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COCA Conference Call Summaries and Slides:
Tularemia (April 27, 2004)

NOTE: This document is provided for historical purposes only and may not provide our most accurate and up-to-date information. The most current Clinician's information can be found on the Clinician Home Page.

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Paul Mead, MD, MPH
Chief of Epidemiology, Microbiology, and Diagnostic Activity
Bacterial Zoonoses Branch, DVBID, NCID, CDC

Jeannine Petersen, PhD
Microbiologist, Diagnostic and Reference Laboratory
Bacterial Zoonoses Branch, DVBID, NCID, CDC

Please note: Data and analysis discussed in these presentations were current when presented. Data collection and analysis are ongoing in many cases, therefore updates may be forthcoming elsewhere on this website, through publications such as CDC's Morbidity and Mortality Weekly Report or other venues. Presentations themselves will not be updated. Please bear this in mind when citing data from these presentations.

OVERVIEW

MICROBIOLOGY

SUBSPECIES OF F. tularensis

Francisella tularensis can be divided into two major groups or subspecies, also known as biovars, on the basis of virulence testing, biochemical testing and epidemiological factors.

ECOLOGY

TRANSMISSION

HIGH RISK OCCUPATIONS

TULAREMIA IN THE UNITED STATES: EPIDEMIOLOGY

CLINICAL PRESENTATION

The clinical presentation of tularemia is extremely variable, and it depends upon the route of inoculation, the dose, and the virulence of the organism. Following an incubation period of about three to five days, patients with tularemia typically present with high fever accompanied by non-specific symptoms such as chills, headaches, myalgias, fatigue, sore throat, cough, shortness of breath, vomiting or diarrhea. A common finding of tularemia is prominent localized lymphadenopathy.

The six principal clinical syndromes of tularemia, include:

These different forms relate to the mode of transmission. Ulceroglandular tularemia is by far the most common form, accounting for approximately 45 to 85 percent of reported cases. It typically results from inoculation into the skin, either through the bite of an arthropod or through handling of contaminated animals or meat. Sometimes hunters will describe cutting themselves while attempting to butcher an animal, and then developing an ulcer at the site, followed by regional lympadenopathy. Oropharyngeal tularemia is acquired primarily through eating contaminated food or drinking contaminated water. Patients develop ulcers in the oropharynx and cervical lymphadenopathy. Pneumonic tularemia is often secondary to some other form of tularemia, but it can also occur through primary respiratory exposure.

Photographs are available that show an ulcer on the thumb of the patient with ulceroglandular tularemia with a large lymph node up in their axilla. There is also one of a patient with cervical lymphadenopathy due to oropharyngeal tularemia, and a chest radiograph for a patient with pulmonary tularemia. This provides a visual of the diverse range of syndromes that may be seen.

LABORATORY DIAGNOSIS

The clinical diagnosis of tularemia is confirmed by isolation of Francisella tularensis. Clinical suspicion is critical in directing the selection of the correct culture media, as well as ensuring the safety of laboratory workers. In addition, materials such as swabs from ulcers or wounds, lymph node aspirates, or tissue can be examined by direct fluorescent antibody. There are serologic assays, although these are generally less useful in the acute diagnosis.

The characteristics that should lead clinical laboratories to suspect Francisella tularensis include:

The organism is slow growing, requiring up to 72 hours, and may be difficult to recover in automated culture systems. Isolates that fit these characteristics should be referred to state laboratories for further work up and evaluation.

There are more specialized tests that can be performed at reference laboratories to presumptively identify Francisella tularensis. The most commonly used and available test is DFA or direct fluorescent antibody. In addition, a single positive serum sample is also used as presumptive diagnosis for tularemia.

Definitive confirmation of tularemia is based on recovery of an isolate grown on cysteine heart agar with the following characteristics: grows well at 37 degrees, but poorly at 25 degrees Celsius; has characteristic of colonial morphology; and tests positive by direct fluorescent antibody. Biochemical testing is considered supplemental.

Alternately, confirmation of tularemia can be based on a four-fold (or greater) titer change in paired sera, taken at least two weeks apart, with at least one of these titers being greater than 1:160 by tube agglutination, or 1:128 by microagglutination.

TREATMENT

PROPHYLAXIS

INFECTION CONTROL FOR PATIENTS

INFECTION CONTROL FOR THE LABORATORY

PREVENTION

Prevention is fairly straightforward, and in reference to ticks and to animal products exposure. It is generally recommended that people:

THREAT OF BIOLOGICAL WARFARE

I will end with this last quotation from Parker from 1934, which is sort of the classic quotation for tularemia. He says, “I know of no other infection of animals communicable to man that can be acquired from sources so numerous and so diverse. In short, one can but feel the status of tularemia, both as a disease in nature and of men is one of potentiality.”

QUESTION AND ANSWER SESSION

Dr. Dan Baden:

Dr. Mead, you mentioned that some of the organisms that were modified for bioweapon use had streptomycin resistance. I thought I heard this at least. In that case, what would be the drug of choice to use?

Dr. Paul Mead:

Well there are several alternatives as mentioned there, and they could include fluoroquinolones, such as ciprofloxacin. Doxycycline would be another alternative. Whether or not cross-resistance to streptomycin would pertain to gentamicin, I'm not entirely sure, but it may be that gentamicin would nevertheless be effective. That's probably the reason why it would be important to get susceptibility testing, particularly if there is any concern in the setting of a bioterrorist event. This is because the organism can be modified. And presumably, someone who went to the effort to intentionally produce and release such an organism might have also engineered some resistances. Although saying that, I think we sometimes overestimate the effort that people put into engineering these things, as indicated by some past events.

Dr. Dan Baden:

You mentioned current clusters. Would you elaborate?

Dr. Paul Mead:

Dr. Dan Baden:

I have a third question, if we could. In some scenarios of use of a bioweapon, like the one you outlined in the ideal conditions, people may not know until patients start showing up with symptoms. Is there any concern or do people who have relatively advanced disease respond fairly well to antibiotic treatment with tularemia?

Dr. Paul Mead:

Well, that's a little bit hard to say because the bioterrorism scenarios are often somewhat different than what you would expect to see normally. Again, tularemia can be a fairly mild illness that patients can have for a while, but under this scenario, it’s presumed that people would have a large exposure to an aerosolized form of tularemia. When you look across the various clinical syndromes of tularemia, certainly pneumonic tularemia has a considerably higher fatality rate, at least without antibiotics, than the other forms of tularemia. Currently, this mortality rate due to naturally occurring tularemia in the United States is under 2%. However, in the absence of antibiotics, pulmonary tularemia can be considerably more fatal, resulting in 50% or so mortality. Whether or not that would happen or whether the rate would be higher following a BT event would again depend a bit upon the dose that people were exposed to, whether or not it had been engineered to have additional virulence factors, whether or not it was antibiotic resistant.

I think in general, it’s reasonable to say that early appropriate treatment improves outcome in most infectious diseases and in tularemia. It’s a little bit less like plague where getting therapy early is critical. Nevertheless, if the patient is already in critical condition when diagnosed, they will likely have a higher mortality rate.

If there are others who would like to listen to the CD on this topic, please e-mail: coca@cdc.gov.

Page last modified July 20, 2004

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