chapter 4 microbial diseases of the skin

CHAPTER 4MICROBIAL DISEASES OF THE SKIN

Miss Rashidah Hj Iberahim

Content

Bacterial skin diseases* Viral skin diseases Fungal skin diseases Wound infection – gas-gangrene*

Bacterial infections

Gram positive infections

Folliculitis and other skin lesions

Scalded skin syndrome

Scarlet Fever Erysipelas

Staphylococcus sp Streptococcus sp

Folliculitis(pimples / pustules)

• S. aureus colonize skin and upper resp. tract of infants within 24 hrs after birth

• Invade thru hair follicle- producing folliculitis (form of pimples and pustules)

• Encapsulated of abcess- x shedding n antibiotic reach the area

• Treatment-surgery

Spread thru hosp personnel, asympt carrier n hosp visitors/catheters and splinters for older patient /nasal droplets and fomites

100 m/org were enough to cause infection in suture

Pathogenesis Transmission

on base of eye lashes – sty

A larger and deeper form – abscess

Exterior abscess – furuncle / boil

Massive lesion - curbuncle

Scalded Skin Syndrome

By certain exotoxin-producing strain of S.aureus (2 types exfoliatins)

Common in infant; adult (toxic shock syndrome)

Exotoxin move thru veins to the skin causing outer layer peeling off in leaflike sheets

Can lead to septicemia and very antigenic

Can cause reinfection – antibiotic very important

1. 1st stage – redness of surrounding area

2. 2nd stage – 1-2 days large, soft and easily ruptured vesicles around the body

3. 3rd stage – the lesion getting dry and scale

Pathogenesis Symptoms

Peeling off skin

Scarlet Fever

Pathogenesis

Also known as scarlatina By Streptococcus pyogenes Contain 3 types of erythrogenic toxin –

reddening The strain was 1st infected by temperate

phage – erythrogenic toxin that leads to rash Only infecting new exposure pt low- virulent strain – glomerulonephritis /

rheumatic fever Reinfection that already defends by previous

antibiotic – leads to strep throat (but carrier of scarlet fever)

Might also caused by fomites

Rash

The best medicine is Penicillin – decrease mortality rate

Erysipelas

Face- small, bright, raised, rubbery lesion.

Beta hemolytic gp A Strept. Always occur after pt

having surgery or wounds Producing hyaluronidase

enzyme and toxin Minor abrasion— sup. Lymph vessels

(causing septicemia, abscess,pneumonia, endocarditis, arthritis, death)

Pathogenesis

Viral Diseases

Rubella

Rashes appear on trunk after 16-21 days after infection

Caused by togavirus 2ndary: arthritis and

arthralgia Can caused

congenital rubella syndrome

Mainly through nasal secresion

Direct contact among children age 5 – 14

Infected infants expose to hospital personnel

The disease Transmission

Rubella

Immunity assessment on pregnant woman

Rubella – specific IgM antibody

Other variety serology test

Currently using rubella vaccine (MMR)

Diagnosis Prevention

Measles/ Rubeola

Caused by Rubeola virus Koplik’s spots – bluish

specks in upper lips and cheek mucosa

Rubella – pink n flat rash Rubeola – red and raised Other complications : Measles encephalitis Subacute sclerosing

panencephalitis (SSPE)

Diagnose by its symptoms

2nd accompanied by bacterial infection

Using the same vaccine as rubella and mumps (MMR)

Diagnosis and prevention

Chicken pox and Shingles

1 virus – 2 diseases CP – varicella, S –

zoster (varicella-zoster virus)

2nd inf by S. aureus In children Damages in blood and

lymphatic drainage During latent period,

stay in ganglia of nerve cells

CP = Causing blood clot and hemorrhage, Cause death

S = pain, burning, prickling of the skin when it reactivate

The disease Symptoms

Disease progression

1. Virus enter upper respiratory tract/ conjuctiva – replicates

2. Carried by blood to various tissues – replicates

3. Release of viruses causes fever and malaise

4. After 14 – 16 days, present of small, irregular, rose-coloured skin lesions

5. Fluid become cloudy, dry and crust over 2-4 days (virus cycle)

6. Rashes start from scalp and trunk, face and limbs, to mouth/throat/ vagina, and may spread to resp tract and GIT

Chicken pox and shingles

CP – Infect between 5-9 yrs old

V – age >45 yrs old

Spread by respiratory secretion and fluid from moist lesion (not the dry lesion)

Using rapid laboratory test

Treatment – antiviral agent (valtrex and neurontin)

Transmission Diagnosis and treatment

Gas gangrene

Wound infection

Gas Gangrene

Caused by more than 1 bacteria = Clostridium sp.

Spores of the bacteria expose during injuries and surgery

The symptoms getting severe because of toxin and enzyme production

Suddent onset = 12-48 hrs after exposure

Foul odour Ferment muscle

carbohydrates “snap, crackle and

pop” High fever, shock,

massive tissue destruction, blackening of tissues

Pathogenesis Symptoms

Photograph before right leg amputation (hemipelvectomy) of a patient with gas gangrene. The right thigh is swollen, edematous and discoloured with necrotic bullae(large blisters). An impressive crepitation is already palpable. At this juncture, the patient is in shock.

Others diseases

1. Wart

Caused by Human Pappiloma Virus (DNA)

Plane wart Plantar wart Face , back of hands sole

Genital wart

Condylomata accuminata

Penile, vulvar skin, perianal area

Sexual partner Child---sexual abuse Some: oncogenic:16, 18

2. Molluscum contagiosum Pox virus Child Face, neck Central punctum Hunderson-patterson bodies

Superficial mycosisDeep mycosis

Fungal

Dermatophyte infection

Skin Hair Nails

Tinea pedisAdult (athlete’s)Toe webs , instepT.rubrum, T.mentagrophytes

Tinea ungum

T.rubrum, T.mentagrophytes

Tinea corporis:

TrunkActive edgeT.rubrum

T.cruris

T.manun

Tinea capitis

Well circumscriped pruritic scaling area of hair loss

Black dot (T.tonsurans) Gray patch (M.audouinii), Kerion (T.verrucosum) Favus (T.schoenleinii)