rabbits. F. tularensis palaearctica (Type B) occurs mainly in aquatic rodents (beavers, muskrats) in North America and in hares and small rodents in northern Eurasia. It is less virulent for humans and rabbits.^[3] The primary vectors are ticks and deer flies, but the disease can also be spread through other arthropods.^[2] The disease is named after Tulare County, California.

Contents 1 History 2 Epidemiology 3 Clinical manifestations and microbiological diagnosis 4 Treatment and prevention 5 Tularemia as a biological weapon 6 Documented outbreaks 7 External links 8 References

History

F. tularensis was discovered in 1911 during an outburst of rabbit fever, when the disease killed a large number of ground squirrels in the area of Tulare Lake in California. Scientists determined that tularemia could be dangerous to humans; a human being may catch the infection after contacting an infected animal. The ailment soon became frequent with hunters, cooks and agricultural workers.[1]

Epidemiology

The disease is endemic in North America, and parts of Europe and Asia. The most common mode of transmission is via arthropod vectors [citation needed]. Rodents, rabbits, hares often serve as reservoir hosts,^[4] but waterborne infection accounts for 5 to 10% of all tularemia in the US.^[5] Tularemia can also be transmitted by biting flies, particularly the deer fly Chrysops discalis. Individual flies can remain infective for 14 days and ticks for over two years. Tularemia may also be spread by direct contact with contaminated animals or material, by ingestion of poorly cooked flesh of infected animals or contaminated water, or by inhalation. The most likely method for bioterrorist transmission is through an aerosol.

In the United States, although records show that tularemia was never particularly common, incidence rates continued to drop over the course of the 20th century so that between 1990 and 2000, the rate was less than 1 per 1,000,000, meaning the disease is extremely rare in the US today.^[6]

Clinical manifestations and microbiological diagnosis

Depending on the site of infection, tularemia has six characteristic clinical syndromes: ulceroglandular (the most common type representing 75% of all forms), glandular, oropharyngeal, pneumonic, oculoglandular, and typhoidal.^[7]

The incubation period for tularemia is 1 to 14 days; most human infections become apparent after 3 to 5 days.^[8] In most susceptible mammals, the clinical signs include fever, lethargy, anorexia, signs of septicemia, and possibly death. Animals rarely develop the skin lesions seen in people. Subclinical infections are common and animals often develop specific antibodies to the organism. Fever is moderate or very high and tularemia bacillus can be isolated from blood cultures at this stage. Face and eyes redden and become inflamed. Inflammation spreads to the lymph nodes, which enlarge and may suppurate (mimicking bubonic plague). Lymph node involvement is accompanied by a high fever. Death occurs in less than 1% if therapy is initiated promptly.

A culture of Francisella tularensis.

The microbiologist must be informed when tularemia is suspected because F. tularensis requires special media for cultivation such as buffered charcoal and yeast extract (BCYE). It cannot be isolated in the routine culture media because of the need for sulfhydryl group donors (such as cystein). Serological tests (detection of antibodies in the serum of the patients) are available and widely used. Cross reactivity with Brucella can confuse interpretation of the results, and for this reason diagnosis should not rely only on serology. Molecular methods such as PCR are available in reference laboratories. The bacteria can 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. It has been contracted from inhaling particles from an infected rabbit ground up in a lawnmower (see below). Tularemia is not spread directly from person to person.^{[citation needed]}

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 pneumoniac and typhoidal forms of the disease, which however account for less than 10% of cases.^[9] Overall mortality was 7% for untreated cases, and the disease responds well to antibiotics with a fatality rate of about 1%. The exact cause of death is unclear, but it is thought to be a combination of multiple organ system failures.

Treatment and prevention

The drug of choice is Streptomycin.^[10] Tularemia may also be treated with gentamicin for ten days, tetracycline-class drugs such as doxycycline for 2–3 weeks,^[11] chloramphenicol or fluoroquinolones. An attenuated, live vaccine is available, but its use is restricted to high risk groups. Its use as post-exposure prophylaxis is not recommended.

Tularemia as a biological weapon

This section appears to contradict itself. Please help fix this problem. (May 2009)

The Centers for Disease Control and Prevention regard F. tularensis as a viable bioweapons agent, and it has been included in the biological warfare programs of the USA, USSR and Japan at various times.^[12] A former Soviet biological weapons scientist, Kenneth Alibek, has alleged that an outbreak of Tularemia among German soldiers shortly before the siege of Stalingrad was due to the release of F. tularensis by Soviet forces, but this claim is rejected by others who have studied the outbreak.^[13] In the US, practical research into using tularemia as a bioweapon took place in 1954 at Pine Bluff Arsenal, Arkansas, an extension of the Camp Detrick program.^[14] It was viewed as an attractive agent because:

• it is easy to aerosolize
• it is highly infective; 10-50 bacteria are required to infect
• it is non-persistent and easy to decontaminate (unlike anthrax)
• it is highly incapacitating to infected persons
• it has comparatively low lethality, which is useful where enemy soldiers are in proximity to non-combatants, e.g. civilians

The Schu S4 strain was standardized as Agent UL for use in the U.S. M143 bursting spherical bomblet. It was a lethal biological with an anticipated fatality rate of 40 to 60 percent. The rate-of-action was around three days, with a duration-of-action of 1 to 3 weeks (treated) and 2 to 3 months (untreated) with frequent relapses. UL was streptomycin resistant. The aerobiological stability of UL was a major concern, being sensitive to sun light, and losing virulence over time after release.^{[citation needed]}

The United States later changed the military symbol for UL to TT (wet-type) and ZZ (dry-type) in an effort to retain security on the identity of military biologicals. When the 425 strain was standardized as agent JT (an incapacitant rather than lethal agent), the Schu S4 strain's symbol was changed again to SR.^{[citation needed]}

No vaccine is available to the general public.^[15] The best way to prevent tularemia infection is to wear rubber gloves when handling or skinning rodents lagomorphs (as rabbits), avoid ingesting uncooked wild game and untreated water sources, wear long-sleeved clothes, and use an insect repellent to prevent tick bites.

Documented outbreaks

In the summer of 2000, an outbreak of tularemia in Martha's Vineyard resulted in one fatality, and brought the interest of the CDC as a potential investigative ground for aerosolized Francisella tularensis. Over the following summers, Martha's Vineyard was identified as the only place in the world where documented cases of tularemia resulted from lawn mowing.^[16]

An outbreak of tularemia occurred in Kosovo in 1999-2000.^[17]

In 2004, three researchers at Boston University Medical Center were accidentally infected with F. tularensis, after apparently failing to follow safety procedures.^[18]

In 2005, small amounts of F. tularensis were detected in the Mall area of Washington, DC the morning after an anti-war demonstration on September 24, 2005. Biohazard sensors were triggered at six locations surrounding the Mall. There were thousands infected however none were reported because health officials were never made aware to test for Tularemia, plus it is actually difficult to be tested, most believed they just contracted a very bad flu.^[19]

Tularemia is endemic in the Gori region of Georgia. Last outbreak was in 2006.^[20]

In 2007, a lab of Boston University's Center for Advanced Biomedical Research, where F. tularensis were being kept for research, was evacuated after smoke set off alarms. An investigation has later determined that an electrical problem was the culprit, and no bacterial contamination was found.

In July 2007, an outbreak was reported in the Spanish autonomous region of Castile and León and traced to the plague of voles infesting the region. Another outbreak had taken place ten years before in the same area.^[21]

External links

• CDC Emergency Preparedness and Response index for tularemia
• Agent Fact Sheet: Tularemia Center for Biosecurity
• BioHealthBase Bioinformatics Resource Center Database of Francisella tularensis sequences and related information.
• Soviet Army used 'rat weapon' during WWII
• Health Officials Vigilant for Illness After Sensors Detect Bacteria on Mall Agent Found as Protests Drew Thousands of Visitors Petula Dvorak Washington Post October 2, 2005
• Test Results Cited in Delay of Mall Alert CDC Explains Why Local Officials Weren't Told for Days About Bacterium Detection Susan Levine and Sari Horwitz Washington Post October 5, 2005
• Detailed CIDRAP overview of tularemia, including fatality statistics
• Biological alarm in Washington Did terrorists attack Washington with a deadly pathogen?

References

1. ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0. 
2. ^ ^{a b} Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 488–90. ISBN 0838585299. 
3. ^ Pearson A (1998). Zoonoses: biology, clinical practice, and public health control (Soulsby EJ, Palmer SL eds.). Oxford [Oxfordshire]: Oxford University Press. pp. 276–9. ISBN 0-19-262380-X. 
4. ^ Mörner T (December 1992). "The ecology of tularaemia". Rev. Sci. Tech. 11 (4): 1123–30. PMID 1305858. 
5. ^ Jellison WL, Owen C, Bell JF, Kohls GM (1961). "Tularemia and animal populations". Wildl Dis 17: 1–22. 
6. ^ Hayes E, Marshall S, Dennis D, et al. (March 2002). "Tularemia--United States, 1990-2000". MMWR 51 (JULIOes=181–4). PMID 11900351. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5109a1.htm. 
7. ^ Plourde PJ, Embree J, Friesen F, Lindsay G, Williams T (June 1992). "Glandular tularemia with typhoidal features in a Manitoba child". CMAJ 146 (11): 1953–5. PMID 1596844. 
8. ^ Office international des épizooties. (2000). Manual of standards for diagnostic tests and vaccines: lists A and B diseases of mammals, birds and bees. Paris, France: Office international des épizooties. pp. 494–6, 1394. ISBN 92-9044-510-6. 
9. ^ "Tularemia: Current, comprehensive information on pathogenesis, microbiology, epidemiology, diagnosis, treatment, and prophylaxis". CIDRAP. http://www.cidrap.umn.edu/cidrap/content/bt/tularemia/biofacts/tularemiafactsheet.html#_Overview_1+CIDRAP. Retrieved 2008-09-29. 
10. ^ Enderlin G, Morales L, Jacobs RF, Cross JT (July 1994). "Streptomycin and alternative agents for the treatment of tularemia: review of the literature". Clin. Infect. Dis. 19 (1): 42–7. PMID 7948556. 
11. ^ "Tularemia: FAQ About Tularemia". CDC. 2003-10-08. http://www.bt.cdc.gov/agent/tularemia/faq.asp. Retrieved 2008-09-29. 
12. ^ Dennis DT, Inglesby TV, Henderson DA, et al. (June 2001). "Tularemia as a biological weapon: medical and public health management". JAMA 285 (21): 2763–73. doi:10.1001/jama.285.21.2763. PMID 11386933. http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=11386933. 
13. ^ Sjöstedt A (June 2007). "Tularemia: history, epidemiology, pathogen physiology, and clinical manifestations". Ann. N. Y. Acad. Sci. 1105: 1–29. doi:10.1196/annals.1409.009. PMID 17395726. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0077-8923&date=2007&volume=1105&spage=1. 
14. ^ Kanti Ghosh, Tushar, Prelas, Mark, Viswanath, Dabir: Science and Technology of Terrorism and Counterterrorism. CRC Press, 2002. Page 97. ISBN 0824708709
15. ^ "Medscape & eMedicine Log In". http://www.medscape.com/viewarticle/431539. 
16. ^ Feldman KA, Enscore RE, Lathrop SL, et al. (November 2001). "An outbreak of primary pneumonic tularemia on Martha's Vineyard". N. Engl. J. Med. 345 (22): 1601–6. doi:10.1056/NEJMoa011374. PMID 11757506. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=11757506&promo=ONFLNS19. 
17. ^ www.cdc.gov
18. ^ Smith S (2005-03-29). "City tells BU to bolster safety of its medical labs". Boston Globe. http://www.boston.com/news/local/articles/2005/03/29/city_tells_bu_to_bolster_safety_of_its_medical_labs/. Retrieved 2007-05-09. 
19. ^ Dvorak P (2005-10-02). "Health Officials Vigilant for Illness After Sensors Detect Bacteria on Mall: Agent Found as Protests Drew Thousands of Visitors". Washington Post. p. C13. http://www.washingtonpost.com/wp-dyn/content/article/2005/10/01/AR2005100101209.html. Retrieved 2007-05-08. "A week after six bioterrorism sensors detected the presence of a dangerous bacterium on the Mall, health officials said there are no reports that any of the thousands of people in the nation's capital Sept. 24 have tularemia, the illness that results from exposure to the bacteria." 
20. ^ According to staff at Georgia's National Center for Disease Control, there was an outbreak of tularemia in the village of Zemo Rene east of Gori in December 2005 and January 2006. 26 persons tested positive for the bacteria, and 45 tested positive for antibodies. There were no fatal cases. The source was deemed to be a water spring. Previous outbreaks were in Tamarasheni (2005) and Ruisi (1997 and 1998).
21. ^ Diagnóstico de un brote de tularemia en Castilla-León (Spanish)

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