Common Bacterial

Infections
By:Dr. Naif Al-Shahrani
Salman bin Abdazziz University

Normal skin flora

NORMAL SKIN FLORA
Class

Organisms

Aerobic cocci

Staphylococcus aureus*, All body sites, especially

S. saprophyticus, S.
intertriginous areas
epidermidis , Micrococcus
luteus, M. roseus, M.
varians
Corynebacterium
Intertriginous areas (e.g.
minutissimum, C.
axillae, groin, toe webs)
lipophilicus, C. xerosis, C.
jeikeium, Brevibacterium
epidermidis
Propionibacterium acnes, Sebaceous glands and
P. granulosum, P. avidum follicles
Acinetobacter spp.
Axillae, perineum,
antecubital fossa
Malassezia furfur
Skin rich in sebaceous
glands (e.g. scalp)

Aerobic coryneform

Anaerobic coryneform
bacteria
Gram-negative bacteria
Yeast

Location on body

Impetigo
It is the most common bacterial infection in
children
Highly contagious, spreading rapidly via direct
person-to-person contact

The primary pathogen is S.aureus and, less

commonly, Streptococcus pyogenes
Non Bullous : usually at site of trauma
Bullous: (considered a localized form of SSSS)

Impetigo
Predisposing factors include
warm temperature, high humidity,
poor hygiene
atopic diathesis
skin trauma (chickenpox, insect bite,
abrasion, laceration, burn)
S. aureus colonization

Treatment
local wound care
Cleansing
removal of crusts
wet dressings
For healthy patients with a few, isolated superficial
lesions and no systemic symptoms:
mupirocin 2% ointment or fusidic acid equally
effective to oral antibiotics

Folliculitis
Folliculitis: infection localized to the hair follicle
Furuncle: entire follicle and surrounding tissue are
involved
Carbuncle : multiple furuncles grouped together
S. aureus is the most common infectious cause of
folliculitis
Gram-ve folliculitis A.V. treated with long
courses of oral antibiotics

Folliculitis
Factors predisposing
occlusion
maceration and hyperhydration with hot and
humid weather,
shaving, plucking or waxing hair
topical corticosteroids
diabetes mellitus
atopic dermatitis.
Obesity
Immunodeficiency
Poor hygiene

Folliculitis
Site: face, chest, back, axillae or buttocks
Superficial folliculitis (Bockhart's
impetigo) are small, 14 mm pustules or
crusted papules on an erythematous base
Gram stain and bacterial cultures in
recurrent or treatment-resistant cases

Folliculitis treatment
Localized:
antibacterial washes
bacitracin or mupirocin 2% may also be used for 7-10
days

Widespread or recurrent:
appropriate -lactam antibiotics, macrolides or
clindamycin

Chronic S. aureus carriage

mupirocin 2% ointment applied twice daily to the nares,
axillae/groin and/or submammary area for 5 days
MONTHLY.

Furuncles, Carbuncles
S. aureus is the most
common causative
organism
Furuncles usually begin as
a hard, tender, red nodule
that enlarges and
becomes painful and
fluctuant; rupture results
in decreased pain,
Systemic symptoms are
usually absent

Furuncles, Carbuncles
Carbuncles are collections of furuncles that extend
deep into the subcutaneous tissue.

The surface usually displays multiple draining sinus

tracts and occasionally ulcerates.
They usually occur in areas with thicker skin (e.g.
nape of neck, back, thigh)
Systemic symptoms are usually present.
Carbuncles are slow to heal scar formation

Treatment
Simple furuncles:
warm compresses may promote maturation, drainage and
resolution of symptoms

Fluctuant lesions
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
(4) lesions not responding to local care

MRSA(methicillin resistance)
Furunculosis is the most frequently
reported manifestation of community
acquired MRSA
MRSA can manifest as :
abscesses or frank cellulitis
impetigo, bullous impetigo, scalded skin
syndrome, nodules or pustules
bacteremia, septic shock and a toxic shocklike syndrome

Treatment MRSA
Emperical treatment with Vancomycin is
indicated in :
patients with severe, life-threatening infection
in patients with a history of MRSA
colonization
in intravenous drug users

Blistering Distal Dactylitis

Children aged 2-16 years
Presents as a localized infection of the volar fat
pad of a finger or a toe
Blister formation and involvement of the nail fold
or more proximal portion of the digit

Darkening of the surrounding skin before blister

formation

Blistering Distal Dactylitis

Group A -hemolytic Streptococcus, S. aureus
and, rarely, S. epiermidis are the responsible
organisms
DDx:
Herpetic whitlow
Thermal or chemical burn
Acute paronychia
Bullous impetigo (vesicles more superficial)
Frictional bullae

Blistering Distal Dactylitis

Treatment
Incision and drainage
plus
a 10-day course of an oral antistaphylococcal
antibiotic (e.g. cephalexin) can prevent
development of new sites of infection as well
as local extension.

Ecthyma
Considered as : ulcerated form of nonbullous impetigo like lesion
Due to either a primary infection with Str.
pyogenes or streptococcal superinfection
of a pre-existing ulceration

Staphylococcal Scalded Skin Syndrome

Staphylococcal toxin-mediated infections
includes:
SSSS
Bullous impetigo
Toxic shock syndrome

Exfoliative toxins (ETs) ETA and ETB are

serine proteases with a very high
specificity for human desmoglein 1 (DG-1)

Staphylococcal Scalded Skin Syndrome

Increased frequency of staphylococcal
scalded skin syndrome in children younger
than 5 years due to :
Absence of antibodies specific for exotoxins
Immature renal function in this age group
may impair clearance
The relative quantity of DG-1 in the skin
differs with age

SSSS clinical features

Severe tenderness of the skin
Erythema
Flaccid bullae within the superficial
epidermis.
In 1-2 days, the bullae are sloughed
moist skin and areas of thin, varnish-like
crust.

SSSS clinical features

The flexural areas are the first to exfoliate.
Scaling and desquamation continue for 3-5 days
Re-epithelialization in 10-14 days, without scarring

The Nikolsky sign is positive.

The mortality rate is 3% for children, over 50% in
adults, and almost 100% in adults with underlying
disease

SSSS work up
Cultures taken from intact bullae are negative
Blood cultures are almost always negative in
children, but may be positive in adults
The leukocyte count may be elevated or normal
Electrolytes and renal function should be followed
closely in severe cases
PCR serum test for the toxin is available.
BIOPSY

SSSS treatment
Localized disease :
Oral treatment with a -lactamase-resistant
antibiotic e.g.dicloxacillin, cloxacillin, for a
minimum of 1 week
Emollient
Isolation
treatment of S. aureus carriers

Extensive, generalized forms of SSSS

hospitalization and parental antibiotics.

Toxic Shock Syndrome

It is a multisystem disease caused by an
exotoxin produced by S. aureus.
Dermatologic manifestations are more
extensive and predictable in staphylococcal
TSS than in streptococcal TSS.

Toxic Shock Syndrome

Sudden onset of high fever with myalgias, vomiting, diarrhea,
headache and pharyngitis
Diffuse macular erythroderma > scarlatiniform eruption with flexural
accentuation

Erythema and edema, then Delayed desquamation of palms

and soles
Hyperemia of conjunctiva and mucous membranes
Strawberry tongue

After recovery, Beau's lines, telogen effluvium may occur

Streptococcal Toxic Shock Syndrome

Rapidly progressive, often fatal illness

Toxins act as superantigens and can cause stimulation

of T cells By binding to the class II MHC of APC
Most common initial symptom is severe local pain in
an extremity
Mortality 30 to 60%

Severe complications of streptococcal TSS include

renal failure, DIC , and adult RDS

Scarlet Fever
Between 1 and 10 years of age
>10 years antibodies prevent rash but not
the sore throat
Caused by toxins types A, B and C by group A
streptococci
Lead to a delayed-type hypersensitivity
reaction

Clinical features
Rash appears 1248 hours after the fever.
The rash starts as erythema of the neck, chest
and axillae, and behind the ears.
After 4-6 hours, the remainder of the body is
involved
spares the face , but cheeks may have flushing

Clinical features
Complications of scarlet fever include

Otitis
Mastoiditis
Sinusitis
Pneumonia
Myocarditis
Meningitis
Arthritis
Hepatitis
Acute glomerulonephritis
Rheumatic fever

Treatment
penicillin is the drug of choice (10-14-day
course)
Antibiotic treatment as long as 10 days
after the onset of symptoms will prevent
the development of rheumatic fever.

Erythromycin can be used in penicillinallergic patients.

Erysipelas
It is an infection of the dermis with significant
lymphatic involvement
Caused by infection with:

group A streptococci and less often by

S. aureus,
Pneumococcus species,
Klebsiella pneumoniae,
Yersinia enterocolitica,
Haemophilus influenzae type

Erysipelas Clinical features

Abrupt onset (clearly demarcated
erythematous plaque) hot, tense, tender and
indurated with non-pitting edema
The lower extremity is the most common
location
.
When the infection resolves, desquamation
and postinflammatory pigmentary changes
may occur

Erysipelas Treatment
The treatment of choice is 10-14-day course
of penicillin
Erythromycin in penicillin-allergic patients
Hospital admission and I.V or I.M. antibiotics
for children and debilitated patients.
prophylaxis with daily penicillin for Recurrent
erysipelas

Cellulitis
Cellulitis is an infection of the deep dermis and
subcutaneous tissue
most commonly Str. pyogenes and S. aureus
In childhood S. aureus >>>> H. influenzae
Diabetic ulcers and decubitus ulcers ( Gram+ve
cocci and Gram-ve and anaerobes)
immunocompetent via break in the skin barrier
immunocompromised bloodborne route is most
common

Cellulitis clinical features

Systemic symptoms: fever, chills and malaise.
4 cardinal signs of inflammation: rubor (erythema),
calor (warmth), dolor (pain), and tumor (swelling).

The lesion usually has ill-defined, non-palpable

borders. In severe infections, vesicles, bullae
Pustules ,necrotic tissue, ascending lymphangitis
and regional lymph node involvement may occur.

Cellulitis clinical features

Children head and neck region
Adults extremities
I.V. drug abusers the upper extremities

Complications include
acute glomerulonephritis (streptococci)
Lymphadenitis
subacute bacterial endocarditis.
Damage to lymphatic recurrent cellulitis

Necrotising Fasciitis
is essentially a severe inflammation of the
muscle sheath that leads to necrosis of the
subcutaneous tissue and adjacent fascia,
that is difficult to diagnose early and
difficult to manage effectively.

Risk factors for NF

>50 years of age

Diabetes mellitus
Peripheral vascular disease
Intravenous drug use
Alcoholism
Immunosuppression
Obesity

Clinical diagnosis of NF
Hx:

minor trauma
insect or human bites
recent surgery
skin infection or ulcers
injection sites and
illicit intravenous drug usage

Many cases, however, remain idiopathic

Clinical diagnosis of NF
Severe pain precedes skin changes by 24 to 48 h in
>97.8% of patients
Mild erythema, cellulitis or swelling overlying the
affected area.
tender area >> smooth, swollen area of skin with
distinct margins progressing to dusky blue/purple,
bruising violaceous plaques, and finally full thickness
necrosis with haemorrhagic bullae

Radiology

MRI are probably the best radiological

adjunctive investigation.