118
P A R T 2
Chemotherapeutic agents
KEY POINTS
■■
Tetracyclines inhibit protein synthesis and prevent
bacteria from multiplying.
■■
Tetracyclines can cause damage to developing teeth
and bones and should not be used with pregnant
women or children.
■■
Monitor the person for GI effects, bone marrow
depression, rash and superinfections. Caution women
that tetracyclines may make oral contraceptives
ineffective.
ANTIMYCOBACTERIALS
Mycobacteria—the group of bacteria that contain the
pathogens that cause tuberculosis and leprosy—are clas-
sified on the basis of their ability to hold a stain even in
the presence of a “destaining” agent such as acid. Because
of this property, they are called “acid-fast” bacteria. The
mycobacteria have an outer coat of mycolic acid that
protects them from many disinfectants and allows them
to survive for long periods in the environment. It may
be necessary to treat these slow-growing bacteria for
several years before they can be eradicated.
Mycobacteria cause serious infectious diseases. The
bacterium
Mycobacterium tuberculosis
causes tubercu-
losis, the leading cause of death from infectious disease
in the world. For several years the disease was thought
to be under control, but with the increasing number
of people with compromised immune systems and the
emergence of resistant bacterial strains, tuberculosis is
once again on the rise.
Mycobacterium leprae
causes leprosy, also known
as Hansen disease, which is characterised by disfigur-
ing skin lesions and destructive effects on the respiratory
tract. Leprosy is also a worldwide health problem; it is
infectious when the mycobacteria invade the skin or res-
piratory tract of susceptible individuals.
Mycobacterium
KEY POINTS
avium-intracellulare
,
which causes mycobacterium
avium complex (MAC), is seen in people with AIDS
or in other people who are severely immunocompro-
mised. Rifabutin (
Mycobutin
), which was developed
as an antituberculosis drug, is most effective against
M. avium-intracellulare.
A
ntituberculosis drugs
Tuberculosis can lead to serious damage in the lungs, the
GU tract, bones and the meninges. Because
M. tubercu-
losis
is so slow growing, the treatment must be continued
for 6 months to 2 years. Using the drugs in combination
helps to decrease the emergence of resistant strains and
to affect the bacteria at various phases during their long
and slow life cycle (Table 9.8).
First-line drugs for treating tuberculosis are used
in combinations of two or more agents until bacterial
conversion occurs or maximum improvement is seen.
The first-line drugs for treating tuberculosis are isoni-
azid (generic),
rifampicin (
Rifadin
), and ethambutol
(
Myambutol
).
If the person cannot take one or more of the first-line
drugs, or if the disease continues to progress because of
the emergence of a resistant strain, second-line drugs
can be used. The second-line drugs include rifabutin
(
Mycobutin
).
In addition, drugs from other antibiotic classes
have been found to be effective in second-line treat-
ment, such as ciprofloxacin (
Ciloxan
,
Ciprol
) which is a
fluoroquinolone.
L
eprostatic drugs
The main antibiotic used to treat leprosy is dapsone
(generic), which has been the mainstay of leprosy treat-
ment for many years, although resistant strains are
emerging (Table 9.8) so other drugs such as clofazimine
(
Lamprene
) are also used. Similar to the sulfonamides,
dapsone inhibits folate synthesis in susceptible bacteria.
In addition to its use in leprosy, dapsone is used to treat
Pneumocystis carinii
pneumonia in people with AIDS
and for a variety of infections caused by susceptible
bacteria, as well as for bites by the brown recluse spider
(rarely found in Australia). Clofazimine is used to treat
multibacillary forms of leprosy but only in combination
with dapsone or rifampicin.
Recently, the hypnotic drug thalidomide (
Thalomid
)
has also been used in erythema nodosum leprosum that
occurs after treatment for leprosy (Box 9.6).
Therapeutic actions and indications
Most of the antimycobacterial agents act on the DNA
and/or RNA of the bacteria, leading to a lack of growth
and eventually to bacterial death (see Figure 9.2).
diarrhoea, cramps or changes in colour of urine
or stool.
Evaluation
■
■
Monitor the person’s response to the drug
(resolution of bacterial infection).
■
■
Monitor for adverse effects (GI effects, rash and
superinfections).
■
■
Evaluate the effectiveness of the teaching plan
(person can name the drug, dosage, possible
adverse effects to expect and specific measures to
help avoid adverse effects).
■
■
Monitor the effectiveness of comfort and safety
measures and compliance with the regimen.
