Tularemia overview
|
Tularemia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Tularemia overview On the Web |
|
American Roentgen Ray Society Images of Tularemia overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Tularemia is a serious infectious disease caused by the bacterium Francisella tularensis. The disease is endemic in North America, and parts of Europe and Asia. The primary vectors are ticks and deer flies, but the disease can also be spread through other arthropods. Animals such as rabbits, prairie dogs, hares and muskrats serve as reservoir hosts. The disease is named after Tulare County, California.
Historical Perspective
Franciscella tularensis was first discovered by George Walter McCoy in 1911. The organism was originally named Bacterium tularense, after Tulare county where the causative agent was first discovered. Expounding upon McCoy's previous research, Dr. Edward Francis furthered global understanding of tularemia, through the discovery of animal reservoirs, vectors, and clinical manifestations. The ailment soon became frequent with hunters, cooks and agricultural workers.[1] Tularemia was later identified as a potential tool for bio-terrorism.
Classification
Tularemia may be classified according the original mode of transmission. The mode of transmission will ultimately dictate the resulting clinical manifestations associated with tularemia infections. There are five common forms of tularemia, they include ulceroglandular, glandular, oculoglandular, oropharyngeal, and pneumonic.[2]
Pathophysiology
Francisella tularensis is an extremely infectious bacteria; 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. 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 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
Francisella is a genus of pathogenic, Gram-negative bacteria.They are small coccobacillary or rod-shaped, non motile organisms, which are also intracellular parasites of macrophages.[3] Francisella colonies bear a morphological resemblance to those of the genus Brucella.[4] 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 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.
Differential Diagnosis
General symptoms reported within the early stages tularemia often resemble those of other tick-borne diseases. These symptoms include fever, chills, headache, and other non-specific flu like symptoms. Later stages of tularemia may include pneumonic clinical manifestations and ulcers in the epidermal tissue.[2]
Epidemiology and Demographics
Tularemia has long been a silent disease plaguing the worldwide community. However, it is difficult to quantify the total worldwide incidence since tularemia is rarely reported. North America and Eurasia are commonly referred to as endemic areas. The majority of cases in the United States have been reported in the South-central and Western states. Seasonal distribution of tularemia infection shows a higher incidence between June and September. A higher incidence has also been reported in children under the age of 10 years.
Risk Factors
The greatest risk factor for contracting tularemia is the bite of an infected tick. Other risk factors include handling contact with infected animals, contamination of water sources, and potential bio-terrorism. Individuals are at a higher risk of infection during the late spring and summer months. Children and males are at a higher risk of infection.
Natural History, Complications & Prognosis
The disease has a very rapid onset, with headache, fatigue, dizziness, muscle pains, loss of appetite and nausea. 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. Complications may include pneumonia, meningitis, endocarditis, hepatitis, sepsis, or osteomyelitis. The prognosis is usual good for common forms of tularemia. However a high mortality rate is associated with pneumonic and typhoidal variations.[2]
History and Symptoms
Symptoms associated with tularemia often include non-specific flu like symptoms. As the disease progresses tularemia will differentiate into five more specific variations. Symptoms and clinical manifestations will differentiate according to the type of tularemia infection.
Physical Examination
Typically signs of tularemia include a biphasic fever, tachycardia, and changes in blood pressure. Depending on the mode of transmission, tularemia may also cause skin ulcers, eye infection, or swelling of the throat.
Laboratory Findings
There are a variety of lab diagnostic tests used to diagnose tularemia including Gram-stains, bacteria cultures,biochemical,and antibody fluorescence tests. Gram-stains and bacteria cultures are useful in identifying F.tularensis. Unfortunately, these diagnostics offer difficult interpretations with extensive procedures. Antibody fluorescence allows for quick and effective testing. This method is extraordinarily important in diagnosing pneumonic variations of tularemia, as these variations are often associated with a higher mortality rate.
Other Diagnostic Findings
Other diagnostic studies for tularemia include the examination of secretions, fluorescent antibody testing, and immunohistochemical staining. These test demonstrate rapid procedures that provide accurate detection of F. tularensis within a few hours of specimen collection.
Medical Therapy
The mainstay of therapy for tularemia is antimicrobial therapy. The drug of choice is Streptomycin. Other pharmacologic therapies for tularemia include Gentamicin, Tetracyclines, Chloramphenicol, or Fluoroquinolones.
Prevention
Tularemia prevention strategies are based on avoiding potentially, infected, tick bites or animal flesh and fecal matter. Avoiding tick bites may be accomplished through limited exposure to endemic areas. However if it is impossible or impractical to avoid these areas, several preventative strategies may be implemented. These strategies are indicated under the Prevention title below. Other prevention strategies include a proper removal of the tick. This process is also outlined below under the title, the best way to remove a tick. Other strategies include daily cleaning, to avoid fecal matter in dust, or proper attire during butchery.
References
- ↑ English Pravda. Tularemia. http://english.pravda.ru/main/18/90/363/14923_tularemia.html
- ↑ 2.0 2.1 Centers for Disease Control and Prevention, Signs and Symptoms of Tularemia. http://www.cdc.gov/tularemia/signssymptoms/index.html Accessed March 1, 2016
- ↑ 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.