Transcript Chapter 4 MICROBIAL DISEASES OF THE SKIN

CHAPTER 4
MICROBIAL DISEASES OF
THE SKIN
Miss Rashidah Hj Iberahim
Content
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Bacterial skin diseases*
Viral skin diseases
Fungal skin diseases
Wound infection – gas-gangrene*
Bacterial infections
Gram positive infections
Staphylococcus sp
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Folliculitis and other
skin lesions
Scalded skin
syndrome
Streptococcus sp
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Scarlet Fever
Erysipelas
Folliculitis(pimples / pustules)
Pathogenesis
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S. aureus colonize skin and
upper resp. tract of infants
within 24 hrs after birth
Invade thru hair follicleproducing folliculitis (form
of pimples and pustules)
Encapsulated of abcess- x
shedding n antibiotic reach
the area
Treatment-surgery
Transmission
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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
on base of eye lashes – sty
A larger and deeper form –
abscess
Exterior abscess – furuncle / boil
Massive lesion - curbuncle
Scalded Skin Syndrome
Pathogenesis
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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
Symptoms
1.
2.
3.
1st stage – redness of
surrounding area
2nd stage – 1-2 days
large, soft and easily
ruptured vesicles
around the body
3rd stage – the lesion
getting dry and scale
Peeling off skin
Scarlet Fever
Pathogenesis
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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
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The best medicine is
Penicillin – decrease
mortality rate
Erysipelas
Pathogenesis
 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)
Viral Diseases
Rubella
The disease
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Rashes appear on
trunk after 16-21
days after infection
Caused by togavirus
2ndary: arthritis and
arthralgia
Can caused congenital
rubella syndrome
Transmission
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Mainly through nasal
secresion
Direct contact among
children age 5 – 14
Infected infants
expose to hospital
personnel
Rubella
Diagnosis
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Immunity assessment
on pregnant woman
Rubella – specific IgM
antibody
Other variety serology
test
Prevention
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Currently using rubella
vaccine (MMR)
Measles/ Rubeola
Diagnosis and prevention
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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)
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Diagnose by its
symptoms
2nd accompanied by
bacterial infection
Using the same vaccine
as rubella and mumps
(MMR)
Chicken pox and Shingles
The disease
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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
Symptoms
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CP = Causing blood
clot and hemorrhage,
Cause death
S = pain, burning,
prickling of the skin
when it reactivate
Disease
progression
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Virus enter upper respiratory tract/
conjuctiva – replicates
Carried by blood to various tissues –
replicates
Release of viruses causes fever and malaise
After 14 – 16 days, present of small,
irregular, rose-coloured skin lesions
Fluid become cloudy, dry and crust over 2-4
days (virus cycle)
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
Transmission
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CP – Infect between 59 yrs old
V – age >45 yrs old
Spread by respiratory
secretion and fluid
from moist lesion (not
the dry lesion)
Diagnosis and treatment
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Using rapid
laboratory test
Treatment – antiviral
agent (valtrex and
neurontin)
Wound infection
Gas gangrene
Gas Gangrene
Pathogenesis
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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
Symptoms
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Foul odour
Ferment muscle
carbohydrates
“snap, crackle and pop”
High fever, shock,
massive tissue
destruction, blackening
of tissues
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
Face , back of hands
Plantar wart
sole
Genital wart
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Condylomata accuminata
Penile, vulvar skin, perianal
area
Sexual partner
Child---sexual abuse
Some: oncogenic:16, 18
2. Molluscum contagiosum
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Pox virus
Child
Face, neck
Central punctum
Hunderson-patterson bodies
Fungal
Superficial mycosis
Deep mycosis
Dermatophyte infection
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Skin
Hair
Nails
Tinea pedis
Adult (athlete’s)
Toe webs , instep
T.rubrum, T.mentagrophytes
Tinea ungum
T.rubrum, T.mentagrophytes
Tinea corporis:
Trunk
Active edge
T.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)