Bacterial Infections
07/02/2011
BY:
MOHAMMED ALSAIDAN
Normal skin flora
NORMAL SKIN FLORA
Class
Organisms
Aerobic cocci
Staphylococcus aureus*, S. All body sites, especially
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-toperson 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) elaborates
several exfoliative toxins (A–D), targeting desmoglein 1
acantholysis in granular layer mimicking P.folaceus
Impetigo
• Predisposing factors include
•
•
•
•
•
warm temperature, high humidity,
poor hygiene
atopic diathesis
skin trauma (chickenpox, insect bite, abrasion, laceration, burn)
S. aureus colonization
Impetigo work up ?
• Diagnosis is usually made clinically
• Exudate from beneath the crust and fluid from intact bullae
can be sent for culture and sensitivity
• Leukocytosis in 50%
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
• Pseudomonas folliculitis  use of hot tubs
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, 1–4
mm pustules or crusted papules on an erythematous base
• Gram stain and bacterial cultures in recurrent or treatmentresistant cases
Folliculitis treatment
• Localized:
• antibacterial washes
• bacitracin or mupirocin 2% may also be used for 7-10 days
• Widespread or recurrent:
• appropriate β-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.
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
• 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 shock-like syndrome
• The major cause of methicillin resistance is the production of
an altered (i.e. reduced affinity) penicillin-βinding protein
(PBP) called PBP2a
Treatment
• 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 β-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 non-bullous 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
Clinical features:
•
•
•
•
•
Prodrome
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.
SSSS work up
• Biopsy: separation of the epidermis at the granular layer. An
inflammatory cell infiltrate is typically not present
• Negative IF
• In (TEN), inflammatory (lymphocytic) infiltrate is present, and
the plane of separation is deeper, at the level of the basement
membrane.
DDx
•
•
•
•
•
sunburn
drug reaction
Kawasaki disease
extensive bullous impetigo
viral exanthem, toxic shock syndrome, GVHD, TEN and
pemphigus foliaceus.
SSSS treatment
• Localized disease :
• Oral treatment with a β-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 toxic shock syndrome toxin-1 (TSST-1). In the
absence of antibodies against TSST-1. TSST-1
• 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
DDx:
•
•
•
•
•
SSSS
scarlet fever
early TEN
Kawasaki disease
Rocky Mountain spotted fever
Treatment
• Remove Foreign bodies and any source of infection
• Beta-lactamase-resistant antibiotics or antibiotics that
suppress toxin production, such as clindamycin, rifampin or
fluoroquinolones.
• In severe cases of shock unresponsive to antibiotics, lowdose corticosteroids
Severe cases of TSS :
• intensive supportive therapy (intravenous fluids and
vasopressor agents).
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
Streptococcal Toxic Shock Syndrome
• Most cases require intensive supportive therapy with
aggressive intravenous fluid and vasopressors.
• Clindamycin inhibit the production of bacterial toxins (the
cause of shock) and is the first-line treatment.
• Early surgical intervention e.g. debridement or fasciotomy
can be life-saving
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
• Prodrome
• Rash appears 12–48 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 (although
some circumoral pallor is characteristic).
Clinical features
• Pastia lines (where the rash runs together in the armpits and
groin) appear and can persist after the rash is gone
• The rash: tiny papules on an erythematous background–
blanches with pressure
• It resembles a ‘sunburn with goose pimples’ and feels like
sandpaper
Extracutaneous manifestation
• The throat is red and edematous and develops an exudate
after 3-4 days
• There is tender cervical adenopathy and palatal petechiae.
• The tongue is initially white with bright red papillae, but later
becomes beefy red (‘red strawberry tongue’).
• After 7-10 days, desquamation affecting the hands and feet
Clinical features
• Complications of scarlet fever include
•
•
•
•
•
•
•
•
•
•
Otitis
Mastoiditis
Sinusitis
Pneumonia
Myocarditis
Meningitis
Arthritis
Hepatitis
Acute glomerulonephritis
Rheumatic fever
Scarlet fever work up
• CBC: elevated leukocyte count with a left shift, mild
hemolytic anemia with reticulocytosis can occur.
• Nose and throat cultures will grow group A streptococci.
• Detection of antistreptolysin O (ASO), antihyaluronidase,
antifibrinolysin and anti-DNase B antibodies are useful in
detecting the streptococcal infection.
• Early in the disease, a mild albuminuria and hematuria can
be seen.
Scarlet fever work up
• The differential diagnosis of scarlet fever includes
•
•
•
•
•
•
hypersensitivity reaction to drugs
Measles
Rubella
toxic shock syndrome
SSSS
Kawasaki disease and toxin-mediated erythema.
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 penicillin-allergic 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 of prodrom  (clearly demarcated
erythematous plaque) hot, tense, tender and indurated with
non-pitting edema
• The lower extremity is the most common location
• LAP , with or without lymphatic streaking.
• Pustules, vesicles, bullae and small areas of hemorrhagic
necrosis may also form.
• When the infection resolves, desquamation and
postinflammatory pigmentary changes may occur
Erysipelas Work up
• 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.
• Anti-DNase B and ASO titers are good indicators of
streptococcal infections.
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
Streptococcal Intertrigo
• Sharply demarcated, erythematous patches or thin plaques
are observed in an intertriginous zone
• Distinct, foul smell is suggestive.
• Infants are particularly vulnerable due to irritation and
frictional forces in moist deep skin folds of the neck, axillae,
antecubital and popliteal fossae, and inguinal region.
• Discrete psoriasiform lesions may also be seen.
• group A streptococci >>> S. aureus and Proteus mirabilis.
Streptococcal Intertrigo
• The differential diagnosis includes
• cutaneous candidiasis
• seborrheic dermatitis
• irritant contact dermatitis.
• Simple intertrigo responds to measures that reduce friction
and minimize moisture
• A 10-day course of oral penicillin is effective in most
instances, with failure of conservative methods
Streptococcal Perianal Disease
• Due to Str. pyogenes
• Sharply demarcated, bright, perianal erythema extending 2–
3 cm around the anal verge
• Patients may complain of painful defecation, blood-streaked
stools, prolonged perianal irritation or pruritus soiling of
undergarments.
• Systemic symptoms are absent.
• The infection may be preceded by a pharyngitis and should
always be considered in patients with guttate psoriasis
Streptococcal Perianal Disease
DDX
• candidiasis, seborrheic dermatitis, pinworm infection,
inflammatory bowel disease, child abuse, and the early
phase of Kawasaki disease.
Rx:
• 10-14-day course of penicillin or erythromycin.
• After treatment, the area should be recultured to exclude
recurrence
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
Cellulitis
LABs:
• WBC is usually normal or only slightly elevated.
• Blood cultures are almost always negative except H. influenzae
• In children and immunocompromised patients, needle
aspiration and skin biopsy may be appropriate for atypical
organisms
DDx :
• DVT, stasis dermatitis, superficial thrombophlebitis,
panniculitis (especially lipodermatosclerosis)
• pseudocellulitis
Cellulitis treatment
• Immobilization and elevation, application of wet dressings to areas
with exudate.
• Mild cases  10-day course of an oral antibiotic that cover . Str.
pyogenes and S. aureus
• Seriously ill or facial cellulitis Hospitalization and I.V antibiotics
• Diabetic or decubitus ulcers  broad-spectrum coverage (e.g.
piperacillin/tazobactam or metronidazole plus ciprofloxacin)
• Antibiotics adjusted according to cultures and sensitivities results
• NO NSAIDs
Pyomyositis
• A primary bacterial infection of the skeletal muscles, most
commonly by S. aureus , untreated disease can progress to
septicemia and septic shock
• Associated with HIV infection, I.V. drug abuse,
immunosuppression and DM
Clinically :
• Myalgias and low-grade fever, progressive over 1-2 weeks 
‘woody’ induration on palpation
• Muscle abscess formation in the second stage of disease, and
frank septicemia may follow.
Pyomyositis
Work up
• MRI as soon as pyomyositis is suspected.
• some cases can be confirmed by ultrasound-guided aspiration.
DDx
• Cellulitis, hematoma, dermatomyositis/polymyositis, HIVassociated myopathies, DVT, osteomyelitis, septic arthritis,
and necrotizing fasciitis
Rx
• Surgical incision and drainage, I.V. antibiotics until clinical
improvement followed by oral antibiotics for a total of 3
weeks
Botryomycosis
• Chronic, purulent and granulomatous bacterial infection, most
commonly caused by S. aureus.
• Cutaneous botryomycosis presents as cutaneous and
subcutaneous nodular masses, abscesses, ulcers or verrucous
plaques. +/– multiple sinuses and fistulae
• Most patients have localized disease on the extremities and it
may be preceded by trauma
Botryomycosis
• The lesions can involve the underlying muscle or bone
• Systemic symptoms are infrequent
• The lungs are the most common extracutaneous site of
involvement, but any organ can be affected
Botryomycosis biopsies
• Biopsy reveal a chronic non-specific inflammatory reaction
with fibrosis. Foreign body type giant cells are commonly
seen.
• 1–3 mm granular bodies which have basophilic centers
representing bacteria, cells and debris.
• The periphery has a homogeneous, eosinophilic, hyaline
appearance secondary to a host immunoglobulin response
(Splendore–Hoeppli phenomenon).
• The granules stain easily with PAS, Gram and Giemsa stains.
At high power, the center of the concretion consists of
basophilic granular material. A brightly eosinophilic band
encases the bacteria.
Botryomycosis work up
• Microscopic examination (fresh mount or 20% KOH) will show
coarse granules with club-like projections.
• Gram staining of crushed granules will usually display masses
of staphylococci.
• Bacterial and fungal cultures should be performed.
• DDx: mycetoma, actinomycosis,, abscesses, dimorphic fungal
infections, orf, tuberculosis and atypical mycobacterial
infections
Treatment
• Excision and debridement.
• Antibiotics usually do not penetrate the lesion adequately.
• The CO2 laser used successfully.
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.
Types
Risk factors for NF
•
•
•
•
•
•
•
>50 years of age
Diabetes mellitus
Peripheral vascular disease
Intravenous drug use
Alcoholism
Immunosuppression
Obesity
GASNF and GAS toxic shock
syndrome (STSS)
• 50% of type II NF cases are associated with STSS.
• STSS is an exotoxin-driven disease that significantly increases
the mortality of streptococcal NF alone from <40% to 67%
with up to half of patients needing amputation
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
• Hx:
• foreign travel >>> resistant or unusual organisms
• trauma involving soil contamination >>> fungal
• Raw seafood ingestion or wound exposure to seawater >>> Vibrio
spp.
• tonsillitis, impetigo, or recent non-steroidal anti-inflammatory
agent (NSAID) >>> streptococcal infection
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
• US findings correlate reasonably well with histological fat
changes in NF
• T2-weighted images on MRI are probably the best radiological
adjunctive investigation, but are more sensitive than specific
Labs
• Blood cultures are positive in 11 to 60% of patients with
GASNF
• Haemoglobinuria is common in GASNF
• Blister fluid is often sterile.
• Tissue biopsy is the investigation of choice for stain and C/S
• Disseminated intravascular coagulation and thrombocytopenia
are common
Labs
• ARF
• CRP levels of >16 mg/dL, with a sensitivity of 89% and
specificity of 90%, have been reported
• Raised serum creatinine kinase (CK) indicates myositis or
myonecrosis
Labs
• CK levels of 600 U/L gave a sensitivity of 58% and a specificity
of 95% for cases of NF.
• 30% hypocalcaemic
• Hypoalbuminaemia and hyponatraemia
• high serum lactate with severe metabolic acidosis
The LRINEC (Laboratory Risk Indicator
for Necrotising Fasciitis)
The LRINEC (Laboratory Risk Indicator
for Necrotising Fasciitis)
• A score of 6 >> raises the suspicion
• A score 8 >> ‘strongly predictive’ of NF
• Predict mortality
Histopathology
• Deep incisional biopsies are more useful than punch biopsies
• Biopsy should include the advancing edge and central necrotic
areas
• Histological examination reveals underlying thrombi, necrosis,
polymorphonuclear infiltrate, microorganisms, and vasculitis.
• Gram staining is important, since a paucity of leucocytes in the
presence of Grampositive cocci may be seen in GASNF or CAMRSA due to leucocidin mediated destruction of WBCs.
Management
Surgical
• Prompt diagnosis
• Aggressive surgery removes the source of infection and toxins
• (VAC) dressing with a continuous pressure of 40 to100 mmHg
is useful for wound coverage and encourages granulation
• the tissue oxygen tension can be measured with a probe using
transcutaneous soft tissue oximetry. lower in NF than cellulitis
Role of hyperbaric oxygen
(HBO)
• HBO switches off a-toxin production from Clostridium spp
• increase the bactericidal action of neutrophils
• Decrease mortality to 12%
Antibiotics
• Broad-spectrum empirical therapy covering most types of NF
• Then >> based on culture data.
• Clindamycin: switching off exotoxin production even in
stationary phase organisms
Empirical protocol
• I.V. clindamycin 1.2 to 1.8 g six-hourly with I.V. imipenem 0.5
to 1 g six-hourly.
• IF MRSA : I.V. linezolid 600 mg BID or daptomycin 6 mg/kg
may be added in preference to vancomycin
• For Vibrio spp. >> doxycycline 100 mg twice daily plus
intravenous ceftazidime 2 g eight-hourly is recommended
I.V.I.G
• IVIG may
• promote clearance of GAS by the immune system
• neutralise streptococcal superantigens
• act as an immunomodulatory agent
• contraindication
• selective IgA deficiency
• history of anaphylaxis with immunoglobulins.
• 2 g/kg, with the option of a second dose if necessary
after 24 h. rate of 20 mL/h, increasing incrementally
after 10 min to a maximum of 160 mL/h.
prognosis
• Bad prognostic factors:










Not type 1
myonecrosis or myositis
STSS
High serum lactate combined with low sodium
Late operation
% BSA
Acidosis
Peripheral vascular disease
Advanced age
Other comorbidities
Antimicrobial prophylaxis for
contacts of GASNF
• 27% of household contacts may be GAS carriers (200 times
more likely to occur)
• CDC, do not recommend routine testing for GAS colonisation
or administration of chemoprophylaxis to household contacts.
• UK Health Protection Agency in 2004, recommend prophylaxis
to mothers and babies if either was infected during the
neonatal period
• Household contacts should be informed about the clinical
manifestations of pharyngeal and GAS infection