Transcript BACTERIAL SKIN INFECTION

LECTURE DELIVERED AT THE NPMCN,
FACULTY OF FAMILY MEDICINE
WORKSHOP ON COMMON SKIN
DISORDERS , AT FMC, BIDA,NIGER
STATE.
BY;
DR. M D. PEMI(MB.,BS., FWACP).
CONSULTANT FAMILY PHYSICIAN,
 Learning
Objectives
 Introduction
 Epidemiology
 Pathogenesis/Predisposing factors
 Symptoms and Signs
 Clinical/Laboratory diagnosis
 Differential diagnosis
 Management, Conclusion,Bibliography
 To
let us know that bacteria skin diseases are
common.
 We should be able to recognize and discuss
differential diagnosis of each.
 To highlight predisposing factors for each.
 To highlight treatment modalities for each
 To highlight prevention/complication
 The
skin has normal flora just like any other
part of the body
 The flora is composed of aerobic cocci,
aerobic and anaerobic coryneform bacteria
etc
 Major function of skin flora is to prevent skin
infections by Providing ecological
competition for pathogenic microorganism
 By hydrolizing lipids of sebum to produce
free fatty acids which are toxic to many
bacteria
 The
ecology of particular areas of the skin is
determined by the availability of moisture,
presence of sebaceous lipids, and gaseous
environment
 The process of infection involves the
interaction between two organisms-the host
and the invader
 The clinical changes depends on the
organisms, its virulence, and patient’s
immunity
 Acute
bacteria infections generally produce
some or all of the classical features of acute
inflammation
 These cardinal signs includes;
erythema(redness), swelling/oedema,
heat/warmth, pain/discomfort
 Bacteria
skin infections are very common in
Family Medicine Practice settings
 Cellulitis, impetigo and folliculitis are the
most common bacteria skin infections seen
by the Family Physicians.
 The percentage office visits for cellulitis was
3.2percent in a cohort of 320,000 health plan
member.
 The
skin has normal flora whose function is
to provide
 Introduction-
folliculitis is infection of the
hair follicles.
 Classification is by the depth of involvement
of the hair follicles which could be
superficial or deep folliculitis.
 Hair follicle can become inflamed by physical
injury, chemical irritation or infection that
leads to folliculitis.
 A furuncle develops when the entire follicle
and surrounding tissues are involved.
 The
most common form is superficial
folliculitis
 It could be multiple or single lesion and can
appear on any skin bearing hair including
head, neck, trunk,buttocks and extremities
 S. aureus is the most common infectious
cause of folliculitis. However,commensal
organisms like yeast can be seen in
immunocompromised.
 Occasionally, gram negative folliculitis can
be seen in acne vulgaris patients treated
with long courses of antibiotics.
 The
use of hot tubs and whirl pools has been
classically associated with Pseudomonas
folliculitis.
 Patients with atopic dermatitis are at
increased risk because of higher rate of
colonization with S. aureus.
 Shaving, plucking or waxing hair, use of
topical corticosteroids, hot and humid
weather, and diabetes mellitus are all
predisposing factors
 The
appearance of the lesions depends on
the depth of follicular involvement.
 Lesions of superficial folliculitis(Bockhart’s
impetigo) are small, 1-4mm pustules or
crusted papules on an erythematous base
 Lesions of superficial folliculitis is usually
tender or painless pustules that heals
without scarring.
 Associated systemic symptoms is rare
A
deep folliculitis appears as large, tender,
erythematous papules, often with a central
pustule.
 The lesions may be pruritic and slighly
tender.
 The lesions are painful and may scar.
 The
diagnosis of bacterial folliculitis is
usually based on clinical inspection.
 Gram stain and bacterial cultures can help to
identify the causative organisms, especially
in recurrent or treatment-resistant cases.
 The differential diagnosis includes other
forms of folliculitis as well as acne vulgaris,
rosacea, ,pseudofolliculitis barbae , and
keratosis pilaris
 Superficial
bacterial folliculitis can be
treated with antibacterial washes that
contain chlorhexidine or triclosan.
 Antibacterial ointments (bacitracin or
mupirocin 2%) may also be used for 7–10 days
for localized lesions.
 When staphylococcal folliculitis is
widespread or recurrent, appropriate oral blactamase inhibitor antibiotics, macrolides
and lincosamides (e.g clindamycin),
flouroquinolones can be used.
 Despite
emerging resistance patterns,
treatment failure of bacterial folliculitis is
uncommon.
 Chronic S. aureus carriage can be treated
with mupirocin 2% ointment applied twice
daily to the nares, axillae/groin and/or
submammary area for 5 days.
 Pseudomonal
folliculitis is associated with
the use of whirlpools, hot tubs and, rarely,
swimming pools.
 P. aeruginosa gains entry via hair follicles or
breaks in the skin.
 The lesions arise 8–48 hours after exposure
and resolve in 7–14 days.
 There
are erythematous, papules and
pustules that rarely scar, but may result in
post inflammatory Hyperpigmentation .
 The lesions frequently occur in sites covered
by bathing suits, and the face and neck are
usually spared.
 Associated
symptoms do not imply systemic
spread of P. aeruginosa,
 These symptoms includes ;
 painful eyes,
 malaise, fever
 The
diagnosis can be confirmed by isolation
of P. aeruginosa, especially serotype O-11,
from lesions.
 The differential diagnosis includes S. aureus
folliculitis, insect bites, papular urticaria,
Majocchi’s granuloma, eosinophilic
folliculitis, miliaria and acne vulgaris.
 Treatment
is generally not indicated in
immunocompetent hosts as it is usually a
self-limited process.
 Lesions usually resolves spontaneously
within seven to ten days
 In the case of widespread eruptions,
recurrences, immunosuppression or
associated systemic symptoms, an oral
fluoroquinolone and topical gentamicin can
be used.
 By
appropriate cleaning of whirlpool or hot
tub.
 By maintaining appropriate chlorine levels
 Bromine/copper solutions are less common
alternatives used. Hand washing is an
important behaviour modification in the
prevention of spread.
 Sports participants should shower regularly
and all personal clothing should not be
shared
 Daily
application of 6.25% aluminium chloride
hexahydrate in completely anhydrous ethyl
alcohol was reported to be very effective in
treatment for chronic folliculitis of
unspecified type, except for scalp lesions.
A
furuncle is a tender, erythematous, firm or
fluctuant mass of walled-off purulent
material arising from the hair follicles.
 It is commonly known as boil or abscess.
 Carbuncles are an aggregate of infected hair
follicles that form broad swollen,
erythematous, deep and painful masses that
usually open and drain through multiple
tracts.
 Furuncles
tend to occur in adolescents and
young adults.
 S. aureus is the most common causative
organism, though recurrent furuncles in the
anogenital region can be secondary to
anaerobic bacteria.
 Five percent of cutaneous abscesses are
sterile, caused by a foreign body reaction
(e.g. ruptured cyst
Predisposing factors include chronic S.
aureus carriage,
 Diabetes mellitus, obesity, poor hygiene,
 Immunodeficiency states, such as in chronic
granulomatous disease and Job syndrome.

 The
most common locations are the face,
neck, axillae, buttocks, thighs and perineum.
Sites prone to friction or minor trauma, such
as the area under a belt, are distinctly
susceptible.
 Furuncles usually begin as a hard, tender,
red nodule that enlarges and becomes
painful and fluctuant; rupture results in
decreased pain.
 Abscesses
are localized collections of pus
that are usually inflamed.
 They can arise in any organ or structure, as
well as at any cutaneous site.
 Furuncles (boils) are acute, inflammatory
abscesses of hair follicles and surrounding
tissue, and, as such, occur only in hairbearing skin.
 Systemic
symptoms are usually absent in
furunculosis
 Carbuncles
are slow to heal and scar
formation is inevitable
 Carbuncles usually occur in area of thicker
skin eg nape of neck, back and thigh
 Biopsy
specimens reveal a dense neutrophilic
infiltrate in the subcutaneous tissue.
 Furuncles are characterized by an acute,
suppurative reaction involving the follicle
below the infundibulum, as well as
perifollicular necrosis with fibrinoid debris
 Diagnosis
is based primarily on clinical
appearance.
 Gram stains and cultures from the lesion
support the diagnosis. Extensive furuncles
and carbuncles can be associated with an
increased leukocyte count.
 A ruptured epidermoid or pilar cyst,
hidradenitis suppurativa (‘acne inversa’) and
cystic acne should be considered in the
differential diagnosis.
 For
simple furuncles oral antibiotics such as
cloxacillin, first generation cephalosporins
are indicated.
 Warm compress may promote maturation
,drainage and resolution of symptoms
 Fluctuant lesions require incision and
drainage
.
Systemic antibiotics should be used in four
instances:
 (1) furuncles around the nose, within the
nares or in the external auditory canal;
 (2) large and recurrent lesions;
 (3) lesions with surrounding cellulitis;
 and (4) lesions not responding to local care .
 INTRODUCTION
 Erysipelas
is primarily an infection of the
dermis with significant lymphatic
involvement.
 It has a distinctive clinical presentation and
is most often caused by Str. pyogenes (group
A streptococci).
 Erysipelas
can be traced back to the Middle
Ages. It was thought to be caused by
ingestion of the fungus Claviceps purpurea,
which produces ergot alkaloids and is found
in contaminated rye.
 The eponymous distinction refers to St
Anthony, an Egyptian monk and healer, who
was believed to be the only person able to
provide relief from the symptoms of
erysipelas
 Erysipelas
is a disease of the very young, the
aged, the debilitated,
 and those with lymphedema or chronic
cutaneous ulcers.
 Women outnumber men, except for very
young patients, where boys are more
commonly affected.
 There is an increased frequency during the
summer months and most cases are isolated.
Most cases of erysipelas are caused by
infection with group A streptococci and less
often by group G, B, C or D.
 S. aureus, Pneumococcus species, Klebsiella
pneumoniae, Yersinia enterocolitica, and
Haemophilus influenzae type b have been
known to cause an erysipelas-like infection

 The
classic lesion of erysipelas, with its welldefined margins, involves the face.
 Nowadays, however, the lower extremity is
the most common location.
 After an incubation period of 2 to 5 days,
there is an abrupt onset of fever, chills,
malaise and nausea.
 A few hours to a day later, a small plaque of
erythema develops that progressively spreads
 The
area is clearly demarcated from
uninvolved tissue, hot, tense and indurated
with non-pitting edema.
 The affected area is painful to palpation and
may burn. Regional lymphadenopathy is
normally present, with or without lymphatic
streaking.
 Pustules, vesicles, bullae and small areas of
hemorrhagic necrosis may also form.
 Complications
of erysipelas are rare and
usually occur in patients with underlying
disease.
 When the infection resolves,desquamation
and postinflammatory pigmentary changes
may occur.
 Biopsy
specimens reveal diffuse edema of the
dermis and a dermal neutrophilic infiltrate.
Involvement of the lymph vessels (dilation),
dermal foci of suppurative necrosis,
 And a dermal–epidermal separation are
commonly seen.
 There is no primary necrotizing vasculitis,
thrombosis or leukocytoclasis
 Diagnosis
is based primarily on clinical
findings.
 Routine laboratory evaluation will show an
elevated leukocyte count with a left shift.
 Blood cultures are positive in only about 5%
of cases.
 Swabs from local ports of entry, pustules or
bullae, the throat, and the nares may be
helpful.
 Culture
of skin biopsy specimens and the
injection-re-aspiration method yield poor
results, especially in immunocompetent hosts
 . Anti- DNase B and ASO titers are good
indicators of streptococcal infections.
 Direct immunofluorescence and latex
agglutination tests can be used to detect
streptococci within skin specimens.
. cellulitis and other soft tissue infections
(e.g. erysipeloid, necrotizing fasciitis)
as well as inflammatory causes of
‘pseudocellulitis’ (e.g. Sweet’s syndrome,
contact dermatitis)
A
10–14-day course of penicillin is the
treatment of choice for erysipelas caused by
streptococci.
 Although macrolides such as erythromycin
may be used in penicillin-allergic patients,
there has been an increase in macrolide
resistance among certain strains of Str.
pyogenes.
 Hospital admission and intravenous or
intramuscular antibiotics should be reserved
for children and debilitated patients.
INTRODUCTION
Cellulitis is an infection of the deep dermis and
subcutaneous tissue caused most commonly
by Str. pyogenes and S. aureus
 Cellulitis
in immunocompetent adults is most
often caused by Str. pyogenes or S. aureus.
The majority of cellulitis in childhood is
caused by S. aureus, and less commonly by
H. influenzae (even less so since the
introduction of the vaccine).
 A mixture of Gram-positive cocci and Gramnegative aerobes and anaerobes is associated
with cellulitis surrounding diabetic ulcers and
decubitus ulcers.
 Bacteria
may gain access to the dermis via an
external or a hematogenous route.
 Usually, in immunocompetent patients, a
break in the skin barrier is responsible
 In
immunocompromised patients, a blood
borne route is most common.
 Lymphedema, alcoholism, diabetes mellitus,
intravenous drug abuse, and peripheral
vascular disease all predispose to cellulitis.
 Recurrent bouts of cellulitis may be caused
by damage to the lymphatic system (e.g.
previous lymph node dissection, saphenous
vein harvest or prior episode of acute
cellulitis)
 Cellulitis
is often preceded by systemic
symptoms, such as fever, chills and malaise.
 The affected area displays all four of the
cardinal signs of inflammation: rubor
(erythema), calor (warmth), dolor (pain),
and tumor (swelling).
 The lesion usually has ill-defined, nonpalpable borders.
 In severe infections, vesicles, bullae,
pustules or necrotic tissue may be present.
.
Ascending lymphangitis and regional lymph
node involvement may occur.
 Children usually have cellulitis of the head
and neck region,
 whereas in adults the extremities are most
often affected
 In
intravenous drug abusers, the upper
extremities are often involved.
 Complications are rare, but include acute
glomerulonephritis (if caused by a
nephritogenic strain of streptococci),
lymphadenitis and subacute bacterial
endocarditis. Damage to lymphatic vessels
can lead to recurrent cellulitis.
A
mild or moderate inflammatory infiltrate
composed mostly of lymphocytes and
neutrophils can be seen throughout the
dermis, occasionally extending into the
subcutaneous fat.
 There is also edema and dilation of
lymphatics and small blood vessels.
 With special stains, the causative organism
may be identified. Subepidermal bullae may
be seen in cases of severe dermal edema
The diagnosis of cellulitis is usually clinical . The
leukocyte count is usually normal or only slightly
elevated.
 Blood cultures are almost always negative in
immunocompetent hosts.
 An important exception is H. influenzae
cellulitis, where there is usually an increased
leukocyte count with a left shift and positive
blood cultures.
 In children and immunocompromised patients,
atypical organisms are more common, and
needle aspiration and skin biopsy may be
appropriate

 The
differential diagnosis of lower extremity
cellulitis includes deep vein thrombosis and
other inflammatory diseases, such as stasis
dermatitis, superficial thrombophlebitis, and
panniculitis (especially lipodermatosclerosis).
 While superficial thrombophlebitis often
presents with redness and tenderness, the
absence of a fever and the presence of a
palpable cord aid in the diagnosis.
 Lipodermatosclerosis, misdiagnosed as
cellulitis, often leads to unnecessary
hospitalizations.
 In
most cases of cellulitis, treatment should
be targeted against
 Str. pyogenes and S. aureus. Mild cases
require a 10-day course of an oral antibiotic
that has good Gram-positive coverage.
 Hospitalization and parenteral antibiotics
should be reserved for patients who are
seriously ill and those who have facial
cellulitis.
 Diabetic
or decubitus ulcers complicated by
cellulitis require broad-spectrum coverage
(e.g. piperacillin/tazobactam or, in
penicillin-allergic patients, metronidazole
plus ciprofloxacin).
 Immobilization
and elevation, as well as the
application of wet dressings to areas with
bullae or exudate, are recommended.
 If signs and symptoms do not improve after
24–36 hours of treatment, cultures and
sensitivities should be obtained and
antibiotics adjusted accordingly.


NSAIDs may mask the signs and symptoms of
deeper necrotizing infections and should be
avoided when treating cellulitis.
 INTRODUCTION:
Impetigo is a common,
highly contagious, superficial skin infection
that primarily affects children.
 The condition presents in both non-bullous
and bullous forms . The primary pathogens in
non-bullous and bullous impetigo are
Staphylococcus aureus and, less commonly,
group A b-hemolytic Streptococcus
(Streptococcus pyogenes).
Worldwide, impetigo is the most common
bacterial skin infection in children.
 It is extremely contagious, spreading rapidly via
direct person to - person contact, though
contact with fomites has also been implicated in
spread of the disease.
 Peak incidence is in summer and fall months.
 Often, adult acquire the infection through close
contact with infected children.
.

Predisposing factors include warm
temperature, high humidity, poor hygiene, an
atopic diathesis and skin trauma.
 Nasal, axillary, pharyngeal and/or perineal S.
aureus colonization imparts an increased risk
for developing impetigo

 Non-bullous
impetigo
 Non-bullous impetigo (or crusted impetigo) is
usually caused by S. aureus and, on occasion,
Str. pyogenes. Infection occurs at minor sites
of trauma (e.g. chickenpox, insect bite,
abrasion, laceration, burn).
 Trauma exposes cutaneous proteins which
allow the bacteria to adhere, invade and
establish infection
Bullous impetigo
 The etiologic agent of bullous impetigo, S.
aureus, elaborates several exfoliative toxins and
bullous impetigo is considered a localized form
of staphylococcal scalded skin syndrome .
 In both diseases, blister formation is mediated
by exfoliative toxin binding to the desmosomal
protein desmoglein 1 and cleaving its
extracellular domain, thus leading to
acantholysis within the epidermal granular layer.

In contrast to non-bullous impetigo, lesions
can occur on intact skin .
 Although the differential diagnosis for nonbullous and bullous impetigo is extensive, the
history , physical examination and ancillary
tests can often establish the diagnosis.

Primary treatment involves local wound care,
including cleansing , removal of crusts, and
application of wet dressings.
 For healthy patients with a few, isolated
superficial lesions and no systemic symptoms ,
either mupirocin 2% ointment or fusidic acid
cream or ointment can be prescribed.
 For patients with limited disease, there is
evidence that these topical medications are at
least equally (if not more) effective than oral
antibiotics

 Although
exotoxin-producing S. aureus is
more sensitive to penicillin,
 meta-analysis of treatment trials found that
traditional penicillin was inferior to
erythromycin and penicillinase-resistant
penicillins for the treatment of impetigo.
 In non-complex cases and in communities
with low levels of resistance, macrolides are
usually effective.

Intravenous therapy should be considered
for more severe or widespread infections, as
well as infections in compromised hosts
 Acne
Keloidalis (Folliculitis keloidalis) is a
chronic, inflammatory process involving the
hair follicles of the nape of the neck and
leading to hypertrophic scarring in papules
and plaques.
 It occurs in males after puberty and is most
frequent between the ages of 14 and 25
years, especially in black males
Acne keloidalis occurs when hairs on the
back of the head and neck grow into the
skin, become inflamed, and cause scar
tissue.
 It is more common in people with stiff or
curly hair and those with darker skin.

•
It is associated with papules and nodules on the
nape of the neck.
A
study from Nigeria reported that 9.4% of all
patients attending dermatology outpatients
had acne keloidalis .
 Many patients have, or have had, significant
acne, and a patient with previous
hidradenitis has been reported .
 No specific organism can be isolated in most
cases , although S. aureus is occassionaly
isolated
 Although
friction from the collar is often
incriminated, the evidence is unconvincing .
 An association between frequent haircuts
(<4 weeks) in high school boys has been
documented
 Associated keloids in other sites seem not to
have been reported, and the process is
regarded as hypertrophic scarring rather than
true keloid.
 The
most frequent histological findings
include chronic perifollicular inflammation,
disappearance of sebaceous glands,
destroyed follicles, lamellar fibroplasia and
acute inflammation around degenerating
follicular components.
 Serial sections may show a foreign-body
reaction to hair and follicular remnants.
 The
pathological findings seen in early
lesions, perilesional skin and clinically
normal skin, suggest that follicular antigens
such as Demodex, bacteria or other skin
flora, stimulate an inflammatory reaction
which then destroys the sebaceous glands
and follicles.
 The end result is scarring .
 Follicular
papules or pustules, often in
irregularly linear groups, develop on the
nape of the neck just below the hair line.
 Less often, they extend upwards into the
scalp, and the name acne keloidalis is thus
preferred to acne keloidalis nuchae
The early inflammatory stage may be
inconspicuous, and the patient may first be
aware of the hard, keloidal papules that follow
the folliculitis.
 The papules may remain discrete, or may fuse
into horizontal bands or irregular plaques.
 In other cases, the inflammatory changes are
persistent and troublesome, with undermined
abscesses and discharging sinuses

 The
condition is extremely chronic and new
lesions may continue to form at intervals for
years.
 Bacterial
infection should be treated if
present, and antiseptics may help to reduce
further or secondary infection.
 No evidence-based reviews of therapy
options are available.
 Avoidance of closely shaven hair on the back
of the scalp may be advised.
 Intralesional
or topical potent steroids may
reduce scarring and inflammation.
 Oral steroids prescribed for another
condition helped, but long-term treatment is
unlikely to be justified
In general, medical treatment is
disappointing, and in troublesome cases
 the affected area may be excised and
grafted, or excised and allowed to heal by
secondary intention.
 Laser therapy followed by secondary
intention healing has been helpful.
 Surgery followed by radiotherapy has also
been advocated previously.

 PFB
is a Chronic Inflammatory disorder of the
hair-bearing skin.
 PFB occurs as a consequence of hair removal
when tightly coiled hair shafts, after being
shaved or plucked, reenter the epidermis or
penetrate the hair follicle wall causing
inflammation
 Sometimes
when men shave, the hair pierces
the epidermis causing irritation and sensitivity
to the hair follicle whose wall is inflamed
after the piercing.
 Beard hair, when shaved closely, causes
inflammation, papules and nodules
 Keratosis
pilaris
 Perioral dermatitis
 Angiofibromas
 Acne keloidalis nuchae
 Folliculitis
 Hidradentis suppurativa
 Basic



skin care
No washing, scrubbing or picking
Cleanse with a gentle soap, may contain
salicylic acid, glycolic acid or benzoyl peroxide
If moisturize use noncomedogenic agent
 Based
on skin type, choose appropriate
vehicle for topical treatments



Oily (solutions, gels, pledgets)
Combination (lotions)
Dry (cream, ointment)
 Tretinoin
(Retin A), Adapalene (Differin),
Tazarotene (Tazorac)






Excellent choice for comedomal acne
Improves follicular desquamation and dyschromia
Anti-inflammatory action (Differin best)
Use at night over entire face, exposure to the sun
increases irritation
Results in six to eight weeks. May increase
concentration over time
Degraded by prolonged exposure to the sun and
when used with benzoyl peroxide (Differin most
photostable)
 Adverse





affects
Irritant potential (Tazorac most irritating,
Differin least)
Sun sensitivity
Pustular eruption after 3-4 weeks
Potential hyper/hypopigmentation in black and
Asian patients
Contraindicated in pregnancy
 Erythromycin,





Clindamycin,
Decrease P.acnes and percentage of free fatty
acids
Slow to act
Resistance often develops over time
Best used in combination with topical
retinoids/benzoyl peroxide
Rare cases of pseudomembranous colitis w/
topical clindamycin
 Bactericidal
effect on P.acnes
 No evidence of resistance
 BP combined with a topical antibiotic may
help decrease the presence of antibiotic
resistant P. acnes
 Mild comedolytic action, decreases free
fatty acids
 Adverse effects



Irritation
Bleaches clothing and hair
Allergic contact dermatitis
 Dicarboxylic
acid that is bacteriostatic
against P.acnes and normalizes keratinization
 Most effective when used with other agents
 Side affects uncommon
 Use in caution in teens w/ dark complexions
due to potential risk of hypopigmentation
 Primarily
used for moderate to severe
inflammatory acne
 Decreases P.acnes
 Reduces amount of free fatty acids
 Preferred agents: Tetracyclin, Doxycyclin,
Minocyclin
 High rates of resistance to Erythromycin
 Oral


contraceptive pills in females
Increases production of sex hormone binding
globulin leading to a decrease of circulating
androgens
Decreases ovarian androgen production
 Ortho
tri-cyclen, Estrostep FDA approved
for the treatment of acne
 Oral antiandrogens (spironolactone) can
be useful
 Oral corticosteroids, short course for
patients with severe inflammatory disease
Systemic retinoid used for nodulo-cystic acne
 Most effective treatment with remission in 60%
after single course (15-24 weeks)
 Reduces sebum production
 Normalizes follicular keratinization
 Decreases inflammation
 Baseline CBC, LFT’s, cholesterol, triglycerides,
urinalysis, pregnancy test. Repeat monthly
 Post pubertal females must be on contraception
and have two sequential negative pregnancy
tests before starting


Adverse effects









Teratogenic (facial dysmorphism, abnormalities of
brain, eye, ear, CV system, thymus) and retinoid
embryopathy can occur with single exposure during
gestation
Drying/chapping of skin and mucous membranes
Myalgias/arthralgias
Photosensitivity
GI effect: transaminitis, lipid abnormalities, pancreatitis
Hematological: leucopenia, elevated platelets and ESR
Neurological: pseudo tumor cerebri
Renal: proteinuria, hematuria
Mood disorders, depression, suicidal ideations and
suicides
 Comedome

May be helpful if comedomes are resistant to
other treatments
 Chemical

removal
peels
Little evidence supporting efficacy
 Intralesional


Used for large inflammatory nodules/cysts
Can be associated with local atrophy
 Topical

steroids
tree oil
One clinical trial documented effectiveness
 Majority
of bacterial skin infection are
caused by Staphylococcus and Streptococcus
species.
 Antibiotics are used emperically with
consideration for resistance pattern
 Gram negative coverage is indicated in
children under 3yrs and patient with diabetes
or immunocompromised
Stulberg DL, Penrod MA, Blatiny RA. Common
bacterial skin conditions. Am Fam Phy 2002:
66(1);119-125.
 Salami T, Omeife H, Samuel S. Prevalence of
acne keloidalis nuchae in Nigerians. Int J
Dermatol 2007; 46: 482.
 George AO, Akanji AO, Nduka EU et al. Clinical,
biochemical and morphologic features of acne
keloidalis in a black population. Int J Dermatol
1993; 32: 714–6.

Khumalo NP, Jessop S, Gumedze J et al.
Hairdressing is associated with scalp disease in
African schoolchildren. Br J Dermatol 2007; 157:
106–10.
 Sperling L, Homoky C, Pratt L et al. Acne
keloidalis is a form of primary scarring alopecia.
Arch Dermatol 2000; 136: 479–84.
 Shah GK. Efficacy of diode laser for treating
acne keloidalis nuchae. Indian J Dermatol
Vernereol Leprol 2005; 71: 31–4.

Daum RS. Skin and soft-tissue infections caused
by methicillin-resistant Staphylococcus aureus. N
Engl J Med. 2007;357:380–90.
 Zetola N, Francis JS, Nuermberger EL, Bishai
WR. Community-acquired meticillin-resistant
Staphylococcus aureus: an emerging threat.
Lancet Infect Dis. 2005;5:275–86.
 Lyon M, Doehring MC. Blistering distal dactylitis:
a case series in children under nine months of
age. J Emerg Med. 2004;26:421–3


Ladhani S, Evans R. Staphylococcal scalded
skin syndrome. Arch Dis Child. 1996;78:85–
8Agerson AN, Wilkins EG. Streptococcal toxic
shock syndrome after breast reconstruction.
Ann Plast Surg. 2005;54:553–6
•O’Loughlin RE, Roberson A, Cieslak PR, et
al.;Active Bacterial Core Surveillance Team.
The epidemiology of invasive group A
streptococcal infection and potential vaccine
implications: United States, 2000–2004. Clin
Infect Dis. 2007;45:853–62..
 Pappas
G, Akritidis N, Bosilkovski M, Tsianos
E. Brucellosis. N Engl J Med. 2005;352:2325–
36.
 Staquet P, Lemee L, Verdier E, et al.
Detection of Neisseria meningitidis DNA from
skin lesion biopsy using real-time PCR:
usefulness in the aetiological diagnosis of
purpura fulminans. Intensive Care Med.
2007;33:1168–72.
 Vignes
S, Dupuy A. Recurrence of
lymphoedema-associated cellulitis
(erysipelas) under prophylactic
antibiotherapy: a retrospective cohort study.
J Eur Acad Dermatol Venereol 2006; 20: 818–
22.
 Koster JB, Kullberg BJ, van der Meer JWM.
Recurrent erysipelas despite antibiotic
prophylaxis: an analysis from case studies.
Neth J Med 2007; 65: 89–94.
THANK


YOU
FOR YOUR

ATTENTION