Bacterial infections
IHAB YOUNIS, MD
Impetigo
Etymology: L. a scabby eruption
Incidence
• The most common skin infection in
children. Approximately 9-10% of all
children presenting to clinics with skin
complaints have impetigo
• The majority (90%) of bullous impetigo
cases occur in children younger than 2
years
Etiology
• Caused by
-Staphylococcus aureus
-Streptococci (group A beta-hemolytic) or
• Staph aureus is cultured consistently from the
lesions, but streptococci are found only
occasionally
• The infection may be caused by a mixture of the
2 organisms
• Strept rarely act as the sole causative agents, as
was believed 10 years ago
• The organisms are thought to enter
through damaged skin and are transmitted
through direct contact
• After infection, new lesions may be seen
on the patient with no apparent break in
the skin
• Usually there is a predisposing factor e.g.
miliaria or scabies
Staphylococci
Streptococci
Clinically
I-Impetigo contagiosa(non-bullous impetigo):
The lesions begin with a single 2- to 4-mm
erythematous macule that rapidly evolves into a
vesicle or a pustule
• This vesicle is very fragile
and ruptures early, leaving
a crusted exudate of a honey
or yellow color over the superficial erosion
• The infection spreads to contiguous and
distal areas through inoculation of other
wounds from scratching
• Regional lymphadenopathy may be found in
impetigo contagiosa
II-Bullous impetigo: presents with small
or large, superficial, fragile bullae on the
trunk and the extremities
• Often, only the remnants of ruptured
bullae are seen at the time of presentation
• Regional lymphadenopathy is rare in
bullous impetigo
• Fever, diarrhea & generalized weakness
may be present in bullous impetigo
• The separation of the epidermis is due to
an exotoxin produced by staphylococci,
which may be the only organism present in
cases of bullous impetigo
III-Common impetigo is the term applied
when the infection occurs in preexisting
wounds
IV-Ecthyma is a deeper, ulcerated
impetigo infection, often occurring with
lymphadenitis
Complications
• Glomerulonephritis due to a nephritogenic
strain of streptococci may occur 3 w from
infection
• Scarlet fever, urticaria and erythema
multiforme may follow impetigo
Histopathology
Subcorneal blister full of neutrofills
Bacteria and neutrophills are
found in the st.corneum
Treatment
• Topical antibiotics: in mild cases i.e. lesions that
are small or few in number
• Systemic antibiotics: If the lesions are widespread or accompanied by lymphadenopathy or
if nephritogenic strept are suspected
• The antibiotic chosen should be active against
staph and strept
Cellulitis&Erysipelas
Etymology: G., fr. [erythros,] red + [pella,] skin
Erysipelas
Normal
Cellulitis
Etiology
• Streptococci (group A) are predominant
• Staph. Aureus are occasional in cellulitis
but rare in erysipelas
Clinically
• Cellulitis most commonly develops on the
legs but can occur anywhere
• The first symptoms are erythema, pain,
and tenderness over an area of skin
• The infected skin becomes hot and slightly
swollen and may look slightly pitted, like
an orange peel
• Most people with cellulitis feel only mildly
ill, but some may have a fever, chills, rapid
heart rate, headache, low blood pressure,
and confusion
• Vesicles or bullae may appear on the
infected skin
• Erysipelas starts abruptly & systemic
symptoms may be severe but responds
rapidly to treatment
• The skin is bright red and noticeably
swollen and the edges of the infected area
are raised. The swelling occurs because
the infection blocks the lymphatic vessels
in the skin
Complications
. Bacteremia with seeding of bone, joints or brain
. Abscesses
.Superinfection
. Lymphangitis . Thrombophlebiti
. Gas-forming cellulitis . Thrombophlebitis
. Necrotizing fasciitis
Differential diagnosis
• Deep vein thrombosis
-Protein level in aspirate of tissue fluid is
>10 g/L
-Phlebography and Doppler
Investigations
• Most patients do not require laboratory study
• Consider the following tests in patients with
moderate to severe cellulitis (ie, patients
requiring admission or requiring parenteral
antimicrobials)
1-CBC counts often show leukocytosis greater
than 13,000 WBC/cc
2-Obtain a blood culture only if the patient is
admitted or has significant systemic
symptoms or if concern of bacteremia exists
 3-Strongly consider culture in all patients

requiring admission or parenteral antibiotics
Treatment
• Penicillin G procaine: 0.6-1.2 million U IM bid for
10 d
• Amoxicillin and clavulanate (Augmentin) for
infections caused by penicillinase-producing
staphylococci: 500-875 mg PO bid
• Erythromycin (Erythrocin) For penicillin sensitive
patients :750-100 mg/d orally for 10 d
Staphylococcal
Scalded Skin
Syndrome SSSS
(Lyell's disease)
Etiology
• Described in 1956 by Alan Lyell as toxic
epidermal necrolysis (TEN)
• Caused by two epidermolytic toxins (A and
B) produced by phage group 2
Staphylococcus aureus
Clinically
• Most common in children (98% are
younger than 6 years). It is rare in adults
• Originates from a focus of infection that
may be a purulent conjunctivitis, otitis
media, or occult nasopharyngeal infection
• Begins with fever, irritability, and a
generalized, faint, orange-red, macular
erythema with cutaneous tenderness
• Within 24-48 hours, the rash progresses
from scarlatiniform to blistering
• Characteristic tissue paper–like wrinkling
of the epidermis is followed by the
appearance of large, flaccid bullae in the
axillae, in the groin and around the body
orifices
• A positive Nikolsky sign (slippage of the
superficial layer of the epithelium on gentle
pressure) can often be elicited at this
stage
• As sheets of epidermis are shed, a moist
erythematous base is revealed
• Healing is usually complete within 5-7d
• In adults, it is frequently followed by
bacteremia and pneumonia, favoring a
poor prognosis
Histopathology
Separation between
gran.&Malpig.layers
Investigations
• ELISA can identify the toxins responsible
• Culture from initial sites
Treatment
•
•
•
•
•
Antibiotics in pediatric doses e.g.:
Penicillin G procaine :600,000-1 million U/d IM
Amoxicillin and clavulanate (Augmentin):
500 mg PO q12h or 250 mg PO q8h
Cephalexin (Keflex): 25-50 mg/kg/d q6h
Gentamicin (Garamycin): <5 years with normal
renal function: 2.5 mg/kg/dose IV/IM q8h
>5 years: 1.5-2.5 mg/kg/dose q8h or 6-7.5
mg/kg/d divided q8h
Erythromycin (Erythrocin): 30-50 mg/kg/d
Erythrasma
Etymology: G. [erythraino,] to redden
Etiology
• The Gram-positive, aerobic diphtheroid
Corynebacterium minutissimum ,which is
present as a normal skin flora
• Corynebacteria invade the upper one-third
of the stratum corneum
• Predisposing factors include excessive
sweating, obesity & diabetes mellitus
Clinically
• The incidence of erythrasma is reported to be
around 4%
• The typical appearance is well-demarcated,
brown-red macular patches
• The skin has a wrinkled appearance with fine
scales
• Infection commonly is located over inner thighs,
axillae, submammary area, periumbilical region,
• Toe web lesions appear as maceration
• Infection commonly is asymptomatic, but it
can be pruritic
• Duration ranges from months to years
• Widespread involvement of trunk and
limbs is possible
Investigations
• Wood’s light examination
• Coral-red fluorescence of lesions is observed
due to to the production of porphyrin by these
diphtheroids
• Results may be negative if
patient bathed prior to presentation
• Gram stain reveals gram-positive rods
Treatment
• Erythromycin (Erythrocin): 500 mg PO bid
for 7-10 d
• Fusidic acid (Fucidin):Apply to affected
area bid for 2 wk
• Miconazole (Daktarin): Apply to affected
area bid for 2 wk
Folliculitis
1-Superficial
folliculitis
Etiology
• It is an inflammation confined to the ostium
of hair follicle
• Caused by coagulase-positive
staphylococci (impetigo of Bockhart) or
Physical (epilation) or Chemical irritation
(mineral oils, tar or adhesive plaster)
Clinically
• The primary lesion is a papule or pustule
with a central hair ,the hair shaft may not
be seen
• Typical body sites affected are the face,
scalp, thighs, axilla, and inguinal area
Treatment
• Topical and oral antibiotics. If a patient
does not improve after a 2-4 week course ,
the case must be investigated (cultures,
Gram stain, KOH prep and biopsy)
• Washing with antibacterial soaps (eg,
Betadine skin cleanser)
• For recurrent and recalcitrant folliculitis,
antibiotic ointment in the nasal vestibule
twice a day for 5 days
2-Pseudofolliculitis
Etiology
• Pseudofolliculitis barbae is a foreign body
inflammatory reaction involving papules and
pustules affecting curly haired males who shave
• Pseudofolliculitis pubis is a similar condition
occurring after shaving pubic hair
• Two mechanisms are involved in the
pathogenesis : (1) extrafollicular penetration
occurs when a curly hair reenters the skin and
(2) transfollicular penetration occurs when the
sharp tip of a growing hair pierces the follicle
wall
Clinically
• The primary lesion is a flesh-colored or
erythematous papule with a hair shaft in its
center. If the hair shaft is gently lifted up, the free
end of the hair comes out of the papule
• Pustules and abscess formation can occur from
secondary infection
• Postinflammatory hyperpigmentation, scarring,
and keloid formation may occur in chronic or
improperly treated cases
Treatment
1-Chemical depilatories:
• They work by breaking the disulfide bonds in hair, which
results in the hair being broken off bluntly at the follicular
opening
• Chemical depilatories should be used every second or
third day because they cause skin irritation
– Barium sulfide powder depilatories 2% paste with
water and applied to the beard area. This paste is
removed after 3-5 minutes
– Calcium thioglycolate preparations come as powder,
lotions, creams, and pastes. They are left for 10-15
minutes; chemical burns result if left on too long. The
mercaptan odor is often masked with fragrance
2-Topically applied tretinoin (Retin-A):
When used nightly, it alleviates
hyperkeratosis removing the thin
covering of epidermis that the hair
becomes embedded in upon emerging
from the follicle
3-Mild topical corticosteroid creams:
Reduce inflammation of papular lesions
4-Topical antibiotics:
In severe cases
Reduce skin bacteria and treat secondary
infection
These topicals include erythromycin
(Acnebiotic), clindamycin (Dalacin-T) and
benzamycin(Akneroxide)
5-Stoping shaving for 4-6 w is the most effective
method but it is temporary
3-Furunccle
(Abcess)
Etymology: L. [furunculus,] a petty thief
Etiology
• It is an acute infection involving an entire hair
follicle and the adjacent subcutaneous tissue
• Caused by Staphylococcus aureus, but as it
is present in the nares&perineum, infection
may reflect a defect in surface defence i.e.
balance between microflora
• Predisposing factors may include
malnutrition but diabetes is doubtful
Clinically
• Most common on the face, neck, armpit,
buttocks and thighs
• Begins as a follicular, tender, red nodule
but ultimately becomes fluctuant
• It may drain spontaneously or surgically,
producing pus
• Furuncles can be very painful (throbbing) if
they occur in areas like the ear canal or
nose
• Furuncles can be single or multiple. Some
people have recurrent bouts
• Less common symptoms include:fever,
fatigue or malaise
Treatment
• Topical and systemic penicillinaseresistant antibiotics
• Warm moist compresses encourage
furuncles to drain, which speeds healing
• Large lesions may need to be drained
surgically
4-Carbuncle
Etymology: L. carbunculus ,small glowing ember
Etiology
• It is a deep infection of a group of
neighboring hair follicles extending to
connective tissue and subcutaneous fat
• Caused by Staphylococcus aureus
• Predisposing factors may include
malnutrition, diabetes, heart failure or
during prolonged steroid therapy
Clinically
• Painful, acutely tender, red, dome-shaped
lump
• It reaches a diameter of 3-10 cm in a few
days
• Suppuration starts and pus is discharged
from multiple follicular orifices
• Constitutional symptoms are severe
• They may be solitary or multiple
• Most leasions are on the back of neck,
shoulders, hips and thighs
• Healing leaves a scar but in debilatated
cases death may occur due to toxemia
Treatment
• Systemic penicillinase-resistant antibiotics
• Large lesions may need to be drained
surgically
• Treatment of predisposing factors
5-Acne kelodalis
Nuchae
(folliculitis keloidalis)
Etiology
• The findings of Sperling et al(2000) indicate that
AK is a primary form of scarring alopecia
• Many of the histologic findings closely resemble
those found in certain other forms of scarring
alopecia
• They claim that overgrowth of microorganisms
does not play an important role in the
pathogenesis
• They also found no association between
pseudofolliculitis barbae and AK
Herzberg et al (1990) provided another
explanation:
•The acute inflammation, whether it begins in the
sebaceous gland or the deep portion of hai
follicle , leads to a weakened follicular wall at
these levels
• This enables the release of hair shafts into the
surrounding dermis. The "foreign" hairs incite
further acute and chronic granulomatous
inflammation
• The localized granulomatous inflammation
manifests itself clinically as a papular
lesion
• Fibroblasts lay down collagen and scars
form in the region of the inflammation
• Distortion and occlusion of the follicular
lumen by fibrosis leads to hair retention in
the inferior follicle and further
granulomatous inflammation and scarring
Older speculations:
• Injury produced by short haircuts (especially
when the posterior hairline is shaved with a
razor
• Curved hair follicles (analogous to
pseudofolliculitis of the beard
• Constant irritation from shirt collars, chronic lowgrade bacterial infections, and an autoimmune
process (AK usually responds to systemic
steroid therapy)
clinically
• Starts after puberty as firm, dome-shaped,
follicular papules or pustules that are 2-4
mm in diameter
• The papules develop on the nape of the
neck and/or on the
occipital part of
the scalp
• Some papules remain discrete but others
coalesce to form keloid-like plaques, which are
usually arranged in a bandlike distribution at or
below the posterior part of the hairline
• Early papular lesions are usually asymptomatic,
but pustular lesions are often pruritic and
occasionally painful
• Scarring alopecia and subcutaneous abscesses
with draining sinuses may also be present
Dermal fibrosis
Hair shafts surrounded by granulomatous inflammation
Larger magnification
Treatment
• Advise patients not to get the occipital part of
their hairline edged with a razor or wear tight
fitting shirts
• Twice-a-day treatment with a combined retinoic
acid (Retin-A) and a strong steroid cream may
be sufficient to relieve all symptomatology and
flatten the existing lesions
• When pustules, crust formation is present, use
topical clindamycin on a twice-daily basis until
the pustules abate and the inflammation
subsides. If the patient does not have significant
improvement in 4-5 days, take a bacterial culture
of the involved area, and start the appropriate
systemic antibiotic
• Intralesional steroid injections (10-40 mg/mL)
are another method of therapy. They seem to be
painful on the posterior part of the scalp, and the
fibrotic tissue is difficult to inject. Injections are
easier if the papules are electrodesiccated and
curetted first. Using a dental syringe or pressure
syringe (Derma-Jet or Meda-Jet) sometimes
makes it easier to inject. Warn patients that the
area injected might become hypopigmented and
stay that way for 6-12 months
• Laser therapy (carbon dioxide or Nd:YAG)
has been successful for some patients.
Postoperative intralesional triamcinolone
injections (10 mg/mL q2-3wk) help prevent
recurrence. Cryotherapy has also proven
to be successful in some cases. The area
is frozen for 20 seconds, allowed to thaw
and is then frozen again a minute later
• Once healing has taken place, apply a
tretinoin-fluorinated steroid mixture to the
occipital part of the scalp twice daily to
help prevent recurrence
• Surgical intervention followed by
intralesional steroids
Pitted keratolysis
Etiology
• Caused by Kytococcus sedentarius,Dermatophilus
congolensis, or species of Corynebacterium and
Actinomyces
• Under appropriate conditions (ie, prolonged
occlusion, hyperhidrosis, increased skin surface
pH), K sedentarius proliferates and produces 2
keratin-degrading proteinases that destroy the
stratum corneum, creating pits
• The malodor associated is presumed to be due to
the production of sulfur by-products, such as thiols,
sulfides, and thioesters
Clinically
• Pits in the stratum corneum ranging from
0.5-7.0 mm in size seen on pressurebearing areas of the plantar surface
• Patients may complain of malodor,
hyperhidrosis and occasionally, soreness
or itching as in military personnel
Treatment
• Limit the use of occlusive footwear
• Absorbent cotton socks must be changed
frequently to prevent excessive foot moisture
• Twice daily applications of erythromycin or
clindamycin are effective. Either solutions or gel
formulations may be used
• Oral erythromycin is another option
• For resistant cases and/or associated with
hyperhidrosis, the use of botulinum toxin
injections has been effective
Anthrax
Etymology: G. anthrax (anthrak-), charcoal
Etiology
• Caused by B anthracis ,a gram-positive bacillus
• Cutaneous anthrax results from exposure to the
spores of Bacillus anthracis after handling sick
herbivorous animals, contaminated wool or hair
• Pulmonary anthrax results from inhaling anthrax
spores
• Intestinal anthrax results from
ingesting meat products that
contain anthrax spores
Clinically
1-Cutaneous anthrax"malignant pustule":
• Begins as a pruritic papule that enlarges in
24-48 hours to form an ulcer with a raised
edematous edge surrounded by a satellite
lesions
• 80% of patients who
are not treated
recover
2-Inhalational anthrax :
• After initial mild symptoms improvement, it
progresses rapidly with high fever, severe
shortness of breath, tachypnea, cyanosis,
profuse diaphoresis, hematemesis, and chest
pain, which may be so severe as
to mimic an acute myocardial
infarction
• It leads to septicemia as the organisms released
from the liver or spleen into the bloodstream
overwhelm host defenses and produce massive
amounts of lethal toxin that result in shock and
death
3-Intestinal anthrax:
Patients complain of nausea, vomiting,
malaise, anorexia, abdominal pain,
hematemesis, and bloody diarrhea, which
are accompanied by fever
Investigations
• The preferred diagnostic procedure for
cutaneous anthrax is staining the ulcer
exudate with methylene blue or Giemsa
stain
• B anthracis readily grows on blood agar
Treatment
• Penicillin G procaine : 600,000-1,000,000 U/d IM
for 60 d
• Doxycycline (Vibramycin) :100 mg PO/IV q12h
for 60 d
• Ciprofloxacin (Ciprobay): 500 mg PO q12h for
60 d (no clinical experience)
• Antimicrobial therapy renders lesions culturenegative within hours, but the lethal effects of
anthrax are related to the effects of the
organism's toxin
Suppurative
hidradenitis
Etiology
Many theories
1-Infective etiology
• Strept., staph. & E. coli have been identified in
the early stages of the disease; however, in the
chronic relapsing stages, anaerobic bacteria and
Proteus species have more commonly been
isolated
• Whether the bacteria are the cause or the result
of the disease has not been determined
2-Hormonal theory: Improvement and relapse
after pregnancy and contraceptive pill intake
suggest that low levels of estrogens predisposes
for hidradenitis suppurativa
3-Immune theory: Immunity in most patients is
intact, but some patients demonstrate a defect in
the T-cell lymphocytes
4-Genetic theory: Increased incidence in
individuals with HLA-A1 and HLA-B8 has been
demonstrated in some patients
The Pathogenesis of Hidradenitis
Suppurativa
Keratin comedones
Occlusion of the apocrine duct
Superimposed inflammation and infection
Abscess formation
Chronic infection and spread
Induration and sinus and fistula formation
Clinically
• It affects skin-bearing apocrine glands :
Axilla,groin, perineum ,perianal
region,buttocks,scrotum submammary region
The onset is usually after puberty, in the
2nd&3rd decades
• Early lesions are solitary, painful pruritic
nodules that may persist for weeks or months
without any change
• The nodules develop into pustules&eventually
rupture, draining purulent material.This leads
to chronic sinus formation, with intermittent
release of serous, purulent, or bloodstained
discharge
• If subcutaneous extension occurs, it may
appear as indurated plaques, which in lax
skin, such as the axilla and groin, manifest
as linear bands. Multiple sites may be
simultaneously affected
• Comedones may be present
Treatment
• Tetracycline and erythromycin may be
helpful on a long-term basis
• Cephalosporins often will help in acute
cellulitis
• Sulfonamide or clindamycin antibiotic are
used in presence of methicillin-resistant
staphylococcus aureus in both short-term
and long-term treatment
• Topical products, such as benzoyl
peroxide, may be helpful
• Retin-A has been found to be helpful in
some patients
• Isotretinoin (Accutane) :
Decreases sebaceous gland size and sebum
production; may also inhibit abnormal
keratinization .Adult Dose 40-60 mg/d PO for
4m
• Topical steroids to modify the body's immune
response
• In severe cases, radical excision of the
pathologic tissue with split-thickness skin
grafts
Actinomycosis
Etymology:G. aktinos, a ray of light + G. myk , fungus, + -osis, condition
Etiology
• Actinomyces israelii is a gram-positive, non–
spore-forming anaerobic bacillus
• Its filamentous growth and mycelia-like colonies
have a striking resemblance to fungi
• They are soil organisms, often found in decaying
organic matter
• It is primarily a commensal
found in normal oral cavities,
in tonsillar crypts, in dental
plaques and in carious teeth
Clinically
•
•
•
•
•
•
1-Cervicofacial actinomycosis:
The most common manifestation, comprising 5070% of reported cases
Occurs following oral surgery or in patients with
poor dental hygiene
In the initial stages soft-tissue swelling of the
perimandibular area occurs
Nodules may be tender in the initial stages, but
typically they are nontender and woody hard in the
later stages
Lymphadenopathy typically is absent.
Fever is variably present
• Direct spread into the adjacent tissues
occurs over time, along with
development of fistulas that discharge
purulent material containing yellow (ie,
sulfur) granules
• Invasion of the cranium or the
bloodstream may occur if the disease is
left untreated
2-Thoracic actinomycosis:
• Presents as a pulmonary infiltrate or mass,
which, if left untreated, can spread to
involve the pleura, pericardium, and chest
wall, ultimately leading to the formation of
sinuses that discharge sulfur granules
3-Actinomycosis of abdomen and pelvis:
• Paients have a history of recent or remote
bowel surgery
• Presents classically as a slowly growing
tumor. Involvement of any abdominal
organ, including the abdominal wall, can
occur by direct spread, with eventual
formation of draining sinuses
Histopathology
"Sulfur granule": colony of
Actinomyces israeli
showing slender,
periph
Gram positive filaments
Investigations
• A Gram-stained smear of the specimen may
demonstrate the presence of beaded,
branched, gram-positive filamentous rods,
suggesting the diagnosis.
• Cultures should be placed immediately under
anaerobic conditions and incubated for 48
hours or longer; the isolation and definitive
identification of actinomycetes may require 23 weeks
• Examining sulfur granules stained with 1%
methylene-blue solution, and examined
microscopically for features characteristic of
actinomycetes
Treatment
• Penicillin G 12-24 million U/d IV by
continuous infusion
• Doxycycline (Vibramycin): For
nonpregnant patients with penicillin
allergy. 100 mg PO q12h
• Clindamycin (Dalacine c) : Alternative in
patients allergic to penicillin. 150-300 mg
PO q8h
• Amoxicillin/Clavulanic Acid (Augmentin):
can be used alone in mild to moderately
severe cases of actinomycosis; covers
both pathogenic actinomycetes and
companion bacteria, which frequently are
resistant to penicillin. 500 mg PO q8h or
875 mg PO q12h