Skin Infections (CH 19) Flashcards
1
Q
What are the key clinical indicators in an infection?
A
- fever
- lymphadenopathy
- skin exam
- labratory diagnostics
- inflammatory markers
- pathogen-specific testing
2
Q
Key clinical indicators of infection: Fever
A
- common hallmark of infection
- core temp =/ >38.3 ( = / > 101F) defines fever of unknown origin
- for every 1C incr in temp, HR raises by 15-20 bpm
3
Q
Key clinical indicators of infection: lymphadenopathy
A
= key infection indicator
- important for noting location, size (<1cm) tenderness, consistency (soft, firm, or rubbery), and matted nodes
- localized: 55% in head/neck; 14% inguinal; 5% axillary
4
Q
Key clinical indicators of infection: Skin Exam
A
- essential for identifying specific rashes that help narrow infection diagnosis –> can determine if infection is localized / systemic
- need full exam of back + front
5
Q
Key clinical indicators of infection: lab diagnostics
A
- serologic tests, antigen tests, molecular diagnostics revolutionizing medical care (PCR)
- tests = complementary, not replacement for hx + physical exam
6
Q
Key clinical indicators of infection: inflammatory markers
A
- ESR (erythrocyte sedimentation rate): indirect measure of inflammation (changes slowly)
- CRP: direct measure of inflammation (changes rapidly)
- serial monitoring helpful for disease progress/resolution
- elevated EST > 100mm/h indicates serious underlying disease (90% predictive value)
- ongoing work to validate other markers (e.g., procalcitonin, serum amyloid A)
7
Q
Key clinical indicators of infection: Pathogen-Specific Testing
A
- sample collection: for accurate diagnosis
- culture: traditional method to identify pathogens
- serology / antigen testing / PCR: for detecting specific pathogens
- radiology: to identify infection-related complications or patterns
8
Q
Structure of Skin: Epidermis
A
superficial layer with 5 layers
1. stratum cornuem
2. stratum lucidum
3. stratum granolusum
4. stratum spinosum
5. stratum basale
- langerhans cells = immune cells
- basal cells = turning + differetiating into keratinocytes
- melanocytes
- dead keratinocytes (keratin)
9
Q
Structure of Skin: Dermis
A
deep layer
- connective tissue
- cells
- blood vessels, nerves, hair follicles, sweat glands
10
Q
Structure of Skin: Hypodermis
A
superficial fascia or subcu layers
- located directly under dermis, consists mostly of adipose and ct
11
Q
What is a rash and what is it caused by?
A
change in color and texture of skin
caused by reaction to toxin produced by:
- the pathogen
- damage to skin by pathogen
- immune response
12
Q
Skin rash: Exanthem
A
widespread skin rash accompanied by systemic symptoms (fever, malaise, headache)
- if rash is in skin
12
Q
skin rash: enanthem
A
- rash on mucous membranes
- if rash in mucosa
13
Q
Viral Rashes - etiology + effects?
A
caused by:
- measles (rubeola) + german measles (rubella)
- fifth disease (erythema infectiosum(
- roseola
- chickenpox
- shingles
- cold sores
- warts
- hand, foot, mouth disease
- smallpox
virus can be cytolytic or cytoproliferation
can lead to rash or warts
14
Q
bacterial infections of skin: conditions + effects?
A
- folliculitis, furnucle, carbuncle
- scalded skin syndrome
- erysipelas
- cellulitis
- acne
can be cytolytic due to toxins or direct contact (lysis/invasion)
leads to rash + pus formation (pyodermas), necrotizing (severe)
15
Q
fungal infections: conditions + effects
A
- dermatophytosis
- tinea versicolor
- candidiasis
can be granulomatous or cytolytic (toxins)
- can lead to rash (mucular) and desquamtive (flaky skin, peeling off)
16
Q
What are the different types of rashes?
A
- macular (erythematous): flat (and red), <1cm in diameter
- papular: small, solid and elevated, < 1cm in diameter (<0.5 cm)
- maculopapular: papule that is reddened
- pustular: skin lesion filled with pus
- vesicular: small blisters formed
17
Q
how are bacterial infections of skin and soft tissues classified as?
A
- primary pyodermas
- infections associated with underlying conditions of the skin
- necrotizing infections (most severe)
17
Q
Types of rashes?
A
- bulla: big vesicle, clear fluid, >1cm
- nodule: big papule; elevated + solid, >1cm
- scales: fungal infection
- petechial rash: microhemorrhagic, caused by toxins killing cells, e.g., meningitis, necrosis fasciitis
- purpuric rash
18
Q
when do skin infections happen?
A
happens when skin’s protective mechanisms fall:
- trauma
- inflammation
- maceration from excessive moisture, poor blood perfusion, or other factors that disrupt the stratum corneum –> creates point of entry for endogenous and exogenous microbial flora
19
Q
What are pyodermas common caused by?
A
are primary cutaneous infections
- commonly caused by narrow spectrum of pyogenic bacteria
- staphylococcus aureus and/or streptococcus pyogenes (group A streptococcus)
19
Q
examples of bacterial infections?
A
- folliculitis, furunculosis, carbuncle
- impetigo
- erysipelas
- cellulitis
- necrotizing fasciitis
- myonecrosis
20
Q
Staphylococcal skin toxin syndromes
SSSS
A
- staphylococcal scalded skin syndrome (SSSS): in neonates, caused by toxin (exofliatin) from S. aureus disrupting skin desmosomes
- caused by S. aureus
21
Q
Staphylococcal Skin Infections: Staphylcocci
A
- staphylococcal epidermis
- staphylococcal aureus
- normal inhabitant of nares - can infect cut and gain access to dermis via hair follicle
- pus forming @ infected sites composed of dead immune cells and bacteria –> can lead to abscess (closed collection of pus)
22
Staphlycoccal Skin Infections: Folliculitis pathogenesis
- s. aureus infection of hair follicle can be superficial or deep
Pathogenesis:
- folliculities: minor infection of hair follicle
- furuncle (boil): boils may rupture and drain pus or develop into carbuncle
- carbuncle: large loculated abscess, particularly in diabetes
23
Staphlycoccal Skin Infections: Folliculitis Dx + Tx
Dx: clinical diagnosis
Tx:
- resovle on its own
- topical abx (mupirocin or fusidic acid)
- abx + drainage
- oral cephalexin or cloxacilin (7-10d) - first line empirical therapies for community-acquired SSTIs
- if MRSA - vancomycin
24
Staphlycoccal Skin Infections: Impetigo
| etiology + epidemiology
= superficial infection of skin (epidermis) --> elevation with pus formation
etiology: s. aureus / group A beta-hemolytic streptococci (sometimes both)
epidemiology: principally associated w/ childhood
25
what are the 2 main types of impetigo?
1. nonbullous:
- starts as superficial bump --> papule and vesicle --> pustules on erythematous skin
- fluid from pustules leak out as they break open --> honey color
2. bullous
- vesicles grow larger and become bullae that are full of clear, yellow fluid
26
Staphlycoccal Skin Infections: Impetigo - clinical features, labs, tx
**clinical features**: honey-coloured crusted lesions develop mainly on face around the nose and spread by autoinoculatoin
**lab diagnosis**: culture of swabs of lesions
**tx:** topical treatment often sufficient (mupirocin)
27
Streptococcal Skin Infections: S. pyogenes
- group A
- human nasopharynx and parts of skin = natural reservoir for S. pyogenes
- has virulence factors:
28
Streptococcal Skin Infections: S. pyogenes virulance factors
exotoxins:
- streptococcal pyogenic exotoxins (SPEs): superantigens; massive amounts --> high levels of inflammation --> shock
- SPEs associated with scarlet fever, streptococcal toxic shock syndrome, necrotizing fasciitis
hemolysin
- lyses RBCs
- these streptococci subclassified into groups A-O according to cell wall antigens
29
Staphlycoccal Skin Infections: Acne vulgaris
| etiology
etiology: propionibacterium acnes
- results from keratin blocked hair, sebaceous follicles/pores called comodones
- can be open or closed
30
Staphlycoccal Skin Infections: Acne vulgaris s/s + tx?
s/s: inflammatory acne
- inflamed macules, papules, pustules, and nodules (severe)
tx: severe case - use tetracylcine combined w/ topical antiseptics
30
Staphlycoccal Skin Infections: Acne vulgaris, development factors
- genetic predisposition
- hormones
- gram-positive bacterium propionbacterium acnes --> organisms use triglycerdies in sebum as nutrient
31
Staphlycoccal Skin Infections: Erysipelas
| etiology + clinical manifestations
- caused by S. pyogenes
acute infection/inflammation
- small, erythematous patch -->
- fiery-red, shiny plaque
- involves upper layer of dermis, then spreads to superficial lymphatics
- swollen lymph nodes, fever, systemic symptoms
- may appear on face, most commonly seen on lower extremities
31
Staphlycoccal Skin Infections: Erysipelas, lab dx + tx
lab dx: blood cultures + skin aspirates may be positive in ~25% pts
tx: benzylpenicillin or macrolide (e.g., erythromycin or clariththromycin) or clindamycin
- aim for cell wall
32
Streptococcal Skin Infections: Necrotizing fasciitis - what are the types?
type 1: polymicrobial (lots of microbes causing infection)
type 2: 1 microorganism, usually S. pyogenes and sometimes S. aureus
- other organisms that can cause necrotizing fasciitis include clostridium perfringens (soil) and vibrio vulnificus (immunocompromised)
33
# ```
Streptococcal Skin Infections: Cellulitis
- uncomplicated, non-necrotizing inflammation of dermis
- characterized by localized pain, swelling, tenderness, **erythema with poorly defined edge**, and warmth
- develops slowly and involves deeper levels of dermis including subcu fat + ct
- often complication of wound infection
- most frequently caused by s. pyogenes, but # of bacterial species can cause this infection
34
Streptococcal Skin Infections: Necrotizing fasciitis, pathogenesis?
bacteria penetrates skin --> prod enzymes and toxins --> local subcu tissue destruction + systemic toxicity
35
Streptococcal Skin Infections: Necrotizing fasciitis - Clinical Features
rapidly spreading cellulitis with necrosis, fever, systemic toxicity, hypotension, and shock
- has high mortality
36
Streptococcal Skin Infections: Necrotizing fasciitis - Treatment
rapid + aggressive surgical removal of affected tissue (debridement)
abx: clindamycin, metronidazole, gentamicin
37
LRINEC score for necrotizing soft tissue infection
- total score of greater than or equal to 6 is associated with high risk of necrotizing infection
- can be used to differentiate between cellulitis – hemorrhagic, regular, or necrotizing
38
Gangrene - Clostridium perfringens process
- highly fermentative - can see, feel, and smell gas
- true saprophyte - thrives in dead tissue, needs it
c. perfringens --> enzymes and exotoxins --> rapid spread --> hemolysis --> gas gangrene or myonecrosis --> septic shock (high rates of mortality if untreated)
38
Gangrene: Dry vs Wet
Dry: occurs when blood supply to tissue is cut off
wet: occurs due to infection
- gas gangrene
- localized necrosis
38
Wet Gangrene - localized necrosis
- can affect internal or external part of body
- anaerobic infections is affecting genital area (Fournier's gangrene) and infections caused by Clostridium species that prod large amounts of gas
39
How can fungal skin infections be diagnosed? treatment?
- clinical appearance
- microscopic examination of potassium hydroxide (KOH) preparations of skin flakes or hair
- fungi can be cultured on special selective medium - Sabouraud agar
- treat with antifungal medications: imidazole compounds such as clotrimazole
39
Gangrene - Clinical features + Tx
- cellulitis with necrotic areas
- bullae with foul-smelling drainage and gas gangrene
- tissue crepitus due to gas production (gas moving in layers of skin)
- fever and toxemia evolve as myositis develop
tx: drain bullae, treat with surgery + abx
40
How is KOH used for diagnosing fungal infections?
it destroys skin cells but not the more resilient walls of mycelia or spores, which can then be seen under a light microscope
40
What do antifungal medications tartget?
aim for regions of metabolism + plasma membrane
41
fungal infections: Dermatophytes - what do they love? what causes majority of infections?
"love" skin
- cool/warm, moist, keratinized tissues (skin, hair follicles, nails)
- epidermophyton, trichophyton, microsporum causes majority of infections
42
How are fungal infections named?
named after location in the body
- tinea capitis (scalp)
- tinea corporis (body)
- tinea cruris (groin/jock itch)
- tinea pedia (foot)
- tinea unguium (nails)
43
Tinea capitis
fungal infection of scalp
- primarily in small children
- ring lesions - lose hair b/c fungi consumes keratin
44
tinea corporis
fungal infection of body skin
- ringworm ring-shaped, itching skin lesions (excluding groin)
- ring expands as fungus grows outward from initial site of infection
45
Tinea versicolor
| where is it prevalent in, pathogenesis, clinical manifestations?
affects melanocytes, loses colour
- LT chronic infection of skin
- prevalent mostly in warm, moist climates
- caused by years of genus Malassezia -> not a dermatophyte
- pathogenesis: round yeast converts to hyphal form --> invades stratum corneum
- lesions of tinea versicolor = small, sharp border, hypopigmented skin (caused by direct lesion to melanocytes)
46
Candida
| The species, what can they infect and where?
candida species - dimorphic yeasts
- part of normal flora of GI tract, vaginal tract, oral cavity, and skin (affect mucous membranes)
- candida albicans can infect: skin, mucous membranes, body organs
- can infect areas where skin touches or rubs together --> candidal intertrigo
