Penicillin Treatment Failure in Group A Streptococcal Tonsillopharyngitis: No Genetic Difference Found between Strains Isolated from Failures and Nonfailures

Abstract

Despite penicillin (pcV) treatment, tonsillopharyngitis caused by group A streptococci (GAS) is associated with bacterial failure rates as high as 25%. The reason for this rate of failure is not fully understood. One explanation might be that certain DNA profiles of GAS strains are responsible for treatment failures. Using arbitrarily primed polymerase chain reaction (AP-PCR), we compared the DNA profiles of GAS strains from 4 patients with several treatment failures following pcV treatment of tonsillopharyngitis with the profiles of strains of the same T type from patients who were clinically and bacteriologically cured after a single course of pcV. The isolates were obtained during the same time period and from the same geographic area. Thirty-seven strains of T types 4, 12, and R28 were investigated. Eleven different DNA profiles could be detected with the AP-PCR technique. Five DNA profiles were identified as T type 12, 3 as T type 4, and 3 as T type R28. The DNA profiles of the strains from the 4 patients with several treatment failures differed, but all isolates from each one of these patients exhibited the same or a very similar profile. The DNA profiles of the failure strains were also represented in nonfailure strains. Treatment failure in these 4 patients therefore seems to be due to insufficient eradication of GAS, rather than to reinfection with a new strain. The finding that the same DNA profile can be present in both failure and nonfailure strains suggests that the treatment failure may be to some extent host-related and not only due to bacterial factors.

Keywords

arbitrarily primed polymerase chain reaction penicillin streptococci tonsillopharyngitis treatment failure

Get full access to this article

View all access options for this article.

References

Stjernquist-Desatnik

Prellner

Christensen

. Clinical and laboratory findings in patients with acute tonsillitis. Acta Otolaryngol (Stockh) 1987; 104: 351–9.

Bengtsson

Ekedahl

Holm

. Acute poststreptococcal glomerulonephritis. A retrospective study. Scand J Infect Dis 1973; 5: 111–4.

Catanzaro

Rammelkamp

Jr Chamovitz

. Prevention of rheumatic fever by treatment of streptococcal infections. N Engl J Med 1958; 259: 51–7.

Strömberg

Schwan

Cars

. Five versus ten days treatment of group A streptococcal pharyngotonsillitis: A ran domized controlled clinical trial with Phenoxymethylpenicillin and Cefadroxil. Scand J Infect Dis 1988; 20: 37–46.

Orrling

Stjernquist-Desatnik

Schalén

Kamme

. Clindamycin in persisting streptococcal pharyngotonsillitis after penicillin treatment. Scand J Infect Dis 1994; 26: 535–41.

Brook

. Role of beta-lactamase-producing bacteria in the failure of penicillin to eradicate group A streptococci. Pediatr Infect Dis 1985; 4: 491–5.

Tunér

Nord

. Emergence of beta-lactamase producing anaerobic bacteria in the tonsils during penicillin treatment. Eur J Clin Microbiol 1986; 5: 399–404.

Kim

Kaplan

. Association of penicillin tolerance with failure to eradicate group A streptococci from patients with pharyngitis. J Pediatr 1985; 107: 681–4.

Orrling

Stjernquist-Desatnik

Schalen

Kamme

. Treatment failure in streptococcal pharyngotonsillitis. An attempt to identify penicillin tolerant Streptococcus pyogenes. Scand J Infect Dis 1996; 28: 143–7.

10.

Stjernquist-Desatnik

Samuelsson

Walder

. Penetration of penicillin V to tonsillar surface fluid in healthy individuals and in patients with acute tonsillitis. J Laryngol Otol 1993; 107: 309–12.

11.

LaPenta

Rubens

Chi

Cleary

. Group A streptococci efficiently invade human respiratory epithelial cells. Proc Natl Acad Sci USA 1994; 91: 12115–9.

12.

Sanders

Harrowe

. Bacterial interference: Effects of oral antibiotics on the normal throat flora and its ability to interfere with group A streptococci. Infect Immun 1976; 13: 808–12.

13.

Orrling

Stjernquist-Desatnik

Schalén

. Clindamycin in recurrent group A streptococcal pharyngotonsillitis — an alternative to tonsillectomy? Acta Otolaryngol (Stockh) 1997; 117: 618–22.

14.

Lancefield

. A serological differentiation of human and other groups of hemolytic streptococci. J Exp Med 1933; 57: 571–95.

15.

Jackson

Cook

. A general method for preparing chromatin containing intact DNA. EMBO J 1985; 4: 913–8.

16.

Österlund

Engstrand

. DNA fingerprinting of Streptococcus pyogenes from patients with recurrent pharyngotonsillitis by means of random amplified polymorphic DNA analysis. Scand J Infect Dis 1995; 27: 119–21.

17.

Bingen

Denamur

Lambert-Zechovsky

Braimi

El Lakany

Elion

. DNA restriction fragment length polymorphism differentiates recurrence from relapse in treatment failures of Streptococcus pyogenes pharyngitis. J Med Microbiol 1992; 37: 162–4.

18.

Tanz

Shulman

Sroka

Marubio

Brook

Yogev

. Lack of influence of beta-lactamase-producing flora on recovery of group A streptococci after treatment of acute pharyngitis. J Pediatr 1990; 117: 859–63.

19.

Stjernquist-Desatnik

Holst

. Tonsillar microbial flora: Comparison of recurrent tonsillitis and normal tonsils. Acta Otolaryngol (Stockh) 1999; 119: 102–6.

20.

Ebenfelt

Lundberg

. Bacterial invasion of the tonsillar tissues in acute pharyngotonsillitis and in the adenoid: A preliminary study. Clin Otolaryngol 1994; 19: 310–3.

21.

Panzer

Brown

Epstein

Lipson

Mahaffey

Atkinson

. Clindamycin levels in various body tissues and fluids. J Clin Pharmacol New Drugs 1972; 12: 259–62.

22.

Norgren

Norrby

Holm

. Genetic diversity in T1M1 group A streptococci in relation to clinical outcome of infection. J Infect Dis 1992; 166: 1014–20.