Vancomycin

Overview

Vancomycin is a glycopeptide antibiotic medication used to treat certain bacterial infections. It is administered intravenously (injection into a vein) to treat complicated skin infections, bloodstream infections, endocarditis, bone and joint infections, and meningitis caused by methicillin-resistant Staphylococcus aureus (medications used to treat MRSA). Blood levels may be measured to determine the correct dose. Vancomycin is also taken orally (by mouth) to treat Clostridioides difficile infections. When taken orally, it is poorly absorbed.[1–5] WP

Common side effects include pain at the injection site and allergic reactions. Occasionally, hearing loss, low blood pressure, or bone marrow suppression occur. Safety in pregnancy is not clear, but no evidence of harm has been found, and it is likely safe for use when breastfeeding. It is a type of glycopeptide antibiotic and works by blocking the construction of a cell wall.[1][6][7] WP

Vancomycin was approved for medical use in the United States in 1958. It is on the World Health Organization's List of Essential Medicines. The WHO classifies vancomycin as critically important for human medicine. It is available as a generic medication. Vancomycin is made by the soil bacterium Amycolatopsis orientalis.[1][3][8][9][10] WP

Uses, dosage and effects

Medical uses

Vancomycin is indicated for the treatment of serious, life-threatening infections by Gram-positive bacteria of both aerobic and anaerobic types that are unresponsive to other antibiotics.[11–14] WP

The increasing emergence of vancomycin-resistant enterococci (VRE) has resulted in the development of guidelines for use by the Centers for Disease Control Hospital Infection Control Practices Advisory Committee. These guidelines restrict use of vancomycin to these indications:[15][16] WP

• treatment of serious infections caused by susceptible organisms resistant to penicillins, such as methicillin-resistant S. aureus (MRSA) and multidrug-resistant S. epidermidis (MRSE),[15][16] WP
• treatment of infections in individuals with serious allergy to penicillins,[15][16] WP
• treatment of pseudomembranous colitis caused by C. difficile; in particular, in cases of relapse or where the infection is unresponsive to metronidazole treatment (for this indication, vancomycin is given orally rather than intravenously),[15][16] WP
• treatment of infections caused by Gram-positive microorganisms in patients with serious allergies to beta-lactam antimicrobials,[16] WP
• antibacterial prophylaxis for endocarditis after certain procedures in penicillin-hypersensitive people at high risk,[16] WP
• surgical prophylaxis for major procedures involving implantation of prostheses in institutions with a high rate of MRSA or MRSE,[16] WP
• early in treatment as an empiric antibiotic for possible MRSA infection while waiting for culture identification of the infecting organism,[15][16] WP
• halting the progression of primary sclerosing cholangitis and preventing symptoms; vancomycin does not cure the patient and success is limited,[15][16] WP
• treatment of endophthalmitis by intravitreal injection for Gram-positive bacteria coverage; it has been used to prevent the condition but is not recommended due to the risk of side effects.[17][18] WP

Spectrum of susceptibility

Vancomycin is a last-resort medication for the treatment of sepsis and lower respiratory tract, skin, and bone infections caused by Gram-positive bacteria. The minimum inhibitory concentration susceptibility data for a few medically significant bacteria are:[19] WP

• S. aureus: 0.25 μg/mL to 4.0 μg/mL[19] WP
• S. aureus (methicillin resistant or MRSA): 1 μg/mL to 138 μg/mL[19] WP
• S. epidermidis: ≤0.12 μg/mL to 6.25 μg/mL[19] WP

Although once described as narrow-spectrum, numerous studies have now shown that vancomycin decreases the levels of a wide spectrum of bacteria, including members of the Gram-negative Bacteroidota that are important in the human gut.[20][21][22] WP

Oral administration

Common side effects associated with oral vancomycin administration (used to treat intestinal infections) include:[23] WP

• gastrointestinal adverse effects (such as abdominal pain and nausea);[23] WP
• dysgeusia (distorted sense of taste), in case of administration of vancomycin oral solution, but not in case of vancomycin capsules.[23] WP

Intravenous administration

Serum vancomycin levels may be monitored in an effort to reduce side effects, but the value of such monitoring has been questioned. Peak and trough levels are usually monitored, and for research purposes the area under the concentration curve is also sometimes used. Toxicity is best monitored by looking at trough values. Immunoassays are commonly used to measure vancomycin levels.[24][25][26] WP

Common adverse drug reactions (≥1% of patients) associated with intravenous vancomycin include: WP

• pain, redness, or swelling at the injection site;[27] WP
• vancomycin flushing syndrome (VFS), previously known as red man syndrome (or "redman syndrome");[23] WP
• thrombophlebitis, which is common when administered through peripheral catheters but not when central venous catheters are used, although central venous catheters are a predisposing factor for upper-extremity deep-vein thrombosis.[28] WP

Damage to the kidneys (nephrotoxicity) and to the hearing (ototoxicity) were side effects of the early, impure versions of vancomycin, and were prominent in clinical trials conducted in the mid-1950s. Later trials using purer forms of vancomycin found nephrotoxicity is an infrequent adverse effect (0.1% to 1% of patients), but this is accentuated in the presence of aminoglycosides.[8][29][30] WP

Rare adverse effects associated with intravenous vancomycin (<0.1% of patients) include anaphylaxis, toxic epidermal necrolysis, erythema multiforme, superinfection, thrombocytopenia, neutropenia, leukopenia, tinnitus, dizziness and/or ototoxicity, and DRESS syndrome.[31] WP

Vancomycin can induce platelet-reactive antibodies in the patient, leading to severe thrombocytopenia and bleeding with florid petechial hemorrhages, ecchymoses, and wet purpura.[32] WP

Historically, vancomycin has been considered a nephrotoxic and ototoxic drug, based on numerous case reports in the medical literature following initial approval by the FDA in 1958. But as its use increased with the spread of MRSA beginning in the 1970s, toxicity risks were reassessed. With the removal of impurities present in earlier formulations of the drug, and with the introduction of therapeutic drug monitoring, the risk of severe toxicity has been reduced.[8] WP

Vancomycin flushing reaction

Vancomycin is recommended to be administered in a dilute solution slowly, over at least 60 min (maximum rate of 10 mg/min for doses >500 mg) due to the high incidence of pain and thrombophlebitis and to avoid an infusion reaction known as vancomycin flushing reaction. This phenomenon has been often clinically referred to as "red man syndrome". The reaction usually appears within 4 to 10 min after the commencement or soon after the completion of an infusion and is characterized by flushing and/or an erythematous rash that affects the face, neck, and upper torso, attributed to the release of histamine from mast cells. This reaction is caused by the interaction of vancomycin with MRGPRX2, a GPCR-mediating IgE-independent mast cell degranulation. Less frequently, hypotension and angioedema occur. Symptoms may be treated or prevented with antihistamines, including diphenhydramine, and are less likely to occur with slow infusion.[15][33][34][35] WP

Routes of administration

In the United States, vancomycin is approved by the Food and Drug Administration for intravenous and oral administration.[23] WP

Intravenous

Vancomycin must be given intravenously for systemic therapy since it is poorly absorbed from the intestine. Vancomycin is a large hydrophilic molecule that partitions poorly across the gastrointestinal mucosa. Due to its short half-life, it is often injected twice daily.[36] WP

Oral

The only approved indication for oral vancomycin therapy is in the treatment of pseudomembranous colitis, where it must be given orally to reach the site of infection in the colon. After oral administration, the fecal concentration of vancomycin is around 500 μg/mL (sensitive strains of Clostridioides difficile have a mean inhibitory concentration of ≤2 μg/mL)[37][38] WP

Inhaled (off-label)

Inhaled vancomycin can also be used off-label, via nebulizer, to treat various infections of the upper and lower respiratory tract.[39–44] WP

Rectal (off-label)

Rectal administration is an off-label use of vancomycin for the treatment of Clostridioides difficile infection.[23] WP

Risks and side effects

Nephrotoxicity

The extent of nephrotoxicity for vancomycin remains controversial. In the 1980s, vancomycin with a purity > 90% was available, and kidney toxicity defined by an increase in serum creatinine of at least 0.5 mg/dL occurred in only about 5% of patients. But dosing guidelines from the 1980s until 2008 recommended vancomycin trough concentrations between 5 and 15 μg/mL. Concern for treatment failures prompted recommendations for higher dosing (troughs 15 to 20 μg/mL) for serious infection, and acute kidney injury (AKI) rates attributable to the vancomycin increased.[30][45][46] WP

Importantly, the risk of AKI increases with co-administration of other known nephrotoxins, in particular aminoglycosides. Furthermore, the sort of infections treated with vancomycin may also cause AKI, and sepsis is the most common cause of AKI in critically ill patients. Finally, studies in humans are mainly associations studies, where the cause of AKI is usually multifactorial.[47–50] WP

Animal studies have demonstrated that higher doses and longer duration of vancomycin exposure correlates with increased histopathologic damage and elevations in urinary biomarkers of AKI.37-38 Damage is most prevalent at the proximal tubule, which is further supported by urinary biomarkers, such as kidney injury molecule-1 (KIM-1), clusterin, and osteopontin (OPN). In humans, insulin-like growth factor binding protein 7 (IGFBP7) as part of the nephrocheck test.[51][52][53] WP

The mechanisms underlying the pathogenesis of vancomycin nephrotoxicity are multifactorial but include interstitial nephritis, tubular injury due to oxidative stress, and cast formation.[46] WP

Therapeutic drug monitoring can be used during vancomycin therapy to minimize the risk of nephrotoxicity associated with excessive drug exposure. Immunoassays are commonly utilized for measuring vancomycin levels.[24] WP

In children, concomitant administration of vancomycin and piperacillin/tazobactam has been associated with an elevated incidence of AKI relative to other antibiotic regimens.[54] WP

Ototoxicity

Attempts to establish rates of vancomycin-induced ototoxicity are even more difficult due to lack of good data. The consensus is that clearly related cases of vancomycin ototoxicity are rare. The association between vancomycin serum levels and ototoxicity is also uncertain. Cases of ototoxicity have been reported in patients whose vancomycin serum level exceeded 80 μg/mL, but cases have also been reported in patients with therapeutic levels. Thus it remains unknown whether therapeutic drug monitoring of vancomycin for the purpose of maintaining "therapeutic" levels prevents ototoxicity. Still, therapeutic drug monitoring can be used during vancomycin therapy to minimize the risk of ototoxicity associated with excessive drug exposure.[24][55][56][57] WP

Interactions

Interactions with other nephrotoxins

Another area of controversy and uncertainty is whether and to what extent vancomycin increases the toxicity of other nephrotoxins. Clinical studies have yielded various results, but animal models indicate that the nephrotoxic effect probably increases when vancomycin is added to nephrotoxins such as aminoglycosides. A dose- or serum level-effect relationship has not been established. WP⚠ Wikipedia itself has flagged this text: citation needed.

Pharmacology

Mechanism of action

Vancomycin targets bacterial cell wall synthesis by binding to the basic building block of the bacterial cell wall of Gram-positive bacteria, whether it is of aerobic or anaerobic type. Specifically, vancomycin forms hydrogen bonds with the D-alanyl-D-alanine (D-Ala-D-Ala) peptide motif of the peptidoglycan precursor, a component of the bacterial cell wall.[11][12] WP

Peptidoglycan is a polymer that provides structural support to the bacterial cell wall. The peptidoglycan precursor is synthesized in the cytoplasm and then transported across the cytoplasmic membrane to the periplasmic space, where it is assembled into the cell wall. The assembly process involves two enzymatic activities: transglycosylation and transpeptidation. Transglycosylation involves the polymerization of the peptidoglycan precursor into long chains, while transpeptidation involves the cross-linking of these chains to form a three-dimensional mesh-like structure.[12] WP

Vancomycin inhibits bacterial cell wall synthesis by binding to the D-Ala-D-Ala peptide motif of the peptidoglycan precursor, thereby preventing its processing by the transglycosylase; as such, vancomycin disrupts the transglycosylation activity of the cell wall synthesis process. The disruption leads to an incomplete and corrupted cell wall, which makes the replicating bacteria vulnerable to external forces such as osmotic pressure, so that the bacteria cannot survive and are eliminated by the immune system.[12] WP

Gram-negative bacteria are insensitive to vancomycin due to their different cell wall morphology. The outer membrane of Gram-negative bacteria contains lipopolysaccharide, which acts as a barrier to vancomycin penetration. This barrier is why vancomycin is mainly used to treat infections caused by Gram-positive bacteria (except some nongonococcal species of Neisseria).[12][58][59] WP

The large hydrophilic molecule of vancomycin is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Under normal circumstances, this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents cell wall synthesis of the long polymers of N-acetylmuramic acid (NAM) and N-acetylglucosamine (NAG) that form the backbone strands of the bacterial cell wall, and prevents the backbone polymers from cross-linking with each other.[60] WP

Research

Research

The combination of vancomycin powder and povidone-iodine lavage may reduce the risk of periprosthetic joint infection in hip and knee arthroplasties.[61] WP

History

History

Vancomycin was first isolated in 1953 by a research team led by chemist Edmund Kornfeld at Eli Lilly, from a soil sample provided by missionary William M. Bouw. The sample had been collected in 1952 within a forest on the island of Borneo, after Bouw took over collection duties from the Reverend William W. Conley, who had been a regular contributor to Lilly's global soil screening program since 1948. This program used a network of Christian and Missionary Alliance members to obtain specimens from remote locations to identify novel microorganisms. The organism within the soil that produced the antibiotic was a previously unknown streptomycete originally named Streptomyces orientalis (later reclassified as Amycolatopsis orientalis).[8][62][63] WP

Initially designated as "compound 05865", the substance was identified as a distinct antibiotic on June 18, 1953, when researcher Marvin Hoehn used paper chromatography to establish its unique "fingerprint." Unlike many contemporaneous samples that resulted in the rediscovery of known agents like chloromycetin, 05865 exhibited a novel chromatographic pattern and was found to be water-soluble. One of the most difficult tasks Kornfeld's team faced was purification. The early purification method employed during that time utilized picric acid (a potentially explosive chemical); because of this, an alternate process was developed. However, this new method yielded material with a purity of only 82% and, when solubilized, produced a brown liquid termed "Mississippi mud".[63][64] WP

The drug's primary indication was the treatment of penicillin-resistant Staphylococcus aureus. The drug was given to a patient who had developed a severe infection on his foot after surgery which had been unresponsive to multiple antibiotics. The surgical staff had recommended amputation or the use of the new antibiotic. His answer was, "Anything that might save my foot". Due to the spread of the bacteria, a high dosage of the antibiotic 05865 was recommended, 100 mg every eight hours, over five days. After the first day, the heat was decreasing, his white cell count was dropping, and the exudate of his wound was less. During the next seven days, the staphylococci disappeared from the wound, and his foot was free from any sign of infection. Two months later, he left the hospital with an intact foot. The drug was fast-tracked for approval by the Food and Drug Administration due to the clinical need for effective anti-staphylococcal agents and an observed lack of resistance development in serial passage in culture media with the drug. The origins of the generic name vancomycin differ; some sources state the name was is linked to the term "vanquish", with others stating it came from the Latin word "vanesco", which means to vanish or disappear. In 1958, Eli Lilly began marketing vancomycin hydrochloride under the trade name Vancocin.[8][29][63][64] WP

Vancomycin never became the first-line treatment for S. aureus for several reasons: WP

• It possesses poor oral bioavailability, so must be given intravenously for most infections. WP
• β-Lactamase-resistant semisynthetic penicillins such as methicillin (and its successors, nafcillin and cloxacillin) were subsequently developed, which have better activity against non-MRSA staphylococci. WP
• Early trials used early, impure forms of the drug ("Mississippi mud"), which were found to be toxic to the inner ear and to the kidneys; these findings led to the relegation of vancomycin to a drug of last resort.[29][65] WP

In 2004, Eli Lilly licensed Vancocin to ViroPharma in the U.S., Flynn Pharma in the UK, and Aspen Pharmacare in Australia. The patent expired in the early 1980s, and the FDA authorized the sale of several generic versions in the U.S., including from manufacturers Bioniche Pharma, Baxter Healthcare, Sandoz, Akorn-Strides, and Hospira.[66] WP

Chemistry

Formula

C66H75Cl2N9O24 PC

CAS number

1404-90-6 PC

Molar mass (g/mol)

1449.2 PC

IUPAC name (computed by PubChem)

(1S,2R,18R,19R,22S,25R,28R,40S)-48-[(2S,3R,4S,5S,6R)-3-[(2S,4S,5S,6S)-4-amino-5-hydroxy-4,6-dimethyloxan-2-yl]oxy-4,5-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-22-(2-amino-2-oxoethyl)-5,15-dichloro-2,18,32,35,37-pentahydroxy-19-[[(2R)-4-methyl-2-(methylamino)pentanoyl]amino]-20,23,26,42,44-pentaoxo-7,13-dioxa-21,24,27,41,43-pentazaoctacyclo[26.14.2.23,6.214,17.18,12.129,33.010,25.034,39]pentaconta-3,5,8(48),9,11,14,16,29(45),30,32,34(39),35,37,46,49-pentadecaene-40-carboxylic acid PC

SMILES

C[C@H]1[C@H]([C@@](C[C@@H](O1)O[C@@H]2[C@H]([C@@H]([C@H](O[C@H]2OC3=C4C=C5C=C3OC6=C(C=C(C=C6)[C@H]([C@H](C(=O)N[C@H](C(=O)N[C@H]5C(=O)N[C@@H]7C8=CC(=C(C=C8)O)C9=C(C=C(C=C9O)O)[C@H](NC(=O)[C@H]([C@@H](C1=CC(=C(O4)C=C1)Cl)O)NC7=O)C(=O)O)CC(=O)N)NC(=O)[C@@H](CC(C)C)NC)O)Cl)CO)O)O)(C)N)O PC

InChIKey

MYPYJXKWCTUITO-LYRMYLQWSA-N PC

PubChem CID

14969

Harm reduction information

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