Mastitis is an inflammatory condition of the breast tissue that often leads to an infection. The inflammation causes localized symptoms such as pain, swelling, and redness in the breast, frequently accompanied by systemic signs like fever and flu-like aches. While inflammation can initially stem from non-infectious causes like milk stasis, the majority of clinical mastitis cases progress rapidly to involve a bacterial infection, requiring timely medical intervention. Understanding the specific bacteria responsible for this infection is paramount for selecting an effective treatment.
Identifying the Main Microbial Causes
The undisputed most common causative agent is Staphylococcus aureus, a bacterium frequently found on healthy skin that can become pathogenic when it gains entry into the breast tissue. This organism is particularly concerning because of its potential for resistance to common antibiotics.
Methicillin-resistant S. aureus (MRSA) is a strain that has developed resistance to beta-lactam antibiotics, including methicillin, penicillin, and related drugs like cephalexin. MRSA possesses a specific gene, mecA, which allows it to produce a modified penicillin-binding protein (PBP2a) that is not effectively targeted by these standard antibiotics. The presence of MRSA necessitates the use of different, targeted antimicrobial agents to clear the infection effectively.
Following S. aureus, various Streptococcus species are the next most frequent cause of infectious mastitis. Group B Streptococcus (Streptococcus agalactiae) is one of the more common streptococcal culprits identified in breast milk cultures from affected individuals. Other bacteria, while less common, can be implicated, including coagulase-negative staphylococci and Gram-negative bacteria like Escherichia coli in severe or hospital-acquired infections. These organisms are typically considered commensal, but they seize the opportunity to multiply rapidly once the environment within the milk ducts becomes compromised.
Pathways for Bacterial Entry and Infection
Bacteria gain access to the interior of the breast through breaks in the skin and nipple tissue. Nipple trauma, such as cracks, fissures, or minor abrasions, provides a direct physical route for bacteria dwelling on the skin or from the infant’s oral flora to enter the underlying milk ducts and glandular tissue. Even microscopic lesions can be sufficient entry points for organisms like S. aureus to invade and establish an infection.
Milk stasis, or incomplete milk removal from the breast, is a major factor promoting infection. When milk is not drained effectively, it becomes stagnant within the ducts, providing an ideal, nutrient-rich environment for any bacteria that have gained entry to multiply rapidly. This buildup of milk and subsequent bacterial proliferation leads to the intense inflammation and systemic symptoms characteristic of clinical mastitis. Risk factors that contribute to milk stasis include an infant’s poor latch, infrequent feedings, or any factor that causes pressure on the breast, restricting milk flow.
Diagnosis and Selecting the Right Antibiotics
The diagnosis of bacterial mastitis is typically made clinically based on the characteristic presentation of localized symptoms combined with systemic signs like fever. However, determining the specific bacteria involved is crucial for treatment success, especially in complex cases. Milk culturing is generally reserved for situations where the infection is severe, recurrent, or fails to improve after 48 hours of initial antibiotic treatment. The culture allows for the identification of the exact organism and, more importantly, provides an antibiotic sensitivity profile, which indicates which medications will be effective against that specific strain.
Because initial treatment cannot wait for culture results, it is often empirical, meaning a broad-spectrum antibiotic is selected based on the assumption that S. aureus is the likely cause. First-line agents typically include penicillinase-resistant penicillins like dicloxacillin or cephalosporins such as cephalexin, which are taken for a full course of 10 to 14 days.
If there are risk factors for MRSA or if the initial empirical treatment fails, the culture results become necessary to guide targeted therapy. In these instances, antibiotics known to be effective against resistant strains, such as clindamycin or trimethoprim-sulfamethoxazole, are selected. Supportive care includes the continued, complete removal of milk from the affected breast, which is safe for the infant and helps clear the infection. Nonsteroidal anti-inflammatory drugs (NSAIDs) are also recommended to manage the pain and reduce the significant inflammation.