Eczema Antibiotics: When They Work and Don't

Your dermatologist just prescribed antibiotics for your eczema. But you don't have an infection. This confuses many patients. Research shows that up to 70% of people with atopic dermatitis are colonized by Staphylococcus aureus bacteria on their skin^[1], yet only a fraction develop obvious infections. Clinical studies reveal that antibiotics work for eczema through mechanisms beyond killing bacteria^[2]. Understanding these pathways opens new treatment possibilities.

You've tried prescription steroids that worked briefly then stopped. Moisturizers helped for hours, not days. Elimination diets disappointed. Each new treatment brought hope, then frustration when symptoms returned. Real-world data shows that over 90% of eczema patients using topical treatments, including steroids, discontinue their use^[3]. The problem isn't your commitment. It's that most approaches address symptoms, not underlying causes.

This guide reveals how antibiotics treat eczema through three distinct mechanisms: reducing harmful bacteria, calming inflammation, and restoring skin microbiome balance. You'll discover why tetracycline-class antibiotics work differently than traditional infection-fighting drugs. We'll examine combination protocols that dermatologists use, including how SmartLotion enhances antibiotic effectiveness. Plus, you'll learn when antibiotics don't work and what alternatives exist. Every recommendation is supported by peer-reviewed research.

What changed the treatment landscape:

A 2023 systematic review revealed that subantimicrobial-dose doxycycline reduces eczema severity by 40% through anti-inflammatory properties alone^[4]. This means the antibiotic effect isn't necessary for improvement. The finding transforms how dermatologists approach eczema treatment, particularly for cases that resist conventional therapy.

Understanding the Eczema-Bacteria Connection

Your skin hosts over 1,000 different bacterial species^[5]. This diverse ecosystem protects against harmful invaders, maintains moisture balance, and communicates with your immune system. Think of it as a microscopic garden where variety equals health. When eczema develops, this garden becomes overrun with weeds.

The Staph Aureus Problem

In atopic dermatitis, the skin's balanced ecosystem is disrupted, allowing Staphylococcus aureus to dominate. While 20% to 30% of healthy individuals carry S. aureus without issue, up to 90% of patients with atopic dermatitis are colonized with it^[6]. The bacteria doesn't just sit there harmlessly. It actively worsens your condition through three mechanisms:

• Produces toxins that trigger immune overreaction
• Forms biofilms that resist treatment
• Crowds out beneficial bacteria that protect your skin

Research demonstrates that colonization density correlates directly with eczema severity^[7]. Patients with severe hand eczema carry significantly higher bacterial loads than those with mild symptoms. The relationship works both ways. Eczema creates the perfect environment for S. aureus, which then makes eczema worse.

How Bacterial Imbalance Triggers Inflammation

S. aureus doesn't need to cause infection to harm your skin. The bacteria produce superantigens, proteins that activate massive immune responses^[9]. Your immune system overreacts to these proteins, creating inflammation that damages healthy tissue. This process occurs even when bacterial counts remain below infection levels.

Dr. Harlan's clinical observations over decades of practice revealed specific patterns in how bacterial overgrowth drives eczema flares:

When eczema is acute and oozy, it almost always has an overgrowth of Staph aureus producing Super-antigens that make eczema worse. The overgrowth of noxious microbes contributes to inflammation and immune dysregulation. Very fortunate people (perhaps 30-40% of us) have rock-solid immune systems that neither overreact nor underreact to environmental insults like bacteria, yeast, and other microbes. Unfortunately, at different times in our lives, the rest of us develop skin disorders caused by the overgrowth of noxious microbes on the skin and runaway inflammation.

- Dr. Steven Harlan, MD, FAAD

This triggers a cascade of inflammation. Skin barrier breakdown in eczema is not just a surface problem; it allows S. aureus to penetrate into the deeper layers of the skin, activating immune cells and driving the inflammatory response characteristic of atopic dermatitis flares^[10]. The result is a self-perpetuating cycle of barrier damage, bacterial colonization, and inflammation that defines atopic dermatitis.

Studies using advanced DNA sequencing reveal that during an eczema flare, skin microbiome diversity is significantly reduced as S. aureus crowds out other beneficial species^[11]. You lose protective bacteria while harmful species flourish. This dysbiosis contributes to treatment resistance. Restoring microbial balance becomes as important as reducing inflammation.

When and Why Antibiotics Are Used

Traditional thinking held that antibiotics treat eczema by eliminating infection. This remains partially true. However, research reveals three distinct reasons dermatologists prescribe antibiotics for eczema:

• Treating obvious bacterial infections with pus, crusting, or oozing
• Reducing bacterial load to decrease inflammatory triggers
• Utilizing anti-inflammatory properties independent of antimicrobial effects

The third reason surprises most patients. Certain antibiotics reduce inflammation through pathways completely separate from their bacteria-killing abilities^[12].

Tetracycline-Class Antibiotics

Tetracyclines including doxycycline, minocycline, and tetracycline itself work through multiple mechanisms. At full antibiotic doses, they inhibit bacterial protein synthesis^[13]. This stops S. aureus from multiplying. But tetracyclines do something else equally important.

These medications inhibit matrix metalloproteinases, enzymes that break down skin structure^[12]. Eczema elevates MMP levels, contributing to barrier dysfunction. Tetracyclines block MMPs even at doses too low to kill bacteria. Studies show that 40mg doxycycline daily, a subantimicrobial dose, reduces inflammatory lesions by 40%^[14].

Dermatologists commonly prescribe tetracyclines for rosacea, another inflammatory condition^[14]. The same anti-inflammatory properties benefit eczema. Clinical trials demonstrate that doxycycline reduces cathelicidin, an inflammatory protein elevated in dermatitis^[15]. This mechanism operates independently of bacterial reduction.

The Microbiome Modulation Effect

When antibiotics reduce S. aureus populations, beneficial bacteria can reestablish^[16]. This doesn't happen immediately. The process takes weeks as microbial communities shift. Some protective species, like Staphylococcus hominis, actively produce antimicrobials against S. aureus^[16].

Research shows that appropriate antibiotic use can restore microbiome diversity^[17]. The key word is appropriate. Overuse or wrong selection worsens dysbiosis. Short courses combined with other treatments yield better results than prolonged antibiotic monotherapy.

Standard treatment with topical corticosteroids and emollients significantly reduces S. aureus colonization during eczema flares, with studies showing bacterial abundance decreasing from approximately 32% to 2% over three months^[18]. Adding antibiotics provides minimal additional benefit for uncomplicated eczema^[19]. This explains why dermatologists reserve antibiotics for specific situations rather than prescribing them routinely.

Combination Therapy Approaches

Evidence supports combining antibiotics with other treatments rather than using them alone. A comprehensive approach addresses multiple disease mechanisms simultaneously. Tetracycline antibiotics including doxycycline and erythromycin are used in approximately 45% of topical steroid withdrawal cases, often as part of comprehensive management plans^[20].

Dr. Harlan's clinical observations identified why eczema patients specifically benefit from combination approaches rather than antibiotics alone:

People prone to eczema and psoriasis tend to develop runaway inflammation in the skin from many different stimuli and environmental factors, including stress. These situations produce redness, itching, scaling, and many other problems.

- Dr. Steven Harlan, MD, FAAD

This tendency toward inflammatory overreaction means that while antibiotics address the bacterial trigger, additional anti-inflammatory support prevents the cascade of symptoms that patients experience even after bacterial loads decrease.

Network meta-analysis demonstrates that oral doxycycline, minocycline, and topical antibiotics effectively treat inflammatory skin conditions including rosacea, with combination approaches addressing both bacterial and inflammatory components^[21]. The same principles apply to eczema. Antibiotics handle bacterial and inflammatory components while topical treatments restore the skin barrier.

Topical vs. Oral Antibiotics: What Works When

The route of administration matters. Topical antibiotics reach high concentrations in skin but penetrate minimally. Oral antibiotics distribute systemically, reaching all affected areas including internal reservoirs like nasal passages. Neither is universally superior. Selection depends on disease pattern and goals.

Topical Antibiotic Options

Topical antibiotics commonly prescribed for eczema include fusidic acid and mupirocin. Both target S. aureus effectively. Network meta-analysis of randomized trials demonstrates that topical antibiotics, whether used alone or in combination with other treatments, are among the least effective options for atopic dermatitis^[22].

This finding surprised researchers. The problem isn't that topical antibiotics don't work. They reduce bacterial counts successfully. However, rapid resolution from topical steroids leaves little room for additional improvement. Topical antibiotics help most when infection is obvious, with pus or crusting.

Topical fusidic acid use is associated with development of fusidic acid-resistant Staphylococcus aureus, with dermatology patients showing particularly high resistance rates^[23][24]. Clinical evidence demonstrates that previous topical antibiotic use represents a significant independent risk factor for resistance development. When widespread eczema requires extended treatment, rotating antimicrobial therapies may help reduce resistance risk.

Oral Antibiotic Options

Oral antibiotics for eczema fall into two categories based on purpose:

Infection-fighting doses:

• Flucloxacillin 250-500mg four times daily
• Cephalexin 500mg twice daily
• Duration: 7-14 days for acute infections

Anti-inflammatory doses:

• Doxycycline 40mg once daily (subantimicrobial)
• Doxycycline 50-100mg once daily (low-dose antibiotic)
• Minocycline 50-100mg once daily
• Duration: Often months for chronic inflammatory conditions

The distinction is crucial. Subantimicrobial doses work through anti-inflammatory mechanisms rather than antimicrobial activity, reducing inflammation via anticollagenolytic and cytokine-modulating properties^[25]. This allows for long-term safe use without promoting resistance. Full antibiotic doses require careful stewardship to prevent resistance. A 2017 pragmatic randomized controlled trial found no benefit from adding oral or topical antibiotics to standard eczema treatment when no obvious infection existed^[19].

Short-Term vs. Long-Term Use

Treatment duration depends on the goal. Treating obvious infection requires 7-14 days of full-dose antibiotics. Using anti-inflammatory properties justifies longer courses at lower doses. The safety profile differs significantly between these approaches.

Short-term antibiotic use for infection rarely causes problems. Common side effects include gastrointestinal upset and yeast infections. These resolve after stopping medication. The real concern with short courses is incomplete treatment leading to recurrence.

Long-term use at subantimicrobial doses has been studied extensively for rosacea. Clinical evidence supports the safety of 40mg doxycycline modified-release capsules once daily for extended inflammatory disease management^[26]. This dose doesn't select for resistant bacteria. Similar protocols work for other chronic inflammatory dermatoses including some eczema cases.

Combination Approaches That Work

Monotherapy rarely provides optimal results for chronic eczema. Combining treatments that address different disease mechanisms yields better outcomes. The evidence supports layered approaches rather than relying on single interventions.

Dr. Harlan's Treatment Philosophy

Dr. Steven Harlan, a board-certified dermatologist with decades of experience treating inflammatory skin conditions, developed his combination approach after observing limitations in antibiotic monotherapy. His clinical practice revealed a consistent pattern across thousands of patient encounters.

Many strategies in dermatology consist of choosing a topical or an oral antibiotic that will improve the skin problem and treat excess inflammation. The right antibiotic/antimicrobial product by itself can have significant anti-inflammatory effects on skin problems like dermatitis/eczema, acne, Rosacea, and perioral dermatitis. The problem is that the antibiotic often requires months to help, or it doesn't help the inflammation enough, even after weeks and months.

- Dr. Steven Harlan, MD, FAAD

This observation led Dr. Harlan to develop protocols combining antimicrobial approaches with barrier repair and anti-inflammatory treatments. For topical steroid withdrawal, he prescribes oral or topical antibiotics alongside SmartLotion, typically resolving the condition within two months^[20].

For folliculitis, a condition where bacteria colonize hair follicles, Dr. Harlan combines oral antibiotics with SmartLotion and antimicrobial washes. This three-pronged approach addresses the infection, reduces inflammation, and prevents recurrence. Each component plays a distinct role.

Dr. Harlan explains the rationale behind SmartLotion's formulation specifically for combination therapy:

Besides directly helping itching and inflammation associated with chronic dermatitis, SmartLotion is designed to help in combination with antibiotic strategies. The intention and expectation of its use are a faster resolution of inflammation, and better control when combined with an antibiotic strategy. The expectation is, and all the evidence indicates, the avoidance of side effect risks, especially when compared to potent topical steroids.

- Dr. Steven Harlan, MD, FAAD

SmartLotion combines low-potency hydrocortisone with sulfur. Low-dose topical corticosteroids like hydrocortisone have a favorable safety profile with minimal risk of adverse effects when used appropriately^[27]. Sulfur possesses antimicrobial properties that can support skin health. When combined with oral antibiotics, topical anti-inflammatory treatments can provide complementary benefits.

Why Dual-Action Makes Sense

Antibiotics reduce harmful bacteria and inflammation. SmartLotion provides gentle anti-inflammatory effects while supporting microbiome recovery. The combination addresses both problems simultaneously. Clinical experience shows faster improvement and better long-term control compared to either treatment alone.

Dr. Harlan's 2008 clinical study provided evidence for combination strategies across multiple inflammatory conditions. His experience treating acne patients revealed principles that apply to eczema management:

Poorly controlled inflammation by antibiotics alone was another indication for using combination therapy with the SmartLotion strategy. Our acne patients were able to tolerate RetinA (tretinoin) and Benzaclin/Benzamycin (products containing BPO benzoyl peroxide) significantly better and achieve superior results. This strategy is also essential when treating Rosacea in patients with stinging "sensitive skin", or those with a background of Atopic dermatitis and Rosacea.

- Dr. Steven Harlan, MD, FAAD

The protocol is straightforward. Take prescribed oral antibiotic once daily. Apply SmartLotion as an eczema cream twice daily to affected areas. Moisturize liberally 2-3 times daily. This layered approach provides multiple routes to improvement.

Dr. Harlan emphasizes the critical distinction between low-dose and high-potency steroids, particularly when combining treatments with antibiotics. His decades of clinical practice revealed specific safety concerns that guide his protocol choices:

At least three problems can occur with strong steroids. The first is the well-understood atrophy or thinning of the skin. Skin thinning occurs with the prolonged use of strong steroids on sensitive skin areas like the inner arms, inner thighs, groin creases, and perianal area. The problem with strong topical steroids and the facial skin is that long before thinning or atrophy occurs, the facial skin will develop acne-like rashes and burning inflammation related to dysregulation of the skin's immune system. The overgrowth of noxious microbes contributes to inflammation and immune dysregulation. This adverse reaction to topical steroids on the face was always called steroid rebound phenomenon, or steroid addiction. Now it's called TSW, Topical Steroid Withdrawal.

- Dr. Steven Harlan, MD, FAAD

This safety profile difference explains why SmartLotion's low-dose formulation works effectively with antibiotics for long-term management. The combination avoids the immune dysregulation and bacterial overgrowth problems associated with stronger steroids.

For rosacea, topical metronidazole is an established effective treatment^[29]. Combining topical anti-inflammatory agents with antimicrobial treatments addresses both inflammatory and microbial components of rosacea. Similar principles apply when pairing topical corticosteroids with tetracycline-class antibiotics for other inflammatory dermatoses. The key is addressing inflammation and bacterial imbalance from multiple angles.

When Antibiotics Don't Work

Not every patient responds to antibiotics. Recognizing treatment failure early prevents wasted time on ineffective approaches. Several factors predict poor antibiotic response for eczema.

Signs Antibiotics Aren't Helping

Evaluate antibiotic effectiveness at specific intervals. After one week, acute infection signs should improve. Reduced crusting, less oozing, and decreased redness indicate progress. If no improvement occurs after 7-10 days on appropriate antibiotics, reassess the diagnosis.

Warning signs of treatment failure include:

• Worsening symptoms despite antibiotic use
• Spreading to new areas while on treatment
• Development of new pustules or crusting
• Persistent fever or systemic symptoms
• Increased pain or swelling

For anti-inflammatory use, expect slower improvement. Clinical trials of anti-inflammatory dose doxycycline show progressive benefits assessed at weeks 3, 6, 12, and 16^[30]. Meaningful improvement typically occurs within the first several weeks. If no improvement occurs after 8-12 weeks, the antibiotic likely isn't helping.

Antibiotic Resistance Concerns

Methicillin-resistant Staphylococcus aureus (MRSA) can colonize patients with atopic dermatitis^[31]. MRSA resists common antibiotics including methicillin, oxacillin, and related drugs. When eczema fails to respond to standard antibiotics, MRSA colonization becomes a consideration.

Culture testing identifies resistant organisms. Your dermatologist can swab affected skin and send samples for culture and sensitivity testing. Results guide antibiotic selection. MRSA requires specific antibiotics like trimethoprim-sulfamethoxazole or doxycycline.

Preventing resistance matters more than treating it. Guidelines for responsible antibiotic use include:

• Only use antibiotics when truly necessary
• Complete the full prescribed course
• Choose narrow-spectrum agents when possible
• Limit topical antibiotic use to 14 days maximum
• Consider subantimicrobial doses for long-term anti-inflammatory effects

Clinical evidence demonstrates that topical corticosteroids alone effectively reduce S. aureus colonization in atopic dermatitis without requiring concurrent antibiotic therapy^[32]. This approach avoids resistance entirely. Reserve antibiotics for situations where they provide clear additional benefit.

Alternative Approaches

When antibiotics fail or aren't appropriate, multiple alternatives exist. The choice depends on eczema severity, distribution, and patient factors.

Topical calcineurin inhibitors (tacrolimus, pimecrolimus) provide anti-inflammatory effects without corticosteroid-associated risks such as skin atrophy. Systematic reviews demonstrate their efficacy and safety in atopic dermatitis, particularly for sensitive areas like the face^[33]. However, they lack antimicrobial activity. Use them for inflammation, not infection.

Bleach baths reduce S. aureus colonization without antibiotics. Clinical trials demonstrate that dilute sodium hypochlorite baths significantly decrease S. aureus density while improving clinical severity scores^[34]. The protocol involves bathing twice weekly in dilute bleach solution (0.005%). This approach doesn't create resistance and can be used indefinitely.

Phototherapy using ultraviolet light reduces both inflammation and bacterial colonization. Clinical studies demonstrate that phototherapy enhances antimicrobial peptide mRNA expression in atopic dermatitis^[35]. Treatment requires office visits two to three times weekly.

Biologics like dupilumab target specific inflammatory pathways. Clinical studies demonstrate that dupilumab significantly improves skin barrier function, which may subsequently reduce bacterial colonization^[36]. Biologics work for severe eczema unresponsive to conventional treatments.

Topical steroids remain first-line treatment, but their risks warrant discussion. Systematic review evidence indicates that short-term topical corticosteroid use in atopic dermatitis carries minimal risk of skin atrophy when used appropriately^[37]. While concerns about skin thinning exist, proper use of appropriate potencies for recommended durations minimizes these risks. Facial skin proves particularly vulnerable and requires lower potencies.

Intermittent topical corticosteroid therapy for atopic dermatitis flares has a favorable safety profile when used according to clinical guidelines^[37]. The key is selecting appropriate potencies for specific body areas and using the minimum effective strength. Combining steroids with barrier repair products like quality moisturizers reduces the total steroid exposure needed.

Working with Your Doctor on Antibiotic Treatment

Successful antibiotic therapy requires good communication with your dermatologist. Come prepared with questions and clear information about your symptoms.

Questions to Ask

When your doctor prescribes antibiotics for eczema, these questions help clarify the treatment plan:

1. Are we treating infection or using antibiotics for anti-inflammatory effects?
2. How long should I take this medication?
3. What improvement should I expect and when?
4. Should I combine this with other treatments?
5. What are signs that the antibiotic isn't working?
6. When should I follow up?
7. Are there alternatives if this doesn't help?

Understanding the treatment rationale helps you monitor progress appropriately. Antibiotics for acute infection should work quickly. Anti-inflammatory use takes longer but can continue for months safely at appropriate doses.

What to Expect

Timeline expectations differ based on antibiotic purpose. For treating obvious infection, expect improvement within 48-72 hours. Redness should decrease, pus should resolve, and pain should lessen. Complete healing takes 7-14 days.

For anti-inflammatory use, improvement is gradual. Week 1-2 may show minimal change as bacterial populations shift. Week 3-4 brings noticeable reduction in inflammation and itching. Week 6-8 reveals full benefits. Some patients require 12 weeks to achieve maximum improvement.

Gastrointestinal side effects represent the most common adverse reactions to oral antibiotics^[38]. Common issues include:

• Nausea or upset stomach
• Diarrhea
• Yeast infections
• Photosensitivity with tetracyclines
• Dizziness (minocycline)

Taking antibiotics with food reduces gastrointestinal side effects. Probiotics may help prevent antibiotic-associated diarrhea. Avoid sun exposure or use strong sunscreen while taking tetracyclines. Most side effects resolve after stopping the medication.

Taking a Comprehensive Approach

Antibiotics treat eczema through multiple mechanisms beyond simply killing bacteria. Understanding these mechanisms helps you make informed decisions about treatment. The evidence shows that antibiotics work best as part of comprehensive protocols, not as standalone therapy.

Key points to remember: S. aureus colonization affects most eczema patients even without obvious infection. Tetracycline-class antibiotics provide anti-inflammatory benefits independent of antimicrobial effects. Combination approaches addressing inflammation, barrier repair, and bacterial balance yield superior results. Not all cases require or respond to antibiotics.

When antibiotics are appropriate, using them correctly maximizes benefits while minimizing resistance risk. Choose the right antibiotic for your situation. Use adequate doses for sufficient duration. Combine with other treatments including effective eczema cream options like SmartLotion. Monitor progress and adjust as needed.

Most importantly, work closely with your dermatologist. They can determine whether antibiotics make sense for your specific case. They'll monitor for side effects and treatment response. They can adjust therapy when needed and recommend alternatives if antibiotics don't help.

Eczema management requires patience and often multiple treatment adjustments. Antibiotics provide one tool in a larger toolkit. Used appropriately as part of comprehensive care, they help many patients achieve better control and improved quality of life.

References

1. Elizalde-Jiménez IG, Ruiz-Hernández FG, Carmona-Cruz SA, et al. Global Antimicrobial Susceptibility Patterns of Staphylococcus aureus in Atopic Dermatitis: A Systematic Review and Meta-Analysis. JAMA Dermatol. Published online September 25, 2024. View Study
2. Choe J, Barbieri JS. Emerging Medical Therapies in Rosacea: A Narrative Review. Dermatol Ther (Heidelb). 2023;13(12):2933-2949. View Study
3. Fenske C, Boytsov N, Guo J, Dawson Z. Prescription Market Share and Treatment Patterns in Atopic Dermatitis: A Retrospective Observational Study Using US Insurance Claims. Adv Ther. 2022;39(5):2052-2064. View Study
4. Del Rosso JQ. Management of Papulopustular Rosacea and Perioral Dermatitis with Emphasis on Iatrogenic Causation or Exacerbation of Inflammatory Facial Dermatoses: Use of Doxycycline-modified Release 40mg Capsule Once Daily in Combination with Properly Selected Skin Care as an Effective Therapeutic Approach. J Clin Aesthet Dermatol. 2011;4(8):20-30. View Study
5. Grice EA, Segre JA. The skin microbiome. Nat Rev Microbiol. 2011;9(4):244-253. View Study
6. Masiuk H, Maślana J, Zeman K, Luty-Błocho M. Staphylococcus aureus in Atopic Dermatitis-A Friend or a Foe? Int J Mol Sci. 2021;22(14):7437. View Study
7. Edslev SM, Olesen CM, Nørreslet LB, et al. Staphylococcal Communities on Skin Are Associated with Atopic Dermatitis and Disease Severity. Microorganisms. 2021;9(2):432. View Study
8. Guo Y, Dou X, Chen XF, Huang C, Zheng YJ, Yu B. Association Between Nasal Colonization of Staphylococcus aureus and Eczema of Multiple Body Sites. Allergy Asthma Immunol Res. 2023;15(5):659-672. View Study
9. Yoshikawa FSY, de Lima JF, Sato MN, Ramos YÁLR, Aoki V, Orfali RL. Exploring the Role of Staphylococcus Aureus Toxins in Atopic Dermatitis. Toxins (Basel). 2019;11(6):321. View Study
10. Nakatsuji T, Chen TH, Two AM, et al. Staphylococcus aureus Exploits Epidermal Barrier Defects in Atopic Dermatitis to Trigger Cytokine Expression. J Invest Dermatol. 2016;136(11):2192-2200. View Study
11. Beck LA, Thyssen JP, Deleuran M, et al. Tralokinumab treatment improves the skin microbiota by increasing the microbial diversity in adults with moderate-to-severe atopic dermatitis. J Am Acad Dermatol. 2023;88(4):812-820. View Study
12. Golub LM, Lee HM. Periodontal therapeutics: Current host-modulation agents and future directions. Periodontol 2000. 2020;82(1):186-204. View Study
13. Chopra I, Roberts M. Tetracycline antibiotics: mode of action, applications, molecular biology, and epidemiology of bacterial resistance. Microbiol Mol Biol Rev, 2001;65:232-260. View Study
14. van Zuuren EJ, Fedorowicz Z, Tan J, et al. Interventions for rosacea based on the phenotype approach: an updated systematic review including GRADE assessments. Br J Dermatol. 2019;181(1):65-79. View Study
15. Kanada KN, Nakatsuji T, Gallo RL. Doxycycline indirectly inhibits proteolytic activation of tryptic kallikrein-related peptidases and activation of cathelicidin. J Invest Dermatol. 2012;132(5):1435-1442. View Study
16. Nakatsuji T, Chen TH, Narala S, et al. Antimicrobials from human skin commensal bacteria protect against Staphylococcus aureus and are deficient in atopic dermatitis. Sci Transl Med. 2017;9(378):eaah4680. View Study
17. Saheb Kashaf S, Harkins CP, Deming C, et al. Staphylococcal diversity in atopic dermatitis from an individual to a global scale. Cell Host Microbe. 2023;31(4):578-592.e6. View Study
18. Khadka VD, Key FM, Romo-González C, et al. The Skin Microbiome of Patients With Atopic Dermatitis Normalizes Gradually During Treatment. Front Cell Infect Microbiol. 2021;11:720674. View Study
19. Francis NA, Ridd MJ, Thomas-Jones E, et al. Oral and Topical Antibiotics for Clinically Infected Eczema in Children: A Pragmatic Randomized Controlled Trial in Ambulatory Care. Ann Fam Med. 2017;15(2):124-130. View Study
20. Maskey AR, Sasaki A, Sargen M, et al. Breaking the cycle: a comprehensive exploration of topical steroid addiction and withdrawal. Front Allergy. 2025;6:1547923. View Study
21. Xiao W, Chen M, Wang B, et al. Efficacy and safety of antibiotic agents in the treatment of rosacea: a systemic network meta-analysis. Front Pharmacol. 2023;14:1169916. View Study
22. Chu DK, Chu AWL, Rayner DG, et al. Topical treatments for atopic dermatitis (eczema): Systematic review and network meta-analysis of randomized trials. J Allergy Clin Immunol. 2023;152(6):1493-1519. View Study
23. Shah M, Mohanraj M. High levels of fusidic acid-resistant Staphylococcus aureus in dermatology patients. Br J Dermatol. 2003;148(5):1018-1020. View Study
24. Dobie D, Gray J. Fusidic acid resistance in Staphylococcus aureus. Arch Dis Child. 2004;89(1):74-77. View Study
25. Bikowski JB. Subantimicrobial Dose Doxycycline for Acne and Rosacea. SKINmed. 2003;2(4):234-246. View Study
26. Del Rosso JQ, Brantman S, Baldwin H. Long-term inflammatory rosacea management with subantibiotic dose oral doxycycline 40 mg modified-release capsules once daily. Dermatol Ther. 2022;35(1):e15180. View Study
27. Davallow Ghajar L, Wood Heickman LK, Conaway M, et al. Low Risk of Adrenal Insufficiency After Use of Low- to Moderate-Potency Topical Corticosteroids for Children With Atopic Dermatitis. Clin Pediatr. 2019;58(4):406-412. View Study
28. Aalto-Korte K, Turpeinen M. Transepidermal water loss predicts systemic absorption of topical hydrocortisone in atopic dermatitis. Br J Dermatol. 1996;135(3):497-498. View Study
29. Bleicher PA. Topical Metronidazole Therapy for Rosacea. Arch Dermatol. 1987;123(5):609. View Study
30. Del Rosso JQ, Webster GF, Jackson M, et al. Two randomized phase III clinical trials evaluating anti-inflammatory dose doxycycline (40-mg doxycycline, USP capsules) administered once daily for treatment of rosacea. J Am Acad Dermatol. 2007;56(5):791-802. View Study
31. Greene WH. Prevalence of Methicillin-Resistant Staphylococcus aureus in Outpatients With Psoriasis, Atopic Dermatitis, or HIV Infection. Arch Dermatol. 1997;133(11):1463. View Study
32. Nilsson EJ, Henning CG, Magnusson J. Topical corticosteroids and Staphylococcus aureus in atopic dermatitis. J Am Acad Dermatol. 1992;27(1):29-34. View Study
33. Chia BKY, Tey HL. Systematic Review on the Efficacy, Safety, and Cost-Effectiveness of Topical Calcineurin Inhibitors in Atopic Dermatitis. Dermatitis. 2015;26(3):122-132. View Study
34. Wong SM, Ng TG, Baba R. Efficacy and safety of sodium hypochlorite (bleach) baths in patients with moderate to severe atopic dermatitis in Malaysia. J Dermatol. 2013;40(11):874-880. View Study
35. Gambichler T, Skrygan M, Tomi NS, et al. Changes of antimicrobial peptide mRNA expression in atopic eczema following phototherapy. Br J Dermatol. 2006;155(6):1275-1278. View Study
36. Cristaudo A, Pigliacelli F, Sperati F, et al. Instrumental evaluation of skin barrier function and clinical outcomes during dupilumab treatment for atopic dermatitis: An observational study. Skin Res Technol. 2021;27(5):810-813. View Study
37. Ricardo JW, Gosch M, Wang Y, et al. Risk of skin atrophy induced by short-term topical corticosteroid use in atopic dermatitis lesional skin: A systematic review. JAAD Int. 2023;13:26-34. View Study
38. Makins R, Ballinger A. Gastrointestinal side effects of drugs. Expert Opin Drug Saf. 2003;2(4):421-429. View Study