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epidermis contents
Stratum corneum – outermost layer – hosts microbiome and made up of flattened dead keratinized cells covered in oil and salt – cells replaced ~ every month.
Stratum granulosum – keratinizes skin and waterproofs it
Stratum spinosum -contains dendritic (Langerhans) cells (phagocytes/APCs) and karatinocytes
Stratum basale – contains basal cells and melanocytes and adheres to Dermis
dermis contents
Contains blood vessels, nerve endings, sebaceous glands (which also harbor microbiota), hair follicles
hypodermis contents
Contains fat cells – subcutaneous and not technically part of the skin, but anchors the skin to underlying tissue
Hyaluronic acid (HA)
glycosaminoglycan found in skin, joints, and tissues as part of the ECM. Capable of retaining moisture and acts as a lubricant to maintain elasticity.
collagen
a protein found in skin that also makes up the main component of connective tissue and the ECM. It’s wound into strong, pliable fibers.
members of skin microbiome
Viruses – (HPVs)
Yeast
Malassezia (eat sebum and can cause hyperpigmentation in immunocompromised people)
Candida albicans - can cause candidiasis (yeast infections) if populations grow out of control
Gram positive bacteria – these tolerate higher salt concentrations
Staphylococcus (most common is Staph epidermidis)
Micrococcus (like M. luteus)
Diphtheroids
Corynebacteria
folliculitis etiology
S. aureus, S. epidermidis — normally doesn’t cause disease unless it “follows” S. aureus
folliculitis mode of transmission
Direct contact, indirect contact via fomites, endogenous infection
folliculitis virulence factors
enzymes and exotoxins like hyaluronidase, coagulase, cytolytic toxins
folliculitis signs/symptoms
Inflamed hair follicles - red, painful and/or itchy bumps or whiteheads near hair follicles; may be clustered or deep. May feel warm to the touch; deep infections may also trigger fever
folliculitis diagnosis
Usually diagnosed clinically by signs/symptoms alone
Bacteria isolated from pus can be cultured
S. aureus differentiated from S. epidermidis by coagulase test – it is coagulase positive (can clot blood)
Staph can be differentiated from Strep using the catalase test – Staph is catalase positive (can break down H2O2)
folliculitis treatment
Pus is drained and skin cleaned, then treated with topical mupirocin (inhibits isoleucyl tRNA-synthetase) or clindamycin/erythromycin (macrolides). Warm compress and OTC analgesics. Oral antibiotics for deeper infection: Clindamycin (macrolide), sulfa, or doxycycline (tetracycline)
MRSA etiology
S. aureus
MRSA mode of transmission
can begin as folliculitis; Direct contact, indirect contact via fomites, endogenous infection
MRSA virulence factors
Staphylococcus aureus strains resistant to penicillin, methicillin, macrolides, aminoglycosides, cephalosporin
MRSA signs/symptoms
You cannot tell by looking at the skin if infection is caused by this
MRSA diagnosis
can be detected from clinical samples via:
Culturing bacteria and performing disk-diffusion assays with various antibiotics
PCR to detect the mecA gene encoding Penicillin Binding Protein (PBP2a)
Agglutination assay to detect PBP2a on the surface of S. aureus cells
MRSA treatment
clindamycin, tetracyclines, sulfa drugs, linezolid, or rifampin (but rifampin is only used in combination with other agents because of resistance)
MRSA prevention
Staph is impossible to eliminate – normal resident of many people
Aseptic treatment of non-intact skin, wounds, and surgical openings, handling of catheters and needles, and hand washing
People with staph lesions should avoid working with food, sharing personal items like towels, clothing, and razors, and should keep them clean and covered until they heal. They should also frequently wash their hands.
Staphylococcal Scalded Skin Syndrome (SSSS) etiology
Staphylococcus aureus
Staphylococcal Scalded Skin Syndrome (SSSS) mode of transmission
Direct person-to-person contact; usually affects infants, but also elderly and immunocompromised patients
Staphylococcal Scalded Skin Syndrome (SSSS) virulence factors
Exfoliative toxin (AKA epidermolysin or exfolatin) in addition to others (like coagulase)
Staphylococcal Scalded Skin Syndrome (SSSS) signs/symptoms
Epidermis separates from underlying tissue – looks like skin that has been boiled/scalded. Skin blisters and peels off in sheets.
Staphylococcal Scalded Skin Syndrome (SSSS) diagnosis
Usually diagnosed clinically. Can also perform a tissue biopsy/histological examination from cultures of the blood, urine, nose, throat, and skin.
Staphylococcal Scalded Skin Syndrome (SSSS) treatment
Hospitalization, IV semisynthetic beta-lactams like flucloxacillin since S. aureus can produce beta-lactamases. May be caused by MRSA – vancomycin (aminoglycoside), linezolid, could be used instead. Skin should be treated as it is for burns.
impetigo etiology
Streptococcus pyogenes, Staphylococcus aureus
impetigo mode of transmission
direct contact from another person or oneself (ex. by wiping runny nose on sleeve); indirect contact less common.
impetigo virulence factors
Strep – M protein; Staph – exotoxins
impetigo signs/symptoms
Flat, red superficial patches/blisters – mostly on face and limbs. Patches ooze pus break and form an itchy honey-colored crust (pyogenic). Rarely causes fever.
impetigo diagnosis
Clinical evaluation; cannot differentiate strep or staph though; can do this in the lab using a catalase test.
impetigo treatment
Applying wet compress, removing scabs, and applying topical mupirocin (targets ribosomes), then covering the sores to prevent spread. Oral amoxicillin (beta- lactam), doxycycline, macrolides are options.
impetigo prevention
Regular hand-washing, clipping children’s fingernails, covering open wounds until they heal
Erysipelas etiology
Streptococcus pyogenes
Erysipelas mode of transmission
Direct or indirect contact
Erysipelas virulence factors
M protein, exotoxins
Erysipelas signs/symptoms
Distinct, raised (edema), bright redness (erythema) on the face and limbs with obvious margin, swollen lymph nodes, fever, chills, and elevated leukocytes
Erysipelas diagnosis
Clinical evaluation; distinct appearance. Cultures only performed if multiple pathogens are suspected.
Erysipelas treatment
Oral penicillin (beta-lactam) first choice, then macrolides (erythromycin)
Erysipelas prevention
practice good hand hygiene and wounds should be cleaned and treated
Necrotizing fasciitis etiology
Streptococcus pyogenes (Group A Strep or GAS)
Necrotizing fasciitis mode of transmission
Direct or indirect contact through breaks in skin or from transient bacteremia (bacteria in the bloodstream). Portal of entry not always defined.
Necrotizing fasciitis virulence factors
Streptolysin S, protease, and DNase, M protein
Necrotizing fasciitis signs/symptoms
Can begin with sunburn-like rash or a small area of red swelling with heat and pain. Pain can either be unusually intense or absent due to neuropathy. Tissue progressively darkens from red→purple→blue→black. Bullae (blisters) form and fill with straw-colored fluid which then becomes bloody. Black necrotic eschar forms as tissue dies. High fever, tachycardia (increased HR) common with more involved infection.
Necrotizing fasciitis diagnosis
Clinical examination, gram stain and culture from samples. CT or MRI can detect subcutaneous or facial edema but should not delay treatment.
Necrotizing fasciitis treatment
Surgeons clean/remove/debride tissue; IV broad-spectrum antibiotics (usually) clindamycin (macrolide) + penicillin (beta-lactam). Maggot Debridement Therapy (MDT) has also been implemented
Necrotizing fasciitis prevention
diabetes, cancer, and chickenpox are risk factors. Prevention means not taking small compromises in skin for granted - issues as harmless as needlesticks and insect bites have been linked to this
acne vulgaris etiology
Cutibacterium acnes (formerly called Propionibacterium acnes)
acne vulgaris mode of transmission
endogenous infection caused by one's own bacteria overgrowing
acne vulgaris virulence factors
lipases, adhesins for biofilm formation, and hyaluronidases
acne vulgaris signs/symptoms
Papules, pustules, nodules, and cysts
acne vulgaris diagnosis
Clinical examination; contributing factors and severity assessed
acne vulgaris treatment
Antibiotics: oral doxycycline (tetracycline) or topical clindamycin (macrolide)
Topicals like benzoyl peroxide: increases cell turnover reduces lipids on skin surface; kills bacteria.
Isotretinoin (Accutane) – vitamin A derivative that inhibits sebum formation but has potentially severe side effects including fetal birth defects, liver effects, increased blood fats, and severe skin drying
Hormonal birth control/estrogens – can affect hormonal acne / sebum production
Spironolactone – not FDA approved for acne but used off-label for blocking androgen hormones since it is an aldosterone antagonist (is used as a diuretic to high blood pressure and edema)
UVB/UVA light can kill bacteria, but can also cause skin damage
Dietary interventions – decreasing consumption of dairy and high glycemic index foods have been linked to improvement
P. aeruginosa (burn infections) etiology
Pseudomonas aeruginosa
P. aeruginosa (burn infections) mode of transmission
direct or indirect contact; often from fomites; ubiquitous and therefore easy to acquire and difficult to avoid
P. aeruginosa (burn infections) virulence factors
Fimbriae and adhesins, Capsule, Neuraminidase, Elastase, Endotoxin (lipid A), Exotoxin A and Exoenzyme S, Pyocyanin
P. aeruginosa (burn infections) signs/symptoms
Fruity, sweet smell emanating from wounds; green pigmentation of dressings and drainage.
P. aeruginosa (burn infections) diagnosis
Samples from infection cultured to confirm; antibiotic susceptibility testing conducted as well.
P. aeruginosa (burn infections) treatment
Treatment can be difficult – bacteria are resistant to numerous drugs and antibacterial agents like soaps (quats)
Usually treated with combination of ceftazidime (beta-lactam) and an aminoglycoside.
P. aeruginosa (burn infections) prevention
Almost impossible to prevent exposure, but isn’t able to invade intact tissue. Proper hand hygiene and frequent hospital cleaning is imperative.
Gas Gangrene etiology
Clostridium perfringens
Gas Gangrene mode of transmission
Transmitted by endospores entering “dirty” trauma wounds. Grows in anaerobic environments like deep tissue.
Gas Gangrene virulence factors
Colonizes wounds and can replicate RAPIDLY ~10 minute generation time
Secretes 17 toxins (alpha toxin and perfringolysin O are the most important). Similar to streptolysin, they lyse erythrocytes and leukocytes, vasodilate blood vessels, and kill cells – necrosis. Also make collagenase, hyaluronidase, hemolysins, to spread more deeply
Gas Gangrene signs/symptoms
Rapid heart rate, fever, low BP and hypoxia, foul-smelling “sickly sweet” discharge from lesions, pain, black, purple, or dark red necrotic tissue with black “bubble” lesions - gas under skin (crepitus).
Gas Gangrene diagnosis
Clinical examination; X-ray, CT, or MRI imaging to look for gas in tissues; culturing and Gram stain to confirm bacteria
Gas Gangrene treatment
IV penicillin (beta-lactam) plus clindamycin (macrolide), surgical debridement/removal of affected tissue, hyperbaric oxygen therapy
Gas Gangrene prevention
Proper debridement of deep wounds
Dermatophytoses etiology
Tinea species
Dermatophytoses mode of transmission
direct contact or indirect contact from fomites
Dermatophytoses virulence factors
lipases and keratinases to digest lipids and keratin
Dermatophytoses signs/symptoms
Red, swollen, itchy and peeling skin; sin can crack and scale as well. often produces a circular spot or produce a bald spot on the scalp.
Dermatophytoses diagnosis
Clinical inspection of the skin; KOH scrapings can be examined microscopically to look for fungal hyphae
Dermatophytoses treatment
Azoles – antifungal drugs. Topical terbinafine or oral griseofulvin for weeks-months in stubborn cases. Avoid steroid creams
Dermatophytoses prevention
Keep active infection covered; keep skin dry and clean; be wary of places like public showers.
Candidiasis etiology
Candida albicans
Candidiasis mode of transmission
Endogenous infection caused by fungal overgrowth; often induced by antibiotic treatment or becoming immunocompromised
Candidiasis virulence factors
Adhesins, dimorphism (grow as pseudohyphae or budding yeast depending on the environment)
Candidiasis signs/symptoms
Patchy rash with redness and intense itching; skin may become cracked, sore.
Candidiasis diagnosis
Clinical examination; KOH skin scrapings can be examined under the microscope or cultured; the KOH destroys normal skin cells leaving the fungi behind. Look for abundant budding yeast and/or pseudohyphae.
Candidiasis treatment
Antifungal azoles or polyenes. Topical miconazole powder or nystatin (polyene) cream. Oral fluconazole. Treatment may take 2-4 weeks
Candidiasis prevention
These fungi thrive in moist skin folds; keeping skin dry and wearing “breathable” garments can help. Beware of signs and symptoms if taking antibiotics
Chickenpox and Shingles etiology
Varicella-Zoster Virus (VZV)
Chickenpox and Shingles mode of transmission
Highly contagious and transmitted in airborne particles or by direct contact with fluid from skin lesions. Most communicable in prodromal period before skin lesions appear.
Chickenpox and Shingles virulence factors
adhesins
Chickenpox and Shingles signs/symptoms
2-3 weeks after infection, patient develops fever and lesions on the trunk, face, and limbs
Macules -> papules -> fluid-filled vesicles -> dry up and crust
Chickenpox and Shingles diagnosis
Clinical examination and antibody-based serologic tests or PCR to confirm. IgM and IgG titers can be done via ELISA
Chickenpox and Shingles treatment
usually self-limiting; can help manage symptoms with antihistamines and acetaminophen; other drugs to reduce severity and duration such as Acyclovir (nucleoside analog)
Chickenpox and Shingles prevention
live attenuated VZV vaccine will protect against this
measles (Rubeola) etiology
Measles virus (MV) or Measles morbillivirus (MeV)
measles (Rubeola) mode of transmission
one of the most contagious viruses – transmitted via airborne respiratory particles and contact with droplets
measles (Rubeola) virulence factors
adhesins that allow attachment to host cells; ability to make syncytia - envelope makes a fusion protein that allows virus to fuse cells together so it can “tunnel” and avoid immune system
measles (Rubeola) signs/symptoms
fever, sore throat, headache, dry cough, conjunctivitis – after 2 days of symptoms Koplik’s spots appear on mucous membranes of mouth (definitive diagnosis). Maculopapular rash appears on face and spreads to the trunk, limbs, and even to palms and soles of feet.
measles (Rubeola) diagnosis
Clinically with presence of Koplik’s spots, but confirmed with serological testing for IgM or testing for virus using RT- PCR in nasopharyngeal samples or serum samples.
measles (Rubeola) treatment
no specific treatments. Hospitalization can support the body if complications arise. Severe cases are treated with vitamin A – this acts as an immunomodulator and support’s the immune system’s functions to improve disease outcomes
measles (Rubeola) prevention
MMR vaccine – live attenuated or MMRV vaccine
Rubella (German measles) etiology
Rubella Virus (RuV) (Rubivirus)
Rubella (German measles) mode of tranmission
vehicle transmission by droplets from respiratory secretions or transplacental transmission. Can be transmitted 2 weeks before and after signs and symptoms appear
Rubella (German measles) virulence factors
adhesins that allow attachment
Rubella (German measles) signs/symptoms
Most cases are mild; swollen lymph nodes, low-grade fever. 50% of those infected experience a widespread pink fine rash after 7-14 days post-infection.
Rubella (German measles) diagnosis
clinical observation and serological testing for anti-RuV IgMs
Rubella (German measles) treatment
no specific treatment; supportive care only