Streptococcus Group A Infections Clinical Presentation

  • Author: Zartash Zafar Khan, MD; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Jan 12, 2012
 

History

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 infections
    • Streptococcal pharyngitis is strongly suggested by the presence of fever, tonsillar exudate, tender enlarged anterior cervical lymph nodes, and absence of cough (Centor criteria).[10] Strep throat has an incubation period of 2-4 days and is characterized by sudden onset of sore throat, cervical lymphadenopathy, malaise, fever, and headache. Younger patients may also develop nausea, vomiting, and abdominal pain.
    • Acute sinusitis manifests as persistent coryza, postnasal drip, headache, and fever.
  • Skin and soft-tissue infections
    • Scarlet fever results from pyrogenic exotoxin released by GAS and is characterized by scarlatiniform rash that blanches with pressure. The rash usually appears on the second day of illness and fades within a week, followed by extensive desquamation that lasts for several weeks.
    • 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 of cases. Lower extremities are commonly affected. The symptoms of erysipelas include erythematous, warm, painful skin lesions with raised borders, commonly associated with fever. With appropriate antibiotics, the lesions resolve in days to weeks, with possible peeling. The condition usually occurs in children or elderly people. See the image below. Streptococcus group A infections. Erysipelas is a Streptococcus group A infections. Erysipelas is a group A streptococcal infection of skin and subcutaneous tissue.
    • Cellulitis is characterized by inflammation of the skin and subcutaneous tissues and is associated with local pain, tenderness, swelling, and erythema. Patients also develop fever, chills, and malaise and may become bacteremic. Intravenous drug abuse, abnormal lymphatic drainage, and breaks in skin integrity (eg, dry cracked skin, tenia pedis) predispose to streptococcal cellulitis. See the image below. Erythema secondary to group A streptococcal cellulErythema secondary to group A streptococcal cellulitis.
    • Impetigo and pyoderma, also called impetigo or impetigo contagiosa, are outbreaks of streptococcal pyoderma that may occur in children of certain population groups and in overcrowded institutions. The mode of spread is via direct contact, environmental contamination, and houseflies. The strains of streptococci that cause pyoderma differ from those that cause exudative tonsillitis.
    • 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 be the first indication of necrotizing fasciitis. Pain may be disproportional to the physical 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 for establishing the diagnosis and directing management.
  • Bacteremia
    • 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 factors for GAS bacteremia include burns, cuts, surgical incisions, childbirth, intravenous drug abuse, and nonpenetrating trauma. Predisposing factors for GAS bacteremia in elderly people include diabetes mellitus, peripheral vascular disease, malignancy, and corticosteroid use.
    • GAS bacteremia usually results from invasive GAS infection. TSS is characterized by early onset of shock and multiorgan failure. Blood cultures results are positive in approximately 60% of STSS cases. These patients usually develop renal failure, acute respiratory distress syndrome, hepatic dysfunction, hematological abnormalities, confusion, skin lesions, and diffuse capillary leak syndrome.
  • Acute rheumatic fever
    • 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 erythrocyte sedimentation rate or C-reactive protein level, and prolonged PR interval on ECG. The presence of two major manifestations or of one major and two minor manifestations, supported by evidence of a preceding GAS infection by positive throat swab or culture results or high serum ASO titers, strongly suggests acute rheumatic fever (ARF).
    • Following the initial pharyngitis, a latent period of 2-3 weeks occurs before the first signs or symptoms of ARF appear.
    • 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 and nephrotic-range proteinuria.
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Physical

  • Physical findings of pharyngitis include erythema, edema, and swelling of the pharynx. The tonsils are enlarged, and a grayish-white exudate may be present. Submandibular and periauricular lymph nodes are usually enlarged and tender to palpation. Patients with pharyngitis may develop chills and fever. Scarlet fever, characterized by diffuse erythematous eruption, fever, sore throat, and a bright red tongue, can accompany pharyngitis in patients who have had prior exposure to the organism. The rash of scarlet fever requires the presence of pyrogenic exotoxin and delayed type skin reactivity to streptococcal toxins. See the image below. Streptococcus group A infections. White strawberryStreptococcus group A infections. White strawberry tongue observed in streptococcal pharyngitis. Image courtesy of J. Bashera, eMedicine, Inc.
  • 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 thick crust. Patients usually do not have systemic symptoms.
  • Local signs of skin erythema, warmth, tenderness and swelling are usually associated with cellulitis and erysipelas. Rash with honey-colored crust is observed with impetigo.
  • In patients with pneumonia, crackles may be found on physical examination. In patients with empyema or pleural effusion, decreased breath sounds and dullness on percussion are observed.
  • 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. Initially, the involved area appears erythematous but progresses rapidly within 24-48 hours, becoming purplish and then often evolving into blisters or bullae that contain hemorrhagic fluid. Frank gangrene and extensive tissue necrosis follows. See the images below. Streptococcus group A infections. Necrotizing fascStreptococcus group A infections. Necrotizing fasciitis rapidly progresses from erythema to bullae formation and necrosis of skin and subcutaneous tissue. Streptococcus group A infections. Necrotizing fascStreptococcus group A infections. Necrotizing fasciitis of the left hand in a patient who had severe pain in the affected area. Streptococcus group A infections. Patient who had Streptococcus group A infections. Patient who had had necrotizing fasciitis of the left hand and severe pain in the affected area (from Image 8). This photo was taken at a later date, and the wound is healing. The patient required skin grafting.
  • Signs of sepsis (eg, fever, tachycardia, tachypnea, hypotension) may be present in invasive infections.
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Contributor Information and Disclosures
Author

Zartash Zafar Khan, MD  Infectious Disease Consultant

Zartash Zafar Khan, MD is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America, and International Society for Infectious Diseases

Disclosure: Nothing to disclose.

Coauthor(s)

Michelle R Salvaggio, MD, FACP  Assistant Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine; Medical Director of Infectious Diseases Institute, Director, Clinical Trials Unit, Director, Ryan White Programs, Department of Medicine, University of Oklahoma Health Sciences Center; Attending Physician, Infectious Diseases Consultation Service, Infectious Diseases Institute, OU Medical Center

Michelle R Salvaggio, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Merck Honoraria Speaking and teaching

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

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

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

Godfrey Harding, MD, FRCP(C) is a member of the following medical societies: American College of Physicians, American Society for Microbiology, Canadian Infectious Disease Society, Canadian Medical Association, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Douglas A Drevets, MD  Assistant Professor, Department of Medicine, Section of Infectious Disease, Oklahoma University Health Sciences Center

Douglas A Drevets, MD is a member of the following medical societies: American Association of Immunologists, American Society for Microbiology, Central Society for Clinical Research, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

John L Brusch, MD, FACP  Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

This article was reviewed by Michelle R. Salvaggio, MD, FACP, Assistant Professor, Associate Fellowship Director of Infectious Diseases, University of Oklahoma Health Science Center.

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Streptococcus group A infections. Necrotizing fasciitis rapidly progresses from erythema to bullae formation and necrosis of skin and subcutaneous tissue.
Streptococcus group A infections. Beta hemolysis is demonstrated on blood agar media.
Streptococcus group A infections. M protein.
Streptococcus group A infections. Erysipelas is a group A streptococcal infection of skin and subcutaneous tissue.
Streptococcus group A infections. White strawberry tongue observed in streptococcal pharyngitis. Image courtesy of J. Bashera, eMedicine, Inc.
Streptococcus group A infections. Streptococcal rash. Image courtesy of J. Bashera, eMedicine, Inc.
Group A Streptococcus on Gram stain of blood isolated from a patient who developed toxic shock syndrome.
Streptococcus group A infections. Necrotizing fasciitis of the left hand in a patient who had severe pain in the affected area.
Streptococcus group A infections. Patient who had had necrotizing fasciitis of the left hand and severe pain in the affected area (from Image 8). This photo was taken at a later date, and the wound is healing. The patient required skin grafting.
Streptococcus group A infections. Gangrenous streptococcal cellulitis in a patient with diabetes.
Erythema secondary to group A streptococcal cellulitis.
 
 
 
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