Origin of infection and the likely bacterial pathogen....

...

IV Catheters:

Gram-positive organisms (staph and strep)

Bacterial Skin and Skin Structure Infections:

Gram-positive organisms (staph and strep)

Respiratory infections:

S. pneumoniae

UTIs

Gram-negative organisms (>50% E. coli)

Abscess/abdominal infection:

Gram-negative organisms and anaerobes

Manipulation (surgery):

Gram-positive organisms (staph and strep)
Consider gram-natives if an intra-abdominal surgery

Papule:

raised lesion less than 10 mm

Plaque:

elevated lesion >10 mm

Pustule or abscess:

Elevated skin lesion containing pus

Vesicle or bulla (blister):

Bubble-like swelling containing air or fluid

Crust--->

hardened, adherent serum on skin surface over lesion

Impetigo:

contagious superficial pyoderma which begins with a superficial flaccid vesicle that ruptures and forms a yellowish crust
MOST COMMON IN CHILDREN ON THE FACE

Folliculitis:

inflammation of a hair follicle
Lesion may be a papule or a pustule

Furuncles:

(folliculitis progresses to furuncles)
localized pyogenic infection starting deep in a hair follicle (boil or abscess)

Carbuncles (multiple furuncles):

deep-seated pyogenic infection of skin and subcutaneous tissues, usually arising in several contiguous hair follicles, with formation of connecting sinuses

Cutaneous abscess:

collection of pus in the dermis and deeper skin tissues

Erysipelas:

acute, superficial cutaneous cellulitis characterized by:
HOT
RED
EDEMATOUS
BRAWNY
SHARPLY DEFINED ERUPTIONS (clearly defined edges)

Cellulitis:

inflammation of subcutaneous, loose connective tissue

Necrotizing fasciitis:

infection of soft tissue with organisms that produce extensive tissue necrosis and local vascular occlusions
MEDICAL EMERGENCY

What are the types of purulent SSTIs?

Furuncles, carbuncles, cutaneous abscess and erysipelas

What are the type of non purulent SSTIS?

Erysipelas, cellulitis and necrotizing fasciitis

What are the infections that occur in the epidermis?

erysipelas, impetigo and folliculitis

What are the infections that occur in the dermis?

Ecthyma, carbunculosis, and furunculosis

What infection occurs in the superficial fascia?

cellulitis

What infection occurs in the subcutaneous tissue?

necrotizing fasciitis

Primary bacterial SSTIs:

infection in regions of formerly healthy skin

Secondary bacterial SSTIs:

infection in areas with already damaged skin

Acute bacterial skin and skin structure infections:

bacterial infection of the skin with a lesion size area of at LEAST 75 cm2

Type of SSTI plus causative agent....

...

Impetigo:

Staph Aureus and group A strep

Folliculitis:

S. aureus and P. aeruginosa

Furuncles/carbuncles/abscess

Staph. aureus

Erysipelas:

Group A strep

Cellulitis:

Group A or other streptococci, S. aureus

Necrotizing fasciitis:

Type I: Anaerobes and facultative bacteria
Type II: Group A strep

Protective factors in healthy skin:

AMPS - antimicrobial peptides
IgG- immunoglobulin G
IgA- immunoglobulin A
APCs- antigen-presenting cells

Pathophysiology- development of SSTI:

1. Bacterial adherence to host cells
2. Invasion of tissue with EVASION of host defenses
3. amplification of toxins

Pathophysiology of impetigo:

Carrier or inoculation by a contaminated object
Organisms become attached to the traumatized area, binding strongly to fibronectin and possibly type 4 collagen and laminin
Early lesion of impetigo is characterized by a split in the epidermis just beneath

Pathophysiology of folliculitis:

infection NOT DUE TO BREAK IN SKIN (portal of entry through hair follicle)
Growth occurs in the OSTIUM of the hair follicle and may progress more deeply around the hair SHAFT
Accumulation of neutrophils, forming an abscess associated with edema of epiderm

Pathophysiology of a furuncle:

-May progress deeper and rupture through the follicular epithelium
Abscess extends into perifollicular dermis and surrounds ENTIRE FOLLICLE
Follicular epithelium and hair shaft with pus form purulent necrotic core furuncle or boil
Healing---> loss of hair

Carbuncle:

Associated with more persistent purulence, fibrosis and granulation tissue
-PANTON-VALENTINE leukocidin- producing strains of S. aureus have been linked to the formation of carbuncles

Pathophysiology of erysipelas and cellulitis:

Minor trauma to skin and invasion of bacteria
Proliferation and spread of bacteria due to virulence factors
Dermal edema and lymphatic dilation follows
Significant neutrophil infiltration with a limited localization around blood vessels

Pathophysiology of necrotizing fasciitis:

-Due to invasive group A B-hemolytic streptococcal infection that produce either pyrogenic exotoxin A or B or both
-Superantigens and cytokines appear to play a critical role in severe group A invasive streptococcal infections
-Impaired recruitment of PMN

Risk factors for impetigo:

-Children 2-5 years old
Climate: hot summers and mild winters/ wet and dry seasons
Infections or injuries that break the skin
Close contact with another person with impetigo (MOST COMMON RF)
-daycare, schools, etc.

Risk factors for folliculitis:

Immunocompromised
Acne or dermatitis
Steroid creams or long-term antibiotic therapy for acne
Being a male with curly hair who shaves
Clothing that traps heat and sweat
Soaking in a hot tub
Damage to hair follicles by shaving, etc.

Risk factors for Erysipelas, cellulitis and skin abscess:

Skin barrier disruption due to trauma (abrasion, penetrating wound, pressure ulcer, etc.
Skin inflammation (eczema, psoriasis, etc.)
Edema due to impaired lymphatic drainage or venous insufficiency
Obesity
Immunosuppression (diabetes or HIV)
Skin breaks b

RF for necrotizing fasciitis:

Major penetrating trauma
Minor laceration or blunt trauma
Skin breach
Recent surgery:
Main ones:
1.MALIGNANCY
2. OBESITY
3. ALCOHOLISM

Clinical presentation of impetigo:

Most common on the face
Classified as bullous or nonbullous

Nonbullous:

Lesions start as small, fluid-filled vesicles
Vesicles quickly turn into pustules that rupture easily
Golden yellow crust forms from purulent discharge

Bullous:

Lesions starting as vesicles, rapidly progress into bullae containing clear yellow fluid
Bullae soon rupture forming thin, light brown crusts
Regional lymphatic nodes may be enlarged

Symptoms of impetigo :

pruritis is common
Minimal systemic signs sand symptoms of infection
Weakness, diarrhea and fever occasionally seen with BULLOUS form

Labs and other diagnostic tests for impetigo:

-cultures should be taken for more severe cases
-crusted tops of lesions should be raised to obtain purulent material at the base for culture
-open, draining pustules should NOT BE CULTURED-COULD BE MIXED WITH NORMAL SKIN FLORA
CBC often performed, leukoc

clinical presentation of folliculitis:

Clustering pruritic papule localized to hair follicles
generally develop in areas SUBJECT TO FRICTION AND PERSPIRATION
Papule are generally less than 5 mm and erythematous
papules evolve into pustules that generally spontaneously rupture in several days
S

Clinical presentation of furuncles:

inflammatory, draining nodule involving a hair follicle
Develop in areas subject to friction and perspiration
Lesions are discrete (singular or multiple nodules)
Lesions starts as a firm, tender, red nodule that becomes painful and fluctuant
SYSTEMIC SIGN

Clinical presentation of carbuncles:

Formed when adjacent furuncles coalesce to form a single inflamed area
Form broad , swollen, erythematous, deep and painful follicular masses
commonly develop on back of neck
COMMONLY ASSOCIATED WITH SYSTEMIC SIGNS (FEVER, CHILLS MALAISE)
Bacteremia with

Clinical presentation of erysipelas:

Lower extremities are most common sites
Symptoms:
-Flu-like symptoms (common in prior to appearance of lesion)
-Very painful/burning pain
Lesion is intensely erythematous and edematous, often with lymphatic streaking
LESION HAS RAISED BORDER, SHARPLY DEMA

Lab tests for erysipelas:

Causative organism can't be cultured from skin surface
Needle aspiration or punch biopsies occasionally identify organism
Cultures considered for more severe cases
C-reactive protein GENERALLY ELEVATED

Clinical presentation of cellulitis:

History of wound from minor trauma, abrasion, ulcer, etc.
Symptoms: Often fever, chills, or malaise....often hot and painful area
-Hypotension, dehydration and altered mental status common
Signs: Erythema and edema of skin
Lesion is painful, non elevated,

Clinical presentation of necrotizing fasciitis:

Frequently involve the abdomen, perineum and lower extremities
RAPID DIAGNOSIS CRITICAL DUE TO AGRESSIVE NATURE AND HIGH MORTALITY (20-50%)
MEDICAL EMERGENCY
Symptoms: systemic symptoms are generally marked
Includes shock and organ failure
More pronounced

Purulent:

Furuncle, carbuncle and abscess
Mild: no signs of systemic infection
Moderate: may have fever, otherwise stable
Severe: Failed incision and drainage plus oral antibiotics
or systemic signs of infection
->38 degrees celsius
-HR> 90 bpm
-RR >24 bpm
-WBC>120

Nonpurulent:

Erysipelas, cellulitis, necrotizing fasciitis
Mild- no signs of systemic infection
Moderate- may have fever, but not otherwise stable
Severe:
Failed oral antibiotic treatment
Systemic signs of infection
Immunocompromised
Clinical signs of deeper infection

Pneumonia classification
CAP-

Pneumonia developing outside the hospital or < 48 hours after hospital admission

HAP-

pneumonia developing >48 hours after hospital admission