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18/04/2023

Antibiotic
(chemical compound)

Antibiotic, chemical substance produced by a living organism, generally a microorganism, that is detrimentalto other microorganisms. Antibiotics commonly are produced by soil microorganisms and probably represent a means by which organisms in a complex environment, such as soil, control the growth of competing microorganisms. Microorganisms that produce antibiotics useful in preventing or treating disease include the bacteria and the fungi.
Antibiotics came into worldwide prominence with the introduction of penicillin in 1941. Since then they have revolutionized the treatment of bacterial infections in humans and other animals. They are, however, ineffective against viruses.
The first antibiotics
In 1928 Scottish bacteriologist Alexander Fleming noticed that colonies of bacteria growing on a culture plate had been unfavourably affected by a mold, Penicillium notatum, which had contaminated the culture. A decade later British biochemist Ernst Chain, Australian pathologist Howard Florey, and others isolated the ingredient responsible, penicillin, and showed that it was highly effective against many serious bacterial infections. Toward the end of the 1950s scientists experimented with the addition of various chemical groups to the core of the penicillin molecule to generate semisynthetic versions. A range of penicillins thus became available to treat diseases caused by different types of bacteria, including staphylococci, streptococci, pneumococci, gonococci, and the spirochaetes of syphilis.
Conspicuously unaffected by penicillin was the tubercle bacillus (Mycobacterium tuberculosis). This organism, however, turned out to be highly sensitive to streptomycin, an antibiotic that was isolated from Streptomyces griseus in 1943. As well as being dramatically effective against tuberculosis, streptomycin demonstrated activity against many other kinds of bacteria, including the typhoid fever bacillus. Two other early discoveries were gramicidin and tyrocidin, which are produced by bacteria of the genus Bacillus. Discovered in 1939 by French-born American microbiologist René Dubos, they were valuable in treating superficial infections but were too toxic for internal use.
In the 1950s researchers discovered the cephalosporins, which are related to penicillins but are produced by the mold Cephalosporium acremonium. The following decade scientists discovered a class of antibiotics known as quinolones. Quinolones interrupt the replication of DNA—a crucial step in bacterial reproduction—and have proven useful in treating urinary tract infections, infectious diarrhea, and various other infections involving elements such as bonesand white blood cells.
Use and administration of antibiotics

The principle governing the use of antibiotics is to ensure that the patient receives one to which the target bacterium is sensitive, at a high enough concentration to be effective but not cause side effects, and for a sufficient length of time to ensure that the infection is totally eradicated. Antibiotics vary in their range of action. Some are highly specific. Others, such as the tetracyclines, act against a broad spectrum of different bacteria. These are particularly useful in combating mixed infections and in treating infections when there is no time to conduct sensitivity tests. While some antibiotics, such as the semisynthetic penicillins and the quinolones, can be taken orally, others must be given by intramuscular or intravenous injection.

Categories of antibiotics
Antibiotics can be categorized by their spectrum of activity—namely, whether they are narrow-, broad-, or extended-spectrum agents. Narrow-spectrum agents (e.g., penicillin G) affect primarily gram-positive bacteria. Broad-spectrum antibiotics, such as tetracyclines and chloramphenicol, affect both gram-positive and some gram-negative bacteria. An extended-spectrum antibiotic is one that, as a result of chemical modification, affects additional types of bacteria, usually those that are gram-negative. (The terms gram-positive and gram-negative are used to distinguish between bacteria that have cell walls consisting of a thick meshwork of peptidoglycan [a peptide-sugar polymer] and bacteria that have cell walls with only a thin peptidoglycan layer, respectively.)

Mechanisms of action
Antibiotics produce their effects through a variety of mechanisms of action. A large number work by inhibiting bacterial cell wall synthesis; these agents are referred to generally as β-lactam antibiotics. Production of the bacterial cell wall involves the partial assembly of wall components inside the cell, transport of these structures through the cell membrane to the growing wall, assembly into the wall, and finally cross-linking of the strands of wall material. Antibiotics that inhibit the synthesis of the cell wall have a specific effect on one or another phase. The result is an alteration in the cell wall and shape of the organism and eventually the death of the bacterium.
Other antibiotics, such as the aminoglycosides, chloramphenicol, erythromycin, and clindamycin, inhibit protein synthesis in bacteria. The basic process by which bacteria and animal cells synthesize proteins is similar, but the proteins involved are different. Those antibiotics that are selectively toxic utilize these differences to bind to or inhibit the function of the proteins of the bacterium, thereby preventing the synthesis of new proteins and new bacterial cells.
Antibiotics such as polymyxin B and polymyxin E (colistin) bind to phospholipids in the cell membrane of the bacterium and interfere with its function as a selective barrier; this allows essential macromolecules in the cell to leak out, resulting in the death of the cell. Because other cells, including human cells, have similar or identical phospholipids, these antibiotics are somewhat toxic.
Some antibiotics, such as the sulfonamides, are competitive inhibitors of the synthesis of folic acid (folate), which is an essential preliminary step in the synthesis of nucleic acids. Sulfonamides are able to inhibit folic acid synthesis because they are similar to an intermediate compound (para-aminobenzoic acid) that is converted by an enzyme to folic acid. The similarity in structure between these compounds results in competition between para-aminobenzoic acidand the sulfonamide for the enzyme responsible for converting the intermediate to folic acid. This reaction is reversible by removing the chemical, which results in the inhibition but not the death of the microorganisms. One antibiotic, rifampin, interferes with ribonucleic acid (RNA) synthesis in bacteria by binding to a subunit on the bacterial enzyme responsible for duplication of RNA. Since the affinity of rifampin is much stronger for the bacterial enzyme than for the human enzyme, the human cells are unaffected at therapeutic doses.
Antibiotic resistance
A problem that has plagued antibiotic therapy from the earliest days is the resistance that bacteria can develop to the drugs. An antibiotic may kill virtually all the bacteria causing a disease in a patient, but a few bacteria that are genetically less vulnerable to the effects of the drug may survive. These go on to reproduce or to transfer their resistance to others of their species through processes of gene exchange. With their more vulnerable competitors wiped out or reduced in numbers by antibiotics, these resistant strains proliferate. The end result is bacterial infections in humans that are untreatable by one or even several of the antibiotics customarily effective in such cases. The indiscriminate and inexact use of antibiotics encourages the spread of such bacterial resistance. (See antibiotic resistance.)
Researchers are continually working to discover new antibiotics as a means of overcoming antibiotic resistance. Some potentially effective compounds that have been discovered include certain bacterial toxins and antimicrobial peptides. Novel treatment strategies, such as combining synergistic antibiotics to boost the killing of bacteria, are also under investigation. It may be possible to introduce compounds into bacterial populations that effectively resensitize the bacteria to existing antibiotic drugs.
Major antibiotics
Each type of antibiotic has a specific application in medicine and can serve as a useful model for exploring the various mechanisms by which antibiotics exert their effects. The following sections focus on the penicillins and cephalosporins, imipenem, the antituberculosis antibiotics, and the agents aztreonam, bacitracin, and vancomycin. These agents and groups of agents further illustrate the chemical and functional diversity found among the antibiotics.
Penicillins
The penicillins have a unique structure, a β-lactam ring, that is responsible for their antibacterial activity. The β-lactam ring interacts with proteins in the bacterial cell responsible for the final step in the assembly of the cell wall.
The penicillins can be divided into two groups: the naturally occurring penicillins (penicillin G, penicillin V, and benzathine penicillin) and the semisynthetic penicillins. The semisynthetic penicillins are produced by growing the mold Penicillium under conditions whereby only the basic molecule (6-aminopenicillanic acid) is produced. By adding certain chemical groups to this molecule, several different semisynthetic penicillins are produced that vary in resistance to degradation by β-lactamase (penicillinase), an enzyme that specifically breaks the β-lactam ring, thereby inactivating the antibiotic. In addition, the antibacterial spectrum of activity and pharmacological properties of the natural penicillins can be changed and improved by these chemical modifications. The addition of a β-lactamase inhibitor, such as clavulanic acid, to a penicillin dramatically improves the effectiveness of the antibiotic. Several naturally occurring inhibitors have been isolated, and others have been chemically synthesized.
The naturally occurring penicillins remain the drugs of choice for treating streptococcal sore throat, tonsillitis, endocarditis caused by some streptococci, syphilis, and meningococcal infections. Several bacteria, most notably Staphylococcus, developed resistance to the naturally occurring penicillins, which led to the production of the penicillinase-resistant penicillins (methicillin, oxacillin, nafcillin, cloxacillin, and dicloxacillin). The use of several of these agents, however, has been severely limited by resistance; methicillin is no longer used, because of the emergence of methicillin-resistant Staphylococcus aureus (MRSA).
To extend the usefulness of the penicillins to the treatment of infections caused by gram-negative rods, the broad-spectrum penicillins (ampicillin, amoxicillin, carbenicillin, and ticarcillin) were developed. These penicillins are sensitive to penicillinase, but they are useful in treating urinary tract infections caused by gram-negative rods as well as in treating typhoid and enteric fevers.
The extended-spectrum agents (mezlocillin and piperacillin) are unique in that they have greater activity against gram-negative bacteria, including Pseudomonas aeruginosa, a bacterium that often causes serious infection in people whose immune systems have been weakened. They have decreased activity, however, against penicillinase-producing Staphylococcus aureus, a common bacterial agent in food poisoning.
The penicillins are the safest of all antibiotics. The major adverse reaction associated with their use is hypersensitivity, with reactions ranging from a rash to bronchospasm and anaphylaxis. The more serious reactions are uncommon.
Cephalosporins
The cephalosporins have a mechanism of action identical to that of the penicillins. However, the basic chemical structure of the penicillins and cephalosporins differs in other respects, resulting in some difference in the spectrum of antibacterial activity. Modification of the basic molecule (7-aminocephalosporanic acid) produced by Cephalosporium acremonium resulted in four generations of cephalosporins.
The first-generation cephalosporins (cefazolin, cephalothin, and cephalexin) have a range of antibacterial activity similar to the broad-spectrum penicillins described above. For instance, they are effective against most staphylococci and streptococci as well as penicillin-resistant pneumococci.
The second-generation cephalosporins (cefamandole, cefaclor, cefotetan, cefoxitin, and cefuroxime) have an extended antibacterial spectrum that includes greater activity against additional species of gram-negative rods. Thus, these drugs are active against Escherichia coliand Klebsiella and Proteus species (though several strains of these organisms have developed resistance). Cefamandole is active against many strains of Haemophilus influenzae and Enterobacter, while cefoxitin is particularly active against most strains of Bacteroides fragilis. Second-generation cephalosporins have decreased activity, however, against gram-positive bacteria.
The third-generation cephalosporins (ceftriaxone, cefixime, and ceftazidime) have increased activity against the gram-negative organisms compared with the second-generation agents. Most Enterobacter species are susceptible to these drugs, as are H. influenzae and various species of Neisseria. The antibacterial spectrum of the fourth-generation compounds (cefepime) is similar to that of the third-generation drugs, but the fourth-generation drugs have more resistance to β-lactamases.
Like the penicillins, the cephalosporins are relatively nontoxic. Because the structure of the cephalosporins is similar to that of penicillin, hypersensitivity reactions can occur in penicillin-hypersensitive patients.
Imipenem
Imipenem is a β-lactam antibiotic that works by interfering with cell wall synthesis. It is highly resistant to hydrolysis by most β-lactamases. This drug must be given by intramuscular injection or intravenous infusion because it is not absorbed from the gastrointestinal tract. Imipenem is hydrolyzed by an enzyme present in the renal tubule; therefore, it is always administered with cilastatin, an inhibitor of this enzyme. Neurotoxicity and seizures have limited the use of imipenem.
Antituberculosis antibiotics
Isoniazid, ethambutol, pyrazinamide, and ethionamide are synthetic chemicals used in treating tuberculosis. Isoniazid, ethionamide, and pyrazinamide are similar in structure to nicotinamide adenine dinucleotide (NAD), a coenzyme essential for several physiological processes. Ethambutol prevents the synthesis of mycolic acid, a lipid found in the tubercule bacillus. All these drugs are absorbed from the gastrointestinal tract and pe*****te tissues and cells. An isoniazid-induced hepatitis can occur, particularly in patients 35 years of age or older. Cycloserine, an antibiotic produced by Streptomyces orchidaceus, is also used in the treatment of tuberculosis. A structural analog of the amino acid D-alanine, it interferes with enzymes necessary for incorporation of D-alanine into the bacterial cell wall. It is rapidly absorbed from the gastrointestinal tract and pe*****tes most tissues quite well; high levels are found in urine. Rifampin, a semisynthetic agent, is absorbed from the gastrointestinal tract, pe*****tes tissue well (including the lung), and is used in the treatment of tuberculosis. Rifampin administration is associated with several side effects, mostly gastrointestinal in nature. The drug can turn urine, f***s, saliva, sweat, and tears red-orange in colour.
Aztreonam, bacitracin, and vancomycin
Aztreonam is a synthetic antibiotic that works by inhibiting cell wall synthesis, and it is naturally resistant to some β-lactamases. Aztreonam has a low incidence of toxicity, but it must be administered parenterally.
Bacitracin is produced by a special strain of Bacillus subtilis. Because of its severe toxicity to kidney cells, its use is limited to the topical treatment of skin infections caused by Streptococcusand Staphylococcus and for eye and ear infections.
Vancomycin, an antibiotic produced by Streptomyces orientalis, is poorly absorbed from the gastrointestinal tract and is usually given by intravenous injection. It is used for the treatment of serious staphylococcal infections caused by strains resistant to the various penicillins. Its use against MRSA led to the emergence of vancomycin-resistant Staphylococcus aureus (VRSA).

18/04/2023

The real story behind penicillin

The discovery of penicillin, one of the world’s first antibiotics, marks a true turning point in human history — when doctors finally had a tool that could completely cure their patients of deadly infectious diseases.

Many school children can recite the basics. Penicillin was discovered in London in September of 1928. As the story goes, Dr. Alexander Fleming, the bacteriologist on duty at St. Mary’s Hospital, returned from a summer vacation in Scotland to find a messy lab bench and a good deal more.

Upon examining some colonies of Staphylococcus aureus, Dr. Fleming noted that a mold called Penicillium notatum had contaminated his Petri dishes. After carefully placing the dishes under his microscope, he was amazed to find that the mold prevented the normal growth of the staphylococci.

It took Fleming a few more weeks to grow enough of the persnickety mold so that he was able to confirm his findings. His conclusions turned out to be phenomenal: there was some factor in the Penicillium mold that not only inhibited the growth of the bacteria but, more important, might be harnessed to combat infectious diseases.

As Dr. Fleming famously wrote about that red-letter date: “When I woke up just after dawn on September 28, 1928, I certainly didn’t plan to revolutionize all medicine by discovering the world’s first antibiotic, or bacteria killer. But I guess that was exactly what I did.”

Fourteen years later, in March 1942, Anne Miller became the first civilian patient to be successfully treated with penicillin, lying near death at New Haven Hospital in Connecticut, after miscarrying and developing an infection that led to blood poisoning.

But there is much more to this historic sequence of events.
Actually, Fleming had neither the laboratory resources at St. Mary’s nor the chemistry background to take the next giant steps of isolating the active ingredient of the penicillium mold juice, purifying it, figuring out which germs it was effective against, and how to use it. That task fell to Dr. Howard Florey, a professor of pathology who was director of the Sir William Dunn School of Pathology at Oxford University. He was a master at extracting research grants from tight-fisted bureaucrats and an absolute wizard at administering a large laboratory filled with talented but quirky scientists.

This landmark work began in 1938 when Florey, who had long been interested in the ways that bacteria and mold naturally kill each other, came across Fleming’s paper on the penicillium mold while leafing through some back issues of The British Journal of Experimental Pathology. Soon after, Florey and his colleagues assembled in his well-stocked laboratory. They decided to unravel the science beneath what Fleming called penicillium’s ”antibacterial action.”

One of Florey’s brightest employees was a biochemist, Dr. Ernst Chain, a Jewish German émigré. Chain was an abrupt, abrasive and acutely sensitive man who fought constantly with Florey over who deserved credit for developing penicillin. Despite their battles, they produced a series of crude penicillium-mold culture fluid extracts.

During the summer of 1940, their experiments centered on a group of 50 mice that they had infected with deadly streptococcus. Half the mice died miserable deaths from overwhelming sepsis. The others, which received penicillin injections, survived.

It was at that point that Florey realized that he had enough promising information to test the drug on people. But the problem remained: how to produce enough pure penicillin to treat people. In spite of efforts to increase the yield from the mold cultures, it took 2,000 liters of mold culture fluid to obtain enough pure penicillin to treat a single case of sepsis in a person.

In September 1940, an Oxford police constable, Albert Alexander, 48, provided the first test case. Alexander nicked his face working in his rose garden. The scratch, infected with streptococci and staphylococci, spread to his eyes and scalp. Although Alexander was admitted to the Radcliffe Infirmary and treated with doses of sulfa drugs, the infection worsened and resulted in smoldering abscesses in the eye, lungs and shoulder. Florey and Chain heard about the horrible case at high table one evening and, immediately, asked the Radcliffe physicians if they could try their ”purified” penicillin.

After five days of injections, Alexander began to recover. But Chain and Florey did not have enough pure penicillin to eradicate the infection, and Alexander ultimately died.

Another vital figure in the lab was a biochemist, Dr. Norman Heatley, who used every available container, bottle and bedpan to grow vats of the penicillin mold, suction off the fluid and develop ways to purify the antibiotic. The makeshift mold factory he put together was about as far removed as one could get from the enormous fermentation tanks and sophisticated chemical engineering that characterize modern antibiotic production today.
In the summer of 1941, shortly before the United States entered World War II, Florey and Heatley flew to the United States, where they worked with American scientists in Peoria, Ill., to develop a means of mass producing what became known as the wonder drug.

Aware that the fungus Penicillium notatum would never yield enough penicillin to treat people reliably, Florey and Heatley searched for a more productive species.

One hot summer day, a laboratory assistant, Mary Hunt, arrived with a cantaloupe that she had picked up at the market and that was covered with a ”pretty, golden mold.” Serendipitously, the mold turned out to be the fungus Penicillium chrysogeum, and it yielded 200 times the amount of penicillin as the species that Fleming had described. Yet even that species required enhancing with mutation-causing X-rays and filtration, ultimately producing 1,000 times as much penicillin as the first batches from Penicillium notatum.

In the war, penicillin proved its mettle. Throughout history, the major killer in wars had been infection rather than battle injuries. In World War I, the death rate from bacterial pneumonia was 18 percent; in World War II, it fell, to less than 1 percent.

From January to May in 1942, 400 million units of pure penicillin were manufactured. By the end of the war, American pharmaceutical companies were producing 650 billion units a month.

Ironically, Fleming did little work on penicillin after his initial observations in 1928. Beginning in 1941, after news reporters began to cover the early trials of the antibiotic on people, the unprepossessing and gentle Fleming was lionized as the discoverer of penicillin. And much to the quiet consternation of Florey, the Oxford group’s contributions were virtually ignored.

That problem was partially corrected in 1945, when Fleming, Florey, and Chain — but not Heatley — were awarded the Nobel Prize in Physiology or Medicine. In his acceptance speech, Fleming presciently warned that the overuse of penicillin might lead to bacterial resistance.

In 1990, Oxford made up for the Nobel committee’s oversight by awarding Heatley the first honorary doctorate of medicine in its 800-year history.
Maybe this September 28, as we celebrate Alexander Fleming’s great accomplishment, we will recall that penicillin also required the midwifery of Florey, Chain and Heatley, as well as an army of laboratory workers.

18/04/2023

The History of Antibiotics

Antibiotics: What’s in a Name?

The term antibiotics literally means “against life”; in this case, against microbes. There are many types of antibiotics—antibacterials, antivirals, antifungals, and antiparasitics. Some drugs are effective against many organisms; these are called broad-spectrum antibiotics. Others are effective against just a few organisms and are called narrowspectrum antibiotics. The most commonly used antibiotics are antibacterials. Your child may have received ampicillin for an ear infection or penicillin for a strep throat.

When a child is sick, parents worry. Even if he has only a mild cold that makes him cranky and restless or an achy ear that only hurts a little, these times can be very stressful. Of course, you want him to get the best possible treatment. For many parents, this means taking him to the pediatrician and leaving the office with a prescription for antibiotics.

But that isn’t necessarily what will happen during the doctor’s visit. After examining your youngster, your pediatrician may tell you that based on your child’s symptoms and perhaps some test results, antibiotics just are not necessary.

Many parents are surprised by this decision. After all, antibiotics are powerful medicines that have eased human pain and suffering for decades. They have even saved lives. But most doctors aren’t as quick to reach for their prescription pads as they once were. In recent years, they’re realizing there is a downside to choosing antibiotics—if these medicines are used when they’re not needed or they’re taken incorrectly, they can actually place your child at a greater health risk. That’s right—antibiotics have to be prescribed and used with care, or their potential benefits will decrease for everyone.

A Look Back
Serious diseases that once killed thousands of youngsters each year have been almost eliminated in many parts of the world because of the widespread use of childhood vaccinations.

In much the same way, the discovery of antimicrobial drugs (antibiotics) was one of the most significant medical achievements of the 20th century. There are several types of antimicrobials—antibacterials, antivirals, antifungals, and antiparasitic drugs. (Although antibacterials are often referred to by the general term antibiotics, we will use the more precise term.) Of course, antimicrobials aren’t magic bullets that can heal every disease. When used at the right time, they can cure many serious and life-threatening illnesses.
Antibacterials are specifically designed to treat bacterial infections. Billions of microscopic bacteria normally live on the skin, in the gut, and in our mouths and throats. Most are harmless to humans, but some are pathogenic (disease producing) and can cause infections in the ears, throat, skin, and other parts of the body. In the pre-antibiotic era of the early 1900s, people had no medicines against these common germs and as a result, human suffering was enormous. Even though the body’s disease-fighting immune system can often successfully fight off bacterial infections, sometimes the germs (microbes) are too strong and your child can get sick. For example,
Before antibiotics, 90% of children with bacterial meningitis died. Among those children who lived, most had severe and lasting disabilities, from deafness to mental retardation.

Strep throat was at times a fatal disease, and ear infections sometimes spread from the ear to the brain, causing severe problems.

Other serious infections, from tuberculosis to pneumonia to whooping cough, were caused by aggressive bacteria that reproduced with extraordinary speed and led to serious illness and sometimes death.
The Emergence of Penicillin

With the discovery of penicillin and the dawning of the antibiotic era, the body’s own defenses gained a powerful ally. In the 1920s, British scientist Alexander Fleming was working in his laboratory at St. Mary’s Hospital in London when almost by accident, he discovered a naturally growing substance that could attack certain bacteria. In one of his experiments in 1928, Fleming observed colonies of the common Staphylococcus aureus bacteria that had been worn down or killed by mold growing on the same plate or petri dish. He determined that the mold made a substance that could dissolve the bacteria. He called this substance penicillin, named after the Penicillium mold that made it. Fleming and others conducted a series of experiments over the next 2 decades using penicillin removed from mold cultures that showed its ability to destroy infectious bacteria.

Before long, other researchers in Europe and the United States started recreating Fleming’s experiments. They were able to make enough penicillin to begin testing it in animals and then humans. Starting in 1941, they found that even low levels of penicillin cured very serious infections and saved many lives. For his discoveries, Alexander Fleming won the Nobel Prize in Physiology and Medicine.

Drug companies were very interested in this discovery and started making penicillin for commercial purposes. It was used widely for treating soldiers during World War II, curing battlefield wound infections and pneumonia. By the mid- to late 1940s, it became widely accessible for the general public. Newspaper headlines hailed it as a miracle drug (even though no medicine has ever really fit that description).

With the success of penicillin, the race to produce other antibiotics began. Today, pediatricians and other doctors can choose from dozens of antibiotics now on the market, and they’re being prescribed in very high numbers. At least 150 million antibiotic prescriptions are written in the United States each year, many of them for children.

Problems With Antibiotics

The success of antibiotics has been impressive. At the same time, however, excitement about them has been tempered by a phenomenon called antibiotic resistance. This is a problem that surfaced not long after the introduction of penicillin and now threatens the usefulness of these important medicines.

Almost from the beginning, doctors noted that in some cases, penicillin was not useful against certain strains of Staphylococcus aureus (bacteria that causes skin infections). Since then, this problem of resistance has grown worse, involving other bacteria and antibiotics. This is a public health concern. Increasingly, some serious infections have become more difficult to treat, forcing doctors to prescribe a second or even third antibiotic when the first treatment does not work.

In light of this growing antibiotic resistance, many doctors have become much more careful in the way they prescribe these medicines. They see the importance of giving antibiotics only when they’re absolutely necessary. In fact, one recent survey of office-based physicians, published in JAMA: The Journal of the American Medical Association in 2002, showed that doctors lowered the number of antibiotic prescriptions they prescribed for children with common respiratory infections by about 40% during the 1990s.

Antibiotics should be used wisely and only as directed by your pediatrician. Following these guidelines, their life-saving properties will be preserved for your child and generations to come.

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18/04/2023

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