Chapter 16

Bacterial infections
 Resident flora of the skin
• The surface of the skin teems with micro-organisms, which are
most numerous in moist hairy areas, rich in sebaceous glands.
• Organisms are found, in clusters
• Mixture of harmless and poorly classified
– Staphylococci: Staphylococcus epidermidis, NOT aureus
– Micrococci
– Diphtheroids:
• Aerobic diphtheroids predominate on the surface
• Anaerobic diphtheroids (Propionibacteria sp.) deep in the
hair follicles.
– Several species of lipophilic yeasts also exist on the skin.
 Erythrasma
• Some diphtheroid members of the skin flora produce
porphyrins.
• Symptom-free macular wrinkled
• Slightly scaly pink
• Brown or macerated white areas
• Found in the armpits, groins or between the toes.
• In diabetics, larger areas of the trunk may be involved.
• Diagnosis (Wood’s light 🡪 coral pink).
• DDx: tinea pedis
• Treatment:
– Topical fusidic acid
– Topical antifungal Miconazole (if it coexists with tenia
pedis)
• Macular wrinkled
• Slightly scaly pink

Wood’s light 🡪 coral

pink
 Pitted keratolysis
• The combination of unusually sweaty feet and
occlusive shoes encourages the growth of
diphtheroid organisms that can digest keratin.
• The result is a cribriform pattern of fine punched-
out depressions on the plantar, coupled with an
unpleasant smell (of methanethiol).
• Fusidic acid ormupirocin ointment is usually
effective, and antiperspirants can also help.
• Occlusive footwear should be replaced by
sandalsand cotton socks if possible.
 Staphylococcal infections
• S.aureus is not part of the resident flora
• Carried in nostrils, perineum or armpits
• Multiply on areas of diseased skin such as eczema
• Cause:
1. Impetigo
2. Ecthyma
3. Furunculosis (boils)
4. Carbuncle
– Scalded skin syndrome
– Toxic shock syndrome
 Impetigo
• Erosions (part of epidermis is lost, so no scar after healing) in
the stratum corneum
• Caused by
– Staphylococci (bullous type)
– Streptococci/ staphylococci (non-bullous/crusted ulcerated)
honey colored crusts
– Both
• S. aureus produce Exfoliative toxins, which cleave the cell adhesion
molecule desmoglein, If the toxin
– Localized 🡪 blisters of bullous impetigo
– Generalized 🡪 widespread blistering as in the staphylococcal
scalded skin syndrome.
• A thin-walled flaccid clear blister
• May become pustular
• If rupture leave
• Extending area of exudation
• Yellowish varnish-like
crusting.
• Multiple
• Particularly around the face.
• More obviously bullous in infants. Fig. 16.2 Widespread
• A follicular type of impetigo impetigo due to Staph.
aureus with erosions
(superficial folliculitis) is also
and cruising. Atypical
common and is also called by staph. presentation, the
. typical is more
localized honey
colored crusted lesions
with erosions around
mouth and nose.
Course:
• Spread rapidly through a family or class.
• Clear even without treatment.
Complications:
• Acute glomerulonephritis (Streptococcal impetigo).
DDx:
• Herpes simplex (color in impetigo honey colored // // causative agent: Herpes simplex by
HSV1, Impetigo: staph aureus or strep // // age group: impetigo: more in children, herpes:
any age group // // recurrence: Herpes: recurrent, impetigo usually not recurrent // //
prodromal symptoms in herpes simplex (itching, tingling, burning sensation before the
appearance of the vesicles, no present in impetigo)
• Eczema.
• Scalp lice (esp. in recurrent impetigo of head & neck which can be due to the head lice)
Investigation:
• Clinically.
• Swab & culture
Treatmant: (after investigation)
• Systemic antibiotics (flucloxacillin, erythromycin or cefalexin)
• penicillin V (nephritogenic strain of streptococcus)
• Removal of crusts by compressing them & application of a topical antibiotic (neomycin,
fusidic acid, mupirocin or bacitracin)
 Ecthyma
• Full thickness ulcer (epidermis and part of dermis is
lost) 🡪 Heals with scarring
• Ulcers forming under a crusted surface infection.
• The site may have been that of
– Insect bite
– Neglected minor trauma
 Folliculitis
• Definition: An inflammation of the hair follicles due to infection(staph), skin injury or irritation.

• Classified into two types:

- Superficial (impetigo of bockhart)
- Deep (furuncles, carbuncles), inflammation of the whole hair follicle and adjacent skin

Superficial Folliculitis:
• Characterized by erythematous follicular based papules and pustules.
• Affects the upper part of the hair follicle and the skin directly next to the follicle.
Treatment:

Mild cases of folliculitis often improve with home care. The following approaches may help
relieve discomfort, speed healing and prevent an infection from spreading:
Apply a warm, moist washcloth or compress. Do this several times a day to relieve discomfort
and help the area drain, if needed. Moisten the compress with a saltwater solution.
Apply over-the-counter antibiotics. Try various nonprescription infection-fighting gels, creams
(mupirocin or clindamycin used for 7–10 days)
and washes (contain chlorhexidine or sodium hypochlorite).
⮚ When staphylococcal folliculitis is widespread or recurrent, oral β-lactam antibiotics,
tetracycline, or (depending on local resistance patterns) macrolides can be prescribed.
Apply soothing lotions.
Try relieving itchy skin with a soothing lotion or an over-the-counter hydrocortisone cream.

Clean the affected skin.

Gently wash the infected skin twice a day with antibacterial soap. Use a clean washcloth and
towel each time and don't share your towels or washcloths. Use hot, soapy water to wash these
items. And wash clothing that has touched the affected area.

Protect the skin.

If possible, stop shaving, as most cases of barber's itch clear up a few weeks after you stop
shaving.
 Furunculosis (boils)
• Acute pustular infection of a hair follicle
• Usually with Staphylococcus aureus
• Adolescent boys are especially susceptible to them.
• Tender, red nodule enlarges, may discharge pus
• its central ‘core’ before healing to leave a scar
• Fever and enlarged draining nodes are rare.
• Most patients have 1-2 boils only, and then clear.
• The sudden appearance of many furuncles suggests a virulent
staphylococcus including strains of community-aquired MRSA. Take a
sample from carrier sites (nostril, groin, axilla) and the pustule itself, and
make sure of antibiotics sensitivity, exclude immunocompromised status
(DM, long term steroid treatment), screen family members. Especially if
recurrent or chronic.
• A few unfortunate persons experience a tiresome sequence of boils (chronic
furunculosis).
• Tender
• Red
• Nodule enlarges
• May discharge pus

Enlarged swollen mass

with purulent material
Fig. 16.3 Chronic furunculosis.
Complications:
• Cavernous sinus thrombosis (boils in central face).
• Septicaemia
• Immunocompromised: cellulitis
• Scalp lesion left untreated: scarring alopecia

DDx:
• Hidradenitis suppurativa (groin and axillae) aka acne inversa.
Multifactorial, exact pathogenesis is not known. We can see sinuses
and tracts.

Investigations in chronic furunculosis

• General examination: skin desease (scabies, pediculosis, eczema).
• Test the urine for sugar. Full blood count.
• Culture swabs from lesions and carrier sites.
• Immunological evaluation only if the patient has recurrent or
unusual internal infections too
Treatment

• Acute episodes:
• Incision & drainage.
• Systemic antibiotics (fever or immunosuppressed).
• Chronic furunculosis
• Topical antiseptic or antibiotic (treat carrier sites twice
daily for 6 weeks).
• Treat family carriers in the same way.
• Stubborn cases
• systemic antibiotic (for 6 weeks)
• Daily bath using an antiseptic soap.
• Improve hygiene and nutritional state, if faulty.
 Carbuncle
• A group of adjacent hair follicles becomes deeply infected
with Staphylococcus aureus
• Swollen painful suppurating area
• Discharging pus from several points.
• More severe than boil.
• Diabetes must be excluded.

Treatment:
• Topical and systemic antibiotics.
• Incision and drainage (speed up healing)

• DDx: fungal kerion in unresponsive carbuncles.

• Swollen painful
• Discharging pus
Chapter 16

Viral infections
 Viral infections
• Viral warts
• Varicella (chickenpox)
• Herpes zoster
• Herpes simplex
 Viral warts
• Highest prevalence in childhood
Cause:
• Human papilloma virus (HPV)
• Types
– HPV-1, 2 & 4 are found in common warts
– HPV-3 is found in plane warts
– HPV-6, 11, 16 & 18 are most common in genital warts.
• Infections occur when
– Wart virus in skin scales comes into contact with breaches
in the skin or mucous membranes
– Immunity is suppressed and dormant viruses escape from
their resting place in the outer root sheaths of hairs.
Warty appearance
• Irregular
hyperkeratotic surface
• Vertical shoulders

Fig. 16.17 Viral warts –

variations on the theme.
 Common warts
• Smooth skin-coloured papule
• Often more easily felt than seen
• Usually occur on the hands, also often on the face and genitals.
• They are more often multiple than single.
• Köbner phenomenon
• Pain is rare.
 Fig. 16.18 Typical common warts
on the fingers.

Fig. 16.19 Multiple hand warts in a

fishmonger showing the Köbner
phenomenon. Linear pattern
 Plane warts
• Smooth flat-topped papules
• Usually skin-coloured or light brown
• Most common on the face, brow, backs of the hands
& shaven legs of women.
• Multiple
• Painless
• Köbner phenomenon.
• Resolve spontaneously by inflammation as a result of
an immunological reaction.
Fig. 16.22 Plane warts
resolving with
inflammation.
 Plantar warts
• Rough surface
• Protrudes slightly from the skin
• Surrounded by a horny collar.
• DDx: corns (bleeding capillary loops allows plantar
warts to be distinguished from corns).
• Multiple
• Painful

Fig. 16.20 Solitary plantar wart on the heel.

Corns
 Facial warts
• Most common in the beard area of
adult males and are spread by shaving.
• Digitate appearance
• Ugly
• Painless
Treated by:
• Electrocautery
• Hyfrecator
• Shaving should be with
– Brushless foam
– Disposable razor
 Anogenital warts
(condyloma acuminata)
• Papillomatous cauliflower-like lesions
• Moist macerated vascular surface
• They may coalesce to form huge fungating
plagues causing discomfort and irritation.
• The vaginal and anorectal mucosae may be
affected.
• Complication: cervical cancer (pap
smear), especially in high risk HPV 16,18
• Anogenital warts in children
– Raises the spectre of sexual abuse, so Fig. 16.23 Multiple
examination and proper history are penile warts in an
immunosuppressed
important (bruises, multiple warts) patient.
– Usually caused by autoinoculation
 Course
• Resolve spontaneously in the healthy
• 30% of patients within 6 months
• 65% within 2 years
• Capillary thrombosis (punctate
blackening): good sign for healing.
Fig. 16.24 Spontaneous resolution of a
• Mosaic warts
group of plantar warts. The blackness
– Slow to resolve is caused by capillary thrombosis.
– Often resist all treatments
• Warts persist and spread in
immunocompromised patients
(recurrence, and higher risk of cancer)
• 70% of renal allograft recipients will have
warts 5 years after transplantation. RCC
Complications
1. Very painful (plantar warts)
2. Epidermodysplasia verruciformis
(not a complication, but a variant
of extensive warts)
3. . Cervical carcinoma
– Rare
– HPV 16 & 18 predisposes to.
– Skin cancer, especially on
light-exposed areas
(immunocompromised
patients)
DDx:
1. Molluscum contagiosum.
2. Plantar corns
– No capillary bleeding on
paring.
– Central keratotic core &
painful.
3. Granuloma annulare lesions
(annular).
4. Condyloma lata (syphilis).
5. Amelanotic melanomas & SCC.
 Treatment
1. No treatment (Resolve spontaneously)
2. Wart paint –keratolytic agents-
– Most contain salicylic acid (12–20%).
– Applied once daily, after
• Moistening the warts in hot water for at least 5 min
• Drying
• Dead tissue and old paint are removed
– Not be applied to
• Facial skin
• Anogenital skin
• Adjacent eczema
3. Cryotherapy (less likely to cause scars)
– Liquid nitrogen (at −196°C)
– Painful
4. Electrosurgery
Anogenital warts
Solitary, stubborn or
• Imiquimod (5% cream).
painful warts
– Irritants & should be used
• cure is not assured & scar
carefully
often follows
– Immune response modifier
• Removed under local
• Podophyllotoxin (0.5% solution anaesthetic with a curette
or 0.15% cream)
• Bleomycin
– Irritant & should be used
carefully
– Not be used in pregnancy
Prevention:
• Vaccine against the relevant
HPV subtypes (prevents the
infection not treat it, some vaccine
cover up to 9 strains and even more)
Fig. 16.25 A wart treated with Fig. 16.26 Multiple scars following the
cryotherapy: area includes a small frozen injudicious surgical treatment of warts.
halo of normal surrounding skin.
 Varicella (chickenpox)
• Cause: herpes virus varicella-zoster
• Spread by the respiratory route
• Incubation period is about 14 days.
Presentation: (polymorphic lesions –vesicles, papules, pustules-
simultaneously //different types of lesions at the same time// )
• Slight malaise, followed by papules, which turn rapidly into clear vesicles on
a pink base (dewdrops on a rose petal).
• Vesicles soon become pustules and then umbilicate.
• Over the next few days the lesions crust and then clear, sometimes leaving
white depressed scars.
• Itchy
• Centripetal (lesions directed toward the center: starts on face and
forehead then spreads to trunk and chest)
• Second attacks are rare.
• Fatal in immunocompromised patients.
Evolution of lesions
Dewdrop on a rose petal: a thin-walled vesicle
with clear fluid forms on a red base.
Characteristic

The vesicle becomes cloudy and depressed in

the center (umbilicated), the border is irregular
(scalloped).

A crust forms in the center and eventually

replaces the remaining portion of the vesicle at
the periphery.
Complications
• Pneumonitis
• Secondary infection of skin lesions.
• Haemorrhagic or lethal chickenpox.
• Scarring.

DDx: Smallpox (mainly centrifugal)

Investigations: Tzanck smear – multinucleated giant Hemorrhagic chickenpox.

cells- Numerous vesicular and
Treatment bullous lesions with
hemorrhage at the base.
• Aciclovir, famciclovir and valaciclovir
– Immunocompromised patients
– prophylactic aciclovir can also be used to prevent
disease if given within a day or two of exposure.
• Calamine lotion topically (in mild attacks)
• A live attenuated vaccine is now available
(prophylactic role, once we have the lesion we can’t
give it)
Numerous lesions on the trunk
(centripetal distribution).
 Herpes zoster (Shingles)
• Caused by the herpes virus varicella-zoster (reactivation)
• The incidence is high, when weaken normal defense
mechanisms in:
– Old age
– Hodgkin’s disease
– AIDS
– Leukaemia
• Shingles does not occur in epidemics
• Patients with zoster can transmit the virus to others in whom it
will cause chickenpox.
 Presentation and course
• Start with a burning pain
• Soon followed by erythema and grouped
• Sometimes blood-filled vesicles scattered over a dermatome.
• The clear vesicles quickly become purulent
• Over the space of a few days burst and crust.
• Scabs usually separate in 2–3 weeks, sometimes leaving depressed depigmented
scars.
• Unilateral
• It may affect more than one adjacent dermatome.
• The thoracic segments and the ophthalmic division of the trigeminal nerve are
involved disproportion often.
• Generalized chickenpox-like eruption accompanying segmental zoster, particularly
if the lesions are unusually haemorrhagic or necrotic, should raise suspicionsately
of:
– Immunocompromised state
– Malignancy`
Herpes zoster may involve >1 adjacent dermatomes

Involvement of a single
mandibular branch of the fifth nerve thoracic dermatome
 Hypertrophic scars
Several scars localized
to a dermatome
Complications:
• Secondary bacterial infection is common.
• Motor nerve involvement is uncommon, but has led to paralysis of
ocular, facial muscles, diaphragm & bladder.
• Corneal ulcers and scarring (zoster of the ophthalmic division of the
trigeminal nerve). A good clinical clue here is involvement of the
nasociliary branch (vesicles grouped on the side of the nose).
• Persistent neuralgic pain, after the acute episode is over, is most
common in the elderly.
DDx:
• Pain (before the rash has appeared)
– Acute appendicitis
– Myocardial infarction
• An early painful red plaque may suggest cellulitis
• Herpes simplex
• Eczema
• Impetigo
Investigations:
• Cultures (only positive in 70%)
• Biopsy or Tzanck smears
– Multinucleated giant cells
– Ballooning degeneration of keratinocytes
Treatment:
• Systemic treatment (within the first 5 days) systemic acyclovir but
check KFT, and tell patient to drink plenty of water to prevent
ARI.
• Early: Famciclovir and valaciclovir
• Late: (supportive)
– Systemic treatment is not likely
– Rest
– Analgesics
– Calamine
– Prevention (|vaccine) better than treatment
 Herpes simplex
• Cause: Herpesvirus hominis
– Ubiquitous
– Carriers continue to shed virus particles in their saliva or
tears
– The virus may become latent, within nerve ganglia
• 2 types:
• Type I are usually extragenitalia (oral cavity)
• Type II virus occur mainly on the genitals
• Route of infection is through
– Mucous membranes
– Abraded skin
Primary infection (acute gingivostomatitis): Recurrent (recrudescent) infections
• Malaise, headache, fever and enlarged • Same place each time.
cervical nodes.
• Precipitated by
• Vesicles, painful & itchy, soon turning into
ulcers, seen scattered over the: – RTI (cold sores)
– Lips – Ultraviolet radiation
– Mucous membranes. – Menstruation
• The illness lasts about 2 weeks. – Stress.
• Heals without scar, Rx: acyclovir (Topical • Common sites
or systemic) – Face
Herpetic whitlow
– Lips (type I)
• Direct inoculation
– Genitals (type II)
• Pus-filled blisters on a fingertip.
– Lesions can occur anywhere.
Primary type II
• Transmitted sexually • Tingling, burning or pain is followed
within a few hours by
• Multiple
• Painful • Erythema and clusters of tense vesicles.
• Genital or perianal blisters which rapidly • Crusting occurs within 24–48 h
ulcerate. • The whole episode lasts about 12 days.
 Evolution of lesions:
Vesicles appear on a red base.

The center becomes depressed

(umbilicated).

Crusts form
The lesions heal with or without scarring.
Fig. 16.29 The grouped vesicles of herpes
simplex, here provoked by sunlight. Those in Primary infections
the lower group are beginning to crust.

A small group of
vesicles on an
erythematous base are
the primary lesion
 Vesicles evolve to pustules and
Sun exposure triggered this extensive recurrence. become

Vesicles of recurrent herpes

 Recurrent oral-labial herpes
Recurrent herpes in an HIV patient.

Herpetic whitlow
Herpes simplex of the skin: vesicular stage. The
uniform size
Eczema herpeticum. Numerous
umbilicated vesicles of the
face.

Eczema herpeticum. First crop of

lesions has formed crusts; a new lesion
has appeared on the ear.

Complications
• Herpes encephalitis or meningitis
• Disseminated herpes simplex
• Eczema herpeticum: patients with
atopic eczema are particularly
susceptible to widespread
cutaneous herpes simplex
infections. Those looking after
patients with atopic eczema
should stay away if they have cold
sores.
• Recurrent dendritic ulcers leading
to corneal scarring.
• Erythema multiforme
Investigations:
• Culture
• Antibody titres rise with primary,
but not with recurrent infections.
Treatment:
• Sunblock
• Dapping with the surgical spirit
• Topical bacitracin, mupirocin,
framycetin or fusidic acid (20
infection)
• Aciclovir cream ( applied 5-6X a
day for the first 4 days of the
episode)
• More effective still is oral aciclovir
200 mg five times daily for 5 days
• Recurrences in the
immunocompromised can usually
be prevented by long-term
treatment at a lower dosage.