Mr. M was 53 years old and lived in rural South Carolina. He complained of a skin lesion that had first appeared on his left ankle 10 days earlier (around the middle of September). Since then the center of the sore had become dark, and Mr. M noted generalized joint pain. Over the past four or five days, the lesion had become increasingly red and painful. He reported no headache or rash.
The patient’s past medical history was significant for osteoarthritis, allergic rhinitis, tension and migraine headaches, hypertension, hypercholesterolemia, and inguinal hernia repair. His current medication regimen included fexofenadine (Allegra) 180 mg daily, duloxetine (Cymbalta) 60 mg daily, bupropion (Wellbutrin) 150 mg daily, telmisartan/hydrochlorothiazide (Micardis) 80/12.5 mg daily, and rizatriptan (Maxalt-MLT) 10 mg as needed. Mr. M had no known drug allergies. There was no history of drug or alcohol abuse, and he had been in a monogamous, heterosexual relationship for more than 20 years.
When Mr. M developed a fever, he went to a nearby urgent-care center. There, an x-ray of the ankle was read as negative, and he was started on amoxicillin clavulanate (Augmentin) 875 mg p.o. b.i.d. and told to follow up with his primary-care clinician. About 16 hours after visiting the urgent-care center, Mr. M came to our office. On presentation, Mr. M weighed 229 lb. His vital signs included temperature 98.6°F, pulse 80 beats per minute, and BP 120/82 mm Hg (respiration rate was not obtained). A well-developed man in no acute distress, the patient was alert and oriented to person, place, and time. His eyes, ears, neck, and throat were unremarkable except for some tenderness over the frontal sinuses. Breathing was unlabored, and lungs were clear to auscultation. S1 and S2 were normal; there were no murmurs, and carotid upstroke was brisk. Trace pitting edema of the ankles was noted, and peripheral pulses were 2+. Joints were nonerythematous, nonswollen, and nontender with free range of motion. No rashes were observed on cutaneous examination.
The lesion on the patient’s left ankle was minimally tender and consisted of a black scab that was circumscribed by a reddish/purplish area up to 0.5 cm in circumference. There was no drainage. Complete blood count (CBC) showed WBCs 5.3×103/µL, hemoglobin 16.3 g/dL, mean corpuscular volume 93.0 fL, mean corpuscular hemoglobin 32.1 pg, mean platelet volume 7.3 fL, platelets 224×103/µL, and erythrocyte sedimentation rate (ESR) 9 mm/hr.
The patient was told to continue the Augmentin and to call the office if he had unusual additional symptoms or if he failed to improve.
Two days after the examination, Mr. M called to say that his condition had worsened. The ankle lesion was growing, and he had begun to run a fever of 103°F, warranting a return to the office. When he arrived, we found that the lesion had increased in circumference to 2.5 cm. CBC was stable. The wound bed was cultured to rule out methicillin-resistant Staphylococcus aureus (MRSA) infection. He was given a prescription for hydrocodone (Vicodin) to relieve continuing joint pain and trimethoprim-sulfamethoxazole (Bactrim) b.i.d. as empiric antibiotic therapy.
At a follow-up appointment three days later, the joint pain had resolved but Mr. M continued to run a fever. And while the lesion was improving, examination revealed scattered petechiae, predominantly on the ipsilateral leg but to a lesser extent on all four extremities (sparing the palms and soles). At this point, we suspected tick-borne disease. Titers for Rocky Mountain spotted fever (RMSF), ehrlichiosis, and Lyme disease were obtained. Results of the RMSF assay showed elevated immunoglobulin M antibodies to be 33 units (normal 0-8). Other titers were negative.
3. Treatment and outcome
Once these findings were known, the Bactrim was discontinued, and a 10-day course of doxycycline 100 mg b.i.d. was started. The local health department was notified. One week later, Mr. M returned for follow-up. The petechial rash, fever, and joint pain had resolved, and the initial tick bite had healed.
RMSF, one of several zoonotic diseases spread through the bite of a tick, is caused by the bacterium Rickettsia rickettsii. According to the CDC, 90% of RMSF cases occur between the months of April and September, and more than half of all U.S. cases occur in the south-Atlantic region (Delaware, Maryland, Washington D.C., Virginia, West Virginia, North Carolina, South Carolina, Georgia, and Florida).1 Nevertheless, RMSF is a rare disease, and Mr. M’s course had some unusual features worth noting. While the victim does not always recall being bitten by a tick, the patient in this case had not spent any significant time in the woods or fields prior to his illness. He did not develop conjunctival redness, headache, or the classic maculopapular rash. In addition, he actually improved somewhat before starting the doxycycline, so the Bactrim most likely offered some coverage.
Our initial differential diagnoses included spider bite, but the lesion did not have the degree of tissue destruction typically seen with such an injury. Mr. M thought he had been bitten by an ant, which certainly could have led to development of localized cellulitis, but the systemic symptoms were not in keeping with this possibility. Given its current preponderance in the community, MRSA had to be included in the differential. The patient’s normal WBC count and ESR made meningitis or endocarditis less likely. In light of Mr. M’s social history, a sexually transmitted infection was only a remote possibility.
Risk factors that can lead to more severe disease or death include absence or late onset of the rash, delay in treatment with an appropriate antibiotic, or age older than 40 years.2 Fortunately, although he met all these criteria, Mr. M’s outcome was excellent.
Ms. Hucks is assistant professor in the department of nursing at Francis Marion University in Florence, S.C.
1. Centers for Disease Control and Prevention. Rocky Mountain Spotted Fever. Accessed May 11, 2009.
2. Heymann DL. Rocky Mountain spotted fever. In: Heymann DL, ed. Control of Communicable Diseases Manual. 18th ed. Washington, D.C.: American Public Health Association; 2004:459-461.