Strep Throat

 

By: Ryan Weber

 

Disease Etiology:

Strep throat is caused by Group A Streptococcus (aka Streptococcus pyogenes).[7] People may carry Group A Streptococci in the throat or on the skin and not be ill.[2] It is most common among children ages 5-15, but adults can get strep throat as well. Infection in children younger than 3 is possible, but usually doesn’t result in throat infections. The disease is most common in the late fall, winter and early spring.[3] While the disease is usually easily treated, the organism has the potential to cause a multitude of other diseases and side effects including scarlet fever, rheumatic fever, postpartum fever, wound infections, pneumonia, streptococcal toxic shock syndrome, necrotizing fasciitis, glomerulonephritis, and impetigo.[4,8]

 

Disease Transmission:

The disease spreads by person-to-person contact through nasal droplets/secretions or saliva.[3,5] The bacteria spread when those secretions come in contact with the mouth, nose, eyes, scrap, or wound. Fomites do not play a major role in the spreading of the disease.[8] Crowding increases transmission as evidenced by common outbreaks in institutional settings, the military, school, etc.[5]

 

Reservoirs:

The human throat and skin are the reservoirs for S. pyogenes.[2]

 

Specific Microbial Characteristics:

S. pyogenes is a gram-positive coccus of approximately 0 .6 – 1.0 micrometers in diameter that occurs in pairs and chains.[4]

 

Specific Tests for Identification:

S. pyogenes is non-motile, non-sporeforming, catalase negative, facultative anaerobe. It requires enriched medium with blood in order to grow. On blood agar it displays beta-hemolysis (complete hemolysis of the red blood cells surrounding the colonies). [4]

 

Many cost effective methods exist involving enzyme immunosorbent assay, latex agglutination, or coagglutination to identify S. pyogenes.[7]

 

Group A streptococci are the only beta-hemolytic streptococci produced from throat culture that produce the enzyme L-pyrrolidonyl-beta-naphthylamide (PYRase). This enzyme can be identified based on the color change of agar to red after inoculation of a disk on an agar plate incubated overnight.[7]

 

Signs and Symptoms

The incubation period is around 2-5 days. Typical symptoms include fever (usually greater than 101.3°F), red throat, sore throat, headache, stomach ache, nausea, chills, malaise, loss of appetite, abnormal taste, swollen lymph nodes in the neck, and difficulty swallowing.[3,5]

 

While a sore throat may be a hallmark symptom of Strep Throat, only 5-10% of all sore throats are caused by bacteria, with Group A Streptococcus being the most common bacterial cause.[5]

 

Historical Information:

In the 5th century BC, the cause of the scarlet fever epidemic described by Hippocrates was probably S. pyogenes. In 1874, Billroth gave the first modern descriptions of Streptococcal infections. Pastuer was the first person to isolate the bacteria from a pregnant woman’s blood who was septic in 1884. In the late 19th century Rosenbach designated the bacteria S. pyogenes. Brown described the blood agar patterns of alpha, beta, and gamma hemolysis of the various Streptococcal species in 1919.[7]

 

Rebecca Lancefield identified distinct serogroups of beta-hemolytic streptococci in the 1930s. These serogroups classified by one letter were based on antigenic differences of group-specific polysaccharides located in the cell wall. More than 20 groups have been identified.[7] The Group A polysaccharide is a polymer of N-acetylglucosamine and rhamnose.[4]

 

Virulence Factors

M protein, fibronectin-binding protein (Protein F), and lipoteichoic acid aid in adherence.[4] Liptoteichoic acid and Protein F aid in adherence by binding to fibronectin on human epithelial cells.[7] A hyaluronic acid capsule, and M protein inhibit phagocytosis.[4] More than 80 M proteins have been identified. The M protein is so important that if it is not present, the bacterium is essentially nonpathogenic. M protein inhibits activation of the alternate complement pathway.[7] The hylauronic acid capsule also acts as an immunological disguse since the chemical composition is similar to host connective tissue. Invasins are also present including streptokinase, streptodornase, hyaluronidase, and streptolysins. Exotoxins include pyrogenic toxin. [4] Two hemolysins produced by the organism are Streptolysin O and Streptolysin S. Streptolysin O is toxic to many cells including the heart, while Streptolysin S is toxic to polymorphonuclear leukocytes and subcellular organelles.[7]

 

Control/Treatment

Treating a person with antibiotics for longer than 24 hours usually caused them to no longer be contagious.[2] Penicillin is still effective against S. pyogenes.[4] For those with penicillin allergy erythromycin is the antibiotic typically used. As a second-line therapy amoxicillin-clavulanate potassium, azithromycin, or a cephalosporin may be used.[5]

 

Prevention/ Vaccines

Preventative measures against S. pyogenes are to wash hands thoroughly and often, and keep wounds clean. One should also get a throat culture for a sore throat with a fever in order to prevent the spread of the disease to others, and to prevent complications like rheumatic fever.[8]

 

A main reason why a vaccine against S. pyogenes is so difficult to make is the fact that the M protein has 80 serotypes, and that the hylauronic acid capsule is chemically similar to our own connective tissue.[4,7] No vaccine has been produced, however specific M-protein vaccines are being tested.[4]

 

Local cases/outbreaks

Strep throat is one of the most common illnesses in children. In the United States, 15-36% of 7.3 million outpatient visits each year among children were due to S. pyogenes.[1] Strep Throat is also more common in the northern area of the United States, however it is seen throughout the nation as well as the world.[7]

 

Global cases/outbreaks

S. pyogenes infections occur worldwide and appear to have no racial, ethnic, or sex-based predispositions.[7]

 

References

[1] World Health Organization. “Group A Streptococcus.” 2010. http://www.who.int/vaccine_research/diseases/soa_bacterial/en/index3.html. 06 March 2010.

 

[2] CDC. “Group A Streptococcal (GAS) Disease.” 03 April 2008. http://www.cdc.gov/ncidod/dbmd/diseaseinfo/groupastreptococcal_g.htm. 06 March 2010.

 

[3] Medline Plus. “Strep Throat.” 10 January 2010. http://www.nlm.nih.gov/medlineplus/ency/article/000639.htm. 06 March 2010.

 

[4] Todar, Kenneth. “Streptococcus pyogenes and Streptococcal Disease.” 2008. http://www.textbookofbacteriology.net/streptococcus.html. 06 March 2010.

 

[5] American Academy of Family Physicians. “Management of Group A Beta-Hemolytic Streptococcal Pharyngitis.” 15 April 2001. http://www.aafp.org/afp/2001/0415/p1557.html. 06 March 2010.

 

[6] Aziz, Ramy K; Kotb, Malak. “Rise and Persistence of Global M1T1 Clone of Streptococcus pyogenes.” 10 Oct 2008. http://www.cdc.gov/eid/content/14/10/pdfs/1511.pdf. 06 March 2010.

 

[7] Schleiss, Mark. “Streptococcal Infection, Group A.” 20 Nov 2009. http://emedicine.medscape.com/article/971097-overview. 06 March 2010.

 

[8] Directors of Health Promotion and Education. “Group A Streptococcus.” 2010. http://www.dhpe.org/infect/strepa.html. 06 March 2010.