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Types of skin lesions

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Types of skin lesions

Macule Papules Plaques Nodules Urticaria (wheals or hives) Vesicles Bullae Pustules Purpura Petechiae Ecchymosis Ulcer Eschar

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Macule

  • Flat lesions

  • change in color of affected skin

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Papules

  • Raised lesion

  • solid

  • less than 5mm in diameter

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Plaques

  • flat with elevated surface (plateau like)

  • more than 5 mm diameter

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Nodules

  • rounded raised lesions

  • more than 5 mm in diameter

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Urticaria (wheals or hives)

  • annular or ring like papules or plaques

  • with pinkish color

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Vesicle

  • circumscribed fluid filled lesions

  • less than 5 mm in diameter

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Bullae

  • circumscribed fluid filled lesions

  • more than 5 mm in diameter

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Pustules

  • circumscribed

  • exudate filled lesions

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Purpura

skin lesions due to bleeding into the skin

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Petechiae

  • type of purpura

  • less than 3mm in diameter

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Ecchymosis

  • type of purpura

  • more than 3mm in diameter

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Ulcer

  • craterlike lesion that may involve the deeper layers of the epidermis and dermis

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Eschar

  • necrotic ulcer covered with a blackened scab or crus

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Bacterial SKIN infections

Staphylococcus aureus Staphylococcus epidermis Streptococcus pyogenes Pseudomonas aeruginosa Clostridium perfringens Bacillus anthracis

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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

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Mode of transmission of Staphylococcus aureus

  • Direct contact

  • person having purulent lesions

  • hands of healthcare of hospital workers

  • fomites

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Clinical findings of Staphylococcus aureus

Folliculitis Furuncle Carbuncle Sty or Hordeolum Impetigo Staphylococcus scalded skin syndrome (Ritter's disease)

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Folliculitis

pyogenic (pus producing)

  • involves the hair follicle

  • localized pain inflammation

  • heals rapidly after draining the pus

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Furuncle (boil)

  • extension of folliculitis

  • larger and painful nodules

  • underlying collection of dead and necrotic tissue

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Carbuncle

  • coalescence of furuncles

  • extends to subcutaneous tissue with multiple sinus tracts

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Sty or Hordeolum

  • folliculitis occurring at the base of the eyelids

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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

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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.

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Exfoliative toxin

  • toxin responsible for manifestation in staphylococcal scalded skin syndrome.

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Laboratory Diagnosis of Staphylococcus Aureus

LABORATORY IDENTIFICATION

  • microscopic examination of gram stained specimen (gram - positive cocci)

  • culture (gray and golden yellow (20- 25 C)

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Catalase POSITIVE Quality of Staphylococcus Aureus

Differentiate it from Streptococci

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Coagulase POSITIVE Quality of Staphylococcus Aureus

Differentiate it from other forms of Staphylococcus

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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

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Staphylococcus Epidermidis

  • part of the normal flora of the skin

  • commonly associated with "stitch abscess", UTI, and endocarditis

  • causes infections in individual with PROTETICS

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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

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Major virulence factor of Streptococcus pyogenes

M protein (anti-phagocytic)

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Mode of transmission of Streptococcus pyogenes

  • Direct contact

  • infected person

  • fomites

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Clinical Findings

  • Pyoderma (Impetigo)

  • Erysipelas (St. Anthony's Fire)

  • Cellulitis

  • Necrotizing Fasciitis (flesh eating or streptococcal gangrene)

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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

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Erysipelas (St. Anthony's Fire)

  • follows respiratory tract or skin infection caused by s. pyogenes

  • DISTINCT FROM NORMAL SKIN

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Manifestation of Erysipelas (St. Anthony's fire)

  • localized areas with pain

  • erythema

  • warmth

  • systemic manifestations -lymphadenopathy

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Cellulitis

  • involves SKIN and SUBCUTANEOUS TISSUE

  • NORMAL SKIN NOT CLEARLY DIFFERENTIATED

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Manifestation of cellulitis

  • local inflammation with systemic signs

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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

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Complications of Streptococcus Pyogenes

  • Acute glomerulonephritis

  • Rheumatic fever

  • Scarlet fever

  • non- supporative, immune mediated complications

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Acute glomerulonephritis

commonly associated with skin infections

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Rheumatic fever

associated with s. pyogenes throat infection

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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

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Laboratory diagnosis of Streptococcus Pyogenes

  • Microscopy

  • Culture

  • Bacitracin test

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Microscopy of Streptococcus Pyogenes

  • infected tissue will show gram-positive cocci in pairs and chains associated with leukocytes

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Culture of Streptococcus Pyogenes

  • positive beta hemolysis in blood agar

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Bacitracin test of Streptococcus Pyogenes

  • antibiotic susceptibility test with (+) zone of inhibition of growth around the Bacitracin disc.

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Treatment and Prevention of Streptococcus Pyogenes

  • DOC (drug of choice): PENICILLIN

  • Alternate drugs: macrolides (erythromycin, azithromycin) or cephalosporin

  • drainage of pus through debridement

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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

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Virulence of Pseudomonas aeruginosa

  • ADHESINS (flagella, pili. LPS, alginate)

  • TOXINS (exotoxin A, pigments)

  • ENZYMES

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Mode of transmission of Pseudomonas aeruginosa

colonization of previously injured skin

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What does Pseudomonas aeruginosa cause to wearers of contact lenses

corneal keratitis

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What does Pseudomonas aeruginosa cause to intravenous drug abusers

endocarditis and osteomyelitis

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What does Pseudomonas aeruginosa cause to healthy individuals?

external otitis (swimmer's ear)

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What does Pseudomonas aeruginosa cause to diabetics

severe external otitis

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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

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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

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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.

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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

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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

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Clostridium perfringens

  • gram positive bacilli

  • anaerobic

  • rarely produce endospores

  • widely distributed in nature

  • associated with soil and water contaminated feces

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4 lethal toxins produced by Clostridium perfringens

  • ALPHA

  • BETA

  • IOTA

  • EPSILON

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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

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Mode of transmission of Clostridium perfringens

  • the colonization of the skin following physical trauma or surgery

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Clinical findings of Clostridium perfringens

  • cellulitis

  • suppurative myositis

  • myonecrosis or gas gangrene

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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

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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.

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Laboratory diagnosis of Clostridium perfringens

MICROSCOPIC: gram-positive bacilli in pairs CULTURE: grow under anaerobic condition

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Treatment and Prevention of Clostridium perfringens

  • Surgical wound debridement

  • high dose penicillin therapy

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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

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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

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EDEMA TOXIN of Bacillus Anthracis

local edema (swelling) and interferes with phagocytosis by macrophages

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LETHAL TOXIN of Bacillus Anthracis

targets and kills macrophages, which disables an essential defense of the host

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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

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Clinical Findings of Bacillus Anthracis

  • disease of the herbivores (sheep and cattle)

  • people at risk are those who handle animals, hides wool

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3 form of Anthrax Disease

Cutaneous anthrax Pulmonary anthrax Gastrointestinal anthrax

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Cutaneous anthrax (skin infection)

  • most common form

  • painless papule at site of inoculation > ulcerative > develop necrotic eschar

  • associated with painful lymphadenopathy and edema.

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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

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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

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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.

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Fungal Skin infections

Superficial Mycoses Cutaneous Mycoses or Dermatophytosis Subcutaneous Mycoses

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Superficial Mycoses

Tinea Versicolor (Pityriasis versicolor) Tinea Nigra

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Tinea Versicolor (Pityriasis versicolor)

  • caused by Malassezia furfur (Pityrosporum orbiculare)

  • more common in tropical regions

  • appear in FACE, NECK TRUNK, ARMS

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Malassezia furfur (Pityrosporum orbiculare)

  • causes Tinea versicolor

  • normal flora of the skin

  • found in areas rich in sebaceous glands

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Lesions of Tinea versicolor (Pityriasis versicolor)

  • irregular

  • discrete hypo- or hyperpigmented macules

  • scaly with a dry, chalky appearance

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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)

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Treatment of Tinea versicolor

  • application of KERATOLYTIC AGENTS containing SELENIUM DISULFIED or SALICYLIC ACID

  • topical ANTIFUNGAL drugs like KETOCONAZOLE

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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

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Hortaea werneckii (formerly Exophiala werneckii)

  • causes tinea nigra

  • dematiaceous fungus

  • produces melanin and grows as mold producing ANNELIDS or ANNELLOCONIDIA

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Lesions of Tinea Nigra

  • gray to black

  • well demarcated macules

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Diagnosis of Tinea Nigra

MICROSCOPIC: skin scraping with potassium hydroxide CULTURE: Sabouraud's dextrose agar medium

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Treatment of Tinea Nigra

  • similar to tinea versicolor

  • application of KERATOLYTIC AGENTS containing SELENIUM DISULFIED or SALICYLIC ACID

  • topical ANTIFUNGAL drugs like KETOCONAZOLE

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Cutaneous Mycoses or Dermatophytosis

  • fungal infection involving keratinized body structures SKIN, HAIR, NAILS

  • caused by group of fungi called DERMATOPHYTES

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Dermatophytes

  • produce keratinase

  • keratinophilic and keratinolytic

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Keratinase

  • enzyme capable of breaking down keratin

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3 genera that cause infection of Cutaneous mycoses or Dermatophytosis

Microsporum Trichophyton Epidermophyton

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Microsporum

  • infect the HAIR and NAILS only

  • produces both MICROCONIDIA and MACROCONIDIA

  • predominant MACROCONIDIA

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Trichophyton

  • infect SKIN, HAIR, NAILS

  • produces predominant MICROCONIDIA

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Epidermophyton

  • infect the SKIN and NAILS only

  • produces SMOOTH-WALLED MACRONIDIA in bundles of 2 and 3

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