Breast implant infections

INTRODUCTION — Augmentation mammoplasty with prosthetic breast implantation is a common surgical procedure used for breast enlargement, for correction of asymmetries, or for reconstruction after mastectomy [1]. In 2019, in the United States, more than 290,000 procedures were performed; this figure represents a 37 percent increase from 2000 [2]. Breast implants are performed both for breast enlargement, as above, and, in women who have undergone mastectomy either for breast cancer or for risk reduction, as part of breast reconstruction.

Today, silicone implants are the implant type used by most surgeons. Saline-filled breast implants used to be the main prostheses used for breast augmentation. Although silicone gel implants provide a more natural appearance and feel, unfounded concerns about risk of connective tissue disease associated with silicone implants led to a moratorium on their use in the United States in 1992. This was lifted in November 2006, after further studies led to the conclusion that silicone gel implants expose patients to no demonstrable risk for connective tissue or rheumatologic disease. (See "Implant-based breast reconstruction and augmentation".)

Both silicone and saline implants have the disadvantages that additional surgery may be necessary, since the implants do not last a lifetime, and that periodic imaging studies may be needed to determine if implant rupture has occurred.

Breast implants in reconstruction are sometimes placed following the use of a tissue expander. In addition, acellular dermal matrix is often used as an adjunct to tissue expander in breast implant reconstructions. This matrix may assist in the shaping of the reconstructed breast and allow either one-stage breast reconstruction with implants or tissue expanders to be filled to higher volumes [3].

Issues related to breast implant infections will be reviewed here. Breast cellulitis, which is another form of breast infection related to breast cancer surgery, is discussed separately. (See "Breast cellulitis and other skin disorders of the breast".)

INCIDENCE AND RISK FACTORS — The risk of infection following breast reconstruction is difficult to estimate due to the lack of high-quality, active surveillance data. Infection rates of 0.2 to 3.2 percent of implanted breasts have been reported in retrospective studies utilizing medical record data, and these studies have methodologic limitations including the heterogeneity of the patient population (eg, post-mastectomy reconstruction versus aesthetic augmentation), surgical procedures (implants versus tissue expanders), and durations of follow-up [4-6].

Risk factors for infection associated with breast implants have not been adequately assessed in prospective studies with long-term follow-up [7]. In addition, the available data do not permit adequate evaluation of the relative importance of risk factors. Despite these limitations, the following factors are thought to be determinants of the risk of infection [7]:

●Surgical technique appears to be important, with a higher infection risk with periareolar and transareolar approaches compared with breast implant insertion through inframammary incisions, as endogenous flora in the nipple area may contaminate the implant.

●Breast reconstruction using implants after mastectomy is associated with as much as a 10-fold increase in the rate of infection compared with breast augmentation alone [8-10]. In a study of over 18,000 commercially insured women who underwent mastectomy between 2004 and 2011, the overall incidence of surgical site infection within 180 days of surgery was 10.3 percent following mastectomy plus breast implantation (compared with 5.1 percent following mastectomy only and 10.7 percent following mastectomy plus flap) [10]. The higher risk with breast reconstruction may be related to the length of procedures, lymph node dissection, tissue scarring, and skin atrophy resulting from prior cancer surgery and radiation therapy [7,11,12]. Acellular dermal matrix use during reconstruction, type II diabetes, and lower median household income (USD <$50,000) are additional risk factors reported in observational studies and a meta-analysis [13-16].

For women undergoing mastectomy with immediate reconstruction (compared with delayed) with implant placement, there is an increased association with infection, perhaps due to contamination of the operative field with endogenous flora during one-stage procedures [10,12]. As an example, in a multistate retrospective cohort study that included over 10,000 women who had reconstruction after mastectomy, the risk of surgical site infection was highest with immediate reconstruction (breast implants, tissue expanders, or immediate repair with autologous tissue within seven days, 8.9 percent risk), followed by delayed reconstruction after seven days (5.7 percent risk), followed by secondary reconstruction (immediate reconstruction followed by additional reconstruction more than seven days later, 3.2 percent risk) [12].

Despite this, immediate breast reconstruction remains the more common approach [17,18].

●The use of acellular dermal matrix as an adjunct to the placement of an implant or tissue expander is associated with higher rates of seroma formation and surgical site infections. In one meta-analysis, acellular dermal matrix use was associated with infection (odds ratio [OR] 1.47, 95% CI 1.04-2.06) but not explantation (OR 1.37, 95% CI 0.89-2.11) [19].

The origin of individual implant-associated infection is often difficult to determine. The major causes are thought to be contamination from endogenous flora in early-onset infections, while seeding of the implant due to secondary bacteremia from remote sites may be important in some late infections [7,9].

Rarely, breast implant infections have resulted from contaminated implants or the use of contaminated saline or contaminated marking solution [20-23]. (See 'Microbiology and epidemiology of infection' below.)

MICROBIOLOGY AND EPIDEMIOLOGY OF INFECTION — Acute and subacute breast implant infections are commonly due to gram-positive pathogens such as coagulase-negative staphylococci, Cutibacterium species, Staphylococcus aureus, and streptococci. However, gram-negative bacteria including Pseudomonas and anaerobes are also important pathogens in many case series [9,24-27]. In a French cohort, Pseudomonas was the second most commonly isolated pathogen in both early and late infection after S. aureus [25]. Case reports of implant infections due to opportunistic pathogens (eg, Prototheca wickerhamii, Scedosporium apiospermum) and atypical exposures (eg, Pasteurella multocida from a cat scratch, Campylobacter fetus from eating undercooked meat) have been reported and should be considered in immunocompromised hosts and patients not responding to empiric antibiotic therapy [28-32].

Implant-associated infections due to nontuberculous mycobacteria usually become apparent several weeks to several months following surgery. Typical clinical features include failure of the primary incision to heal or early dehiscence of a portion of the incision and odorless serous or seropurulent drainage of fluid that is culture-negative on routine bacterial cultures. Acid-fast stains and cultures should be obtained in all cases of subacute infection, even when routine culture reveals skin flora.

Contaminated skin marking solution and tap water have been implicated as potential sources in small outbreaks of nontuberculous mycobacterial infections [23,33], but a source is not identified in most cases [34].

In another small outbreak, black sediment in the saline implants of patients undergoing revision surgery was due to contamination with Curvularia [20]. This dematiaceous mold was isolated from the sterile supply room where saline used to fill implants had been stored in bottles under a water-damaged ceiling.

PATHOGENESIS

General principles of implant infection — The pathogenesis of prosthetic implant infections involves a complex interaction between the host, the device, and the bacteria causing the infection. In animal models, the presence of a subcutaneous foreign body reduces the minimal inoculum of S. aureus required to cause infection by a factor of more than 100,000, to as little as 100 colony-forming units [35]. At least two factors contribute to this increase in risk: foreign bodies do not have a microcirculation, which is crucial for both host defense and the delivery of antibiotics [35], and the interaction of neutrophils with the foreign body can induce a neutrophil defect that may enhance the susceptibility to infection [36].

Adherent bacteria multiply and elaborate exopolysaccharides, also known as glycocalyx. Eventually, microcolonies of bacteria encased in glycocalyx coalesce to form a structure known as a biofilm [37,38].

A majority of implant infections are caused by microorganisms that grow in biofilms such as coagulase-negative staphylococci (eg, Staphylococcus epidermidis) and S. aureus. Microcolonies of bacteria in biofilms form complex communities, with intraspecies communication and adaptation through a process called quorum-sensing, which regulates both virulence and biofilm formation [39].

Bacteria near the surface of the biofilm are usually metabolically active and have access to nutrients that diffuse through the upper surface of the biofilm. In comparison, organisms deep within the biofilm are metabolically inactive or in various stages of dormancy and are protected from host defenses such as phagocytes and antimicrobial penetration. (See "Prosthetic joint infection: Epidemiology, microbiology, clinical manifestations, and diagnosis", section on 'Biofilm'.)

Microbiology of the breast — The breast contains endogenous flora derived from the nipple ducts. Bacteria colonizing the nipple ducts may gain access to deeper breast tissue, particularly during surgical or biopsy procedures. In samples obtained from women undergoing breast augmentation or reduction, coagulase-negative staphylococci were the predominant organism, being isolated from 53 percent of specimens [40]. Other aerobic organisms, each of which was present in less than 10 percent of specimens, were diphtheroids, lactobacilli, enterococci, and alpha-hemolytic streptococci (3 percent). The major anaerobe was Cutibacterium (formerly Propionibacterium) acnes.

The endogenous flora can contaminate the prosthesis during implantation and be responsible for subsequent acute infections. (See 'Clinical manifestations' below.)

CLINICAL MANIFESTATIONS — Breast implant infections usually present in a bimodal fashion: during the acute postoperative period (six days to six weeks after surgery) or with late onset (more than six months after surgery). In a single center study of 1473 breast cancer patients who underwent mastectomy and immediate implant-based breast reconstruction or placement of a tissue expander, the median time between surgery and infection was 70 days (interquartile range [IQR]: 34 to 190 days) [5].

●Early-onset infections of breast implants are typically associated with fever, breast pain, erythema, and purulent fluid or drainage at the site of the incision. However, some patients develop systemic signs and symptoms of infection at a time when the primary surgical site manifests little or no evidence of infection [41]. As an example, toxic shock syndrome is a rare complication in the early postoperative period; it results from S. aureus infection that is usually acquired during surgery [7,42]. Symptoms in patients with toxic shock syndrome may begin as early as 12 to 24 hours after surgery, but the median time is four days after surgery [41]. Despite the severe systemic manifestations, the surgical site typically shows neither inflammation nor purulence. (See "Staphylococcal toxic shock syndrome".)

Among individuals who underwent implantation using acellular dermal matrix, erythema of the breast within the first weeks postoperatively could also reflect "red breast syndrome." It can be distinguished from infection in that the erythema only overlies the acellular dermal matrix and leukocytosis or systemic signs of infection are absent. It is felt to be an immune response and is self-limited. One particular acellular dermal matrix, AlloDerm, appears to be the main culprit [43].

●Subacute infections usually present with chronic pain, persistent drainage of serous or purulent fluid, failure of a portion of the incision to heal or remain healed, and/or migration or extrusion of the implant.

●Late infections, occurring several months to years after implantation, are rare and usually result from secondary bacteremia due to a focus of infection at another body site or an invasive procedure. Early treatment of any potentially severe bacterial infection may limit this risk.

●The role of infection in the genesis of capsular contracture (contraction of the scar around the soft implant) is unproven but suggested by the high incidence of bacteria grown in culture from these capsules [7,44,45]. Some have proposed an important role for biofilm from coagulase-negative staphylococci [46]. (See 'General principles of implant infection' above.)

DIAGNOSIS — The diagnosis of breast implant infection is typically first suspected from the clinical features of fever and erythema of the breast.

If the breast increases in size or a seroma is suspected based on physical exam, ultrasonography should be performed to see if there is a fluid collection. If fluid is present, aspiration should be performed under ultrasound guidance, since blind aspiration may lead to perforation and leakage of the implant. Aspirated fluid should be sent for Gram stain, aerobic and anaerobic bacterial cultures, and fungal and acid-fast bacilli cultures.

If tissue is removed, it should be sent for histopathologic examination and cultures. Special stains to reveal acid-fast organisms should be routinely performed and a portion of the specimen should be sent for both bacterial and mycobacterial culture [7].

TREATMENT — The initial treatment of breast implant infections is antibiotic therapy. In patients with deep infections, surgical intervention, including implant removal, is often necessary. There are no randomized trials or large cohort studies evaluating the management of breast implant infections, and our approach outlined below is based on small case series and clinical experience.

A systematic review of observational studies including 1044 patients found the following [47]:

●Twenty-nine percent of patients had a mild infection (ie, warmth, swelling, cellulitis) and were exclusively treated with antibiotics. Of these, 81 percent (95% CI:58 to 97) were successfully treated without surgical intervention.

●Thirty-nine percent underwent a one-stage replacement, of whom 85 percent (95% CI: 75 to 92) were successfully treated without infection recurrence.

●Thirty-five percent underwent explantation, of which 39 percent (95% CI:24 to 55) had delayed reimplantation (mean duration between explantation and reimplantation was 5.75 months);five percent of patients who underwent delayed reimplantation experienced recurrence of infection requiring removal of implant.

Mild, superficial cellulitis — Mild, superficial cellulitis describes patients with no systemic symptoms and with a limited area of erythema overlying the breast.

Choice of antibiotics — An empiric antibiotic regimen should include coverage for methicillin-resistant S. aureus (MRSA), coagulase-negative staphylococcus, and streptococci. A mild superficial cellulitis may be treated exclusively with oral antibiotics. For oral therapy, we prefer antibiotics such as trimethoprim-sulfamethoxazole (two double-strength tablets twice daily), clindamycin (450 mg three times daily), or the combination of doxycycline (100 mg twice daily) and amoxicillin (875 mg twice daily).

Response to therapy — In cases of superficial infections that promptly respond to oral antibiotic therapy, therapy should be continued for 10 to 14 days.

A lack of response to therapy within 48 hours should prompt re-evaluation for deeper sites of infection and any need for surgical intervention or alterations of the antibiotic regimen. Patients initially treated with oral antibiotics should be changed to an intravenous regimen. (See 'Extensive cellulitis and/or deep infections' below.)

Extensive cellulitis and/or deep infections — Extensive cellulitis describes patients with a larger area of erythema overlying the breast with or without systemic symptoms. Deep infections involve the prosthesis with abscess or draining wound.

Choice of antibiotics — Extensive cellulitis and/or deeper infections should be treated with intravenous antibiotics.

●For patients with extensive cellulitis without involvement of the prosthesis, empiric therapy should include coverage for MRSA, coagulase-negative staphylococci, and streptococci. We prefer vancomycin (table 1). (See "Vancomycin: Parenteral dosing, monitoring, and adverse effects in adults".)

●For patients with involvement of the prosthesis, abscess, or draining wound, surgery is indicated and empiric antibiotics should target MRSA, coagulase-negative staphylococci, and streptococci. In this case, initial parenteral therapy is vancomycin (table 1). Based on the Gram stain or clinical suspicion of gram-negative organisms, vancomycin should be combined with a cephalosporin or fluoroquinolone with pseudomonal activity. (See 'Indications for immediate surgical intervention' below and "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Antibiotics with antipseudomonal activity'.)

Empiric antibiotic therapy can ultimately be tailored to target the organism(s) recovered at the time of surgery or from aspiration (if performed) based on culture and susceptibilities. If no gram-negative organisms are recovered on Gram stain or culture(s) remain negative, antibiotic therapy should be tailored to cover MRSA, coagulase-negative staphylococci, and streptococci. If S. aureus or coagulase-negative staphylococcus are cultured, we would add oral rifampin (600 mg daily) for biofilm coverage.

Patients not requiring immediate surgical intervention — For patients without systemic symptoms who have an extensive cellulitis and/or ultrasound findings of a fluid collection that is nonpurulent on aspiration, close observation on intravenous antibiotics is reasonable. For patients who have had aspiration of fluid, antibiotics can be tailored to culture results. If there is clinical response to initial therapy, patients can be switched to suitable oral alternatives as described above (see 'Choice of antibiotics' above). The duration of intravenous antibiotic therapy is usually 10 to 14 days. Surgical intervention is required for infections that do not resolve on intravenous antibiotics after 48 to 72 hours.

Indications for immediate surgical intervention — For patients with systemic signs of infection and extensive cellulitis, or drainage from a wound that connects to the implant, purulent drainage from ultrasound-guided aspiration, threatened implant exposure, or wound breakdown, immediate surgical intervention is warranted.

Surgical intervention — The intent of surgery is to drain purulent fluid, resect necrotic tissue, and explore the condition of the pocket to determine if it would be possible to immediately replace an implant (one-stage replacement). Otherwise, the implant is removed with a plan for delayed reimplantation. A third approach is explantation of infected material and immediate autologous free flap breast reconstruction. This approach has been used in patients at high risk for prosthetic-related complications (eg, morbidly obese, undergoing radiation or chemotherapy for breast cancer) [48,49].

●One-stage replacement – In the absence of purulent, malodorous discharge and granulation tissue in the pocket, a one-stage implant replacement followed by antibiotic therapy is usually attempted in order to prevent the discomfort, cost, and disability required for removal, treatment, and delayed replacement of a new implant. If a decision is made to pursue a one-stage replacement, close follow-up is necessary to assure that adequate resolution of all signs of infection occurs.

●Delayed implantation – Findings that would favor immediate implant removal with a need for delayed reimplantation would be malodorous or frankly purulent discharge and granulation tissue in the pocket. In the case of sepsis, the implant is removed and the wound left open to expedite resolution of the infection. Reimplantation would be considered months later when all edema has resolved.

Additionally, conversion from a one-stage replacement to delayed implantation is necessary if any of the following factors occur over the course of the infection:

•Nontuberculous mycobacterial infection (see "Rapidly growing mycobacterial infections: Mycobacteria abscessus, chelonae, and fortuitum", section on 'Treatment')

•Fungal infections

•A prompt and lasting response to antibiotic therapy has not occurred

The timing of reimplantation if a two-stage replacement is being attempted is dependent upon the degree of infection and the causative organism [7]. Some experts recommend four to six months or more before reimplantation, although there are no published trials to support this approach.

A specialized wound vac dressing that facilitates instillation of antimicrobial solutions for 7 to 10 days before reimplantation has been studied in several small uncontrolled case series of patients who underwent two-stage breast implant replacement [50-55]. However, the optimal type, side effects, and concentration of antimicrobial solutions remains unknown. Randomized studies with long-term follow-up are needed before we can recommend this approach.

The potential efficacy of treating breast implant infection with a one-stage implant replacement has been evaluated in retrospective studies [56-62]. As an example, in a study of 43 patients with infections where salvage was attempted with a one-stage replacement, 76.7 percent were successful with a mean follow-up of 18.4 months [59]. Salvage procedures included debridement, lavage, immediate prosthesis (eg, expander or permanent implant) replacement, and systemic antibiotics for four to six weeks tailored to culture and susceptibility results from the time of surgery.

In another retrospective cohort study of 73 microbiologically confirmed implant infections, implant pocket salvage was attempted in 43 patients, with either antibiotic therapy alone for approximately two weeks (n = 35) or antibiotics for three to four days followed by a one-stage replacement and additional antibiotics (n = 8) [63]. Successful salvage, defined as retention of implant ≥12 months after surgery, was higher with a one-stage replacement (100 percent) versus antibiotics alone (57 percent; p = 0.035). Successful salvage was higher in patients with infected tissue expanders versus implants. Given the small sample size and retrospective design, important limitations include treatment selection bias and lack of standardization in the outcome measures. For example, it is unclear whether any subjects with implant retention showed signs of a recurrence, chronic pain, or disfigurement [50-55].

Duration of antibiotic therapy — Duration of therapy depends on the severity of infection and the surgical procedure employed. The initial course of intravenous antibiotics can be followed by a transition to oral therapy at 7 to 10 days if clinical improvement has occurred. The choice of subsequent oral antibiotic therapy, if indicated, is based on culture and sensitivity data recovered at the time of the surgical procedure.

●For deep infections treated with "one-stage" replacement, lavage, and/or debridement, we typically treat for two to four weeks. However, if S. aureus or coagulase-negative staphylococcus are cultured, the duration of antibiotic therapy should be extended to four to six weeks.

●For deep infections treated with implant removal and debridement with plan for delayed reimplantation, we typically treat for 10 to 14 days for bacterial infections and three to six months for mycobacterial infections.

PREVENTION — We suggest against the routine use of antimicrobial prophylaxis for the prevention of surgical site infections. This is in agreement with a guidelines from multidisciplinary expert groups in the United States [64]. For patients with particular risk factors for infection (eg, diabetes mellitus, obesity, tobacco use, coexisting infections elsewhere, known colonization with microorganisms, immunocompromised), we and others administer prophylactic antibiotics. Many surgeons routinely give an intravenous antibiotic immediately prior to the procedure regardless of underlying risk factors. (See "Antimicrobial prophylaxis for prevention of surgical site infection in adults", section on 'Breast surgery'.)

If prophylaxis is given for surgical site infection, it should cover the most common organisms responsible for wound infection, particularly staphylococci (see 'Microbiology and epidemiology of infection' above). The first-generation cephalosporin cefazolin (1 to 2 g intravenously) has been effective for most clean procedures [65]. A single dose should be given within 60 minutes prior to the surgical incision. (See "Antimicrobial prophylaxis for prevention of surgical site infection in adults", section on 'Antibiotic selection'.)

The risk of surgical site infections with breast augmentation or reconstruction surgery is generally low. The estimated mean incidence of postoperative surgical site infection following augmentation surgery is 1.4 percent (range 0 to 1.7 percent) [66]. Infection rates are higher when all forms of breast reconstruction are included, ranging from 0 to 29 percent (average, 5.8 percent).

Several observational studies have explored the risk of infection with the use of perioperative antibiotics in breast implant surgery, with conflicting results [66,67]. With breast augmentation, perioperative antibiotic prophylaxis does not appear to reduce infection rates [66]. In a systematic review evaluating all forms of breast reconstruction, short courses (24 hours or less) of antibiotics were associated with reduced infection rates compared to no antibiotics [67]. However, longer courses of antibiotics were not associated with further reduction in rates of infection even when drains were in place [68,69].

The use of topical antimicrobials and antiseptics for irrigation of the surgical pocket at the time of implantation has been suggested, but there are limited prospective clinical trials to support this practice [70]. Retrospective studies and limited prospective cohort studies have reported lower rates of surgical site infections and capsular contractures following irrigation of the implant pocket with a combination of antibiotics (eg, cefazolin, bacitracin, and gentamicin) and antiseptics (half-strength povidone iodine) [71,72]. One retrospective, single center study reported a low (0.5 percent) incidence of deep surgical site infection following primary breast augmentation without pocket irrigation. However, the study excluded breast cancer patients, all patients received one dose of perioperative systemic antibiotics, and the study did not include a comparator arm that received pocket irrigation [73]. Although not proven in controlled clinical trials, pocket irrigation with an antibiotic solution is commonly performed by most plastic surgeons.

For women with existing breast implants, there are no well-established strategies to reduce the risk of subsequent implant infection. Although prophylactic antibiotics are commonly given to such women prior to dental procedures, there are no data to support the practice [74] and we do not advise it, even with invasive dental procedures. For women with breast implants who need to undergo surgical procedures, the antibiotics typically given for that procedure to prevent surgical site infection should suffice. (See "Antimicrobial prophylaxis for prevention of surgical site infection in adults".)

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: Breast surgery".)

SUMMARY AND RECOMMENDATIONS

●Infections of breast implants occur in approximately 2 to 2.5 percent of cases. Postmastectomy implantation is associated with a higher risk of infection compared with breast augmentation alone. The use of particular surgical approaches or acellular dermal matrix may also increase the risk of infection. (See 'Incidence and risk factors' above.)

●Most acute and subacute breast implant infections are due to gram-positive pathogens such as coagulase-negative staphylococci, Cutibacterium species, Staphylococcus aureus, and streptococci. Nontuberculous mycobacteria are also an important cause of subacute infections. Both gram-positive and gram-negative (eg, Pseudomonas) bacteria have been associated with late-onset infections, often secondary to bacteremia. (See 'Microbiology and epidemiology of infection' above.)

●Breast implant infections usually have a bimodal presentation, during the acute postoperative period (six days to six weeks after surgery) or late onset (generally more than six months after surgery). Acute infections are usually associated with fever and breast pain, erythema, and drainage. Subacute infections may present with chronic pain, persistent drainage, failed healing of the incision site, or migration of the implant. (See 'Clinical manifestations' above.)

●The diagnosis of breast implant infection is typically first suspected from the clinical features of fever and erythema of the breast. If the breast is increased in size or a seroma is suspected based on physical exam, an ultrasound should be performed. Any fluid present around the implant should be aspirated under ultrasound guidance and sent for Gram stain, aerobic and anaerobic bacterial cultures, and fungal and acid-fast bacilli smears and cultures. (See 'Diagnosis' above.)

●Some bacterial breast implant infections can be treated successfully with medical therapy alone. For those requiring surgical intervention, one-stage implant replacement is an option depending on the operative findings. However, implant removal with delayed reimplantation may be necessary for cure, particularly for mycobacterial and fungal infections. (See 'Treatment' above.)

●For patients with mild, superficial cellulitis (eg, no systemic symptoms and with a limited area of erythema overlying the breast), the oral empiric regimen should target methicillin-resistant S. aureus (MRSA), coagulase-negative staphylococcus, and streptococci. (See 'Mild, superficial cellulitis' above.)

●For patients with extensive cellulitis without involvement of the prosthesis, empiric therapy should be parenteral and include coverage for MRSA, coagulase-negative staphylococci, and streptococci. Surgical intervention is not necessary unless the patient fails to improve after 24 to 48 hours of antibiotics. (See 'Extensive cellulitis and/or deep infections' above.)

●For patients with breast implant infections who have evidence of systemic toxicity, involvement of the prosthesis, abscess or draining wound, we favor an empiric parenteral antibiotic therapy with a regimen effective against MRSA, coagulase-negative staphylococcus, and streptococci. If Gram stain or cultures reveal gram-negative organisms, coverage should be expanded to also cover gram-negative bacteria. Immediate surgical evaluation is also warranted in these cases. Duration of therapy depends on the infecting organism as well as the surgical approach. (See 'Duration of antibiotic therapy' above.)

●For patients with a purulent, malodorous discharge or granulation tissue in the pocket, or with mycobacterial or fungal infection, a two-stage implant replacement with delayed reimplantation is favored. In the absence of these findings, a one-stage implant replacement with continued antibiotic therapy is usually attempted. (See 'Surgical intervention' above.)

●For patients undergoing breast augmentation or reconstructive surgery, we suggest against the routine use of antimicrobial prophylaxis for the prevention of surgical site infections (Grade 2C). For patients with particular risk factors for infection (eg, diabetes mellitus, obesity, tobacco use, coexisting infections elsewhere, known colonization with microorganisms, immunocompromised), we do administer prophylactic antibiotics. (See 'Prevention' above and "Antimicrobial prophylaxis for prevention of surgical site infection in adults".)