COMPLETE CLINICAL DETAILS FOR ANTHRAX CASE 8  



about Epidemiology & the department

Epidemiology academic information

Epidemiology faculty

Epidemilogy resources

sites of interest to Epidemiology professionals



Last Updated

06 Nov 2002

Source: Freedman A et al. Cutaneous Anthrax associated with microangiopathic hemolytic anemia and coagulopathy in a 7-month-old infant. JAMA 287(7), 869-874, 2002 (Feb. 20, 2002).

October 1, 2001

A 7-month-old, previously healthy, white male infant was admitted to the hospital on October 1, 2001. Two days prior to admission (September 29, 2001) he was noted to have a painless red macule on the proximal medial aspect of the left upper extremity with associated swelling. During the next 24 hours, the arm became increasingly edematous, the macule evolved to a papule, and a slight serous drainage began. However, the patient remained afebrile and without apparent pain or other systemic symptoms. His primary pediatricians treated him with amoxicillin/clavulanate potassium for presumed cellulitis, but he required admission to the hospital after the third dose, due to increased swelling and drainage of the lesion, and his difficulty in tolerating oral medication.

The infant did not have a significant medical history but he had recently played outdoors in a New York park and had also visited his mother at her workplace, the offices of a national television news organization, for an hour the day before his symptoms began. Anthrax spores were subsequently found at his mother's workplace.

On admission, the infant was alert, afebrile, and in no apparent distress. Laboratory studies revealed significant leukocytosis and hyponatremia (click for daily Table).

Blood was not sent for culture, but intravenous ampicillin/sulbactam was initiated. Surgical incision and drainage performed under local anesthesia revealed no underlying abscess, but dark red fluid was expressed from the lesion. Bacterial cultures were not performed.

October 2, 2001

On hospital day 2, the left arm showed massive, nonpitting, nontender edema with a dark red macule approximately 2 to 3 cm in diameter. There was copious, yellow serous drainage from the wound and paler erythema extending across the anterior thorax to the sternum. No axillary adenopathy was palpable. The hyponatremia was managed with fluid restriction and clindamycin was added to the antibiotic regimen. An infectious disease consultation was obtained. A gram stain of the wound drainage showed neither white blood cells nor organisms. Differential diagnoses considered were infection of bone, soft tissue, or both; arachnid bite; and obstructive mass lesion. Ultrasound of the left upper extremity revealed diffuse inflammation without abscess, and minimal axillary lymphadenopathy. Doppler studies excluded deep vein thrombosis or other vascular compromise to the limb. Later that day, the patient became febrile (39.2°C) and developed significant thrombocytopenia.

During the next 2 days, the arm edema decreased slightly, a 3-mm area of central necrosis was noted at the wound site, and petechiae appeared on the left anterosuperior thorax and axilla. The patient's hematocrit decreased to 23.3%, and low-grade fever, hyponatremia, thrombocytopenia, and leukocytosis persisted, now with a significant number of band forms. Due to loss of intravenous access, the antibiotic regimen was changed to oral cephalexin and clindamycin.

October 5, 2001

By hospital day 5, the fever resolved and the arm edema had decreased considerably. The lesion appeared as a circumscribed erythematous plaque (4.5-5 cm) with a central eschar of less than 1 cm (see Figure 1A). A magnetic resonance image of the upper extremity (previously published) revealed extensive soft tissue inflammation extending from the left lateral chest wall to the hand, but there was no bone involvement, soft tissue gas or fluid collection, or mass lesion. The hematocrit decreased to 18.7%. The glucose-6-phosphate dehydrogenase enzyme level was normal, but the peripheral blood smear revealed schistocytes and fragmented red blood cells. A serum lactate dehydrogenase level of greater than 5000 U/L, along with evidence of mild increases in serum urea nitrogen and creatinine levels, supported a diagnosis of microangiopathic hemolytic anemia.

At this point, the working diagnosis was cutaneous and systemic loxoscelism, as the clinical course and the evolution of the skin lesion seemed more consistent with envenomation than an infectious process. Dermatologic consultation concurred with this diagnosis. Oral prednisolone was begun and antibiotics were discontinued.

While the patient's arm edema improved and he remained afebrile, his hematologic status worsened during the next few days. The hematocrit decreased to 14.3% with accompanying tachycardia, necessitating 2 transfusions of 15 mL/kg of packed red blood cells. Coagulopathy was evident, with ongoing thrombocytopenia and elevated D-dimer levels and fibrin degradation products. A persistent hypofibrinogenemia required transfusion of 4 U of cryoprecipitate. Renal insufficiency, with elevated serum urea nitrogen, hematuria, proteinuria, transient oliguria, and hypertension (systolic blood pressure of 130 mm Hg and diastolic blood pressure of 85 mm Hg), were present. By hospital day 12, these laboratory abnormalities were resolving and the patient was clinically stable. However, a 2-cm black eschar was present in the center of the cutaneous lesion (see Figure 1B).

October 12, 2001

That day, the first case of cutaneous anthrax in New York (see case 2) was reported and the New York Department of Health was notified that this infant was potentially infected with anthrax. Two skin biopsies of the lesion were performed the next day, and these, as well as blood obtained on hospital day 2, were sent to the Centers for Disease Control and Prevention for polymerase chain reaction diagnosis and immunohistology, respectively. Two days later, these tests were reported as positive for B anthracis, with significant anthrax DNA present in the serum sample and immunohistochemical detection of fragmented anthrax bacilli in the biopsy tissue. Western blot testing of serum samples from day 13 of illness revealed both an IgM response to the 83-kd protective factor and an IgG response (Figure 2).

October 18, 2001

On day 20 of the patient's illness, the IgM response decreased but the IgG response intensified and extended to the edema and lethal factors band of 89 to 93 kd. The patient was discharged home on day 17 of illness (October 15, 2001), receiving oral ciprofloxacin, the treatment recommended by the Centers for Disease Control and Prevention. His platelet count and fibrinogen level were normal, but evidence of a mild hemolysis persisted. After 2 weeks of ciprofloxacin, when the other anthrax isolates were shown to be susceptible to penicillin, amoxicillin was used as the antibiotic. Hematuria, anemia, and elevated D-dimer levels slowly resolved over the next 2 weeks, 30 days after admission. Serum urea nitrogen and creatinine levels were normal at 12 days after admission and the skin lesion healed with little evidence of scarring by day 60 (see Figure 1C).

Return to Case 8