Derm micro 12/3/25

This flashcard set covers key vocabulary and definitions from the lecture on dermatology, focusing on various skin infections, their causative agents, and relevant treatment options.

yeast

malassezia furfur

monomorphic molds

Dermatophytes:

• Microsporum

• Trichophyton

• Epidermophyton

dimorphic molds

Blastomyces dermatididis (skin lesions only)

dna, non enveloped viruses

• Parvovirus B19

• Human Papilloma Virus (warts)

dna enveloped viruses

• Herpes Simplex Virus

• HHV6 (roseola)

• HHV8 (Kaposi's)

• Varicella Zoster Virus

• Molluscum Contagiosum Virus

rna non enveloped virus

coxsackievirus (HFMD)

rna enveloped virus

• Measles (Rubeola)

• Rubella (rash only)

parvoviridae

non-enveloped, ssDNA, linear

• Parvovirus B19

papillomaviridae

non-enveloped, dsDNA, circular

• Human Papilloma Virus

herpesviridae

enveloped, dsDNA, linear

• Herpes Simplex Virus

• HHV6 (roseola)

• HHV8

• Varicella Zoster Virus

poxviridae

enveloped, dsDNA, linear, replicates in cytoplasm

• Molluscum Contagiosum Virus

picornaviridae

non-enveloped, ssRNA, positive, non-segmented

• Coxsackievirus

paramyxoviridae

enveloped, ssRNA, negative, non-segmented

• Measles (Rubeola)

matonaviridae

enveloped, ssRNA, positive, non-segmented

• Rubella

gram positive cocci

• Staphylococcus aureus – including MRSA

• Streptococcus pyogenes (Group A Streptococcus)

gram positive rods

• Cutibacterium acnes

• Bacillus anthracis

• Clostridium perfringens

gram negative rods

• Eikenella corrodens

• Pasteurella multocida

• Pseudomonas aeruginosa

• Vibrio vulnificus

spirochetes

borrelia burgdorferi

intracellular

rickettsia ricketsii

staph aureus

cocci in clusters, catalase positive, coagulase positive

strep pyogenes

cocci in chains, catalase negative, beta-hemolytic, bacitracin sensitive

clostridium perfringens

obligate anaerobe, spore-forming

types of SSTIs image

malassezia furfur

§ Normal flora (low levels)

§ Lipophilic: feeds on skin lipids

• Production by sebocytes and keratinocytes

§ Sebum: moisturize and protect skin and hair

• Protective barrier

• Prevents water loss

• Shields against microbes (some), friction, UV radiation

§ Stratum corneum only

• Scalp, face, chest, and back

pityriasis (tinea) versicolor

malassezia fungal infection.

§ Hypo- or hyper-pigmented

§ Finely scaly macules/patches

§ Trunk, neck, upper arms

§ More visible after sun exposure

folliculitis

malassezia fungal infection

§ Rarer, may be misdiagnosed as acne

§ Itchy follicular papules/pustules

• Chest, back, shoulders, or face

§ Worse with heat, humidity, or steroid use

malassezia diagnosis

§ Wood lamp: Yellow/Silver “glow”

§ KOH prep of skin scraping

• Round yeast forms and short “hyphal” forms (pseudohyphae)

• “Spaghetti and meatballs”

malassezia treatment

Topical (also for maintenance):

§ Selenium sulfide lotion/shampoo

§ Zinc pyrithione shampoo (head and shoulders)

§ First line azoles: ketoconazole, clotrimazole, miconazole cream

§ Terbinafine (allylamine) cream

dermatophytes

Macroconidia on microscopy → diagnostic

§ Monomorphic molds

• Soil, animals (including pets), humans

• Contagious

§ Produce keratinases

• Break down keratin, allow invasion into lower layers of epidermis

• ONLY grow on keratinized structures

§ Scaling skin

§ Loss of hair (can be permanent)

§ Crumbling nails

§ Itching

epidermophyton

• Infects skin and nails but does not infect hair

• Causes common infections like jock itch and athlete’s foot

• Person-to-person; indirectly through contaminated surfaces/objects

microsporum

• Primarily infect skin and hair

• Zoonotic transmission (e.g., dogs)

• Ectothrix hair invasion (infection outside the hair shaft)

trichophyton

• Infect skin, hair, and nails

• More common in chronic, persistent infections

• Some are zoonotic (dogs, cats, cattle, horses)

only contagious fungal infections (human to human):

dermatophytes

dermatophyte infections

§ Tinea capitis: capit = head

• Common in children

§ Tinea corporis: corpus = body

• “ring worm”

§ Tinea cruris: cruris = groin (jock itch)

§ Tinea pedis: ped = foot (athlete’s foot)

§ Tinea unguium: unguis = nail

• Onychomycosis: nail infection

§ Tinea barbae: beard

tinea corporis

body.

§ “Traditional” “ ringworm”

§ Clearing, scaling and raised, red edges; dry

§ Expands out = Hyphae only seen on edges

§ Treatment: Topical 2-4 weeks

• Terbinafine

• Miconazole

• Clotrimazole

dermatophytes diagnosis

§ Skin or nail scraping, hair plucking

• KOH prep

• Look for branched, septate hyphae

§ Wood lamp → especially for Tinea capitis

• Look for fluorescence … not always positive

macroconidia clues

Microsporum = Spindle shaped

Epidermophyton = Beaver’s tail

Trichophyton = Cigar shaped

dermatophyte treatment

§ Cutaneous mycoses can be cured with topical therapy

• Exception: Tinea capitis/barbae (drug must penetrate hair follicles) → Oral griseofulvin … microtubule inhibition, concentrates in keratinized structures

§ Topical

• Imidazoles (clotrimazole, ketoconazole)

§ Oral

• Terbinafine, azoles (fluconazole and itraconazole)

• Usually for cases that aren’t responding/resistant

blastomycosis

§ Blastomyces dermatitidis

• Mississippi River basin, Great Lakes, NE

• Hunters, forestry workers, farmers, campers

§ Can disseminate to almost any tissue

• Skin especially → chronic, painless, rough (verrucous)

§ Diagnosis

• Broad-budding yeast in sputum, urine, tissues

• Confirm by culture

§ Treatment

• Itraconazole

• Liposomal amphotericin B – life-threatening, CNS

HPV skin manifestation

• Verrucous warts (skin)

• Serotypes 1 and 2

HSV skin manifestation

• Grouped fluid-filled vesicles on an erythematous base

• Small, painful

• Can reactivate

HHV8 skin manifestation

• Dark red/brown raised nodules or patches

• Kaposi sarcoma

• In HIV/AIDS patients, CD4 <200

molluscum contagiosum skin manifestation

• Raised, round, skin-colored bumps with central umbilication

• Painless

-Henderson Paterson bodies on microscopy

VSV skin manifestation

• Lesions go through a progression; all can be seen at the same time during infection

• Macular to papular to vesicular lesions before crusting

• Shingles within single dermatome

coxsackievirus skin manifestation

• Hand Foot Mouth Disease

• Painful, blister-like lesions

• Redness surrounding

HSV diagnostics

Clinical

§ Characteristic grouped vesicles on an erythematous base that may ulcerate

§ Pain/tingling/burning prior to lesion appearance

§ History of similar symptoms

Laboratory

§ Gold standard = PCR on clinical specimen

§ Eye = Fluorescein staining for characteristic dendritic lesions in cornea

§ PANCE (historical test) = Tzanck smear

• Scraping of lesion, Wright or Giemsa stain, multinucleated giant cells

HSV vs HFMD lesions

HSV

• Any age, recurrent (reactivation), common

• Prodrome of pain/burning/tingling

• Lesions surround each other at 1 spot

• Can have high fever

• Lesions very painful

• Can confirm with PCR or Tzanck smear (multinucleated giant cells)

HFMD

• Kids usually, palms, soles, around mouth; buttocks sometimes

• May have prodrome of sore throat, decreased appetite

• Low-grade or no fever

• Lesions “shallow” and “grey”; not as painful as HSV

6 childhood exanthems chart

rubeola vs rubella vs roseola infantum graphic

congenital virus complications

Parvovirus B19

§ Aplastic crisis (infects RBCs)

§ Hydrops fetalis/fetal death

Rubella

§ Congenital: triad of cataracts, heart defects, deafness

Varicella

§ Congenital: Cicatricial (scar-like) skin lesions (dermatomal distribution), limb hypoplasia, microcephaly etc.

Measles

§ Sub-acute sclerosing panencephalitis (SSPE)

HSV treatments

§ Acyclovir, valacyclovir (less doses)

§ Can also be used to prevent reactivation

varicella treatment

IV acyclovir in immunocompromised

zoster treatments

Oral acyclovir, valacyclovir

human papilloma virus (HPV)

Microbe characteristics

• Papillomaviridae – non-enveloped, dsDNA (circular)

• DNA remains in nucleus

• Integration occurs

• E6 and E7 viral protein are made

• Oncogenic

Reservoir/s and transmission

• Human-only pathogen

• Transmission is by direct contact: Fomites

Epidemiology

• Worldwide; MC STI in US – 18-59 yrs

• Different serotypes, different diseases

HPV replication strategy

§ Complex, tied to epithelial cell development

§ Attachment, endocytosis

• Basal cell infection FIRST

§ Viral DNA is transported into nucleus

• Can integrate into chromosome; mechanisms not known

• Necessary for HPV-related cancer events

• E6 and E7 proteins are oncoproteins –bind to and inhibits p53 and Rb, causing uncontrolled cell cycle

HPV oncogenic process

§ GENOME INTEGRATION

§ SYNTHESIS OF E6 and E7 proteins

§ Interact with p53 and pRb → cause their degradation (and inactivation)

§ P53 can’t work: no apoptosis

§ Rb can’t stop cell cycle proliferation

• Regulate G1/S transition of cell cycle

condyloma acuminata (anogenital warts), laryngeal papillomas

§ HPV 6 and 11

§ “Cauliflower shaped” – can get large and interfere with defecation etc. in immunocompromised

cutaneous warts (verrucae)

§ HPV 1 and 2

§ Rough, raised bumps on hands, fingers, and soles of feet

§ Most resolve, may need surgical removal (e.g., plantar warts)

§ Will reappear if not completely “excised”

• Basal cells infected!

HPV wart treatments for immunocompetent

§ Topical salicylic acid, several weeks

• Keratolytic; softens and removes infected keratinocytes

• Requires patient compliance; can cause mild irritation

§ Cryotherapy (liquid nitrogen)

§ Electrosurgery / curettage

• Physical removal of the wart

viruses w/ vaccines

Measles, mumps, rubella (MMR)

• Live, attenuated

Varicella

• Live, attenuated

Zoster

• Shingrix: Recombinant, surface glycoprotein E

HPV

• Recombinant, virus-like particles

• Capsid proteins of HPV 6, 11, 16, 18, 31, 33, 45, 52, 58

leishmania major, braziliensis, mexicana

Microbe characteristics

• Flagellated protozoan

Reservoir/s and transmission

• Sandfly vector

• Injects promastigotes during feeding

• No human-to-human contact, even cutaneous

Epidemiology

• Endemic: India, Bangladesh, Sudan, Ethiopia, and Brazil

leishmaniasis

Sandfly bite during blood meal

• Injects promastigotes

Promastigotes (flagellated)

• Phagocytosed (preferentially) by macrophages

• Transform into amastigotes –DIAGNOSTIC inside macrophages

Sandfly bite

• Ingests infected macrophages

• Amastigotes

cutaneous leishmaniasis

§ Weeks/months after sandfly bite

§ Skin/mucosal papules that progress to nodule or ulcer

§ Raised, well-demarcated border “Volcano”

§ Painless OR painful

§ Can be destructive

§ Leaves a scar

cutaneous leishmaniasis diagnosis

• Gold standard: Direct visualization of amastigotes (Leishman-Donovan bodies) Giemsa-stained Bone marrow biopsy, skin lesion biopsy

• Amastigotes inside macrophages

• Urine antigen test

scalded skin syndrome cause

• Staphylococcus aureus toxin breaks apart desmosomes

• Life-threatening, admit

Penicillinase-resistant, anti-staphylococcal –nafcillin, oxacillin etc; Vanc for MRSA

impetigo causes

• Streptococcus pyogenes (GAS)

• Staphylococcus aureus (bullous)

folliculitis causes

• Staphylococcus aureus

• Pseudomonas aeruginosa (hot-tub)

erysipelas cause

Streptococcus pyogenes (GAS)

with staph aureus always consider:

MRSA

carbuncles/furuncles MC causes

• Staphylococcus aureus

• Furuncle = 1

• Carbuncle = multiple coalesce

skin abscesses MC cause

staph aureus

cellulitis MC cause

Streptococcus pyogenes (GAS), S. aureus

type 1 NF MC cause

• Polymicrobial

• Anaerobes (e.g. Bacteroides)

• Spontaneous

type 2 NF MC causes

• Streptococcus pyogenes (GAS)

• Staphylococcus aureus

myonecrosis MC cause

Clostridium perfringens

• Other Clostridial normal flora

acne vulgaris

white heads, black heads etc.

Cutibacterium acnes

Mild/moderate: topical benzoyl peroxide or topical clindamycin

cutaneous anthrax

Painless black eschar, surrounding edema (extensive)

Bacillus anthracis

Oral ciprofloxacin

scarlet fever

Fine, sandpaper-like rash, starts on trunk, spares palms and soles; ”strawberry tongue”

Group A Streptococcus

Penicillin OR amoxicillin

lyme disease

primary “Bullseye” rash – erythema migrans

Borrelia burgdorferi; tick bite

Doxycycline as soon as suspected

rocky mountain spotted fever

rash – wrists/ankles, moves inwards (centripetal)

Rickettsia rickettsii; tick bite

Doxycycline as soon as suspected

toxic shock syndrome

widespread, “sunburn-like” rash, skin peeling (palms and soles) after; bad vitals, vomiting, multi-organ involvement

Group A Streptococcus or Staphylococcus aureus expressing superantigen

Tx Directed (cultured): penicillin for GAS; clindamycin + nafcillin for MSSA; clindamycin + vanc for MRSA

uncomplicated vs complicated SSTIs

UC: Impetigo, erysipelas, simple cellulitis, simple abscess

§ Localized

§ Respond to I&D or short-course oral antibiotics

§ Streptococcus pyogenes, Staphylococcus aureus (MSSA/MRSA)

C: Deep abscesses, infected ulcers, diabetic foot infections, postoperative wound infections, necrotizing fasciitis

§ Extend deeper layers

§ May be immunocompromised

§ Often need surgical intervention, IV empiric and definitive antibiotics

§ Polymicrobial (Gram-positive, Gram-negative, anaerobes), MRSA, Enterobacteriales, Pseudomonas

MRSA risk factors

§ Prior MRSA infection

§ Recent antibiotic use (broad-spectrum); community or hospital

• Esp. fluoroquinolones or B-lactams

§ Close quarters, contact sports, sharing personal items

§ Recent hospitalization or surgery / frequent healthcare contact

§ Residence in long-term care facility

§ Chronic wounds/ulcers

§ IVDU

impetigo

§ Highly infectious

§ Very common

§ Usually in children

§ Red sores on the face: nose and mouth / hands and feet

• Over a week, sores burst and develop honey-colored crusts

• Itchy

§ S. pyogenes MC cause

§ S. aureus strains that express exfoliative toxin → bullous impetigo (fluid-filled blisters)

• Not systemic toxins like scalded skin syndrome

impetigo treatment

Mild: Topical mupirocin (protein synthesis inhibitor)

folliculitis

• Small, erythematous papules or pustules centered on hair follicles

• May have a surrounding erythema

• May spread deeper to cause furuncles/carbuncles

• Localized, often on beard area (face), scalp, arms, legs, trunk, or buttocks

• Mild pruritus or tenderness

• Pain is uncommon

• S. aureus most common cause by far

• Shaving, tight clothing, friction

• Mild: topical mupirocin

• Hot tub folliculitis

• Pseudomonas aeruginosa, exposure to contaminated water

• Most cases resolve on their own

abscesses, carbuncles, furuncles

§ Furuncle: infection of hair follicle, surrounding skin and deep underlying subcutaneous tissue

• Carbuncle: multiple furuncles have fused L

§ MC cause: MSSA and MRSA

§ Painful, erythema, mild edema

§ Pus can leak

§ Can have a fever

Management

§ Incision and drainage

• Will be left open to heal

• Drain pus, keep moist

§ Culture and sensitivity, especially if moderate/severe infection like MRSA

erysipelas

§ Malaise, fever, chills 48 hours before onset of rash

§ Infection of superficial dermis

• Can extend to superficial cutaneous lymphatics

• Peau d’orange (orange peel skin)

§ Area of erythema is well demarcated, raised

§ Fast development

§ Often affects the lower extremities

• Face second most common

§ Burning, pain, itchy

§ Group A Strep

§ Outpatient: Penicillin or amoxicillin

cellulitis

MSSA, MRSA, GAS

§ Bacterial invasion extending into reticular dermis and subcutaneous fat

• Does not extend past subQ fat

• Usually a good prognosis

§ Risk factors (local to site)

• Skin trauma: Barrier disruption (abrasion, wound, ulcer, insect bite, IVDU)

• Skin inflammation

• Breaks in the skin between the toes

• Preexisting skin infection: tinea pedis, impetigo, varicella

§ Risk factors (person)

• Age

• Edema (stretching of skin)

• Obesity (stretching of skin)

• Immunosuppression

§ Clinical fx

• Warmth, erythema, pain, edema

• Swelling can cause skin to break

• Vitals usually OK

• Borders ill-defined

• Lower extremities most affected

• Unilateral

• Progresses slowly

• Purulent or non-purulent, purulent suggests Staph

• Abscesses can form: nodules are fluctuant

• Vesicles, bullae (large fluid-filled cavities)

§ Complications

• Bacteria can invade surrounding blood vessels

• Bacteremia, endocarditis, osteomyelitis, metastatic infection, sepsis, toxic shock syndrome

cellulitis diagnosis

• Usually clinically – history, physical exam

• Rule out others

• Erysipelas – well-defined borders, more superficial

• NF – poor vitals, fast-progressing, necrotic signs

• Culturing is not required if uncomplicated/routine

• Skin swabs = normal flora, not involved in infection

• MRSA, treatment failure (rarer cause?), C&S may be required

• Imaging is not helpful, except to visualize an abscess / differential DVT

cellulitis treatment

§ Mark margins to track spread

§ Early treatment essential

§ Therapy directed to Streptococcus pyogenes first

• Cephalexin(covers MSSA too), or dicloxacillin / oxacillin

§ MSSA 2nd

§ If purulent, I&D may be needed

§ Cellulitis may appear to worsen the first 24-48 hours despite antibiotics → bacterial cell lysis

If MRSA suspected, but GAS most likely, mild: TMP-SMX and cephalexin, oral.

TMP-SMX not for GAS

eikenella corrodens tx

§ Oral Amoxicillin-clavulanate

§ * Consider polymicrobial infections with human bite wounds

pasteurella multocida tx

Oral Amoxicillin-clavulanate

pseudomonas aeruginosa tx

IV Piperacillin-tazobactam or Ceftazidime or Cefepime

vibrio vulnificus tx

§ IV … has ability to progress to sepsis FAST

§ Doxycycline AND a 3rd gen ceph (ceftriaxone, cefotaxime, ceftazidime)

if anaerobe probability, tx:

metronidazole, clindamycin

necrotizing fasciitis

§ Rare, but life-threatening infection of fascial planes and overlying subcutaneous fat

§ Muscle is usually spared (early stages) due to good blood supply and immune system

• Clostridium doesn’t care

§ Risk factors similar to cellulitis plus:

• Major penetrating trauma, recent surgery, malignancy

• Diabetes: lower extremities, perineum (Fournier gangrene), head and neck region

necrotizing fasciitis mortality rates

§ Group A Streptococcus (monomicrobial): 25–30%

§ MSSA: 15-30%

§ MRSA: 20-40%, esp. if empiric therapy doesn’t cover

§ Polymicrobial (type I): 20–35%

§ Vibrio vulnificus: up to 50% or higher

• Esp. in patients with liver disease

§ Aeromonas: 30–50%

§ Factors that increase:

• Delayed diagnosis or inadequate surgical intervention (>24 hrs)

• Chronic liver disease, diabetes, or immunosuppression

• Septic shock at presentation

§ Despite optimal management, mortality remains high

necrotizing fasciitis symptom progression

§ Acute, RAPID progressing

• Extensive destruction of affected tissue

• Necrosis

§ Systemic toxicity

• Tachycardia, fever, hypotension, tachypnea

§ Ill-defined erythema and borders

§ Edema that extends beyond erythema

§ Severe pain out of proportion to physical exam (early on)

§ Crepitus (popping/cracking, air under skin) … depends on cause

§ Bruising (ecchymoses) – ”dusky” color

§ Bullae – dark red/black

Type 1 necrotizing fasciitis

Polymicrobial – most common

• Aerobic and anaerobic

• At least one anaerobic species (e.g., Bacteroides) is isolated in combination with Enterobacteriaceae

• Streptococcus, Staphylococcus

• Post-surgery, diabetic foot infection, Fournier’s