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Various combined preparations of calcium and vitamin D are available; a common choice is Adcal D3® two tablets daily (each tablet contains calcium 600 mg and colecalciferol 400 units) medications zoloft side effects 500 mg secnidazole with amex. Given the urgency of the situation symptoms joint pain fatigue cheap secnidazole online mastercard, it is acceptable to administer the treatment frst and write the prescription later medicine kim leoni 500mg secnidazole sale. You should seek expert guidance for the management of severe or symptomatic hypocalcaemia; vitamin D defciency; and in the use of calcium and vitamin D in severe chronic kidney disease symptoms 4 days before period order secnidazole 500 mg without prescription. Doses should be separated from potentially interacting medicines (see Important interactions) by about 4 hours. They may also interact with certain foods, including spinach, bananas and whole cereals; about 2 hours separation is required if these have been consumed. Communication Explain the rationale for treatment as appropriate for the clinical indication. Advise patients to seek medical advice if they develop side effects such as abdominal pain and limb pain, as these may be a sign of high calcium levels, requiring a blood test. Monitoring Patients with severe hyperkalaemia require continuous cardiac monitoring. For any patient receiving calcium or vitamin D supplements, check serum calcium levels at regular intervals or if they develop symptoms of hypercalcaemia. Cost Oral calcium and vitamin D preparations are relatively inexpensive on an individual patient basis, but at a population level they account for substantial healthcare spending. Clinical tip—Hyperkalaemia is common among hospital inpatients and is potentially life threatening. All calcium channel blockers can be used to control symptoms in people with stable angina; β-blockers are the main alternative. Diltiazem and verapamil are used to control cardiac rate in people with supraventricular arrhythmias including supraventricular tachycardia, atrial futter and atrial fbrillation. Mechanisms of Calcium channel blockers decrease Ca2+ entry into vascular and cardiac action cells, reducing intracellular calcium concentration. This causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure. Reduced cardiac rate, contractility and afterload reduce myocardial oxygen demand, preventing angina. Dihydropyridines, including amlodipine and nifedipine, are relatively selective for the vasculature, whereas non-dihydropyridines are more selective for the heart. Of the non-dihydropyridines, verapamil is the most cardioselective, whereas diltiazem also has some effects on the vessels. Important Common adverse effects of amlodipine and nifedipine include ankle adverse effects swelling, fushing, headache and palpitations, which are caused by vasodilatation and compensatory tachycardia. Verapamil commonly causes constipation and less often, but more seriously, can cause bradycardia, heart block and cardiac failure. As diltiazem has mixed vascular and cardiac actions, it can cause any of these adverse effects. Warnings Verapamil and diltiazem should be used with caution in patients with poor left ventricular function as they can precipitate or worsen heart failure. Amlodipine and nifedipine should be avoided in patients with unstable angina as vasodilatation causes a refex increase in contractility and tachycardia, which increases myocardial oxygen demand. In patients with severe aortic stenosis, amlodipine and nifedipine should be avoided as they can provoke collapse. Important Non-dihydropyridine calcium channel blockers (verapamil and diltiazem) interactions should not be prescribed with β-blockers except under close specialist supervision. Both drug classes are negatively inotropic and chronotropic, and together may cause heart failure, bradycardia, and even asystole. Amlodipine has a plasma half-life of 35–50 hours and is suitable for once daily administration. By contrast, the half-lives of nifedipine (2–3 hours), verapamil (2–8 hours) and diltiazem (6–8 hours) are relatively short. Administration Modifed-release and long-acting preparations should be swallowed whole, and not crushed or chewed as this will interfere with the slow release of the drug. Communication Explain why the calcium channel blocker has been prescribed depending on indication. As appropriate, discuss other measures to reduce cardiovascular risk, including smoking cessation. For diltiazem and nifedipine, only the longer-acting preparations are licensed to treat hypertension. Clinical tip—The different longer-acting preparations of nifedipine and diltiazem may not be bioequivalent. You should therefore request a specifc brand when prescribing either of these drugs. Trigeminal neuralgia, as frst choice treatment to control pain and reduce frequency and severity of attacks. Bipolar disorder, as an option for prophylaxis in patients resistant to or intolerant of other medication. Mechanisms of the mechanism of action of carbamazepine is incompletely understood. This may inhibit spread of seizure activity in epilepsy, control neuralgic pain by blocking synaptic transmission in the trigeminal nucleus and stabilise mood in bipolar disorder by reducing electrical kindling in the temporal lobe and limbic system. Important the most common dose-related adverse effects are gastrointestinal adverse effects upset (e. Carbamazepine hypersensitivity affects about 10% of people taking the drug and most commonly manifests as a mild maculopapular skin rash. Antiepileptic hypersensitivity syndrome affects about 1 in 5000 people taking carbamazepine or phenytoin, usually within 2 months of starting treatment. Stevens–Johnson syndrome, toxic epidermal necrolysis), fever and lymphadenopathy with systemic (e. Other common adverse effects include oedema and hyponatraemia due to an antidiuretic hormone-like effect. Warnings Carbamazepine exposure in utero is associated with neural tube defects, cardiac and urinary tract abnormalities and cleft palate. Women with epilepsy planning pregnancy should discuss treatment with a specialist and start taking high-dose folic acid supplements before conception. Prior antiepileptic hypersensitivity syndrome is a contraindication to both carbamazepine and phenytoin, due to potential cross-sensitivity. Carbamazepine should be prescribed with caution in patients with hepatic, renal or cardiac disease, due to increased risk of toxicity. Important Carbamazepine induces cytochrome P450 enzymes, reducing plasma interactions concentration and effcacy of drugs that are metabolised by P450 enzymes (e. Carbamazepine is itself metabolised by these enzymes, so its concentration and adverse effects are increased by cytochrome P450 inhibitors (e. Complex interactions occur with other antiepileptic drugs as most alter drug metabolism. The effcacy of antiepileptic drugs is reduced by drugs that lower the seizure threshold (e. As tolerance develops to adverse effects, the dose is increased gradually to a usual maximum of 1. Treatment should not be stopped suddenly, but should be withdrawn gradually under medical supervision, due to risk of seizure recurrence. Administration Oral carbamazepine is available as immediate- or modifed-release tablets, chewable tablets and oral suspension. As carbamazepine bioavailability differs between formulations, switching between them is best avoided. Use of rectal suppositories should be limited to short periods when oral administration is not possible as rectal irritation may occur with prolonged use. Warn the patient to look out for signs of severe hypersensitivity, including skin rashes; bruising, bleeding, a high temperature or mouth ulcers (blood toxicity); reduced appetite or abdominal pain (liver toxicity). Advise patients that they must not drive unless they have been seizure-free for 12 months (or have at least a three-year pattern of seizures while asleep only).
How- ever symptoms joint pain fatigue 500 mg secnidazole visa, some patients are especially sensitive to tyramine and so all patients should be advised to avoid tyramine-rich foods and indirect-acting sympathomimetic amines treatment 4s syndrome purchase secnidazole mastercard. It is completely absorbed from the gut but undergoes signiﬁcant ﬁrst-pass metabolism resulting in an oral bioavailability of 60–80% treatment tendonitis order secnidazole pills in toronto. It is metabolized in the liver by cytochrome P450 and up to 2% of the Caucasian and 15% of the Asian pop- ulation have been shown to be slow metabolizers medicine 95a pill order 500 mg secnidazole with visa. Linezolid is a new antibiotic indicated for methacillin-resistant Staphlococcus aureus and vancomycin-resistant enetrococci. However, the newer agents may con- trol depression more effectively and reduce the chance of a serious peri-operative drug interaction. Atypical agents Mianserin Mianserin is a tetracyclic compound used in depressive illness, especially where sedation is required. It does, however, block presynaptic α2-adrenoceptors, which reduces their negative feedback, resulting in increased synaptic concentrations of neurotransmitters. It has very little ability to block muscarinic and peripheral α-adrenoceptors and as such causes less in the way of antimuscarinic effects or postural hypotension. Its important side effects are agranulocytosis and aplastic anaemia, which are more common in the elderly. Lithium carbonate Lithium is used in the treatment of bipolar depression, mania and recurrent affective disorders. Inexcitable cells, lithium imitates Na+ and decreases the release of neurotransmitters. It may increase generalized muscle tone and lower the seizure threshold in epilep- tics. Many patients develop polyuria and polydipsia due to antidiuretic hormone antagonism. Lithium prolongs neuromuscular blockade and may decrease anaesthetic requirements as it blocks brain stem release of noradrenaline and dopamine. The thyroid gland may become enlarged and underactive and the patient may experience weight gain and tremor. Above the therapeutic level patients suffer with vomiting, abdominal pain, ataxia, convulsions, arrhythmias and death. It may be given orally or intravenously but the dose must be tailored to the individual patient as wide interpatient variation exists (about 9% of the population are slow hydroxylators) and blood assays are useful in this regard. Mechanism of action the action of phenytoin is probably dependent on its ability to bind to and stabilize inactivated Na+ channels. This prevents the further generation of action potentials that are central to seizure activity. Effects r Idiosyncratic – acne, coarsening of facial features, hirsutism, gum hyperplasia, folate-dependent megaloblastic anaemia, aplastic anaemia, various skin rashes and peripheral neuropathy. Rapid undiluted intravenous administration is associated with hypotension and heart block. Its metabolism may be inhibited by metronidazole, chloramphenicol and isoniazid leading to toxic levels. Furthermore phenytoins metabolism may be induced by carbamazepine or alcohol resulting in reduced plasma levels. Kinetics the oral bioavailability is approximately 90% and it is highly plasma protein bound (90%). It undergoes saturable hepatic hydroxylation resulting in zero-order kinetics just above the therapeutic range. Effects r Central nervous system – mild neurotoxic effects including headache, diplopia, ataxia, vomiting and drowsiness are common and often limit its use. Kinetics Carbamazepine is well absorbed from the gut with a high oral bioavailability. It is approximately 75% plasma protein bound and undergoes extensive hepatic metabolism to carbamazepine 10,11-epoxide, which retains about 30% of carba- mazepines anticonvulsant properties. Sodium valproate Uses Sodium valproate is used in the treatment of various forms of epilepsy including absence (petit mal) seizures and in the treatment of trigeminal neuralgia. Itisalong-actingbarbituratethatinduceshepatic enzymes and interacts with other agents (warfarin, oral contraceptives, other anti- convulsants). Other agents Vigabatrin,gabapentin,lamotrigine and pregabalin are newer agents that are used in the control of persistent partial seizures. It interacts with phenytoin reducing its concentration by about 25% by an unknown mechanism. Lamotrigine acts on the presynaptic neuronal membrane and stabilizes the inac- tive Na+ channel leading to a reduction in excitatory neurotransmitter release. Its rate of metabolism is increased by other enzyme-inducing drugs (carbamazepine and phenytoin) but reduced by sodium valproate. Gabapentins mode of action is uncertain but it may bind to Ca2+ channels within the brain. It is not plasma protein bound and has a terminal elimination half-life of 5–7 hours. It is excreted unchanged in the urine and does not interfere with other anticonvulsants as it does not affect hepatic enzyme systems. Pregabalin is a potent ligand for the alpha-2-delta subunit of voltage-gated cal- cium channels in the central nervous system. Once bound there is a reduction in calcium inﬂux leading to a reduction of excitatory neurotransmitter release. In a manner similar to gabapentin it is not metabolized so that it does no interact with other anticonvulsants. In previous decades anaesthesia was almost synonymous with vomiting, but with the advent of new anaesthetic agents and more aggressive treatment the incidence of vomiting has decreased. However, even the latest agents have failed to eradicate this troublesome symptom encountered in the peri-operative period. It has no discrete anatomical site but may be considered as a collection of effector neurones situated in the medulla. This collection projects to the vagus and phrenic nerves and also to the spinal motor neuronessupplyingtheabdominalmuscles,whichwhenactingtogetherbringabout the vomiting reﬂex. While the administration of antiemetics forms a vital part of treat- ment, attention should also be given to minimizing the administration of opioids by the use of non-steroidal anti-inﬂammatory drugs and avoiding unnecessary anti- cholinesterase administration. Dopamine antagonists Phenothiazines Phenothiazines are the main group of anti-psychotic drugs (neuroleptics) and have onlyalimitedroleinthetreatmentofvomiting. Theyaredividedintothreegroupson the basis of structure, which confers typical pharmacological characteristics (Table 18. Chlorpromazine Chlorpromazines proprietary name Largactil hints at the widespread effects of this drug. Uses Chlorpromazine is used in schizophrenia for its sedative properties and to cor- rect altered thought. Its effects on central neural pathways are complicated but are thought to involve isolating the reticular activating system from its afferent con- nections. This results in sedation, disregard of external stimuli and a reduction in motor activity (neurolepsy). It is sometimes used to control vomiting or pain in ter- minal care where other agents have been unsuccessful. It1 also has membrane-stabilizing properties and prevents noradrenaline uptake into sympathetic nerves (uptake 1). Ithasvariableeffectson hypothalamic function, reducing the secretion of growth hormone while increas- ing the release of prolactin (dopamine functions as prolactin release inhibitory factor). While it has been shown to be an adequate antiemetic, its other effects have limited this role. Cholestatic jaundice, agranulocytosis, leucope- nia, leucocytosis and haemolytic anaemia are all recognized. Kinetics Absorption from the gut is good but due to a large hepatic ﬁrst-pass metabolism (limiting its oral bioavailability to about 30%), it is often given parenterally. The large number of hepatic metabolites is excreted in the urine or bile, while a variable but small fraction is excreted unchanged in the urine.
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The distinguishing feature of partial agonists is that they fail to achieve a maximal effect even in very high dose treatment 3 cm ovarian cyst generic secnidazole 500mg online. Partial agonists may act as either agonists or antagonists depending on circumstances treatment nail fungus purchase 500mg secnidazole. When combined with a full agonist they produce additive effects at low doses of the full agonist medicine 75 buy genuine secnidazole on-line, but this switches to competitive antagonism as the dose of full agonist increases; the full agonist needs todisplacethepartialagonistinordertorestoremaximumeffect medicine 666 secnidazole 500 mg for sale. Inthecaseofpartial agonists the equilibrium between active and inactive forms can never be entirely in favour of the active conformation, so the link between activation of receptor and effect is only a fraction of that seen with full agonists. Inverse agonists It is possible for a drug to bind and exert an effect opposite to that of the endogenous agonist. The mechanism of inverse agonism is related to a constitutive action of receptors; some receptors can show a low level of activity even in the absence of a ligand, since the probability of taking up an active conformation is small but mea- surable. Inverse agonists bind to these receptors and greatly reduce the incidence of the active conformation responsible for this constitutive activity, as a result inverse agonists appear to exert an opposite effect to the agonist. Competitive antagonists For competitiveantagoniststheeffectoftheantagonistmaybeovercomebyincreas- ing the concentration of the agonist – the two molecules are competing for the same receptor and the relative amounts of each (combined with receptor afﬁnity) deter- mine the ratios of receptor occupation. In the presence of a competitive inhibitor the log[dose] versus response curve is shifted to the right along the x-axis; the extent of this shift is known as the dose-ratio (Figure 3. It deﬁnes the factor by which agonist concentration must be increased in order to produce equivalent responses in the presence and absence of a competitive inhibitor. The pA2 value, the negative logarithm of the concentration of antagonist required to produce a dose-ratio of 2, is used to compare the efﬁciency of competitive antagonism for different antagonists at a given receptor. Examplesofcompetitiveinhibitionincludethenon-depolarizingmusclerelaxants competing with acetylcholine for cholinergic binding sites at the nicotinic receptor of the neuromuscular junction and β-blockers competing with noradrenaline at β-adrenergic receptor sites in the heart. Note the parallel shift to the right in the presence of competitive inhibitor, with preservation of maximum response. In the presence of the non-competitive inhibitor the curve is not shifted to the right, but the maximum obtainable response is reduced. As a general principle, ﬁrst postulated by Bowman, weaker antagonists at the neuromuscular junction have a more rapid onset of action. This is because they are given in a higher dose for the same maximal effect so that more molecules are available to occupy receptors, and the receptor occupancy required for full effect is achieved more rapidly. Rocuronium, a non-depolarizing muscle relaxant, has only 36 3 Drug action (c) 100 A 80 60 A + C 40 C 20 0 10−10 10−9 10−8 10−7 10−6 10−5 10−4 10−3 Concentration (mol/l) Figure 3. The dotted line, A + C, shows the dose-response curve for A in the presence of a sub-maximal dose of C. At low concentration of A the combination results in a greater effect than with A alone but as the dose of A is increased there comes a point at which the effect of A + Cisless than with A alone. This is because at the crossover point the only way A can increase the response is by competing for receptors occupied by C. The relative ﬂooding of the receptors means that the threshold receptor occupancy is achieved more rapidly, with a clear clinical beneﬁt. Non-competitive antagonists Non-competitive antagonists do not bind to the same site as the agonist, and clas- sically they do not alter the binding of the agonist. Their antagonism results from preventing receptor activation through conformational distortion. Recentclassiﬁcationofantagonistsnowgroupsnon-competitiveinhibitors and negative allosteric modulators (see later) together. This is because most non- competitive inhibitors, when investigated carefully, do alter agonist binding. Allosteric modulation of receptor binding Not all drugs with reversible activity will produce effects that ﬁt neatly into either the competitive or non-competitive category. Some drugs can bind to sites distant from the agonist receptor site, yet still alter the binding characteristics of the agonist. Irreversible Irreversible antagonists may either bind irreversibly to the same site as the ago- nist or at a distant site. Whatever the nature of the binding site, increasing agonist concentration will not overcome the blockade. A clinical example is that of phenoxy- benzamine that irreversibly binds to and antagonizes the effects of catecholamines at α-adrenoceptors. This is why aspirin should be stopped 7–10 days before surgery where surgical bleeding must be minimized. However, only a fraction of these recep- tors needs to be occupied to produce a maximal pharmacological effect. As a result there are spare receptors, which provide some protection against failure of transmission in the presence of toxins. This can be demonstrated as follows: if a small dose of an irreversible inhibitor is given then a proportion of the receptors are bound by the inhibitor and rendered unavailable so the log[dose] versus response curve for acetylcholine is shifted to the right because a higher fraction of the remaining receptors must be occupied to produce the orig- inal response. If a further irreversible antagonist is used more receptors are made unavailable and results in a further right-shift of the log[dose] versus response curve. Tachyphylaxis, desensitization and tolerance Repeated doses of a drug may lead to a change in the pharmacological response, which may be increased or decreased for the same dose. The most common mechanism is the decrease of stores of a transmitter 38 3 Drug action beforeresynthesiscantakeplace. Anexampleisthediminishingresponsetorepeated doses of ephedrine, an indirectly acting sympathomimetic amine, caused by the depletion of noradrenaline. Desensitization Desensitization refers to a chronic loss of response over a longer period and may be caused by a structural change in receptor morphology or by an absolute loss of receptor numbers. An example is the loss of β-adrenergic receptors from the myocardial cell surface in the continued presence of adrenaline and dobutamine. Tolerance Tolerance refers to the phenomenon whereby larger doses are required to produce the same pharmacological effect, such as occurs in chronic opioid use or abuse. This reﬂectsanalteredsensitivityofthereceptorsofthecentralnervoussystemtoopioids – the mechanism may be a reduction of receptor density or a reduction of receptor afﬁnity. Tolerance occurs if nitrates are given by continuous infusion for prolonged periods as the sulphydryl groups on vascular smooth muscle become depleted. A drug holiday of a few hours overnight when the need for vasodilatation is likely to be at its lowest allows replenishment of the sulphydryl groups and restoration of the pharmacological effect. Sometimes these inter- actions result in unwanted effects, but some interactions are beneﬁcial and can be exploited therapeutically. Drug interaction can be described as physicochemical, relating to the properties of the drug or its pharmaceutical preparation, pharmacokinetic due to alterations in the way the body handles the drug or pharmacodynamic where the activity of one drug is affected. The chance of a signiﬁcant interaction increases markedly with the number of drugs used and the effects of any interaction are often exaggerated in the presence of disease or coexisting morbidity. About one in six inpatient drug charts contain a signiﬁcant drug interaction, one- third of which are potentially serious. An uncomplicated general anaesthetic for a relatively routine case may use ten or more different agents that may interact with one another or, more commonly, with the patients concurrent medication. Pharmaceutical these interactions occur because of a chemical or physical incompatibility between the preparations being used. Sodium bicarbonate and calcium will precipitate out of solution as calcium carbonate when co-administered in the same giving set. How- ever, one agent may inactivate another without such an overt indication to the observer; insulin may be denatured if prepared in solutions of dextrose and may, therefore, lose its pharmacological effect. Drugs also may react with the giving set or syringe and therefore need special equipment for delivery, such as a glass syringe forparaldehydeadministration. Glyceryltrinitrateisabsorbedbypolyvinylchloride; therefore, special polyethylene administration sets are preferred. Pharmacokinetic Absorption In the case of drugs given orally, this occurs either as a result of one drug bind- ing another in the lumen of the gastrointestinal tract or by altering the function of the gastrointestinal tract as a whole. Charcoal can adsorb drugs in the stomach, preventing absorption through the gastrointestinal tract (charcoal is activated by steam to cause ﬁssuring, thereby greatly increasing the surface area for adsorption). Distribution Drugs that decrease cardiac output (such as β-blockers) reduce the ﬂow of blood carrying absorbed drug to its site of action. The predominant factor inﬂuencing the time to onset of fasciculation following the administration of suxamethonium is cardiac output, which may be reduced by the prior administration of β-blockers. In addition, drugs that alter cardiac output may have a differential effect on regional blood ﬂow and may cause a relatively greater reduction in hepatic blood ﬂow, so slowing drug elimination. Chelating agents are used therapeutically in both the treatment of overdose and of iron overload in conditions such as haemochromatosis.
Although fungi are ubiquitous medicine 4h2 cheap secnidazole 500 mg without a prescription, there is great the Candida bloodstream infection medications guide discount secnidazole online master card, candidaemia internal medicine purchase secnidazole now. Prior antibiotic use infection caused by the yeast Candida symptoms after embryo transfer purchase secnidazole line, and is the most is one of the common risk factors for Candida common cause of fungal infection worldwide (35-37). Over 20 species of Candida can cause receiving intensive antibacterial therapy, such as those infection. Response to antifungal therapy difers by in intensive care or receiving immunosuppressive Candida species. Other examples of common fungal infections demonstrated a marked shift in causative organisms are aspergillosis, histoplasmosis and dermatophytosis of candidaemia towards species of Candida that have (commonly known as ringworm). Also, many of the existing Azoles are used most frequently to treat Candida data are limited to single-centre reports, which may infections, but some Candida species are inherently bias results towards certain patient populations. Antifungal susceptibility testing methods have Echinocandins, when available, are the empiric changed over time, making trend comparisons di´cult. Formulations of amphotericin B are Antifungal susceptibility testing is not performed available in many countries, but this agent has higher in most resource-limited countries, and resistance toxicity than azoles and echinocandins. Although many azole- There are also only limited available data on how resistant Candida infections can be treated with drugs antifungal drug laboratory values correspond to of a dierent class, signiﬁcant cost, toxicity and absence how patients respond to the drug, especially among of an oral formulation can present barriers to their use. Moreover, the standard design of In some developing countries only a single class of surveillance programmes is to collect the ﬁrst isolate antifungal drug is available and, if resistance develops, from each episode of infection, and generally before there are no other treatment options. This method would not capture limitations of available antifungal drugs, the following isolates that developed resistance after exposure to resistance proﬁles are of particular concern: antifungal drugs. For these reasons, resistance might • resistance to azoles, especially fluconazole, be greater than is currently being detected or reported. Figure 21 Fluconazole drug resistance, by Candida, species and country (12, 37, 39-45) % resistant to ﬂuconazole - C. Data are compiled from prior published reports of Economic impact candidaemia in hospitalized patients among state Invasive Candida infections have been reported to be or national surveillance projects, and prospective associated with high morbidity and mortality (mortality laboratory surveillance projects. In most countries of approximately 35%), as well as higher health-care where data are available, drug resistance appears to costs and prolonged length of hospitalization (46, 47). Although it is suspected that resistant infections greatly increase these costs, In some locations, candidaemia is the most common few data exist on the economic impact of resistant cause of all bloodstream infections related to vascular Candida infections. Inappropriate antifungal therapy is associated with increased mortality, increased attributable costs, and increased burden of fuconazole non-susceptible Candida species (46). Resistance to azoles is probably • Resistance to the newest class of antifungal agents, increasing, and resistance to the echinocandins is the echinocandins, is emerging in some countries. It is likely that the global burden will increase with increasing populations of immunocompromized • There are large gaps in information on antifungal patients as economies develop and health care resistance and the global burden of antifungal- improves. Reports of Joint Committee on the Use of Antibiotics in Animal Husbandry and Veterinary Drug (Swann Committee). Norm Norm-Vet Report: A report on usage of antimicrobial agents and occurence of antimicrobial resistance in Norway in animals and humans. Consumption of antimicrobial agents and antimicrobial resistance among medically important bacteria in the Netherlands and Monitoring of antimicrobial resistance and antibiotic usage in animals in the Netherlands in 2012. Solna, Sweden, Swedish Institute for Communicable Disease Control and National Veterinary Institute, 2012. The European Union Summary Report on antimicrobial resistance in zoonotic and indicator bacteria from humans, animals and food in 2011. Global principles for the containment of antimicrobial resistance in animals intended for food. Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. High-density livestock operations, crop ﬁeld application of manure, and risk of community-associated methicillin-resistantStaphylococcus aureus infection in Pennsylvania. High-level technical meeting to address health risks at the human-animal-ecosystems interfaces. Mexico City, Food and Agriculture Organization of the United Nations/World Organisation for Animal Health/World Health Organization, 2011. Frequency of voriconazole resistance in vitro among Spanish clinical isolates of Candida spp. According to breakpoints established by the Antifungal Subcommittee of the European Committee on Antimicrobial Susceptibility Testing. Increasing incidence of candidemia: results from a 20-year nationwide study in Iceland. Nationwide study of candidemia, antifungal use, and antifungal drug resistance in Iceland, 2000 to 2011. A 1-year prospective survey of candidemia in Italy and changing epidemiology over one decade. Excess mortality, hospital stay, and cost due to candidemia: a case-control study using data from population-based candidemia surveillance. Changes in incidence and antifungal drug resistance in candidemia: results from population-based laboratory surveillance in Atlanta and Baltimore, 2008-2011. It is essential to take appropriate measures to preserve the e´cacy of the Whether plentiful or scarce, data on the resistance existing drugs so that common and life-threatening patterns for the bacteria of public health importance infections can be cured. Treatment failure due to resistance to available surveillance and collaboration exist. It is also unclear to what Many of the submitted data sets were collected in 2011 extent dierences in reported data for some bacteria– or earlier. More recent data are needed at all levels antibacterial drug combinations reﬂect real dierences to systematically monitor trends, to inform patient in resistance patterns, or are attributable to dierences treatment guidelines and to inform and evaluate in sampling of patients, laboratory performance and containment eorts. To improve the quality and There is no common coordinated widely agreed strategy comparability of data, international collaboration based or public health goal among identiﬁed surveillance on standardized methodology is needed. The tables in Annex 2 illustrate the variety of sources for the data available for this report. This entails major Timely information sharing pitfalls, such as lack of representativeness and ability Surveillance systems need to be fexible and adaptable to measure impact in the population. Surveillance systems infections (particularly health-care associated should also be able to deliver information promptly infections and those for which frst-line treatment to avoid any delay in public health actions at the failed), community-acquired and uncomplicated local, national, regional and global level. This imbalance is a widely used and freely available software supporting likely to result in higher reported resistance rates than laboratory-based surveillance, can be useful for this would be found for the same bacteria in community purpose in stand-alone laboratories in resource- or population-based samples, as was shown in some limited settings where commercial information reports with data submitted separately for these technology systems are not accessible. In addition, lack of information on the provides a platform for management and sharing source (patient) may lead to overrepresentation of a of data. Treatment guided by limited and biased information may increase the risk of unnecessary use of broad- 6. This will increase the antimicrobial drug resistance in economic impact and accelerate the emergence of disease-specific programmes resistance to last-resort antibacterial drugs. The programmes are supported through broad prolonged illness and excessive mortality, or how much stakeholder engagement, including by governments, of the population or which patient groups are afected, public health institutes, reference laboratories and and so on. After years of sustained efort, on defned populations and epidemiological samples the programmes have been able to deliver surveillance would be necessary to provide the information needed data to inform strategic planning and further actions. Data were sought from the following sources: on a denominator of at least 30 tested isolates. Presentation of data in maps and tables: However, the tables in Annex 2 present all data obtained • Because the focus of this report is to describe the from national sources, surveillance networks or sites, status of national surveillance, priority was given to and data that were received in parallel. The aim with the literature review was to see whether it could add any information on A1. Whenever possible, a sense of the population studied is provided, to give • Whenever available, information on the type of some information on the variety of settings. The questionnaires and technical points, was sent to a few national and were then passed on for completion by the designated international surveillance networks. Scientifc journal databases, giving a total of 6566 papers, which were articles on resistance rates in human isolates of the stored in two databases. Published reports that were excluded were those that: the retrieved abstracts were reviewed by one person. The minimal information considered necessary • did not fulﬁl the inclusion criteria; was the proportion of resistance, number of tested • were posters, conference abstracts or similar; isolates, and information that either data collection or year of publication was 2008 or later. If any of this • did not include original data, such as reviews, information was missing from the abstract, the full policy or position papers, treatment guidelines paper was¢evaluated. This deﬁnition does not imply that the data collected is representative for that country as a whole because information gaps are likely. This deﬁnition does not imply that the data collected is representative for that country as a whole because information gaps are likely. For data from time periods of several years, or where data from a subset of year(s) were available, the format (2001)–2011, indicates the ﬁrst year of data collection within parenthesis, and the most recent year with separate data outside the parenthesis.