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 erysipelas CHRONIC 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 antibiotics The 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 INFECTION 1- 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

Tissue destructive modalities 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 Recurrence Orbital infection 2- GENITAL ( HSV II ) Initial Recurrence

Incubation period : 7- 10 days 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- CHICKENPOX Incubation period : 2 weeks Presentation : 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 ZOSTER After 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 appear 2- 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 )

SERIOUS involvement It is almost always DERMATOMAL SPINAL (Thoracic ) CRANIAL ( Trigeminal) SERIOUS involvement 1. 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 )

Treatment HERPES SIMPLEX Acyclovir 200 mg five time a day for a week HERPES ZOSTER Acyclovir 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.

FUNGAL Two main groups : 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

Inflammatory pedis Tinea Pedis

Tinea corporis / Tinea cruris 1. Hyperkeratotic type (T 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 Tinea Capitis ( affect the scalp ) 1.Hyperkeratotic (black dot) usually due to T. tonsurans 2. Inflammatory (Kerion)  how mycotic absess usually due to M. canis complex 3. 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- YEAST Candidosis Due to candida albicans It 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

It is weak organism So it affect the wet isolated areas only 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 miconazole Systemic Antifungal Use 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 Cutaneous Not localized Multiple non-ulcerated nodules Caused by : L. maxican 3- Mucocutaneous Caused 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

Mite called sarcoptes scabei 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 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

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