CUTANEOUS INFECTIONS AND INFESTATIONS Fahad Al Sudairy, M.D.
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Transcript of CUTANEOUS INFECTIONS AND INFESTATIONS Fahad Al Sudairy, M.D.
CUTANEOUS INFECTIONS AND INFESTATIONS
Fahad Al Sudairy, M.D.
OBJECTIVES 1. General understanding of the causative
organisms of common skin infection(CSI).
2. Focus on CSI ( common skin infections ) clinical presentation.
3. Overview of the basic investigations done and general knowledge of first line therapy.
BACTERIA (impetigo , erysipelas &cellulits )
VIRUS (wart ,herpes simplex & herpes zoster)
FUNGUS (Tinea , candidasis)
PARASITE (Lieshmaniasis ,scabies & pediculosis)
BACTERIAL
The most common cause is Gram + ( like strept and staph )
Classification of skin infections according to the site : 1- superficial - Epidermis - ( ex Impetigo ) : and it
divided to : A-non follicular if the hair follicles are intact
(Impetigo)B- follicular if the hair follicles are involved (the
infection here is called folliculitis 2- deep infections – dermis - ( ex erysipelas &
cellulits ) )
I. Impetigo Superficial non-follicular infection due to
staphylococcus and streptococcus Children not sick ( No fever or any general symptoms ) pustule (honey-colored crust ) Face and Acral areas it could be :- Primary : if there are no previous lesions of the skin - or secondary : if the infection occur on previous
skin lesion (superinfection of severe ecsema “impetigo on top of ecsema”)
II. Erysipelas deep cutaneous infection (Dermal) due to streptococcus after penetrating trauma ( CHRONIC LYMPHEDEMA) sick ( the pt, come with fever , malaise and lymphoadenopathy ) Face and Acral areas ( unilateral ) Unilateral sharply demarcated edematous red plaque Prompt response to
full doses of oral peneicillin is the useful diagnosic test for erysipelasCHRONIC LYMPHEDEMA : ( repeated soft tissue infection lead to
damage lymph cause chronic lymphedema the lymphedema is perfect environment for infections ) So always treat the lymphoedema
III. Cellulitis deep cutaneous infection (up to SC FAT) due to streptococcus after penetrating trauma ( CHRONIC
LYMPHEDEMA) sick ( the pt, come with fever , malaise and lymphoadenopathy )
Face and Acral areas clinical presentation : Unilateral Diffuse (NOT well demarcated)
edematous red plaque always do Blood Culture in immuocompramized and Immunocompetent pts.
Rx : full doses of systemic antibioticsThe complications of soft tissue infections : 1- chronic lymphodema 2- septicemia
The clinical presentation difference between erysipelas and cellulitis is “the border”. Erysipelas affects the upper part of dermis, its border is clear and you can feel it without seeing! Cellulitis has no border, it’s diffuse and ill defined!
Viral Infection
Fahad Alsudairy , M.D.
VIRAL INFECTION1- WART (common benign self-limited cutanous tumors) causative agent : Human papilloma virus (HPV) , Separated by Direct contact Asymptomatic transmition ( at the transmission there are no any
symptoms the symptoms may appear later or they may never occur )
Delay in presentation (up to 10 years) Oncogenic potential (HPV 16 and 18) High recurrence rate ( because it is latent at the basal layer of the
skin )
HPV CUTANOUS ( HPV 1 and 3 ) common wart (found on the hands, in children 5-10
y/o, demonstrate the Koebner phneomenon)
flat wart
planter wart
GENITAL (HPV 6 and 11) :
classic
condyloma acuminata
Common warts
flat warts
Classic genetal warts
condyloma acuminata : elevated lesions ( more than 1 cm ) it look like papules
GENITAL WART
*they are the MOST COMMON STD
*it is Oncogenic HPVs ( Cervical cancer)
*Usually more persistent and difficult to treat .
If pt come with genetal Wart - always exam the whole genetoanal area- Investigate – analyze - the urine - Do serology for ( syphilis and the 3 H ( hepatitis – herpes
– HIV ) - Check the sexual partner
TREATMENT ( 2 methods : • Tissue destructive modalities • Keratolytic (salicylic acid and podophyllin) Cryotherapy ( Liquid nitrogen) Electrotherapy CO2 laser
* Immunotherapy
2- HERPES SIMPLEX
Causative agent : Human Herpes virus I and II
It separated by : Direct contact
Asymptomatic transmition
Latency ( delay presentation )
High recurrence rate
Type 2 virus has high association with cervical cancer
1 - CUTANEOUS ( HSV I - 98% of population ) Could be ( Initial Or recurrent ) orolibialis Initial Herpatic whitlow Recurrence( inflamation of the proximal nail folds – paronychia - )
herpes ophtalmicus RecurrenceOrbital infection
2- GENITAL ( HSV II )
Initial Recurrence
Incubation period : 7- 10 days. Presentation : After 24-48 hours of burning and tingling sensation the patient develop grouped vesicles on erythematous base which ulcerate within 24 hours. Hall mark
At presentation the pt usually have Erosions ( secondary lesions ) because the dz has fast progression .
The whole illness is around 7-10 days.
Topical steroid should not be applied to herpes simplex lesions
It appear as GROUPED infection
Investigations
1- Tzank smear
The Microscope will show ( Multinuculated Gaint cells ) This test not spesific to the type of the virus
2- Direct fluorescent antibody test very specific to the type of the virus
3- Viral culture
4- Blood serology used to check the partner
3- VARICELLAE ZOSTER VIRUS (VZV) Also called Human herpes 3
Transmission : Airborn ( respiratory droplets )
It cause :
CHICKENPOX ( Children)
HERPES ZOSTER (Adult) is due to reactivation of VZV which was dorminant in nerve root ganglion
A- CHICKENPOXIncubation period : 2 weeksPresentation : A- Prodrom of respiratory coryza ( Same
URTI ) followed by B- disseminated red macules with central
vesicles. ( in the Trunk sparing the Extremities )
The whole illness : 3 weeks The patient contagious 5 days before and 5
days after skin eruption
Classic presentation : red macules with central vesicles.
B- HERPES ZOSTERAfter 24-48 hours of burning and tingling
sensation the patient develop grouped vesicles on erythematous base which ulcerate within 24 hours.
The whole illness is around 7-10 days.
Post-herpetic neuralgia (PHN) which usually persist for around 4 weeks.
Types ( phases ) of Pain : 1- early : burning before the vesicles appear2- middle : tingling sensation when the visicles appear 3- late : Post-herpetic neuralgia (PHN) which usually persist for around 4 weeks after the vesicles Disappear . treat if it last longer than 1 moth
It usually unilateral and it is Dermatome ( follow the dermatome )
The commonest dermatomes : ( Spinal ( thoracic ) – Cranial (trigeminal )
It is almost always DERMATOMAL
SPINAL (Thoracic )
CRANIAL ( Trigeminal)
SERIOUS involvement1. Ophthalmic herpes :ex Ophthalmic division of
trigeminal nerve.
2. Risk of motor Nueropathy : ex Geniculate ganglia (Ramsey-hunt syndrome) which affect the External ear and it could cause Ipsilateral Facial palsy
3.Sacral ganglia.
4. Immunocomprimised Pt. : ex usually have Dissemanated Herpes
All these cases should treated by immediate IV antiviral ( acyclovir )
TreatmentHERPES SIMPLEX Acyclovir 200 mg five time a day for a
weekHERPES ZOSTERAcyclovir 800 mg five time a day for a
week
Molluscum Contagiosum
Poxvirus.
Dome-shaped pearly papuels with central umbilication.
Spontaneous resolution.
Treatment …
Fungal Infection
Fahad Alsudairy , M.D.
FUNGALTwo main groups :
1- DERMATOPHYTE 1- DERMATOPHYTE which cause :
A- Tinea Pedis (most common)
This Dz have many forms like :
1.Erosive interdigitalis
2. Hyperkeratotic type(T. rubrum) ( dry type ) this type trasfares from human to human ( anthrophilic )
3. Inflammatory type(T.mentagrophyte) ( wet type ) this type is Zoophelic
Tinea Pedis Inflammatory pedis
Tinea corporis / Tinea cruris 1.Hyperkeratotic type (T. rubrum) well-demarcated annular red
hyperkeratotic plaque with central clearing (Ring worm) classic pic
2.Inflammatory type (T.mentagrophyte) well-demarcated edematous red
plaque with superimposed pustules
well-demarcated annular red hyperkeratotic plaque with central clearing (Ring worm ) show central clearing Which type ?
Tinea Capitis ( affect the scalp ) 1.Hyperkeratotic (black dot) usually due to T. tonsurans2. Inflammatory (Kerion) how mycotic absess usually due to M. canis complex3. Favus * Due to T. schoenleinii * it characterized by the presence of
Scutulae ( golden crust ) .
1.Hyperkeratotic (black dot)
Inflammatory (Kerion) how mycotic abscess Show soft nodules and abcess
Favus : inflamed and eroded area
2- YEASTCandidosisDue to candida albicansIt is a commensal flora of the gut
which become pathogenic when the immune status of the person changed
When does it become pathological
physiological (old age , neonate and pregnancy)
pathological ( DM, HIV and organ transplant)
Itrogenic (long course of Antibiotics)
Locations
MUCOSAL
1. Oral
oral thrush
angular chilitis
2. Genital
valvuvaginitis
CUTANEOUS
it favor wet areas and the most common types are :
Candidal intertrigo
peripherally spreading glazed red patch with scaly border and satellite pustules
Candidal paronychia ( Nails )
It is weak organism So it affect the wet isolated areas only
Witch plaques on the tongue
2- pityriasis versicolor ( very common ) Due to Malassezia furfur ( previously
called : protrosposim oval )
Asypmtomatic
Well-demarcated brown patches with branny over the trunk and upper extremities
Well-demarcated brown patches with branny
Diagnosis
1. Scraping ,Clipping and Hair blucking
KOH/microscopy Culture
2. Skin biopsy Histopathology . ( Rare to be requested )
Treatment Topical Antifungal Nystatin preparation (oral thrush) for mucosal Candida Imidazoles e.g. cotrimazole and miconazoleSystemic AntifungalUse it for :- Tinea Capitis - onychomycosis (fungal nail infection) - Any Resistant infection Imidazoles e.g. Itraconazole and fluconazole Allylamine e.g. Terbinafine Griseovulvin
PROTOZOA
1- Lieshmaniasis
Protozoa called Lieshmania
Has 2 form :
At the Sand fly (premastigote )
At the Macrophage (Amastigote) it called Lieshman-Donovan bodies
Transmistion : sand fly
Presentation 1- Localized Cutaneous – most common Well-demarcated ulcerated nodule over the exposed
areas after a trip to an endemic area ( H/o of insect bite)
It caused by : ( L. tropical – L. major ) 2- Disseminated CutaneousNot localized Multiple non-ulcerated nodules Caused by : L. maxican 3- MucocutaneousCaused by : L. brazelai 4- Visceral ( kakazar )
Well-demarcated ulcerated nodule over the exposed areas ( classical presentation )
Investigations
Skin biopsy
Histopathology with Gimsa stain
Lieshman-Donovan bodies
Culture
PCR for DNA
Liesmanin test
Treatment
Resolve spontaneously leaving a scar
Antimony (Pentostam (( sodiume stepogluconate )) either Intralesional ( if localized ) or Intramuscular( if separated ) to shrink the lesion
2- Scabies Mite called sarcoptes scabei which residue in burrows in the
stratum corneum laying eggs then dieing and the eggs will maturate in 2 weeks period and the cycle repeated.
Skin lesions are Secondary eczematous eruption due to immune reaction to the mite and eggs
Show eczema only – no specific sign
When to suspect scabies ?
1.pruritus mainly at night
2. Other member of the family also having severe pruritus
3. Pruritus and skin eruption is more severe in the flexors
Document See the mite or eggs
Treatment
Permethrin cream ( 1st line )
Lindane cream
Malathion lotion
2.5% sulphur ointment
Instructions for treatment
1- treat all family members and close contacts even if they do not have symptoms
2- Do special cleaning for all the pt, ‘s belongs ( clothes and bed ) by Dry cleaning or bag it in well closed bag for 10 days
3- Use active treatment ( cover all the body specially the flexses ) put the cream and leave it for 24h then repeat it after 1 week to kill the eggs
3- PEDICULOSIS
Head lice (Pediculosis Capitis)
Children
Body lice (Pediculosis Corporis)
Homeless people and vagrants
Pubic lice (Pediculosis Pubis)
STD ( partner should be treated)
Diagnosis and treatment
The diagnosis can be conformed by seeing the lice eggs ( NITs)
Best treatment is SHAVING for head ( if boy ) and pubic lice. Alternatives:
Permethrin creame rinse ( 1st line )
Malathion lotion
Instructions for treatment
Ask the pt to use Permethrin Shampoo daily
Use special combs daily
Use active treatment- 1st line - ( for 24 h ) then repeat in 1 week
No need to treat the whole family
THANK YOU