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Bio-Terror Agents

    TULAREMIA

    BIOTERRORBIBLE.COM: There is an ever expanding list of potential bio-terror agents that could be used in a bio-terror attack, but anthrax, smallpox and flu are the only “threats” the government appears worried about. These 3 agents will likely be used the same way that they were used in the U.S. government bio-terror war-games entitled Dark Winter and Atlantic Storm.

    Title: Tularemia
    Date: 2012
    Source: Wikipedia

    Abstract: Tularemia (also known as Pahvant Valley plague, rabbit fever, deer fly fever, and Ohara's fever:286) is a serious infectious disease caused by the bacterium Francisella tularensis. A Gram-negative, nonmotile 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 in 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. The primary vectors are ticks and deer flies, but the disease can also be spread through other arthropods. The disease is named after Tulare County, California.

    History


    Ancient

    F. tularensis has been identified as the cause of human outbreaks in ancient Canaan in about 1715 BC and in 1075 BC. A long-lasting epidemic that plagued the eastern Mediterranean in the 14th century BC was also traced back to a focus in Canaan along the Arwad-Euphrates trading route. According to Siro I. Trevisanato, this epidemic contaminated an area stretching from Cyprus to Iraq, and from Israel to Syria, sparing Egypt (due to a quarantine) and Anatolia (owing to effective political boundaries). Subsequently, wars are believed to have spread the same disease into central Anatolia, from whence it was deliberately introduced into western Anatolia, in acts constituting the first known record of biological warfare.[6]. Finally, Aegean soldiers fighting in western Anatolia returned home to their Greek islands, further spreading the same epidemic.

    Modern
    The tularemia bacterium was first isolated by G.W. McCoy of the U.S. Public Health Service plague lab and reported in 1912. Scientists determined 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.

    Epidemiology

    The disease is endemic in North America, and parts of Europe and Asia. The most common mode of transmission is via arthropod vectors. Ticks involved include Amblyomma, Dermacentor, Haemaphysalis, and Ixodes.[10] Rodents, rabbits, and hares often serve as reservoir hosts, but waterborne infection accounts for 5 to 10% of all tularemia in the US. 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.

    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 between 1990 and 2000, the rate was less than 1 per 1,000,000, meaning the disease is extremely rare in the US today.[13]
    Clinical manifestations and microbiological diagnosis

    Clinical Manifestations & 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.

    The incubation period for tularemia is one to 14 days; most human infections become apparent after three to five days.In most susceptible mammals, the clinical signs include fever, lethargy, anorexia, signs of septicemia, and possibly death. Nonhuman mammals 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 bacilli can be isolated from blood cultures at this stage. The 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.

    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 cysteine). 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, so 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.

    Francisella tularensis is an intracellular bacterium, meaning it is able to live as a parasite within host cells. It primarily infects macrophages, a type of white blood cell, thus is able to evade the immune system. The course of disease involves the spread of the organism to multiple organ systems, including the lungs, liver, spleen, and lymphatic system. The course of disease is different depending on the route of exposure. Mortality in untreated (before the 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.[16] 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 & Prevention
    The drug of choice is streptomycin. Tularemia may also be treated with gentamicin for ten days, tetracycline-class drugs such as doxycycline for two to three weeks, chloramphenicol or fluoroquinolones. An attenuated, live vaccine is available, but its use is only for high risk groups. Its use as postexposure prophylaxis is not recommended.

    Tularemia as a Biological Weapon
    The Centers for Disease Control and Prevention (CDC) regard F. tularensis as a viable biological warfare agent, and it has been included in the biological warfare programs of the United States, Soviet Union and Japan at various times. 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. Others who have studied the pathogen "propose that an outbreak resulting from natural causes is more likely". In the US, practical research into using rabbit fever as a biological warfare agent took place in 1954 at Pine Bluff Arsenal, Arkansas, an extension of the Camp Detrick program.

    It was viewed as an attractive agent because:

    1. It is easy to aerosolize,
    2. It is highly infective; 10-50 bacteria are required to infect,
    3. It is nonpersistent and easy to decontaminate (unlike anthrax),
    4. It is highly incapacitating to infected persons,
    5. It has comparatively low lethality, which is useful where enemy soldiers are in proximity to noncombatants, e.g. civilians.

    The Schu S4 strain was standardized as "Agent UL" for use in the United States M143 bursting spherical bomblet. It was a lethal biological warfare agent with an anticipated fatality rate of 40 – 60%. The rate-of-action was around three days, with a duration-of-action of one to three weeks (treated) and two to three months (untreated), with frequent relapses. UL was streptomycin resistant. The aerobiological stability of UL was a major concern, being sensitive to sunlight, and losing virulence over time after release. 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.

    Both wet and dry types of F. tularensis (identified by the codes TT and ZZ) were examined during the "Red Cloud" tests, which took place from November 1966 to February 1967 in the Tanana Valley, Alaska.

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

    Documented Outbreaks
    From May to October 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.

    An outbreak of tularemia occurred in Kosovo in 1999-2000.

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

    In 2005, small amounts of F. tularensis were detected in the Mall area of Washington, DC the morning after an antiwar demonstration on September 24, 2005. Biohazard sensors were triggered at six locations surrounding the Mall. While thousands of people were potentially exposed, no infections were reported. The detected bacteria likely originated from a natural source, not from a bioterror attempt.

    Tularemia is endemic in the Gori region of the Eurasian country of Georgia. The last outbreak was in 2006.

    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.

    In August 2009, a Swedish tourist was bitten by an unidentified insect at Point Grey, Vancouver, BC, Canada. It was not until after return to Sweden that he was diagnosed with tularemia, despite seeking medical treatment in Vancouver.[citation needed]

    In Jan 2011, researchers searching for brucellosis among feral hog populations in Texas discovered widespread tularemia infection or evidence of past infection in feral hog populations of at least 2 Texas counties, even though tularemia is not normally associated with pigs at all. Precautions were recommended for those who hunt, dress, or prepare feral hogs. Since feral hogs roam over large distances, there is concern that tularemia may spread or already be present in feral hogs over a very wide geographic area.

    In June 2011, in Armenia, Mrgahovit village of Lori Marz two people were infected.[citation needed]

    In November 2011, it was found in Tasmania, Australia. Reports claimed it to be the first in the southern hemisphere. However, the causative organism was documented to have been isolated from a foot wound in the Northern Territory, Australia in 2003 
    (Wikipedia, 2012).