It was shown, somewhat surprisingly, that many women with potential pathogens in their breast milk, even at high bacterial counts, either recovered spontaneously from mastitis or did not have any symptoms of mastitis (as seen among control women). Furthermore, it was demonstrated that increasing bacterial counts did not influence the clinical manifestation of mastitis. The breast milk of women who were given antibiotics because of their symptoms, did not contain higher bacterial counts than those who were not given antibiotics. These results and the finding that so many healthy women harboured potential pathogens in their breast milk may indicate that the division of mastitis into infective or non-infective forms may not be practically feasible. Although only 15% of women with mastitis were given antibiotics, most of them recovered spontaneously with few cases of recurrent symptoms within 6 weeks requiring antibiotic treatment.
The diagnostic criteria for mastitis used in this study consisted of clinical signs and symptoms, which are in the main subjective. This implies that the scope of illness reported in the case group may have been quite broad, ranging from mild to very severe. However, the 6% incidence of mastitis in the breastfeeding population was low compared to the range reported by WHO (2.6% – 33%), which suggests that the women in the RCT were correctly diagnosed. The incidence of 3.3% of breast abscess development in the group with mastitis can be compared to data from a recent study from Australia, which showed that 14.5% of breastfeeding women were treated with antibiotics and 2.9% of the women with mastitis developed an abscess [11]. Leukocyte counts have previously been used as a marker of infective mastitis [5]. However, it was not possible in the present study to measure leukocyte levels since the cases were originally included in a RCT of care interventions where measurement of infection was not the primary aim. Bacterial content in breast milk may vary over time and by geographical location and therefore the findings of this study may not be applicable to all communities.
Our analysis suggested that the two most abundant bacterial species or groups found, CNS and viridans streptococci, were not linked to clinical mastitis; these are well established as major components of the resident skin or throat flora and possibly of importance for protection against pathogens [12]. Interestingly, Heikkilä and Saris found that human breast milk contains commensal bacteria that inhibit S. aureus and may prevent maternal breast infections [13]. Two potentially pathogenic species, S. aureus and GBS, were recovered more frequently in mastitis cases as compared to controls, indicating an active role in mastitis. In particular, S. aureus has earlier been reported as a primary causative organism in mastitis [14–16] and might conceivably be expected to give rise to breast abscess. The breast milk samples of five of the seven women with a breast abscess was positive for S. aureus, but these figures are too small to allow any conclusions to be drawn. The inflammation in mastitis occurs in the connective tissue of the breast and for this reason causative organisms may be difficult to isolate from breast milk.
It was stated in a WHO review on mastitis that antibiotic treatment is indicated if either cell or bacterial colony counts are available and indicate infection or symptoms are severe from the beginning or a nipple fissure is visible or symptoms do not improve after 12–24 hours of improved milk removal [2]. If these criteria had been followed, many more than the 15% of cases, as reported here, would have received antibiotics. Reports from industrialised countries such as Australia [17–19] and USA [20, 21] have shown that 77% – 97% of women with lactational mastitis are prescribed antibiotics. The findings of our study do not appear to support this extensive use of antibiotic treatment for mastitis during lactation. It is important for all communities to avoid imprudent use of antibiotics because of the spread of methicillin resistant S. aureus (MRSA) and other multi-resistant pathogens. It has also been considered that maternal antibiotic therapy might disturb the commensal flora of the upper airways in breastfed infants [22].
The major rationale for treatment of mastitis by antibiotics is to avoid the development of breast abscess. However, empirical evidence for a continuum from mastitis to abscess is not readily available and the WHO review suggests that breast abscess may occur seemingly spontaneously, irrespective of previous mastitis [2]. Nonetheless, lactational mastitis has the potential for serious sequelae such as breast abscess and in rare cases septicaemia [1] and if clinical signs and symptoms and bacterial culture of breast milk are unhelpful, we need to consider how to aid in the decision to prescribe antibiotics. In order to select which women will not recover without antibiotic treatment, it is necessary to maintain daily contacts with the women to assure that symptoms are subsiding. Although, as reported earlier [4] the mean number of contact days with a breastfeeding clinic was 5 (± 2.9), it is important, in our opinion, that symptoms improve within 24 to 48 hours after initiation of care interventions. Scales to measure symptoms may assist clinicians in judging whether improvement has occurred. Continuity of care provider will also ensure that women are adequately treated. Those not improving will need a new consultation with a view to antibiotic treatment. At this time, results of bacterial culture may be of value for choice of antibiotic.
The frequent occurrence of GBS in both cases and healthy mothers was notable. GBS is a leading cause of serious infection in neonates [23] but no such infections were reported in the context of this study. Whether certain components of breast milk may protect infants and mothers from invasive GBS infection will be an important area for future research. Another avenue for investigation might be to consider why many women who harbour S. aureus do not develop mastitis. Knowledge of how often breast abscess occurs during lactation without any noticeable episode of preceding breast inflammation might also give us more understanding of the process. Well-designed RCTs of antibiotic therapy for treatment of lactational mastitis would help define the optimal level of such treatment for this group. New research could also include measurement of leukocyte levels.
Comments
View archived comments (1)