795.51 Nonspecific reaction to tuberculin skin test without active tuberculosis
ICD10
A15.7 Primary respiratory tuberculosis
A15.9 Respiratory tuberculosis unspecified
R76.11 Nonspecific reaction to skin test w/o active tuberculosis
TULAREMIA Scott Bentz BASICS DESCRIPTION
Tularemia is an acute febrile illness caused by the small aerobic gram-negative pleomorphic intracellular coccobacillus Francisella tularensis :
Organism is highly infectious.
Person-to-person transmission has not been reported.
Humans become infected through different environmental exposures:
Bites from infected tick, deerfly, mosquito, or other infected insect
Direct contact with infectious animal tissue or fluid
Contact with or ingestion of contaminated food, water, or soil
Inhalation of infected aerosols (e.g., cutting grass with power mowers, which may aerosolize the organism)
The 4 major strains of the bacterium have different virulence and geographic location:
2 subspecies cause human infection in North America: F. tularensis subspecies tularensis (type A, more virulent) and F. tularensis subspecies holartica (type B, less virulent)
Natural hosts:
Lagomorphs and other rodents
Found in species of wild animals (insects, rabbits, hares, ticks, flies, muskrats, beavers, mice), domestic animals (sheep, cattle, cats), ticks, and water and soil contaminated by infected animals
Natural vectors:
Ticks
Biting flies
Mosquitoes
Wild rabbits
Weaponization of tularemia was accomplished during the Cold War:
Because of its virulence and ability to be aerosolized, it remains a potential biologic agent for mass destruction.
Lab technicians handling culture specimens are at high risk:
F. tularensis cultures should be manipulated only in a biosafety level 3 facility.
Also known as “rabbit fever” or “deerfly fever”
ETIOLOGY
Individuals who spend time outdoors in endemic areas are at higher risk:
Farmers
Hunters
Forest workers
Those who handle animal carcasses are at highest risk (taxidermists and butchers).
Two-thirds of cases occur in males.
Although tularemia can occur worldwide, it is endemic in the northern hemisphere:
Reported nationwide except in Hawaii
States with the highest incidence include Missouri, Arkansas, Kansas, South Dakota, and Oklahoma.
Few hundred cases annually in US, although probably underreported
Peak season is June–October.
Mortality is 5–15%. Appropriately treated patients have mortality as low as 1%.
Pediatric Considerations
25% of cases occur in children 1–14 yr of age.
Children who spend time outdoors in endemic rural areas are at highest risk.
DIAGNOSIS SIGNS AND SYMPTOMS
Tularemia has different presentations based on route of entry:
Primary route of entry is through skin; most often a cutaneous ulcer develops.
Incubation is 3–5 days, range 1–14 days. Lesion usually begins as papule, often with fever.
6 forms of illness:
Ulceroglandular:
Most common presentation (70–80% of cases)
Inoculated cutaneously (scratch, abrasion, insect bite) with as few as 50 organisms
Initially, a local cutaneous papule at point of entry
Followed by tender regional adenopathy and constitutional symptoms to include fever, chills, myalgias, and headaches
Associated with pneumonia in 30% of cases
Glandular:
Rare form
Gains access to lymphatic system or bloodstream through inapparent abrasion
Tender regional lymphadenopathy with no local lesions
Oculoglandular:
Rare form
Organism enters through a splash of infected blood/fluid to the eye or is introduced by eye rubbing after handling infectious materials (e.g., rabbit carcass).
Edema, conjunctivitis, injection, chemosis with periauricular, submandibular, or cervical lymphadenopathy
Pharyngeal:
Rare form
From ingestion of contaminated food or water
Severe throat pain with exudative pharyngitis and regional lymphadenitis
Pneumonic:
Secondary to inhalation
Seen in sheep shearers, farmers, landscapers, and lab technicians
Fever, dry cough, and pleuritic chest pain develop.
Pneumonia can occur in 30% of patients with ulceroglandular tularemia
Typhoidal:
Historically, the typhoidal form defined as devoid of skin or mucous membrane lesion or remarkable lymph node enlargement.
No known point of entry (probably oral or respiratory).
Only when no route of infection can be established may the term still be acceptable.
In North America, where type A is prevalent, fulminant manifestations are reported, including severe sepsis, meningitis, endocarditis, hepatic failure, and renal failure.
Septicemia associated with type A tularemia is usually extremely severe and potentially fatal. High fever, abdominal pain, and diarrhea may occur early in the course of disease.
History
Exposure and epidemiologic risk factors can be helpful.
Sudden fever, chills, headaches
Progression of components of signs and symptoms may be useful in defining form of illness.
Physical-Exam
Fever
Tender, well-demarcated cutaneous ulcer
Tender regional lymphadenopathy; lymph nodes can develop fluctuance and spontaneously drain.
Exudative pharyngitis (with pharyngeal tularemia)
Ulcerations of the conjunctiva with pronounced chemosis (with oculoglandular tularemia)
DIAGNOSIS TESTS & NTERPRETATION Lab
No rapid diagnostic test available
Routine lab studies nonspecific:
CBC can be normal.
ESR might be slightly elevated.
CSF: May have increased protein or mild pleocytosis
LFTs are often abnormal.
Gram stain, cultures, and tissue biopsies:
Often negative
Blood cultures usually negative because of specific growth requirements
Enzyme-linked immunosorbent assay and polymerase chain reaction are available through reference labs.
Serum antibody titers:
Typically do not reach diagnostic levels until ≥10 days after the onset of illness
A single titer of at least 1:160 for tube agglutination is diagnostic for F. tularensis infection.
May not be elevated before day 11 of illness and generally are diagnostic after 16th day.
Imaging
Chest radiograph for:
Consolidative process, pleural effusions, and hilar adenopathy