Case Letter

Primary Herpes Simplex Virus Infection of the Nipple in a Breastfeeding Woman

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Practice Points

  • Herpes mastitis should be included in the differential diagnosis for breast pain during lactation.
  • Children of breastfeeding women diagnosed with herpes mastitis require immediate evaluation for a possible source of the infection, as complications of herpes viral infection in infants can be severe and life threatening.



To the Editor:

A 33-year-old woman presented with tenderness of the left breast and nipple of 2 weeks’ duration and fever of 2 days’ duration. The pain was so severe it precluded nursing. She rented a hospital-grade electric breast pump to continue lactation but only could produce 1 ounce of milk daily. The mother had been breastfeeding her 13-month-old twins since birth and did not report any prior difficulties with breastfeeding. Both twins had a history of mucosal sores 2 months prior and a recent outbreak of perioral vesicles following an upper respiratory tract illness that was consistent with gingivostomatitis, followed by a cutaneous outbreak secondary to herpes simplex virus (HSV) type 1 infection. The patient had no known history of HSV infection. Prior to presentation the patient was treated with oral dicloxacillin and then cephalexin for suspected bacterial mastitis. She also had used combination clotrimazole-betamethasone cream for possible superficial candidiasis. The patient had no relief with these treatments.

Physical examination revealed approximately 20 microvesicles (<1 mm) on an erythematous base clustered around the left areola (Figure). Erythematous streaks were noted from the medial aspect of the areolar margin extending to the central sternum. The left breast was firm and engorged but without apparent plugged lactiferous ducts. There was no lymphadenopathy. No lesions were present on the palms, soles, and oral mucosa.

Herpes simplex virus of the left nipple.

The patient was empirically treated with valacyclovir, trimethoprim-sulfamethoxazole, and nonsteroidal anti-inflammatory drugs while awaiting laboratory results. Bacterial cultures were negative. Viral titers revealed positive combination HSV-1 and HSV-2 IgM (4.64 [<0.91=negative, 0.91–1.09=equivocal, >1.09=positive]) and negative HSV-1 and HSV-2 IgG (<0.91[<0.91=negative, 0.91–1.09=equivocal, >1.09=positive]), which confirmed the diagnosis of primary HSV infection. Two months later viral titers were positive for HSV-1 IgG (1.3) and negative for HSV-2 IgG (<0.91).

At 1-week follow-up the patient reported that the fever had subsided 1 day after initial presentation. After commencement of antiviral therapy, she continued to have some mild residual tenderness, but the vesicles had crusted over and markedly improved. Upon further questioning, the patient’s husband had a history of oral HSV-1 and was likely the primary source for the infection in the infants.


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