150: Superficial Cutaneous Infections and Pyodermas Flashcards
What are the two major groups of Staphylococci and their characteristics?
- Coagulase-negative Staphylococci (e.g., S. epidermidis): Primarily harmless commensals, can cause superficial and invasive infections, especially on implanted foreign materials.
- Coagulase-positive Staphylococci (e.g., S. aureus): Can be harmless commensals but also aggressive pathogens, commonly associated with pyodermas and skin infections.
What is the significance of S. aureus in pyodermas and skin infections?
S. aureus is the most common cause of primary pyodermas, SSTIs, and secondary infections on disease-altered skin.
It can be found colonizing the skin in up to 37% of patients with purulent community-acquired MRSA infections.
What are the common sites of colonization for S. aureus?
Common sites of colonization include:
- Inguinal region: Moist area, prone to colonization.
- Axillae: Moist area, prone to colonization.
- Perirectal skin: Moist area, prone to colonization.
- Nasal mucosa: Permanent colonization in ~30% of population.
- Pharynx: Potential site of transient carriage.
- Rectal mucosa: Potential site of transient carriage.
What conditions predispose individuals to S. aureus colonization?
Conditions predisposing to S. aureus colonization include:
1. Atopic dermatitis
2. Diabetes mellitus
3. Renal insufficiency (patients on dialysis)
4. Intravenous drug use
5. Liver dysfunction
6. Certain genetic or acquired immunosuppressive disorders, including HIV infection.
What are the two clinical patterns of impetigo recognized?
- Nonbullous impetigo
- Bullous impetigo
What is the primary cause of cutaneous pyodermas?
Staphylococcus aureus or group A Streptococcus (GAS).
What is the role of S. epidermidis in human skin?
It is primarily a harmless commensal but can cause infections in certain conditions.
How is S. aureus commonly transmitted?
By contact with skin of other persons or fomites rather than through the air.
What percentage of the population has S. aureus colonized in their anterior nares?
Approximately 30%.
What are the clinical implications of S. aureus being the most common cause of primary pyodermas and SSTIs?
The clinical implications include:
- Increased risk of infections: S. aureus is a leading cause of skin infections, necessitating prompt diagnosis and treatment to prevent complications.
- Need for effective infection control measures: Understanding its transmission routes (contact with skin or fomites) is crucial for preventing outbreaks, especially in healthcare settings.
- Consideration of antibiotic resistance: The prevalence of S. aureus, particularly MRSA strains, requires careful selection of antibiotics and monitoring for resistance patterns in treatment protocols.
What is the most common cause of impetigo and how does it typically present?
Impetigo is most commonly caused by S. aureus (70% of cases), but can also be caused by GAS or both. It typically presents as erythematous papules that evolve into vesicles and pustules, leading to honey-colored crusted papules on an erythematous base, especially around the nares or on the face after trauma.
What are the characteristics of bullous impetigo and its common demographic?
Bullous impetigo is caused by S. aureus strains that express exfoliative toxins, leading to clusters of thin-roofed bullae and vesicles. It occurs most commonly in newborns and older infants and is characterized by rapid progression from vesicles to flaccid bullae.
What is ecthyma and how does it differ from impetigo?
Ecthyma is caused by S. aureus and/or GAS, evolving from untreated impetigo that is occluded by footwear and clothing. It produces ‘punched-out’ ulcers that extend deeply into the dermis, often healing with scarring, unlike impetigo which typically does not.
What are the key elements in the pathogenesis of ecthyma?
Key elements in the pathogenesis of ecthyma include poor hygiene and neglect, often occurring in neglected elderly patients, children, and individuals with diabetes.
How is folliculitis classified and what is its starting point?
Folliculitis begins within the hair follicle and is classified according to the depth of invasion (superficial and deep) and microbial etiology.
A 5-year-old child presents with honey-colored crusted papules around the nares. What is the most likely diagnosis, and what is the causative organism?
The most likely diagnosis is nonbullous impetigo, commonly caused by Staphylococcus aureus or Group A Streptococcus (GAS).
A newborn develops flaccid bullae that rupture to form thin, golden-yellow crusts. What is the diagnosis, and what toxin is responsible?
The diagnosis is bullous impetigo, caused by Staphylococcus aureus strains that express exfoliative toxins (ETA and ETB).
A patient with diabetes presents with indurated, violaceous ulcers on the lower extremities. What is the diagnosis, and what are the key elements in its pathogenesis?
The diagnosis is ecthyma, caused by Staphylococcus aureus and/or GAS. Poor hygiene and neglect are key elements in its pathogenesis.
What percentage of impetigo cases are caused by S. aureus or GAS?
70% of impetigo cases are caused by S. aureus or GAS, or both in combination.
What is the typical progression of nonbullous impetigo lesions?
Nonbullous impetigo starts as erythematous papules that become vesicles and pustules, leading to honey-colored crusted papules on an erythematous base.
What are the common areas where impetigo arises?
Impetigo often arises on the face, especially around the nares, or on extremities after trauma.
What characterizes bullous impetigo?
Bullous impetigo is characterized by clusters of thin-roofed bullae, vesicles, and/or pustules that arise on normal skin and easily rupture.
What is the typical appearance of bullae in bullous impetigo?
Bullae initially contain clear yellow fluid that becomes dark yellow and turbid, with sharply demarcated margins without an erythematous halo.
What is ecthyma and how does it evolve?
Ecthyma is caused by S. aureus and/or GAS and evolves from untreated impetigo occluded by footwear and clothing, extending more deeply.
What are the characteristics of ulcers produced by ecthyma?
Ecthyma produces ‘punched-out’ ulcers that are indurated, raised, and violaceous, with a granulating base extending deeply into the dermis.
What are the common risk factors for developing ecthyma?
Ecthyma occurs most commonly on the lower extremities of children, neglected elderly patients, and individuals with diabetes, with poor hygiene and neglect being key elements in pathogenesis.
What is the classification of folliculitis based on?
Folliculitis is classified according to the depth of invasion (superficial and deep) and microbial etiology.
What are the clinical features and common causes of nonbullous impetigo, and how does it typically present on the skin?
Nonbullous impetigo is characterized by:
- Etiology: Primarily caused by S. aureus (most common) or GAS.
- Demographics: More prevalent in children, but can also occur in adults.
- Presentation: Begins as erythematous papules that evolve into vesicles and pustules. These rupture, leading to honey-colored crusted papules on an erythematous base.
- Location: Commonly arises on the face (especially around the nares) or extremities after trauma.
- Symptoms: Associated with pruritus or soreness in carriers of S. aureus.
Describe the pathogenesis and clinical presentation of bullous impetigo, including its common demographic and distinguishing features.
Bullous impetigo is characterized by:
- Etiology: Caused by S. aureus strains that produce exfoliative toxins cleaving desmoglein 1 in the epidermis.
- Demographics: Most commonly occurs in newborns and older infants.
- Presentation: Features clusters of thin-roofed bullae, vesicles, and/or pustules on normal skin that easily rupture, leading to crusted erosions.
- Fluid Characteristics: Initially contains clear yellow fluid that becomes dark yellow and turbid.
- Nikolsky Sign: Absent in bullous impetigo.
- Progression: Rapid progression from vesicles to flaccid bullae; lesions may collapse within days, forming light-brown to golden-yellow crusts.
What are the key clinical features and complications associated with ecthyma, and how does it differ from impetigo?
Ecthyma is characterized by:
- Etiology: Caused by S. aureus and/or GAS.
- Pathogenesis: Evolves from untreated impetigo that is occluded by footwear and clothing, leading to deeper skin involvement.
- Presentation: Produces punched-out ulcers with grayish-yellow crust and purulent material. Lesions are indurated, raised, and violaceous with surrounding edema.
- Complications: Untreated lesions can enlarge over weeks to months, often healing with scarring.
- Demographics: Commonly occurs on the lower extremities of children, neglected elderly patients, and individuals with diabetes.
- Distinction: Should be differentiated from ecthyma gangrenosum, which is caused by Pseudomonas aeruginosa.
How does folliculitis develop, and what factors influence its classification and microbial etiology?
Folliculitis develops as:
- Origin: Begins within the hair follicle.
- Classification: Classified according to the depth of invasion (superficial and deep) and microbial etiology.
- Factors Influencing Development:
- Microbial agents: Various bacteria, fungi, or viruses can cause folliculitis.
- Skin conditions: Conditions like atopic dermatitis or abrasions can predispose individuals to folliculitis.
- Hygiene: Poor hygiene practices can increase the risk of developing folliculitis.
What is the definition of superficial folliculitis and where is it commonly found?
Superficial folliculitis, also known as follicular or Bockhart impetigo, is often found on the scalps of children and in the beard area, as well as the axillae, extremities, and buttocks of adults.
What are the characteristics of furuncles?
Furuncles start as hard, tender, red folliculocentric nodules in hair-bearing skin that enlarge and become painful and fluctuant. They may rupture, discharging pus and necrotic material, and can occur as solitary or multiple lesions, particularly in areas subject to friction and perspiration.
What are some noninfectious and inflammatory differentials of folliculitis that are more common in black men?
- Pseudofolliculitis barbae - occurs on the lower beard area.
- Folliculitis keloidalis - occurs on the nape of the neck.
- Perifolliculitis capitis - occurs on the scalp.
What systemic host factors are associated with furunculosis?
Systemic host factors associated with furunculosis include conditions that impair immune function, such as diabetes mellitus, obesity, and other chronic illnesses.
What are the characteristics of furuncles?
Furuncles start as a hard, tender, red folliculocentric nodule that enlarges and becomes painful and fluctuant.
What can complicate the occurrence of furuncles?
Preexisting lesions such as atopic dermatitis, excoriations, abrasions, scabies, or pediculosis.
What is the typical presentation of a furuncle?
A hard, tender, red nodule that may rupture and discharge pus.
What is superficial folliculitis also known as?
Follicular or Bockhart impetigo.
What areas are commonly affected by superficial folliculitis?
Scalps of children and the beard area, axillae, extremities, and buttocks of adults.
What is sycosis barbae?
A deep folliculitis with perifollicular inflammation occurring in the bearded areas of the face and upper lip.
What is a common cause of hot tub folliculitis?
Pseudomonas aeruginosa.
What are some noninfectious and inflammatory differentials of folliculitis that are more common in black men?
Pseudofolliculitis barbae, folliculitis keloidalis, and perifolliculitis capitis.
What are the systemic host factors associated with furunculosis?
Obesity, blood dyscrasias, defects in neutrophil function, and immunosuppression.
What are the clinical features and common sites of occurrence for furuncles?
Furuncles start as a hard, tender, red folliculocentric nodule in hair-bearing skin. They enlarge and become painful and fluctuant after several days, leading to abscess formation. They may occur as solitary lesions or multiple lesions, commonly found in areas such as the buttocks, neck, face, axillae, and buttocks.
What are the characteristics and clinical implications of carbuncles?
More extensive, deeper, and serious inflammatory lesions that develop when multiple closely set furuncles coalesce. Commonly occur on the nape of the neck, back, or thighs. Symptoms include fever and malaise, with the patient appearing quite ill.
What is botryomycosis and what are its predisposing factors?
Botryomycosis is a rare pyogenic disease presenting as a purulent, chronic, subcutaneous infection. Predisposing factors include trauma, immunosuppression, chronic alcoholism, and diabetes mellitus.
What are the clinical features of Staphylococcal paronychia?
Predisposition in individuals exposed to hand trauma or chronic moisture. Caused primarily by S. aureus, often around the fingernails, originating from a break in the skin.
What distinguishes Staphylococcal Whitlow from herpetic whitlow?
Feature | Staphylococcal Whitlow | Herpetic Whitlow |
|———|———————–|——————|
| Cause | S. aureus | Herpes simplex virus |
| Symptoms | Red, hot, tender finger bulb with possible abscess formation | Grouped hemorrhagic vesicles that may become confluent |
What systemic signs may indicate a serious infection requiring immediate antibiotic therapy?
Signs of systemic infection may include temperature higher than 38°C or lower than 36°C, tachypnea exceeding 24 breaths per minute, tachycardia exceeding 90 beats per minute, and abnormal white blood cell counts.
What complications can arise from S. aureus infections?
Can lead to cellulitis, lymphangitis, and bacteremia, which may result in life-threatening infections in various organs.
What is a carbuncle and how does it develop?
A carbuncle is a more extensive, deeper, and serious inflammatory lesion that develops when multiple closely set furuncles coalesce.
What are the common sites for abscess formation?
Abscesses occur at sites of trauma, foreign bodies, burns, or sites of insertion of intravenous catheters.
What is the major infectious cause of acute paronychia?
The major infectious cause of acute paronychia is Staphylococcus aureus.
What are the signs of systemic infection in skin infections?
Signs of systemic infection may include temperature higher than 38°C, tachypnea exceeding 24 breaths per minute, tachycardia exceeding 90 beats per minute, and abnormal white blood cell counts.
What are the potential complications of untreated staphylococcal infections?
Untreated staphylococcal infections can lead to serious complications, including cellulitis, lymphangitis, and bacteremia.
What are the risk factors for S. aureus skin and soft tissue infections?
Risk factors include colonization in mucosal sites and skin, preexisting tissue injury, immunodeficiency disorders, and conditions resulting in defective neutrophil function.
What are the virulence factors of S. aureus that promote colonization and infection?
Virulence factors include pore-forming toxins that lyse host cells, such as α-hemolysin.
What are the genetic or acquired deficiencies that affect neutrophil number or function?
Genetic disorders (e.g., chronic granulomatous disease) or acquired conditions (e.g., diabetes, cancer patients on chemotherapy).
What is a genetic or acquired deficiency of interleukin (IL)-17 responses?
Job’s syndrome.
What are the virulence factors of S. aureus that promote colonization and infection?
Virulence factors include pore-forming toxins, exfoliative toxins, superantigens/enterotoxins, inhibition of neutrophil function, and other factors like catalase and protein A.
How does S. aureus evade the immune system?
S. aureus evades the immune system through production of inhibitory proteins, pore-forming toxins, superantigens, catalase, and protein A.
What laboratory tests are recommended for diagnosing impetigo and ecthyma?
Gram stain and culture of pus or exudates to identify S. aureus (including MRSA) and/or GAS.
What is the role of antimicrobial peptides in the immune response to S. aureus?
Antimicrobial peptides are produced by keratinocytes and other immune cells, helping to kill bacteria and modulate the immune response.
What diagnostic tests are recommended to confirm the causative organism in a skin abscess?
Gram stain and culture of pus or exudates.
What virulence factor inhibits neutrophil chemotaxis?
The chemotaxis inhibitory protein of Staphylococcus aureus (CHIPS).
What virulence factor blocks antibody-mediated phagocytosis?
Protein A on the surface of Staphylococcus aureus.
What virulence factor degrades neutrophil extracellular traps (NETs)?
Staphylococcal nuclease (Nuc).
What virulence factor targets desmoglein 1?
Exfoliative toxins (ETA, ETB, and ETD).
What virulence factor is associated with toxic shock syndrome?
Toxic shock syndrome toxin-1 (TSST-1).
What virulence factor is responsible for the golden color of Staphylococcus aureus colonies?
Staphyloxanthin, a yellow carotenoid pigment.
What virulence factor targets ADAM10?
Alpha-toxin (α-toxin).
What virulence factor targets C5a receptors?
Panton-Valentine leukocidin (PVL).
What virulence factor targets CCR5, CXCR1, and CXCR2?
Leukocidin ED (LukED).
What virulence factor blocks P-selectin and ICAM-1?
Staphylococcal superantigen-like proteins (SSL5 and SSL11) and extracellular adherence protein (Eap).
What virulence factor nonspecifically activates T cells?
Superantigens interact with human leukocyte antigen-DR molecules.
What virulence factor inhibits reactive oxygen-mediated killing?
Catalase, alkyl hydroperoxide reductase, and staphyloxanthin.
What virulence factor is associated with increased severity of atopic dermatitis?
Staphylococcus aureus superantigens, especially SEB.
What virulence factor is associated with community-acquired MRSA?
Alpha-toxin (α-toxin) and Panton-Valentine leukocidin (PVL).
What virulence factor correlates with protection against recurrent infections?
High serum antibody titers against alpha-toxin (α-toxin).
What virulence factor is located in Staphylococcus aureus bacteriophages?
Exfoliative toxins ETA and ETB.
What virulence factor is located in the bacterial chromosome?
Exfoliative toxin ETD.
What virulence factor blocks complement and formyl peptide receptors?
Chemotaxis inhibitory protein of Staphylococcus aureus (CHIPS).
What virulence factor blocks CXCR2 neutrophil-attracting chemokines?
Staphopain A (ScpA).
What virulence factor prevents NETosis-mediated killing?
Adenosine synthase A (AdsA) and staphylococcal nuclease (Nuc).
What virulence factor is responsible for staphylococcal scalded-skin syndrome?
Exfoliative toxins (ETA and ETB).
What virulence factor is responsible for toxic shock syndrome?
Toxic shock syndrome toxin-1 (TSST-1).
What are the risk factors for S. aureus skin and soft tissue infection?
Colonization in mucosal sites and skin, preexisting tissue injury or inflammation, immunodeficiency disorders, and genetic or acquired deficiency of interleukin (IL)-17 responses.
What are pore-forming toxins associated with S. aureus?
Single-component α-hemolysin and biocomponent leukotoxins like Panton-Valentine leukocidin (PVL).
What is the role of exfoliative toxins in S. aureus infections?
They are serine proteases that target desmoglein 1.
How do superantigens affect T cells in S. aureus infections?
They nonspecifically activate T cells by interacting with human leukocyte antigen-DR molecules.
What is the significance of IL-1β in S. aureus infections?
IL-1β induces neutrophil recruitment and abscess formation.
What laboratory tests are recommended for diagnosing impetigo and ecthyma?
Gram stain and culture of pus or exudates to identify S. aureus or GAS.
What is the recommended approach for large furuncles, carbuncles, and abscesses?
Culture of pus following incision and drainage is strongly recommended.
What is the purpose of biopsy or aspiration in patients with extensive furuncles or abscesses?
To perform histologic evaluation and microbiology cultures.
What are the risk factors associated with S. aureus skin and soft tissue infections?
Colonization, preexisting tissue injury, immunodeficiency disorders, defective neutrophil function, and genetic deficiency of IL-17 responses.
How do pore-forming toxins contribute to the virulence of S. aureus?
Pore-forming toxins like α-hemolysin and PVL lyse host immune cells, impairing the immune response.
What role do superantigens play in S. aureus infections?
Superantigens nonspecifically activate T cells, leading to increased cytokine release and severe inflammatory responses.
How does the activation of the inflammasome contribute to the immune response against S. aureus infections?
Pore-forming toxins induce phagosomal rupture, activating caspase-1 and promoting IL-1β release.
What histological findings are characteristic of a furuncle?
A dense polymorphonuclear inflammatory process in the dermis and subcutaneous fat.
What are the clinical implications of untreated S. aureus skin infections?
Untreated infections can lead to invasive spread, cellulitis, lymphangitis, and bacteremia.
What is the recommended treatment for localized impetigo?
Mupirocin 2% topical ointment or retapamulin 1% ointment twice daily for 5 to 7 days.
What should be considered when imaging is indicated in cases of furuncles or carbuncles?
Imaging is indicated in febrile neutropenic patients with extensive lesions.
What is the first-line oral antibiotic treatment for impetigo caused by methicillin-sensitive S. aureus?
Dicloxacillin or cephalexin.
What are the recommended initial empiric antibiotics for suspected CA-MRSA?
Doxycycline, clindamycin, or TMP-SMX.
What is a suitable substitute for treating impetigo in a patient with a penicillin allergy?
Erythromycin is suitable, but resistance is common.
What does histologic examination of a furuncle reveal?
A dense polymorphonuclear inflammatory process.
What is the typical imaging indication for furuncles and carbuncles?
Imaging is not typically indicated except in febrile neutropenic patients.
What is the potential consequence of untreated S. aureus infections?
Invasive spread of the infection.
What is the recommended topical treatment for impetigo?
Mupirocin 2% topical ointment or retapamulin 1% ointment.
What is the typical imaging indication for furuncles and carbuncles?
Imaging is not typically indicated except in febrile neutropenic patients with extensive furuncles, carbuncles, or abscesses.
What is the potential consequence of untreated S. aureus infections?
There is a potential for invasive spread of the infection, resulting in cellulitis, lymphangitis, and bacteremia.
What is the recommended topical treatment for impetigo?
Mupirocin 2% topical ointment or retapamulin 1% ointment twice daily for 5 to 7 days.
What oral antibiotic is commonly recommended for methicillin-sensitive S. aureus infections?
Dicloxacillin or cephalexin.
What should be done if CA-MRSA is suspected in a patient?
Doxycycline, clindamycin, or TMP-SMX are recommended for initial empiric therapy.
What is the importance of continuing oral antibiotic treatment for skin infections?
Oral antibiotic treatment should be continued for 7 days (10 days if streptococci are isolated).
What are the side effects of fusidic acid when used for localized impetigo?
Fusidic acid has few adverse side effects.
What is the clinical significance of S. aureus in skin infections?
S. aureus can disseminate and cause infections of many organs and tissues, such as osteomyelitis and pneumonia.
What histological findings are characteristic of a furuncle and carbuncle caused by Staphylococcus aureus?
A furuncle shows a dense polymorphonuclear inflammatory process in the dermis and subcutaneous fat. In carbuncles, there are multiple abscesses separated by connective-tissue trabeculae present in the dermis, especially along the edges of hair follicles, reaching the skin surface through openings in the undermined epidermis.
What are the potential complications of untreated Staphylococcus aureus skin infections?
If untreated, Staphylococcus aureus skin infections can lead to invasive spread resulting in: 1. Cellulitis 2. Lymphangitis 3. Bacteremia 4. Infections of various organs such as osteomyelitis, septic arthritis, endocarditis, pneumonia, and sepsis.
What is the recommended management for impetigo caused by Staphylococcus aureus?
The management for impetigo includes: 1. Topical treatment: Mupirocin 2% ointment or retapamulin 1% ointment twice daily for 5 to 7 days. 2. Physical removal: Gentle cleansing of the affected area with soap and water. 3. Oral antibiotics: Dicloxacillin or cephalexin for adults; for children, appropriate dosing based on weight is recommended. 4. Alternative options: For penicillin-allergic patients, erythromycin can be used, but resistance is common. Other options include amoxicillin with clavulanic acid or clindamycin for children.
What imaging considerations should be taken into account for patients with extensive furuncles or carbuncles?
Imaging is not typically indicated except in cases of febrile neutropenic patients with extensive furuncles, carbuncles, or abscesses. It is important if there is a concern for underlying osteomyelitis or if there is an indolent pulmonary site of Staphylococcus aureus infection, which can spread to the overlying skin and soft tissues.
What are the first-line oral antibiotics for treating folliculitis caused by Staphylococcus aureus?
The first-line oral antibiotics for treating folliculitis include: 1. Dicloxacillin: 250 to 500 mg orally 4 times a day for adults. 2. Cephalexin: 500 mg orally 4 times a day for adults; for children, 50 to 100 mg/kg/day divided 3 to 4 times per day. 3. Erythromycin: Can be used for patients allergic to penicillin, but resistance is common.
What is the recommended treatment for simple furuncles, carbuncles, and abscesses?
Incision and drainage (I&D) is often performed and is likely adequate, but additional antibiotic coverage has a better cure rate.
What adjunctive therapy should be considered for patients with severe or extensive disease after I&D?
Adjunctive antibiotic therapy should be added if there is severe or extensive disease with multiple sites of infection, surrounding cellulitis, or signs of systemic infection or inflammation.
What should be done for severe infections or infections in dangerous areas?
Maximal antibiotic dosage should be employed by the parenteral route.
What is the role of vancomycin in treating serious purulent infections?
Vancomycin or other systemic parenteral agents with anti-CA-MRSA activity are indicated for patients with serious purulent infections.
What is the recommended duration for antibiotic treatment in cases of furuncles, carbuncles, and abscesses?
Antibiotic treatment should be continued for at least 7 to 14 days and until all evidence of inflammation has regressed.
What preventive measures should be taken to avoid reinfection of draining wounds?
Draining wounds should be kept clean and covered with clean and dry bandages, and frequent hand cleansing is important after contacting infected skin.
What should be done to decolonize patients with recurrent S. aureus SSTIs?
Nasal decolonization can be achieved with mupirocin ointment administered to the nares twice daily for 5 to 10 days, along with body decolonization using chlorhexidine or bleach baths.
