Types of skin lesions
Macule Papules Plaques Nodules Urticaria (wheals or hives) Vesicles Bullae Pustules Purpura Petechiae Ecchymosis Ulcer Eschar
Macule
Flat lesions
change in color of affected skin
Papules
Raised lesion
solid
less than 5mm in diameter
Plaques
flat with elevated surface (plateau like)
more than 5 mm diameter
Nodules
rounded raised lesions
more than 5 mm in diameter
Urticaria (wheals or hives)
annular or ring like papules or plaques
with pinkish color
Vesicle
circumscribed fluid filled lesions
less than 5 mm in diameter
Bullae
circumscribed fluid filled lesions
more than 5 mm in diameter
Pustules
circumscribed
exudate filled lesions
Purpura
skin lesions due to bleeding into the skin
Petechiae
type of purpura
less than 3mm in diameter
Ecchymosis
type of purpura
more than 3mm in diameter
Ulcer
craterlike lesion that may involve the deeper layers of the epidermis and dermis
Eschar
necrotic ulcer covered with a blackened scab or crus
Bacterial SKIN infections
Staphylococcus aureus Staphylococcus epidermis Streptococcus pyogenes Pseudomonas aeruginosa Clostridium perfringens Bacillus anthracis
Staphylococcus aureus
common pathogen in humans
gram positive cocci
arranged individually, pairs, short chains, clusters
FOUND in the SKIN and NASOPHARYNX
produce gray or golden yellow colonies
coagulase positive
catalase positive
produces enzymes and toxins responsible for invasiveness and pathogenicity
most dangerous among all common staphylococcus
Mode of transmission of Staphylococcus aureus
Direct contact
person having purulent lesions
hands of healthcare of hospital workers
fomites
Clinical findings of Staphylococcus aureus
Folliculitis Furuncle Carbuncle Sty or Hordeolum Impetigo Staphylococcus scalded skin syndrome (Ritter's disease)
Folliculitis
pyogenic (pus producing)
involves the hair follicle
localized pain inflammation
heals rapidly after draining the pus
Furuncle (boil)
extension of folliculitis
larger and painful nodules
underlying collection of dead and necrotic tissue
Carbuncle
coalescence of furuncles
extends to subcutaneous tissue with multiple sinus tracts
Sty or Hordeolum
folliculitis occurring at the base of the eyelids
Impetigo
common in young children
INVOLVES the FACE and LIMBS
starts as flat red spot (macules) later becomes pus-filled vesicle = ruptures form crust
can be caused by S. AUREUS and S. PYOGENES
Stapylococcal scalded skin syndrome (Ritter's disease)
found in newborns and young children
sudden onset of perioral (surrounding the mouth) erythema, covers body in 2 days
slight pressure applied = skin displacements = postivie NIKOLSKY SIGN
bullae and cutaneous blister will follow later under go desquamation (peeling of the skin)
antibodies are produce after 7 to 10 days
only outer layer of epidermis is affected, no scarring.
Exfoliative toxin
toxin responsible for manifestation in staphylococcal scalded skin syndrome.
Laboratory Diagnosis of Staphylococcus Aureus
LABORATORY IDENTIFICATION
microscopic examination of gram stained specimen (gram - positive cocci)
culture (gray and golden yellow (20- 25 C)
Catalase POSITIVE Quality of Staphylococcus Aureus
Differentiate it from Streptococci
Coagulase POSITIVE Quality of Staphylococcus Aureus
Differentiate it from other forms of Staphylococcus
Treatment and Prevention
treatment of choice is BETA-LACTAM ANTIBIOTICS like PENICILLIN
S. Aureus develop resistance to penicillin and other penicillin derivatives (methicillin and nafcillin)
OXACILLIN only penicillin derived antibiotic ACTIVE against S. aureus
incision and drainage of skin is necessary
Staphylococcus Epidermidis
part of the normal flora of the skin
commonly associated with "stitch abscess", UTI, and endocarditis
causes infections in individual with PROTETICS
Streptococcus pyogenes
gram positive cocci
arrange in pairs or in chains
belongs to group A streptococci
beta hemolytic (cause rupture of blood)
produces enzymes and toxins to protect from phagocytosis
associated with sever systemic infection
Major virulence factor of Streptococcus pyogenes
M protein (anti-phagocytic)
Mode of transmission of Streptococcus pyogenes
Direct contact
infected person
fomites
Clinical Findings
Pyoderma (Impetigo)
Erysipelas (St. Anthony's Fire)
Cellulitis
Necrotizing Fasciitis (flesh eating or streptococcal gangrene)
Pyoderma (Impetigo)
purulent skin infection
localized common involves FACE, UPPER and LOWER EXTREMITIES
vesicle > pustules > rupture = honey-colored crust
may have enlargement of lymph node
NO SIGN F SYSTEMIC INFECTION
Erysipelas (St. Anthony's Fire)
follows respiratory tract or skin infection caused by s. pyogenes
DISTINCT FROM NORMAL SKIN
Manifestation of Erysipelas (St. Anthony's fire)
localized areas with pain
erythema
warmth
systemic manifestations -lymphadenopathy
Cellulitis
involves SKIN and SUBCUTANEOUS TISSUE
NORMAL SKIN NOT CLEARLY DIFFERENTIATED
Manifestation of cellulitis
local inflammation with systemic signs
Necrotizing Fasciitis (flesh eating or streptococcal gangrene)
involves DEEP SUBCUTANEOUS TISSUE
cellulitis > bullous and gangrenous > spread to fascia > muscle and fat
become systemic and cause multi-organ failure leading to death
Complications of Streptococcus Pyogenes
Acute glomerulonephritis
Rheumatic fever
Scarlet fever
non- supporative, immune mediated complications
Acute glomerulonephritis
commonly associated with skin infections
Rheumatic fever
associated with s. pyogenes throat infection
Scarlet fever
develops in some people who have strep throat.
manifested by STRAWBERRY TONGUE
bright red rash that covers most of the body, sore throat and fever
Laboratory diagnosis of Streptococcus Pyogenes
Microscopy
Culture
Bacitracin test
Microscopy of Streptococcus Pyogenes
infected tissue will show gram-positive cocci in pairs and chains associated with leukocytes
Culture of Streptococcus Pyogenes
positive beta hemolysis in blood agar
Bacitracin test of Streptococcus Pyogenes
antibiotic susceptibility test with (+) zone of inhibition of growth around the Bacitracin disc.
Treatment and Prevention of Streptococcus Pyogenes
DOC (drug of choice): PENICILLIN
Alternate drugs: macrolides (erythromycin, azithromycin) or cephalosporin
drainage of pus through debridement
Pseudomonas aeruginosa
gram negative bacilli
arranged in PAIRS ENCAPSULATED
opportunistic pathogen
common cause of NASOCOMICAL INFECTIOSN
capable of producing water soluble PIGMENTS (pyocyanin - blue)
resistant to most antibiotic
affects extensive skin burns
Virulence of Pseudomonas aeruginosa
ADHESINS (flagella, pili. LPS, alginate)
TOXINS (exotoxin A, pigments)
ENZYMES
Mode of transmission of Pseudomonas aeruginosa
colonization of previously injured skin
What does Pseudomonas aeruginosa cause to wearers of contact lenses
corneal keratitis
What does Pseudomonas aeruginosa cause to intravenous drug abusers
endocarditis and osteomyelitis
What does Pseudomonas aeruginosa cause to healthy individuals?
external otitis (swimmer's ear)
What does Pseudomonas aeruginosa cause to diabetics
severe external otitis
Clinical Findings of Pseudomonas aeruginosa
BLUE-GREEN pus that exudes a SWEET GRAPE-like odor
folliculitis and secondary infections in individuals with acne
nail infections from immersion in contaminated water
Osteochondritis
Osteochondritis in Pseudomonas aeruginosa
one of the clinical finding of Pseudomonas aeruginosa
most common cause of inflammation of the bone and a cartilage of the foot following a penetrating injury
Laboratory Diagnosis of Pseudomonas aeruginosa
GRAM STAINING: gram negative bacilli, individual or in pairs CULTURE: flat colonies with green pigmentation with sweet grape like odor OXIDASE TEST: Positive, aerobic and can use oxygen as a terminal electron acceptor in respiration.
Acronym AERUGINOSA
A: aerobic E: Exotoxin A R: Rod/ resistance U: UTI, burns, injuries G: green-blue dressing I: iron-containing lesions N: negative gram O: odor of grapes S: slime capsule sometimes A: Adherin pili
Treatment and prevention of Pseudomonas aeruginosa
resistant to most antibiotics, culture and sensitivity must be done
prevent contamination of sterile hospital equipment and instruments
prevent cross-contamination of patients by hospital personnel
Clostridium perfringens
gram positive bacilli
anaerobic
rarely produce endospores
widely distributed in nature
associated with soil and water contaminated feces
4 lethal toxins produced by Clostridium perfringens
ALPHA
BETA
IOTA
EPSILON
Most lethal toxin produced by Clostridium perfringens
ALPHA TOXIN
acts as LECITHINASE cause lysis of erythrocytes (RBC), platelets, and leukocytes (WBC)
cause massive hemolysis
bleeding and tissue destruction
Mode of transmission of Clostridium perfringens
the colonization of the skin following physical trauma or surgery
Clinical findings of Clostridium perfringens
cellulitis
suppurative myositis
myonecrosis or gas gangrene
Suppurative myositis in Clostridium perfringens
acute intramuscular infection that develops secondary to hematogenous microorganism spread into the body of skeletal muscle, manifested by abscess formation of large muscle groups
Myonecrosis or Gas gangrene
life threatening infection following physical trauma or surgery
characterized by massive tissue necrosis with gas formation, shock, renal failure, and death within two days of onset.
Laboratory diagnosis of Clostridium perfringens
MICROSCOPIC: gram-positive bacilli in pairs CULTURE: grow under anaerobic condition
Treatment and Prevention of Clostridium perfringens
Surgical wound debridement
high dose penicillin therapy
Bacillus Anthracis
gram positive bacilli
arrange individually or in pairs or long serpentine chains describe as "bamboo fishing rod" or "medusa's head"
aerobic, spore forming, encapsulated
can affect SKIN, LUNGS, GASTROINTESTINAL TRACTS
can be used in bioterrorism
produces ANTHRAX TOXIN resulting in an ulcer with a black eschar.
deadly disease to livestock and, occasionally, to humans.
only permanent (obligate) pathogen within the genus Bacillus.
Endospores survive in soil tests for up to 60 years
Virulence of Bacillus Anthracis
POLYPEPTIDE CAPSULE
responsible for evading phagocytosis EDEMA and LETHAL TOXINS
both inhibit the host's immune response
LETHAL TOXINS
targets and kills macrophages, which disables an essential defense of the host
EDEMA TOXIN of Bacillus Anthracis
local edema (swelling) and interferes with phagocytosis by macrophages
LETHAL TOXIN of Bacillus Anthracis
targets and kills macrophages, which disables an essential defense of the host
Mode of transmission of Bacillus Anthracis
inoculation into open skin from either soil or infected animal products
ingestion of infected meat or milk
inhalation of aerosolized spores
Clinical Findings of Bacillus Anthracis
disease of the herbivores (sheep and cattle)
people at risk are those who handle animals, hides wool
3 form of Anthrax Disease
Cutaneous anthrax Pulmonary anthrax Gastrointestinal anthrax
Cutaneous anthrax (skin infection)
most common form
painless papule at site of inoculation > ulcerative > develop necrotic eschar
associated with painful lymphadenopathy and edema.
Laboratory diagnosis of Bacillus Anthracis
GRAM STAINING: peripheral blood contains a large number of B. anthracis BLOOD TEST: detects inhalation and cutaneous cases of anthrax within an hour CULTURE: spores observe only in low carbon dioxide tension DEMONSTRATION of spores can be done through DORNER STAIN or WIRTZ CONKLIN STAIN
Treatment and prevention of Bacillus Anthracis
DOC: PENICILLIN and DOXYCYLINE
CIPROFLOXACIN recommended in RESISTANT CASES
prevention through VACCINATION ANIMALS (1 dose, live attenuated vaccine)
VACCINATION HUMANS: individual at risk such as animal handlers, military personnel, slaughter houses (1 dose, inactivated antigen)
3 doses over 4 weeks of vaccine to persons exposed to Bacillus Anthracis
Patient care of Bacillus anthrax
Standard Precautions
Add Contact Precautions for cutaneous anthrax patient if there is a large amount of uncontained drainage.
Use soap, water for handwashing; alcohol does not have sporicidal activity.
Fungal Skin infections
Superficial Mycoses Cutaneous Mycoses or Dermatophytosis Subcutaneous Mycoses
Superficial Mycoses
Tinea Versicolor (Pityriasis versicolor) Tinea Nigra
Tinea Versicolor (Pityriasis versicolor)
caused by Malassezia furfur (Pityrosporum orbiculare)
more common in tropical regions
appear in FACE, NECK TRUNK, ARMS
Malassezia furfur (Pityrosporum orbiculare)
causes Tinea versicolor
normal flora of the skin
found in areas rich in sebaceous glands
Lesions of Tinea versicolor (Pityriasis versicolor)
irregular
discrete hypo- or hyperpigmented macules
scaly with a dry, chalky appearance
Laboratory diagnosis of Tinea versicolor
Microscopic: visualization of "spaghetti and meatball" appearance of M. furfur with ALKALINE STAIN OF 10% KOH or NaOH DEMONSTRATED with Periodic AcidSchiff stain (PAS stain) or hematoxyllineosin stain (H & E stain)
Treatment of Tinea versicolor
application of KERATOLYTIC AGENTS containing SELENIUM DISULFIED or SALICYLIC ACID
topical ANTIFUNGAL drugs like KETOCONAZOLE
Tinea Nigra
caused by caused by Hortaea werneckii (formerly Exophiala werneckii)
appears in PALMS and SOLES
common in tropical and subtropical regions
seen in ADOLESCENTS, YOUNG ADULTS, FEMALES
Hortaea werneckii (formerly Exophiala werneckii)
causes tinea nigra
dematiaceous fungus
produces melanin and grows as mold producing ANNELIDS or ANNELLOCONIDIA
Lesions of Tinea Nigra
gray to black
well demarcated macules
Diagnosis of Tinea Nigra
MICROSCOPIC: skin scraping with potassium hydroxide CULTURE: Sabouraud's dextrose agar medium
Treatment of Tinea Nigra
similar to tinea versicolor
application of KERATOLYTIC AGENTS containing SELENIUM DISULFIED or SALICYLIC ACID
topical ANTIFUNGAL drugs like KETOCONAZOLE
Cutaneous Mycoses or Dermatophytosis
fungal infection involving keratinized body structures SKIN, HAIR, NAILS
caused by group of fungi called DERMATOPHYTES
Dermatophytes
produce keratinase
keratinophilic and keratinolytic
Keratinase
enzyme capable of breaking down keratin
3 genera that cause infection of Cutaneous mycoses or Dermatophytosis
Microsporum Trichophyton Epidermophyton
Microsporum
infect the HAIR and NAILS only
produces both MICROCONIDIA and MACROCONIDIA
predominant MACROCONIDIA
Trichophyton
infect SKIN, HAIR, NAILS
produces predominant MICROCONIDIA
Epidermophyton
infect the SKIN and NAILS only
produces SMOOTH-WALLED MACRONIDIA in bundles of 2 and 3