Group A streptococcal infection

Group A streptococcal infection
Classification and external resources

Streptococcus pyogenes
ICD-10 B95.0
eMedicine article/971097

The group A streptococcus bacterium (Streptococcus pyogenes, or GAS) is a form of β-hemolytic Streptococcus bacteria responsible for most cases of streptococcal illness. Other types (B, C, D, and G) may also cause infection. Several virulence factors contribute to the pathogenesis of GAS, such as M protein, hemolysins, and extracellular enzymes.

Contents

Types of infection

Infections are largely categorized by the location of infection:

(Note that some of these diseases can be caused by other infectious agents as well.)

Complications

Acute rheumatic fever

Acute rheumatic fever (ARF) is a complication of respiratory infections caused by GAS. The M-protein generates antibodies that cross-react with autoantigens on interstitial connective tissue, in particular of the endocardium and synovium, that can lead to significant clinical illness. Although common in developing countries, ARF is rare in the United States, possibly secondary to improved antibiotic treatment, with small isolated outbreaks reported only occasionally. It is most common among children between 5 and 15 years old and occurs 1–3 weeks after an untreated GAS pharyngitis. ARF is often clinically diagnosed based on Jones Criteria, which include: pancarditis, migratory polyarthritis of large joints, subcutaneous nodules, erythema marginatum, and sydenham chorea (involuntary, purposeless movement). The most common clinical finding is a migratory arthritis involving multiple joints. Other indicators of GAS infection such as a DNAase or ASO serology test must confirm the GAS infection. Other minor Jones Criteria are fever, elevated ESR and arthralgia. Of the most serious complications is pancarditis, or inflammation of all three heart tissues. A fibrinous pericarditis can develop with a classic friction rub that can be auscultated. This will give increasing pain upon reclining. Further endocarditis can develop with aseptic vegetations along the valve closure lines, in particular the mitral valve. Chronic rheumatic heart disease mostly affects the mitral valve, which can become thickened with calcification of the leaflets, often causing fusion of the commissures and chordae tendineae. Other findings of ARF include erythema marginatum (usually over the spine or other bony areas) and a red expanding rash on the trunk and extremities that recurs over weeks to months. Because of the different ways ARF presents itself, the disease may be difficult to diagnose. A neurological disorder, Sydenham chorea, can occur months after an initial attack, causing jerky involuntary movements, muscle weakness, slurred speech, and personality changes. Initial episodes of ARF as well as recurrences can be prevented by treatment with appropriate antibiotics. It is important to distinguish ARF from rheumatic heart disease. ARF is an acute inflammatory reaction with pathognomonic Aschoff bodies histologically and RHD is a non-inflammatory sequelae of ARF.

Post-streptococcal glomerulonephritis

Post-streptococcal glomerulonephritis (PSGN) is an uncommon complication of either a strep throat or a streptococcal skin infection. It is classified as a type III hypersensitivity reaction. Symptoms of PSGN develop within 10 days following a strep throat or 3 weeks following a GAS skin infection. PSGN involves inflammation of the kidney. Symptoms include pale skin, lethargy, loss of appetite, headache, and dull back pain. Clinical findings may include dark-colored urine, swelling of different parts of the body (edema), and high blood pressure. Treatment of PSGN consists of supportive care.

Severe streptococcal infections

Some strains of group A streptococci (GAS) cause severe infection. Those at greatest risk include children with chickenpox; persons with suppressed immune systems; burn victims; elderly persons with cellulitis, diabetes, blood vessel disease, or cancer; and persons taking steroid treatments or chemotherapy. Intravenous drug users also are at high risk. GAS is an important cause of puerperal fever worldwide, causing serious infection and, if not promptly diagnosed and treated, death in newly delivered mothers. Severe GAS disease may also occur in healthy persons with no known risk factors.

All severe GAS infections may lead to shock, multisystem organ failure, and death. Early recognition and treatment are critical. Diagnostic tests include blood counts and urinalysis as well as cultures of blood or fluid from a wound site.

Severe Group A streptococcal infections often occur sporadically but can be spread by person-to-person contact. [1] Close contacts of people affected by severe Group A streptococcal infections, defined as those having had prolonged household contact in the week before the onset of illness, may be at increased risk of infection. This increased risk may be due to a combination of shared genetic susceptibility within the family, close contact with carriers, and the virulence of the Group A streptococcal strain that is involved.[2]

Public Health policies internationally reflect differing views of how the close contacts of people affected by severe Group A streptococcal infections should be treated. Health Canada [3] and the US CDC recommend close contacts see their doctor for full evaluation and may require antibiotics;[4] current UK Health Protection Agency guidance is that, for a number of reasons, close contacts should not receive antibiotics unless they are symptomatic but that they should receive information and advice to seek immediate medical attention if they develop symptoms.[2]

Treatment

Once group A streptococcus is documented as the cause of infection, treatment with penicillin should be started. Erythromycin or another macrolide can be used in patients allergic to penicillin. Treatment with ampicillin/sulbactam is appropriate if deep oropharyngeal abscesses are present. In cases of streptococcal toxic shock syndrome, treatment consists of penicillin and clindamycin, given with intravenous immunoglobulin., August 2010 

Relation with tics and OCD

In recent years, subsets of children with acute, rapid-onset of tic disorders and obsessive compulsive disorder (OCD) hypothesized to be due to an autoimmune response to group A beta-hemolytic streptococcal infection (PANDAS) have been identified.[5]

References

  1. ^ Gamba MA, Martinelli M, Schaad HJ, Streuli RA, DiPersio J, Matter L, et al. Familial transmission of a serious disease producing group A streptococcus clone:case reports and review. Clin Infect Dis 1997; 24: 1118-21.
  2. ^ a b Health Protection Agency, Group A Streptococcus Working Group (2004). Interim UK guidelines for management of close community contacts of invasive group A streptococcal disease. Commun Dis Public Health 2004; 7(4): 354-61. Available at: http://www.hpa.org.uk/cdph/issues/CDPHVol7/no4/guidelines1_4_04.pdf
  3. ^ Guidelines for management of contacts of cases of invasive group A streptococcal disease (GAS) including streptococcal toxic shock syndrome (STSS) and necrotising fasciitis. Toronto, Ontario: Ministry of Health; 1995. Available at: http://www.microbiology.mtsinai.on.ca/protocols/pdf/k5b.pdf
  4. ^ [1]
  5. ^ History of Treatment of OCD. Stanford School of Medicine. Retrieved on 2007-04-12 [2]

Note: Elements of the original text of this article are taken from the NIH Fact Sheet "Group A Streptococcal Infections", dated March 1999. As a work of the U.S. Federal Government without any other copyright notice, this is assumed to be a public domain resource.

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