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Key Diagnostic Tests.

Tularemia can present in several different ways depending upon the path of infection. In the case of an aerial attack, the most likely form will be pulmonary tularemia. Symptoms include a nonproductive cough, dyspnea (difficulty breathing) and pleuritic chest pain. However, a standard physical examination looks normal. Chest X-rays may reveal patchy infiltration and there may be development of lobar pneumonia.

In nature, infection is usually through the skin and mucous membranes (mouth, nose, lungs, eyes) by contamination with body fluids from infected animals or insects (the ulceroglandular form of the disease), or by being bitten by infected deer flies, mosquitoes, or ticks. Infection by inhalation of contaminated dust, or ingestion of contaminated food or water (the typhoidal form) is rarer. Fever and enlargement of the liver and spleen (hepatosplenomegaly) are common and a rash may be seen. Inflammation, ulceration or nodulation may be seen at the site of an infection.

• Recovery of the bacterium. This is difficult, as it is fastidious and grows very slowly in culture even in its preferred medium (glucose-cysteine-blood agar) and cultures have to be considered dangerous.
• Detection of antigens or antibody to the agent in the blood (serology) although some cross reactions are known, especially to Brucella;
• Agglutination tests
• Direct observationin blood: Gram stain is often unsuccessful and a modified Dieterle stain or immunofluorescence must be used.

Symptoms and effects.

After an incubation period of 2-10 days, the disease develops rapidly. Ulceroglandular tularemia begins with fever, chills, headaches, and malaise with a skin ulcer forming at the site of infection. Some 5-10% of cases do not give rise to a skin ulcer and the disease is then known as glandular tularemia. Typhoidal tularemia has symptoms of fever, prostration (extreme exhaustion), and weight loss but without the  ulceration of the skin. These non-specific symptoms make typhoidal tularemia difficult to diagnose. The disease can progress to the lungs and give rise a pneumonia (filling of the lungs with fluid). A key sign is lymphadenopathy that is usually more extensive than in other diseases.

In the event of the organism being used as an aerosol weapon, pneumonic tularemia is most likely. Common symptoms of this form are a dry cough, difficulty breathing and pleurisy-like chest pain. In some cases these symptoms are not seen and the disease progresses directly to a systemic infection.

A tularemia skin ulcer. Photograph: R. Brachman, courtesy of the Public health Image Library, Centers for Disease Control.

 Medical and Physical Countermeasures.

 Vaccination (Immunoprophylaxis)

A live attenuated vaccine that can give significant protection against typhoidal tularemia is at an advanced stage of development. It is administered by scarification, the method used for smallpox vaccines.

Antibiotics

The disease responds well to antibiotics. Intramuscular injection of streptomycin (1 gram every 12 hours for 10-14 days) is the treatment of choice. Gentamicin (3-5 milligrams per kilogram of body weight per day for 10-14 days) is also effective. Tetracyclines and chloramphenicol are useful, but the disease often returns after treatment has ended.

Antibiotic resistance

Supportive care

Treatment of symptoms including maintaining fluids and the use of antipyretics are helpful.

Decontamination

The bacterium is sensitive to heat and is killed by heating to 55°C for 10 minutes and with standard disinfectants.

Agent Properties and Potential Uses

Francisella tularensis is one of the most infective agents known with the effective dose needed to develop the disease is in the range of a few tens of bacteria. Typically, 90-100% of those exposed to the bacterium develop disease. This means that an attack with this agent against an unprotected populace would be extremely disabling and could cause a large number of deaths. The mortality rate for typhoidal tularemia is 30-60%. The most likely method of delivery is as an aerosol. The result of this would be an epidemic of pneumonic tularemia.

The bacterium is tolerant of low temperatures and can survive in surface waters.

Terrorist Acquisition and Attempted Use.

• None known

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The History and Natural History of Tularemia.

There are two forms or biotypes of F. tularensis. Type A, which is the more virulent, is found in rabbits and their relatives (the lagomorphs) and is common in North America and type B, also known as Francisella tularemia palaearctica is found in Europe and Asia and uses rodents (rats, mice and their relatives) as hosts. Natural sources of transmission include the bites of blood sucking ticks and insects or from water contaminated by infected animals. The commonest source of human infection is from contaminated rabbit meat. An outbreak of a mild form of the disease in Kosovo in the winter and spring of early 2000 was due to an increase in the rat population as a result of the breakdown of garbage collection af the war of separation from Yugoslavia.

The bacterium prefers cooler weather and its natural homes are north of the tropics. It is not found in Mexico or south of the Mediterranean. Ken Alibek (formerly Kanatjan Alibekov) a former senior scientist in the Soviet BW program reports that the Soviet Union was working on the use of the organism before World War II and he believes that an outbreak of tularemia in German forces in Russia may have been as a result of deliberate use of the agent. Alibek himself may have been a victim of the disease during an accident involving a leak in a fermentor.

It is actually difficult to perceive of a Soviet Union with its industrial base either in ruins or being moved east of the Urals being able to find the resources to mount an effective biological attack. The real explanation may be more mundane. Eric Croddy of the Monterey Institute of International Studies, has examined health records from the time. He found that tularemia was already rampaging in the local populace when the deadlock at Stalingrad set in. Fighting had prevented harvesting of crops and the rodent populations that act as carriers for the disease had exploded. The fighting had also destroyed the public health infrastructure. The two circumstances together cleared the way for an epidemic. It also turns out that the disease attacked not only German soldiers, but also Soviet forces and seriously crippled Soviet air forces at one point. Infection may have been higher in German forces because they had always been trained to turn over hay before sleeping on it. The fine dust suspension containing rodent urine and feces could have increased the efficiency of transmission.

The extremely low infectious dose and the crippling symptoms have made this organism an extremely attractive candidate as a biological weapon, even though it is relatively difficult to culture.

Not to be used as a substitute for an official Material Safety Data Sheet.

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