This document provides an overview of various skin infections. It discusses bacterial infections like cellulitis, erysipelas, folliculitis, impetigo and furunculosis. It also covers fungal infections such as tinea, candidiasis, pityriasis versicolor and deeper fungal infections. Viral infections including warts and herpes are mentioned. Finally, it summarizes parasitic infestations like scabies, larva migrans and head lice. For each condition, it provides details on pathogenesis, clinical features, diagnosis and treatment.

1. Overview of Skin infections
By
Dr Bolaji Otike-Odibi

2. Introduction
• Skin infections are dermatological conditions caused by bacteria,
viruses, fungi and parasites. They are numerous and tend to increase
in humid areas and can be associated with poor hygiene and
underdevelopment.
• It is important for us to know how to diagnose and treat some of
these skin infections because they would present commonly in our
clinics.

3. Bacterial Skin infections
1) Cellulitis
2) Erysipelas
3) Folliculitis
4) Impetigo
5) Furunculosis

4. Cellulitis
• Are soft tissue infections characterized by an acute, diffuse,
spreading edematous, suppurative inflammation of the dermis and
subcutaneous tissues often associated with systemic symptoms of
malaise, fever and chills.
• Differentiated from erysipelas by
1) Lesions of cellulitis are not raised and demarcation from uninvolved
skin is indistinct.
2) Skin is hard on palpation and is extremely painful.

5. • Staph Aureus and GAS are by far the most common aetiologic agents.
• Other bacteria are GBS, Pneumococcus and a variety of gram negative
bacilli.
Risk Factors: Drug and alcohol abuse, cancer and cancer chemotherapy,
DM, cirrhosis, nephritic syndrome, malnutrition, renal failure.
I.P- Few days
Prodrome: Malaise, anorexia, fever, chills can develop rapidly before
cellulitis is apparent clinically. Higher fever (38.5%) and chills usually
associated with GAS.

6. Distribution: Lower leg following interdigital tinea, arm in young male
consider i.v drug use, face following rhinitis and conjunctivitis.
Treatment: B-lactam antibiotics with activity against penicillinase
producing S.aureus are the usual drugs of choice.
Indications for i.v use- rapidly spreading lesions
- Systemic symptoms eg fever, chills
- Immune compromise
- Oral therapy- Healthy individuals with early symptoms in the absence of
systemic symptoms.

8. Erysipelas
• Distinct type of superficial cutaneous cellulitis with marked dermal
lymphatic vessel involvement presenting as a painful, bright red, raised,
oedematous, indurated plaque with advancing raised borders sharply
marginated from the surrounding normal skin.
- Caused by GAS, very uncommonly group C or G streptococcus and
rarely due to Staph aureus
- Sites: Face, lower legs, areas of preexisting lymphedema, umbilical
stump.
- Rx is like cellulitis

9. •

10. Folliculitis
• Infectious folliculitis occurs in the upper hair follicle, characterized by
a follicular papule, pustule, erosion, or crust at the follicular
infundibulum; infection can extend deeper into the entire length of the
follicle.
Variants- S.Aureus Folliculitis: Can be superficial(infundibular) or deep
(sycosis) extension beneath infundibulum with abscess formation.
Gram-Negative Folliculitis: Occurs in individuals with acne vulgaris
treated with oral antibiotics. Characterized by small follicular pustules
and /or larger abscesses on the cheeks and by the nostrils.

11. • Hot tub folliculitis: Occurs in the trunk after immersion in spa water.
Caused by P.aeroginosa. Multiple follicular pustules occur few days
after bathing in hot tub.
Investigations: Direct microscopy for S.aureus gram positive.
KOH Preparation: To rule out dermatophytes.
Prophylaxis: Correct underlying predisposing condition. Washing with
antibacterial soap or benzoyl peroxide preparation.
Bacterial folliculitis- Penicillins, cephalosporins,macrolides,tetracyclines

12. • Gram negative folliculitis- Discontinue current antibiotics. Wash with
benzoyl peroxide. Use ampicillin, trimethoprim-sulfamethoxazole qid,
• Isotretinoin.

13. Impetigo
• S.aureus and GAS (S.pyogenes) can cause superficial infection of the
epidermis (impetigo) which may extend into the dermis (ecthyma)
xterized by crusted erosions or ulcers.
They may arise as primary infections in minor superficial breaks in the
skin or as secondary infections of preexisting
dermatoses.(impetiginiztion or secondary infection).
Lab invs- Gram stain, culture, dermatopathology.
Rx-Prevention-daily bath, benzyl peroxide wash
Topical-mupirocin 3x dly for7-10days, cephalosporin,erythromycin

15. Fungal infections
• Superficial :
• 1) Tinea corporis
• Tinea unguim
• Tinea Cruris
• Tinea Capitis
• Candidal infections
• Pityriasis Versicolor

16. Superficial fungal infections
• They are the most common of all mucocutaneous infections. Often
caused by overgrowth of transient or resident flora associated with a
change in the microenvironment of the skin.
The fungi causing these are dermatophytes, candida spp and
malassezia furfur.
Dermatophytes are made up of Epidermophyton, Trichophyton and
Microsporon. They are a unique grp of fungi capable of infecting
nonviable keratinized cutaneous structures including statum corneum,
nails and hair.

17. • Dermatophytoses of keratinized epidermis: Tinea facialis, corporis,
cruris, manus and pedis.
• Dermatophytoses of nail apparatus: Tinea unguim (toenails,
fingernails)
• Dermatophytoses of hair and hair follicle: Tinea capitis and tinea
barbae.
• Pathogenesis: Dermatophytes synthesize keratinases that digest
keratin and sustain existence of fungi in keratinized structures.

18. • Clinical features: Tinea Pedis
• Interdigital-1) Dry scaling
• 2)Maceration, peeling and fissuring of toe webs.
• Moccasin type- Well demarcated erythema with minute papules on
margin, fine white scaling and hyperkeratosis. (Confined to heels,
soles, lateral borders of feet.)
• Inflammatory/Bullous type- Vesicles or bullae filled with clear fluid
• -sole,instep, webspaces

19. • Tinea Manuum- Well demarcated scaling patches, hyperkeratosis and
scaling confined to palmar creases, fissures on palmar hand. Borders
well demarcated, central clearing.
• Tinea Cruris- Large scaling, well demarcated dull red/tan/brown
plaques. Central clearing. Papules, pustules may present at margins.
• Tinea corporis- Sharply marginated plaque with central clearing.
• Tinea capitis- A large round hyperkeratotic plaque of alopecia due to
breaking off of hair shafts close to the surface. Circular in shape.

20. • Host factors that facilitate dermatophyte infections: atopy, topical and
systemic glucocorticoids, ichthyosis, collagen vascular dx.
Local factors favoring dermatophyte infection: sweating, occlusion,
occupational exposure, geographic location, high humidity (tropical or
semitropical climates.
Investigations: KOH 5 to 20% ,Wood’s lamp, Fungal Cultures

21. Treatment
Topical antifungals- may be effective for treatment of dermatophytosis
of the skin but not for hair or nails.
Examples are Terbinafine, miconazole,ketoconazole.
Systemic antifungal- infection of keratinized skin: use if lesions are
extensive or if infection has failed to respond to topical preparations.
Required for treatment of tinea capitis and unguim.
1) Terbinafine 250mg dly
2) Azole/imidazoles- itraconazole-100mg, fluconazole
100,150,200mg,ketoconazole- 200mg
3) Griseofulvin-250-500mg

23. Pityriasis Versicolor
• Characterized by well dermacated scaling patches with variable
pigmentation.
• Occurring most commonly on the trunk.
• Most common in young adults.
• Predisposing factors - High temp, relative humidity, oily skin,
hyperhydrosis, steroid Rx.
• No symptoms most of the time, rarely mild pruritus. Mainly a
cosmetic concern

25. • Lesions present as sharply marginated macules, off white or brown of
varying intensities.
• 0ccurs mostly on the upper trunk, upper arms, neck, abdomen,
axillae, groins, thighs and genitalia.
• Infection can persist for years if predisposing conditions persist.

26. • Dyspigmentation persist for mths after infection has been cleared.
• Management- Topical
• Selenium sulphide shampoo
• Ketoconazole shampoo
• Systemic therapy , Fluconazole,
• Itraconazole

27. • Deep:
• 1) Mycetoma
• 2) Chromomycosis
• 3) Sporotrichosis

28. Subcutaneous mycoses
Are a heterogenous group of fungal infections that develop at the site
off transcutaneous trauma. Infection slowly evolves as the aetiologic
agent survives and adapts to adverse host environment. The diagnosis
rests on clinical presentation, histopathology and culture of the
aetiologic agents. Eg Mycetoma,Chromomycosis and sporotrichosis.
Mycetoma is a chronic suppurative infection originating in
subcutaneous tissue characterized by the presence of grains, which are
are tightly clumped colonies of the causative agent. Painless swelling,
woody induration and sinus tracts that discharge pus intermittently are
characteristic.

29. • Pathogenesis- Pathogens live in soil and enter through breaks in the
skin. Only organisms that can survive at body temperature can
produce mycetoma.
• Lab investigations- Smear of pus from lesion granules show medlar
bodies visualized on KOH preparations as microbial colonies.
• Dermatopathology- Pseudoepitheliomatous hyperplasia of epidermis.
Grains are found in purulent foci surrounded by fibrosis and
mononuclear cell inflammatory cell response.
Culture- Isolate organism. Imaging: CTscan and echosonography define

30. • the extent of involvement. Xray of bone shows multiple osteolytic
lesions (cavities) periosteal bone formation.
• Mgt- Surgery
• Medicosurgical Approach- bulk reduction with effective antimicrobial
agent given.
Systemic Antimicrobial therapy: Usually continued for 10months

31. Mycetoma

32. • Chromomycosis: Is a chronic localized invasive fungal infection of skin
and subcutaneous tissues caused by pigmented (dematiaceous or
dark-walled) fungi. Verrucous plaques usually occur on the leg or
foot. Fonsecaea pedrosoi, F.compacta.
• Lab investigations- Smear of Pus from lesion. Medlar bodies visualized
in 10 to 20% KOH preparation as black dots. Hyphal forms can be seen
in crusts, pus and exudate.
• Dermatopathology-Warty granuloma, medlar bodies
• Culture- Organism in sabouraud’s agar show velvety green to black,
restricted, slow growing colonies.

33. • Treatment- Rx is continued for at least 1year.
• Sporotrichosis- commonly follows accidental inoculation of the skin
and is characterized by ulceronodule formation at the inoculation
site.
• Aetiology- Sporothrix schenckii, a dimorphic fungus, living as a
saprophyte on plants in many areas of the world.
• Touch Preparation- KOH solution added to smear from lesional skin
biopsy helps visualize multiple yeast forms.

34. Chromomycosis

35. • Management- Oral antifungal agents

36. Spsorotrichosis

37. Parasitic infestations
1) Scabies
2) Cutaneous Larva Migrans
3) Head Lice

38. Scabies
• Is an infestation by the mite sarcoptes scabiei, usually spread by skin
to skin contact, characterized by generalized intractable pruritus,
papules, nodules and post inflammatory hyperpigmentation.
• Pathogenesis: Hypersensitivity of both immediate and delayed types
occurs in the development of lesions other than burrows.
• For pruritus to occur sensitization of S.scabiei, must take place.
• Clinical Features: pruritus intense widespread, interferes with sleep.
• Often present in family members
• Intraepidermal burrows,scabetic nodules-penis,scrotum,axilla,waist.

39. • buttocks, areola
• Investigations- Microscopy- Scabetic mites,eggs and faecal pellet
• Dermoscopy- Jet with contrail sign
• Dermatopathology- Scabietic burrow
• Treatment- Permethrin cream from neck downwards leave for 8hrs
then wash off. Repeat in 1wk
• Benzyl benzoate 10% and 25%- several regimen recommended.
• Systemic ivermectin: 200ug/kg PO ,2 doses I week apart.
• Washing of beddings and underwears 2x, 1 week apart

40. • Treatment of close contacts.
• Treatment of secondary bacterial infection.
• Treatment of pruritus.

41. Pediculosis capitis (Head Lice)
• Is an infestation of the scalp by head louse, which feeds on the scalp
and neck and deposits its eggs in the hair.
• Few symptoms but is a major cause of concern.
• Transmission is by shared hats, caps, brushes, combs, head to head
contact.
• Symptoms are pruritus of the back and sides of scalp. Scratching and
secondary infection associated with occipital and /or cervical
lymphadenopathy.

42. • Microscopy- Louse or nit on a hair shaft can be examined to confirm
the gross examination of the scalp and hair
• Fomite/environmental control: Avoid contact with possibly
contaminated items such as hats, headsets, bedding. They should be
washed and dried on the hot cycle of a drier.
• Combs and brushes should be soaked in rubbing alcohol for 1hr.
• Rx- Permethrin 1% over the counter, 5% prescription. Apply to
infected areas then wash off after 10mins. Repeat 7 to 14days.
• Malathion 0.5% in 78% isopropyl alcohol

43. Viral infections
• 1) Warts- Common
2) Genital
3) Herpes Simplex 1 and 2

44. Warts
• 3 clinical manifestations of cutaneous Human papilloma virus
infection.
• Common Warts ( Verruca vulgaris)
• Plantar warts
• Flat warts
• Human papillomavirus are double-stranded DNA, some types
commonly infect keratinized skin. Warts are a discrete benign
epithelial hyperplasia with varying degrees of surface hyperkeratosis

45. • Manifested as minute papules to large plaques. Lesions may become
confluent forming a mosaic. The extent of lesions is determined by the
immune status of the host.
Verruca vulgaris (common warts): Firm papules, 1-10mm or rarely
larger, hyperkeratotic, clefted surface with vegetations. Palmar lesions
disrupt the normal line of fingerprints. Xteristic red or brown dots are
better seen with hand lens and are pathognomonic, representing
thrombosed capillary loops.

46. • Verruca plantaris (Plantar Warts) : Early small shiny sharply
marginated papule---plaque with rough hyperkeratotic surface
studded with brown black dots.
• Verruca Plana (Flat warts): Sharply defined flat papules, flat surface.
The thickness of the lesion is 1 to 2mm skin colored or light brown.
• Epidermodysplasia verriciformis: Flat topped papules. Pityriasis
versicolor like lesions, particularly on the trunk. Skin colored, light
brown, pink, hypopigmented.
• Dermatopathology: Acanthosis, papillomatosis, hyperkeratosis.
Characteristic feature is foci of vacuolated cells.

47. • Treatment: Aggressive therapies which are often quite painful and
may be followed by scarring are usually to be avoided because the
natural hx of cutaneous HPV infection is spontaneous resolution in
months or years.
• Patient initiated therapy: 10-20% salicylic acid and lactic acid in
collodion. 40% salicylic acid plaster for 1wk.
• Cryosurgery
• Electrosurgery
• Co2 laser

48. Genital warts
• When clinically symptomatic, lesions are barely visible papules to
nodules to confluent masses occurring on the anogenital area caused
by a mucosal HPV type.
• Aetiology- HPV is a DNA papovavirus that multiplies in the nuclei of
infected epithelial cells. More than 20 types of HPV can infect the
genital tract: types 6 and 11 most commonly.
Transmission: Through sexual contact: genital-genital, oral-genital,
genital-anal

49. Clinical features: 4 types
-Small papular
-Cauliflower-floret
-Keratotic warts
-Flat topped papules/plaques
Lab investigations-Acetowhitening
-Pap smear
-Dermatopathology
- Detection of HPV DNA

50. • Serology
• Rx- Imiquimod 5% cream, applied 3x a week usually at bedtime
• Podofilox- podophyllin
• Podophyllin 10-20%
• Electrodessication
• Carbon dioxide laser and electrodessication

53. Herpes virus 1 and 2
• Genital herpes is a chronic sexually transmitted viral infection,
characterized by symptomatic and asymptomatic viral shedding.
• In most cases both primary infection and recurrences are
asymptomatic.
• When symptomatic primary GH may present with grouped vesicles at
the site of inoculation associated with significant pain and regional
lymphadenopathy.
• Recurring outbreak of vesicles at the same site
• Shedding rate is higher from HSV-2 than HSV-1.

54. • Risk Factors- increases with no of sexual partners.
• Most clinical lesions are minor breaks in the mucocutaneous
epithelium presenting as erosions, abrasions, fissures.
• Management: First clinical episode- Acyclovir 400mg tid or 200mg 5x
a day for 7-10days.
• Recurrent episodes 400mg 5x a day for10days.

56. • THANK
YOU