Ulceroglandular tularemia is the most common clinical form of tularemia, caused by the gram-negative intracellular coccobacillus Francisella tularensis. It is characterized by a cutaneous ulcer at the inoculation site with painful regional lymphadenopathy, typically following a tick bite or direct contact with infected animals. [1-3] It is a CDC Category A bioterrorism agent due to its extremely low infectious dose (~10 organisms) and ease of aerosolization. [4-5]
The following figure illustrates the various modes of acquisition and their corresponding clinical syndromes:
1. History
- Exposure history is paramount: Ask about tick bites (most common US vector, ~69% of cases), handling rabbits/hares/rodents, skinning or butchering wild game, cat bites/scratches, deer fly bites, mowing over animal carcasses, and contaminated water exposure [2][5][7]
- Incubation period: Typically 3–5 days (range 1–21 days) [1][8-9]
- Symptom characterization: Abrupt onset of fever (38–40°C), chills, headache, malaise, myalgia, and anorexia, followed by development of a skin lesion at the inoculation site and painful swollen lymph nodes [1-2][5]
- Timing: Patients seek care after a median of 3 days of illness [7]
- Important negatives: No person-to-person transmission; no respiratory symptoms (distinguishes from pneumonic form); no pharyngitis (distinguishes from oropharyngeal form) [2][5]
2. Alarm Features
- High fever with systemic toxicity (rigors, prostration, confusion) — suggests progression to typhoidal or septic tularemia [5]
- Respiratory symptoms (cough, dyspnea, pleuritic pain) — any form can develop secondary pneumonia via hematogenous spread [5][9]
- Pulse-temperature dissociation — noted in up to 42% of patients; should raise suspicion [5][10]
- Suppurative lymphadenopathy with fluctuance — occurs in ~30% and may require surgical drainage [9][11]
- Immunocompromised patients — at risk for severe, atypical, and disseminated disease [2][12]
- Delayed treatment >2–3 weeks from onset — associated with higher treatment failure and relapse rates [11]
3. Medications
Effective treatments:
- Mild-moderate disease (outpatient):
- Ciprofloxacin 500–750 mg PO BID × 10–14 days [1][13-14]
- Levofloxacin 500 mg PO daily × 10–14 days [1]
- Doxycycline 100 mg PO BID × 14–21 days (higher relapse rate with shorter courses) [1][13]
- Severe disease (inpatient):
- Gentamicin 5 mg/kg/day IV (or 1.5 mg/kg q8h) — first-line for severe tularemia [1][4]
- Streptomycin 15 mg/kg IM q12h (max 2 g/day) — historical gold standard [1][15]
- Step-down: Parenteral aminoglycoside until clinical improvement, then oral fluoroquinolone or doxycycline to complete 10–14 days [1]
Contraindicated/ineffective:
- Beta-lactams — F. tularensis is intrinsically resistant; empiric use is a common cause of treatment failure [1][11]
- Most macrolides — generally ineffective [11]
- Anti-tuberculosis agents — ineffective [11]
Cautions:
- Doxycycline and tetracyclines are bacteriostatic → higher relapse rates, especially with courses <7–10 days [1]
- Aminoglycosides require renal dose adjustment and monitoring [1]
- The 2025 CDC guidelines now designate fluoroquinolones and doxycycline as first-line for outbreaks of any size [13]
4. Diet
- No specific dietary triggers or restrictions
- Ensure adequate hydration, especially in febrile patients with systemic symptoms
- Avoid consumption of untreated water from natural sources in endemic areas (potential transmission route) [2][5]
- Ensure thorough cooking of wild game meat
5. Review of Systems
- Constitutional: Fever, chills, rigors, night sweats, weight loss, fatigue, anorexia [2][5]
- Skin: Ulcer or eschar at bite/contact site; erythema nodosum or erythema multiforme (rare) [8-9]
- Lymphatic: Painful regional lymphadenopathy (inguinal/femoral for lower extremity bites; axillary for upper extremity; cervical for head/neck) [3][10]
- Respiratory: Cough, dyspnea, pleuritic chest pain (screen for secondary pneumonia) [5]
- GI: Nausea, vomiting, diarrhea, abdominal pain [2][5]
- Musculoskeletal: Myalgia, arthralgia, low back pain [5][9]
- Neurologic: Headache; confusion/stupor in severe typhoidal forms [9]
- Ophthalmologic: Photophobia, conjunctivitis (if oculoglandular form suspected) [2]
6. Collateral History and Family History
- Occupational exposure: Hunting, trapping, butchering, farming, landscaping/mowing, veterinary work, laboratory work [5][16]
- Recreational exposure: Hiking, camping, outdoor activities in endemic areas during summer months [7][16]
- Animal contact: Recent contact with rabbits, hares, rodents, or domestic cats; dead animal sightings near home [2][5]
- Geographic context: Residence or travel to endemic areas (Arkansas, Missouri, Oklahoma, South Dakota, Montana; Scandinavia, former Soviet Union) [5][17]
- Household contacts: No person-to-person transmission, but shared environmental exposures may indicate cluster/outbreak [5]
- Family history is generally not relevant (no hereditary predisposition)
7. Risk Factors
- Tick exposure — most common US vector (~69% of cases); peak incidence in summer months [7][16]
- Direct animal contact — handling infected rabbits, hares, rodents, or their carcasses [2][5]
- Male sex — 65% of cases; reflects occupational/recreational exposure patterns [7][17]
- Age bimodal distribution — highest incidence in children aged 5–9 years and men >55 years [17]
- Rural residence in endemic states [5]
- Occupational risk: Hunters, trappers, farmers, landscapers, laboratory workers [5]
- Immunocompromised status — anti-TNF-α therapy, other immunosuppression → risk of severe/disseminated disease [12]
- Cat bites/scratches — increasingly recognized transmission route [1][18]
8. Differential Diagnosis
Cannot-miss diagnoses:
- Plague (bubonic) — similar ulcer + lymphadenopathy; more rapid progression, higher mortality; exposure to rodent fleas
- Anthrax (cutaneous) — painless black eschar with surrounding edema; no significant lymphadenopathy initially
- Necrotizing soft tissue infection — rapidly progressive; systemic toxicity disproportionate to local findings
Most important alternatives:
- Cat scratch disease (Bartonella henselae) — lymphadenopathy with cat exposure; typically less systemic toxicity; no ulcer at inoculation site [19]
- Sporotrichosis — nodular lymphangitis pattern; gardening/soil exposure; chronic course
- Staphylococcal/streptococcal lymphadenitis — responds to beta-lactams (tularemia does not)
- Tuberculosis — chronic lymphadenopathy with caseating granulomas; tularemia can mimic TB histologically [20]
- Lymphoma — painless lymphadenopathy; B symptoms; tularemia lymphadenopathy can mimic malignancy on PET/CT [20-21]
- Other tick-borne diseases — RMSF, ehrlichiosis, Lyme disease (different rash patterns, different lymph node involvement) [3]
- Mycobacterium marinum — if water exposure; chronic granulomatous skin lesion
Key distinguishing feature: Failure to respond to beta-lactam antibiotics in a patient with ulcer + lymphadenopathy should raise strong suspicion for tularemia [11][22]
9. Past Medical History
- Immunosuppression — HIV, organ transplant, anti-TNF-α therapy, chemotherapy → increased risk of severe/disseminated disease [2][12]
- Prior tularemia — cellular immunity is long-lasting; reinfection tends to be localized [10]
- Chronic kidney disease — impacts aminoglycoside dosing [1]
- Prior tick-borne illness — suggests ongoing arthropod exposure risk
- Splenectomy — increased susceptibility to encapsulated and intracellular organisms
10. Physical Exam
Vital signs:
- Fever 38–40°C (often high-grade) [5]
- Pulse-temperature dissociation (relative bradycardia) in up to 42% [5][10]
- Tachycardia if septic; hypotension in severe cases
Focused exam:
- Skin: Tender papule → pustule → punched-out ulcer with raised borders and necrotic base (eschar) at inoculation site; typically on lower extremities (tick bite), upper extremities (animal handling), or trunk [1][3]
- Lymph nodes: Tender, enlarged regional lymphadenopathy — inguinal/femoral (lower extremity inoculation), axillary (upper extremity), cervical (head/neck); may be fluctuant if suppurated [1][3][9]
- Lungs: Usually clear in ulceroglandular form; crackles or decreased breath sounds if secondary pneumonia develops [5]
- Abdomen: Hepatosplenomegaly possible in systemic disease [10]
- Skin rashes: Erythema nodosum, erythema multiforme (uncommon complications) [8-9]
11. Lab Studies
Recommended:
- Tularemia serology (microagglutination test) — preferred diagnostic method; seroconversion or 4-fold rise in paired sera is confirmatory; single titer ≥1:128 is presumptive [1][9]
- 1–2 weeksLancet Infect Dis[9]
- PCR for F. tularensis — from ulcer swab, lymph node aspirate, or biopsy; rapid and highly sensitive/specific [9][12]
- Blood cultures — low yield (<10%), but should be obtained; must notify lab of tularemia suspicion (biosafety risk) [1][9][15]
- CBC — may show leukocytosis or normal WBC; nonspecific
- CMP — mild hepatitis (elevated transaminases) is common [10]
- CRP/ESR — typically elevated; nonspecific
Key lab pearl: Routine cultures are often negative unless cysteine-supplemented media are used. Unsuspected growth of F. tularensis poses a serious laboratory-acquired infection risk — always alert the microbiology lab [1][15][19]
12. Imaging
- Ulceroglandular form: Imaging is generally not necessary for straightforward presentations
- Ultrasound of lymph nodes — useful to assess for suppuration/abscess formation requiring drainage [9]
- Chest X-ray — obtain if respiratory symptoms present; findings are nonspecific (infiltrates, hilar lymphadenopathy, pleural effusion) [15][23]
- CT chest — if pneumonic involvement suspected; may show mediastinal lymphadenopathy, pulmonary nodules, pleural effusion [21]
- PET/CT — can show intensely hypermetabolic lymph nodes mimicking lymphoma; avoid unnecessary biopsy if tularemia is in the differential [21]
13. Special Tests
- Tularemia microagglutination test — gold standard serologic method; paired sera 2–4 weeks apart [9]
- PCR (F. tularensis-specific) — from wound swab, lymph node aspirate; faster than serology [9][12]
- Immunofluorescence staining — can be performed on tissue specimens [15]
- Culture on cysteine heart agar with 9% chocolate blood or chocolate agar — growth in 24–48 hours at 37°C; requires BSL-3 precautions [9]
- Lymph node FNA or biopsy — may show necrotizing granulomatous inflammation; can mimic TB (caseating granulomas) [20]
- Point-of-care: No rapid bedside test currently available
14. ECG
- Not routinely indicated for ulceroglandular tularemia
- Cardiovascular complications are very rare but reported: myocarditis, pericarditis (usually with concomitant pneumonia), and extremely rare endocarditis [18][24-25]
- Obtain ECG if: chest pain, dyspnea out of proportion to exam, new arrhythmia, or signs of myocarditis (elevated troponin, new heart failure)
- If myocarditis suspected: look for diffuse ST changes, low voltage, new conduction abnormalities [18]
15. Assessment
Clinical summary: Ulceroglandular tularemia presents as an acute febrile illness with a skin ulcer at the inoculation site and painful regional lymphadenopathy, typically 3–5 days after tick bite or animal contact. It is the most common form, accounting for ~37–47% of all tularemia cases in the US. [7][22]
Severity stratification:
- Mild-moderate: Localized ulcer + lymphadenopathy, low-grade fever, non-toxic appearance → outpatient oral therapy
- Severe: High fever, systemic toxicity, suppurative nodes, immunocompromised host, concern for secondary pneumonia or sepsis → inpatient IV therapy
Typical vs. atypical:
- Typical: Ulcer + regional adenopathy + fever after tick/animal exposure
- Atypical: Ulcer may be healed/inconspicuous at presentation ("glandular" form); granulomatous lymphadenitis mimicking TB or lymphoma [1][20]
Complications:
- Lymph node suppuration (~30%) [9][11]
- Secondary pneumonia via hematogenous spread [5]
- Sepsis (rare in ulceroglandular form)
- Meningitis, brain abscess (very rare) [9]
- Myocarditis, pericarditis (very rare) [18][25]
- Erythema nodosum, erythema multiforme [8-9]
16. Treatment Plan
Initial stabilization:
- IV access, fluid resuscitation, and antipyretics for febrile/toxic patients
- Obtain cultures and serology before starting antibiotics, but do not delay treatment while awaiting results
Mild-moderate ulceroglandular (outpatient):
- Ciprofloxacin 500 mg PO BID × 10–14 days, OR
- Doxycycline 100 mg PO BID × 14–21 days (longer course to reduce relapse) [1][13]
Severe disease (inpatient):
- Gentamicin 5 mg/kg/day IV divided q8h (adjust for renal function), OR
- Streptomycin 1 g IM q12h [1]
- Step down to oral fluoroquinolone or doxycycline once clinically improved; total course 10–14 days [1]
Suppurative lymph nodes:
- Lancet Infect Dis + 1[9][11]
Special populations:
- Children: Gentamicin 6 mg/kg/day IV divided q8h for severe disease; ciprofloxacin or doxycycline for mild disease [1]
- Pregnancy: Gentamicin preferred for severe disease; ciprofloxacin may be considered for mild disease (risk-benefit discussion) [13]
- Immunocompromised: Lower threshold for aminoglycoside therapy and longer treatment courses [13]
17. Disposition
Admission criteria:
- Systemic toxicity, hemodynamic instability, or sepsis
- Pneumonic or typhoidal features
- Inability to tolerate oral medications
- Immunocompromised host with moderate-severe disease
- Need for IV aminoglycoside therapy
- Suppurative lymphadenopathy requiring surgical intervention
- Diagnostic uncertainty with concern for dangerous mimics (plague, anthrax)
Discharge criteria (outpatient management appropriate if):
- Non-toxic appearance, stable vitals
- Localized ulceroglandular disease without systemic complications
- Able to tolerate oral antibiotics
- Reliable follow-up available
- Immunocompetent
Observation:
Specialist consultation triggers:
- Infectious disease — all confirmed/suspected cases (uncommon disease, complex treatment decisions)
- Surgery — suppurative lymph nodes requiring drainage
- Pulmonology — if pneumonic involvement suspected
- Public health notification — tularemia is a nationally notifiable disease; report to local/state health department [16-17]
18. Follow Up / Return Precautions
Follow-up timing:
- Recheck in 48–72 hours after initiating antibiotics to assess clinical response
- Repeat serology at 2–4 weeks for paired sera confirmation [9]
- Follow-up at 2 weeks to assess ulcer healing and lymph node regression
Symptoms requiring immediate reassessment:
- Worsening fever or new rigors despite 48–72 hours of appropriate antibiotics
- New respiratory symptoms (cough, dyspnea, chest pain) — concern for secondary pneumonia
- Increasing lymph node size, fluctuance, or new drainage — may need I&D
- Altered mental status, neck stiffness — concern for meningitis
- Rash progression (erythema nodosum, erythema multiforme)
Patient counseling:
- No person-to-person transmission — standard precautions are sufficient [5][15]
- Ulcer healing may take weeks to months; lymphadenopathy can persist for months [9]
- Relapse is possible, especially with bacteriostatic agents (doxycycline) or short courses — complete the full antibiotic course [1][11]
- Tick prevention: DEET-based repellents, permethrin-treated clothing, daily tick checks, prompt tick removal [2]
- Avoid handling sick/dead wild animals without gloves [5]
Expected recovery:
- With appropriate antibiotics, clinical improvement typically occurs within 48–72 hours [7]
- Overall mortality for ulceroglandular form is low (<2% with treatment) [8][14]
- Untreated fatality rate for all forms can reach up to 60%, though ulceroglandular carries the best prognosis among tularemia subtypes [4][10]
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