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Letters to the Editor
has already been suggested, and could be related to an inhibitory effect of S. pneumoniae on S. aureus via the pro- duction of hydrogen peroxide.7 These findings raise the question of whether oropharyngeal carriage may be asso- ciated with a risk for developing ACS with S. aureus. In the general population, an increase in the prevalence of S. aureus carriage over a prolonged period has been suggest- ed after pneumococcal vaccination.8 Moreover, S. aureus infection might be more common in patients who are colonized.9 Some series have highlighted the risk of S. aureus oropharyngeal carriage and the risk of S. aureus infection in the general population9 as well as in the crit- ical care setting.10 A sickle-cell pediatric series suggested that S. aureus colonization was also associated with a subsequent risk of S. aureus infection, without specifying the site of infection.11 In our study, a history of S. aureus infection was associated with the subsequent occurrence of ACS associated with this microorganism. This finding may also suggest a chronic carriage of S. aureus in this population, and the subsequent risk for developing another S. aureus infection.
S. aureus has been implicated in influenza LRTI.12 In our study, 24% of the ACS episodes associated with S. aureus occurred during the flu season, a rate that did not differ from that of the other ACS episodes. The viral co-infection rate was 10%, but influenza was identified in only one episode, despite a broad search using mPCR (66% of patients with S. aureus documentation). In addi-
Table 2. Genotypic markers of Staphylococcus aureus.
tion, the ACS episodes associated with S. aureus were not preponderant during the flu season.
We identified two MRSA, accounting for 3% of the S. aureus strains, a rate higher than that usually reported in community-acquired pneumonia,4 but lower than the 16% rate in a recent series concerning community acquired pneumoniae.13 SCD patients are regularly hospi- talized and exposed to repeat antimicrobial therapies, which could partly explain this proportion. Nevertheless, a pediatric series suggested a similar rate of MRSA oropharyngeal carriage between SCD and non-SCD pop- ulations.14
Despite a higher initial clinical severity, the S. aureus group had similar short-term outcomes to the control group, a finding that may be related to the fact that early antimicrobial treatments 5 were administered to all patients, as recommended.
Genotypic analysis demonstrated a significant clonal diversity, with a 62% rate of toxin genes, similarly to col- onizing and pathogenic S. aureus strains.15 While the PVL strains may be involved in necrotizing community- acquired pneumonia,13 the two ACS episodes were not associated with necrotizing pulmonary lesions, and had favorable outcomes.
Our study has limitations inherent to all retrospective monocentric studies, and our results should be extrapo- lated with caution. The selection criteria may have underestimated the prevalence of S. aureus, but also the prevalence of other microorganisms, in particular intra- cellular bacteria. In some patients, the vaccination pro- gram may have been just initiated before the ACS episode, precluding any formal conclusion about the rela- tionship between S. aureus ACS and the pneumococcal vaccination strategy. Last, the distinction between S. aureus colonization and S. aureus infection may have been difficult in some cases.
Whether the identification of S. aureus is associated with colonization in ACS, and whether this colonization is associated with a subsequent risk for developing a new infection is uncertain. In order to answer this, it would be necessary to take sequential samples at baseline and dur- ing episodes of ACS. In this context, and due to the lim- itations of the current diagnostic tests, the value of quan- titative PCR may help to distinguish between coloniza- tion and deep pulmonary infection. Moreover, deconta- mination of the S. aureus carriage sites could be useful. Finally, antibiotic therapy targeting MSSA on admission of patients with ACS having a prior S. aureus infection may be warranted.
Alexandre Elabbadi,1 Guillaume Voiriot,1,2 Anne Tristan,3,4 Aude Gibelin,1 Charlotte Verdet,5 Michel Djibré,1
Aline Santin,6 Etienne-Marie Jutant,1 Julien Lopinto,1 François Vandenesch,3,4 François Lionnet6
and Muriel Fartoukh1,2
1Sorbonne Université, Assistance Publique - Hôpitaux de Paris, Service de Médecine Intensive Réanimation, Hôpital Tenon, Paris; 2Groupe de Recherche Clinique CARMAS, Collegium Galilée, Créteil; 3Centre National de Référence des Staphylocoques, Institut des Agents Infectieux, Hospices Civils de Lyon, Lyon; 4Centre International de Recherche en Infectiologie, INSERM U1111, Université Lyon 1, École Normale Supérieure de Lyon, Lyon; 5Sorbonne Université, Assistance Publique - Hôpitaux de Paris, Service de Bactériologie, Hôpital Saint- Antoine, Paris and 6Sorbonne Université, Assistance Publique - Hôpitaux de Paris, Service de Médecine Interne, Centre de Référence de la Drépanocytose, Hôpital Tenon, Paris, France
Correspondence:
ALEXANDRE ELABBADI - alexandre.elabbadi@aphp.fr
Variables, n (%)
Toxin
TSST-1 Enterotoxins§ PVL
Exfoliative toxin
agr allele I
II
III
IV 1(5)
Clonal Complex CC15 MSSA CC12 MSSA CC8 MSSA CC8 MRSA CC398 MSSA CC188 MSSA CC152 MSSA CC121 MSSA CC97 MSSA CC96 MSSA CC88 MSSA CC45 MSSA CC30 MSSA
¶
Strains, n=21
13 (62) 2 (10) 11 (52) 2 (10) 1 (5)
5 (24) 2 (10) 2 (10) 2 (10) 2 (10) 1 (5) 1 (5) 1 (5) 1 (5) 1 (5) 1 (5) 1 (5) 1 (5)
10 (48) 7 (33) 3 (14)
TSST: toxic shock syndrome toxin; PVL: Panton-Valentine leucocidin; agr: accessory gene regulator; MSSA: methicillin-sensitive Staphylococcus aureus; MRSA: methi- cillin-resistant Staphylococcus aureus; CC: clonal complexes. §SEA (n=2); SEB (n=3); SEC (n=2); SED (n=1); SEG (n=3); SEI (n=3); SEJ (n=1); SEL (n=2); SEM (n=1); SEN (n=1); SEO (n=1); SEP (n=4); SEJ (n=2); SEQ (n=1); SER (n=2); SEU (n=2); ¶ETA (n=1).
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haematologica | 2021; 106(12)