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
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
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
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
31.
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.
35.
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
38.
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-papulepapulevesicle (clear dropvesicle (clear drop
like)like)pustulepustuledry scabdry scabnoscar 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
44.
45.
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 )