Streptococcus Group A Infections Author: Zartash Zafar Khan, MD, Fellow in Infectious Diseases, University of Oklahoma Health Science Center

Coauthor(s): Michelle R Salvaggio, MD, Assistant Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine; Medical Director of Infectious Diseases Institute, University of Oklahoma Health Sciences Center; Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital; Godfrey Harding, MD, FRCP(C), Program Director of Medical Microbiology, Professor, Department of Medicine, Section of Infectious Diseases and Microbiology, St Boniface Hospital, University of Manitoba, Canada Contributor Information and Disclosures Updated: Sep 23, 2009
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Background

Streptococcus pyogenes is beta-hemolytic bacterium that belongs to Lancefield serogroup A, also known as group A streptococci (GAS). GAS, a ubiquitous organism, causes a wide variety of diseases in humans and is the most common bacterial cause of acute pharyngitis, accounting for 15%-30% of cases in children and 5%-10% of cases in adults.1 During the winter and spring in temperate climates, up to 20% of asymptomatic school-aged children may be GAS carriers.2
GAS usually causes pharyngitis or impetigo but, in rare cases, can also cause invasive diseases such as cellulitis, bacteremia, necrotizing fasciitis, and toxic shock syndrome (TSS). Along with Staphylococcus aureus, GAS is one of the most common pathogens responsible for cellulitis . Historical perspectives

S pyogenes was 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 pyogenes in 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 streptococci by serotyping based on M-protein precipitin reactions. Lancefield established the critical role of M protein in disease causation. In the early 1900s, Dochez, George, and Dick identified hemolytic streptococcal infection as the cause of scarlet fever. The epidemiological studies of the mid 1900s helped establish the link between GAS infection and acute rheumatic fever (ARF) and acute glomerulonephritis.3

and catalase-negative. or both. The antigenic components of the cell are the virulence factors.51. which encodes the cell surface M protein. in the postantibiotic period. exotoxin B. Thus. hepatic failure. generally following pharyngitis. Pathophysiology Streptococci are a large group of gram-positive. This gene-typing system is based on sequence analysis of the emm gene. which is based on serotyping. They often grow in pairs or chains and are oxidase. non–spore-forming cocci about 0. among others. The most common forms of S pyogenes disease include respiratory and skin infections. and skin findings. allowing the bacterium to escape recognition by the host as an offending agent. However. This is predominantly associated with M types 1 and 3 that produce pyrogenic exotoxin A. allowing it to colonize. 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.2 µm in size. The cell wall of S pyogenes is very complex and chemically diverse. diseases due to streptococcal infections are well-controlled and uncommonly cause death. Spectrum of diseases due to group A streptococcal infections In the preantibiotic era. the bacterium escapes phagocytosis by neutrophils or macrophages. neurological symptoms. with different strains usually responsible for each form. has been replaced by emm typing. 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 multiorgan failure. nonmotile. The extracellular components responsible for the disease process include invasins and exotoxins. S pyogenes tends to colonize the upper respiratory tract and is highly virulent as it overcomes the host defense system. which has a chemical structure resembling host connective tissue.4 Scarlet fever: This is characterized by upper-body rash. acute renal failure. with manifestations of respiratory failure. GAS can cause a diverse variety of both suppurative diseases and nonsuppurative postinfectious sequelae. Lipoteichoic acid and M . hematological abnormalities. The outermost capsule is composed of hyaluronic acid. streptococci frequently caused significant morbidity and were associated with significant mortality rates.The traditional Lancefield M-protein classification system. defined by Jones criteria) Rheumatic heart disease (chronic valvular damage. Approximately 200 emm types have been identified by the Centers for Disease Control and Prevention (CDC) thus far.

This is also true when compared with other streptococci. The second step is firm irreversible adhesion mediated by tissue-specific M protein. or FBP54. M protein. Acquisition of prophages . S pyogenes possesses additional virulence factors. protein F. The most recent theory proposed in the process of adhesion is a two-step model. Protein F mediates adhesion to Langerhans cells. fibronectin-binding proteins (eg. Streptococcus group A infections. The R and T proteins are used as epidemiologic markers and have no known role in virulence. whereas FBP54 mediates adhesion to buccal cells. Bacterial adherence factors At least 11 different surface components of GAS have been suggested to play a role in adhesion. the major virulence factor. Bacterial virulence factors The cell wall antigens include capsular polysaccharide (C-substance). The C-substance is composed of a branched polymer of L-rhamnose and N -acetyl-Dglucosamine. and cell-bound streptokinase. which destroys the chemotactic signals by cleaving the complement component of C5A. peptidoglycan and lipoteichoic acid (LTA). such as C5A peptidase. and various surface proteins. and initiate disease process. This allows survival of the organism by inhibiting phagocytosis. is a macromolecule incorporated in fimbriae present on the cell membrane projecting on the bacterial cell wall. type-specific antibodies develop against M protein activity in some cases. but not to HEp-2 cells.5 The M protein binds the host fibrinogen and blocks the binding of complement to the underlying peptidoglycan.proteins located on the cell membrane traverse through the cell wall and project outside the capsule. Strains that contain an abundance of M protein resist phagocytosis. M protein. among others. multiply rapidly in human tissues. Once adherence has occurred. More than 50 types of S pyogenes M proteins have been identified based on antigenic specificity. the streptococci resist phagocytosis. The initial step of overcoming the electrostatic repulsion of the bacteria from the host is mediated by LTA rendering weak reversible adhesion. Hasty and Courtney proposed that GAS express different arrays of adhesins in various environmental niches. M protein mediates adhesion to HEp-2 cells in humans. and begin to invade the local tissues. proliferate. and the M protein is the major cause of antigenic shift and antigenic drift among GAS. protein F).6 GAS show enormous and evolving molecular diversity. fimbrial proteins. In 1997. Based on their review. In addition to M protein. It may have a role in increased invasive capacity. but not keratinocytes. but not buccal cells. including M protein. After an acute infection. driven by horizontal transmission among various strains. R and T proteins.

hyaluronic acid. B.9 Frank disease occurs based on degree of bacterial virulence after colonization of the upper respiratory tract. is an oxygen-stable leukocidin toxic to polymorphonuclear leukocytes. hyaluronidase (which digests host connective tissue. lipoproteinase. and STSS. nicotinamide adenine dinucleotidase. a 28 residue peptide. D) assist in the liquefaction of pus and help to generate substrate for growth. The other common cause of impetigo is S aureus. RBCs.5 These toxins act as superantigens and are responsible for inciting systemic immune response and acute disease caused by the sudden and massive release of T-cell cytokines into the blood stream. Impetigo The bacterial toxins cause proteolysis of epidermal and subepidermal layers. The superantigens bypass processing by antigen presenting cells and cause T-cell activation by binding class II MHC molecules directly and nonspecifically. Accurate diagnosis is essential for appropriate antibiotic selection. C. Necrotizing fasciitis . Pneumonia Invasive GAS can cause pulmonary infection. C).7 Pyrogenic exotoxins GAS produce 3 different types of exotoxins (A. Measurement of antistreptolysin O (ASO) antibody titer in humans is used as an indicator of recent streptococcal infection. Extracellular products and toxins Various extracellular growth products and toxins produced by GAS are responsible for host cell damage and inflammatory response. and the organism's own capsule). and cardiohepatic toxin. thereby causing blisters or purulent lesions. Other extracellular products include NADase (leukotoxic). pyrogenicity. Streptolysin S is responsible for RBC lysis observed on sheep blood agar.accounts for much of the diversity. conferring not only virulence via phage-associated virulence factors but also increased bacterial survival against host defenses.8 Nucleases Four antigenically distinct nucleases (A. streptococci produce proteinase. Other enzymes In addition. The streptococcal pyrogenic exotoxins (SPEs) are responsible for causing scarlet fever. adenosine triphosphatase. Streptolysin S. streptokinases (proteolytic). B. Suppurative Disease Spectrum Streptococcal pharyngitis S pyogenes causes up to 15%-30% of cases of acute pharyngitis. neuraminidase. and streptodornase A-D (deoxyribonuclease activity). The mechanism is similar to that of staphylococcal TSS. and platelets. allowing the bacteria to spread quickly along the skin layers. often with rapid progression to necrotizing pneumonia. Streptolysin O is an oxygen-labile leukocidin that is toxic to neutrophils and induces a brisk antibody response.

local tissue factors (eg. interactions among organisms (synergistic infections).10 Although GAS is often isolated in cases of necrotizing fasciitis. T cells can recognize streptococcal M5 protein peptides and produce various inflammatory cytokines (eg. Reports of obsessivecompulsive disorder (OCD). this disease state is frequently polymicrobial. and therefore may lead to autoimmune rheumatic carditis (rheumatic fever) following acute infection. and other neuropsychiatric symptoms that occur in association with group A beta-hemolytic streptococcal infections suggest that various CNS sequelae may be triggered by poststreptococcal autoimmunity. and necrosis occur. tic disorders. They are caused by spread of organisms via the eustachian tube (otitis media) and direct spread to sinuses (sinusitis). Nonsuppurative Complications Acute rheumatic fever Certain M types are considered rheumatogenic. collagenase. which could be responsible for progressive fibrotic valvular lesions.12 Frequency United States . chronic illness. Subepithelial deposits of immunoglobulin can be observed with immunofluorescent staining. interleukin [IL]–10. Streptococcal toxic shock syndrome Severe GAS infections associated with shock and organ failure have been reported with increasing frequency. vascular occlusion. with subsequent spread through superficial and deep fascial planes. IL-4). tissue ischemia. as they contain antigenic epitopes related to heart muscle. Cross-reactivity between cardiac myosin and group A beta-hemolytic streptococcal M protein has been adequately demonstrated and may contribute to pathogenesis. and general host factors (eg. hyaluronidase. PSGN results from deposition of antigen-antibody-complement complexes on the basement membrane of renal glomeruli. The spread of organisms is aided by bacterial toxins and enzymes (eg. lipase. Cardiac myosin has been defined as a putative autoantigen recognized by autoantibodies in patients with rheumatic fever. surgery).Necrotizing fasciitis is caused by bacterial invasion into the subcutaneous tissue. Otitis media and sinusitis These are common suppurative complications of streptococcal tonsillopharyngitis. streptokinase). decreased blood and oxygen supply). predominantly in North America and Europe. STSS is a severe systemic immune response mediated by superantigens. interferon [IFN]–gamma. CD4+ T cells are probably the ultimate effectors of chronic valve lesions in rheumatic heart disease. As the infection spreads deep along the fascial planes. immunocompromised state. as described above (see Pyrogenic exotoxins). tumor necrosis factor [TNF]–alpha.11 Poststreptococcal glomerulonephritis Poststreptococcal glomerulonephritis (PSGN) is caused by infection with specific nephritogenic strains of GAS (types 12 and 49) and may occur in sporadic cases or during an epidemic. the neurologic manifestation of rheumatic fever. Central Nervous System Diseases The primary evidence for poststreptococcal autoimmune CNS disease is provided by studies of Sydenham chorea.

A crude rate of 2.31 in the United Kingdom. Mexico. Venezuela. in Maracaibo.6% to 3. ARF is commonly seen in young adults or children aged 4-9 years. PSGN accounted for 2. .3-1. In China and Singapore. More than 10 million noninvasive GAS infections (primarily throat and superficial skin infections) occur annually.000 individuals per year.000 population). In contrast.500 cases of invasive GAS disease (3. and Italy. but only 9 cases were reported between 1992 and 1994. while necrotizing fasciitis may result in amputation. invasive GAS infections carry a mortality rate of 10%15%. reported the epidemiology of severe S pyogenes disease in Europe during the 2000s.5 per 100. PSGN is more common in persons older than 60 years and in children younger than 15 years.According to a CDC report dated April 3.58 in Denmark. Cyprus. the rates of reports in the more central and southern countries. Mortality/Morbidity As reported by the CDC in April 2008.000 population was reported in Finland. By 1980.7% of all primary glomerulopathies from 1987-1992.000 population) occur each year in the United States. were substantially lower (0. although rheumatic mitral stenosis is more common in females. STSS may also result in organ system failure. The incidence of PSGN ranges from 9.2-3.000 population from 1862-1962. the disease has virtually disappeared since 1999. and elsewhere in the 1980s and into the 1990s was thoroughly documented and has heightened public awareness about this organism.000 population. the incidence ranged from 0. approximately 9. attributed to poor diagnostic microbiological investigative methods in these countries.5-28.23-1.46 cases per 100. and 3. Sex GAS infections have no sexual predilection. Age • • • Strep throat is more common in school-aged children and teens.1 in Sweden. 2008.5 new cases per 100.000 population to 100 cases per 100. Europe.14 The Strep-EURO program.88 cases per 100. 2. In Denmark. In Guadalajara. 3.13 Race GAS infections have no racial predilection. the incidence of sporadic PSGN decreased from 90-110 cases per year from 1980-1985 to 15 cases per year from 2001-2005. with STSS and necrotizing fasciitis carrying fatality rates of over 35% and approximately 25%.13 International The resurgence of GAS as a cause of serious human infections in the United States. the Czech Republic. Romania. which analyzed data gathered in 11 participating countries. the incidence of PSGN has decreased in the past 40 years. In Chile.000-11. and. the incidence of rheumatic fever decreased from 250 cases per 100. STSS and necrotizing fasciitis each accounted for approximately 6%-7% of cases. the combined data from two hospitals showed a reduction in cases of PSGN from 27 in 1992 to only 6 in 2003. Disease resurgence coupled with the lack of a licensed GAS vaccine and ongoing concern about acquisition of penicillin resistance remain a major concern. respectively.9 per 100.

severe systemic disease. pyoderma. pneumonia. necrotizing fasciitis. abscess). it now accounts for 20% or less of cases. commonly associated with fever. and fever. the face was the most commonly involved site of infection. however. With appropriate antibiotics. and malaise and may become bacteremic. postnasal drip. The condition usually occurs in children or elderly people. Streptococcus group A infections. dry cracked skin. rheumatic fever. skin and softtissue infections (eg. The rash usually appears on the second day of illness and fades within a week. the lesions resolve in days to weeks. headache. In the past. tenia pedis) predispose to streptococcal cellulitis. and erythema. o Erysipelas is an acute infection of the skin. cellulitis. warm. malaise.9 Strep throat has an incubation period of 2-4 days and is characterized by sudden onset of sore throat. erysipelas. painful skin lesions with raised borders. Younger patients may also develop nausea. o Acute sinusitis manifests as persistent coryza. Erysipelas is a group A streptococcal infection of skin and subcutaneous tissue. Lower extremities are commonly affected. Patients also develop fever. tenderness. osteomyelitis. with possible peeling. and abdominal pain. The symptoms of erysipelas include erythematous. 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. and absence of cough (Centor criteria). tonsillar exudate. followed by extensive desquamation that lasts for several weeks. o Cellulitis is characterized by inflammation of the skin and subcutaneous tissues and is associated with local pain. swelling. acute glomerulonephritis). and headache. including strep throat. myositis. Intravenous drug abuse. and long-term nonsuppurative complications (eg. abnormal lymphatic drainage. chills. . • • Head and neck infections o Streptococcal pharyngitis is strongly suggested by the presence of fever. cervical lymphadenopathy. fever.Clinical History Group A streptococci (GAS) can cause various diseases. vomiting. tender enlarged anterior cervical lymph nodes. and breaks in skin integrity (eg.

confusion.Erythema secondary to group A streptococcal cellulitis. malignancy. varicella virus infection. Pain may be disproportional to the physical findings. These patients usually develop renal failure. o GAS bacteremia usually results from invasive GAS infection. and nonpenetrating trauma. Blood cultures results are positive in approximately 60% of STSS cases. and anorexia may also be present. polyarthritis. Hypotension may develop initially or over time. myalgias. risk factors include burns. erythema marginatum. The mode of spread is via direct contact. Fever. and subcutaneous nodules. hepatic dysfunction. The minor criteria include fever. skin lesions. and immunosuppression. and prolonged PR interval on ECG. The presence of two major manifestations or of one major and two minor manifestations. Bacteremia o The risk factors for GAS bacteremia vary with age. also called impetigo or impetigo contagiosa. elevated erythrocyte sedimentation rate or C-reactive protein level. o Following the initial pharyngitis. TSS is characterized by early onset of shock and multiorgan failure. and corticosteroid use. o Rheumatic heart disease is a sequela of ARF that manifests as valvular heart disease 10-20 years after the causative episode of ARF. peripheral vascular disease. intravenous drug abuse. Predisposing factors for GAS bacteremia in elderly people include diabetes mellitus. cuts. surgical incisions. the risk factors for GAS bacteremia include burns. strongly suggests acute rheumatic fever (ARF). environmental contamination. Acute rheumatic fever o The Jones criteria are used to diagnose rheumatic fever. are outbreaks of streptococcal pyoderma that may occur in children of certain population groups and in overcrowded institutions. o • • • . diarrhea. chorea. Unexplained and rapidly progressing pain may be the first indication of necrotizing fasciitis. Impetigo and pyoderma. 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. Surgical exploration is critical for establishing the diagnosis and directing management. Poststreptococcal glomerulonephritis: This manifestation occurs rapidly within days after streptococcal pharyngitis and is characterized by acute renal failure with hematuria and nephrotic-range proteinuria. malignant neoplasm. arthralgia. hematological abnormalities. Among individuals aged 40-60 years. Erythema may be diffused or localized or may be absent. and diffuse capillary leak syndrome. The strains of streptococci that cause pyoderma differ from those that cause exudative tonsillitis. childbirth. acute respiratory distress syndrome. supported by evidence of a preceding GAS infection by positive throat swab or culture results or high serum ASO titers. a latent period of 2-3 weeks occurs before the first signs or symptoms of ARF appear. malaise. and houseflies. Among children younger than 2 years. The 5 major criteria include carditis.

sore throat. Submandibular and periauricular lymph nodes are usually enlarged and tender to palpation. and swelling of the pharynx. eMedicine. Initially. tenderness and swelling are usually associated with cellulitis and erysipelas. can accompany pharyngitis in patients who have had prior exposure to the organism. and a grayish-white exudate may be present. Inc. characterized by diffuse erythematous eruption. Rash with honey-colored crust is observed with impetigo. Necrotizing fasciitis rapidly progresses from erythema to bullae formation and necrosis of skin and subcutaneous tissue. White strawberry tongue observed in streptococcal pharyngitis. In patients with pneumonia. and a bright red tongue. crackles may be found on physical examination.Physical • Physical findings of pharyngitis include erythema. Streptococcus group A infections. Patients usually do not have systemic symptoms. The tonsils are enlarged. Local signs of skin erythema. decreased breath sounds and dullness on percussion are observed. edema. Patients with pharyngitis may develop chills and fever. fever. Streptococcus group A infections. . Necrotizing fascitis is an extensive and rapidly spreading infection of the subcutaneous tissue and fascia accompanied by necrosis and gangrene of the skin and underlying structures. • • • • Pyoderma begins as a small papule and evolves into a vesicle surrounded by erythema. Image courtesy of J. The vesicle turns into a pustule and then breaks down over 4-6 days to form a thick crust. the involved area appears erythematous but progresses rapidly within 24-48 hours. warmth. In patients with empyema or pleural effusion. Frank gangrene and extensive tissue necrosis follows. The rash of scarlet fever requires the presence of pyrogenic exotoxin and delayed type skin reactivity to streptococcal toxins. Scarlet fever. becoming purplish and then often evolving into blisters or bullae that contain hemorrhagic fluid. Bashera.

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