Moreover, chloroquine is not listed among the four treatments studied as part and those given hydroxychloroquine plus the antibiotic azithromycin, the results Afterwards, in terms of adverse effects, at increased doses, it is.
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There are concerns that use of azithromycin-chloroquine for IPT could encourage the emergence and spread of resistance to a variety of organisms. Pathogens that need to be considered include malaria parasites, organisms causing STIs, and the pneumococcus. Apart from clinical trials, azithromycin has never been used operationally for treatment or prevention of malaria.
The susceptibility of azithromycin-chloroquine for selecting parasites resistant to azithromycin is, therefore, unknown. The declining use of chloroquine throughout sub-Saharan Africa is likely to lead to reversal of resistance as witnessed in Malawi where parasite sensitivity returned five years after suspending its use.
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It is possible the re-introduction of chloroquine with azithromycin as a partner drug may prevent re-selection of parasites carrying the pfcrt resistance mutation. However, rigorous surveillance would be needed to verify this assumption.
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Azithromycin sensitivity patterns in high-income countries do not suggest that its use in IPTp would rapidly induce resistance in N. Sensitivity of the gonococcus remains relatively high, even in the presence of growing penicillin resistance. In the United States, minimum inhibitory concentrations MICs of azithromycin exposed to gonococcal isolates have increased modestly since when tracking began. In , 0. In the case of C. There is greater concern regarding syphilis.
Azithromycin has been used, for example, since in San Francisco USA for chemoprophylactic 1, mg and curative 2, mg purposes against syphilis. By , a mutation associated with T. The rapid decline in sensitivity is likely attributable, in large part, to underlying erythromycin resistance which has been in general use for over 50 years.
Erythromycin-resistant T. Indeed, a risk factor for being infected with azithromycin-resistant syphilis is having used azithromycin or other macrolides in the recent past [ , ]. The potential for rapid induction of T. In Madagascar, the mutation was not found in analysis of T. Because neither macrolide has been deployed on any scale in focus countries of IPTp, azithromycin may be less vulnerable to rapid loss of sensitivity as has been witnessed in high-income countries.
Pneumococcal resistance to macrolides occurs by two primary mechanisms, each with distinct genetic markers: ribosomal methylation ermB or ermA genes and efflux pump mutation mefA or mefE genes. Based on experience in mass treatment of trachoma with azithromycin, there is concern that use of the azithromycin-chloroquine combination for IPTp might increase the prevalence of azithromycin- and erythromycin-resistant pneumococci.
Trachoma eradication campaigns using azithromycin among vulnerable groups of children in Australia and Nepal found that one-time treatment may select macrolide-resistant pneumococcal strains in the nasopharynx [ , ] and conjunctiva [ ]. Selection, however, was transient. In Australia, By six months, Selection of azithromycin-resistant strains, however, has not always followed trachoma treatment campaigns. Very high macrolide sensitivity of nasopharyngeal pneumococci was observed in Tanzania when samples were obtained at three weeks, two months and six months post-treatment.
Of 4, pneumococcal swabs tested, only one demonstrated pneumococcal resistance to azithromycin. Curiously, the resistant sample was collected at six months, not earlier, as might be expected with a treatment-induced mutation [ ]. A number of steps could be taken to reduce the chances that azithromycin use in IPT might enhance macrolide resistance in bacteria responsible for several major infections. Considerations include the following:. A counter-selective dose — the minimum dosage necessary to prevent the emergence of drug resistance — can be used instead of the conventional minimum required dose to achieve adequate clinical and parasitological cure.
Such a dose, set just above the resistance breakpoint of target micro-organisms, would suppress most pathogens during initial drug exposure and sustain concentrations sufficient to inhibit mutant progeny that might survive and select for resistance. Breakpoints and a counter-selective dose for azithromycin-chloroquine can be modelled using pharmacokinetic and pharmacodynamic parameters in IPTp target countries.
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While there will always be the potential for inducing resistance, a multi-national, multi-centre surveillance study over 10 years has shown that treatment of respiratory tract infections to the point of bacterial eradication minimizes potential for selecting and maintaining resistant strains [ ]. If azithromycin-chloroquine is limited to IPT, made available only through health facilities, and not simultaneously used for treatment purposes, then drug pressure can be kept to a minimum.
Coordinated resistance surveillance of pneumococci should become a regional objective if countries choose to adopt azithromycin-chloroquine for IPT. Regional networks already exist for monitoring malaria and pneumococcal resistance, and could collaborate on this objective. Monitoring, however, can be a source of controversy as the relevance of in vitro macrolide sensitivity to clinical outcomes is not well established. There has not been a concomitant rise in S. A similar paradox has been seen with penicillin-resistant S.
Multiple reasons may contribute to these discordant trends. In the case of newer macrolides, including azithromycin, drug concentrations are able to reach higher levels in the intracellular tissue and in the epithelial lining fluid of the lung than concentrations measured in blood [ , ]. Azithromycin, therefore, may have superior pharmacokinetics in vivo to inhibit S.
However, macrolide efflux pump mutations have been identified in S. The in vitro-in vivo paradox may be better understood with improved surveillance that involves analysis of in vitro MICs and in vivo treatment outcomes that include morbidity markers — not just morbidity rates — which may be more sensitive in detecting the effect of in vitro changes in macrolide resistance on clinical outcomes [ ]. Evidence to date suggests that azithromycin-chloroquine is a potential alternative for SP for IPTp and its evaluation in clinical trials is warranted.
Several scientific and programmatic questions need to be addressed, however, so that policymakers and programme managers are able to consider the merits of azithromycin-chloroquine in IPTp. Key questions include:. The combination has demonstrated synergism in vivo against P. Preliminary results of studies in non-pregnant adults in sub-Saharan Africa have shown that azithromycin-chloroquine is not inferior to mefloquine, a compound currently under consideration for IPTp.
The azithromycin-chloroquine combination may be safely administered at any time in pregnancy. The secondary benefits of the combination, clearing of symptomatic and asymptomatic STIs, may be as important to maternal, foetal and neonatal health as the clearance and prevention of malaria. Close monitoring of antibiotic resistance markers would need to be an essential part of any IPTp programme using azithromycin-chloroquine. MC structured the review and wrote the paper. RP reviewed the early manuscript and contributed to the writing of the paper.
BG reviewed the early manuscript and contributed to the writing of the paper. DC refined the structure of the review and contributed to the writing of the paper.
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All authors read and approved the final version. Read article at publisher's site DOI : Expert Opin Pharmacother , 19 16 , 05 Oct Cited by: 0 articles PMID: Parasitol Res , 9 , 04 Jul Cited by: 2 articles PMID: Int J Antimicrob Agents , 50 4 , 29 Jun PLoS One , 11 11 :e, 18 Nov To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation.
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Chandramohan D. Affiliations All authors 1. Share this article Share with email Share with twitter Share with linkedin Share with facebook. This review summarizes key in vitro and in vivo evidence of azithromycin and chloroquine activity against Plasmodium falciparum and Plasmodium vivax, as well as the anticipated secondary benefits that may result from their combined use in IPTp, including the cure and prevention of many sexually transmitted diseases.
Free full text. Malar J. Published online Dec PMID: Author information Article notes Copyright and License information Disclaimer. Corresponding author. R Matthew Chico: ku. Received Jul 28; Accepted Dec This article has been cited by other articles in PMC. Go to:. Azithromycin monotherapy for treatment and prevention of malaria Pharmacokinetics Azithromycin is a slow-acting anti-malarial macrolide [ 19 ], an analogue of erythromycin with a nitrogen atom inserted into the macrolide nucleus.
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Safety and tolerability Doses of azithromycin between mg and 2, mg have been used in all trimesters of human pregnancy for the treatment of upper and lower respiratory tract infections, skin diseases, Chlamydia trachomatis , mycoplasma and group B streptococci infections among women allergic to other antibiotics. Efficacy The in vitro anti-malarial activity of azithromycin increases fold against P.
Table 1 Chemoprophylactic effect of azithromycin monotherapy against Plasmodium falciparum in semi-immune non-pregnant adults. Open in a separate window. Chloroquine as monotherapy for the treatment and prevention of malaria Pharmacokinetics Chloroquine has been the first-line treatment of malaria in much of the world for most of the past 60 years.