Breast Infection in a Woman With Diabetes

A 42-year-old woman has had tenderness and pain in the upper outer quadrant of her right breast, several centimeters below the axilla, for about a week. These symptoms have worsened, and she has noted progressive redness, induration, and swelling of the breast. For the past 48 hours, she has also had a fever.

HISTORY

The patient has insulin-dependent type 2 diabetes; her blood glucose level is moderately well controlled. Four months earlier, she had folliculitis with abscess formation in the same breast/axillary area. Surgical drainage and several weeks of dressing changes were required to achieve resolution. When the patient was younger, she used intravenous drugs and alcohol excessively, but she has not done so for several years.

PHYSICAL EXAMINATION

Temperature is 38.5°C (101.3°F); heart rate, 108 beats per minute, with regular rhythm and no gross murmurs; respiration rate, 14 breaths per minute, with oxygen saturation of 98% on room air; and blood pressure, 130/88 mm Hg. Examination of the head, ears, eyes, nose, and throat reveals no abnormalities. Chest is clear.

The right breast is swollen, red, and warm. On the lateral side of the breast, there is a shiny and very tender indurated area that suggests localization; however, an obvious abscess has not yet formed. Several soft, tender lymph nodes are palpable in the axilla.

LABORATORY RESULTS

Results of a chemistry panel are normal except for the blood glucose level, which is 330 mg/dL. There is no anion gap. Hemoglobin level is 12.8 g/dL, and the white blood cell (WBC) count is 19,800/µL, with 6% band forms.

Which of the following is most appropriate for this patient?
A. Oral linezolid.
B. Intravenous cefazolin.
C. Oral trimethoprim/sulfamethoxazole (TMP/SMX).
D. Intravenous vancomycin.

Staphylococcal infections seen today differ in 2 major ways from those of previous decades. First, methicillin- resistant staphylococci now appearing in the community are not the result of the spread of infections associated with hospitals, nursing homes, or dialysis centers. Second, bacteriologic studies of these staphylococci seem to indicate that they are genetically fundamentally different from nosocomial methicillin-resistant clones seen in the past.

Before 2000, almost all methicillin-resistant Staphylococcus aureus (MRSA) infections were nosocomial; they occurred in patients with such established risk factors as a hospital stay of 2 or more days, recent surgery, dialysis, or the presence of indwelling tubes or devices.¹ Since then, a multitude of studies involving all regions of the United States have demonstrated that between 8% and 20% of S aureus infections in patients in the community who have none of the traditional nosocomial-related risk factors are now caused by MRSA strains.^1,2

These new infections have their own epidemiology, characteristic risk factors, and clinical manifestations. They are predominantly skin infections (77%); abscesses, cellulitis, and folliculitis are common. However, invasive infection with these strains is not rare; in 6% of patients, bacteremia, arthritis, and osteomyelitis complicated the infection.¹ A recent study from California reported necrotizing fasciitis associated with the new strain in 14 patients over a 15-month period in a single institution.³

The resistant Staphylococcus clones also have a unique biology. The organisms are resistant to methicillin and to the entire class of b-lactam antibiotics. Molecular analysis of the isolates appears to confirm a community origin rather than spillage from nosocomial reservoirs. All are examples of the clone designated "USA300" by the CDC. All USA300 organisms contain pri genes that encode the novel and characteristic Panton-Valentine leukocidin, a staphylococcal membrane toxin that targets WBCs. This may explain how a methicillin-resistant clone (which would be expected to be less able to compete with wild strains in the community) has prevailed and become virulent.⁴

The increasing prevalence and virulence of these resistant strains are resulting in changes in the treatment of clinically obvious, community-acquired S aureus infections. A much lower threshold for obtaining cultures of mundane abscesses to detect MRSA is clearly warranted. Similarly, a more aggressive approach to selection of antibiotics is evolving, as is a lower threshold for admission of patients to the hospital.

This patient has a serious breast abscess and exhibits several clues associated with heightened risk of MRSA infection. These include:

• A skin-related infection.
• Previous skin infection.
• Diabetes.
• Intravenous drug use (she has at least a remote history).

All of these are risk factors for community-associated MRSA infection.¹ Thus, MRSA infection is a distinct enough possibility that a b-lactam antibiotic, such as cefazolin (choice B), is inappropriate here.

Based on the presence of systemic signs and clinical progression, her infection seems sufficiently serious to warrant hospitalization. Oral antibiotics (choices A [linezolid] and C [TMP/SMX]) are probably not aggressive enough therapy for this potentially dangerous infection. In addition, clinical experience with linezolid in this setting is limited, and its high cost militates against outpatient use.^1,4 Both linezolid and TMP/SMX show in vitro efficacy against MRSA, and in a less noxious situation (eg, an afebrile patient with folliculitis), oral TMP/SMX would be a reasonable choice. However, most experts would use parenteral vancomycin (choice D) here; this agent is preferred for both empiric coverage and definitive therapy for MRSA infections.

Outcome of this case. The patient was admitted; parenteral vancomycin was administered and warm compresses were applied. On the third day, the abscess pointed and was surgically drained. By day 5, she was afebrile and the infection had begun to resolve. Cultures revealed MRSA; gene sequencing eventually confirmed the presence of the USA300 clone. She was discharged on day 11.

References

1. Fridkin SK, Hageman JL, Morrison M, et al. Methicillin-resistant Staphylococcusaureus disease in three communities. N Engl J Med. 2005;352:1436-1444.
2. Herold BC, Immergluck LC, Maranan MC, et al. Community-acquired methicillin-resistant Staphylococcus aureus in children with no identified predisposingrisk. JAMA. 1998;279:593-598.
3. Miller LG, Perdreau-Remington F, Reig G, et al. Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles.N Engl J Med. 2005;352:1445-1453.
4. Chambers HF. Community-associated MRSA—resistance and virulence converge. N Engl J Med. 2005;352:1485-1487.