Group A beta-hemolytic streptococcal pharyngitis: current clinical concepts

Author: Daria Kiselica
Date: April, 1994

Group A beta-hemolytic streptococcus (GABHS) is responsible for 10 to 30 percent of the cases of sore throat treated by health care providers. GABHS pharyngitis typically occurs in patients aged five to 11 years and is uncommon in children under three years of age. Attack rates are particularly high in closed populations, such as day care centers and military barracks.

Over the past 10 years, infections caused by GABHS have become increasingly prevalent and alarmingly virulent. Not only has there been a resurgence of acute rheumatic fever, a medically significant complication of GABHS pharyngitis, but the incidence of other severe and potentially life-threatening Streptococcus pyogenes infections has increased in the United States and elsewhere. These severe infections include a toxic-shock-like illness (toxic strep syndrome), GABHS bacteremia, streptococcal deep tissue infections and streptococcal cellulitis[1-3] The increased frequency of these infections is thought to reflect changes in, and the evolution of, various strains of GABHS.[2,3]

Properties of GABHS

The cell wall of the GABHS organism has several pathogenetic features. The M protein, the chief virulence factor of GABHS, is anchored in the cell membrane and wall, and it exerts an antiphagocytic effect that allows GABHS to multiply rapidly in human blood.[4] Lipoteichoic acid is critical for GABHS colonization,[5] and the hyaluronate capsule is antiphagocytic.[6] Overall, GABHS organisms, which are heavily encapsulated and of particular M-protein serotypes, are readily transmitted and tend to produce severe infection.[1]

Extracellular products may also play a role in pathogenicity. Pyrogenic exotoxins (erythrogenic toxins) are responsible for the rash in scarlet fever and enhanced susceptibility to endotoxic shock. These exotoxins also alter T-cell functioning.[1]

Other extracellular products, specifically streptolysin O, deoxyribonuclease B and hyaluronidase, induce antibody formation seven to 10 days following acute GABHS infection. Serologic evidence of these antic-bodies may be used, for example, to confirm the occurrence of recent streptococcal infection in

patients with acute glomerulonephritis or acute rheumatic fever.

Clinical Features of GABHS Pharyngitis

In patients who present with pharyngitis, the major goal of the physician is to distinguish between GABHS infection, which has potentially serious medical sequelae, and other causes of pharyngitis.

Classic clinical features of GABHS infection include sudden onset of sore throat, fever and tender, swollen anterior cervical lymph nodes, typically in a child five to 11 years of age. Abdominal pain, nausea and vomiting may occur, although these symptoms are more characteristic of GABHS infection in children than in adults. Headache may be present, but cough, rhinorrhea and hoarseness are generally absent.

Physical examination may reveal erythema and swelling of the pharynx, enlarged and erythematous tonsils, tonsillar exudate and palatal petechiae. The rash of scarlet fever, which is characterized by a fine, blanching appearance, sandpaper texture, circumoral pallor and hyperpigmentation in the skin creases, is highly suggestive of GABHS infection. An elevated white blood cell count and the presence of tonsillar exudate are more reliable indicators of GABHS infection in adults than in children (Table 1).

TABLE 1Classic Clinical Signs of Group ABeta-Hemolytic Streptococcal PharyngitisClinical sign CommentsFever, usually 38.3 [degrees] C to May also occur in viral infections; 40.0 [degrees] C unreliable (101 [degrees] F to for diagnosis of GABHS pharyngitis 104 [degrees] F)Enlarged, erythematous Unreliable for diagnosis of GABHS tonsils pharyngitisTonsillar exudate More common in adults than in children; unreliable for diagnosis of GABHS pharyngitisEnlarged, tender One of the most useful clinical anterior cervical findings lymph nodes suggestive of GABHS pharyngitis, but may also occur in viral infectionsPalatal petechiae May also occur in viral infections; unreliable for diagnosis of GABHS pharyngitisRash of scarlet fever May be considered diagnostic of GABHSElevated peripheral More common in adults than in children; white blood cell count unreliable for diagnosis of GABHS pharyngitisGABHS = group A beta-hemolytic streptococcus.

The majority of patients with GABHS pharyngitis do not have the classic symptoms. The triad of fever, pharyngeal exudate and anterior cervical adenopathy is present in only 15 percent of cases.[7] Exudate occurs in fewer than 50 percent of patients with GABHS pharyngitis; culture of an exudative pharyngitis leads to a diagnosis of GABHS infection in 25 to 50 percent of patients.[8] Pharyngeal erythema is an unreliable indicator of GABHS infection, since it may occur in both infected and noninfected patients.

Tonsillar size does not correlate with either current infection or the frequency of past infections. Duration of symptoms is not helpful, because most patients with GABHS pharyngitis become asymptomatic in three or four days, even without treatment. It is important to remember that other organisms that infect the pharynx, including viruses and non-group A streptococci (specifically those from groups B, C and G), may also cause the symptoms generally considered to be typical of GABHS pharyngitis.[9,10]

The clinical diagnosis of GABHS infection is, in fact, not straightforward. Numerous studies have shown that experienced medical personnel are correct in only 50 to 75 percent of cases when they make a decision about the etiology of pharyngitis based on clinical criteria alone. In one study,[11] physician overestimated the probability of a culture being positive for GABHS in 81 percent of the patients, and the impact on treatment decisions was significant. Therefore, a throat culture or a rapid streptococcal test is required to confirm the presence of GABHS in the pharynx of symptomatic patients.

Complications

The complications of GABHS pharyngitis may be classified as suppurative and nonsuppurative. Suppurative complications occur when the infection spreads to adjacent or nearby structures. These complications include otitis media, sinusitis, cervical adenitis and retropharyngeal or peritonsillar abscess. Nonsuppurative complications, such as acute glomerulonephritis and acute rheumatic fever, involve responses to GABHS at other sites.

The development of acute glomerulonephritis can follow GABHS pharyngitis by about 10 days or can follow GABHS skin infections by about three weeks.[12] This complication has been linked to a limited number of GABHS serotypes that have certain M proteins in the cell wall; these serotypes are termed "nephritogenic strains." Little or no evidence shows that antibiotic treatment prevents acute glomendonephritis.

Acute rheumatic fever usually occurs about 18 days after GABHS pharyngitis.[12] This illness has not been associated with GABHS skin infections. In epidemics of GABHS pharyngitis, acute rheumatic fever may develop in up to 3 percent of untreated patients; in endemic infections, fewer cases probably occur.[13] While the pathogenetic mechanisms responsible for the development of acute rheumatic fever are unclear, epidemiologic data suggest that certain serotypes of GABHS are rheumatogenic.[14]

Adequate antibiotic treatment of GABHS pharyngitis can minimize the risk of acute rheumatic fever. Such therapy may be initiated as late as nine days after the onset of pharyngitis and still be effective.[15] The incidence of acute rheumatic fever declined dramatically from the early part of the 20th century through the 1970s. However, multifocal outbreaks and clusters of acute rheumatic fever cases occurred in various areas of the United States between 1984 and 1988. Unexpected features in these epidemics, in comparison with previous outbreaks, included a substantial proportion of patients not able to recall recent pharyngitis symptoms,[16-18] a higher incidence of carditis[1,17,18] and the occurrence of outbreaks primarily in suburban or rural middle-class white neighborhoods.[16-19]

Strains of GABHS recovered in the recent epidemics were heavily encapsulated, and well-recognized rheumatogenic serotypes were involved.[1,14,18-20] While the reasons for the apparent resurgence of acute rheumatic fever are unknown, investigators believe that changes in the virulence of certain strains are involved, as are changes in host characteristics, such as the immunogenetic factors that influence susceptibility to acute rheumatic fever.[21]

Diagnosis

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A statement for health professionals by the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, the American Heart Association. Circulation 1988;78:1082-6. [14.] Kaplan EL, Johnson DR, Cleary PP. Group A streptococcal serotypes isolated from patients and sibling contacts during the resurgence of rheumatic fever in the United States in the mid-1980s. J Infect Dis 1989;159:101-3. [15.] Catanzaro FT, Stetson CA, Morris AI, Chamovitz R, Rammelkamp CH, Stolzer BL, et al. The role of the streptococcus in the pathogenesis of rheumatic fever. Am J Med 1954;17:749-56. [16.] Wald ER, Dashefsky B, Feidt C, Chiponis D, Byers C. Acute rheumatic fever in western Pennsylvania and the tristate area. Pediatrics 1987;80:371-4. [17.] Hosier DM, Craenen JM, Teske DW, Wheller JJ. Resurgence of acute rheumatic fever. Am J Dis Child 1987;141:730-3. [18.] Veasy LG, Wiedmeier SE, Orsmond GS, Ruttenberg HD, Boucek MM, Roth SJ, et al. 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DARIA KISELICA, M.D. is assistant professor in the department of internal medicine and student health at the University of Virginia Health Sciences Center, Charlottesville, Dr. Kiselica graduated from Pennsylvania State University College of Medicine in Hershey and completed a residency in internal medicine at the University of Massachusetts Medical School in Worcester.

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