Types of Antibiotics

Penicillins and Cephalosporins

Most bacterial cells have double layers on their outside. The outermost layer - the "cell wall" - is similar to the outer layer of plant cells, but is missing in human and animal cells. This wall must grow along with the cell, or the growing cell will eventually become too big for the wall and burst and die. the Antibiotics class of Penicillins and Cephalosporins kill bacteria by destroying or interfering with their wall-building system. Since we don't have cell walls, and plants have a different wall-building system, neither we, nor animals, nor plants are affected by the medicine.

There are a types of bacteria that don't have cell walls. These germs are immune to penicillins and cephalosporins for the same reasons we are. Most bacteria do have cell walls, but many have changed their wall-building systems so that penicillins can't interfere, or have come up with ways to break down the medicines before the medicines can work. These are resistant bacteria or "super germs".

Penicillins and cephalosporins usually don't cause many problems for a patient. Like all antibiotics, they can cause mild side effects like diarrhea. Less common side effects include rashes and Hives; however an outbreak of Hives usually means you're allergic to the medicine.

Macrolides

Erythromycin is an antibacterial produced by a mold. There are a couple of new Erythromycin-related macrolides of - Azithromycin and Clarithromycin - that work the same way, but kill more bacteria and have slightly fewer side effects. The Erythromycin-like antibiotics are known as Macrolides.

Macrolides works by blocking the bacterial cell's machinery for making new proteins. Since proteins both make up much of the cell's structure and make the enzymes that direct all the cell's chemical reactions, blocking protein manufacturing makes the cell unable to function. Erythromycin in low doses will stop bacteria from growing and multiplying, but a higher concentration is required to kill the bacteria. However, if the drug can stop growth until the body's immune system kicks in, that will help you get rid of the infection.

Since all protein making is affected, Erythromycin can slow down or kill any bacteria, even those without cell walls. Because of this, we use the Erythromycins for several diseases, including bacterial bronchitis, chlamydia, and whooping cough, that penicillins and cephalosporins can't treat.

Macrolides don't have allergy problems we see with the penicillins and cephalosporins, although there are rare people who have reactions to it. The biggest problem with these medicines is that they can irritate the stomach; this irritation seems to happen most often when someone tries to take the medicine on an empty stomach. Always take Erythromycin with food or milk; the same holds for Clarithromycin. Azithromycin doesn't irritate the stomach nearly as much as the other Macrolides.

Sulfanilamides or Sulfonamides

The Sulfas ("sulfanilamides" or "sulfonamides") were the first synthetic antibiotics to be developed; they are completely man-made. Sulfas interfere with certain "manufacturing" systems in the bacterial cell, including ones that bacteria use to produce new DNA for new bacteria. Sulfanilamides can stop bacteria from growing, but they cannot actually kill the bacteria.

When they were first used, Sulfonamides worked against many kinds of bacteria. Unfortunately, as with Penicillin, the more we used the Sulfas the more bacteria became resistant to it. Sulfonamides also have a tendency to produce allergic reactions including some that are rare but life-threatening. Because of this we don't use sulfas nearly as much we used to in the past, and most often when we use sulfas it's in combination with another drug which attacks a different part of the bacteria - an attack on two fronts is usually better than an attack on one. The drugs we usually combine with sulfas are either Erythromycin or Trimethoprim; these combinations usually can kill bacteria rather than just slowing them down.

Trimethoprim

Trimethoprim (TMP) is another synthetic antibiotic. Like the Sulfas, TMP blocks an important step in the bacteria's system for making new DNA. By itself, Trimethoprim can kill bacteria, but very slowly. Usually, though, we use TMP in combination with Sulfamethoxazole (SMX), and the combination of TMP and a Sulfa kills bacteria better. In fact, bacteria that are partly resistant to either TMP or SMX can still be killed by the combination of the two. The side effects of the combination are the same as those of the two separate components.

Nitrofurantoin

Nitrofurantoin is another synthetic antibiotic, used mainly for urinary tract infections. Nitrofurantoin stops bacteria from growing, and can kill bacteria with a high enough level, by blocking the bacteria's ability to use energy it makes by digesting nutrients like sugar, and by blocking other chemical reactions that use the same system. It is not usually used for infections other than UTIs, and there are several side effects, ranging from stomach upset to (very rarely) malfunctioning nerves, which limit its use.

Aminoglycosides

The Aminoglycosides are drugs which stop bacteria from making proteins; they work by attaching permanently to the protein machinery. Since they attach permanently, the bacterial cell will die if it gets enough of the drug. Aminoglycosides can be used by themselves, or along with Penicillins or Cephalosporins to give a two-pronged attack on the bacteria.

Aminoglycosides work quite well, but bacteria are prone to becoming resistant to them. Since Aminoglycosides are broken down easily in the stomach, they can't be given by mouth and must be injected or given intravenously (although we can use them as eyedrops for conjuctivitis). When injected, their side effects include possible damage (temporary or permanent) to the ears and to the kidneys; this can be minimized by checking the amount of the drug in the blood and adjusting the dose so that there is enough drug to kill bacteria but not too much of it. Generally, Aminoglycosides are given for short time periods, and in the hospital where we can clinically check both the drug levels and the bacteria's sensitivity.

Quinolones

The Quinolones, of which the best known is Ciprofloxacin (Cipro®), interfere with an enzyme called DNA gyrase that is essential for duplication of bacterial DNA. Bacteria have only one long chromosome (DNA molecule) and this chromosome gets twisted during replication and the chromosome can become so twisted that nothing more can be done with it. DNA gyrase is the "untwisting" enzyme for the bacterial chromosome. This interference by Quinolones is completely different from the interference of other antibiotics with bacterial "machinery", and so bacteria that are resistant to other antibiotics will be vlunerable to the Quinolones.

However, bacteria have been known to develop resistance to the Quinolones too. Also, researchers have found that young animals given quinolones can have damage to their cartilage; resultantly we have avoided using quinilones in children because of this finding, but we sometimes have to give some children quinolones when there is no alternative antibiotic available.

Types of Antivirals

Antibacterial antibiotics will do nothing to help get rid of viruses, and giving antibacterial antibiotics when there is a viral infection will likely do nothing except help other bacteria in the body to become resistant; which makes the next bacterial infection much harder to treat. In case of viral infections, only Antiviral Agents can help mitigate the viral infection. However, antiviral drugs, even more than the antibacterials, are specialized and can only specifically attack the kind of viruses they are intended to attack.

Since viruses can't live outside the host (infected person or animal) they infect, they are much harder to kill off. Our immune system can find and kill many of the viruses that attack us, but sometimes a virus can multiply and overwhelm the immune system before the immune system kicks in to full force. We immunize or vaccinate people against diseases so that their immune systems do have that head start. That seems to be the most succesful way to kill viruses permanently. An example is smallpox, which has been eradicated due mainly to the use of vaccines against it. Some viruses, such as HIV, which specifically attacks the immune system, are very hard to become immune to, but a great deal of research is being aimed at producing a working vaccine for those diseases.

Unfortunately, since viruses are completely dormant outside a host the immune system can't go after the virus unless it's in the body, and all of the antiviral medicines we have work only when the virus is trying to reproduce in the body. We can destroy viruses in the environment if we know they are there, for example using household bleach to kill HIV that might be on equipment contaminated with body fluids. But once the virus is in the body, all we can do is let the immune system do its work or give drugs that slow down the infection so that the body can clear it out more easily.

Acyclovir

One commonly-used Antiviral medicine is Acyclovir (Ganciclovir and Valciclovir are similar to Acyclovir). These Antiviral drugs slow down infections with viruses of a certain family, which include both varicella (chickenpox and shingles) and the herpes viruses. Acyclovir slows down the virus multiplication and therefore slows down the infection. The problem is that the varicella and herpes viruses are never actually eradicated; they stay in the body forever and reactivate later, sometimes years later. The recurrent sores of herpes, and the appearance of shingles years after you have chickenpox, are examples of reactivation, and although Aciclovir can help you get over the reactivation infection, it can't actually get rid of the viruses permanently.

Reverse-Transcriptase Inhibitors

A well-known Antiviral agent is Triazidothymidine, better known as Zidovudine or AZT. This drug, and others like it, are used to inhibit an enzyme called "reverse transcriptase" which HIV uses to copy its own genes into the genes of the cells it infects. Once the HIV genes are copied, the infected cell and all its offspring can produce more HIV. This is why an AIDS patient cannot actually get rid of all of the virus once infected: the virus may lie dormant as inactive genes for months or years, and the anti-AIDS drugs cannot get to the gene copies. Like bacteria, viruses can mutate, changing their structure so that drugs that used to work no longer help; this explains why AZT and other reverse-transcriptase inhibitors eventually lose their effectiveness in many patients.

Protease Inhibitors

A newer class of Anti-AIDS drugs, the protease inhibitors, work by blocking a different HIV enzyme. HIV uses reverse transcriptase to copy its genes into the cell it's infecting but it uses protease - an enzyme that breaks down protein - to get into the cell in the first place. Many people with AIDS have been able to almost eliminate the virus from their bloodstream by using both reverse-transcriptase inhibitors and protease inhibitors at the same time.

However, since the virus has copied itself into cells where neither kind of drug can attack it, a patient must keep taking the drugs forever to keep the virus from reactivating.