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PRESENTEDPRESENTEDBYBYDR. HUSSEIN ABOUL FOTOUHDR. HUSSEIN ABOUL FOTOUHMB.Bch.MS.Sc. DERMATOLOGY& ANDROLOGYMB.Bch.MS.Sc. DERMATOLOGY& ANDROLOGYCAIRO UNIVERSITYCAIRO UNIVERSITYPH. D. ALAZHAR UNIVERSITYPH. D. ALAZHAR UNIVERSITY..
COMMON SKINCOMMON SKININFECTIONSINFECTIONSBy Dr. Hussein AboulBy Dr. Hussein AboulFotouhFotouhDermatologistDermatologistM.G.HM.G.H
• *the skin is the first line of defense of the*the skin is the first line of defense of thehuman 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 ofenvironmental 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 systemicbacterial disease e.g. bacteraemia & E.Nbacterial disease e.g. bacteraemia & E.N
THE COMMON pyogenic SKINTHE COMMON pyogenic SKININFECTIONSINFECTIONSare:(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 abscessPrimary, Secondary And systemicPrimary, Secondary And systemicPrimaryPrimary
11..Scarlet fever 1. Staph Bacteraemia &Scarlet fever 1. Staph Bacteraemia &EndocarditisEndocarditis2. S B E 2. S S S S2. S B E 2. S S S S3. E.N 3. Bullous Impetigo3. E.N 3. Bullous Impetigo4. E. Marginatum4. E. Marginatum5. E. M. like lesion5. E. M. like lesionSystemicSystemic
*The follicular occlusion triad*The follicular occlusion triad-Hydradenitis suppurativa-Hydradenitis suppurativa-acute conglobata-acute conglobata-Perifolliculitis capitis abscedens et-Perifolliculitis capitis abscedens etsuffodens (dissecting cellulites of the scalp.suffodens (dissecting cellulites of the scalp.Some common G -ve)Some common G -ve)-Erythraosma corynebacterium-Erythraosma corynebacteriumminutissimumminutissimum-Actinomycosis --Actinomycosis -israelliiisraelliibovisbovis
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, henceno metabolism of their own. They must use theno metabolism of their own. They must use thehost cell for their replication ----host cell for their replication ----disturbing thedisturbing themetabolism of the host cell, so acting as themetabolism of the host cell, so acting as thepathogen.pathogen.• -Structure: outside the cell they are called virion-Structure: outside the cell they are called virionwhich 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 MAYOCCUR 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 epidermis2. systemic infections; the skin lesion2. systemic infections; the skin lesionproduced by systemic viral infection areproduced by systemic viral infection arecalled exanthemata & occur duringcalled exanthemata & occur duringviraemiaviraemia
HERPES SIMPLEXHERPES SIMPLEX• There are 2 types of H.S.V which show noThere are 2 types of H.S.V which show nocross 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 lesionsdue to orogenital sexdue to orogenital sex
**Pathogenesis: (1) infection: occurs in individuals**Pathogenesis: (1) infection: occurs in individualswho are infected Primary for the first time & havewho are infected Primary for the first time & haveno specific neutralizing antibodies it isno specific neutralizing antibodies it isEither subclinical 90%Either subclinical 90%Clinical 10%Clinical 10%After primary infection the virus is not eliminatedAfter primary infection the virus is not eliminatedfrom the body but stays dormant in one of thefrom the body but stays dormant in one of thesensory gangliasensory ganglia(2)recurrent H.S.: occurs in(2)recurrent H.S.: occurs inindividuals 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 byfever, trauma, menstruation….fever, trauma, menstruation….
******Clinical Features: PRIMARY HERPESClinical Features: PRIMARY HERPESSIMPLEXSIMPLEX-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 togroupinggrouping-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 secondaryinfectioninfection
CLINICAL TYPESCLINICAL TYPES• 1. Gingivostomatitis: the most common Primary1. Gingivostomatitis: the most common Primaryinfectioninfection• 2. Keratoconjunctivitis: recurrent dendritic ulcer2. Keratoconjunctivitis: recurrent dendritic ulcer• 3. Herpes progenitalis: it is usually due to3. Herpes progenitalis: it is usually due toH.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..Kaposis Varicelliform eruption= H.S.V. infectionKaposis Varicelliform eruption= H.S.V. infectionin atopic individualsin atopic individuals5. Herpetic whitlow= inoculation HS5. Herpetic whitlow= inoculation HSPainfull deep seated vesicles limited toPainfull deep seated vesicles limited toparonychial or volar aspects of distal phalanx ofparonychial or volar aspects of distal phalanx ofthe 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 male7. H.S pneumonia-7. H.S pneumonia- from aspirated HS offrom aspirated HS ofmouth----mouth----FatalFatal8. H.S encephalitis--8. H.S encephalitis-- very high mortalityvery high mortality9. 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 considerablesince 1% of pts in pregnancy clinics have HSv2since 1% of pts in pregnancy clinics have HSv2infection by culture from vagina & 1/2 of theseinfection by culture from vagina & 1/2 of thesehave lesionshave lesions..
VARICELLA & ZOSTERVARICELLA & ZOSTER•******Varicella (chicken pox) & H.Z (Shingles) areVaricella (chicken pox) & H.Z (Shingles) arecaused 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 withoutresistance to this virus---resistance to this virus---chicken poxchicken pox•--after subsidence of the primary attack, the virusafter subsidence of the primary attack, the virusremains 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 thevirus 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 dropletinfection-infection-viraemia -viraemia -skin exanthema [mildskin exanthema [mildprodroma, fever 1-2 daysprodroma, fever 1-2 days• --macule-macule-papulepapulevesicle (clear dropvesicle (clear droplike)like)pustulepustuledry scabdry scabnoscar except ifnoscar except ifsecondary 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 + Hgicvesicle)vesicle)
COMPLICATIONSCOMPLICATIONS::•11..Pneumonia (14% adultsPneumonia (14% adults((•22..Reyes syndrome: fatal encephalopathyReyes syndrome: fatal encephalopathyassociated with varicellaassociated with varicella•33..Neonatal varicella: fatal if mother hasNeonatal varicella: fatal if mother hascontracted the infection 5 days before deliverycontracted the infection 5 days before delivery•44..Secondary infectionSecondary infection•55..Cutaneous gangreneCutaneous gangrene dermatitisdermatitisgangrenasegangrenase•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 debilitatingconditions. think of HIV , if recurrent in youngconditions. think of HIV , if recurrent in youngadults.adults.• *Pain 2-3 days grouped vesicles on an*Pain 2-3 days grouped vesicles on anerythematous base along the course of alongerythematous base along the course of alongsensory nerve & strictly unilateral ( never crosssensory nerve & strictly unilateral ( never crossthe 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 inimmunocompromised 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 nonintact 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, liquidnitrogen, cotton swabsnitrogen, cotton swabs• 7.) Anogenital in children: sexual abuse-mothers genital7.) Anogenital in children: sexual abuse-mothers genitaltract – or non sexualtract – or non sexual
CLINICAL CLASSIFICATIONCLINICAL CLASSIFICATION• 1. Verruca vulgaris = common warts1. Verruca vulgaris = common wartsincluding 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 ofLutz (1922) inherited disorder (A.R): wideLutz (1922) inherited disorder (A.R): widespread & 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 )