Q&A
| Q&A |
|
|
|
November 2005 Q. We always culture for beta-streptococci group A for throat cultures. When Staphylococcus aureus is the predominant organism, should it be reported to the physician? If it is clinically significant, should a full minimum inhibitory concentration be done? A. Pharyngitis is caused by a variety of organisms, but most cases are due to an upper respiratory viral infection.1 Common viruses implicated in acute pharyngitis include coronavirus, rhinovirus, respiratory syncytial virus, influenza A and B, parainfluenza virus types 1, 2, and 3, and adenovirus. In addition, patients may be co-infected with an upper respiratory virus and have secondary pharyngeal invasion due to bacteria. It is difficult to differentiate between viral and bacterial causes because the clinical signs and symptoms may be identical.1–3 However, according to the clinical index developed by McIsaac and colleagues,2 patients with bacterial pharyngitis are more likely to present with a history of or measured temperature greater than or equal to 38°C, absence of cough, tender anterior cervical adenopathy, tonsillar swelling or exudates, and age younger than 15 years. Patients with a viral upper respiratory tract infection may also have conjunctivitis, coryza, cough, and diarrhea. The vast majority of cases of acute bacterial pharyngitis are due to beta-hemolytic streptococci, specifically group A streptococci. The Infectious Diseases Society of America, or IDSA, recommends that clinical laboratories analyze throat swabs for group A streptococci alone.1 Throat swabs for group A streptococci detection may be cultured or tested using a non-culture method.1 Commercial methods, including nucleic acid hybridization or a rapid direct group A strep, or GAS, antigen test,1,4,5 are available. Comparative performance studies have shown that non-culture-based methods have similar performance for detecting moderate to heavy amounts of GAS.4–8 However, sensitivity may decrease when small amounts of GAS are present. Laboratories may primarily test adults using a non-culture-based method without secondarily culturing all GAS-negative specimens.1,3,6 However, due to the higher incidence of GAS infection in children, particularly those younger than five years, all throat swabs from children who are GAS negative using a non-culture method should be secondarily cultur ed so as not to miss small amounts.1,3 Despite current guidelines, many laboratories still isolate and report moderate to heavy amounts of other beta-hemolytic streptococci, specifically large colony group C and group G isolates. Although several reports have shown that group C streptococci may cause acute pharyngitis during outbreaks in young adults, 9 in general they do not indicate that group C or group G streptococci are clinically important endemic path o gens in this context. 1,10–13 The routine isolation and reporting of group C or G streptococci from a throat swab is not recommended1 because beta-hemolytic streptococci other than group A are part of the normal oropharyngeal bacterial flora and there is limited evidence in specific populations that group C or G streptococci result in non-infectious sequelae such as rheumatic fever.14 S. aureus is also part of the normal upper respiratory flora. Although the presence of organisms other than group A streptococci, including S. aureus, has been implicated as one explanation for the failure of penicillin alone to prevent recurrent episodes,15 there is no evidence that this organism causes acute pharyngitis. Its presence should, therefore, not be reported, even if isolated in a moderate to heavy amount, because it may encourage indiscriminate antimicrobial therapy. However, colonization with S. aureus may be clinically significant in patients with recurrent skin and soft tissue infection or an acute invasive infection such as bacteremia or pneumonia. Physicians should screen these patients for colonization with S. aureus by collecting nasal and rectal swabs. From these sites, clinical laboratories should report any amount of this organism and perform antibiotic susceptibility testing to determine whether the strain is methicillin resistant. Several studies have documented that physicians empirically start antimicrobial therapy for suspected acute pharyngitis and may not collect a swab for throat culture.1,16 However, the IDSA recommends that a throat swab be collected to confirm the presence of group A streptococci and thus avoid unnecessary treatment and the development of antimicrobial resistance. References 1. Bisno AL, Gerber MA, Gwaltney ME Jr., et al. Diagnosis and management of group A streptococcal pharyngitis: a practice guideline. Infectious Diseases Society of America. Clin Infect Dis. 1997; 25: 574–583. 2. McIsaac WJ, Goel V, To T, et al. The validity of a sore throat score in family practice. CMAJ. 2000;163: 811– 815. 3. McIsaac WJ, Kellner JD, Aufricht P, et al. Empirical validation of guidelines for the management of pharyngitis in children and adults. JAMA. 2004;29: 1587–1595. 4. Chapin KC, Blake P, Wilson CD. Performance characteristics and utilization of rapid antigen test, DNA probe, and culture for detection of group A streptococci in an acute care clinic. J Clin Microbiol. 2002;40:4207–4210. 5. Heiter BJ, Bourbeau PP. Comparison of the Gen-Probe group A streptococcus direct test with culture and a rapid streptococcal antigen detection assay for diagnosis of streptococcal pharyngitis. J Clin Microbiol. 1993;3:2070–2073. 6. Gerber MA, Shulman ST. Rapid diagnosis of pharyngitis caused by group A streptococci. Clin Microbiol Rev. 2004; 17: 571–580. 7. Mayes T, Pichichero ME. Are follow-up throat cultures necessary when rapid antigen detection tests are negative for group A streptococci? Clin Pediatr (Phila). 2001;40:191–195. 8. Nerbrand C, Jasir A, Schalen C. Are current rapid detection tests for group A streptococci sensitive enough? Scand J Infect Dis. 2002;34:797–799. 9. Turner JC, Fox A, Fox K, et al. Role of group C beta-hemolytic streptococci in pharyngitis: epidemiologic study of clinical features associated with isolation of group C streptococci. J Clin Microbiol. 1993;31(4):808–811. 10. Lewis RF, Balfour AE. Group C streptococci isolated from throat swabs: a laboratory and clinical study. J Clin Pathol. 1999;52:264–266. 11. Meier FA, Centor RM, Graham L Jr., et al. Clinical and microbiological evidence for endemic pharyngitis among adults due to group C streptococci. Arch Intern Med. 1990;150(4): 825–829. 12. Schwartz RH, Shulman ST. Group C and group G streptococci. In-office isolation from children and adolescents with pharyngitis. Clin Pediatr (Phila). 1986; 25: 496–502. 13. Zaoutis T, Attia M, Gross R, et al. The role of group C and group G streptococci in acute pharyngitis in children. Clin Microbiol Infect. 2004;10:37–40. 14. Haidan A, Talay SR, Rohde M, et al. Pharyngeal carriage of group C and group G streptococci and acute rheumatic fever in an Aboriginal population. Lancet. 2000;356:1167–1169. 15. Brook I. Penicillin failure and copathogenicity in streptococcal pharyngotonsillitis. J Fam Pract. 1994;38(2):175–179. 16. McIsaac WJ, Goel V, To T, et al. Effect on antibiotic prescribing of repeated clinical prompts to use a sore throat score: lessons from a failed community intervention study. J Fam Pract. 2002;51: 339–444. Deirdre Church, MD, PhD Resource Committee |
|||
|
|
