1. CUTANEOUS INFECTIONS AND INFESTATIONS
Fahad Al Sudairy, M.D.

2. 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.

3. BACTERIA (impetigo , erysipelas &cellulits ) VIRUS (wart ,herpes simplex & herpes zoster) FUNGUS (Tinea , candidasis) PARASITE (Lieshmaniasis ,scabies & pediculosis)

4. 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 ) )

5. 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”)

7. 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

9. 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

10. 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!

11. Viral Infection
Fahad Alsudairy , M.D.

12. 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 )

13. 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

14. Common warts

15. flat warts

16. Classic genetal warts

17. condyloma acuminata : elevated lesions
( more than 1 cm ) it look like papules

18. 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

19. Tissue destructive modalities
TREATMENT ( 2 methods :
Tissue destructive modalities
Keratolytic (salicylic acid and podophyllin)
Cryotherapy ( Liquid nitrogen)
Electrotherapy
CO2 laser
* Immunotherapy

20. 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

21. 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

22. Incubation period : 7- 10 days
Incubation period : days. Presentation : After 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

24. It appear as
GROUPED
infection

25. 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

26. 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

27. 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

28. Classic presentation : red macules with central vesicles.

29. B- HERPES ZOSTER
After 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

30. It usually unilateral and it is Dermatome ( follow the dermatome )
The commonest dermatomes : ( Spinal ( thoracic ) –
Cranial (trigeminal )

31. 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 )

32. 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

33. Molluscum Contagiosum
Poxvirus.
Dome-shaped pearly papuels with central umbilication.
Spontaneous resolution.
Treatment …

37. Fungal Infection
Fahad Alsudairy , M.D.

38. 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

39. Inflammatory pedis
Tinea Pedis

40. 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

41. well-demarcated annular red hyperkeratotic plaque
with central clearing (Ring worm )  show central
clearing
Which type ?

42. 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 ) .

43. 1.Hyperkeratotic (black dot)

44. Inflammatory (Kerion)  how mycotic abscess
Show soft nodules and abcess

45. Favus : inflamed and eroded area

46. 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

47. When does it become pathological
physiological (old age , neonate and pregnancy) pathological ( DM, HIV and organ transplant) Itrogenic (long course of Antibiotics)

48. Locations
MUCOSAL 1. Oral oral thrush angular chilitis 2. Genital valvuvaginitis

49. 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

50. Witch plaques on the tongue

53. 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

54. Well-demarcated brown patches with branny

55. Diagnosis
1. Scraping ,Clipping and Hair blucking KOH/microscopy Culture 2. Skin biopsy Histopathology . ( Rare to be requested )

56. 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

57. 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

58. 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 )

59. Well-demarcated ulcerated nodule over the exposed areas ( classical presentation )

60. Investigations
Skin biopsy Histopathology with Gimsa stain Lieshman-Donovan bodies Culture PCR for DNA Liesmanin test

61. Treatment
Resolve spontaneously leaving a scar Antimony (Pentostam (( sodiume stepogluconate )) either Intralesional ( if localized ) or Intramuscular( if separated ) to shrink the lesion

62. 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

64. Show eczema only – no specific sign

66. 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

67. Treatment
Permethrin cream ( 1st line ) Lindane cream Malathion lotion 2.5% sulphur ointment

68. 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

69. 3- PEDICULOSIS Head lice (Pediculosis Capitis) Children Body lice (Pediculosis Corporis) Homeless people and vagrants Pubic lice (Pediculosis Pubis) STD ( partner should be treated)

72. 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

73. 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

74. THANK YOU