Molecular basis and clonal nature of increasing pneumococcal macrolide resistance in South Africa, 2000–2005

Wolter, Nicole; Gottberg, Anne von; Plessis, Mignon du; Gouveia, Linda de; Klugman, Keith P.

doi:10.1016/j.ijantimicag.2008.01.013

Cited by 18 publications

(8 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MDR VREs increase VRE‐associated mortality rates above figures caused by sensitive enterococci strains . As well, the evolution of macrolide resistance in drug‐resistant streptococci is limiting treatment options and resulting in high mortalities . These data support the need to prioritize antibiotic stewardship and increase One Health molecular studies across Africa to quickly identify and preempt full‐scale outbreaks and dissemination of pathogens.…”

Section: Discussionmentioning

confidence: 92%

Molecular epidemiology and mechanisms of antibiotic resistance inEnterococcusspp.,Staphylococcusspp., andStreptococcusspp. in Africa: a systematic review from a One Health perspective

Sekyere

Mensah

2019

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

A systematic review of antibiotic‐resistant Gram‐positive bacteria in Africa from a One Health perspective is lacking. Here, we report result from a search for English‐language articles on the resistance mechanisms and clonality of Gram‐positive bacteria in Africa between 2007 and 2019 reported in PubMed, Web of Science, ScienceDirect, and African Journals OnLine; 172 studies from 22 different African countries were identified. Resistance genes, such as mecA, erm(B), erm(C), tet(M), tet(K), tet(L), vanB, vanA, vanC, and tet(O), were found to be common. Staphylococcus spp., Enterococcus spp., and Streptococcus spp. were the main species reported by the studies, with clones such as Staphylococcus aureus ST5 (n = 218 isolates), ST8 (n = 127 isolates), ST80 (n = 133 isolates), and ST88 (n = 117 isolates), and mobile genetic elements such as IS16 (n = 28 isolates), IS256 (n = 96), Tn916 (n = 107 isolates), and SCCmec (n = 4437 isolates) identified. SCCmec IV (n = 747 isolates) was predominant, followed by SCCmec III (n = 305 isolates), SCCmec II (n = 163 isolates), SCCmec V (n = 135 isolates), and SCCmec I (n = 79 isolates). Resistance to penicillin (n = 5926 isolates), tetracycline (n = 5300 isolates), erythromycin (n = 5151 isolates), rifampicin (n = 3823 isolates), gentamycin (n = 3494 isolates), sulfamethoxazole/trimethoprim (n = 3089 isolates), and ciprofloxacin (n = 2746 isolates) was common in most reports from 22 countries. Clonal dissemination of resistance across countries and between humans, animals, and the environment was observed. Resistance rates ranged from 1.4% to 100% for 15 of the studies; 10 were One Health–related studies. Strict infection control measures, antimicrobial stewardship, and periodic One Health epidemiological surveillance studies are needed to monitor and contain the threat of increasing antibiotic resistance in Africa.

show abstract

Section: Discussionmentioning

confidence: 92%

Molecular epidemiology and mechanisms of antibiotic resistance inEnterococcusspp.,Staphylococcusspp., andStreptococcusspp. in Africa: a systematic review from a One Health perspective

Sekyere

Mensah

2019

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

show abstract

“…Constitutive MLS B resistance can be conferred by a variety of mutations in the leader sequence (Sutcliffe and Leclercq 2002;Subramaniam et al 2011), and includes deletions of the entire attenuator region for erm(C) in clinical isolates of S. epidermidis and S. aureus (Lampson and Parisi 1986) and for erm(B) in E. faecalis, S. agalactiae, and S. pneumoniae (Martin et al 1987;Rosato et al 1999;Wolter et al 2008b) as well as tandem duplications in the attenuator of erm(C) of S. aureus and S. equorum (Oliveira et al 1993;Lodder et al 1997), which either destabilize the hairpin structure sequestering the initiation sequences for the methyltransferase or duplicate the initiation sequences, leaving one unsequestered and available for translation. Notably, constitutive erm(B)-containing pneumococcal isolates with a higher percentage of 23S rRNA methylation were telithromycin-resistant (Douthwaite et al 2005;Wolter et al 2008a).…”

Section: Inducible or Constitutive Mls B Phenotypementioning

confidence: 99%

Resistance to Macrolide Antibiotics in Public Health Pathogens

Fyfe

Grossman

Kerstein

et al. 2016

Cold Spring Harb Perspect Med

163

140

View full text Add to dashboard Cite

Macrolide resistance mechanisms can be target-based with a change in a 23S ribosomal RNA (rRNA) residue or a mutation in ribosomal protein L4 or L22 affecting the ribosome's interaction with the antibiotic. Alternatively, mono-or dimethylation of A2058 in domain V of the 23S rRNA by an acquired rRNA methyltransferase, the product of an erm (erythromycin ribosome methylation) gene, can interfere with antibiotic binding. Acquired genes encoding efflux pumps, most predominantly mef(A) þ msr(D) in pneumococci/streptococci and msr(A/B) in staphylococci, also mediate resistance. Drug-inactivating mechanisms include phosphorylation of the 2 0 -hydroxyl of the amino sugar found at position C5 by phosphotransferases and hydrolysis of the macrocyclic lactone by esterases. These acquired genes are regulated by either translation or transcription attenuation, largely because cells are less fit when these genes, especially the rRNA methyltransferases, are highly induced or constitutively expressed. The induction of gene expression is cleverly tied to the mechanism of action of macrolides, relying on antibiotic-bound ribosomes stalled at specific sequences of nascent polypeptides to promote transcription or translation of downstream sequences. Macrolide antibiotics are polyketides composed of a 14-, 15-, or 16-membered macrocyclic lactone ring (14-, 15-, and 16-membered) to which several sugars and/or side chains have been attached by the producing organism or as modifications during semisynthesis in the laboratory (Figs. 1 and 2). Newer semisynthetic derivations, like ketolides telithromycin, and solithromycin, have a C3-keto group in place of the C3 cladinose (akin to naturally occurring pikromycin) (Brockmann and Henkel 1950) and an 11,12-cyclic carbamate with an extended alkyl -aryl side chain that increases the affinity of the antibiotic for the ribosome by 10-to 100-fold (Hansen et al. 1999;Dunkle et al. 2010); in the case of solithromycin, a fluorine substituent at C2 provides an additional ribosomal interaction (Llano-Sotelo et al. 2010). Macrolides continue to be important in the therapeutic treatment of community-acquired pneumonia (Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and atypicals Legionella pneumophila, Mycoplasma pneumoniae, Chlamydia pneumoniae), sexually transmitted diseases (Neiserria gonorhoeae, Chlamydia trachomatis, Mycoplasma genitalium), shigellosis, and salmonellosis. With solithromycin heading for a new drug application (NDA) filing in 2016 and having the in vitro potency to treat erythromycin-resistant

show abstract

“…The prevalence of macrolide resistance mechanisms differs considerably among countries, as shown in Table 2 [44–58]. The emergence of pneumococci that carry both ermB and mefE macrolide resistance genes is a cause for concern, especially in Asian countries, Russia, South Africa, and the USA [52,59].…”

Section: Macrolidesmentioning

confidence: 99%

Changes in antimicrobial resistance, serotypes and genotypes in Streptococcus pneumoniae over a 30-year period

Liñares

Ardanuy

Pallarés

et al. 2010

Clinical Microbiology and Infection

267

160

View full text Add to dashboard Cite

Over the past three decades, antimicrobial resistance in Streptococcus pneumoniae has dramatically increased worldwide. Non-susceptibility to penicillin in S. pneumoniae was first described in Australia in 1967, and later in New Guinea (1974), South Africa (1977), and Spain (1979). Most of these strains showed resistance to multiple antibiotics and belonged to serotypes 6A, 6B, 19A, 19F, and 23F. By the late 1980s and 1990s, the emergence and rapid dissemination of antibiotic-resistant pneumococci was observed in southern and eastern Europe, North America, South America, Africa, and Asia. Great geographical variability, both in serotype distribution and in the prevalence of resistant pneumococci, has been reported. However, the highest rates of resistance to penicillin and erythromycin worldwide were found in serotypes 6B, 6A, 9V, 14, 15A, 19F, 19A, and 23F. The introduction of the seven-valent pneumococcal conjugate vaccine (PCV7) in the 2000s and a reduction in antimicrobial use were associated with a significant decline in the incidence of invasive pneumococcal infections and in rates of antibiotic resistance in the USA. However, an increase in the incidence of infections caused by non-PCV7 serotypes, especially multiresistant serotype 19A pneumococci, has been observed in many countries over the last 5 years. The dynamic character of serotypes and antibiotic resistance in S. pneumoniae should be controlled by a policy of prudent antibiotic use and by implementation of the new generation of conjugate vaccines.

show abstract

Molecular basis and clonal nature of increasing pneumococcal macrolide resistance in South Africa, 2000–2005

Cited by 18 publications

References 18 publications

Molecular epidemiology and mechanisms of antibiotic resistance inEnterococcusspp.,Staphylococcusspp., andStreptococcusspp. in Africa: a systematic review from a One Health perspective

Molecular epidemiology and mechanisms of antibiotic resistance inEnterococcusspp.,Staphylococcusspp., andStreptococcusspp. in Africa: a systematic review from a One Health perspective

Resistance to Macrolide Antibiotics in Public Health Pathogens

Changes in antimicrobial resistance, serotypes and genotypes in Streptococcus pneumoniae over a 30-year period

Contact Info

Product

Resources

About