streptococcus group A infections

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Fellow in Infectious Diseases, University of OklahomaHealth Science Center

Assistant Professor, Department of InternalMedicine, Section of Infectious Diseases, University of Oklahoma College of Medicine; MedicalDirector of Infectious Diseases Institute, University of Oklahoma Health Sciences Center;

Professor and Head, Division of Pulmonary Medicine, Department ofInternal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St BonifaceGeneral Hospital; Program Director of Medical Microbiology,Professor, Department of Medicine, Section of Infectious Diseases and Microbiology, StBoniface Hospital, University of Manitoba, CanadaContributor Information and Disclosures

Updated: Sep 23, 2009

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Streptococcus pyogenesis beta-hemolytic bacterium that belongs to Lancefield serogroup A,also known as group A streptococci (GAS). GAS, a ubiquitous organism, causes a wide varietyof diseases in humans and is the most common bacterial cause ofacute pharyngitis, accountingfor 15%-30% of cases in children and 5%-10% of cases in adults.1During the winter and springin temperate climates, up to 20% of asymptomatic school-aged children may be GAS carriers.2

GAS usually causes pharyngitis orimpetigo but, in rare cases, can also cause invasive diseasessuch as cellulitis, bacteremia, necrotizing fasciitis, and toxic shock syndrome (TSS). Along withStaphylococcus aureus, GAS is one of the most common pathogens responsible for cellulitis .

S pyogeneswas first described by Billroth in 1874 in patients with wound infections. In 1883,Fehleisen isolated chain-forming organisms in pure culture from perierysipelas lesions.Rosebach named the organism S pyogenesin 1884. Studies by Schottmueller in 1903 and J.H.Brown in 1919 led to knowledge of different patterns of hemolysis described as alpha, beta,and gamma hemolysis.

A later development in this field was the Lancefield classification of beta-hemolytic streptococciby serotyping based on M-protein precipitin reactions. Lancefield established the critical role ofM protein in disease causation. In the early 1900s, Dochez, George, and Dick identified

hemolytic streptococcal infection as the cause ofscarlet fever. The epidemiological studies ofthe mid 1900s helped establish the link between GAS infection and acute rheumatic fever (ARF)and acute glomerulonephritis.3
http://emedicine.medscape.com/article/228936-printmailto:enter%20email%20address%20here?Subject=eMedicine%20Article%20-%20Streptococcus%20Group%20A%20Infections&Body=I%20thought%20you%20might%20be%20interested%20in%20this%20article%20from%20eMedicine.%20You%20may%20either%20click%20on%20the%20following%20link%20or%20copy%20and%20paste%20it%20into%20your%20browser.%0Dhttp://emedicine.medscape.com/article/228936-overview%0D%0A%0D%0AeMedicine%20is%20the%20leading%20provider%20of%20clinical%20medical%20information%20for%20medical%20professionals%20and%20consumers.%20To%20explore%20eMedicine%20today,%20visit%20http://emedicine.medscape.comhttp://emedicine.medscape.com/article/225243-overviewhttp://emedicine.medscape.com/article/219473-overviewhttp://emedicine.medscape.com/article/219473-overviewhttp://emedicine.medscape.com/article/214222-overviewhttp://emedicine.medscape.com/article/961169-overviewhttp://emedicine.medscape.com/article/1054438-overviewhttp://emedicine.medscape.com/article/169177-overviewhttp://emedicine.medscape.com/article/228816-overviewhttp://emedicine.medscape.com/article/228816-overviewhttp://emedicine.medscape.com/article/188988-overviewhttp://emedicine.medscape.com/article/1053253-overviewhttp://emedicine.medscape.com/article/333103-overviewhttp://emedicine.medscape.com/article/239278-overviewmailto:enter%20email%20address%20here?Subject=eMedicine%20Article%20-%20Streptococcus%20Group%20A%20Infections&Body=I%20thought%20you%20might%20be%20interested%20in%20this%20article%20from%20eMedicine.%20You%20may%20either%20click%20on%20the%20following%20link%20or%20copy%20and%20paste%20it%20into%20your%20browser.%0Dhttp://emedicine.medscape.com/article/228936-overview%0D%0A%0D%0AeMedicine%20is%20the%20leading%20provider%20of%20clinical%20medical%20information%20for%20medical%20professionals%20and%20consumers.%20To%20explore%20eMedicine%20today,%20visit%20http://emedicine.medscape.comhttp://emedicine.medscape.com/article/228936-printhttp://emedicine.medscape.com/article/228936-printmailto:enter%20email%20address%20here?Subject=eMedicine%20Article%20-%20Streptococcus%20Group%20A%20Infections&Body=I%20thought%20you%20might%20be%20interested%20in%20this%20article%20from%20eMedicine.%20You%20may%20either%20click%20on%20the%20following%20link%20or%20copy%20and%20paste%20it%20into%20your%20browser.%0Dhttp://emedicine.medscape.com/article/228936-overview%0D%0A%0D%0AeMedicine%20is%20the%20leading%20provider%20of%20clinical%20medical%20information%20for%20medical%20professionals%20and%20consumers.%20To%20explore%20eMedicine%20today,%20visit%20http://emedicine.medscape.comhttp://emedicine.medscape.com/article/228936-diagnosishttp://emedicine.medscape.com/article/228936-treatmenthttp://emedicine.medscape.com/article/228936-followuphttp://emedicine.medscape.com/article/228936-mediahttp://emedicine.medscape.com/article/225243-overviewhttp://emedicine.medscape.com/article/219473-overviewhttp://emedicine.medscape.com/article/214222-overviewhttp://emedicine.medscape.com/article/961169-overviewhttp://emedicine.medscape.com/article/1054438-overviewhttp://emedicine.medscape.com/article/169177-overviewhttp://emedicine.medscape.com/article/228816-overviewhttp://emedicine.medscape.com/article/188988-overviewhttp://emedicine.medscape.com/article/1053253-overviewhttp://emedicine.medscape.com/article/333103-overviewhttp://emedicine.medscape.com/article/239278-overview


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The traditional Lancefield M-protein classification system, which is based on serotyping, hasbeen replaced by emmtyping. This gene-typing system is based on sequence analysis of theemmgene, which encodes the cell surface M protein. Approximately 200 emmtypes have beenidentified by the Centers for Disease Control and Prevention (CDC) thus far.

In the preantibiotic era, streptococci frequently caused significant morbidity and wereassociated with significant mortality rates. However, in the postantibiotic period, diseases dueto streptococcal infections are well-controlled and uncommonly cause death. GAS can cause adiverse variety of both suppurative diseases and nonsuppurative postinfectious sequelae.

The suppurative spectrum of GAS diseases includes the following:

Pharyngitis with or without tonsillopharyngeal cellulitis or abscess Impetigo (purulent honey-colored crusted skin lesions) Pneumonia Necrotizing fasciitis Streptococcal bacteremia Osteomyelitis Otitis media Sinusitis Meningitis or brain abscess (a rare complication resulting from direct extension of an ear

or sinus infection or from bacteremic spread)

The nonsuppurative sequelae of GAS infections include the following:

Acute rheumatic fever (ARF; defined by Jones criteria) Rheumatic heart disease (chronic valvular damage, predominantly mitral valve) Acute glomerulonephritis

Superantigen-mediated immune response may result in the following entities:

Streptococcal TSS (STSS): This is characterized by systemic shock with multiorganfailure, with manifestations ofrespiratory failure, acute renal failure, hepatic failure,neurological symptoms, hematological abnormalities, and skin findings, among others.This is predominantly associated with M types 1 and 3 that produce pyrogenic exotoxinA, exotoxin B, or both.4

Scarlet fever: This is characterized by upper-body rash, generally following pharyngitis.

Streptococci are a large group of gram-positive, nonmotile, nonspore-forming cocci about 0.5-1.2 m in size. They often grow in pairs or chains and are oxidase- and catalase-negative.

S pyogenestends to colonize the upper respiratory tract and is highly virulent as it overcomesthe host defense system. The most common forms ofS pyogenesdisease include respiratoryand skin infections, with different strains usually responsible for each form.

The cell wall ofS pyogenesis very complex and chemically diverse. The antigenic componentsof the cell are the virulence factors. The extracellular components responsible for the disease

process include invasins and exotoxins. The outermost capsule is composed of hyaluronic acid,which has a chemical structure resembling host connective tissue, allowing the bacterium toescape recognition by the host as an offending agent. Thus, the bacterium escapesphagocytosis by neutrophils or macrophages, allowing it to colonize. Lipoteichoic acid and M
http://emedicine.medscape.com/article/300157-overviewhttp://emedicine.medscape.com/article/785020-overviewhttp://emedicine.medscape.com/article/764006-overviewhttp://emedicine.medscape.com/article/232915-overviewhttp://emedicine.medscape.com/article/212946-overviewhttp://emedicine.medscape.com/article/333103-overviewhttp://emedicine.medscape.com/article/891897-overviewhttps://connect.ouhsc.edu/med/,DanaInfo=www.emedicine.com+TOPIC879.HTMhttp://emedicine.medscape.com/article/167981-overviewhttp://emedicine.medscape.com/article/243492-overviewhttp://emedicine.medscape.com/article/300157-overviewhttp://emedicine.medscape.com/article/785020-overviewhttp://emedicine.medscape.com/article/764006-overviewhttp://emedicine.medscape.com/article/232915-overviewhttp://emedicine.medscape.com/article/212946-overviewhttp://emedicine.medscape.com/article/333103-overviewhttp://emedicine.medscape.com/article/891897-overviewhttps://connect.ouhsc.edu/med/,DanaInfo=www.emedicine.com+TOPIC879.HTMhttp://emedicine.medscape.com/article/167981-overviewhttp://emedicine.medscape.com/article/243492-overview


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proteins located on the cell membrane traverse through the cell wall and project outside thecapsule.

The cell wall antigens include capsular polysaccharide (C-substance), peptidoglycan andlipoteichoic acid (LTA), R and T proteins, and various surface proteins, including M protein,fimbrial proteins, fibronectin-binding proteins (eg, protein F), and cell-bound streptokinase.

The C-substance is composed of a branched polymer of L-rhamnose and N-acetyl-D-glucosamine. It may have a role in increased invasive capacity. The R and T proteins are usedas epidemiologic markers and have no known role in virulence.

M protein, the major virulence factor, is a macromolecule incorporated in fimbriae present onthe cell membrane projecting on the bacterial cell wall. More than 50 types ofS pyogenesMproteins have been identified based on antigenic specificity, and the M protein is the majorcause of antigenic shift and antigenic drift among GAS.5The M protein binds the host fibrinogenand blocks the binding of complement to the underlying peptidoglycan. This allows survival of

the organism by inhibiting phagocytosis. Strains that contain an abundance of M protein resistphagocytosis, multiply rapidly in human tissues, and initiate disease process. After an acuteinfection, type-specific antibodies develop against M protein activity in some cases.

In addition to M protein, S pyogenespossesses additional virulence factors, such as C5Apeptidase, which destroys the chemotactic signals by cleaving the complement component ofC5A.

At least 11 different surface components of GAS have been suggested to play a role inadhesion. In 1997, Hasty and Courtney proposed that GAS express different arrays of adhesinsin various environmental niches. Based on their review, M protein mediates adhesion to HEp-2cells in humans, but not buccal cells, whereas FBP54 mediates adhesion to buccal cells, but notto HEp-2 cells. Protein F mediates adhesion to Langerhans cells, but not keratinocytes.

The most recent theory proposed in the process of adhesion is a two-step model. The initialstep of overcoming the electrostatic repulsion of the bacteria from the host is mediated by LTArendering weak reversible adhesion. The second step is firm irreversible adhesion mediated bytissue-specific M protein, protein F, or FBP54, among others. Once adherence has occurred, the

streptococci resist phagocytosis, proliferate, and begin to invade the local tissues.6GAS showenormous and evolving molecular diversity, driven by horizontal transmission among variousstrains. This is also true when compared with other streptococci. Acquisition of prophages


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accounts for much of the diversity, conferring not only virulence via phage-associated virulencefactors but also increased bacterial survival against host defenses.

Various extracellular growth products and toxins produced by GAS are responsible for host celldamage and inflammatory response. Streptolysin S, a 28 residue peptide, is an oxygen-stableleukocidin toxic to polymorphonuclear leukocytes, RBCs, and platelets. Streptolysin S isresponsible for RBC lysis observed on sheep blood agar. Streptolysin O is an oxygen-labileleukocidin that is toxic to neutrophils and induces a brisk antibody response. Measurement ofantistreptolysin O (ASO) antibody titer in humans is used as an indicator of recent streptococcalinfection. Other extracellular products include NADase (leukotoxic), hyaluronidase (whichdigests host connective tissue, hyaluronic acid, and the organism's own capsule), streptokinases(proteolytic), and streptodornase A-D (deoxyribonuclease activity).7

GAS produce 3 different types of exotoxins (A, B, C).5These toxins act as superantigens and are

responsible for inciting systemic immune response and acute disease caused by the sudden andmassive release of T-cell cytokines into the blood stream. The superantigens bypass processingby antigen presenting cells and cause T-cell activation by binding class II MHC moleculesdirectly and nonspecifically.

The streptococcal pyrogenic exotoxins (SPEs) are responsible for causing scarlet fever,pyrogenicity, and STSS. The mechanism is similar to that of staphylococcal TSS.8

Four antigenically distinct nucleases (A, B, C, D) assist in the liquefaction of pus and help to

generate substrate for growth.

In addition, streptococci produce proteinase, nicotinamide adenine dinucleotidase, adenosinetriphosphatase, neuraminidase, lipoproteinase, and cardiohepatic toxin.

S pyogenescauses up to 15%-30% of cases of acute pharyngitis.9Frank disease occurs basedon degree of bacterial virulence after colonization of the upper respiratory tract. Accuratediagnosis is essential for appropriate antibiotic selection.

The bacterial toxins cause proteolysis of epidermal and subepidermal layers, allowing thebacteria to spread quickly along the skin layers, thereby causing blisters or purulent lesions.The other common cause of impetigo is S aureus.

Invasive GAS can cause pulmonary infection, often with rapid progression to necrotizing

pneumonia.


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Necrotizing fasciitis is caused by bacterial invasion into the subcutaneous tissue, withsubsequent spread through superficial and deep fascial planes. The spread of organisms isaided by bacterial toxins and enzymes (eg, lipase, hyaluronidase, collagenase, streptokinase),interactions among organisms (synergistic infections), local tissue factors (eg, decreased bloodand oxygen supply), and general host factors (eg, immunocompromised state, chronic illness,surgery). As the infection spreads deep along the fascial planes, vascular occlusion, tissue

ischemia, and necrosis occur.10

Although GAS is often isolated in cases of necrotizing fasciitis,this disease state is frequently polymicrobial.

These are common suppurative complications of streptococcal tonsillopharyngitis. They arecaused by spread of organisms via the eustachian tube (otitis media) and direct spread tosinuses (sinusitis).

Certain M types are considered rheumatogenic, as they contain antigenic epitopes related toheart muscle, and therefore may lead to autoimmune rheumatic carditis (rheumatic fever)following acute infection. CD4+ T cells are probably the ultimate effectors of chronic valvelesions in rheumatic heart disease. T cells can recognize streptococcal M5 protein peptides andproduce various inflammatory cytokines (eg, tumor necrosis factor [TNF]alpha, interferon[IFN]gamma, interleukin [IL]10, IL-4), which could be responsible for progressive fibroticvalvular lesions. Cardiac myosin has been defined as a putative autoantigen recognized byautoantibodies in patients with rheumatic fever. Cross-reactivity between cardiac myosin andgroup A beta-hemolytic streptococcal M protein has been adequately demonstrated and maycontribute to pathogenesis.11

Poststreptococcal glomerulonephritis (PSGN) is caused by infection with specific nephritogenicstrains of GAS (types 12 and 49) and may occur in sporadic cases or during an epidemic. PSGNresults from deposition of antigen-antibody-complement complexes on the basementmembrane of renal glomeruli. Subepithelial deposits of immunoglobulin can be observed withimmunofluorescent staining.

Severe GAS infections associated with shock and organ failure have been reported with

increasing frequency, predominantly in North America and Europe. STSS is a severe systemicimmune response mediated by superantigens, as described above (see Pyrogenic exotoxins).

The primary evidence for poststreptococcal autoimmune CNS disease is provided by studies ofSydenham chorea, the neurologic manifestation of rheumatic fever. Reports ofobsessive-compulsive disorder (OCD), tic disorders, and other neuropsychiatric symptoms that occur inassociation with group A beta-hemolytic streptococcal infections suggest that various CNSsequelae may be triggered by poststreptococcal autoimmunity.12
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According to a CDC report dated April 3, 2008, approximately 9,000-11,500 cases of invasiveGAS disease (3.2-3.9 per 100,000 population) occur each year in the United States. STSS andnecrotizing fasciitis each accounted for approximately 6%-7% of cases. More than 10 millionnoninvasive GAS infections (primarily throat and superficial skin infections) occur annually.13

The resurgence of GAS as a cause of serious human infections in the United States, Europe,and elsewhere in the 1980s and into the 1990s was thoroughly documented and hasheightened public awareness about this organism. Disease resurgence coupled with the lack ofa licensed GAS vaccine and ongoing concern about acquisition of penicillin resistance remain amajor concern.

In Denmark, the incidence of rheumatic fever decreased from 250 cases per 100,000 populationto 100 cases per 100,000 population from 1862-1962. By 1980, the incidence ranged from0.23-1.88 cases per 100,000 population.

The incidence of PSGN ranges from 9.5-28.5 new cases per 100,000 individuals per year. PSGN

accounted for 2.6% to 3.7% of all primary glomerulopathies from 1987-1992, but only 9 caseswere reported between 1992 and 1994. In China and Singapore, the incidence of PSGN hasdecreased in the past 40 years. In Chile, the disease has virtually disappeared since 1999, and,in Maracaibo, Venezuela, the incidence of sporadic PSGN decreased from 90-110 cases per yearfrom 1980-1985 to 15 cases per year from 2001-2005. In Guadalajara, Mexico, the combineddata from two hospitals showed a reduction in cases of PSGN from 27 in 1992 to only 6 in2003.14

The Strep-EURO program, which analyzed data gathered in 11 participating countries, reportedthe epidemiology of severe S pyogenesdisease in Europe during the 2000s. A crude rate of2.46 cases per 100,000 population was reported in Finland, 2.58 in Denmark, 3.1 in Sweden,and 3.31 in the United Kingdom. In contrast, the rates of reports in the more central andsouthern countries, the Czech Republic, Romania, Cyprus, and Italy, were substantially lower(0.3-1.5 per 100,000 population), attributed to poor diagnostic microbiological investigativemethods in these countries.

As reported by the CDC in April 2008, invasive GAS infections carry a mortality rate of 10%-15%, with STSS and necrotizing fasciitis carrying fatality rates of over 35% and approximately25%, respectively. STSS may also result in organ system failure, while necrotizing fasciitis mayresult in amputation.13

GAS infections have no racial predilection.

GAS infections have no sexual predilection, although rheumatic mitral stenosis is more commonin females.

Strep throat is more common in school-aged children and teens. PSGN is more common in persons older than 60 years and in children younger than 15

years. ARF is commonly seen in young adults or children aged 4-9 years.
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Group A streptococci (GAS) can cause various diseases, including strep throat, skin and soft-tissue infections (eg, pyoderma, erysipelas, cellulitis, necrotizing fasciitis, myositis,osteomyelitis, pneumonia, abscess), severe systemic disease, and long-term nonsuppurative

complications (eg, rheumatic fever, acute glomerulonephritis).

Head and neck infectionso Streptococcal pharyngitis is strongly suggested by the presence of fever, tonsillar

exudate, tender enlarged anterior cervical lymph nodes, and absence of cough(Centor criteria).9Strep throat has an incubation period of 2-4 days and ischaracterized by sudden onset of sore throat, cervical lymphadenopathy,malaise, fever, and headache. Younger patients may also develop nausea,vomiting, and abdominal pain.

o Acute sinusitis manifests as persistent coryza, postnasal drip, headache, and

fever. Skin and soft-tissue infections

o Scarlet fever results from pyrogenic exotoxin released by GAS and is

characterized by scarlatiniform rash that blanches with pressure. The rashusually appears on the second day of illness and fades within a week, followedby extensive desquamation that lasts for several weeks.

o Erysipelas is an acute infection of the skin. In the past, the face was the most

commonly involved site of infection; however, it now accounts for 20% or less ofcases. Lower extremities are commonly affected. The symptoms of erysipelasinclude erythematous, warm, painful skin lesions with raised borders, commonlyassociated with fever. With appropriate antibiotics, the lesions resolve in days toweeks, with possible peeling. The condition usually occurs in children or elderly

people.

o Cellulitis is characterized by inflammation of the skin and subcutaneous tissues

and is associated with local pain, tenderness, swelling, and erythema. Patientsalso develop fever, chills, and malaise and may become bacteremic. Intravenousdrug abuse, abnormal lymphatic drainage, and breaks in skin integrity (eg, drycracked skin, tenia pedis) predispose to streptococcal cellulitis.
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o Impetigo and pyoderma, also called impetigo or impetigo contagiosa, are

outbreaks of streptococcal pyoderma that may occur in children of certainpopulation groups and in overcrowded institutions. The mode of spread is viadirect contact, environmental contamination, and houseflies. The strains ofstreptococci that cause pyoderma differ from those that cause exudativetonsillitis.

o Necrotizing fasciitis is a rapidly invasive GAS infection that may arise following

minor trauma or from hematogenous spread of GAS from the throat to a site of

blunt trauma or muscle strain. Unexplained and rapidly progressing pain may bethe first indication of necrotizing fasciitis. Pain may be disproportional to thephysical findings. Erythema may be diffused or localized or may be absent.Fever, malaise, myalgias, diarrhea, and anorexia may also be present.Hypotension may develop initially or over time. Surgical exploration is critical forestablishing the diagnosis and directing management.

Bacteremiao The risk factors for GAS bacteremia vary with age. Among children younger than

2 years, risk factors include burns, varicella virus infection, malignant neoplasm,and immunosuppression. Among individuals aged 40-60 years, the risk factorsfor GAS bacteremia include burns, cuts, surgical incisions, childbirth, intravenous

drug abuse, and nonpenetrating trauma. Predisposing factors for GASbacteremia in elderly people include diabetes mellitus, peripheral vasculardisease, malignancy, and corticosteroid use.

o GAS bacteremia usually results from invasive GAS infection. TSS is characterized

by early onset of shock and multiorgan failure. Blood cultures results are positivein approximately 60% of STSS cases. These patients usually develop renalfailure, acute respiratory distress syndrome, hepatic dysfunction, hematologicalabnormalities, confusion, skin lesions, and diffuse capillary leak syndrome.

Acute rheumatic fevero The Jones criteria are used to diagnose rheumatic fever. The 5 major criteria

include carditis, polyarthritis, chorea, erythema marginatum, and subcutaneous

nodules. The minor criteria include fever, arthralgia, elevated erythrocytesedimentation rate or C-reactive protein level, and prolonged PR interval on ECG.The presence of two major manifestations or of one major and two minormanifestations, supported by evidence of a preceding GAS infection by positivethroat swab or culture results or high serum ASO titers, strongly suggests acuterheumatic fever (ARF).

o Following the initial pharyngitis, a latent period of 2-3 weeks occurs before the

first signs or symptoms of ARF appear.o Rheumatic heart disease is a sequela of ARF that manifests as valvular heart

disease 10-20 years after the causative episode of ARF. Poststreptococcal glomerulonephritis: This manifestation occurs rapidly within days after

streptococcal pharyngitis and is characterized by acute renal failure with hematuria andnephrotic-rangeproteinuria.
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Physical findings of pharyngitis include erythema, edema, and swelling of the pharynx.The tonsils are enlarged, and a grayish-white exudate may be present. Submandibularand periauricular lymph nodes are usually enlarged and tender to palpation. Patientswith pharyngitis may develop chills and fever. Scarlet fever, characterized by diffuse

erythematous eruption, fever, sore throat, and a bright red tongue, can accompanypharyngitis in patients who have had prior exposure to the organism. The rash of scarletfever requires the presence of pyrogenic exotoxin and delayed type skin reactivity tostreptococcal toxins.

Pyoderma begins as a small papule and evolves into a vesicle surrounded by erythema.The vesicle turns into a pustule and then breaks down over 4-6 days to form a thickcrust. Patients usually do not have systemic symptoms.

Local signs of skin erythema, warmth, tenderness and swelling are usually associatedwith cellulitis and erysipelas. Rash with honey-colored crust is observed with impetigo.

In patients with pneumonia, crackles may be found on physical examination. In patientswith empyema or pleural effusion, decreased breath sounds and dullness on percussionare observed.

Necrotizing fascitis is an extensive and rapidly spreading infection of the subcutaneoustissue and fascia accompanied by necrosis and gangrene of the skin and underlyingstructures. Initially, the involved area appears erythematous but progresses rapidlywithin 24-48 hours, becoming purplish and then often evolving into blisters or bullaethat contain hemorrhagic fluid. Frank gangrene and extensive tissue necrosis follows.


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Signs of sepsis (eg, fever, tachycardia, tachypnea, hypotension) may be present ininvasive infections.

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