Infections of the skin. All types of infections included. Bacterial, Viral, etc... Overview on infections.

1. Infections of the skin
Dr. Mumux Mirani (MPT Sports)
Asst. Professor
S. R. C. P.

3. Skin infections
The skin always has some amount of bacteria, fungus
and viruses living on it.
Occur when there are breaks in the skin and the
organisms have uncontrolled growth

4. Types of infections of the skin:
Fungal
Bacterial
Viral
Parasitic

5.  Fungal infections are caused by non--
photosynthetic vegetable parasites called
fungi.
 Depending on whether the species resides
in soil, animals or human beings, it is said
to be geophilic, zoophilic or anthrophilic.
 Infection with zoophilic are often
suppurative.

7. Superficial Mycoses
Dermatophytosis (Ringworm)
 There are three genera of dermatophytes:
Trichophyton, Microsporum and
Epidermophyton.
 They are grouped according to their natural
habitat as geophilic (soil), zoophilic
(animals), and anthrophilic (humans).
 Transmission may be indirect (via
desquamated epithelium) or direct through
bodily contact.

8.  Predisposing factors – Warm, humid climate, poor
nutrition and hygiene, obesity, diabetes mellitus and
debilitating illness.
 Common symptom is pruritus in all types of dermato-
phytosis.
 In AIDS patients, dermatophytosis leads to wide spread or
atypical infections and rapidly spreading white
onychomycosis involving the whole nail plate.

10. Tinea Uguium Tinea Pedis

11. T. Capitis scalp
T. cruris groin
T. pedis foot
T. unguim nail

12. •T. corporis• — Ringworm of the body
Tinea/ dermatophyte infections caused by
Trichophyton, Epidermophyton and Microsporum
•T. corporis :ltchy, annular patch, well defined edge,
scaling more obvious at the edges( central clearing)
T.pedis / Athlete's foot
•T. unguim : onycholysis, subungual hyperkeratosis,
dystrophy/pigmentary changes
•T.capitis:

13. Tinea Capitis: Capital region: Scalp

14. Treatment:
•Topical terbinafine/ azole x nearly 4 wks
Oral tx for T. capitis, Onychomycosis — need at least 6 — 12 wks
tx
•Topical nystatin not effective against Tinea. It works for
Candida.
•Griseofulvin — is cheap, but has more side effects and needs
longer duration of tx

15. Onychomycosis
 Onychomycosis includes all infections of the nail caused by any fungus
including non-dermatophytes and yeasts.
 Nail plate is yellow and thick with subungual hyperkeratosis, which is friable
over here: Toe nails are frequently involved.

16. Paronychia – is inflammation of nail folds.

17. a. Acute paronychia – Swollen, tender red nail fold with
visible pus under it.
b. Chronic paronychia – Inflammatory dermatosis of nail
folds with secondary effects on nail matrix and nail growth.
Predisposing factors – Network as in domestic workers, house
wives, DM, candidal vulvo vaginitis.Cl. Fs. Swollen nail head.
Adjacent nail plate becomes ridged and discoloured.

18. 5. Shampoo the hair immediately after visit to the barber’s shop.

21. Candidiasis / Candidosis
 Superficial candidiasis
 Cutaneous Candidiasis
 Mucosal candidiasis
Caused by Candida Albicans
Common sites: the mouth, vagina and GI tract

22. Candidal intertrigo-breasts, groin, web spaces

25. Bacterial infections:
Impatigo / Boil???

26. Bacterial skin infections:
 Very common.
 Ranging from irritation to deadly
infections.
 Mostly caused by Staph. Aureus and Strep.

27. Folliculitis
 Infection of hair follicle
 Usually heals without scarring
 Caused by Staph. Aureus
 Tx: Warm saline compresses. If does not
resolve spontaneously in 1-2 weeks, topical
mupirocin. Oral dicloxacillin (Very rare)

29. Hot tub folliculitis
 Caused by Pseudomonas aeruginosa, commonly found in contaminated
water pools, hot tubs, water slides or physiotherapy pools.
 Rash can erupt anywhere on the body that has been in contact with
contaminated water.
 Most cases resolve on their own, tx: silvadene cream, cipro (for
widespread cases)
 Prevention: frequent changing of water, continuous water filtration,
monitoring of disinfectant levels (chlorination) in pools.
 Showering after contact does not prevent infection.

30.  Young male presenting
with pruritic
erythematous macules
that progressed to
papules and pustules. 3
days ago he has been
to a whirl pool for
physio therapeutical
treatment.

31. Staph skin infections
Furuncle/ Boil
 Infection of pilosebaceous unit(hair follicle and surrounding tissue)
 Usually must drain before they heal- takes less than 2 wks
 Complicated boils- over middle of face/spine or with fever
Carbuncle
 Several furuncles that are densely packed together
 Common in diabetes
 Tx: Severe cases, first I&D (Incision and drainage)
 Oral abx(antibiotics) (dicloxacillin or cephalexin) if fever.

32. Furuncle Carbuncle

33. Impetigo
 Non-bullous (MC form) — principal pathogen is Staph aureus. Group A beta
haemolytic strep minority of cases.
 Bullous form is nearly caused by Staph aureus (common in infants and
children <2yrs)
 Honey crusted lesions/large vesicles
 Tx: topical mupirocin as effective as oral abx
 Oral abx for nonlocalized cases - dicloxacillin, 1st gen cephalosporin,
augmentin. Macrolides not adequate given increasing resistance.
 Complication: Strep glomerulonephritis
 Nasal carriage, source for recc, tx w/ topical mupirocin x 5 d.
 Very contagious, appropriate hygiene for prevention.

34. Impetigo contagiosa (Non bullous form)

35. Impetigo (Bullous form)

36. Viral infections of the skin:
Herpes Zoster Eczema
 Eczema herpeticum (EH) is a painful, blistering rash caused by the herpes
simplex virus.
 EH is also called Kaposi varicelliform eruption, as the person who first
described it believed it to resemble chicken pox, which is caused by the
varicella zoster virus.

39.  Sites – The thoracic and lumbar dermatomes are most
commonly affected.
 An eruption in the mandibular or maxillary distribution of
trigeminal nerve is associated with oral, palatal and
pharyngeal lesions.
 If the ophthalmic division is affected, there may be
keratitis or uveitis, with vesicles in the nose.
 In Ramsay-Hunt syndrome, the geniculate ganglion is
affected.
 Pain in the ear and throat is followed by vesicles in and
around the external auditory meatus associated with
lower motor neuron facial paralysis.

41. complications
 Post-herpetic neuralgia – Risk factors –
(a) Age > 50 years.
(b) Sex - Female
(c) Presence of a prodrome(early symptoms).
(d) Severe or disseminated rash.
(e) Severe pain at presentation.
(f) Ophthalmic zoster.
(g) PCR detect able varicella zoster viraemia.
 Keratitis and corneal ulceration – when the trigeminal nerve is
involved.
 Neurological – including encephalitis, meningitis and myelitis.

44. Acne Vulgaris

45.  Acne vulgaris is a common chronic skin disease involving blockage
and/or inflammation of hair follicles and their accompanying
sebaceous gland. Acne can be present as non-inflammatory lesions,
inflammatory lesions, or a mixture of both, and it is characterised
by:
 Open comedones (Black heads)
 Closed comedones (white heads)
 Papules
 Enlarged pores of hair follicles-
 Cysts
 Pustules
 Scars (occasionally)

46. It distributes to…
 Face
 Upper back-
 Chest and arms-
 Medial sides of thighs-
 Buttocks (rarely)
 (The condition is commonly seen in adolescents)

47. Pathophysiology
 Disease of genetic and hormonal factors
 Increased androgens
 Increased sebaceous gland activity
 Propioni bacterium acne organisms

48. Treatment
 a) Comedolytics
 Tretinoin (trans-retinoic acid)
 Benzoyl peroxide (BenoxyIR, PersoleforteR)
 Combination of Tretinoinand Benzoyl peroxide
 B) chemotherapy
 (c) exfoliant like element sulphur, salicylic acid
 (D) comedone extraction
 (E) corticosteroids (intralesional)
 (F) estrogens and anti-androgens

49.  (G) Vitamin A
 (H) NSAIDs
 (I) acne surgery (incision & drainage)
 (J) cryotherapy
 (K) UV rays (UVB)
 (L) diet
 (M) cosmetic surgery

50. Alopecia areata
 It is a type of hair loss that occurs when the immune system mistakenly
attacks hair follicles.
 The Damage to the follicle is usually not permanent and the condition is
characterized by:
 Lesions are well defined, single or multiple, round or oval areas of complete
hair loss
 A svmptomatic, non-inflammatory and non-scarring lesions.

51. Common sites – affected…
 Scalp
 Eyebrows
 Beard region
 Any hair bearing area

52. Types:
 Alopecia Areata – Local patches
 Alopecia totalis – Whole scalp
 Alopecia universalis – scalp and body

53. Other features
 Nail changes
 Family history
 Ophiasis (primary patch develops in occipital region in children)

54. Patchy

55. Totalis

56. Universalis

57. Treatment
 Topical corticosteroids (Clobetasol)
 Intra lesional corticosteroid (Triamcinolone hexa-acetomide)
 Contact allergens/Topical sensitizes (di-nitro-chloro-benzene) (squaric-acid
di-butyl ester)
 Non-antigenic agents like phenol,resorcin
 PUVA (twice a week) Oral methoxypsoralen or Topical oxsoralen ointment +
UVA

58. Psoriasis

59.  It is a papulo-squamous disorder of skin. Character-zed by erythemato-
squamous lesions, vary in size from pinpoint to large plaques. May be
localized or generalised with pustular eruptions. It may affect the
joints/nails.
 1-3% of population is affected
 Affects both sexes equally in 3rd decade.
 Heredity factors plays a major role.
 HLA antigen (HLA-CW6) is the most important genetic marker.
 HLA-BW17- For higher familial incidence and advanced clinical disease
 HLA-B13 - For more reversible disease
 HLA-B27 - For psoriatic sacroilitis
 HLA-BW38 - For psoriasis and distal arthritis

60. Pathogenesis
 It’s debatable
 Rapid epidermal transit time, i.e., 3 4 days in contrast to the normal 26 to 28
days
 Shortened cell cycle time (37 hours rather than 163hours)
 Recruitment of the resting cells into the active cell cycle
 Accelerated epidermopoiesis
 Lack of cell maturation and keratinization henceforth will lead to the
condition clinically, histologically and chemically

61. Psoriasis can be precipitated by:
 Trauma
 Infection
 Endocrine factors
 Climate
 Emotional stress
 Drugs (chloroquine, lithium, carbonate, steroids, beta-blockers, etc…)

62. Psoriasis patient have:
 Decrease in T cells
 Increased in arachidonic acid
 Increase polyamines
 High concentration of lipid and phospholipids
 Increase acid muco-polysaccharides

63. Clinical features:
 characterized by well circumscribed, sharply demarcated erythematous
papules and/or plagues.
 These are covered by silvery or grayish white scales.
 Woronoff's ring - a white blanching ring around the lesion.
 After grattage of scales, candle grease sign can be observed› Berkley's
membrane (thin peel like membrane) comes off-> A surface, which is wet
with multiple pinpoint bleeding is revealed(Auspitz's sign).
 Elbows, knees, scalp and lumbosacral area mainly affected.
 Nail involvement is common.

64. Psoriasis may be present as any one of
the following clinical variants:
1. Chronic plaque psoriasis
2. Guttate psoriasis
3. Flexural psoriasis
4. Erythrodermic psoriasis
5. Pustular psoriasis
6. Psoriasis of the scalp : (Psoriasis vulgaris)
7. Palmo plantar psoriasis
8. Psoriatic arthritis
DIAGNOSIS : Purely Clinical

65. Treatment:
 Corticosteroids
 PUVA
 Methotrexate (MTX)
 Retinoids – synthetic derivative of Vitamin A – It inhibits inflammation,
proliferation and terminal differentiation
 Cyclosporine – A (Latest drug) – Increases suppressor T-helper cell population

66. Leukoderma /
Vitiligo

67. Vitiligo
 These are (irregular) white patches of the skin.
Theories may involve:
1. Mistake theory (malformation)
2. Chemical theory (destruction of melanin)
3. Neurogenic theory

68. Causes:
 Mental disorders
 Chronic gastrointestinal disorders
 Hepatic dysfunction
 Tight clothes
 Occupational hazards
 Tattoos, gloves
 Neurogenic destruction
 Post burn/Trauma

69. Differential Diagnosis (D.D.)
 Worm infection
 Calcium deficiencies
 Vitamin deficiencies
 Allergies (Food)

70. Symptoms
 Alopecia / Greying of hair
 Pale-brown-white patches
 Hands, neck, back, wrist are affected

71. Treatment:
 PUVA
 Avoiding dying of hair
 Antioxidants
 Avoid citrus fruits, tamarind, fish, lobsters, crabs and prawns.

72. Leprosy

73. World Leprosy day???

74. Leprosy
 Chronic infectious disease caused by Mycobacterium Laprae
 First discovered in 1873 by Norwegian physician.
 First known written evidence related leprosy found in egyptician dynasty in
around 1500 B.C.
 It also well recognised in old literatures in ancient India and China.
 As per WHO reports India continuous to record highest number of new leprosy
cases in the world.

83. Thank you…