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Lecture: Erysipelas

- Is a super ficial cutaneous disease -> to dermis

- Have lymphatic involvement
- Distinguished by other forms of skin inf by 2 features:
 Elevation on level of surrounding skin
 Have clear line of demarcation of uninvolved tissue
- > common in infants, young child, & older adult
- In our hospital (Moscow) ->older adult
- By β-hemolytic streptococci
- In most cases, inf agent is in group A β- hemolytic streptococci
- Can be also caused by group C & G
- Rarely group B & Staphylococcus aureus
- Was described involved the “ Butterfly area of face”
- Have in lower extremities ( > freq)
- In pt with facial erysipelas have history of streptococci sore throat & mode of its transmission to
skin is still unknown. (ophthal & antrum)
- Incl. surgical incision, trauma / incision & kin dis / psoriasis & local fungal inf. (> freq)
- Cutaneous lesion has localized erythema & swelling with changed red margin that raised & well
demarcated from a normal young zone. < yaziki flamani> - demarcation zone is not level
- Have marked edema often with _________ formation & erysipelas have swollen eyes
- Can demonstrated ___________
- Cutaneous manifestation have chill, fever & intoxication

Basic clinical principles:

- From stable high case rate, charac. of all region of the country, tendency to go to clinical chronic
- Evaluation of clinical course o disease with ↑ of dis. With hemorrhagic erysipelas with longer
fever & slowdown of reparation in the locus of an inflame
- The special place with contagious__________, hereditary determinant reaction of organism of
pt with streptococcus group A. Onset of ___________ intra & extracellular factor of virulence
(will be late)

Provoking factors:
1. Disturbances of integrity of integument as fracture, lesion, change T’ ,sharp trauma etc
2. Emotional stress & insolation & ↓ T’
3. Trauma of field / bruises with erysipelas ( Intercurrent dis angina, bronchitis etc.)
Contribution factors:
1. Concommitant diseases:
- DM, obesity, chronic venous failure (varicose dis of veins), chronic failure of absorbent vessels
(lymphostasis), eczema, psoriasis & other skin diseases (mycosis of the auto- podium)
2. Presence of the locuses of chronic streptococci inf contamination (tonsillitis, otitis, sinusitis,
karies, paradontitis) -> lead to oftenly to erysipelas of the foot, osteomyelitis, trophic ulcer etc.
3. Profesion trauma (bone trauma) with increasing of contamination of integument with________
(sportsman,drivers etc)
4. Chronic somatopathy with immunodeficiency (in advance ages)
5. End stage of pathogeny of erysipelas

Clinical classification of Erysipelas (V.I Cherkasov; 1986)

1. On character of aboriginal exhibiting :

- Erythematic
- Erythematic – bullous
- Erythematic – hemorrhagic
- Bullous – hemorrhagic

2. On a degree of gravity : Mild (I), Moderate (II), Severe (III)

3. On frequency rate of course:

- Primary
- Repeated (arising in 2 years, other localization of process)
- Relapsing (at presence not less than 3 relapses of an erysipelas for a year expediently
determining “often relasing erysipelas” )

4. On prevalence of aboriginal exhibiting:

- Localized erysipelas
- Abundance erysipelas
- Metastatic erysipelas with the advent of remote from each other the locuses of an inflammation

5. Complications of an erysipelas:

a) Aboriginal (an abscess, phlegmon, necrosis,phlebitis,periadenitis etc.)

b) Common (a sepsis, toxic shock,thomboemboli of pulmonary arteries etc.)

6. Consequences erysipelas:

a) Resistant lymphostasis (lymphatic edema)

b) Secondary elephantitis (fibredema)
Features of pathogens of dev of erysipelas:
- Making up of the resistant locus of a streptococcal infection contamination in an organism of
the patient ( L-form ):
 A derma
 Lymph nodes
 Bone marrow (osteal brain)
- Depression of functional condition status of neutrophil
- Fluctuation of a level of cellular & humoral immunodefense
- The high level of an allergization (cell- mediated type IV hypersensitivity to group A β –
hemolytic streptococci.

Localization of the locus of an inflammation :

- Lower extremities : 60 -80%
- Face : 15 -25%
- Upper extremities: 5 -8 %
- Other localization (perineum,trunk etc): 1 -3%

Pathogenesis of Erysipelas:
- Introduction of a streptococcus in a skin as a result of its damage (at a primary erysipelas) or by
a becoming infected from the locus of a dosing infection contamination can descend & is
immediate from the locus of independent disease of a streptococcal etiology (a pharyngitis,
sinusitis, otitis etc.)
- Breeding of streptococcus in lymphatic capillary vessel dermas
- Development bacteriemia, toxemias, that leads to originating symptoms to an intoxication (the
acute beginning of disease from rise in temperature, a cold fit,delicacy etc)
- Development of the aboriginal locus of an infectious – allergic inflammation of a skin with
participation of immune- complex process (are formed perivascular) the located cell – bound
immune complexes containing C-3 fraction of a complement).
- Disturbance capillary flows of lymph in a skin & microcirculation with formation of a
lymphostasis, possible formation of hemorrhages & bladders with serous & hemorrhagic
- Formation of the locuses of a chronic streptococcal infection contamination in a skin & partial
lymphonduses with presence of bacterial & L –forms of a streptococcu that leads at a part of
patients in development of relapse of disease (chronic course of erysipelas)
- Elimination of bacterial forms of a streptococcus by means of an engulment & formation of cell-
bound immune complexes both other immune mechanism & convalescence of the patient.
Indications for obligatory hospitalization in infectious diseases hospitals
(abjointings) are:

- Serious current of an erysipelas with sharply expressed intoxication or the widespread lesion of
a skin (especially at bullous – hemorrhagic to the form of an erysipelas)
- Frequent relapses of an erysipelas, irrespective of a degree of an intoxication, character of
aboriginal process
- Presence of serious general concomitant diseases
- Senile children’s age of patients

Incubation period:-

- From several hour till 3 – 5 days. At patients with relapsing course of the erysipelas,
development of the next attack of disease is preceded often with a frigorism, stress. At the
depressing majority o patients disease begins was acutely.

The initial stage of disease:-

- Is characterized by fast development of signs of an intoxication which more than at half of

patients (it is usual at localization of an erysipelas on the lower extremities) for the term of from
several hours till 1 -2 daysadvance originating aboriginal exhibiting of disease.
- The headache, the general delicacy, a cold fit, muscular pains is marked, 25 – 30% of patients
have nausea & a vomiting.
- At the 1st hourof disease the temperature increase upto 38 – 40 ‘ C.
- On fields of a skin in the field of the future local exhibiting at of some patients are felt
parasthesia, sense strutting or burning sensations, not intensive. Quite often there are alo pains
in the field of enlarged partial lymph nodes.

The height of disease:-

- Comes in terms from several hours till 1- 2 days after the first exhibiting disease. Reach the
maximum general – toxic exhibiting & a fever. There are characteristic aboriginal exhibiting an
- More often inflammatory process is localized on the lower extremities (60 -70%), less often on
the face (20 -30%) and the top extremities ( 4 -7%), is rare only on a trunk, in the field of
mammary gland, perineum, outside of reproductive organs.
- From the beginning of the treatment and uncomplicated character of an erysipelas the fever
usually does not exceed 5 day. At 10 -15% of patients the fever is keptover 7days that is
observed usually at the widespread process & not enough a high grade causal treatment.
- The longest feverish period at bullous – hemorrhagic to the erysipelas. From above, 70% that
sizk of erysipelas, it is marked a lymphadenitis educing at all forms of disease.
The period of reconvalescence:-

- Normalization of temperature & decreasing of intoxication are observed at an erysipelas earlier,

than the previous ly shown
- Acute presentation of disease are kept till 5 -8 days at hemorrhagic forms till 12 -18 day and
more. To the residual phenomena of an erysipelas kept during several weeks & months, concern
pastose and xanthopathy, a stagnant hyperemia on a place of the quenched erythema, dense
dry crusted on a place of bullas, a hydropic syndrome.
- The kept enlarged & morbid lymph nodes, infiltrates of a skin in the field of the quenched locus
of an inflammation, subfebrile temperature have unfavourable prognostic value ( probability of
development of early relapse).
- Prognostically unfavourable also long conservation of a lymphatic edema (lymphostasis) which
should be surveyed as an early stage (lymphatic edema) a secondary elephantitis.
- The hyperpigmentation of fields of a skin on the lower extremities at the patients, who have
tolerated bullous – hemorrhagic an erysipelas, can be kept for life.

Diagnostic criteria of an erysipelas: (are based only on a characteristic clinical

pattern of disease, laboratory methods of diagnostics are not used)
- The acute beginning of disease with the expressed igns of an intoxication
- Primary localization aboriginal inflame process on the lower extremities and the face
- Development of typical aboriginal exhibiting with a characteristic erythema, possible aboriginal
hemorrhagic syndrome
- Development partial a lymphadenitis
- Absence of the expressed pains in the locus of an inflammation in rest

*Infectious – allergic and immunocomplex mechanisms of the inflammation at the erysipelas cause its
serous- hemorrhagic character. Apposition of a purulent inflame testifies to the complicated disease.

Differential diagnosis:
- erysipelas should be compared with more than with 5 -10 diseases, concerning clinical features
of surgical, dermal and contagious and intrinsic diseases.
- First of all,we need t exclude abscess, phlegmon, supurative hematom, thrombophlebitis
(phlebitis), dermatitis,eczema, surrounding erysipeloid, a nodulose erythema.
Treatment of an erysipelas:

(I) Etiological treatment:

Treatment in hospital ;
- a preparation of choice – is Benzylpenicilin daily dose 6 -12 million U, IM for 10 days
- reserve preparation is cephalosporin I generation (Cefazolinum etc.) – in a daily dose 1,2 – 2,4 g
and more,IM) are appointed at the serious omplicated course of erysipelas
- In the serious course of disease, development of complications (an abscess, phlegmon etc) the
combination Benzylpenicillin (in the specified dosage) & gentamycin (240 mg – once daily,IM).
- Penicillin (in the specified dosage) & ciprofloxacin (400 – 800 mg IV drip)
- Penicillin & clindamycin (in specified dosages)
- Purpose of the combined antibacterial therapy is justified & at bullous hemorrhage of erysipelas
with an abundant exudates of fibrin.

Treatment for out-patient;

- Give one of the drugs(antibiotics) below perorally:
o Spiramycin 3 million ME 2x/d for 10 days
o Azithromycin- in 1st day 0,5 g, then within 4 days on 0,25g 1x/d for 0,5g for 5 days
o Roxithromycin - 0,15 g 2x/day for 10 days
o Ciprofloxacin – 0,5g 2-3x/day for 10 days
o Cefaclor 0,5 g 3x/day for 10 days
o Use new Quinolones (Levofloxacin, gatifloxacin, moxifloxacin) are also possible

(II) Pathogenetic treatment:

- Disintoxication therapy (if necessary IV) , with use of diuretic & cardiovascular preparations
- Anti inflammatory therapy (Indomethacin, Butadionum, Aspirinum etc) – precaution to DM pt
- Desensitization therapy (under indication) – anti allergic (Suprastin etc)

(III) Local therapy:

- Apply bandages with 0,02% furosilinum / 0,1% solution of Rivanolum, shanging them sometimes
within day (erythematic erysipelas carrying out of aboriginal therapy is not required)

(IV) Physiotherapy:
- Use ultraviolet radiation on range of the locus of an inflammation & an electric current of
ultrahigh frequency on range regional lymph nodes
- Conservation in the period of a reconvalescence of an infiltration of a skin, hydropic syndrome,
regional a lymphadenitis are appointed an ozocerite or a bandage with warm taftaleneum
ointment (to the lower extremities), paraffin (on the face), electrophoresis of lydasum
(especially in initial stages of formation of an elephantitis), sodium chloridum of calcium, radon
baths, a magneto therapy
- Last year high efficacy low-energy laserotherapy in treatment of an thermal inflammatory
syndrome is established at varius clinical forms of an erysipelas.
- Laser radiance,as in red, and in infra-red range is used.

Anti recurrent therapy:

(I) Consecutive 2- course antibioticotherapy

(It is desirable in a hospital at developing an acute episode of disease)

1st course:

- Benzylpenicillin daily 6 -12 million U, IM for 10 days

- Cephalosporin (I) generation (Cefazolin in a daily dose of 3 -6 g IM for 10 days

2nd course:

- Lincomycin (30% a solution -2,0 ml – 3x /day, IM) or 0,5g 3x/day perorally for 7 – 10 days

(II) Bicillinum prophylaxis (outside of an acute episode of disease)

After the tolerated primary, recurring or repeated erysipelas

- Bicilinum 5 -1,5 million U or Benzathine benzylpenicillin (Retarpen, Extenvilline) 2,4 million U,

in/m once in 2 -3 weeks( the drug is appointed after careful finding out of the anamnesis
excluding had survivability of Peniccilinum)

Variant Indications Course

Continuous Frequent (not less than 3 for last Till 2nd year and more
year) relapses of an erysipelas
In season Distinctly expressed seasonal The beginning 1 month prior to a
prevalence of relapses season of relapse, within 3 -4
Course Preserving significant residual Within 3 -6 months after an
the phenomenon in the season extact frm hospital
of a reconvalescence at the
patients which have tolerated a
relapsing, repeated or primary
Prophylaxis of relapse it is necessary (it is our patient or in specialized
1. The well-timed and high grade antibiotic therapies of primary disease and relapses
2. Treatment of the expressed residual phenome (the erosion, kept puffiness in the field of the
aboriginal focus), consequences of an arysipelas (a non perishable lymphostasis an elephantitis)
3. Treatment is long and persistently proceeding chronic diseases the skins leading disturbances of
its trophicity and appearance of entrance hiluses for an infection contamination
4. Treatment of the locuses of a chronic streptococcal infection contamination (chronic tonsillitis,
sinusitis, otitis etc)
5. Treatment of disturbances of a flow of lymph & a circulation in a skin as a result of primary and
secondary lymphostasis and an elephantiasis, chronic diseases of peripheral vessels.
6. Treatment of an obesity, a diabetes mellitus (which frequent decompensation is observed in

Morphology of group Streptococci:

- Streptococci is a gram (+), catalae (-), non-motile, non-spore forming have in chains or in pairs of
- Individual cells are round to avoid cocci; 0,6 – 1,0 micrometer in diameter.
- Streptococci divide in 1 plane and thus occur in pairs or (especially in liquid media or clinical
material) in chains of varying lengths. The metabolism of Streptococci is fermentative
- Nutrition of bac needs complex media and it prefers supplemental blood for best grows.
- Homeofermentative lactic acid without production of gas at major end – product. Aerobic &
- It doesn’t use oxygen metabolically

The classification of streptococci (The type of hemolytic reaction displayed on

blood agar)
1. β –hemolytic Streptococci (assoc. with complete lysis of red cells surrounding the colony)
2. α – hemolytic Streptococci ( a partial or “green” hemolysis assoc. with ↓ of red cell Hb)
3. γ – hemolytic Streptococci (non-hemolytic colonies) -> no changes in blood agar
- The cell wall of streptococci is composed of repeating unit of N – Acetylglucosamine
(polysaccharide). Historically, the definitive identification f treptococci has rested on the
serologic reactivity of <cell wall>. Polysaccharide antigens as originally described by Rebecca
Lancefield (1930s). 20 groups- specific antigens (Lancefield goups) were established (A,B,C,D etc)
Classification of Streptococci Most commonly assoc woth human diseases
Lance field group Species Most common Human diseases
A (β –hemolytic) Streptococcus pyogenes Pharyngitis, skin infection,
wound inf, pneumonia, post inf
glomerulonephritis, rheumatic
B ( β & γ- hemolytic) Streptococcus agalactiae Neonatal septicaemia,
meningitis, osteomyelitis,
C (β- hemolytic) Streptococcus equisimilis , dysgalactiae Wound inf, puerperal
septicaemia, cellulitis,
endocarditis, epidemic
pharyngitis, pyogenic arthritis
Streptococcus bovis Subacute endocarditis,
D (α & γ hemolytic) bacteremia of hepatobiliary
origin, malignant lesions of the
G (α,β,γ hemolytic) Streptococcus canis Puerperal infection, skin
&wound inf, endocarditis,
pyogenic arthritis
Viridans streptococci Streptococcus pneumonia Pneumonia, otitis media,
(α,β,γ hemolytic) sinusitis, meningitis
Streptococcus mutans, S. oralis, sanguis, Endocarditis, septicaemia, dental
gordonii, crista, salivarius, anginosus, infection inf (caries),
vestibularis intravascular catheter – related

Comparison of Early-Onset & Later-Onset Group B Streptococcal Infectious:

Feature Early onset Late-onset Very late onset
Age range < 7 days 7 to 89 days  3 months
Median age at onset 1 hour 27 days Unknown
Maternal obstrectic Common Uncommon Varies
Frequency of gestation Frequency (30%) Uncommon Common
<37 weeks
Usual clinical Septicaemia (35 - 55%) Meningitis (25 – 35%) Bacteremia without
presentations Meningitis (5-10%) Bacteremia without focus (common)
Resp dis (pneumonia) focus (40-60%) Bacteremia with a focus
(35-55%) Osteoarhtitis (5%) (occasional)
Common serotypes I (Ia,Ib,Ia/c), II, III, V III ( 75%) Unknown
Mortality rate 5 – 70% 2 -6 % Low
Streptococcus Group D infections
1. Echocardiography
- Transthoracic / transesophageal (> sensitive), echocardiography frequently permits visualization
of vegetations.
2. Liver ultrasonography & CT scanning
- Usually liver US is performed 1st, followed by CT scanning
3. Barium enema (detecting malignant lesions in the colon)
- Barium enema should be performed on patients with S. bovis bacteremia or endocarditis
- The only alternative to a barium enema is a colonoscopy

Cell surface stucture of Streptococcus pyogenes & secreted products involved in


Group A Streptococcal M-Types ( >120) often associated ith nonsuppurative &

toxin-mediated sequalae:

Sequela M-Types
Acute rheumatic fever 1, 3, 5,6, 18
Postpharyngeal 1-4, 12, 15
Postpyoderma 49, 52, 55, 59, 60, 61
Streptococcal toxic shock syndrome 1, 3 predominantly; severa others

Mucosal immunity Against Group A Streptococci:

Factor of Virulence Group A streptococci (Streptococcus pyogenes)
Components of a cellular wall
A polysaccharide (group carbohydrate Ag or Autoimmune reactions, formation of immune
substance C) complexes, necrosis & a generation of collagenic
fibres, a damage of lysosome macrophages
M- protein ( > 120) Oppresion phagocytosis, autoimmune reactions
(synovial membrane,skin, valve of heart, kidneys
etc), formation of immune complexes factor of
invasion, superantigen (invasion forms)
Peptidoglycan Pyrogenic reactions, necrosis of tissue, activation
of an internal way of hemostasis, activation
kallikrein – kinin system
Lipoteichoic acid Factors of adhesion, damage of platelets,
Hyaluronic acid capsule, fibronectin binding Factors of adhesion
Protein F1 Factors of invasion
Extracellular Products
Streptococcal pyrogenic exotoxins (SpeA, SpeB, Pyrogenic reactions, superantigens (streptococcal
SpeC etc), SSA toxic shock syndrome (Strep TSS), necrotizing
fasciitis, and other severe infections), scarlatinal
toxins (SpeA & SpeC)
Streptolysin O Autoimmune reactions damage the membranes of
polymorphonuclear leukocytes, platelets,
erythrocytes ad subcellular organelles, cardiotoxic
Streptolysin S Cytotoxic action (polymorphonuclear
leukocytes,platelets, erythrocytes)
Hyaluronidase Damage of the basic substance of a connecting
fabric, endothelium of vessels (spread thru tissues)
Streptokinase Activation fibrinolysis, cytotoxic action (skin
DNases A,B,C,D Cytotoxic action
C5a / peptidase Streptococcal inhibitor of complement (oppression
pagocytosis, blocks migration of
Polymorphonuclear leukocytes)

Summary of diseases caused by Streptococcus pyogenes:

1. Supurative conditions (active infections assoc with pus) occur in throat, skin and

Throat Streptococcal pharyngitis is acquired by inhaling aerosols emitted by infected

individuals. The symptoms reflect the inflammatory events at the ite of infection. A
few (1- 3%) people develop rheumatic fever weeks after the infection has cleared
Skin Impetigo involves the infection of epidermal layer of skin. Pre-pubertal children are
the most susceptible. Cellulitis occurs when the infection spreads subcutaneous
tissues. Erysipelas is the infection of the dermis. About 5% of patients will develop
more disseminated disease. Necrotizing fasciitis involves infection of the fascia &may
proceed rapidly to underlying muscle.

2. Systemic

Scarlet fever Is caused by production of erythrogenic toxin by a few strains of the organism.
2 of the most severe, but least common, forms of invasive GAS disease are called
“necrotizing fasciitis” and “streptococcal toxic shock syndrome” (STSS)

3. Non – supurative sequelae

- Some of the antibodies produced during the above infections cross-react with certain host
tissues. These can indirectly damage host tissues even after the organisms have been cleared
and cause non-supurative complications

Rheumatic fever M protein cross reacts with sarcolemma Antibodies cross reacts with heart
tiua, fix complement and cause damage
Glomerulonephritis Antigen-Antibody complexes may be deposited in kidney, fix complement,
and damage glomeruli. Only a few M-types are nephritogenic.

- Is an initially vesicular, later crusted, superficial inf of the skin.. Most cases occur in children.
Histopathologically, impetigo consists of a superficial intra epidermal, unilocular vesicopustule.
- In epidemiological studies, group A streptococcal acquisition on normal skin antedates the
appearances of impetigo by about 10 days.
- During that time,minor trauma (eg:insect bite,abrasion) predisposes to the development of
infected lesions.
- Impetigo is most common during hot, humid summer weather. 2 -3 weeks after skin acquisition
of streptococci, pharyngeal colonization by the same organism occurs in about 30% of children
with skin lesions.
- The sporadic cases of the facial impetigo occur in colder climates probably result from
contagious spread from an initial nasopharyngeal infection, and the serotypes involved are
those commonly causing pharyngeal disease.
- In contrast, in the case of staphylococcal impetigo,(in case of only S. aureus is the pathogen),
nasal colonization precedes that of the normal skin; skin lesions then occur after such
Classification of Bacterial superficial infections of the skin

Type of lesion Etiological agents

Impetigo Staphylococcus aureus, group A streptococci
Follicullitis S. aureus, Candida, Pseudomonas aeruginosa,
Pityrosporum ovale
Furuncles & carbuncles S. aureus
Paronychia S. aureus, group A streptococci, Candida, P.
Ecthyma Group A streptococci

- Erysipelas involves the more superficial layers of the skin & cutaneous lymphatic, whereas
cellulitis extens more deeply into the subcutaneous tissues.
- This anatomical distinction is the basis for the clinical differentiation of the 2 entities.
- In typical erysipelas, the area of inflammation is raised above the surrounding skin, and there is
a distinct demarcation between involved & normal skin. In cellulitis, neither of these clear
distinction between infected nor not infected one is present.

Specific Anatomical Variant of Cellulitis & Cause Predispoition to the Condition

Predisposing condition Etiological agent

Periorbital cellulitis Staphylococcus aureus, pneumococcus, group A
Bucal cellulitis Haemophilus influenza
Perianal cellulitis Group A streptococcus
Cellulitis complicating body piercing (ear, nose, S. aureus, group A streptococcus
Mastectomy (with axillary – node dissection) for Non-group A hemolytic streptococcus
breast cancer
Harvest of saphenous vein for coronary bypass Group A or non- group A hemolytic streptococcus
Liposuction (thigh, abdominal wall) Group A streptococcus, peptostreptococus
Postoperative (very early) wound infection Group A streptococcus
(abdomen, chest hip)
Injection of drugs used (“skin popping”) – S. aureus, streptococci (groups A,C,F,G)
extremities, neck
Gas gangrene, crepitant cellulitis Clostridium perfringens and other clostridial
species: Bacteroides,peptostreptococci, Klebsiella,
E. coli
Necrotizing fasciitis:
- is an infection of the dermal of the dermal, fascial and subcutaneous layers of the skin
- it is characterized by microbial & leucocytic infiltrates leading to vasculitis, thrombosis and
tissue necrosis
- the infection is commonly acute, fulminant process but may follow a subacute, progressive
- Necrosis may become widespread, with signs of systemic toxicity appearing unless the infection
is treated in its earliest stages.
- Mortality rates upto 76% have been reported without early intervention.

Etiologic Agents of Necrotizing Fasciitis:

Predisposing Condition Etiological agent

None Group A streptococcus
Diabetes mellitus Bacteroides fragilis (other gram negative anaerobic
bacilli), Enterobacteriaceae, Staphylococcus
aureus, Streptococcus sp.
Prior surgery Bacteroides sp. , Clostridium sp, Staphylococcus
aureus, Group D streptococcus
Immunosuppression & malignancy Pseudomonas aeruginosa, Enterobacteriaceae
Arterioclerosis Streptococcus sp, Clostridium sp
Odontogenic infection Prevotella sp, Porphyromonas sp, Fusobacterium
Varicella infection Group A streptococcus
Streptococcal gangrene & necrotizing fasciitis Group A streptococci, mixed infections with
Enterobacteriaceae & anaerobes
Definition of Streptococcal toxic shock-like syndrome:

(I) Isolation of GAS from:

A) a normally sterile site (eg: blood,CSF, pleural fluid or peritoneal fluid, tissue biopsy, surgical
wound etc.)
B) a non sterile site (eg: throat, sputum, vagina, superficial skin lesion etc)

(II) Clinical signs of severity:

A) Hypotensive : systolic BP ≤ 90 mmHg in adult and <5% for children

B) ≥ 2 of the following signs

i) Renal impairment: creatinine ≥ 177 µM for adults or ≥ 2 of the upper limit of normal age. N
patients with pre-existing renal disease, in ≥ 2-fold elevation over the baseline level.
ii) Coagulopathy: platelets ≤ 100 x 109 /L or disseminated intravascular coagulation defined by
prolonged clotting times, low fibrinogen level and the presence of fibrin degradation
iii) Liver involvement: alanine aminotransferase, aspartate aminotransferase or total bilirubin
levels ≥2 x the upper limit of normal age. In patients with preexisting liver disease, a ≥ 2-fold
elevation over the baseline level
iv) Adult resp distress syndrome defined by acue onset of diffuse pulmonary infiltrates &
hypoxemia in the absence of cardiac failure or evidence of diffuse capillary leak manifested
by acute onset of generalized edema or pleural or peritoneal effusions with
v) A generalized erytematous macular rash that may desquamate
vi) Soft tissue necrosis, including necrotizing fasciitis or myositis or gangrene

An illness fulfilling criteria IA and II (A and B) is defined as definitive case. An illness fulfilling criteria IB
and II (A and B) is defined as a probable case if no other etiology for the disease is identified.