Antibiotics.

(ready)
Dr. Sayeed Ahmad D. I. Hom. (London)

Antibiotic is a substance produced by certain bacteria or fungi that kills other

cells or interferes with their growth. In nature, these substances help some microbes
survive by limiting the multiplication of other microbes that share the same environment.
Antibiotics that attack pathogenic (disease-causing) microbes without severely harming
normal body cells are useful as drugs.

Antibiotics are especially useful for treating infections caused by bacteria.

Antibiotics came into widespread use during the 1940's. At that time, they were often
called "wonder drugs" because they cured many bacterial diseases that were once fatal.
The number of deaths caused by meningitis, pneumonia, tuberculosis, and scarlet fever
declined drastically after antibiotics became available. Today, physicians prescribe
antibiotics to treat many diseases caused by bacteria.

In addition, some antibiotics are effective against infections caused by fungi and
protozoa, and a few are useful in treating cancer. Antibiotics are also used to treat
infectious diseases in animals. Farmers sometimes add small amounts of antibiotics to
livestock feed. The antibiotics support the animals' growth for reasons that are not
entirely understood.

Antibiotics are not effective against colds, influenza, or other viral diseases. In
addition, the effectiveness of antibiotics is limited because both pathogenic microbes and
cancer cells can become resistant to them.

Kinds of antibiotics :

Antibiotics are selectively toxic-that is, they damage some types of cells without
harming others. Medically useful antibiotics attack infectious microbes or cancer cells
without excessively hurting human cells. Antibiotics fight different types of illnesses in a
variety of ways.

Antibacterial antibiotics. Antibiotics are selectively toxic against bacteria because

bacterial cells differ greatly from human cells. One of the chief differences is that
bacteria, unlike animal cells, have a cell wall. This wall is a rigid structure that forms the
cell's outer boundary.

The type of cell wall a bacterium has is one factor that determines which
antibiotics can kill it. Scientists use a process called Gram staining to classify cell walls
of bacteria. Hans C. J. Gram, a Danish bacteriologist of the late 1800's, developed the
process. This method classifies bacteria as gram-positive (G+) or gram-negative (G-).

Some antibiotics selectively kill either gram-positive bacteria or gram-negative

bacteria. These substances are called narrow spectrum antibiotics. The antibiotic
Vancomycin selectively kills such gram-positive bacteria as Staphylococcus,
Streptococcus, and Enterococcus). Aztreonam is a narrow spectrum antibiotic that kills
only gram-negative bacteria, such as Escherichia coli and Pseudomonas aeruginosa.
Other antibiotics can kill both gram-positive and gram-negative bacteria. These drugs are
called broad spectrum antibiotics. Ceftriaxone is one example of a broad spectrum
antibiotic. No broad spectrum antibiotic can kill all bacteria, and no narrow spectrum
antibiotic can kill all gram-positive or all gram-negative bacteria.

Other kinds of antibiotics. Some antibiotics are effective against infections caused
by fungi and protozoans, whose cells differ from human cells. Antibiotics that fight fungi
include miconazole and amphotericin. Paromomycin is used to treat amebiasis, an
intestinal disease caused by a protozoan.

Anticancer antibiotics attack cells while they are dividing. These drugs are
somewhat selectively toxic because cancer cells generally divide much more frequently
than do normal cells. But some normal cells-such as blood-forming cells-divide rapidly.
Anticancer antibiotics also affect these cells. The antibiotic doxorubicin is used to treat
certain types of leukemia, breast cancer, and other tumors.

Some widely used antibiotics :

Antibiotic --> Some infections and diseases treated :

Ampicillin: G+ and G- infections, including respiratory infections and urinary tract

infections.
Azithromycin: Many kinds of pneumonia, and certain other G+ infections.
Ceftriaxone: G+ and G- infections, including gonorrhea.
Chloramphenicol: Rocky Mountain spotted fever and G+ and G- infections, including
meningitis.
Ciprofloxacin Urinary tract infections and acute diarrheal diseases caused by certain G-
infections.
Dicloxacillin Penicillin-G resistant, methicillin-sensitive staphylococcal infections.
Doxycycline Pneumonia, G+ and G- infections, bite wounds, acne.
Fluconazole Fungus infections of the skin, mucous membranes, blood, and brain.
Gentamicin Serious infections, especially G- infections.
Neomycin G+ and G- infections, especially skin infections and those resulting from
burns.
Penicillin G Syphilis, strep throat, and other G+ infections.
Rifampin Tuberculosis.
Streptomycin Tuberculosis and bubonic plague.
Vancomycin Serious staphylococcal, enterococcal, and streptococcal infections that
resist other drugs.

How antibiotics work :

Antibiotics fight microbes and cancer cells by interfering with normal cell
functions. In most cases, this interference occurs in one of three ways: (1) prevention of
cell wall formation, (2) disruption of the cell membrane (covering), and (3) disruption of
chemical processes.
Prevention of cell wall formation.

Penicillins and some other antibiotics destroy microbes by interfering with their
cell wall formation. Animal cells do not form walls. As a result, these antibiotics do not
damage them.

Disruption of the cell membrane. All cells have a membrane that controls the
movement of substances in and out of the cell. Some antibiotics, including amphotericin
B and nystatin, disrupt the cell membrane of certain microbes. A damaged membrane
might allow vital nutrients to escape or poisonous substances to enter and kill the cell.
These antibiotics do not harm human cells because the drugs affect membrane
components found only in microbial cells.

Disruption of chemical processes. All cells produce proteins and nucleic acids,
which are vital to life. Human cells produce these substances in much the same way as
microbial cells do. But in some cases, these processes differ enough so that antibiotics
interfere with the chemical activities in microbial cells, but not in human cells. For
example, streptomycin and tetracycline prevent certain kinds of microbes from producing
proteins, and rifampin interferes with the formation of nucleic acids.

Dangers of antibiotics:
Many antibiotics are regarded among the safest drugs when properly used. But
antibiotics can sometimes cause unpleasant or dangerous side effects. The three main
dangers are (1) allergic reactions, (2) destruction of helpful microbes, and (3) damage to
organs and tissues.

Allergic reactions, in most cases, are mild and produce only a rash or fever. But
severe reactions can occur, and can even cause death. All antibiotics are able to produce
allergic reactions, but such reactions occur most often with penicillins. A physician
usually asks if a patient has ever had an allergic reaction to an antibiotic before
prescribing that drug. Most people who are allergic to one antibiotic can take other
antibiotics that have significantly different chemical compositions.

Destruction of helpful microbes. Certain areas of the body commonly harbor both
harmless and pathogenic microbes. These two types of microbes compete for food, and
so the harmless microorganisms help restrain the growth of those that cause disease.
Many antibiotics-especially broad spectrum drugs-do not always distinguish between
harmless and dangerous microbes. If a drug destroys too many harmless microorganisms,
the pathogenic ones will have a greater chance to multiply. This situation can lead to a
new infection called a superinfection. Physicians usually prescribe a second drug to
combat a superinfection.

Damage to organs and tissues is rare in people using antibiotics that act only
against the cells of pathogenic microbes. Extensive use of some antibiotics, however,
may damage tissues and organs. For example, streptomycin has caused kidney damage
and deafness. Physicians prescribe drugs with such known risks only if no other drug is
effective.
 Anticancer antibiotics act against all cells that divide rapidly, and so can affect
normal cells as well as cancer cells. For example, cells in the bone marrow divide
constantly to produce fresh blood cells. Anticancer antibiotics can damage the bone
marrow. Such damage increases the risk of infection by reducing the number of white
blood cells, which help the body fight disease.

Resistance to antibiotics. Some pathogenic microbes develop an ability to resist

the effects of certain antibiotics. The most widespread and worrisome resistance in
pathogenic microbes occurs in bacteria.

Bacteria can become resistant to antibiotics through a type of evolution. In

bacteria-as in other living things-genes carry instructions controlling life processes.
Occasionally, a gene in a bacterium naturally changes in a way that enables the microbe
to resist the effects of an antibiotic. Such a change is called a mutation. The change may
provide resistance to one specific antibiotic or to a group of chemically similar
antibiotics-for example, the penicillins. Bacteria can also acquire resistance from other
bacteria by transferring genetic material. In some cases, these exchanges enable bacteria
to acquire resistance to more than one type or more than one group of antibiotics.

Bacteria also can become resistant to antibiotics by producing an enzyme that

breaks down the drug. This occurs with Staphylococcus, which may resist penicillins and
cephalosporins. Bacteria can also change their cell membranes so that antibiotics can not
penetrate them. An example of this kind of bacteria is Pseudomonas. Pseudomonas may
develop resistance to the quinolone antibiotics this way. Enterococcus, a gram-positive
bacteria, can become resistant to vancomycin by changing the proteins to which
vancomycin usually binds. Streptococcus can resist penicillins and cephalosporins in this
way.

Testing and producing antibiotics:

Testing.

Every year, scientists test thousands of natural and chemically modified microbial
substances for potential use as antibiotics. First, they test these substances against
harmful microbes or cancer cells that have been grown either in test tubes or on
laboratory plates.

A substance that shows strong antibiotic activity against pathogenic microbes or

cancer cells undergoes extensive tests in laboratory animals. If it produces no harmful
effects in the animals, scientists test the antibiotic in human beings. In the United States,
the Food and Drug Administration (FDA) must approve human testing. If the drug proves
to be safe and effective, it is referred to the FDA for approval. Finally, if the FDA
approves the antibiotic, the developer begins to produce it for sale.

Production of antibiotics involves several steps. First, cultures of antibiotic-

producing microbes are grown in flasks and then transferred to huge fermentation vats.
The microbes multiply rapidly in the vats because the environment is controlled to
stimulate their growth. After fermentation, the antibiotic substance is extracted from the
culture and purified.

Some natural antibiotic substances are modified chemically to produce

semisynthetic antibiotics. Many such drugs are more effective than the natural antibiotics
from which they were developed.

Drug companies conduct special tests on antibiotics during and after production to
ensure their quality. Finally, manufacturers make the purified antibiotic substances into
pills, liquids, and ointments for medical use.

History:

For more than 2,500 years, people have treated certain skin infections with molds
that form antibiotics. However, modern scientific study of these substances did not begin
until the late 1800's. At that time, the French chemist Louis Pasteur discovered that
bacteria spread infectious diseases. Then Robert Koch, a German bacteriologist,
developed methods of isolating and growing various kinds of bacteria. Koch also
identified specific bacteria that cause certain diseases.

Scientists then began working to develop drugs that could destroy pathogenic
microbes, but the substances they produced proved either ineffective or dangerous. A
historic breakthrough came in 1928, when British bacteriologist Alexander Fleming
observed that a mold of the genus Penicillium produced a substance that destroyed
bacteria. He called the substance penicillin.

In the early 1940's, American bacteriologist Selman A. Waksman tested about

10,000 types of soil bacteria for antibiotic activity. In 1943, he discovered that some
Streptomyces a type of fungi, produced a substance that had potent antibiotic properties.
A new antibiotic called streptomycin resulted from Waksman's research. Thousands of
antibiotic substances have been found in nature or have been produced chemically.
Relatively few antibiotic substances, however, have proved safe and effective.

Since the 1990's, resistance to antibiotics has been a growing threat to public
health. Widespread use of antibiotics to treat human infections increases the number of
resistant bacteria. Antibiotic use in livestock promotes the development of resistant
bacteria that can spread to humans. For example, studies in the Netherlands, Spain, the
United States, and the United Kingdom in the late 1990's revealed that many chickens
were infected with antibiotic resistant strains of a bacterium called Campylobacter. When
people cooked the meat of these chickens, some of the Campylobacter microbes survived,
and the people became infected.

Certain kinds of Enterococcus bacteria are especially troublesome because of their

resistance. In Europe, drug-resistant strains (types) of Enterococcus that originated in
livestock have spread to people. In the United States, Enterococcus resistant to multiple
antibiotics has caused human infections that are difficult or impossible to treat. Infections
caused by antibiotic-resistant varieties of Enterococcus occur mostly in patients who are
already seriously ill.
 In the 1990's, scientists combined the antibiotics quinupristin and dalfopristin to
create a drug that works against resistant strains of Enterococcus. In 2000, the FDA
approved linezolid, the first entirely new type of antibiotic developed in more than 30
years. The antibiotic, sold under the brand name Zyvox, is effective against gram-positive
bacteria, including Enterococcus, that have become resistant to all other antibiotics. But
experts believe antibiotic-resistant Enterococcus remains a major threat to public health.

ANTIBIOTICS AND HOMŒOPATHIC ANTIDOTES

Adverse Effects of Penicillin

Fever with cold feet. ----- Bell., Cupr-ac.

Wheezing and Pseudoasthmatic attack. ----- Aspidosperma (Quebracho)
When skin eruptions are simultaneously present ----- Grind.
Anorexia (with Mycin group of drugs like Aureomycin) ----- Abrot.
Peripheral Neuritis. ----- Ant-t.
Brachiaglia Nocturna (with the pronounced symptoms of pins and needles). ----- Sec.,
Act-s.
Pruritus. ----- Apis and Grind. 10 drops mixed in a cup of milk and applied locally.
Skin lesions from Penicillin. ----- Agar., Sulph.
Chronic cough after Penicillin. ----- Penicillin 3x or 30, Seneg. 30 or 200.
In cases when Srepto Peniciliin had been used. Streptococcin 30 or Staphelococcin 30
(as an intercurrent remedy).
Heart depressing effects of Penicillin. ----- Ars-a.
Harmful effects of Penicillin. ----- Ars-a., Thuj., Nux-v., Sil.
Specific to counteract the effects of Penicillin. ----- Ars-a.
Diarrhœa from Antibiotics (especially Mycins). ----- Nit-ac.
Allergic reactions to Antibiotics. ----- Sulph., Penicillin, Streptomycin.
Headache due to Streptomycin. ----- Bell.
Ill effects of Chloromycetin: cases of typhoid (where Chloromycetin was given). -----
Chloromycetin 30, 200 or 1M (according to patient’s Constitution). With Placebo for a
week. In second week ----- Typhoidinum 200 or 1M (with Placebo for a fortnight).
Intestinal effects of Aureomycin. ----- Aureomycin leaves a very weak liver and severe
trouble with the bowels. In this case, a pure constitutional treatment with careful
observation of idiosyncrasies is most effective.
Ill effects of Allergy (in general). Ill effects of Penicillin. ----- Carb-v. (Dilutions used:
2x, 3x, 6x, 12x).

References:
World Book 2003.
Homœopathy and Adverse Reactions of Allopathic Drugs, by Dr. Sayeed Ahmad.
Antibiotics & Homeopathic Antidotes.
Dr. Sayeed Ahmad D. I. Hom. (London)

I. - INTRODUCTION

Antibiotics (Greek anti,"against;"bios,"life") are chemical compounds used to kill

or inhibit the growth of infectious organisms. Originally the term antibiotic referred only
to organic compounds, produced by bacteria or molds, that are toxic to other
microorganisms. The term is now used loosely to include synthetic and semisynthetic
organic compounds. Antibiotic refers generally to antibacterials; however, because the
term is loosely defined, it is preferable to specify compounds as being antimalarials,
antivirals, or antiprotozoals. All antibiotics share the property of selective toxicity: They
are more toxic to an invading organism than they are to an animal or human host.
Penicillin is the most well-known antibiotic and has been used to fight many infectious
diseases, including syphilis, gonorrhea, tetanus, and scarlet fever. Another antibiotic,
streptomycin, has been used to combat tuberculosis.

II. – HISTORY

Although the mechanisms of antibiotic action were not scientifically understood

until the late 20th century, the principle of using organic compounds to fight infection has
been known since ancient times. Crude plant extracts were used medicinally for
centuries, and there is anecdotal evidence for the use of cheese molds for topical
treatment of infection. The first observation of what would now be called an antibiotic
effect was made in the 19th century by French chemist Louis Pasteur, who discovered
that certain saprophytic bacteria can kill anthrax bacilli. In the first decade of the 20th
century, German physician and chemist Paul Ehrlich began experimenting with the
synthesis of organic compounds that would selectively attack an infecting organism
without harming the host organism. His experiments led to the development, in 1909, of
salvarsan, a synthetic compound containing arsenic, which exhibited selective action
against spirochetes, the bacteria that cause syphilis. Salvarsan remained the only effective
treatment for syphilis until the purification of penicillin in the 1940s. In the 1920s British
bacteriologist Sir Alexander Fleming, who later discovered penicillin, found a substance
called lysozyme in many bodily secretions, such as tears and sweat, and in certain other
plant and animal substances. Lysozyme has some antimicrobial activity, but it is not
clinically useful.

Penicillin, the archetype of antibiotics, is a derivative of the mold Penicillium

notatum. Penicillin was discovered accidentally in 1928 by Fleming, who showed its
effectiveness in laboratory cultures against many disease-producing bacteria. This
discovery marked the beginning of the development of antibacterial compounds produced
by living organisms. Penicillin in its original form could not be given by mouth because it
was destroyed in the digestive tract and the preparations had too many impurities for
injection. No progress was made until the outbreak of World War II stimulated renewed
research and the Australian pathologist Sir Howard Florey and German-British
biochemist Ernst Chain purified enough of the drug to show that it would protect mice
from infection. Florey and Chain then used the purified penicillin on a human patient
who had staphylococcal and streptococcal septicemia with multiple abscesses and
osteomyelitis. The patient, gravely ill and near death, was given intravenous injections of
a partly purified preparation of penicillin every three hours. Because so little was
available, the patient's urine was collected each day, the penicillin was extracted from the
urine and used again. After five days the patient's condition improved vastly. However,
with each passage through the body, some penicillin was lost. Eventually the supply ran
out and the patient died.

The first antibiotic to be used successfully in the treatment of human disease was
tyrothricin, isolated from certain soil bacteria by American bacteriologist Rene Dubos in
1939. This substance is too toxic for general use, but it is employed in the external
treatment of certain infections. Other antibiotics produced by a group of soil bacteria
called actinomycetes have proved more successful. One of these, streptomycin,
discovered in 1944 by American biologist Selman Waksman and his associates, was, in
its time, the major treatment for tuberculosis.

Since antibiotics came into general use in the 1950s, they have transformed the
patterns of disease and death. Many diseases that once headed the mortality tables—such
as tuberculosis, pneumonia, and septicemia—now hold lower positions. Surgical
procedures, too, have been improved enormously, because lengthy and complex
operations can now be carried out without a prohibitively high risk of infection.
Chemotherapy has also been used in the treatment or prevention of protozoal and fungal
diseases, especially malaria, a major killer in economically developing nations. Slow
progress is being made in the chemotherapeutic treatment of viral diseases. New drugs
have been developed and used to treat shingles and chicken pox. There is also a
continuing effort to find a cure for acquired immunodeficiency syndrome (AIDS), caused
by the human immunodeficiency virus (HIV).

III. - CLASSIFICATION

Antibiotics can be classified in several ways. The most common method classifies
them according to their action against the infecting organism. Some antibiotics attack the
cell wall; some disrupt the cell membrane; and the majority inhibit the synthesis of
nucleic acids and proteins, the polymers that make up the bacterial cell. Another method
classifies antibiotics according to which bacterial strains they affect: staphylococcus,
streptococcus, or Escherichia coli, for example. Antibiotics are also classified on the
basis of chemical structure, as penicillins, cephalosporins, aminoglycosides, tetracyclines,
macrolides, or sulfonamides, among others.

A. Mechanisms of Action

Most antibiotics act by selectively interfering with the synthesis of one of the
large-molecule constituents of the cell—the cell wall or proteins or nucleic acids. Some,
however, act by disrupting the cell membrane (see Cell Death and Growth Suppression
below). Some important and clinically useful drugs interfere with the synthesis of
peptidoglycan, the most important component of the cell wall. These drugs include the Â-
lactam antibiotics, which are classified according to chemical structure into penicillins,
cephalosporins, and carbapenems. All these antibiotics contain a Â-lactam ring as a
critical part of their chemical structure, and they inhibit synthesis of peptidoglycan, an
essential part of the cell wall. They do not interfere with the synthesis of other
intracellular components. The continuing buildup of materials inside the cell exerts ever
greater pressure on the membrane, which is no longer properly supported by
peptidoglycan. The membrane gives way, the cell contents leak out, and the bacterium
dies. These antibiotics do not affect human cells because human cells do not have cell
walls.

Many antibiotics operate by inhibiting the synthesis of various intracellular

bacterial molecules, including DNA, RNA, ribosomes, and proteins. The synthetic
sulfonamides are among the antibiotics that indirectly interfere with nucleic acid
synthesis. Nucleic-acid synthesis can also be stopped by antibiotics that inhibit the
enzymes that assemble these polymers—for example, DNA polymerase or RNA
polymerase. Examples of such antibiotics are actinomycin, rifamicin, and rifampicin, the
last two being particularly valuable in the treatment of tuberculosis. The quinolone
antibiotics inhibit synthesis of an enzyme responsible for the coiling and uncoiling of the
chromosome, a process necessary for DNA replication and for transcription to messenger
RNA. Some antibacterials affect the assembly of messenger RNA, thus causing its
genetic message to be garbled. When these faulty messages are translated, the protein
products are nonfunctional. There are also other mechanisms: The tetracyclines compete
with incoming transfer-RNA molecules; the aminoglycosides cause the genetic message
to be misread and a defective protein to be produced; chloramphenicol prevents the
linking of amino acids to the growing protein; and puromycin causes the protein chain to
terminate prematurely, releasing an incomplete protein.

B. Range of Effectiveness

In some species of bacteria the cell wall consists primarily of a thick layer of
peptidoglycan. Other species have a much thinner layer of peptidoglycan and an outer as
well as an inner membrane. When bacteria are subjected to Gram's stain, these
differences in structure affect the differential staining of the bacteria with a dye called
gentian violet. The differences in staining coloration (gram-positive bacteria appear
purple and gram-negative bacteria appear colorless or reddish, depending on the process
used) are the basis of the classification of bacteria into gram-positive (those with thick
peptidoglycan) and gram-negative (those with thin peptidoglycan and an outer
membrane), because the staining properties correlate with many other bacterial
properties. Antibacterials can be further subdivided into narrow-spectrum and broad-
spectrum agents. The narrow-spectrum penicillins act against many gram-positive
bacteria. Aminoglycosides, also narrow-spectrum, act against many gram-negative as
well as some gram-positive bacteria. The tetracyclines and chloramphenicols are both
broad-spectrum drugs because they are effective against both gram-positive and gram-
negative bacteria.

C. Cell Death and Growth Suppression

 Antibiotics may also be classed as bactericidal (killing bacteria) or bacteriostatic
(stopping bacterial growth and multiplication). Bacteriostatic drugs are nonetheless
effective because bacteria that are prevented from growing will die off after a time or be
killed by the defense mechanisms of the host. The tetracyclines and the sulfonamides are
among the bacteriostatic antiobiotics. Antibiotics that damage the cell membrane cause
the cell's metabolites to leak out, thus killing the organism. Such compounds, including
penicillins and cephalosporins, are therefore classed as bactericidal.

IV - TYPES OF ANTIBIOTICS

Following is a list of some of the more common antibiotics and examples of some
of their clinical uses. This section does not include all antibiotics nor all of their clinical
applications.

Penicillins

Penicillins are bactericidal, inhibiting formation of the cell wall. There are four
types of penicillins: the narrow-spectrum penicillin-G types, ampicillin and its relatives,
the penicillinase-resistants, and the extended spectrum penicillins that are active against
pseudomonas. Penicillin-G types are effective against gram-positive strains of
streptococci, staphylococci, and some gram-negative bacteria such as meningococcus.
Penicillin-G is used to treat such diseases as syphilis, gonorrhea, meningitis, anthrax, and
yaws. The related penicillin V has a similar range of action but is less effective.
Ampicillin and amoxicillin have a range of effectiveness similar to that of penicillin-G,
with a slightly broader spectrum, including some gram-negative bacteria. The
penicillinase-resistants are penicillins that combat bacteria that have developed resistance
to penicillin-G. The antipseudomonal penicillins are used against infections caused by
gram-negative Pseudomonas bacteria, a particular problem in hospitals. They may be
administered as a prophylactic in patients with compromised immune systems, who are at
risk from gram-negative infections.

Side effects of the penicillins, while relatively rare, can include immediate and
delayed allergic reactions—specifically, skin rashes, fever, and anaphylactic shock,
which can be fatal.

B. Cephalosporin

Like the penicillins, cephalosporins have a Â-lactam ring structure that interferes
with synthesis of the bacterial cell wall and so are bactericidal. Cephalosporins are more
effective than penicillin against gram-negative bacilli and equally effective against gram-
positive cocci. Cephalosporins may be used to treat strains of meningitis and as a
prophylactic for orthopedic, abdominal, and pelvic surgery. Rare hypersensitive reactions
from the cephalosporins include skin rash and, less frequently, anaphylactic shock.
C. Aminoglycosides

Streptomycin is the oldest of the aminoglycosides. The aminoglycosides inhibit

bacterial protein synthesis in many gram-negative and some gram-positive organisms.
They are sometimes used in combination with penicillin. The members of this group tend
to be more toxic than other antibiotics. Rare adverse effects associated with prolonged
use of aminoglycosides include damage to the vestibular region of the ear, hearing loss,
and kidney damage.

D. Tetracyclines

Tetracyclines are bacteriostatic, inhibiting bacterial protein synthesis. They are

broad-spectrum antibiotics effective against strains of streptococci, gram-negative bacilli,
rickettsia (the bacteria that causes typhoid fever), and spirochetes (the bacteria that causes
syphilis). They are also used to treat urinary-tract infections and bronchitis. Because of
their wide range of effectiveness, tetracyclines can sometimes upset the balance of
resident bacteria that are normally held in check by the body's immune system, leading to
secondary infections in the gastrointestinal tract and vagina, for example. Tetracycline
use is now limited because of the increase of resistant bacterial strains.

E. Macrolides

The macrolides are bacteriostatic, binding with bacterial ribosomes to inhibit

protein synthesis. Erythromycin, one of the macrolides, is effective against gram-positive
cocci and is often used as a substitute for penicillin against streptococcal and
pneumococcal infections. Other uses for macrolides include diphtheria and bacteremia.
Side effects may include nausea, vomiting, and diarrhea; infrequently, there may be
temporary auditory impairment.

F. Sulfonamides

The sulfonamides are synthetic bacteriostatic, broad-spectrum antibiotics,

effective against most gram-positive and many gram-negative bacteria. However,
because many gram-negative bacteria have developed resistance to the sulfonamides,
these antibiotics are now used only in very specific situations, including treatment of
urinary-tract infection, against meningococcal strains, and as a prophylactic for rheumatic
fever. Side effects may include disruption of the gastrointestinal tract and
hypersensitivity.

V. - PRODUCTION

The production of a new antibiotic is lengthy and costly. First, the organism that
makes the antibiotic must be identified and the antibiotic tested against a wide variety of
bacterial species. Then the organism must be grown on a scale large enough to allow the
purification and chemical analysis of the antibiotic and to demonstrate that it is unique.
This is a complex procedure because there are several thousand compounds with
antibiotic activity that have already been discovered, and these compounds are repeatedly
rediscovered. After the antibiotic has been shown to be useful in the treatment of
infections in animals, larger-scale preparation can be undertaken.

Commercial development requires a high yield and an economic method of

purification. Extensive research may be needed to increase the yield by selecting
improved strains of the organism or by changing the growth medium. The organism is
then grown in large steel vats, in submerged cultures with forced aeration. The naturally
fermented product may be modified chemically to produce a semisynthetic antibiotic.
After purification, the effect of the antibiotic on the normal function of host tissues and
organs (its pharmacology), as well as its possible toxic actions (toxicology), must be
tested on a large number of animals of several species. In addition, the effective forms of
administration must be determined. Antibiotics may be topical, applied to the surface of
the skin, eye, or ear in the form of ointments or creams. They may be oral, or given by
mouth, and either allowed to dissolve in the mouth or swallowed, in which case they are
absorbed into the bloodstream through the intestines. Antibiotics may also be parenteral,
or injected intramuscularly, intravenously, or subcutaneously; antibiotics are
administered parenterally when fast absorption is required.

In the United States, once these steps have been completed, the manufacturer may
file an Investigational New Drug Application with the Food and Drug Administration
(FDA). If approved, the antibiotic can be tested on volunteers for toxicity, tolerance,
absorption, and excretion. If subsequent tests on small numbers of patients are successful,
the drug can be used on a larger group, usually in the hundreds. Finally a New Drug
Application can be filed with the FDA, and, if this application is approved, the drug can
be used generally in clinical medicine. These procedures, from the time the antibiotic is
discovered in the laboratory until it undergoes clinical trial, usually extend over several
years.

VI. - RISKS AND LIMITATIONS

The use of antibiotics is limited because bacteria have evolved defenses against
certain antibiotics. One of the main mechanisms of defense is inactivation of the
antibiotic. This is the usual defense against penicillins and chloramphenicol, among
others. Another form of defense involves a mutation that changes the bacterial enzyme
affected by the drug in such a way that the antibiotic can no longer inhibit it. This is the
main mechanism of resistance to the compounds that inhibit protein synthesis, such as the
tetracyclines.

All these forms of resistance are transmitted genetically by the bacterium to its
progeny. Genes that carry resistance can also be transmitted from one bacterium to
another by means of plasmids, chromosomal fragments that contain only a few genes,
including the resistance gene. Some bacteria conjugate with others of the same species,
forming temporary links during which the plasmids are passed from one to another. If
two plasmids carrying resistance genes to different antibiotics are transferred to the same
bacterium, their resistance genes can be assembled onto a single plasmid. The combined
resistances can then be transmitted to another bacterium, where they may be combined
with yet another type of resistance. In this way, plasmids are generated that carry
resistance to several different classes of antibiotic. In addition, plasmids have evolved
that can be transmitted from one species of bacteria to another, and these can transfer
multiple antibiotic resistance between very dissimilar species of bacteria.

The problem of resistance has been exacerbated by the use of antibiotics as

prophylactics, intended to prevent infection before it occurs. Indiscriminate and
inappropriate use of antibiotics for the treatment of the common cold and other common
viral infections, against which they have no effect, removes antibiotic-sensitive bacteria
and allows the development of antibiotic-resistant bacteria. Similarly, the use of
antibiotics in poultry and livestock feed has promoted the spread of drug resistance and
has led to the widespread contamination of meat and poultry by drug-resistant bacteria
such as Salmonella.

In the 1970s, tuberculosis seemed to have been nearly eradicated in the developed
countries, although it was still prevalent in developing countries. Now its incidence is
increasing, partly due to resistance of the tubercle bacillus to antibiotics. Some bacteria,
particularly strains of staphylococci, are resistant to so many classes of antibiotics that the
infections they cause are almost untreatable. When such a strain invades a surgical ward
in a hospital, it is sometimes necessary to close the ward altogether for a time. Similarly,
plasmodia, the causative organisms of malaria, have developed resistance to antibiotics,
while, at the same time, the mosquitoes that carry plasmodia have become resistant to the
insecticides that were once used to control them. Consequently, although malaria had
been almost entirely eliminated, it is now again rampant in Africa, the Middle East,
Southeast Asia, and parts of Latin America. Furthermore, the discovery of new
antibiotics is now much less common than in the past.
ANTIBIOTICS AND HOMOEOPATHIC ANTIDOTES

Adverse Effects of Penicillin

Fever with cold feet. Bell., Cupr-ac.

Wheezing and Pseudoasthmatic attack. Aspidosperma (Quebracho)

When skin eruptions are simultaneouslypresent. Grind.

Anorexia (with Mycin group of drugs likeAureomycin). Abrot.

Peripheral Neuritis. Ant-t.

Brachiaglia Nocturna (with the pronounced symptoms of pins and

needles). Sec., Act-s.

Pruritus. Apis and Grind. 10 drops mixed in a cup of milk andapplied

locally.

Skin lesions from Penicillin. Agar., Sulph.

Chronic cough after Penicillin. Penicillin 3x or 30, Seneg. 30 or 200.

In cases when Srepto Peniciliin had been used. Streptococcin 30 or

Staphelococcin 30 (as an intercurrent remedy.

Heart depressing effects of Penicillin. Ars-a.

Harmful effects of Penicillin. Ars-a., Thuj., Nux-v., Sil.

Specific to counteract the effects of Penicillin. Ars-a.

Diarrhœa from Antibiotics (especially Mycins). Nit-ac.

Allergic reactions to Antibiotics. Sulph., Penicillin, Streptomycin.

Headache due to Streptomycin. Bell.

#. Effects of Chloromycetin: cases of typhoid (where Chloromycetin

was given). ----- Chloromycetin 30, 200 or 1M (according to patient’s
Constitution). With Placebo for a week. In second week Typhoidinum
200 or 1M (with Placebo for a fortnight).

Intestinal effects of Aureomycin. Aureomycin leaves a very weak liver

and severe troublewith the bowels. In this case, a pure constitutional
treatment with careful observation of idiosyncrasies is most effective.
#. Effects of Allergy (in general). Ill effects of Penicillin. ----- Carb-v.
(Dilutions used: 2x, 3x, 6x, 12x).

References:

1. Contributed by Dr. M. Maureen Dale and Dr. Joel Mandelstam (MS

Encarta Encylopædia 2002).

2. Homœopathy and Adverse Reactions of Allopathic Drugs by Dr.

Sayeed Ahmad.