COMMON BACTERIAL&

VIRAL INFECTIONS OF SKIN

 DIRECT DIRECT
STAPHYLOCOCCAL STREPTOCOCCAL
Direct infection of skin and adjacent tissue

INFECTIONS INFECTIONS
 Impetigo  Impetigo
 Ecthyma  Ecthyma
 Cellulitis
 Cellulitis
 Erysipelas
 Folliculitis (superficial/deep)
 Vulvovaginitis
 Carbuncle  Perianal infections
 Sycosis  Streptococcal ulcers
 Blistering distal dactylitis
 Necrotising fascitis
 IMPETIGO

 Contagious superficial pyogenic infection of the skin

 Causative – Staph/ Streptococi
 Nonbullous – blister formation is slight and transient
 Complications – Infective / PSGN
/Urticaria/Scarlet fever
Impetigo

NON BULLOUS BULLOUS

 Thin walled transient  Less transient and larger
vesicle over an bullae
erythematous base  Clear latter turbid
 Yellowish brown crusts  Thin flat brownish crust
 Gradual peripheral irregular  Circinate lesions
extension without central
 Face > anywhere
healing
 Crust dry and separate
leaving erythema , fades
without scarring
A) Non bullous impetigo B) Bullous impetigo
 HPE - Epidermal split below stratum
granulosum
Large blisters, having Neutrophils ,
cocci
Upper dermal infiltrates of neutrophils
and
lymphocytes
 ECTHYMA
 Pyogenic infection of the skin characterized by the formation
of adherent crusts, beneath which ulceration occurs
 Bullae or pustules on erythematous base
 Hard adherant crust of dried exudates
 Peripheral accreation
 Healing with scarring
 Causative - Group A Streptococcus such as S. pyogenes,
Pseudomonas aeruginosa and Staphylococcus aureus.
 CELLULITIS AND
ERYSIPELAS
 Cellulitis - an acute, subacute or chronic
inflammation of loose connective tissue
 Erysipelas - bacterial infection of the dermis
and upper subcutaneous tissue; its hallmark is a
well‐defined raised edge reflecting the more
superficial (dermal) involvement.
Causative – Group A beta haemolytic
streptococci, group B ( Under 3 months and after
surgery ) and others H.Influenzae ,
Pseudomonas
CELLULITIS ERYSIPELAS
SUPERFICIAL FOLLICULITIS

 Subacute or chronic inflammatory changes

confined to the ostium /extend only slightly
below
 Heals without scar formation
 Predisposing factor – potent topical steroid
use
 Heals within 7-10 days
 Causative – Staph aureus > Pseudomonas
Acute folliculitis of face
 FURUNCLE
 An acute, usually necrotic,
infection of a hair follicle
with S. aureus
 Small, follicular,
inflammatory nodule
 Soon becoming pustular and
then necrosis
 Heal with violaceous
macule and a permanent
scar
 CARBUNCLE
 Deep infection of a group
of contiguous follicles
with S. aureus,
accompanied by intense
inflammatory changes in
the surrounding and
underlying connective
tissues
 Painful hard red lump
 Multiple follicular orifices
 Necrosis of intervening
skin leads to crateriform
nodules
 STAPHYLOCOCCAL SCALDED
SKIN SYNDROME

 Exfoliative dermatosis
 Exfoliative toxin of Staphylococcous phage
group 2
 Selectively cleaves desmoglein 1
 Starts as a localized staphylococcal infection
 Fever, irritability and skin tenderness.
 Erythematous eruption ….blister formation…
painful raw areas….heals within 7-14 days
SSSS
TOXIC SHOCK SYNDROME
 This is a serious life‐threatening illness characterized by
fever, acute erythema followed by desquamation, circulatory
shock and multisystem disease which is mediated by
bacterial toxins
 Toxic shock syndrome toxin 1 (staphylococcal enterotoxin F
) / pyrogenic exotoxin C
 More recently, staphylococcal enterotoxin B
 T‐lymphocyte proliferation- non‐antigen‐specific manner
 Acute onset fever and widespread macular erythema
 Vomiting, diarrhoea and multiple organ involvement and
Circulatory shock
 scarlatiniform and papulopustular eruptions are also
described
 Mucous membrane erythema – more in conjuctiva
 Blistering associated
with TSS

TREATMENT:

• Hemodynamic
resuscitation

• IV clindamycin and/or
benzyl penicillin
sodium or vancomycin

• Severe cases - IVIG

DISEASES CAUSED BY
CORYNEBACTERIUM
 PITTED KERATOLYSIS

 A superficial infection
of the skin producing
circular erosions on
the soles
 Invade keratin
softened by sweat
 Causative –
corynebacterium
species
 ERYTHRASMA
• Mild chronic localized
superficial infection of the
skin caused by a group of
closely related aerobic
coryneform bacteria,
usually known as C.
minutissimum.
• Predominantly flexural
area
• WOODS LAMP….. CORAL RED
PSEUDOMONAS
INFECTIONS
ECTHYMA GANGRENOSUM

 Bullae in moist areas such

as the axillae, perineum and
the buttocks.
 These may rapidly rupture
to give necrotic ulcers
PARONYCHIAL CHANGES

 Perionychial pustules
may be formed .
 The presence of
Pseudomonas spp.
(Pyocyanin/ pyoverdin )
beneath nails with
onycholysis gives rise to
characteristic green
discoloration .
PSEUDOMONAS INFECTION OF FOOT

 The sharply
demarcated areas
of maceration and
tender erosions
sometimes tinged
with green, and
showing green
fluorescence under
Wood’s light
 EXTERNAL OTITIS

 Common in swimmers
 Swelling, maceration, and
pain with pustular discharge

 Malignant external otitis,

occurs in elderly patients with
diabetes or in those
immunocompromised with
HIV infection, on
chemotherapy, or living with
organ transplants.
PSEUDOMONAS FOLLICULITIS

 Pruritic follicular
,maculopapular, vesicular, or
pustular lesions occurring
within
1–4 days after bathing in a hot
tub, whirlpool, or public
swimming pool
 complaints may include
earache, sore throat,
headache, fever, and malaise
 Hot tube folliculitis
VIRAL INFECTIONS OF
SKIN
 Herpes Simplex Virus
 2 types

 HSV-1

 HSV-2
 Herpes Simplex Virus-1

• Spread predominantly through infected

saliva or active perioral lesions

• Divides more efficiently in

Oral
Facial
Ocular area
• Pharynx
• intraoral sites Sites
• Lips involved
• most
Eyes
fr equ ent ly
• skin above waist
 Clinical Features

• initial exposure to a n individual

without antibodies to virus is called
p r i m a r y i nfect i on

• typically occurs a t a young age

• often asymptomatic
• does not cause significant
morbidity

• virus is taken up by sensory nerves

• transported to associated
sensory or less frequently
a u t o n o m i c g an gl i a

• virus remains in a latent state

• all primary infections occur
from contact with a n infected
person who is releasing the
virus

• usual incubation period is

3-9 days
 acquired from contact
with contaminated:

• saliva
• active perioral lesions
• crowding
• poor oral hygiene
 Acute Herpetic Gingivostomatitis
(primary herpes)

• most common pattern of

symptomatic primary HSV
infection

• arise between ages of 6

months and 5 years

• peak prevalence occurring between

2 and 3 years of age

• onset is abrupt
 accompanied by:

• anterior cervical
lym pha denopat h y
• chills
• fever (103 to 105 F)
• Nausea
• Anoxeria
• Irritability
• sore mouth lesions
• initially affected mucosa develops
numerous pinhead vesicles, which
rapidly collapse to form erosions and
ulcers.

• both movable + attached oral mucosa can

be affected

• in all cases, gingiva is:

• enlarged
• painful
• extremely erythematous
• mild cases usually resolve
within 5-7 days

• severe cases may extend

to 2 weeks
Herpes Simplex Virus-2

• adapted best to the genital zones

• predominantly through sexual

contact

• typically involves

• genitalia
• skin below waist
• antibodies to HSV-1 decrease the
chance of infection with HSV-2 or lessen
severity of clinical manifestation.

• dramatic increase seen in HSV-2 due

to:

• partly to lack of prior exposure

to HSV-1

• increased sexual activity

• lack of barrier conception

 Treatment & Prognosis

• if infection is diagnosed early,

antiviral medications can have
significant influence
 Varicella (Chickenpox)

 similar to herpes
simplex virus (HSV)

 chickenpox represents
primary infection with VZV

 latency ensues, and

recurrence is possible as
h e r p e s z ost e r often after
many yesterday
 Etiology

 presumed to be
spread through air
droplets

 direct contact with

active lesions

 arise between ages

of 5 and 9
 Clinical Features

 symptomatic phase usually

begins with:

• malaise
• pahryngitis
• rhinitis
 Clinical Features

 in older children +
adults, additional
symptoms:

• headache
• myalgia
• nausea
• anorexia
• vomiting
 Clinical Features

 r as h begins on face +
t r un k followed by
involvement of extremeties

 each lesion rapidly progresses

through stages of:
• erythema
• vesicle
• pustule
• hardened crust
 Clinical Features

 lesions typically continue

to erupt for 4 days

 some cases, exanthem’s

arrival may extend to 7
or more days

 affected individuals are

contagious from 2 days
before exanthem until all
lesions crust
 Clinical Features

 vermillion border of
lips + palate are
most common sites
of involvement

 followed by buccal
mucosa

 occasionally, gingival lesions

resemble those with
 Clinical Features

 lesions of varicella tend

to be painless

 lesions begin as 3-to-4-mm

white opaque vesicles

• rupture to form
1-to-3-mm ulcerations
 Clinical Features

 mild cases: often only

1 or 2 oral ulcers are evident

• these heal within

1-3 days

 severe cases:
almost
always have oral ulcerations
upto 30 lesions

• persist for 5-10 days

 Treatment & Prognosis

 warm bath with

soap or baking soda

 application of calamine
lotion

 systemic
diphenhydramine

• to relieve pruritus
  Treatment & Prognosis

antipyretics should be
given to reduce fever

use of peroral antiviral

medications such as:

• acyclovir been shown

• valacyclovir to reduce duration + severity
• famciclovir if administered within first 24
hrs of ra s h
 Herpes Zoster (Shingles)

 after initial infection with

chickenpox, virus is
tr a n sp o r t e d u p t h e sensory
nerves

 presumably
establishes latency
in dorsal spinal
ganglia

 occurs after reactivation

of virus, with
involvement
of t h e distribution of
 predisposing factors
for reactivation:

 immunosuppresion
 HIV-infection
 trea t me nt with cytoxic
or immunosuppresive
drugs
 radiation
 presence of malignancies
 old age
 alcohol abuse
 stress (emotional or
physical)
 Clinical Features

 can be grouped into

3 phases:

• (1) prodome
• (2) acute
• (3) chronic
 Clinical Features

 (1) Prodome

• during initial viral replication

active ganglionitis develops
with resultant

neuronal necrosis
severe neuralgia
 Clinical Features

 (1) Prodome

• inflammatory reaction
is responsible for padromal
symptoms of intense
pain t h a t precedes
ras h in more t h a n
90% of cases
 Clinical Features

 (1) Prodome

• as virus travels down

the nerve, pain
intensifies:

burning
tingling
itching
Boring
prickly or knifelike
 Clinical Features

 (1) Prodome

• pain develops in area of

epithelium innervated by
affected sensory nerve
(dermatome)
  Clinical Features

 (1) Prodome

• accompanied by:

fever normally present

malais 1-4 days before
e
 headache development of
cutaneous
or mucosal lesions
 Clinical Features

 (2) Acute

• begins as involved skin

develops clusters of vesicles
set on erythematous base

• within 3-4 days, vesicles

become pustular + ulcerate
with crusts developing
after 7-10 days
 Clinical Features

 (2) Acute

• oral lesions occur with

trigeminal nerve involvement

• may be present on
movable or bound mucosa
 Clinical Features

 (2) Acute

• lesions often extend to

midline

• frequently are present in

conjunction with involvement
of skin overlying affected
quadrant
 Clinical Features

 (2) Acute

• most cases, significant

bone necrosis with loss
of teeth in areas
involved with herpes
zoster
 Clinical Features

 (3) Chronic

• approximately 15% of affected

patients progress to chronic
phase of herpes zoster

characterized by pain
(postherpetic neuralgia)
persists longer t h a n 3
months
 Clinical Features

 (3) Chronic

• pain is
described as:

burning
throbbin
g
aching
itching
stabbing
 Treatment & Prognosis

 antipyretics

 antipruritics such as
diphenhydramine

• can be administered
to decrease itching
 Treatment & Prognosis

 skin lesions should be

kept dry + clean

• prevent secondary
infection

 antibiotics to tre at secondary

infections
Treatment & Prognosis

antiviral medications:

• acyclovir accelerate healing

• valacyclovir of cutaneous + mucosal
• famciclovir lesions;
reduce duration
of acute pain
effective if initiated within
72 hours after development
of 1 s t vesicle
MOLLUSCUM CONTAGIOSUM

 Caused by molluscipox virus

 Pearly white umbilicated papules.

 Incubation period – 14 days to 6 months

 TREATMENT:

 Caustic destruction
 Chemical or surgical
irritants
 Surgical removal
 Cidofovir, paclitaxel