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We believe that patients with se- 2. Casanova JL, Jouanguy E, Lamhamedi - vere combined immunodefi ciency S, Blanche S, Fischer A. Immunological conditions of children with BCG dissemi- resistant and any form of mild local changes nated infection. Lancet. 1995;346:581. at the BCG injection site should be 3. Casanova JL, Blanche S, Emile JF, Streptococcus given single or double anti-TB ther- Jouanguy E, Lamhamedi S, Altare F, pneumoniae apy, which should be continued until et al. Idiopathic disseminated bacillus Calmette-Guérin infection: a French na- complete immunologic reconstitution tional retrospective study. Pediatrics. To the Editor: Antimicrobial occurs after bone marrow transplant. 1996;98:774–8. medications classifi ed as Severe local BCG infection with re- 4. Fieschi C, Dupuis S, Catherinot E, Fein- (e.g., ) and gional lymph node involvement needs berg J, Bustamante J, Breiman A, et al. (e.g., clindamycin) show strong ac- Low penetrance, broad resistance, and at least triple anti-TB therapy followed favourable outcome of interleukin 12 tivity against streptococci and are by long-term prophylaxis. Dissemi- receptor β1 defi ciency: medical and im- commonly used to treat community- nated BCG infection needs anti-TB munogical implications. J Exp Med. acquired infections caused by Strepto- therapy, including >4 anti-TB drugs, 2003;197:527–35. coccus pneumoniae. Moreover, these 5. Liberek A, Korzon M, Bernatowska E, until the patient fully recovers. Kurenko-Deptuch M, Rydlewska M. drugs are the recommended alterna- Vaccination-related Mycobacterium bo- tives for patients who cannot tolerate Acknowledgments vis BCG infection. Emerg Infect Dis. β-lactams. 2006;12:860–2. Two main -resistant S. E.A.B. thanks Peter Folb, Dina Pfeif- 6. Heyderman RS, Morgan G, Levinsky pneumoniae phenotypes have been re- er, and Adwoa Bentsi-Enchill for encour- R, Strobel S. Successful bone marrow transplantation and treatment of BCG in- ported (1). The fi rst has a high level agement in writing this article. fection in two patients with severe com- of resistance to all macrolides, lincos- The investigation was supported by bined immunodefi ciency. Eur J Pediatr. amides, , and 1991;150:477–80. grant EURO-POLICY-primary immuno- 7. Gonzalez B, Moreno S, Burdach R, Va- B due to ribosomal dimethylation, 23S defi ciency SP23-CT-2005-006411 and na- lenzuela MT, Herinquez A, Ramos MI. rRNA mutations, or ribosomal protein Clinical presentation of bacillus Calmette- tional project no. PBZ-KBN-119/PO5/04. mutations (MLSB, MSB, ML, MKSB, Guérin infections in patients with immu- and K phenotypes). The second is nodefi ciency syndromes. Pediatr Infect Ewa Anna Bernatowska,* Dis J. 1989;8:201–6. characterized by a low-level resistance Beata Wolska-Kusnierz,* 8. Wolska-Kusnierz B, Pac M, Pietrucha (e.g., MIC 2–4 mg/L) to only 14- and Malgorzata Pac,* B, Heropolitanska-Pliszka E, Klaudel- 15-member ring macrolides (M phe- Dreszler M, Kurenko-Deptuch M, et notype) because of mef gene–medi- Magdalena Kurenko-Deptuch,* al. Twenty fi ve years of investigation Zofi a Zwolska,† into primary immunodefi ciency dis- ated active drug effl ux mechanism. Jean-Laurent Casanova,‡ eases in the Department of Immunol- In January 2005, an erythromy- Barbara Piatosa,* ogy, Children’s Memorial Health Insti- cin-susceptible but clindamycin-resis- tute, Warsaw. Central European Journal tant pneumococcal strain was obtained Jacques van Dongen,§ of Immunology. 2005;30:104–14 [cited Kazimierz Roszkowski,† 2007 Mar 19]. Available from http://www. from a conjunctival swab of a 10- Bozena Mikoluc,¶ termedia.pl/magazine.php?magazine_ month-old female outpatient attending Maja Klaudel-Dreszler,* id=10&article_id=6799&magazine_ the daycare center of the Clinic and subpage=ABSTRACT. Laboratory of Infectious Diseases, and Anna Liberek¶ 9. Bonilla FA, Bernstein IL, Khan DA, Bal- *Children’s Memorial Health Institute, War- las ZJ, Chinen J, Frank MM, et al. Practice Siena University, Siena, Italy. To our saw, Poland; †National Institute of Tubercu- parameter for the diagnosis and the man- knowledge, such a phenotype has not agement of primary immunodefi ciency. losis and Lung Diseases, Warsaw, Poland; been reported in the international lit- Ann Allergy Asthma Immunol. 2005;94 erature for S. pneumoniae, although a ‡University Rene Descartes, Paris, France; (5 Suppl 1):S1–63. §University Medical Center, Rotterdam, the 10. Folb PI, Bernatowska E, Chen R, Clemens similar phenotype of S. agalactiae was Netherlands; and ¶Medical University of J, Dodoo AN, Ellenberg SS, et al. A global described by Malbruny et al. (2). perspective on vaccine safety and public Bialystock, Bialystock, Poland The S. pneumoniae isolate was health: the Global Advisory Committee identifi ed by standard procedures (3) on Vaccine Safety. Am J Public Health. 2004;94:1926–31. and confi rmed by PCR for the com- References mon capsule gene cpsA (4). Serotyp- 1. Newport MJ, Huxley CM, Huston S, Address for correspondence: Ewa Anna ing, performed by Quellung reaction, Hawrylowicz CM, Oostra BA, William- Bernatowska, Children’s Memorial Health showed a 35F serotype. Susceptibility son R, et al. A mutation in the interferon– testing was carried out by disk dif- gamma–receptor gene and susceptibility Institute, Department of Immunology, Av. to mycobacterial infection. N Engl J Med. Dzieci Polskich, 20 Warsaw, 04-730 Mazovia, fusion and confi rmed with E-test ac- 1996;335:1941–9. Poland; email: [email protected] cording to Clinical and Laboratory

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 13, No. 5, May 2007 801 LETTERS

Standards Institute standards (5,6) for genes with primers described by Canu 5. Clinical and Laboratory Standards Insti- penicillin, ceftriaxone, ciprofl oxacin, et al. (10). Although these fi ndings are tute. Performance standards for antimi- crobial disk susceptibility tests, 9th ed. erythromycin, clindamycin, , preliminary and the molecular basis Approved standard M2–A9. Wayne (PA): and quinupristin-dalfopristin. For for resistance is the subject of ongoing The Institute; 2006. telithromycin, because an E-test strip investigation, the identifi cation of this 6. Clinical and Laboratory Standards Insti- was unavailable, a microbroth dilution S. pneumoniae phenotype may affect tute. Performance standards for antimi- crobial susceptibility testing, 16th Infor- method was used. clinical management of pneumococcal mational Suppl. M100–S16. Wayne (PA): The strain was susceptible to cef- infections, especially in the treatment The Institute; 2006. triaxone (MIC 0.125 mg/L), ciprofl ox- of patients intolerant of β-lactams. 7. Brenwald NP, Martin JG, Wise R. acin (MIC 0.125 mg/L), erythromycin Prevalence of a putative effl ux mecha- nism among fl uoroquinolone-resistant (MIC 0.125 mg/L), linezolid (MIC 1.5 Acknowledgments clinical isolates of Streptococcus pneu- mg/L), quinupristin/dalfopristin (MIC moniae. Antimicrob Agents Chemother. We thank Elisabetta Mantengoli for 0.5 mg/L), and telithromycin (MIC 1998;42:2032–5. useful suggestions on gene sequencing <0.0035 mg/L); it was not susceptible 8. Oster P, Zanchi A, Cresti S, Lattanzi M, and Sanofi Aventis for providing telithro- Montagnani F, Cellesi C, et al. Patterns to penicillin (MIC 0.125 mg/L) and mycin. of macrolide resistance determinants was resistant to clindamycin (MIC among community-acquired Streptococ- 1 mg/L). A triple disk–diffusion test Strain serotyping was performed at cus pneumoniae isolates over a 5-year with erythromycin, clindamycin, and Streptococcal Reference Unit of Respira- period of decreased macrolide susceptibil- ity rates. Antimicrob Agents Chemother. was performed to test resis- tory and Systemic Infection Laboratory, 1999;43:2510–2. tance inducibility. No inducible pat- Centre for Infections, Health Protection 9. Cresti S, Lattanzi M, Zanchi A, Mon- tern was shown. Agency, London, UK. tagnani F, Pollini S, Cellesi C, et al. To understand the possible resis- Resistance determinants and clonal di- versity in group A streptococci collected tance mechanism, MICs for 2 lincos- Francesca Montagnani,*1 during a period of increasing macrolide amides (clindamycin and ) Alessandra Zanchi,*1 resistance. Antimicrob Agents Chemother. were determined by using a micro- Lucia Stolzuoli,* 2002;46:1816–22. broth dilution method in the presence 10. Canu A, Malbruny B, Coquemont N, Da- Leonardo Croci,* vies TA, Appelbaum PC, Leclercq R. Di- and absence of 10 mg/L of the ef- and Carla Cellesi* versity of ribosomal mutations conferring fl ux pump inhibitor reserpine (Sigma *Clinica e Laboratorio di Malattie Infettive, resistance to macrolides, clindamycin, , and telithromycin in Strep- Chemicals, St Louis, MO, USA), as Università degli Studi di Siena, Italy described (7); S. pneumoniae ATCC tococcus pneumoniae. Antimicrob Agents Chemother. 2002;46:125–31. 49619 and S. mitis 21A29 (mefE+) were used as controls (8). The MICs References Address for correspondence: Francesca remained unchanged in the presence 1. Edelstein PH. Pneumococcal resistance to Montagnani, Clinica e Laboratorio di Malattie of reserpine: 1 mg/L for clindamycin macrolides, lincosamides, ketolides, and Infettive, Dipartimento di Biologia Molecolare, streptogramin B agents: molecular mecha- and 4 mg/L for lincomycin. Università di Siena, Ospedale Le Scotte, Piano nisms and resistance phenotype. Clin In- The strain was screened for er- 0 lotto IV, Viale Bracci, 16, 53100 Siena, Italy; mTR, ermB or mefA, and mefE deter- fect Dis. 2004;38:S322–7. 2. Malbruny B, Werno AM, Anderson TP, email: [email protected] minants as described (8,9). All PCR Murdroch DR, Leclercq R. A new phe- controls gave the expected results. notype of resistance to lincosamide and No PCR product was obtained for the streptogramin A-type in Strep- studied isolate. tococcus agalactiae in New Zealand. J Antimicrob Chemother. 2004;54:1040–4. Preliminary data did not show 3. Rouff KL, Whiley RA, Beighton D. classic macrolide resistance determi- Streptococcus. In: Murray PR, Baron EJ, nants for S. pneumoniae. Low-level Jorgensen JH, Pfaller MA, Yolken RH, lincosamide resistance suggests the editors. Manual of clinical microbiology. 8th ed. Washington: American Society for presence of some effl ux mechanism, Microbiology; 2003. p. 405–21. even if no inhibition by reserpine was 4. Lawrence ER, Griffi ths DB, Martin SA, observed. Moreover, no mutations of George RC, Hall LM. Evaluation of semi- ribosomal proteins and of known bind- automated multiplex PCR assay for deter- mination of Streptococcus pneumoniae se- ing sites for lincosamides in rRNA (1) rotypes and serogroups. J Clin Microbiol. were shown by sequencing of L22, 2003;41:601–17. L4, and 23S rRNA domain II and V 1Contributed equally to this work.

802 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 13, No. 5, May 2007