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PRESENTEDPRESENTED
BYBY
DR. HUSSEIN ABOUL FOTOUHDR. HUSSEIN ABOUL FOTOUH
MB.Bch.MS.Sc. DERMATOLOGY& ANDROLOGYMB.Bch.MS.Sc. DERMATOLOGY& ANDROLOGY
CAIRO UNIVERSITYCAIRO UNIVERSITY
PH. D. ALAZHAR UNIVERSITYPH. D. ALAZHAR UNIVERSITY..
COMMON SKINCOMMON SKIN
INFECTIONSINFECTIONS
By Dr. Hussein AboulBy Dr. Hussein Aboul
FotouhFotouh
DermatologistDermatologist
M.G.HM.G.H
• *the skin is the first line of defense of the*the skin is the first line of defense of the
human body against micro organismshuman body against micro organisms
(Bacteria, Fungi, viruses & others)(Bacteria, Fungi, viruses & others)
• *It is well adapted to a wide range of*It is well adapted to a wide range of
environmental changes (mechanical &environmental changes (mechanical &
thermal injury) throughout its anatomical,thermal injury) throughout its anatomical,
physiological & immunological make up.physiological & immunological make up.
11..BACTERIA INFCETIONSBACTERIA INFCETIONS
• 1. Primary infections ( pyoderma) e.g.1. Primary infections ( pyoderma) e.g.
Impetigo, erysiplase; single organism.Impetigo, erysiplase; single organism.
• 2. Secondary infection in damaged skin2. Secondary infection in damaged skin
(mixture of organisms)(mixture of organisms)
• 3. Cutaneous involvement in systemic3. Cutaneous involvement in systemic
bacterial disease e.g. bacteraemia & E.Nbacterial disease e.g. bacteraemia & E.N
THE COMMON pyogenic SKINTHE COMMON pyogenic SKIN
INFECTIONSINFECTIONS
are:(Gram +veare:(Gram +ve((
• StreptococciStreptococci StaphylococciStaphylococci
• 1. Impetigo & Ecthyma 1. Impetigo(10% of cases1. Impetigo & Ecthyma 1. Impetigo(10% of cases
• 2. Erysiplase 2. Bullous Impetigo2. Erysiplase 2. Bullous Impetigo
• 3. Cellulites 3.3. Cellulites 3. superficial & deep Follicullitissuperficial & deep Follicullitis
• 4. Lymphangitis 4. Sweat gland abscess4. Lymphangitis 4. Sweat gland abscess
Primary, Secondary And systemicPrimary, Secondary And systemic
PrimaryPrimary
1. Complicating scabies 1. Complicating1. Complicating scabies 1. Complicating
Ulcers 'Bullous eruptionUlcers 'Bullous eruption
Eczema, insect biteEczema, insect bite
2- Intertrigo 2. intertrigo2- Intertrigo 2. intertrigo
3- Necrotizing cellulites3- Necrotizing cellulites
3. Infectious gangrene 4. decubitus & phagedenic ulcer3. Infectious gangrene 4. decubitus & phagedenic ulcer
SecondarySecondary
11..Scarlet fever 1. Staph Bacteraemia &Scarlet fever 1. Staph Bacteraemia &
EndocarditisEndocarditis
2. S B E 2. S S S S2. S B E 2. S S S S
3. E.N 3. Bullous Impetigo3. E.N 3. Bullous Impetigo
4. E. Marginatum4. E. Marginatum
5. E. M. like lesion5. E. M. like lesion
SystemicSystemic
**Generally speaking : StaphylococciGenerally speaking : Staphylococci
commonly attack skin appendages ( haircommonly attack skin appendages ( hair
follicle, sweat glands, periungual tissuefollicle, sweat glands, periungual tissue
while streptococci attack the skin properwhile streptococci attack the skin proper..
*The follicular occlusion triad*The follicular occlusion triad
-Hydradenitis suppurativa-Hydradenitis suppurativa
-acute conglobata-acute conglobata
-Perifolliculitis capitis abscedens et-Perifolliculitis capitis abscedens et
suffodens (dissecting cellulites of the scalp.suffodens (dissecting cellulites of the scalp.
Some common G -ve)Some common G -ve)
-Erythraosma corynebacterium-Erythraosma corynebacterium
minutissimumminutissimum
-Actinomycosis --Actinomycosis -israelliiisraellii
bovisbovis
2-Fungal Infections2-Fungal Infections
• Superficial DeepSuperficial Deep
• Dermatophytosis SporotrichosisDermatophytosis Sporotrichosis
• Pityriasis versicolor MycetomaPityriasis versicolor Mycetoma
• Candidiasis paracoccidiosisCandidiasis paracoccidiosis
• T.nigra chromomycosisT.nigra chromomycosis
• Piedra blastomycosisPiedra blastomycosis
• Moulds coccidiomycosisMoulds coccidiomycosis
• cryptococosiscryptococosis
• nocardiosisnocardiosis
33..VIRAL INFECTIONSVIRAL INFECTIONS
• -Viruses are obligatory intracellular parasites-Viruses are obligatory intracellular parasites
• -They are not cell as they lack organells, hence-They are not cell as they lack organells, hence
no metabolism of their own. They must use theno metabolism of their own. They must use the
host cell for their replication ----host cell for their replication ----disturbing thedisturbing the
metabolism of the host cell, so acting as themetabolism of the host cell, so acting as the
pathogen.pathogen.
• -Structure: outside the cell they are called virion-Structure: outside the cell they are called virion
which is composed of:which is composed of:
• 1. Central core of DNA or RNA = viral genome1. Central core of DNA or RNA = viral genome
• 2. Capsid surrounds the nucleoprotein2. Capsid surrounds the nucleoprotein
The subunit of the capsid = capsomer =The subunit of the capsid = capsomer =
mainantegenic component of the viruses.mainantegenic component of the viruses.
VIRAL INFECTIONS OF THE SKIN MAYVIRAL INFECTIONS OF THE SKIN MAY
OCCUR IN 3 DIFFERENT WAYS:OCCUR IN 3 DIFFERENT WAYS:
1. Direct inoculation : e.g. Molluscum, orf---1. Direct inoculation : e.g. Molluscum, orf---
replicate directly in the epidermisreplicate directly in the epidermis
2. systemic infections; the skin lesion2. systemic infections; the skin lesion
produced by systemic viral infection areproduced by systemic viral infection are
called exanthemata & occur duringcalled exanthemata & occur during
viraemiaviraemia
EXANTHEMTAEXANTHEMTA
• -Macular : Rubelle & I.M.-Macular : Rubelle & I.M.
• -Maculopapular: measles-Maculopapular: measles
• -Maculopapular-vesicular: echo & coxsackie-Maculopapular-vesicular: echo & coxsackie
• -maculopapular-petecheal: togo virus-maculopapular-petecheal: togo virus
• -Urticaria : Hepatitis B-Urticaria : Hepatitis B
• -Vesicular : chicken pox-Vesicular : chicken pox
• -Vesiculopustular: H.S & H. Z-Vesiculopustular: H.S & H. Z
33..Local spread from an internal focus: recurrent H.S & H.ZLocal spread from an internal focus: recurrent H.S & H.Z
CUTANEUS VIRALCUTANEUS VIRAL
INFECTIONSINFECTIONS
1.Herpes Virus grp. 2.Pox Virus grp. 3.Papovirus grp. 4.Picorna virus grp.
D N A RNA
Intranuclear Intracytoplasmic Intranucelear
1.Herpes Simplex V 1.Small pox 1Verruca 1.Hand, foot,mouth
2.Varicella/zoster 2.Monkey pox 2.Focai epithelial 2.Foot & mouth
3.Cytomegalovirus 3.Molluscum contagiosum 3.Hepatitis A
4.E.B. Virus 4.Orf
5.Human Herpes V. 5.Milker's nodule
(HHV6)
hyperplasiahyperplasia
HERPES SIMPLEXHERPES SIMPLEX
• There are 2 types of H.S.V which show noThere are 2 types of H.S.V which show no
cross immunitycross immunity
• *H.S.V.(1) attack the skin & oral mucosa*H.S.V.(1) attack the skin & oral mucosa
• (most of infections above the waist)(most of infections above the waist)
• *H.S.V.(2) attack the genital area*H.S.V.(2) attack the genital area
• (most of infections below the waist)(most of infections below the waist)
However HSv1 may be found in genital lesionsHowever HSv1 may be found in genital lesions
due to orogenital sexdue to orogenital sex
**Pathogenesis: (1) infection: occurs in individuals**Pathogenesis: (1) infection: occurs in individuals
who are infected Primary for the first time & havewho are infected Primary for the first time & have
no specific neutralizing antibodies it isno specific neutralizing antibodies it is
Either subclinical 90%Either subclinical 90%
Clinical 10%Clinical 10%
After primary infection the virus is not eliminatedAfter primary infection the virus is not eliminated
from the body but stays dormant in one of thefrom the body but stays dormant in one of the
sensory gangliasensory ganglia
(2)recurrent H.S.: occurs in(2)recurrent H.S.: occurs in
individuals previously infected with H.S.V. &individuals previously infected with H.S.V. &
possesses specific neutralizing antibodies.possesses specific neutralizing antibodies.
reactivation of the dormant virus is triggered byreactivation of the dormant virus is triggered by
fever, trauma, menstruation….fever, trauma, menstruation….
******Clinical Features: PRIMARY HERPESClinical Features: PRIMARY HERPES
SIMPLEXSIMPLEX
-It affects children (2-5y.o) with fever &-It affects children (2-5y.o) with fever &
malaisemalaise
-Large vesicle which show no tendency to-Large vesicle which show no tendency to
groupinggrouping
-Regional L.N.: enlarged & tender-Regional L.N.: enlarged & tender
-Vesicle--Vesicle-rupture-rupture-erosionserosions
-Spontaneous resolution after 1-2 wks-Spontaneous resolution after 1-2 wks
-No scarring except in case of secondary-No scarring except in case of secondary
infectioninfection
CLINICAL TYPESCLINICAL TYPES
• 1. Gingivostomatitis: the most common Primary1. Gingivostomatitis: the most common Primary
infectioninfection
• 2. Keratoconjunctivitis: recurrent dendritic ulcer2. Keratoconjunctivitis: recurrent dendritic ulcer
• 3. Herpes progenitalis: it is usually due to3. Herpes progenitalis: it is usually due to
H.S.V.2 but rarely H.S.V.1 (after orogenital sex)H.S.V.2 but rarely H.S.V.1 (after orogenital sex)
= 20% in adults after sexual intercourse= 20% in adults after sexual intercourse
• -I.P 2-7 usually 5 days-I.P 2-7 usually 5 days
• -Site: glans & shaft of penis in male; vulva,-Site: glans & shaft of penis in male; vulva,
vagina, cervix in femalevagina, cervix in female
• -vesicles on erythematous base--vesicles on erythematous base-rupture-rupture-
painful erosions last-painful erosions last-2-6wks2-6wks
• -Fever & malaise-Fever & malaise
• -Enlarged regional L.N.-Enlarged regional L.N.
44..Kaposi's Varicelliform eruption= H.S.V. infectionKaposi's Varicelliform eruption= H.S.V. infection
in atopic individualsin atopic individuals
5. Herpetic whitlow= inoculation HS5. Herpetic whitlow= inoculation HS
Painfull deep seated vesicles limited toPainfull deep seated vesicles limited to
paronychial or volar aspects of distal phalanx ofparonychial or volar aspects of distal phalanx of
the finger, more in medical paersons by type (1) &the finger, more in medical paersons by type (1) &
(2)(2)
6. Herpatic Folliculitis: of beard region in male6. Herpatic Folliculitis: of beard region in male
7. H.S pneumonia-7. H.S pneumonia- from aspirated HS offrom aspirated HS of
mouth----mouth----FatalFatal
8. H.S encephalitis--8. H.S encephalitis-- very high mortalityvery high mortality
9. Neo-natal (congenital) H.S:9. Neo-natal (congenital) H.S:
The potential of congenital H.S is considerableThe potential of congenital H.S is considerable
since 1% of pts in pregnancy clinics have HSv2since 1% of pts in pregnancy clinics have HSv2
infection by culture from vagina & 1/2 of theseinfection by culture from vagina & 1/2 of these
have lesionshave lesions..
VARICELLA & ZOSTERVARICELLA & ZOSTER
•******Varicella (chicken pox) & H.Z (Shingles) areVaricella (chicken pox) & H.Z (Shingles) are
caused by the same virus. Varicella zoster viruscaused by the same virus. Varicella zoster virus
= DNA intranuclear= DNA intranuclear..
•--Primary infection occurs in patients withoutPrimary infection occurs in patients without
resistance to this virus---resistance to this virus---chicken poxchicken pox
•--after subsidence of the primary attack, the virusafter subsidence of the primary attack, the virus
remains dormant in one of the sensory gangliaremains dormant in one of the sensory ganglia
(latency period(latency period((
•--Reactivation of the latent virus--Reactivation of the latent virus--sread of thesread of the
virus to tha skin supplied by the affected root -virus to tha skin supplied by the affected root -
H.zosterH.zoster
VARICELLA = CHICKEN POXVARICELLA = CHICKEN POX
• I.P: 2-3 WKS, 90 % children. Skin &I.P: 2-3 WKS, 90 % children. Skin &
affection. Epidemic, transmitted by dropletaffection. Epidemic, transmitted by droplet
infection-infection-viraemia -viraemia -skin exanthema [mildskin exanthema [mild
prodroma, fever 1-2 daysprodroma, fever 1-2 days
• --macule-macule-papulepapulevesicle (clear dropvesicle (clear drop
like)like)pustulepustuledry scabdry scabnoscar except ifnoscar except if
secondary infection supervene.secondary infection supervene.
• -New lesions continue to develop-New lesions continue to develop
(Pleomorphism) in contrast to variola.(Pleomorphism) in contrast to variola.
• - Haemorrhagic varicella ( high fever + Hgic- Haemorrhagic varicella ( high fever + Hgic
vesicle)vesicle)
COMPLICATIONSCOMPLICATIONS::
•11..Pneumonia (14% adultsPneumonia (14% adults((
•22..Reye's syndrome: fatal encephalopathyReye's syndrome: fatal encephalopathy
associated with varicellaassociated with varicella
•33..Neonatal varicella: fatal if mother hasNeonatal varicella: fatal if mother has
contracted the infection 5 days before deliverycontracted the infection 5 days before delivery
•44..Secondary infectionSecondary infection
•55..Cutaneous gangreneCutaneous gangrene  dermatitisdermatitis
gangrenasegangrenase
•66..Thrombocytopenic purpuraThrombocytopenic purpura
•77..Viral arthritisViral arthritis
H.ZOSTER ( SHINGLESH.ZOSTER ( SHINGLES((
• *In adults: attack maybe PPT by debilitating*In adults: attack maybe PPT by debilitating
conditions. think of HIV , if recurrent in youngconditions. think of HIV , if recurrent in young
adults.adults.
• *Pain 2-3 days grouped vesicles on an*Pain 2-3 days grouped vesicles on an
erythematous base along the course of alongerythematous base along the course of along
sensory nerve & strictly unilateral ( never crosssensory nerve & strictly unilateral ( never cross
the midline)the midline)
• *Thoracic H.Z 53% > cervical 20 % > Trigeminal*Thoracic H.Z 53% > cervical 20 % > Trigeminal
• *Regional L.N. are enlarged & tender*Regional L.N. are enlarged & tender
• *Healing within 2-3 weeks*Healing within 2-3 weeks
• *lesions may be Hgic or necrotic or ulcerated*lesions may be Hgic or necrotic or ulcerated
• *Disseminated H.Z may be fatal: occurs in*Disseminated H.Z may be fatal: occurs in
immunocompromised pts.immunocompromised pts.
COMPLICATIONCOMPLICATION
• 1. Post herpetic neuralgia1. Post herpetic neuralgia
• 2. Secondary infection2. Secondary infection
• 3. Gangrene3. Gangrene
• 4. H.Z ophthalmicus (Gasserian ganglion)4. H.Z ophthalmicus (Gasserian ganglion)
• 5. Ramsey – Hunt Ssyndrome5. Ramsey – Hunt Ssyndrome
• Ear: pain-tinitus-deafnessEar: pain-tinitus-deafness
• Tongue: out 2/3: loss of taste sensationTongue: out 2/3: loss of taste sensation
• Face: facial palsy : maybe permanentFace: facial palsy : maybe permanent
VERRUCAE (WARTSVERRUCAE (WARTS((
• -HPV : papovirus DNA intranuclear 55 types-HPV : papovirus DNA intranuclear 55 types
• Incubation period weeks up to a yearIncubation period weeks up to a year
• -All types have tropism to squamous epithelial cells.-All types have tropism to squamous epithelial cells.
• -Mode of transmission: by direct & indirect routes of non-Mode of transmission: by direct & indirect routes of non
intact skinintact skin
• 1.) plantar w: swimming pools or shower rooms floor1.) plantar w: swimming pools or shower rooms floor
• 2.) Common hands warts2.) Common hands warts
• 3.) Shaving -3.) Shaving - beard areabeard area
• 4.) Occupational: handlers of meat & fish4.) Occupational: handlers of meat & fish
• 5.) Genital: sexual or non-sexual5.) Genital: sexual or non-sexual
• 6.) Iatrogenic: HPV detected in vaginal specula, liquid6.) Iatrogenic: HPV detected in vaginal specula, liquid
nitrogen, cotton swabsnitrogen, cotton swabs
• 7.) Anogenital in children: sexual abuse-mother's genital7.) Anogenital in children: sexual abuse-mother's genital
tract – or non sexualtract – or non sexual
CLINICAL CLASSIFICATIONCLINICAL CLASSIFICATION
• 1. Verruca vulgaris = common warts1. Verruca vulgaris = common warts
including filariform wartsincluding filariform warts
• 2. Deep hyperkeratotic palmoplantar warts2. Deep hyperkeratotic palmoplantar warts
• 3. Superficial – mosaic type3. Superficial – mosaic type
• 4. Verruca plana (plane warts)4. Verruca plana (plane warts)
• 5. Candyloma acuminata5. Candyloma acuminata
• 6. Epidermo dysplasia verruciformis of6. Epidermo dysplasia verruciformis of
Lutz (1922) inherited disorder (A.R): wideLutz (1922) inherited disorder (A.R): wide
spread & persistent infection with HPVspread & persistent infection with HPV
44--OthersOthers
• Others like parasitic infestationOthers like parasitic infestation
(scabies – Pediculosis corporis and pubis )(scabies – Pediculosis corporis and pubis )
Common skin infections
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Common skin infections

  • 1. PRESENTEDPRESENTED BYBY DR. HUSSEIN ABOUL FOTOUHDR. HUSSEIN ABOUL FOTOUH MB.Bch.MS.Sc. DERMATOLOGY& ANDROLOGYMB.Bch.MS.Sc. DERMATOLOGY& ANDROLOGY CAIRO UNIVERSITYCAIRO UNIVERSITY PH. D. ALAZHAR UNIVERSITYPH. D. ALAZHAR UNIVERSITY..
  • 2. COMMON SKINCOMMON SKIN INFECTIONSINFECTIONS By Dr. Hussein AboulBy Dr. Hussein Aboul FotouhFotouh DermatologistDermatologist M.G.HM.G.H
  • 3. • *the skin is the first line of defense of the*the skin is the first line of defense of the human body against micro organismshuman body against micro organisms (Bacteria, Fungi, viruses & others)(Bacteria, Fungi, viruses & others) • *It is well adapted to a wide range of*It is well adapted to a wide range of environmental changes (mechanical &environmental changes (mechanical & thermal injury) throughout its anatomical,thermal injury) throughout its anatomical, physiological & immunological make up.physiological & immunological make up.
  • 4. 11..BACTERIA INFCETIONSBACTERIA INFCETIONS • 1. Primary infections ( pyoderma) e.g.1. Primary infections ( pyoderma) e.g. Impetigo, erysiplase; single organism.Impetigo, erysiplase; single organism. • 2. Secondary infection in damaged skin2. Secondary infection in damaged skin (mixture of organisms)(mixture of organisms) • 3. Cutaneous involvement in systemic3. Cutaneous involvement in systemic bacterial disease e.g. bacteraemia & E.Nbacterial disease e.g. bacteraemia & E.N
  • 5. THE COMMON pyogenic SKINTHE COMMON pyogenic SKIN INFECTIONSINFECTIONS are:(Gram +veare:(Gram +ve(( • StreptococciStreptococci StaphylococciStaphylococci • 1. Impetigo & Ecthyma 1. Impetigo(10% of cases1. Impetigo & Ecthyma 1. Impetigo(10% of cases • 2. Erysiplase 2. Bullous Impetigo2. Erysiplase 2. Bullous Impetigo • 3. Cellulites 3.3. Cellulites 3. superficial & deep Follicullitissuperficial & deep Follicullitis • 4. Lymphangitis 4. Sweat gland abscess4. Lymphangitis 4. Sweat gland abscess Primary, Secondary And systemicPrimary, Secondary And systemic PrimaryPrimary
  • 6. 1. Complicating scabies 1. Complicating1. Complicating scabies 1. Complicating Ulcers 'Bullous eruptionUlcers 'Bullous eruption Eczema, insect biteEczema, insect bite 2- Intertrigo 2. intertrigo2- Intertrigo 2. intertrigo 3- Necrotizing cellulites3- Necrotizing cellulites 3. Infectious gangrene 4. decubitus & phagedenic ulcer3. Infectious gangrene 4. decubitus & phagedenic ulcer SecondarySecondary
  • 7. 11..Scarlet fever 1. Staph Bacteraemia &Scarlet fever 1. Staph Bacteraemia & EndocarditisEndocarditis 2. S B E 2. S S S S2. S B E 2. S S S S 3. E.N 3. Bullous Impetigo3. E.N 3. Bullous Impetigo 4. E. Marginatum4. E. Marginatum 5. E. M. like lesion5. E. M. like lesion SystemicSystemic
  • 8. **Generally speaking : StaphylococciGenerally speaking : Staphylococci commonly attack skin appendages ( haircommonly attack skin appendages ( hair follicle, sweat glands, periungual tissuefollicle, sweat glands, periungual tissue while streptococci attack the skin properwhile streptococci attack the skin proper..
  • 9. *The follicular occlusion triad*The follicular occlusion triad -Hydradenitis suppurativa-Hydradenitis suppurativa -acute conglobata-acute conglobata -Perifolliculitis capitis abscedens et-Perifolliculitis capitis abscedens et suffodens (dissecting cellulites of the scalp.suffodens (dissecting cellulites of the scalp. Some common G -ve)Some common G -ve) -Erythraosma corynebacterium-Erythraosma corynebacterium minutissimumminutissimum -Actinomycosis --Actinomycosis -israelliiisraellii bovisbovis
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  • 15. 2-Fungal Infections2-Fungal Infections • Superficial DeepSuperficial Deep • Dermatophytosis SporotrichosisDermatophytosis Sporotrichosis • Pityriasis versicolor MycetomaPityriasis versicolor Mycetoma • Candidiasis paracoccidiosisCandidiasis paracoccidiosis • T.nigra chromomycosisT.nigra chromomycosis • Piedra blastomycosisPiedra blastomycosis • Moulds coccidiomycosisMoulds coccidiomycosis • cryptococosiscryptococosis • nocardiosisnocardiosis
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  • 26. 33..VIRAL INFECTIONSVIRAL INFECTIONS • -Viruses are obligatory intracellular parasites-Viruses are obligatory intracellular parasites • -They are not cell as they lack organells, hence-They are not cell as they lack organells, hence no metabolism of their own. They must use theno metabolism of their own. They must use the host cell for their replication ----host cell for their replication ----disturbing thedisturbing the metabolism of the host cell, so acting as themetabolism of the host cell, so acting as the pathogen.pathogen. • -Structure: outside the cell they are called virion-Structure: outside the cell they are called virion which is composed of:which is composed of: • 1. Central core of DNA or RNA = viral genome1. Central core of DNA or RNA = viral genome • 2. Capsid surrounds the nucleoprotein2. Capsid surrounds the nucleoprotein
  • 27. The subunit of the capsid = capsomer =The subunit of the capsid = capsomer = mainantegenic component of the viruses.mainantegenic component of the viruses. VIRAL INFECTIONS OF THE SKIN MAYVIRAL INFECTIONS OF THE SKIN MAY OCCUR IN 3 DIFFERENT WAYS:OCCUR IN 3 DIFFERENT WAYS: 1. Direct inoculation : e.g. Molluscum, orf---1. Direct inoculation : e.g. Molluscum, orf--- replicate directly in the epidermisreplicate directly in the epidermis 2. systemic infections; the skin lesion2. systemic infections; the skin lesion produced by systemic viral infection areproduced by systemic viral infection are called exanthemata & occur duringcalled exanthemata & occur during viraemiaviraemia
  • 28. EXANTHEMTAEXANTHEMTA • -Macular : Rubelle & I.M.-Macular : Rubelle & I.M. • -Maculopapular: measles-Maculopapular: measles • -Maculopapular-vesicular: echo & coxsackie-Maculopapular-vesicular: echo & coxsackie • -maculopapular-petecheal: togo virus-maculopapular-petecheal: togo virus • -Urticaria : Hepatitis B-Urticaria : Hepatitis B • -Vesicular : chicken pox-Vesicular : chicken pox • -Vesiculopustular: H.S & H. Z-Vesiculopustular: H.S & H. Z 33..Local spread from an internal focus: recurrent H.S & H.ZLocal spread from an internal focus: recurrent H.S & H.Z
  • 29. CUTANEUS VIRALCUTANEUS VIRAL INFECTIONSINFECTIONS 1.Herpes Virus grp. 2.Pox Virus grp. 3.Papovirus grp. 4.Picorna virus grp. D N A RNA Intranuclear Intracytoplasmic Intranucelear 1.Herpes Simplex V 1.Small pox 1Verruca 1.Hand, foot,mouth 2.Varicella/zoster 2.Monkey pox 2.Focai epithelial 2.Foot & mouth 3.Cytomegalovirus 3.Molluscum contagiosum 3.Hepatitis A 4.E.B. Virus 4.Orf 5.Human Herpes V. 5.Milker's nodule (HHV6) hyperplasiahyperplasia
  • 30. HERPES SIMPLEXHERPES SIMPLEX • There are 2 types of H.S.V which show noThere are 2 types of H.S.V which show no cross immunitycross immunity • *H.S.V.(1) attack the skin & oral mucosa*H.S.V.(1) attack the skin & oral mucosa • (most of infections above the waist)(most of infections above the waist) • *H.S.V.(2) attack the genital area*H.S.V.(2) attack the genital area • (most of infections below the waist)(most of infections below the waist) However HSv1 may be found in genital lesionsHowever HSv1 may be found in genital lesions due to orogenital sexdue to orogenital sex
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  • 32. **Pathogenesis: (1) infection: occurs in individuals**Pathogenesis: (1) infection: occurs in individuals who are infected Primary for the first time & havewho are infected Primary for the first time & have no specific neutralizing antibodies it isno specific neutralizing antibodies it is Either subclinical 90%Either subclinical 90% Clinical 10%Clinical 10% After primary infection the virus is not eliminatedAfter primary infection the virus is not eliminated from the body but stays dormant in one of thefrom the body but stays dormant in one of the sensory gangliasensory ganglia (2)recurrent H.S.: occurs in(2)recurrent H.S.: occurs in individuals previously infected with H.S.V. &individuals previously infected with H.S.V. & possesses specific neutralizing antibodies.possesses specific neutralizing antibodies. reactivation of the dormant virus is triggered byreactivation of the dormant virus is triggered by fever, trauma, menstruation….fever, trauma, menstruation….
  • 33. ******Clinical Features: PRIMARY HERPESClinical Features: PRIMARY HERPES SIMPLEXSIMPLEX -It affects children (2-5y.o) with fever &-It affects children (2-5y.o) with fever & malaisemalaise -Large vesicle which show no tendency to-Large vesicle which show no tendency to groupinggrouping -Regional L.N.: enlarged & tender-Regional L.N.: enlarged & tender -Vesicle--Vesicle-rupture-rupture-erosionserosions -Spontaneous resolution after 1-2 wks-Spontaneous resolution after 1-2 wks -No scarring except in case of secondary-No scarring except in case of secondary infectioninfection
  • 34. CLINICAL TYPESCLINICAL TYPES • 1. Gingivostomatitis: the most common Primary1. Gingivostomatitis: the most common Primary infectioninfection • 2. Keratoconjunctivitis: recurrent dendritic ulcer2. Keratoconjunctivitis: recurrent dendritic ulcer • 3. Herpes progenitalis: it is usually due to3. Herpes progenitalis: it is usually due to H.S.V.2 but rarely H.S.V.1 (after orogenital sex)H.S.V.2 but rarely H.S.V.1 (after orogenital sex) = 20% in adults after sexual intercourse= 20% in adults after sexual intercourse • -I.P 2-7 usually 5 days-I.P 2-7 usually 5 days • -Site: glans & shaft of penis in male; vulva,-Site: glans & shaft of penis in male; vulva, vagina, cervix in femalevagina, cervix in female • -vesicles on erythematous base--vesicles on erythematous base-rupture-rupture- painful erosions last-painful erosions last-2-6wks2-6wks • -Fever & malaise-Fever & malaise • -Enlarged regional L.N.-Enlarged regional L.N.
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  • 36. 44..Kaposi's Varicelliform eruption= H.S.V. infectionKaposi's Varicelliform eruption= H.S.V. infection in atopic individualsin atopic individuals 5. Herpetic whitlow= inoculation HS5. Herpetic whitlow= inoculation HS Painfull deep seated vesicles limited toPainfull deep seated vesicles limited to paronychial or volar aspects of distal phalanx ofparonychial or volar aspects of distal phalanx of the finger, more in medical paersons by type (1) &the finger, more in medical paersons by type (1) & (2)(2) 6. Herpatic Folliculitis: of beard region in male6. Herpatic Folliculitis: of beard region in male 7. H.S pneumonia-7. H.S pneumonia- from aspirated HS offrom aspirated HS of mouth----mouth----FatalFatal 8. H.S encephalitis--8. H.S encephalitis-- very high mortalityvery high mortality 9. Neo-natal (congenital) H.S:9. Neo-natal (congenital) H.S: The potential of congenital H.S is considerableThe potential of congenital H.S is considerable since 1% of pts in pregnancy clinics have HSv2since 1% of pts in pregnancy clinics have HSv2 infection by culture from vagina & 1/2 of theseinfection by culture from vagina & 1/2 of these have lesionshave lesions..
  • 37. VARICELLA & ZOSTERVARICELLA & ZOSTER •******Varicella (chicken pox) & H.Z (Shingles) areVaricella (chicken pox) & H.Z (Shingles) are caused by the same virus. Varicella zoster viruscaused by the same virus. Varicella zoster virus = DNA intranuclear= DNA intranuclear.. •--Primary infection occurs in patients withoutPrimary infection occurs in patients without resistance to this virus---resistance to this virus---chicken poxchicken pox •--after subsidence of the primary attack, the virusafter subsidence of the primary attack, the virus remains dormant in one of the sensory gangliaremains dormant in one of the sensory ganglia (latency period(latency period(( •--Reactivation of the latent virus--Reactivation of the latent virus--sread of thesread of the virus to tha skin supplied by the affected root -virus to tha skin supplied by the affected root - H.zosterH.zoster
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  • 39. VARICELLA = CHICKEN POXVARICELLA = CHICKEN POX • I.P: 2-3 WKS, 90 % children. Skin &I.P: 2-3 WKS, 90 % children. Skin & affection. Epidemic, transmitted by dropletaffection. Epidemic, transmitted by droplet infection-infection-viraemia -viraemia -skin exanthema [mildskin exanthema [mild prodroma, fever 1-2 daysprodroma, fever 1-2 days • --macule-macule-papulepapulevesicle (clear dropvesicle (clear drop like)like)pustulepustuledry scabdry scabnoscar except ifnoscar except if secondary infection supervene.secondary infection supervene. • -New lesions continue to develop-New lesions continue to develop (Pleomorphism) in contrast to variola.(Pleomorphism) in contrast to variola. • - Haemorrhagic varicella ( high fever + Hgic- Haemorrhagic varicella ( high fever + Hgic vesicle)vesicle)
  • 40. COMPLICATIONSCOMPLICATIONS:: •11..Pneumonia (14% adultsPneumonia (14% adults(( •22..Reye's syndrome: fatal encephalopathyReye's syndrome: fatal encephalopathy associated with varicellaassociated with varicella •33..Neonatal varicella: fatal if mother hasNeonatal varicella: fatal if mother has contracted the infection 5 days before deliverycontracted the infection 5 days before delivery •44..Secondary infectionSecondary infection •55..Cutaneous gangreneCutaneous gangrene  dermatitisdermatitis gangrenasegangrenase •66..Thrombocytopenic purpuraThrombocytopenic purpura •77..Viral arthritisViral arthritis
  • 41. H.ZOSTER ( SHINGLESH.ZOSTER ( SHINGLES(( • *In adults: attack maybe PPT by debilitating*In adults: attack maybe PPT by debilitating conditions. think of HIV , if recurrent in youngconditions. think of HIV , if recurrent in young adults.adults. • *Pain 2-3 days grouped vesicles on an*Pain 2-3 days grouped vesicles on an erythematous base along the course of alongerythematous base along the course of along sensory nerve & strictly unilateral ( never crosssensory nerve & strictly unilateral ( never cross the midline)the midline) • *Thoracic H.Z 53% > cervical 20 % > Trigeminal*Thoracic H.Z 53% > cervical 20 % > Trigeminal • *Regional L.N. are enlarged & tender*Regional L.N. are enlarged & tender • *Healing within 2-3 weeks*Healing within 2-3 weeks • *lesions may be Hgic or necrotic or ulcerated*lesions may be Hgic or necrotic or ulcerated • *Disseminated H.Z may be fatal: occurs in*Disseminated H.Z may be fatal: occurs in immunocompromised pts.immunocompromised pts.
  • 42. COMPLICATIONCOMPLICATION • 1. Post herpetic neuralgia1. Post herpetic neuralgia • 2. Secondary infection2. Secondary infection • 3. Gangrene3. Gangrene • 4. H.Z ophthalmicus (Gasserian ganglion)4. H.Z ophthalmicus (Gasserian ganglion) • 5. Ramsey – Hunt Ssyndrome5. Ramsey – Hunt Ssyndrome • Ear: pain-tinitus-deafnessEar: pain-tinitus-deafness • Tongue: out 2/3: loss of taste sensationTongue: out 2/3: loss of taste sensation • Face: facial palsy : maybe permanentFace: facial palsy : maybe permanent
  • 43. VERRUCAE (WARTSVERRUCAE (WARTS(( • -HPV : papovirus DNA intranuclear 55 types-HPV : papovirus DNA intranuclear 55 types • Incubation period weeks up to a yearIncubation period weeks up to a year • -All types have tropism to squamous epithelial cells.-All types have tropism to squamous epithelial cells. • -Mode of transmission: by direct & indirect routes of non-Mode of transmission: by direct & indirect routes of non intact skinintact skin • 1.) plantar w: swimming pools or shower rooms floor1.) plantar w: swimming pools or shower rooms floor • 2.) Common hands warts2.) Common hands warts • 3.) Shaving -3.) Shaving - beard areabeard area • 4.) Occupational: handlers of meat & fish4.) Occupational: handlers of meat & fish • 5.) Genital: sexual or non-sexual5.) Genital: sexual or non-sexual • 6.) Iatrogenic: HPV detected in vaginal specula, liquid6.) Iatrogenic: HPV detected in vaginal specula, liquid nitrogen, cotton swabsnitrogen, cotton swabs • 7.) Anogenital in children: sexual abuse-mother's genital7.) Anogenital in children: sexual abuse-mother's genital tract – or non sexualtract – or non sexual
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  • 46. CLINICAL CLASSIFICATIONCLINICAL CLASSIFICATION • 1. Verruca vulgaris = common warts1. Verruca vulgaris = common warts including filariform wartsincluding filariform warts • 2. Deep hyperkeratotic palmoplantar warts2. Deep hyperkeratotic palmoplantar warts • 3. Superficial – mosaic type3. Superficial – mosaic type • 4. Verruca plana (plane warts)4. Verruca plana (plane warts) • 5. Candyloma acuminata5. Candyloma acuminata • 6. Epidermo dysplasia verruciformis of6. Epidermo dysplasia verruciformis of Lutz (1922) inherited disorder (A.R): wideLutz (1922) inherited disorder (A.R): wide spread & persistent infection with HPVspread & persistent infection with HPV
  • 47. 44--OthersOthers • Others like parasitic infestationOthers like parasitic infestation (scabies – Pediculosis corporis and pubis )(scabies – Pediculosis corporis and pubis )