Lactational mastitis

INTRODUCTION — Lactational mastitis is inflammation of the breast tissues associated with breastfeeding. Mastitis can occur any time during lactation but is most common in the first four to six weeks of breastfeeding. Nipple injury appears to be an inciting factor, although the exact mechanisms are debated. Lactational mastitis is characterized by localized pain, swelling and, often, redness. In some patients, the initial inflammatory process leads to bacterial infection, which may result in fever and malaise. Bacterial infection can progress to local abscess formation if not treated promptly.

Issues, etiology, diagnosis, and treatment of lactational mastitis will be reviewed here. General issues related to lactation and discussions of other breast infections are presented separately.

●(See "Initiation of breastfeeding".)

●(See "Breastfeeding: Parental education and support".)

●(See "Primary breast abscess".)

In this topic, when discussing study results, we will use the terms "woman/en" or "patient(s)" as they are used in the studies presented. We encourage the reader to consider the specific counseling and treatment needs of transgender and gender-expansive individuals.

EPIDEMIOLOGY AND PATHOGENESIS

Epidemiology — Lactational mastitis has been estimated to occur in 2 to 20 percent of breastfeeding patients [1-3]. Meta-analysis of pooled incidence data from three studies reported 11.1 episodes per 1000 breastfeeding weeks (95% CI 10.2-12.0) from birth to postpartum week 25 [2]. Episodes are most common in the first four to six weeks of breastfeeding [2]. The incidence of mastitis requiring hospitalization is low; in one cohort including 136,459 new mothers, 127 patients were hospitalized for mastitis, an incidence of 9 per 10,000 deliveries [4].

The risk of recurrence of mastitis in individuals with prior history of lactational mastitis is higher than in patients with no prior history. (See 'Recurrence' below.)

Pathogenesis — The pathogenesis of lactational mastitis is not well defined as the disease represents a spectrum of conditions and may include poorly understood interactions between the mammary-associated microbiota and host-specific genetic factors [5,6]. Breastfeeding factors, including nipple trauma, breastfeeding challenges, and hyperlactation appear to contribute to its development [6]. The roles of dysbiosis and breast pump use are debated [6,7].

Lactational mastitis follows ductal narrowing that can develop in response to a variety of factors; the ductal narrowing then results in poor milk drainage from the part of the breast drained by the affected duct. Milk stasis that persists beyond 12 to 24 hours is believed to be an inciting factor for bacterial growth and resultant infectious mastitis.

●Cascade of events – The primary event appears to be ductal narrowing (figure 1). Duct narrowing leads to poor milk drainage. Resultant swelling can lead to inflammation, edema, and compression of additional milk ducts. If the ductal narrowing persists, stagnant milk can become infected with bacteria, and this infection can spread into the surrounding breast tissue, resulting in infectious mastitis, and, in some patients, abscess (figure 2) [8].

●Associated risk factors – Lactational mastitis often occurs in the setting of breastfeeding challenges that may contribute to problems with milk drainage [6]. Its etiology is complex and risk factors include [2,5]:

•Breastfeeding difficulties (see "Common problems of breastfeeding and weaning")

•Nipple injury, including excoriation or cracking (see "Common problems of breastfeeding and weaning", section on 'Nipple injury')

•Breast pump use (see "Initiation of breastfeeding", section on 'Milk expression')

•Hyperlactation (see "Common problems of breastfeeding and weaning", section on 'Milk overproduction')

•History of mastitis (See 'Recurrence' below.)

Microbiology — Most episodes of bacterial lactational mastitis are caused by Staphylococcus aureus, followed by streptococci species [8-12]. There is no evidence that yeast plays an important part in infection or nipple pain associated with breast feeding [13,14].

●Prevalence of Staph and Strep – In one study comparing milk from 192 patients with mastitis with milk from 466 unaffected donors, S. aureus and group B Streptococci were recovered significantly more frequently from patients with mastitis (S. aureus 45 versus 31 percent and Group B streptococci 21 versus 10 percent) [8]. That 31 percent of patients without mastitis also had S. aureus in their milk highlights the limits of solely using milk culture for diagnosing mastitis.

●Impact of MRSA – Methicillin-resistant S. aureus (MRSA) has become an important pathogen in cases of lactational mastitis [1,12,15]. In one study of 127 patients hospitalized for mastitis, MRSA was the most common pathogen isolated from women with mastitis alone (24 of 54 specimens) or mastitis and abscess (18 of 27 specimens) [15]. In a different study of 535 lactating patients (316 with infectious mastitis and 219 with breast abscess), 70 patients (34.5 percent) had MRSA [12].

●Less common – Less frequent pathogens include Streptococcus pyogenes (group A or B), Escherichia coli, Bacteroides species, Corynebacterium species, and coagulase-negative staphylococci (eg, Staphylococcus lugdunensis) [6].

Risk reduction — The risk of developing lactational mastitis can be reduced by frequent on-demand feeding (or milk expression) and by optimizing breastfeeding technique [16]. Breastfeeding education and light breast massage may be helpful, but supporting data are of limited quality [17,18]. (See "Initiation of breastfeeding", section on 'Principles of breastfeeding'.)

CLINICAL MANIFESTATIONS — Lactational mastitis presents on a clinical spectrum ranging from early, focal disease to, in rare cases, systemic illness.

●Lactational mastitis – Patients with lactational mastitis typically present with a swollen and tender region of the breast that may also be red (ie, erythematous) (picture 1) [5,19]. Lactational mastitis is most common in the first three months of breastfeeding. The erythema and induration can progress beyond the initial quadrant and effect the entire breast. Systemic symptoms such as fever, chills, and tachycardia may be present. Patients with symptoms lasting more than 24 hours should be evaluated. (See 'Diagnostic evaluation' below.)

●Infectious lactational mastitis – Patients with infectious lactational mastitis typically present with a firm, red, painful, swollen area of one breast associated with fever >38.3ºC; milk secretion can be diminished. Systemic complaints may include myalgia, chills, malaise, and flu-like symptoms. Rarely, patients with severe mastitis can develop sepsis. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis".)

●Sepsis from advanced infection – Rarely, patients with severe infectious lactational mastitis can develop symptoms of sepsis, including hypotension, tachycardia, tachypnea, fever, leukocytosis, and/or evidence of end organ dysfunction. These patients require immediate evaluation and resuscitative management, as discussed in detail elsewhere.

•(See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis".)

•(See "Evaluation and management of suspected sepsis and septic shock in adults".)

DIAGNOSTIC EVALUATION

History and physical examination — Lactational mastitis is diagnosed by physical examination confirming a swollen and tender breast in a lactating patient with history of breast pain and/or swelling (picture 1). Red coloration may be present but is not required for the diagnosis; red coloration may be absent in patients with darker skin tone until later in the process. In the early stages, the presentation can be subtle with few clinical signs. Low-grade fever may be present. Laboratory tests and imaging studies are not indicated for the diagnosis of lactational mastitis.

Patients with bacterial infection generally present with a large area of breast swelling with overlying skin erythema and fever >38.3°C. Reactive axillary lymphadenopathy may be associated with axillary pain and swelling. Systemic complaints may include myalgia, chills, malaise, and flu-like symptoms. Rarely, patients may have evidence of sepsis (table 1).

Laboratory evaluation — While routine laboratory tests are not helpful for diagnosing lactational mastitis, cultures can be helpful for patients with suspected bacterial infection, infection that does not respond to initial treatment, or patients with evidence of sepsis (table 1).

●Milk culture – While not done routinely, culture of the breast milk can be useful to guide selection of antibiotics. Culture can be helpful in the setting of infection that is particularly severe, hospital acquired, or unresponsive to initial empiric antibiotics [16,20].

To perform breast milk culture, the nipple and areola are cleaned with either topical antiseptic or washed with soap and water [5]. After sterile gloves are donned, milk is expressed from the breast into a sterile collection tube without having the breast and tube connect. Approximately 5 to 10 mL of milk is collected and labeled as "body fluid culture."

●Blood culture – Blood cultures are warranted in the setting of severe infection (eg, hemodynamic instability, progressive erythema) but are otherwise not routinely necessary.

Imaging studies — Imaging studies are useful if lactational mastitis does not respond within 48 to 72 hours to supportive care and/or antibiotics. Ultrasound is the most effective method of differentiating mastitis from breast abscess [21-25]. (See "Primary breast abscess".)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of abnormalities of the lactating breast include engorgement, plugged ducts, galactocele, abscess, and, rarely, cancer. The differential diagnosis of mastitis unrelated to lactation is reviewed separately. (See "Nonlactational mastitis in adults".)

●Engorgement – Engorgement occurs due to interstitial edema with onset of lactation or, at other times, with accumulation of excess milk. Postpartum engorgement is physiologic bilateral breast fullness that generally occurs on postpartum days three to five [26,27]; onset may be one to two days later for patients who undergo cesarean delivery [26]. Secretion of mature milk is believed to distend the alveolar ducts, which results in vascular and lymphatic compression. Typical symptoms are bilaterally full and tense breasts which may be painful. Some patients experience "flu-like" malaise as well. Symptoms are self-limited and generally improve in 24 hours. (See "Overview of the postpartum period: Normal physiology and routine maternal care".)

Multiple treatments have been studied, but efficacy has not been established [28]. Care is generally supportive. For patients with persistent symptoms, we advise meeting with a lactation specialist, wearing a supportive breast-feeding bra that does not constrict, and using ibuprofen or acetaminophen as needed for discomfort. (See "Overview of the postpartum period: Normal physiology and routine maternal care", section on 'Management of breast engorgement and lactation suppression'.)

Severe engorgement may be distinguished from mastitis in that engorgement is bilateral with generalized involvement while mastitis is localized and generally affects only one breast [1]. (See "Common problems of breastfeeding and weaning", section on 'Engorgement'.)

●Focal duct narrowing ("Plugged duct") – "Plugged ducts" are localized areas of congested mammary tissue (picture 2). These can be mistaken for infection. (See "Common problems of breastfeeding and weaning" and "Common problems of breastfeeding and weaning", section on 'Ductal narrowing'.)

●Breast abscess – Roughly 3 to 11 percent of patients with lactational mastitis will progress to an infected fluid collection (ie, abscess) [29]. Physical examination findings suggestive of abscess include a palpable, tender, and well-defined fluctuant area of the breast; the skin may or may not be compromised (picture 3A-B) [5]. Ultrasonography may aid in diagnosis and facilitate guided drainage (preferred treatment) (image 1) [5,21,24,25,30]. (See "Primary breast abscess".)

●Galactocele – A galactocele (also known as a milk retention cyst) is a cystic collection of fluid that is usually caused by obstructed or narrowed milk ducts [31]. Galactoceles present as soft cystic masses (picture 4); they are not tender and are not associated with systemic manifestations. Ultrasonography may demonstrate a simple milk cyst or a complex mass (image 2). The diagnosis can be made on the basis of the clinical history and ultrasound examination. Occasionally, needle aspiration may be used for diagnosis, which yields a milky substance. (See "Common problems of breastfeeding and weaning", section on 'Galactocele'.)

●Inflammatory breast cancer – Inflammatory breast cancer (IBC) should be considered if mastitis does not resolve with appropriate treatment. Erythema may improve to some degree with antibiotics in patients with IBC, but there are usually other manifestations of IBC present; IBC may be differentiated from mastitis by clinical manifestations of skin thickening due to edema, erythema, and peau d'orange appearance (picture 5A-B). It is often associated with palpable axillary lymphadenopathy due to metastatic nodal involvement. The diagnosis is established with core biopsy. (See "Inflammatory breast cancer: Clinical features and treatment".)

TREATMENT

Clinical management — Physiological breastfeeding and anti-inflammatory measures are the key interventions to resolve ductal narrowing and prevent bacterial mastitis.

●Candidates – All patients with lactational mastitis should be educated about this approach, even if additional treatment with antibiotics is warranted. Patients who are candidates for clinical management only include those with focal breast findings and mild systemic symptoms. Improvement should be seen within 24 to 48 hours.

●Approach – Initial management of nonsevere lactational mastitis consists of several interventions aimed at relieving pain and maintaining milk flow through the milk ducts of the breast [32]. We provide the following guidance to patients [5,10,11,16,19,20,22,32,33]:

•Feed the infant on cue or express the volume of milk that the child needs.

•Minimize breast pump usage if possible and avoid use of nipple shields.

•For pain relief:

-Topical – Warm or cold compresses (ie, soak a cloth in warm or cold water and place it on the breast). While use of either heat or cold may reduce pain, applying cold may decrease associated tissue edema and inflammation [5]. Supporting data for both interventions are limited [28].

-Systemic – Acetaminophen or ibuprofen can be used to relieve pain and reduce inflammation and fever (aspirin should be avoided [32]).

•Rest and drink plenty of fluids.

•Avoid deep massage (light sweeping of the skin similar to that for manual lymphatic drainage may be helpful [34,35]).

•Wear an appropriately fitting supportive bra (ie, not too tight).

•Keep patients and infants together if feasible.

●Unclear benefit of probiotics – Data on the use of probiotic use to treat or prevent mastitis are inconsistent. Two different reviews were unable to make definitive recommendations due to the limitations of available trials and low quality of evidence [17,36].

●Warning signs for bacterial infection – If symptoms persist beyond 24 to 48 hours or are accompanied by fever or systemic symptoms, treatment additionally includes antibiotic therapy with activity against S. aureus [11,13,19,21,22,36,37]. (See 'Antibiotic therapy' below.)

Antibiotic therapy

Approach and patient counseling — Antibiotic use is reserved for patients with evidence of bacterial infection. This reflects a change from the historical approach of starting antibiotics quickly for all patients with lactational mastitis [19]. If available, milk culture results can guide antibiotic selection. Infection can progress to local abscess formation if not treated promptly.

Antibiotic treatment is given in addition to the clinical approach above. In one observational study, when infectious lactational mastitis was treated with a combination of antibiotics and breast emptying, the rate of symptom resolution within two weeks increased from 50 to 96 percent [10]. Thus, continued breast feeding should be encouraged in the presence of infective lactational mastitis, including abscess [16,38,39]. (See 'Clinical management' above.)

Antibiotic selection — As high quality data specific to treatment of infectious mastitis are limited [33], treatment is based on that for cellulitis and other soft tissue infections (algorithm 1). Empiric therapy should include activity against S. aureus [10,33]. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Acute cellulitis'.)

●Nonsevere infection – Patients with nonsevere disease are treated based on their risk factors for methicillin-resistant S. aureus (MRSA) (table 2). Nonsevere disease includes patients with typical clinical signs of infectious mastitis (eg, pain, redness, fever, myalgia) who are hemodynamically stable, immunocompetent, and have not previously been treated with antibiotics for mastitis. Drug selection is based on availability, cost, patient allergies and prior treatment response (if applicable), culture results (if available), and local antibiotic resistance patterns. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Selecting an antibiotic regimen'.)

•Nonsevere without MRSA risk factors – Patients without MRSA risk factors are offered (algorithm 1) [5,33]:

-Dicloxacillin 500 mg orally four times daily.

Or

-Flucloxacillin 500 mg orally four times daily.

Or

-Cephalexin 500 mg orally four times daily.

For patients with beta-lactam hypersensitivity, options include antibiotics that are often used for MRSA infections, as described below (eg, trimethoprim-sulfamethoxazole, clindamycin).

•Nonsevere with MRSA risk factors – In the setting of nonsevere infection with risk for MRSA (table 2), effective oral antibiotics compatible with lactating patients include (table 3):

-Trimethoprim-sulfamethoxazole (TMP-SMX; 1 double-strength tablet orally twice daily).

TMP-SMX may be used in patients who are breastfeeding healthy, full-term infants who are at least one month old. The drug should be avoided in patients who are breastfeeding newborn infants (<1 month old) or infants with glucose-6-phosphate dehydrogenase deficiency, and it should be used cautiously in patients who are breastfeeding infants who are jaundiced, premature, or ill [37]. (See "Trimethoprim-sulfamethoxazole: An overview", section on 'Pregnancy and breastfeeding'.)

Or

-Clindamycin 450 mg orally three times daily.

Clindamycin has been associated with Clostridioides difficile colitis and increasing rates of resistance among staphylococci. (See "Clostridioides difficile infection in adults: Epidemiology, microbiology, and pathophysiology", section on 'Antibiotic use'.)

●Severe infection – Patients with severe infection (eg, fever, hypotension, tachycardia), rapid expansion of infection, or infection that progresses despite appropriate oral antibiotics warrant intravenous treatment that provides coverage of both Gram-positive and Gram-negative organisms. In this scenario, intravenous antibiotics are typically given in an inpatient setting. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Indications for parenteral therapy'.)

We use the following initial approach:

•Initial empiric inpatient therapy with intravenous vancomycin (table 4).

Plus

•Either ceftriaxone (2 g intravenously once daily) or piperacillin-tazobactam (3.375 g intravenously every six hours).

If beta-lactam agents are not an option, vancomycin can be combined with an aminoglycoside (eg, gentamicin). Aminoglycosides are used in this setting because of their safety in breastfeeding. Dosing is discussed in detail separately. (See "Dosing and administration of parenteral aminoglycosides".)

Subsequent drug selection should be tailored to culture and sensitivity results from breast milk and/or blood cultures.

●Evidence of sepsis – Patients with evidence of sepsis, including fever, hypotension, tachycardia, tachypnea, leukocytosis, and/or evidence of end organ dysfunction, require immediate evaluation and management with resuscitative therapy. The management of patients with suspected sepsis is presented in detail elsewhere. (See "Evaluation and management of suspected sepsis and septic shock in adults".)

Duration of treatment — The optimal duration of antibiotic treatment is not clear and varies, in part, by severity of initial disease and speed of patient response. Treatment durations are extrapolated from other types of cellulitis. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Duration of antibiotic therapy'.)

●Nonsevere infection – In general, patients with uncomplicated infection respond fully within five to six days of oral antibiotics. Symptomatic improvement is typically seen within 24 to 48 hours. Patients who do not respond fully may require additional antibiotic treatment for a total of 10 to 14 days.

Additional discussions with presentation of supporting data are available in related content:

•(See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Duration of antibiotic therapy'.)

•(See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Monitoring response to therapy'.)

●Severe infection – In patients with severe or initially progressive infection, intravenous drugs are transitioned to oral antibiotics once there are signs of clinical improvement and no evidence of systemic toxicity. This usually occurs after 48 to 72 hours. The optimal duration of oral therapy in this setting is not known; in general, five to six days of therapy is appropriate for patients whose condition has improved. Extension of antibiotic therapy (up to 14 days) may be warranted in the setting of severe infection, slow response to therapy, or immunosuppression.

Minimal or no clinical response — If there is minimal or no clinical improvement on antibiotic treatment within 48 to 72 hours, we evaluate with ultrasound imaging to determine if there is an underlying abscess. If abscess is not present, milk cultures should be obtained to further inform antibiotic selection. We also consider the possibility of a noninfectious process. (See "Primary breast abscess" and 'Differential diagnosis' above.)

Lactation professionals — Lactation professionals, including lactation consultants, are often involved in early assessment of patients who develop mastitis (table 5). Their role is to provide advice on optimal feeding strategies, to support lactating parents, and to provide education. Their advice may include the use of nonsteroidal anti-inflammatory agents, keeping the area cool, and medical referral of those with signs and symptoms of bacterial mastitis for antibiotics [5]. (See "Breastfeeding: Parental education and support", section on 'Programmatic approaches and professional resources'.)

BREAST IMPLANTS — Patients with breast implants can breastfeed but lower rates of success have been reported compared with individuals without implants (82 versus 88 percent in a meta-analysis of 11 observational studies) [40]. The presence of implanted foreign bodies may predispose to bacterial infection, including lactational mastitis [41-43]. An observational study of over 28,000 postpartum women reported infectious mastitis occurred in 8.3 percent of patients with implants versus 6.6 percent of those without (OR 1.22, 95% CI 1.09-1.35) [44]. However, the absolute rate of infection below 10 percent in both groups was overall reassuring. Patients with breast implants who develop lactational or infectious mastitis receive the same treatment as those without implants. Patients with implants may benefit from antibiotic use until redness and related symptoms are gone or nearly resolved.

RECURRENCE — There is no consensus definition of recurrent lactational mastitis. Repeat episodes of lactational mastitis may result from ongoing breastfeeding problems, inability to remediate breastfeeding technique that is leading to incomplete milk drainage, and/or inappropriate or incomplete antibiotic therapy. Repeat episodes of lactational mastitis are treated in the same manner as discussed above. Consultation with a lactation professional may be beneficial to manage underlying causes.

●(See 'Treatment' above.)

●(See 'Lactation professionals' above.)

Patients that have repeated episodes in the same location of the breast and/or do not respond to antibiotic therapy are evaluated for inflammatory breast carcinoma. (See 'Differential diagnosis' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Breastfeeding and infant nutrition".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Mastitis (The Basics)" and "Patient education: Common breastfeeding problems (The Basics)")

●Beyond the Basics topic (see "Patient education: Common breastfeeding problems (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Pathogenesis – Lactational mastitis is inflammation of the breast tissues associated with breastfeeding. The primary event appears to be ductal narrowing (figure 1) that leads to poor drainage and subsequent inflammation, edema, and compression of additional milk ducts. Breast milk can contain bacteria; incomplete breast emptying may result in organisms growing and proliferating into infectious mastitis. (See 'Epidemiology and pathogenesis' above.)

●Microbiology – Most episodes of infectious lactational mastitis are caused by Staphylococcus aureus or Streptococcus species. Methicillin-resistant S. aureus (MRSA) has become an important pathogen. (See 'Microbiology' above.)

●Clinical manifestations – Patients with lactational mastitis typically present with a swollen and tender region of the breast, which may also be red in patients with lighter skin tone (picture 1). Systemic complaints may include myalgia, chills, malaise, and flu-like symptoms. It is most common during the first three months of breastfeeding. (See 'Clinical manifestations' above.)

●Diagnostic evaluation

•History and physical examination – Lactational mastitis is diagnosed by physical examination confirming a swollen and tender breast in a lactating patient with history of breast pain and/or swelling (picture 1). Erythema (redness) may or may not be present.

•Laboratory evaluation – Laboratory tests and imaging studies are not indicated for the diagnosis of lactational mastitis. By contrast, milk and/or blood cultures can be helpful for patients with suspected bacterial infection, infection that does not respond to initial treatment, or patients with evidence of sepsis.

•Imaging studies – Breast imaging, typically with ultrasound, is useful to exclude abscess in patients who do not respond to treatment within 48 to 72 hours. (See 'Diagnostic evaluation' above.)

●Differential diagnosis – The differential diagnosis includes severe breast engorgement, plugged duct, galactocele, breast abscess, and inflammatory breast cancer. (See 'Differential diagnosis' above.)

●Treatment

•Clinical management – All patients with lactational mastitis are counseled on treatment to reduce pain and swelling (eg, nonsteroidal inflammatory agents, cold compresses) and emptying of the breast, ideally via ongoing breastfeeding and/or hand expression. (See 'Clinical management' above.)

•Antibiotic therapy – Management of infectious lactational mastitis includes the above measures plus administration of antibiotic therapy with activity against S. aureus. Drug selection is similar to that for cellulitis and other soft tissue infections (algorithm 1), with preference for drugs that are compatible with breastfeeding. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Acute cellulitis'.)

-Nonsevere infection – For patients with nonsevere infectious mastitis and no MRSA risk factors, we suggest treatment with dicloxacillin, flucloxacillin, or cephalexin rather than other agents (Grade 2C). The dosing for each of these drugs is 500 mg orally given four times a day. (See 'Antibiotic selection' above.)

For patients with MRSA risk factors (table 2) or patients unable to tolerate beta-lactams, we suggest treatment with trimethoprim-sulfamethoxazole (TMP-SMX) or clindamycin rather than other agents (Grade 2C). Dosing is TMP-SMX one double-strength tablet orally twice daily or clindamycin 450 mg orally three times per day. (See 'Antibiotic selection' above.)

-Severe infection – For patients with evidence of severe infection (eg, fever, hypotension) or those not improving with appropriate oral antibiotics, we suggest treatment with intravenous vancomycin and either ceftriaxone or piperacillin-tazobactam rather than treatment with other agents (table 4) (Grade 2C). Inpatient treatment is typically warranted. Subsequent treatment decisions are based on culture results. (See 'Antibiotic selection' above.)

-Evidence of sepsis – The rare patient with infectious lactational mastitis and evidence of sepsis, including hypotension, tachycardia, tachypnea, fever, leukocytosis, and/or evidence of end organ dysfunction, requires immediate evaluation and supportive management, as discussed in detail separately.

(See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis".)

(See "Evaluation and management of suspected sepsis and septic shock in adults".)

•Duration of treatment – The optimal duration of antibiotic treatment is not clear and varies, in part, by severity of initial disease and speed of patient response.

-Nonsevere infection – The general treatment duration for patients receiving oral antibiotics is five to seven days. Patients who do not respond fully may require longer duration of treatment, up to 10 to 14 days.

-Severe infection – Patients hospitalized with severe infection that warrants intravenous antibiotics are transitioned to oral antibiotics once there are signs of clinical improvement and no evidence of systemic toxicity; this usually occurs after 48 to 72 hours. In general, treatment for five to seven days is reasonable in patients with rapid response to treatment but extended treatment may be required. (See 'Duration of treatment' above.)