case study mastitis

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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

StatPearls [Internet].

Acute mastitis.

Melodie M. Blackmon ; Hao Nguyen ; Pinaki Mukherji .

Affiliations

Last Update: July 21, 2023 .

Continuing Education Activity

This activity for healthcare professionals aims to enhance clinicians' competence in diagnosing and managing acute mastitis. Lactational and non-lactational mastitis, including periductal mastitis and idiopathic granulomatous mastitis, are discussed. The activity will cover etiology, pathophysiology, epidemiology, histopathology, evaluation, treatment, and complications of mastitis. Clinicians will learn to differentiate mastitis from other breast conditions and apply evidence-based guidelines for appropriate management. The activity will emphasize the importance of continuing breastfeeding during mastitis, early recognition of abscess formation, and educating patients on preventive measures to reduce mastitis incidence. An interprofessional approach will be highlighted to improve healthcare outcomes.

Screen individuals presenting with breast pain, erythema, swelling, or systemic symptoms to identify those at risk for acute mastitis.
Differentiate lactational mastitis, periductal mastitis, and idiopathic granulomatous mastitis based on clinical presentation, risk factors, and diagnostic criteria.
Implement evidence-based treatment strategies, including antibiotic therapy, supportive measures, and pain management for each subtype of acute mastitis,
Collaborate with the interprofessional team to improve outcomes for patients affected by lactational mastitis.
Introduction

Mastitis is inflammation of the breast and can be categorized into lactational and non-lactational mastitis. Lactational mastitis is the most common form of mastitis. Non-lactational mastitis includes periductal mastitis and idiopathic granulomatous mastitis (IGM).

Lactational mastitis, or puerperal mastitis, is typically due to prolonged engorgement of milk ducts, with infection from bacterial entry through breaks in the skin. Patients can develop a focal area of erythema, pain, and swelling and can have associated systemic symptoms, most notably fever. This occurs most often in the first 6 weeks of breastfeeding but can occur at any time during lactation, with most cases decreasing after 3 months. [1]

Periductal mastitis is a benign inflammatory condition affecting the subareolar ducts and occurs most commonly in reproductive-aged women. Alternatively, IGM is a rare benign inflammatory condition that can clinically mimic breast cancer and occurs primarily in parous women ordinarily within 5 years of giving birth. [1]

Lactational mastitis is most commonly caused by bacteria that colonize the skin, with Staphylococcus aureus being the most common. Methicillin-resistant S aureus (MRSA) has become an increasingly frequent cause of mastitis, and risk factors for MRSA should be considered. Other causative organisms include Streptococcus pyogenes , Escherichia coli , Bacteroides species, and coagulase-negative staphylococci. Risk factors for lactational mastitis include a prior history of mastitis, nipple cracks and fissures, inadequate milk drainage, maternal stress and lack of sleep, tight-fitting bras, and the use of antifungal nipple creams. [2] [3]

The cause of periductal mastitis is not clear. Smoking may be associated with the development of the condition through direct damage to the ducts and subsequent inflammation. Bacteria are isolated in cultures in 62% to 85% of patients with periductal mastitis, and the most common causative organisms include S aureus , Pseudomonas aeruginosa , and Enterococcus , Bacteroides , and Proteus species. [4] Obesity and diabetes have also been proposed as possible risk factors. [5]

The etiology of IGM remains unclear. Autoimmune disease, trauma, lactation, oral contraceptive pill use, and hyperprolactinemia have all been suggested as possible causes. [6] There may also be an association with Corynebacterium , particularly in patients with histological findings of cystic neutrophilic granulomatous mastitis. [7]

Epidemiology

Worldwide, lactational mastitis occurs in 2% to 30% of breastfeeding women. [8] In the United States, the reported incidence is between 7% to 10%. [2] [9] The incidence peaks during the first 3 weeks postpartum. [10]

Periductal mastitis is most often found in reproductive-aged females and is almost exclusively associated with tobacco use. [10] Periductal mastitis occurs in 5% to 9% of women worldwide. [11]

IGM is very rare, and its true prevalence is unknown. [12] IGM occurs in parous women, usually within the first 5 years postpartum. Most affected patients report a history of breastfeeding and develop symptoms 6 months to 2 years after the cessation of breastfeeding. [13] The mean age of onset is 32 to 34. [13] Several studies have shown a higher incidence of IGM in Hispanic populations. [14] [15] [16] [12]

Pathophysiology

Lactational mastitis occurs due to the inadequate drainage of milk and the introduction of bacteria. Common scenarios leading to poor milk drainage include infrequent feeding, an oversupply of milk, rapid weaning, illness in the mother or child, and a clogged duct. [3] The inadequately drained milk stagnates, and organisms grow, leading to infection. Bacteria, usually from the infant’s mouth or mother’s skin, possibly enter the milk via cracks in the nipple. [2]

The pathophysiology of periductal mastitis remains unclear. Smoking is thought to play a role by directly or indirectly damaging the ducts leading to subsequent necrosis and infection. [17] Squamous metaplasia is found in patients with this condition, and it is thought that desquamated metaplastic cells may form a plug leading to blockage of the duct and subsequent infection. [18] One recent study showed an upregulation of IFN- γ, and IL-12A in patients with periductal mastitis compared to controls. [5] These are cytokines secreted by T helper 1 cells and play a role in eradicating foreign pathogens. The upregulation of these cytokines suggests that immune responses may play a role in the pathogenesis of periductal mastitis.

The pathophysiology of IGM remains unclear. Still, the most widely accepted theory points to autoimmune destruction initiated by a specific trigger, such as trauma, bacteria, or extravasated milk. [14] This causes leakage of secretions from the ducts into the breast tissue, and inflammatory cells infiltrate, causing a granulomatous response. [19]

Histopathology

A biopsy is not routinely recommended to evaluate periductal mastitis or lactational mastitis.

Non-caseating granulomas with epithelioid histiocytes and multinucleated giant cells in the breast lobules characterize IGM. The classic histologic features of the cystic neutrophilic granulomatous mastitis subtype are non-caseating granulomas with characteristic cystic spaces lined by neutrophils containing gram-positive cocci. [20] [21]

History and Physical

Lactational mastitis is often preceded by either engorgement or a focally blocked duct. Patients may give a history of these associated symptoms before developing the classic features of mastitis. Lactational mastitis is characterized by a focal, firm, erythematous, swollen, and painful area of one breast, plus a fever with a temperature ≥100.4 °F (38 °C). Patients often experience systemic symptoms such as chills, myalgias, and malaise.

Features of periductal mastitis include a periareolar or subareolar mass which may be associated with pain and erythema. Patients may present with nipple inversion, a thick nipple discharge, a breast abscess, or draining fistulas. [22]

IGM typically presents with a firm, unilateral breast mass. Other findings may include nipple retraction, skin thickening, axillary adenopathy, ulceration, and abscess formation. [23] Many of these features overlap with the presenting features of breast malignancy, which may, at times, lead to an early misdiagnosis. Patients with IGM can also experience extramammary manifestations, including arthralgias, episcleritis, and skin changes. [24]

The diagnosis of lactational mastitis is made based on history and clinical findings. If there is concern that the patient may have a breast abscess, a breast ultrasound can be obtained. Hypoechoic areas of purulent material will be seen if an abscess is present. A breast milk culture can guide appropriate antibiotic selection for patients with a severe infection unresponsive to initial antibiotic therapy. However, this is not typically necessary. Similarly, blood cultures should be obtained if there is a concern for bacteremia in a patient with severe mastitis. Blood cultures are also not a part of the routine workup. [11]

Periductal mastitis is primarily a clinical diagnosis. If nipple drainage is present, a gram stain and culture should be obtained to identify any associated organisms. An ultrasound or mammography should be ordered if there is a breast mass or concern for malignancy. [11]

Given the clinical features of IGM overlap with those of breast cancer, a breast biopsy must be performed to make this diagnosis. Core needle biopsy or excisional biopsy are acceptable options. Due to the proposed association between hyperprolactinemia and IGM, a prolactin level may be obtained. Ultrasound and mammography alone cannot distinguish IGM from breast malignancy. [13]

Treatment / Management

The initial management of lactational mastitis is symptomatic treatment. [25] Emptying the breasts fully has been shown to decrease the duration of symptoms in patients treated with and without antibiotics. Patients should be encouraged to continue to breastfeed, pump, or hand express. [19] [8] [9] If the patient stops draining the milk, further stasis occurs, and the infection will progress. Non-steroidal anti-inflammatory drugs (NSAIDs) can be used for pain control. Heat applied to the breast before emptying can help increase milk letdown and facilitate emptying. [25] Cold packs applied to the breast after emptying can help reduce edema and pain.

If the symptoms of lactational mastitis persist beyond 12 to 24 hours, antibiotics should be administered. [8] [9] Antibiotic therapy should be tailored accordingly, with S. aureus as the most common cause. In mild infections without MRSA risk factors, outpatient treatment can be initiated with dicloxacillin or cephalexin. If the patient has a penicillin allergy, erythromycin can be utilized. If the patient has risk factors for MRSA infection, treatment options include trimethoprim-sulfamethoxazole (TMP-SMX) or clindamycin. TMP-SMX should be avoided in women who are breastfeeding infants younger than 1 month and in infants who are jaundiced or premature. If a patient requires hospitalization, empiric treatment with vancomycin should be initiated until culture and sensitivity results return. There are insufficient studies on the appropriate duration of outpatient antibiotic treatment, but most sources recommend a 10 to14 day course. [10]

Periductal mastitis is treated empirically with amoxicillin-clavulanate. Alternative options include dicloxacillin plus metronidazole or cephalexin plus metronidazole. If an abscess is present, ultrasound-guided needle aspiration plus antibiotic therapy is the preferred management choice. [11] Periductal mastitis is often a recurring condition. Surgical excision of the inflamed ducts may be required if a patient has multiple recurrent infections. [26]

The treatment of IGM remains controversial. Current treatment strategies vary broadly, including observation, corticosteroids, immunosuppressants, antibiotics, and surgery. [23] IGM is a benign condition that typically resolves without treatment in an average of 5 months. [23] A recent study showed that the time to resolution of symptoms did not differ between patients managed with medications and those managed with observation and supportive care alone. [23] Surgical excision is an option, but there is a reported 10% recurrence, even with surgical treatment. If IGM is complicated by secondary infection, antibiotics should be chosen based on culture and sensitivity results.

Differential Diagnosis

The differential diagnosis of the 3 forms of mastitis varies significantly. The common differential diagnoses for each are as follows:

Lactational Mastitis

Breast engorgement
Clogged duct
Breast abscess
Galactocele
Inflammatory breast carcinoma

Periductal Mastitis

Duct ectasia
Breast carcinoma

Idiopathic Granulomatous Mastitis

Wegener granulomatosis
Tuberculosis
Sarcoidosis

Most patients with mastitis will recover with appropriate treatment. The recurrence rate for each type of mastitis is as follows:

Lactational mastitis: 8% to 30% [27] [28]
Periductal mastitis: 4% to 28% [17]
Idiopathic granulomatous mastitis (IGM): 20% to 78% [29] [30]

One study reported that 38% of patients with IGM reported significant scarring, and 29% reported long-term pain. [30]

Complications

One of the most common breastfeeding complications is lactational mastitis resulting in early termination of breastfeeding. The infection of the breast and associated pain are the most commonly cited reasons for early cessation. [25] [31] A breast abscess is a complication of lactational mastitis and occurs in 3% to 11% of patients. [32] [25] The development of a breast abscess is more common if mastitis is not treated early in its course.

Periductal mastitis and IGM can be complicated by an abscess or fistula formation. Both forms of non-lactational mastitis are associated with recurrence and can lead to scarring and deformity of the breast tissue.

Deterrence and Patient Education

Lactational mastitis frequently develops after a period of incomplete drainage and milk stasis. Educating patients on ways to limit potential stasis to prevent mastitis is crucial. Topics to discuss may include the appropriate feeding frequency and proper infant latching technique. Nipple pain is common in breastfeeding women and may lead to less frequent nursing. This increases milk stasis, thus increasing the patient's risk of developing mastitis. It is essential to counsel patients on decreasing or managing their pain. Patients with lactational mastitis may feel inclined to stop breastfeeding due to discomfort or pain and the concern of passing the infection to their infant. Clinicians should reassure the patient that breastfeeding with mastitis is safe and should recommend the patient continue if desired. [33] If the patient does not wish to continue breastfeeding, she should be counseled on the importance of emptying the breasts and taught alternative methods, such as using a breast pump or manual expression.

In addition to patient education, the education of health care professionals is also essential. One small study showed that some clinicians are misinforming patients with mastitis that they must stop breastfeeding while infected. [28] Not only does this error increase the likelihood of the patient developing an abscess, but it also contributes to the early termination of breastfeeding, eliminating the associated benefits to both the patient and the infant. [33]

Periductal mastitis is found almost exclusively in smokers. Encouraging smoking cessation is essential and may help reduce the risk of recurrent inflammation.

Pearls and Other Issues

Take-Home Points

One of the most critical considerations in the treatment of lactational mastitis is the need to continue to empty the breasts. Therefore, patients should be encouraged to continue breastfeeding if desired and, if not, to use a breast pump or express by hand.
Lactational mastitis can be managed conservatively with supportive measures for the first 12 to 24 hours. If symptoms do not improve after this period, antibiotics should be started.
If symptoms of lactational mastitis do not improve in 24 to 28 hours, consider the possibility of a breast abscess, and obtain a breast ultrasound.
IGM is a rare condition often mistaken for breast carcinoma. A biopsy must be performed to diagnose this condition and to rule out malignancy.
The majority of patients with mastitis can be managed as outpatients. Examples in which a patient may require hospitalization include hemodynamic instability, intolerance to oral intake, severe dehydration, and recurrent infection that has failed outpatient management.
Enhancing Healthcare Team Outcomes

Lactational mastitis is a common condition among breastfeeding women. There are several modifiable risk factors discussed in this article, such as feeding too infrequently, the use of certain nipple creams, poor latching techniques, and tight-fitting bras, that predispose women to this condition. Education soon after delivery to raise maternal awareness of these risk factors could decrease mastitis incidence. An interprofessional team approach should be taken when educating postpartum women. Input from physicians, advanced practice practitioners, nursing staff, and lactation consultants should be incorporated in a consolidated effort to help decrease the incidence of lactational mastitis.

While patients with lactational mastitis may seek care from their obstetrician, it is not uncommon for these patients to present to urgent care facilities, emergency departments, or family practice physicians for evaluation. For this reason, healthcare professionals in each of these settings must be aware of the appropriate management. All medical staff caring for patients with mastitis need to be aware of the recommendation that these patients continue to breastfeed and that sudden cessation of breastfeeding increases the risk of abscess formation. [33]

For patients seeking care in the emergency department, where there are often long wait times, pumping or nursing may be necessary during the waiting period. Some hospitals have breast pumps that can be checked out to patients in the emergency department. Emergency department clinicians should know their hospital policy to obtain a breast pump if needed. This can often be coordinated with the lactation consulting or obstetrics teams.

When a physician is unsure whether or not an antibiotic is appropriate to take while breastfeeding, a pharmacist's expertise can be requested to ensure the patient is prescribed a medication that will allow her to continue safely breastfeeding.

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Disclosure: Melodie Blackmon declares no relevant financial relationships with ineligible companies.

Disclosure: Hao Nguyen declares no relevant financial relationships with ineligible companies.

Disclosure: Pinaki Mukherji declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Cite this Page Blackmon MM, Nguyen H, Mukherji P. Acute Mastitis. [Updated 2023 Jul 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Case Report
Open access
Published: 15 September 2020

Case report: characterization of a persistent, treatment-resistant, novel Staphylococcus aureus infection causing chronic mastitis in a Holstein dairy cow

Ellie J. Putz 1 , 2 ,
Mitchell V. Palmer 1 ,
Eduardo Casas 2 ,
Timothy A. Reinhardt 2 &
John D. Lippolis ORCID: orcid.org/0000-0003-2314-4384 2

BMC Veterinary Research volume 16 , Article number: 336 ( 2020 ) Cite this article

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Mastitis is the most common health concern plaguing the modern dairy cow and costs dairy producers estimates of two billion dollars annually. Staphylococcus aureus infections are prevalent, displaying varied disease presentation and markedly low cure rates. Neutrophils are considered the first line of defense against mastitis causing bacteria and are frequently targeted in the development of treatment and prevention technologies. We describe a case of naturally occurring, chronic mastitis in a Holstein cow (1428), caused by a novel strain of S. aureus that was not able to be cleared by antibiotic treatment.

Case presentation

The infection was identified in a single quarter, 2 months into the cow’s first lactation. The infection persisted for the following 20 months, including through dry off, and a second calving and lactation. This case of mastitis was associated with a consistently high somatic cell count, however presented with no other clinical signs. This cow was unsuccessfully treated with antibiotics commonly used to treat mastitis, consisting of two rounds of treatment during lactation and an additional round at the beginning of dry off. The chronic infection was also unchanged through an experimental mid-lactation treatment with pegylated granulocyte-colony stimulating factor (PEG-gCSF) and an additional periparturient treatment with PEG-gCSF. We isolated milk neutrophils from 1428 and compared them to two cows challenged with experimental S. aureus, strain Newbould 305. Neutrophils from 1428’s milk had higher surface expression of myeloperoxidase compared to experimental Newbould challenged animals, as well as increased presence of Neutrophil Extracellular Traps. This suggests a heightened activation state of neutrophils sourced from 1428’s naturally occurring infection. Upon postmortem examination, the affected quarter revealed multifocal abscesses separated by fibrous connective tissues. Abscesses were most common in the gland cistern and collecting duct region. Microscopically, the inflammatory reaction was pyogranulomatous to granulomatous and consistent with botryomycosis. Colonies of Gram-positive cocci were found within the eosinophilic matrix of the Splendore-Hoeppli reaction within granulomas and intracellularly within the acinar epithelium.

Conclusions

Collectively, we describe a unique case of chronic mastitis, the characterization of which provides valuable insight into the mechanics of S. aureus treatment resistance and immune escape.

Mastitis is estimated to cost the US dairy industry $2 billion per year [ 1 ]. One of the most common mastitis causing pathogens remains Staphylococcus aureus ( S. aureus ), which can appear in both chronic and acute varieties, with markedly low cure rates [ 2 , 3 ]. S. aureus is known to escape immune clearance by adhering and infiltrating epithelial cells of the mammary gland which contributes to the difficulty to treat an infection [ 4 , 5 ]. S. aureus can also be associated with walled-off aggregates seen histologically as Splendore-Hoeppli phenomena [ 6 ]. Strain specific phenotypes are also associated with S. aureus infections in cattle, including varying degrees of epithelial invasiveness, and inflammatory responses [ 5 , 7 , 8 ].

Neutrophils are a primary immune effector cell in response to an intramammary infection [ 9 , 10 , 11 ]. Circulating neutrophils express the cell adhesion molecule CD62L (L-selectin) on their cell surface. In response to an infection, local vascular signaling molecules interact with CD62L. This activation causes CD62L to be cleaved and shed from the cell surface, which facilitates cell migration into the tissue and helps target CD62L expressing immune cells, such as neutrophils, to the site of infection [ 10 , 12 , 13 , 14 ]. An additional adhesion molecule, CD62E (E-selectin), is differentially expressed on vascular endothelial cells at the site of infection. Neutrophils have been shown to upregulate their surface expression of myeloperoxidase (MPO) in response to stimulus [ 15 , 16 ]. Glycovariants of surface MPO are thought to bind to E-selectin [ 17 ] and maybe part of the mechanism that allows the movement of the neutrophils from the circulation into the mammary gland. Treatment of cows with PEGg-CSF can cause shedding of surface CD62L and up-regulation of cell surface MPO in neutrophils [ 18 ]. Experimental infection of the mammary gland has resulted in the appearance of neutrophils in the milk with the high surface level of CD62L and MPO, suggesting their translocation from the blood into the mammary gland of infected cows [ 18 ].

When they encounter a pathogen, neutrophils have multiple antimicrobial mechanistic weapons at their disposal. They can produce reactive oxygen species, phagocytose the bacteria, or eject their genomic material to capture the bacterium in what are called Neutrophil Extracellular Traps (NETs) that contain antimicrobial proteins [ 19 , 20 , 21 ]. The presence of neutrophil NETs in milk from infected cows can be observed by DNA stains of the milk fat. Of the three antimicrobial mechanisms employed by neutrophils, NETs have been shown to have a longer efficacy in milk than the others [ 20 ].

While antibiotics are the most common treatment for mastitis cases, alternative approaches do exist including preventative cytokine therapeutics such as pegylated granulocyte-colony stimulating factor (PEG-gCSF) (Imrestor/Pegbovigrastim, Elanco, IN USA). These alternative approaches have been shown to boost circulating neutrophil numbers, lower disease severity against mastitis challenge, and reduce the naturally occurring incidence of mastitis when administered during the periparturient period [ 22 , 23 ].

We describe the case of a three-year old Holstein dairy cow (1428) who presented with a naturally-occurring, subclinical mastitis infection in her left hindquarter, approximately two months into her first lactation. Milk samples from cows in our research herd are periodically monitored for bacterial growth and changes in SCC (Somatic Cell Count) to monitor animal and udder health. Additional samples are collected if naturally occurring mastitis is suspected or for various scientific uses. Cow 1428 was born and raised on the USDA campus within the Holstein research herd. Mastitis was observed at a routine daily milking and culture of the sample was performed. Milk from quarters of interest was aseptically collected, by hand milking, and SCC sample values were determined by Dairy Lab Services (IA, USA). For bacterial counts, aseptically collected milk samples were plated on Trypticase Soy Agar with 5% sheep blood plates (BD Biosciences, CA, USA Cat. No.221261), and incubated overnight at 37 °C, prior to colony counting. An isolated colony was typed by the Iowa State University Veterinary Diagnostic Laboratory (ISU VDL) and identified as S. aureus . The S. aureus strain was sequenced and designated as SA1428 [ 24 ]. The infection remained subclinical, with no identifiable drop in milk yield, no visual signs of inflammation including teat hardening, redness, or milk chunkiness, but was continuously identifiable by moderately increased SCC and bacterial culture. Multiple SCC and bacterial counts were determined over the course of several months. At the initial detection of the infection SCC in the infected quarter were 3.8 × 10 6 cells/ mL with bacteria counts > 3000 cfu/mL. Other quarters had no detectable bacteria and SCC below 7.5 × 10 4 cells/ mL. Cow 1428 was not isolated from the herd, however, no other cows became naturally infected with the novel S. aureus pathogen to our knowledge.

Cow 1428 was treated with antibiotics, daily for five days, with cephapirin sodium (ToDAY, Boehringer Ingelheim, MO, USA) twice daily, and additionally pirlimycin hydrochloride (PIRSUE, Zoetis, NJ, USA) once daily. In our herd, this treatment has been successful at clearing experimentally induced S. aureus infections (Newbould 305 strain). When antibiotics did not clear the infection (as confirmed by bacterial culture) an additional round of antibiotics was completed two months later, which also failed to clear 1428’s infection. Numerous rounds of antibiotic treatment may not be a common commercial practice, but was appropriate within our research herd where previously we have been able to clear experimental S. aureus infections with this specific treatment and where milk is not used for human consumption. Interestingly, susceptibility testing of SA1428 by the ISU VDL, revealed susceptibility to several antibiotics (Ampicillin, Ceftiofur, Cephalothin, Erythromycin, Oxacillin, Penicillin, Penicillin/Novobiocin, Pirlimycin, Sulfadimethoxine, and Tetracycline). Mid-lactation, cow 1428 was treated off-label with a cytokine-based, PEG-gCSF therapy (Imrestor/Pegbovigrastim, Elanco, IN, USA), which was administered in two subcutaneous doses of 2.7 mL of 15 mg PEG-gCSF 7 days apart. While on-label use is designed for periparturient administration, our group was interested if the PEG-gCSF targeted neutrophil expansion would have an effect on 1428’s chronic infection. After PEG-gCSF treatment, circulating blood neutrophils increased from 2× 10 9 cells per liter of blood to 54 × 10 9 cells per liter of blood at their peak, 2 days post the second PEG-gCSF injection. In her infected quarter, cow 1428’s SCC also increased, from 1.11 × 10 6 cells per milliliter of milk to 5.17 × 10 6 cells per milliliter of milk, peaking 4 days post the second PEG-gCSF injection. Despite the increased presence of circulating neutrophils and milk SCC, cow 1428 did not clear the S. aureus infection. After being bred and confirmed pregnant, cow 1428 was dried off approximately 60 days prior to calving. In accordance with general dry-off practice, she was treated with cephapirin benzathine (ToMORROW, Boehringer Ingelheim, MO, USA). Seven days prior to cow 1428’s calving date she was treated again with an injection of PEG-gCSF, and again on the day of calving, as directed by on-label use of the product. Despite this treatment, 1428’s S. aureus infection presented immediately with the start of her second lactation.

We sought to characterize the infected mammary gland environment to identify phenotypes associated with SA1428 infection as compared to experimentally infected S. aureus . For the experimentally infected samples, we utilized resident Holsteins five weeks post experimental infection with S. aureus Newbould 305. For another ongoing study on the USDA National Animal Disease Center campus, eight Holstein cows were challenged by intramammary infusion in a single quarter with 150 CFU of S. aureus (Newbould). Subclinical, chronic infections developed in all cows. Five weeks after challenge, the Newbould infected cow with consistently high SCC values, and the Newbould infected cow with consistently low SCC values had milk samples collected for comparison along with milk from 1428’s naturally occurring infection. Over three consecutive days, 1428’s SCC for her infected quarter averaged 3.02 ± 0.78 × 10 6 cells per milliliter of milk, the high SCC cow averaged 12.59 ± 6.55 × 10 6 cells per milliliter of milk, and the low SCC cow averaged 0.24 ± 0.08 × 10 6 cells per milliliter of milk.

From S. aureus infected quarters 100–150 mL of milk was collected into 50 mL conical tubes. Samples were spun for 40 min, at 10,000 x g, at 4 °C to separate for pelleted milk cells for flow analysis and milk fat. Top milk fat layers were scraped into separate tubes, washed with PBS and protease inhibitor, and frozen for subsequent NET analysis.

Milk from the centrifuged samples was poured off, and cell pellets were placed on ice and resuspended in 1 mL media (L-glutamine, 10% FBS supplemented complete RPMI). Cell suspensions were layered over density gradients (Histopaque 1077, Sigma Aldrich, MO, USA, Cat No. 10771-500ML) spun for 20 min at 1500 x g, and had buffy coats removed leaving a highly neutrophil enriched cell pellet. Cell pellets were washed once with PBS and live cell counts were determined by cell counter (TC20 automated cell counter, BioRad, CA, USA). We used flow cytometry to evaluate the surface expression of MPO and L-selectin on neutrophils sourced from milk from infected quarters. To compare MPO and L-selectin expression over a range of SCC, we sampled milk from the Newbould infected cows with the highest and lowest SCC to compare with milk from cow 1428. Live milk cells were washed and resuspended in flow buffer (BioLegend, CA, USA, Cat. No. 420201). Individual primary, secondary, and directly conjugated antibodies were added to cell suspensions and incubated at room temperature for 15 min in the dark, with a flow buffer wash step between each antibody set. Samples were run on a Becton Dickinson LSR II flow cytometer and all analyses were performed with FlowJo software (FlowJo LLC, Ashland, OR, USA). Neutrophil gating was determined by forward and side scatter. Live, singlet milk cells were gated for CD45 (Monoclonal Antibody Center, Washington State University, USA. Cat. No. BOV2039). CD45 + cells were separately assessed for MPO (BioRad, Hercules, CA, USA Cat. No. VPA00193) and CD62L (BioLegend, San Diego, CA, USA Cat. No. 304824) surface expression. Flow cytometry of milk derived neutrophils from the three cows showed that cow 1428 had the greatest MPO surface expression (Fig. 1 a). Between the Newbould infected cows, the high SCC cow also showed higher surface MPO expression compared to the low SCC cow (Fig. 1 a). Surface expression of L-selectin revealed comparable levels on 1428 and the high SCC Newbould infected cow, but both were reduced compared to the low SCC Newbould infected cow (Fig. 1 b).

Flow cytometry and microscopy of NETs sourced from chronically S. aureus infected milk from 1428 and two Newbould infected cows (high and low somatic cell responders). Flow Cytometry of neutrophils isolated from infected milk was analyzed for surface expression of ( a ) myeloperoxidase and ( b ) CD62L (L-selectin). The red histogram depicts cell isolated from 1428 milk, dark gray is from a chronic Newbould challenged low SCC cow, and light gray represents a chronic Newbould challenged high SCC cow. Milk fat was additionally evaluated for the presence of Neutrophil Extracellular Traps (NETs). ( c ) 1428 S. aureus infected milk fat shows increased NET presence compared to both high ( d ) and low ( e ) SCC cows challenged with Newbould. Control NET staining shows DNAse treatment of 1428’s infected milk fat ( f ), and staining of clean healthy quarter milk fat from cow 1428

Neutrophils are known to produce NETs with activation which results in cell death. To capture information about NET-forming neutrophils, we stained milk fat for DNA as described previously [ 16 ], which is indicative of NET formation from all three cows. Microscopy showed that 1428 had the greatest NET presence (Fig. 1 c), compared to both Newbould infected cows (Fig. 1 d, e). DNAse treated and healthy milk fat controls are shown in Fig. 1 f, g. Samples were analyzed via confocal microscopy imaging using a Nikon A1R+ laser scanning microscope and NIS-Elements imaging software. Slide images are shown at the 20X objective, 75 numerical aperture, as imaged using a GaASP detector, 561 laser.

Cow 1428 was euthanized approximately 20 months after the first identification of infection by lethal injection of barbiturates by our institutional veterinarian. Gross pathology of the infected quarter of the mammary gland can be seen in Fig. 2 a, b . The infected quarter was systematically sampled by obtaining samples from 12 different sites; 3 each from the proximal and distal gland body of the gland, 3 from the collecting duct region and 1 each from the gland cistern, teat cistern and streak canal as illustrated in Fig. 2 c. Gross examination revealed multifocal abscesses and increased amounts of fibrous connective tissue, most notably in the collecting duct and gland cistern regions. Tissue samples (≤0.5 cm thick) were fixed by immersion in 10% neutral buffered formalin for 24 h, then transferred to 70% alcohol followed by standard paraffin embedding techniques. Paraffin embedded samples were cut to 4 μm thick sections, transferred to Superfrost Plus™ charged microscope slides (Thermo Fisher, MA, USA) and stained with hematoxylin and eosin (H&E). Adjacent sections were stained by the Hucker-Twort technique for visualization of Gram-positive and Gram-negative bacteria. Microscopically, samples from the teat sphincter and teat cistern were normal, with minimal if any inflammation (Fig. 2 c) and no bacteria present, confirmed by Gram stain. Samples from the gland cistern and collecting duct regions contained multifocal suppurative to pyogranulomatous infiltrates. Some regions contained distinct infiltrates of only neutrophils surrounding colonies of Gram-positive cocci embedded in a brightly eosinophilic, homogenous matrix, which radiated outward; interpreted to be Splendore-Hoeppli reaction (Fig. 3 a, b). In these same regions, there were also pyogranulomatous to granulomatous infiltrates arranged in nodules separated by prominent bands of fibrous connective tissue (Fig. 3 c). These nodular infiltrates contained variable numbers of extracellular Gram-positive cocci. In the alveolar duct and body regions of the gland, numerous acini contained infiltrates of large numbers of neutrophils (Fig. 3 d). In such acini, Gram-positive cocci were found both individually and in small colonies (Fig. 3 e). Some glands were absent of inflammatory infiltrates, but one to several Gram-positive cocci could still be found adhered to or within epithelial cells (Fig. 3 f).

Gross pathology and necropsy collection outline detailing levels of inflammation. Gross pathology of 1428’s infected quarter ( a , b ). Note multifocal purulent exudate found in abscesses surrounded by fibrous connective tissue. The mammary gland was sampled as detailed in ( c ), capturing tissue from physiologically meaningful regions of the mammary gland. Also depicted, general levels of inflammation found at each section level ( c ). Diagram in ( c ) adapted from [ 25 ]

Photomicrographs of mastitic quarter from 1428. (A) Pyogranulomatous infiltrate. Note colonies of basophilic cocci (white arrows) within brightly eosinophilic and radiating matrix of Splendore-Hoeppli reaction (black arrows). H&E 20X. (B) Cocci within eosinophilic matrix are Gram-positive. Gram stain 40X. (C) Granulomas with abundant peripheral fibrosis and central areas of dystrophic mineralization. H&E 4X. (D) Acini containing numerous neutrophils. H&E 10X. (E) Intraluminal Gram-positive cocci within acinus. Gram stain 40X. (F) Intracellular Gram-positive cocci. Gram stain 20X

To further document S. aureus strain SA1428, its genome was sequenced. The genome sequencing data have been deposited in NCBI Sequence Read Archive under accession number PRJNA609126. The de novo genome assembly is available at NCBI with the accession number CP048431-CP048432.

Discussion and conclusions

This unique case report sheds light on important host and pathogen interactions that should be further investigated to be utilized in the development of mastitis treatment and preventative technologies. The presence of heightened immune cell activation in the mammary gland identified by present neutrophils, but lack of bacterial clearance, raises questions about the mechanisms of inflammation regulation and immune escape strategies of S. aureus as a mastitis causing pathogen. Low cure rates of S. aureus mastitis have been attributed to components of host and pathogen genetics, environmental exposure, and antibiotic resistance [ 26 ]. Additionally, while it’s known that S. aureus can evade neutrophil killing and gain intracellular access to epithelial cells [ 26 ], much more needs to be understood about why the immune response is ineffective and how S. aureus escape mechanisms function. In this work we demonstrate a correlation between infections caused by two strains of S. aureus and differences in surface expression of proteins of interest on milk neutrophils. Milk neutrophils sourced from cow 1428 had substantially increased surface expression of MPO (Fig. 1 a), which has been associated with cell activation [ 16 ] as well as accumulation within mastitic mammary glands [ 18 ]. Also consistent with neutrophil activation, levels of surface CD62L were comparable between 1428 cells and the high SCC Newbould cow, but both appeared to have increased shedding of CD62L compared to the low SCC cow (Fig. 1 b). These observations are consistent with the role of CD62L as an adhesion molecule important for the targeting cells to the site of infection. These observations are also supportive of the hypothesis that MPO expressed on the cell surface may be a ligand for E-selectin and potentially plays a role in cell migration to localized infections. Lastly, imaging showed more NETs present in 1428’s milk fat than in either of the Newbould challenged cows (Fig. 1 c, d, e). Collectively these findings suggest that cow 1428 had heightened neutrophil activation within the mammary gland compared to cells from experimentally infected animals. It is also clear that this activation is not driven strictly by accumulated cell numbers as the high SCC Newbould infected cow had four-fold higher SCC numbers than 1428. Of interest, between the two Newbould experimentally-infected animals, the high SCC Newbould infected cow had higher surface expression of MPO compared to the low SCC Newbould infected cow (Fig. 1 a), reduced surface expression of CD62L (Fig. 1 b), and increased NET presence (Fig. 1 d,e), which is supportive that these parameters are capturing biological activation. These findings should be further validated in the context of hypothesis driven experimental studies.

Many different strains of S. aureus exist that are capable of causing mastitis in dairy cattle. Variations in mastitis-causing strains include differences in the genotypic expression of virulence factors, biofilm production, cellular infiltration, and antimicrobial activity [ 27 ]. Comparison of an infection by SA1428 and SA Newbould highlights the phenotypic variation between strains that can be observed, both in terms of host immune cell response and response to antibiotic treatment; Newbould being successfully cleared and SA1428 persisting. The antibiotic susceptibility results of S. aureus SA1428, but failure to treat in vivo, suggests that the persistence of 1428’s infection may be contributed to physical escape by the bacteria. Histologically, inflammation of 1428’s infected quarter can be considered chronic in nature with pyogranulomatous and granulomatous lesions and increased fibrosis. The largest numbers of Gram-positive cocci were seen within the eosinophilic matrix of the Splendore-Hoeppli reaction associated with pyogranulomatous lesions and the nodular granulomatous infiltrates surrounded by large bands of fibrous connective tissue. Both settings provide protection from antibiotic treatment.

The naturally occurring, chronic case of S. aureus mastitis of cow 1428 describes the identification of strain SA1428, and describes an associated treatment-resistant phenotype. Our unique evaluation of activation levels of mammary sourced neutrophils, and detailed look at weakly characterized histology phenomena, contributes to the general knowledge of the behavior of chronic S. aureus infections, and offers several opportunities for hypothesis driven research to explore these findings.

Availability of data and materials

The genome sequencing data for SA1428 has been deposited in NCBI Sequence Read Archive (accession number PRJNA609126), and the de novo genome assembly is available at NCBI (accession number CP048431-CP048432). All additional datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Abbreviations

Somatic Cell Count

Myeloperoxidase

Pegylated granulocyte-colony stimulating factor

Neutrophil extracellular trap

Hematoxylin and eosin

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Acknowledgements

Our greatest appreciation goes to Duane Zimmerman, Tera Nyholm, Adrienne Shircliff, and Judi Stasko of the USDA Microscopy Service team, as well as to the animal and veterinary care staff for the excellent care of animals. Mention of trade names, proprietary products, or specified equipment do not constitute a guarantee or warranty by the USDA and does not imply approval to the exclusion of other products that may be suitable. USDA is an Equal Opportunity Employer.

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EJP wrote the manuscript and performed neutrophil characterization. MP was the case pathologist, responsible for necropsy sample collection, interpretation of histological results, and helped write and edit the manuscript. HM was responsible for the processing of sequence data. JDL and TAR helped interpret results, contributed to writing and editing the manuscript, and aided in designing characterization methods. The author(s) read and approved the final manuscript.

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Putz, E.J., Palmer, M.V., Ma, H. et al. Case report: characterization of a persistent, treatment-resistant, novel Staphylococcus aureus infection causing chronic mastitis in a Holstein dairy cow. BMC Vet Res 16 , 336 (2020). https://doi.org/10.1186/s12917-020-02528-8

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Breast Pumps and Mastitis in Breastfeeding Women: Clarifying the Relationship

Leon r mitoulas, riccardo davanzo.

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Received 2022 Jan 17; Accepted 2022 May 23; Collection date 2022.

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Mastitis is a debilitating condition that can impact around 20% of mothers and is characterized by fever, flu-like symptoms and tender, swollen areas of the breasts. Despite the emerging evidence that breast milk dysbiosis is an underlying cause of mastitis, breast pumps have been implicated as a predisposing risk factor in the pathophysiology of mastitis in breastfeeding mothers. Previous studies have suggested that the use of a breast pump increases a mother's risk for developing mastitis, however, incidence rates of mastitis over the stages of lactation do not match breast pump usage rates. Furthermore, breast pumps, even when used at low vacuum, still promote some breast drainage, thus avoiding milk stasis, which is considered a key factor in the development of mastitis. As a consequence, these data suggest that the literature association of breast pumps with mastitis is more a case of reverse causation and not direct association. Moreover, it is important to note that breast pumps are actually a part of the conservative management of mastitis. In combination, these data show that the breast pump should not be considered a driver in the pathophysiology of mastitis in women.

Keywords: mastitis, human milk, breastfeeding, breast pump, breast milk expression

Introduction

Lactational mastitis, characterized by fever, flu-like symptoms and tender, swollen areas of the breasts ( 1 ), is a debilitating condition experienced by many breastfeeding mothers ( 2 ). The incidence rate of mastitis varies throughout the literature, with some texts suggesting up to 33% of mothers will experience mastitis ( 2 ). Indeed, the variability exhibited in the literature may result from the changing incidence rate associated with stage of lactation and the lack of standardization in the timing of studies ( Figure 1 ) ( 3 ). Despite this known variability, the Academy of Breastfeeding Medicine ( 4 ) suggests that the true range is more likely from 3-20%, indicating that up to one in five mothers can expect to suffer at least one episode of mastitis over the course of their lactation ( 5 ).

Incidence of mastitis over the course of lactation [Data adapted from Wilson et al. ( 3 )].

Whilst an emerging understanding suggests that an underlying cause of mastitis is due to an unbalanced breast milk microbiota ( 6 ), a contributing factor in many cases of non-infective and infective mastitis is recognized to be milk stasis ( 2 ). Blocked ducts, engorgement and injury to the breast can all result in milk stasis and precipitate non-infective mastitis, whereas cracked nipples and other trauma that disrupt the integrity of the breast may result in infective mastitis ( 7 ). Infective mastitis can be caused by bacteria associated with the skin and the infant's mouth. These bacteria are able to gain entry to the breast via cracks in the nipple ( 8 ) or by retrograde flow from the nipple back to the alveoli ( 9 ). In one study, more women with mastitis were found to have S. aureus and Group B streptococci in their milk than those mothers without symptoms ( 10 ). Notably, a growing percentage of S. aureus infections have been found to be methicillin-resistant ( 11 , 12 ). In addition, coagulase-negative staphylococci have also been commonly found associated with mastitis ( 8 ).

Currently, there is no consensus on the pathophysiology of mastitis, which can be inflammatory, with or without the presence of infection ( 4 ). Given the lack of consensus, studies have looked to define predisposing factors and areas of risk, in an effort to provide mothers with information to minimize their likelihood of developing mastitis. In this regard, the use of a breast pump has been, in recent years, associated with a reported increased risk for the development of mastitis ( 13 ). Therefore, it is important to outline the role that the breast pump plays in the pathophysiology of mastitis in women so that policy makers and institutions alike can provide mothers and clinicians with up-to-date and appropriate support.

Predisposing Factors and Treatment

The risk and predisposing factors for mastitis are many and varied although the evidence for their association is weak ( 4 ). Of these, it can be noted that the majority are situations that promote or result in the increased likelihood of milk stasis, with the exception of damaged nipples, which is more associated with direct infection. In these situations, milk stasis results in the development of an inflammatory response ( 14 ) or provides the time and environment for the growth of pathogenic bacteria. Abou-Dakn and coworkers ( 15 ) suggest that measurement of leucocytes and pathogenic bacteria in the milk can be used to differentiate the two causes, although this approach requires the availability of laboratory resources.

Treatment options nearly always focus on the optimization of milk removal with methods to promote the frequent and effective milk removal suggested as a first line, conservative management strategy ( 4 , 15 ). These care options include ensuring effective and comfortable positioning and latch during breastfeeding whilst paying attention to breastfeeding positions. The incorporation of massage is also recommended. The expression of milk remaining in the breast by the use of hand expression or a breast pump is also suggested and may augment breast drainage and decrease the time to resolution ( 4 ). The warming of the breast by wrapping in a warm, moist towel or by taking a warm bath or shower, can activate the oxytocin reflex and promote breast milk flow, whereas the application of cold after milk expression may provide an analgesic/anti inflammatory effect. Pharmacologic management is suggested for cases that do not resolve conservatively, if infectious mastitis is confirmed, or if clinical conditions do not suggest delay ( 4 , 15 ). In these instances, amoxicillin-clavulanate, dicloxacillin and flucloxacillin, as well as cephalexin (if penicillin intolerance) or clarithromycin (if beta-lactam allergy) are the empiric therapy of choice and are frequently prescribed ( 4 , 16 ). More recently, the prophylactic supplementation of the mother with a specific probiotic during pregnancy and lactation has also shown to reduce the risk of mothers developing mastitis ( 6 ), although such recommendations might better focus on women with a previous history of lactational mastitis.

Breast Pump and Breast Milk Expression

Previous studies have implicated the breast pump as a potential contributor to the condition of lactational mastitis. Foxman and colleagues ( 17 ) reported that for women without a history of mastitis, using a manual breast pump increased the risk of mastitis by 2.1 times, although interestingly, there was no association in women with a history of mastitis. These data are at odds with the perception that the breast pump is a causative factor in the development of mastitis, given that a history of mastitis, itself, is associated with an elevated odds ratio for the development of the condition ( 17 ). It would, therefore, be expected that the use of the pump would have been a greater risk factor in this population as well, if it was a causative element for the pathophysiology of mastitis.

It is also of interest to note that the incidence density for mastitis ( Figure 1 ) shows an increase in the likelihood of mastitis in the early, puerperal, stages of lactation. Breast pump usage does occur in the first four weeks postpartum ( 18 ) and remains quite high over the first 6 months of lactation ( Figure 2 ) ( 19 ). Despite this, the incidence density for mastitis from various studies published in the literature tends to decrease as stage of lactation progresses ( 3 ). Although circumstantial and even when accounting for the decrease in the percentage of mothers breastfeeding over the first six months of lactation, it would be expected that if the breast pump was a causative factor for the development of mastitis the incidence rate would remain high throughout the duration of lactation, following breast pump usage rates.

Percent of mothers who pumped or tried to pump milk by infant age, among mothers who breastfed at each age [Data adapted from Centers for Disease Control and Prevention. Results: Breastfeeding and Infant Feeding Practices ( 19 )].

Another report, by Mediano and coworkers ( 20 ), also noted that the use of a breast pump was associated with mastitis, however, the authors went on to suggest that this may be a consequence rather than a cause. Indeed, it was also noted that those studies that had observed a relationship between breast pump usage and the incidence of mastitis used retrospective data pooling, thus making it unclear if breast pump usage was a cause or a consequence of mastitis ( 21 ). In this connection, it was suggested that expressing milk by hand or by pump actually reduced the risk of mastitis and was therefore a useful technique for the prevention of mastitis during episodes of oversupply ( 22 ). This position is further bolstered by the frequent protocol recommendation to promote breast drainage via the use of hand expression or a breast pump ( 4 , 15 , 23 ). As such, the apparent reverse causation was considered more likely than a direct association, due to the confounding provided by the increased use of the breast pump by the mother with nipple damage when caused as a consequence of breastfeeding ( 3 ). This has been further supported by more recent studies finding no statistically significant correlation between the usage of a breast pump and acute mastitis ( 24 , 25 ).

Lastly, in a study analyzing 1,844 breast pump using mothers ( 13 ) who contributed to the Infant Feeding Practices II survey ( 26 ), it was suggested that mothers could reduce their risks of problems and injury by choosing breast pumps of better quality and by learning breast pump skills from a person rather than following written or video instructions. In particular, skilled support for breast shield sizing is recommended in order not to negatively impact the amount of breast milk expressed ( 27 ). The above data by Qi and coworkers also showed that for mothers using a breast pump, approximately 15% cited any pump-related injury, with only 2.2 % indicating nipple injury, leading to only 0.3% reporting any infection. These data, nevertheless, are below the recognized incidence rate for nipple trauma in the breastfeeding population, which is reported as varying between 29 and 76% ( 28 ), suggesting that an appropriate pump usage does not increase the risk of nipple trauma and further supporting the reverse causality proposed by Wilson and coworkers ( 3 ).

The Effect of Vacuum on Milk Removal

One area targeted in the implication of a breast pump being a causative factor in the pathophysiology of mastitis has been low vacuum, in particular with respect to the potential poor vacuum performance of a misused or faulty breast pump and the ensuing poor milk removal. The connection between vacuum and milk removal is well established with research on the breastfeeding infant showing that vacuum is, indeed, the main driver of milk removal ( 29 ). Furthermore, the relationship between strength of vacuum and milk removal has been extended to the mother using the breast pump ( 30 ). This has led to the development of protocols that allow the mother using the breast pump to define her individual maximum comfortable vacuum and then subsequently to use this vacuum setting for all expression episodes ( 30 ). Whilst this practice will optimize milk removal, it should be noted that a reduction in vacuum of the breast pump did not result in the complete failure of the breast pump to remove any milk ( Figure 3 ).

Volume of milk removed when pumping at maximum comfortable vacuum (MCV; −190.7 ± 8.0 mm Hg), 75% of MCV (−143.0 ± 8.8 mm Hg), −125 and −75 mm Hg [Data adapted from Kent et al. ( 30 )].

These data suggest that even with less than optimal vacuum, some milk removal is achieved. Indeed, with vacuums as weak as −75 mm Hg, Kent and colleagues ( 30 ) observed mothers removing, on average, 73.9 mL, suggesting that some milk drainage is achievable when vacuum is low and that complete milk stasis is avoided.

Despite the observation that even low vacuum will result in some milk removal, mothers should be provided anticipatory guidance on hand expression techniques and/or the optimal use of a breast pump as a critical management step in the treatment of mastitis is the frequent and effective removal of milk ( 4 ). With regard to the use of a breast pump, this includes practical aspects such as actual pump selection, relative to maternal needs, as well as evidence based characteristics specific to optimizing individualized pump performance ( 31 , 32 ). These include the use of correctly sized breast shields ( 27 ), double pumping ( 33 ), when possible and the determination of the mother's maximum comfortable vacuum ( 30 ).

It is important to note that with the key role of milk stasis acknowledged as a driver for the pathophysiology of mastitis, the suggested use of the breast pump has become a complementary strategy of the conservative management approach ( 4 , 15 , 34 ). In situations of poor infant positioning and attachment that remain unresponsive to skilled breastfeeding counseling, the inefficient drainage of the breast by the breastfeeding infant can be overcome with the use of hand expression and/or, particularly when the expression is required for a prolonged time, the breast pump, facilitating milk removal and hastening the resolution of the problem ( 4 ). Furthermore, in situations of extreme nipple pain from direct breastfeeding, the proper use of hand and/or breast pump expression, in order not to create or amplify any nipple issues, can prove to be less painful ( 35 ), and provides the mother with another option to maintain milk removal as the core issue of nipple pain is being resolved.

Given the emerging evidence in the literature regarding the underlying role of mammary gland microbiota dysbiosis in the development of mastitis ( 6 ), these data rather suggest that the use of a breast pump is unlikely to be a driver of the pathophysiology of mastitis in women and that the associations presented in the literature are most likely due to reverse causation. In support of this is the decreasing incidence density of mastitis over the course of lactation, despite breast pump usage remaining relatively high over the same timeframe. Moreover, one of the major pathways in the development of mastitis, milk stasis, has been shown to be avoided even in situations of low pump vacuum, as a result of the choice of the mother or in the case of pump misuse. In this connection, in addition to hand expression, the breast pump, when used appropriately in terms of indication and correctness of use, should be considered a valuable tool in the treatment of mastitis, facilitating the drainage of the breast when the mother is unable to breastfeed.

Data Availability Statement

The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding author.

Author Contributions

LRM conceptualized and drafted the initial manuscript. LRM and RD reviewed and edited the manuscript. Both authors contributed to the article and approved the submitted version.

Conflict of Interest

LRM is an employee of Medela AG, Switzerland. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Women's experience of lactational mastitis--I have never felt worse

Affiliation.

1 Mother and Child Health Research, La Trobe University, Melbourne, Victoria. [email protected]
PMID: 16969450

Background: Mastitis is a common problem for breastfeeding women in the postpartum period.

Methods: Ninety-four breastfeeding women participating in a case control study of mastitis provided a free text comment about their experience of mastitis. Women were recruited from the emergency department, wards or breastfeeding clinics of the Mercy Hospital for Women and the Royal Women's Hospital, Melbourne, in 2002-2004.

Results: The main themes which emerged from the free text comments were: acute physical illness; negative emotions; life disrupted; to continue breastfeeding or not? A minor theme was 'support for mastitis research'.

Discussion: Women with mastitis often experience a rapid onset physical illness accompanied by strong negative feelings, which leads some women to consider stopping breastfeeding while others are determined to persevere. General practitioners need to provide emotional support for women with mastitis and acknowledge that breastfeeding may be difficult for new mothers.