Pneumonia
by Bruce Mirken
Pneumocystis carinii pneumonia (PCP)
was one of the first identified manifestations of AIDS. Although improved
strategies for prevention and treatment of PCP have greatly reduced the
number of cases and deaths, PCP and other pneumonias remain a major cause
of illness and death among people with AIDS, and account for roughly one-third
of AIDS deaths. Because bacterial pneumonias and other respiratory problems
can sometimes produce similar symptoms, diagnosis of PCP can be tricky.
Today, use of prophylactic treatment to prevent PCP in persons with fewer
than 200 CD4 cells/mm3 is universally regarded as one of the
most effective medical interventions available.
History and Trends
Pneumonia -- infection and inflammation
of the lungs in which parts of the lungs may fill with fluid -- can be
caused by a wide variety of organisms, including bacteria, viruses and
fungi. Whatever the cause, pneumonia can be debilitating and often deadly.
Until the 1980s pneumonia caused by Pneumocystis
carinii was extremely rare: only about 50 cases were reported in 1970.
Although the organism--long regarded as a protozoan, but now understood
to be more like a fungus--is quite common, it is harmless in individuals
with healthy immune systems. Before AIDS, the few instances of PCP disease
occurred in people whose immune systems had been seriously weakened. Cases
were reported in malnourished World War II orphans and, more recently,
in organ transplant recipients receiving immunosuppressive anti-rejection
therapy and in people with cancer undergoing chemotherapy.
When PCP began appearing in 1980 and 1981
in young gay men with none of the usual risk factors, alarms went off
at the Centers for Disease Control (CDC).
In the early 1980s, doctors had little experience
treating PCP; the death toll was astonishing, and an average patient had
only a 50% chance of surviving an episode of the disease. Among those
whose illness was severe enough to require a breathing tube and ventilatory
support, the incidence of death reached 80%. For many years, PCP remained
the number one killer of people with AIDS. Even those who recovered from
a first episode of PCP generally saw their health continue to decline.
In over 60% of cases, PCP recurred, often with increasing severity.
Despite recent progress, PCP is still cause
for concern. As San Francisco physician Lisa Capaldini, MD, put it recently,
"If someone gets PCP out of the blue, they're likely to have a progressive
decline in their health, because a rip-roaring pneumonia can really knock
your socks off."
Fortunately, progress on all fronts against
PCP has made the outlook more hopeful since the late 1980s. Improved diagnostic
and treatment methods began to increase survival. Perhaps most importantly,
increasing use of prophylactic medications to prevent PCP began to reduce
the number of cases.
An analysis by CDC researchers of HIV-related
causes of death listed on death certificates from 1987-1992 illustrates
the point dramatically. While the rates of death involving most other
opportunistic infections remained fairly constant, PCP-related mortality
dropped from 32.5% of HIV-related deaths in 1987 to 13.8% by 1992. In
that same period, deaths due to bacterial pneumonia increased from 1.2%
to 2.1%. Unspecified pneumonias remained constant at about 18%. Some of
these unspecified pneumonias no doubt represent undiagnosed cases of PCP,
while others represent divergent causes. The researchers believe the decline
in PCP canceled out increases in other types of pneumonia in this "unidentified"
group.
A similar trend has been seen in another
CDC study, the Adult Spectrum of Disease Project, which collected data
from 100 inpatient and outpatient medical facilities in 10 U.S. cities
from 1990-1995. Although only some of the data have been released, figures
through 1993 show a gradual but steady decline in PCP incidence among
gay and bisexual men. In contrast, PCP rates increased among injection
drug users (IDU), although the increase did not quite achieve statistical
significance. Fewer of the IDU were receiving PCP prophylaxis, and the
researchers theorize that those who were may not have adhered to their
prophylactic regimens as well as the gay and bisexual men. Data on other
causes of pneumonia in this study have not yet been released.
The incidence of PCP in San Francisco has
more or less conformed to the national trend. Annual PCP cases peaked
at 1,095 in 1987, leveled off for a few years, and dropped to 613 by 1994.
Data for 1995 are still incomplete. According to Kevin McKinney of the
city's AIDS Office, reliable figures are not available for other types
of pneumonia.
Still, for a city as renowned for state-of-the-art
HIV care as San Francisco, PCP is far from vanquished. John Stansell,
MD, Medical Director of the AIDS Program at San Francisco General Hospital,
notes, "We still see a very large number of PCP cases here. Per month
it's probably gone from a high of about 30 cases to about 20-25. It's
true that there's been somewhat of a decline, but it's by far still the
most frequent opportunistic infection that we encounter here at San Francisco
General."
About half of those cases, Stansell continues,
occur in people who were not receiving PCP prophylaxis. Most of the others
occurred in persons who did not take their medication as scheduled or
who were on aerosolized pentamidine or dapsone, which are considered weaker
PCP preventatives than trimethoprim-sulfamethoxazole (TMP-SMX, brand names
Bactrim and Septra). Stansell believes that true "breakthrough"
infections while on TMP-SMX are "very rare" (see below for a
detailed discussion of PCP prophylaxis).
Stansell is part of the team conducting
the long-term Pulmonary Complications of HIV Infection study, which recruited
patients at 6 sites around the country beginning in 1987 and followed
them for 5 years. The study enrolled 1130 HIV positive participants and
167 HIV negative controls matched for age and gender. Stansell calls it
"the first study that really aimed at enrolling a cohort that looked
like the AIDS epidemic" in terms of demographics. Much of the data
are still awaiting publication, but some appeared last September in the
New England Journal of Medicine (333(13): 845-51. September 28,
1995).
"The incidence of bacterial pneumonia
was about 10-fold higher among HIV-infected people than it was in uninfected
individuals," Stansell says. Although the rates of bacterial pneumonia--caused
by various organisms including Streptococcus pneumoniae and Haemophilus
influenzae--increased as CD4 counts declined, HIV positive persons with
normal CD4 counts still had significantly higher rates than the uninfected
controls. The explanation, Stansell suspects, is that "there are
probably qualitative differences in the ability of the body to rid itself
of pathogens if you're HIV-infected. The immune cells, even if they're
there, probably don't work as well."
Smoking was also associated with higher
rates of bacterial pneumonia. Strikingly, PCP prophylaxis with TMP-SMX
was associated with a two-thirds reduction in bacterial pneumonia, in
addition to a decrease in PCP.
Overall, those who experienced any type
of pneumonia had a mortality rate 4 times higher than those who did not.
Equally distressing, Stansell notes, is that "the people who have
bacterial pneumonia appear to have a greater risk of rapid progression
in their HIV disease. Those data are just being ferreted out now, but
it looks like it's a very bad prognostic indicator."
Prophylaxis
PCP prevention has been one of the areas
of greatest progress in HIV care over the years. Some precautions can
be taken to reduce the risk of bacterial pneumonias as well.
The first line of defense, and one not to
be underestimated, is to see a physician who is knowledgeable about HIV
disease. An assessment of HIV care provided by primary care doctors published
last year in Archives of Internal Medicine found that large numbers
of physicians did not prescribe or recommend the most basic elements of
HIV care. For example, only half indicated that they would start appropriate
PCP prophylaxis.
If there is anything that AIDS-experienced
physicians agree upon, it is that PCP prophylaxis works. Standard practice
is to recommend prophylaxis for any HIV-infected person with 200 or fewer
CD4 cells/mm3 or whose CD4 percentage is less than 14% of total
lymphocytes. PCP prophylaxis is also recommended for anyone, regardless
of CD4 count, who is experiencing a sharp decline in CD4 counts or persistent,
unexplained fevers or thrush (shown in some studies to be independent
predictors of high risk for PCP). Anyone who has already had 1 or more
bouts of PCP should also receive prophylaxis. Study after study has demonstrated
that effective prophylaxis sharply reduces the incidence of PCP in such
individuals.
The CDC has developed specific PCP prophylaxis
guidelines for infants and children. The agency recommends prophylaxis
for all infants born to HIV-infected mothers starting at age 4-6 weeks,
to be discontinued if HIV antibody testing after 4 months of age indicates
that the child is HIV-uninfected. For HIV-infected children aged 1-5 years,
prophylaxis is recommended for those with fewer than 500 CD4 cells/mm3
or a CD4 percentage less than 15%. TMP-SMX, an oral antibiotic, is the
preferred drug. (For more on pediatric HIV infection, see HIV/AIDS
in Children, this issue.)
TMP-SMX is the prophylactic drug of choice
for adults as well. Other regimens, notably dapsone, another oral drug,
and aerosolized pentamidine (AP), inhaled in mist form through a device
called a nebulizer, are also used extensively. Besides being extremely
effective at preventing PCP, TMP-SMX has 2 other advantages: it is inexpensive,
and it also helps to prevent other diseases such as toxoplasmosis (a brain
infection) and bacterial infections including pneumonia. However, TMP-SMX
can produce a number of toxic side effects, including rash, fever, nausea,
vomiting and neutropenia (loss of white blood cells). Life-threatening
reactions, including severe anaphylactic reactions or Stevens-Johnson
syndrome (a condition involving severe blistering and sloughing of skin
and mucous membranes) can occur, but are rare. Aerosolized pentamidine
does not prevent extrapulmonary PCP.
The scales were definitively tipped towards
TMP-SMX by a study known as ACTG 021, in which 1 double-strength tablet
of TMP-SMX daily was compared to 300 mg of AP given once per month to
HIV positive persons who had already had PCP at least once. PCP recurred
in the AP group more than twice as frequently as in the TMP-SMX group.
Based on this study, the U.S. Public Health Service recommended this dose
of TMP-SMX for PCP prophylaxis.
A later study, ACTG 081, published in the
March 16, 1995 New England Journal of Medicine, seemed to muddy
the picture a bit. This trial compared a higher dose of TMP-SMX (1 double-strength
tablet twice daily) to dapsone (50 mg twice daily) to AP (300 mg every
4 weeks) in people with fewer that 200 CD4 cells/mm3 and no prior history
of PCP. Those who had serious (grade 3) toxic effects had their doses
reduced and/or were switched to a different therapy. Although TMP-SMX
was more active against PCP than the other drugs, toxicity forced 79%
of those receiving it to reduce the dose or switch to another drug.
The "intent-to-treat" analysis--comparing
the groups based on the drug they were originally assigned, regardless
of later changes--showed only statistically insignificant differences
in the risk of developing PCP among the 3 groups. Over 36 months, the
risk was 18% in the dapsone group, 17% in the TMP-SMX group and 21% in
the AP group. For those with fewer than 100 CD4 cells/mm3,
though, the difference was more pronounced: the risks of developing PCP
were 22%, 19% and 33%, respectively.
However, an "as-treated" analysis--looking
at the therapy the patient was actually receiving at the time of the PCP
episode--tells a somewhat different story. Only 4 of 34 treatment failures
in the TMP-SMX group occurred among people still taking the drug at the
original dose, and none occurred in those whose dose was reduced to once
daily. The failures overwhelmingly occurred after patients had switched
drugs. By contrast, 21 of 33 dapsone treatment failures occurred while
on that drug, and the failure rate increased 4-fold at the first dose
reduction. Few AP patients switched drugs, and 37 of 38 failures occurred
while on AP.
The researchers concluded that although
TMP-SMX is clearly stronger against Pneumocystis (P.) carinii,
use of this drug as the first prophylactic strategy did not produce significantly
better results than starting with dapsone or AP. The reason, the researchers
write, is that "because of continuing cross-overs and dose reductions
as the trial progressed, more patients were receiving less adequate treatments
even as their vulnerability to P. carinii increased" due to
declining CD4 counts.
The impact of this study is somewhat uncertain.
Clearly 2 double-strength TMP-SMX tablets per day showed no advantage
over one. Just as clearly, 100 mg per day of dapsone per day performed
better than 50 mg. Overall the researchers found "similar effectiveness,"
no matter which drug patients started with. An accompanying editorial
went further, suggesting that AP, with its low toxicity, might be the
drug of choice for those with CD4 counts over 100 cells/mm3,
and TMP-SMX the preferred prophylaxis for those with fewer than 100 cells/mm3.
That suggestion goes against the generally
accepted recommendation to use TMP-SMX as first-line prophylaxis across
the board. There seems not to have been a general move in favor of AP
since the study was published. A meta-analysis of 35 randomized PCP prophylaxis
trials that appeared in the January 22, 1996 Archives of Internal Medicine
sheds more light on the situation.
The researchers pooled and analyzed the
results from all 35 studies, which looked at a variety of drugs--including
TMP-SMX, AP and dapsone--and dosing regimens. Some of the studies combined
dapsone with pyrimethamine.
Such an analysis has limitations. In comparing
results from different trials, it is impossible to completely adjust for
all of the differences in trial methodology. Still, the researchers found
clear patterns that allowed them to draw some fairly solid conclusions.
"Regardless of dose," they wrote,
"TMP-SMX was almost universally effective for patients who tolerated
it" [emphasis added]. Overall, the drug was 42% more effective than
AP in preventing PCP. The difference between TMP-SMX and dapsone was not
statistically significant, though the trend favored TMP-SMX. A dose of
100 mg of dapsone was more effective than 50 mg. Overall, AP had the fewest
side effects while TMP-SMX had the most.
There were few treatment failures on TMP-SMX,
most of which occurred after the drug had been discontinued. Most striking
were the dose-response relationships uncovered. For example, increasing
the daily dose of TMP-SMX seemed to hurt more than it helped; in fact,
there was a trend toward more failures at the highest dose tried (2 double-strength
tablets per day, the regimen used in ACTG 081). AP, meanwhile, did better
when given twice monthly instead of the standard once monthly dose.
Thus, reduced dosing of TMP-SMX--such as
1 double-strength tablet 3 times per week--might minimize the need to
discontinue therapy due to toxicity, with little loss in efficacy. The
scientists caution that relatively little data exists to support using
this regimen in people with lower CD4 counts or those who have already
had PCP.
Another approach to dealing with the toxicity
of TMP-SMX is known as desensitization. This involves starting with tiny,
diluted doses of the drug and building up to the regular dose over a period
of days, so that the body gradually learns to tolerate it. Many different
desensitization protocols exist. One version offered by Project Inform
takes 8 days; others take more or less time. Considerable success has
been reported with desensitization, although it is generally considered
too risky to attempt with persons who have had a severe anaphylactic reaction
to sulfa drugs or who have had Stevens-Johnson syndrome.
What is less clear is which protocol is
best. "There's no standard," observes San Francisco clinician
and AIDS researcher Gifford Leoung, MD. "It's all arbitrary; there
are no published data from well-organized trials. In fact," he continues,
"there's a paper that came out last year that suggested you don't
even need to desensitize people." Instead, you can "just give
them a single dose--directly challenge them right up-front." Leoung
is protocol chair of an American Foundation for AIDS Research-financed
trial that is now comparing this direct-rechallenge approach with gradual
desensitization.
In any case, Stansell declares, "The
most important thing you can do for yourself is to take PCP prophylaxis."
Whatever treatment you're on, it is critical to do it right. That means
taking your pills as scheduled, and if side effects make that difficult,
talking with your doctor about ways to manage the problem, rather than
haphazardly skipping doses. If you are using AP, follow the instructions
you are given about posture and breathing during the treatment. Slouching
and breathing shallowly will prevent the medication from getting all the
way into the lungs, reducing the benefit.
For protection against bacterial pneumonia,
the CDC recommends vaccination with pneumococcal vaccine as soon as possible
after testing HIV positive, a recommendation the agency calls "especially
pertinent in light of the increasing incidence of invasive infections
with drug-resistant strains of Streptococcus pneumoniae."
Vaccination against Haemophilus influenzae "may be considered,
but data are insufficient to recommend the use of this vaccine in HIV-infected
adults at this time."
As Stansell points out, TMP-SMX seems to
offer some protection against bacterial pneumonias as well as PCP. Although
the CDC suggests this be considered when choosing PCP prophylaxis, it
warns that "indiscriminate use of this drug 'when not indicated for
PCP prophylaxis or other specific reasons' may promote the development
of resistant organisms." In addition, the drug will not protect against
drug-resistant strains.
Diagnosis
A constellation of symptoms, including fever,
cough, fatigue and shortness of breath, can signal the onset of pneumonia.
Some or all of these symptoms may be present. Of course, many other conditions,
such as bronchitis and the common cold, can produce some of the same effects.
If symptoms continue beyond a few days or worsen, it is essential to seek
medical evaluation. Caught early, most pneumonias can be successfully
treated, often on an outpatient basis, but if allowed to worsen, they
can be life-threatening.
It is important to be able to describe your
symptoms in as much detail as possible, including the length of time they
took to appear, because these details will help your physician to narrow
down a diagnosis. Symptoms can be clues to the cause of the pneumonia.
For example, bacterial pneumonias tend to develop rapidly, often within
24 hours or less, while other lung infections, including Aspergillus
or Mycoplasma infections, tend to have a slower onset. PCP also
tends to come on slowly. Leoung says symptoms may be barely perceptible
at first but then worsen slowly over a period of weeks.
The cough can also be an important clue.
A classic PCP cough is dry, with little or no sputum; any sputum that
is produced is likely to be clear. Bronchitis, on the other hand, can
often produce large amounts of sputum; and bacterial pneumonias produce
greenish, rust-colored, bloody or yellow-tinged sputum.
Often a doctor will listen to the patient's
chest with a stethoscope. Pneumonias often produce a characteristic breathing
sound called "rales," while bronchitis usually does not; PCP
may or may not produce recognizable chest sounds.
Chest X-rays are often used to make a diagnosis
because different illnesses produce characteristically different patterns.
However, a certain amount of natural variation occurs on X-rays, and PCP
may not always be visible. Further testing is required to confirm a diagnosis
made by X-ray.
Along with identifying the cause of the
problem, Leoung notes, it is important to quickly make other key determinations.
"How sick is this person? Do they need to be in the hospital? That's
the real next question. If they're not getting enough oxygen they can't
go home. Is this illness serious enough to require IV antibiotics, as
opposed to oral antibiotics? If so, the person most likely needs to be
hospitalized."
One important measure of the seriousness
of any type of pneumonia is its effect on the amount of oxygen that gets
into the blood. Two different tests are commonly used for making this
determination. The simplest but crudest is known as pulse oximetry, which
involves placing a device that resembles a clothes pin on a finger to
measure the amount of oxygen under the skin. Although oximetry is simple
and fast, Stansell dismisses it as "very inexact." A far more
precise method is to draw arterial blood and measure the gases it contains.
Unfortunately, arterial blood gas measurement can be painful, because
arteries tend to have more nerve endings than the veins used for most
other blood tests.
Aside from these test results, the decision
to hospitalize or not can involve what Leoung calls a somewhat subjective
evaluation of "how much you think this person can tolerate in terms
of getting worse. If there's a lot of leeway, you can go home because
there's time to get you back in here. But if you're close to the edge,
I don't want to send you home. Sometimes I rely on my gut feelings; the
numbers may look great, but the person just does not look good."
As with prophylaxis, these judgment calls tend to be most reliably made
by an HIV-experienced physician.
If the symptoms, history and X-rays seem
to point in one direction--PCP, for example--the physician will probably
recommend beginning treatment immediately. Even so, standard practice
in San Francisco is to make a confirmatory test for the responsible organism.
Unusual symptomology can occur, and sometimes more than one condition
may be present at once, with one set of symptoms partly masking another.
The least invasive way to confirm a diagnosis
is through a procedure called sputum induction. The patient breathes a
saline mist which provokes coughing, hopefully bringing up sputum which
can be examined for P. carinii, bacteria, fungi or whatever organisms
the symptoms and X-rays suggest. Patients are advised not to eat for 8
hours before the procedure, nor to use toothpaste or mouthwash, all of
which can interfere with the results. Stansell calls sputum induction
"a technically difficult procedure," which not everyone manages
to do well. At San Francisco General Hospital, where the procedure is
frequently used, over 70% of PCP diagnoses are made this way, but facilities
that use the technique less are not usually this successful.
If sputum induction fails to enable a diagnosis,
the next, more invasive step is bronchoscopy. In this procedure, a tube
is inserted through the mouth or nose into the breathing tubes. The patient
is generally sedated and the throat numbed, which makes bronchoscopy "a
very quick, very easy, painless procedure," according to Stansell.
Still, the invasive procedure is not easy to tolerate. One or both lungs
are washed out (lavaged) to flush out the organisms, and brushings of
the bronchial walls may also be done. The fluid and brushings are then
examined by microscope.
Fortunately, bronchoscopy tends to be extremely
accurate at producing a confirmed diagnosis. A far more invasive approach,
a surgical procedure called an open-lung biopsy, is now only very rarely
used to diagnose HIV-related pneumonia.
Recently, researchers from the National
Institutes of Health have advocated treatment for AIDS-related pneumonia,
including PCP, without necessarily looking for the Pneumocystis organism,
if cost-effective facilities for PCP testing are not available (see Research
Notes, this issue).
Treatment
General guidelines for treatment of all
pneumonias emphasize adequate hydration to help clear secretions. If a
patient is so sick that adequate intake of fluids by mouth is difficult,
intravenous supplementation may be needed.
The drug therapy used depends on the organism
responsible. Pneumonias caused by fungi such as Cryptococcus or
Histoplasma are treated with the same antifungals, such as amphotericin
B, itraconazole and fluconazole, that are used to treat other ailments
caused by these organisms. Similarly, the relatively rare pneumonia caused
by cytomegalovirus (CMV) is treated with the familiar anti-CMV drugs ganciclovir
and foscarnet.
Treatment of bacterial pneumonias may require
any of numerous antibiotics, including penicillin, amoxicillin, TMP-SMX,
clarithromycin, azithromycin and the cephalosporins, depending on the
specific bacteria involved. A potential source of difficulty is the increasing
occurrence of drug-resistant strains, and the CDC recommends drug sensitivity
testing to ensure that an appropriate therapy is chosen.
Although PCP treatment has improved steadily
over time, the picture has not changed dramatically since BETA published
"Guidelines for Treatment of Pneumocystis carinii Pneumonia,"
by editor Ronald Baker, PhD, in March, 1993. TMP-SMX remains the first-line
treatment, whether administered intravenously for severe cases or orally
for milder ones. The drug's toxicities may be problematic, but can often
be controlled with dose adjustments and/or use of antihistamines and fever-reducing
drugs. Still, in some cases it is necessary to switch to another drug.
In severe cases that require intravenous
(IV) therapy, IV pentamidine remains the second-line drug of choice. Like
TMP-SMX, it is extremely effective against PCP. However, IV pentamidine
can produce serious, sometimes irreversible side effects, such as abnormally
low blood pressure, or blood sugar level abnormalities including diabetes,
pancreatitis (pancreas inflammation), kidney toxicity and loss of white
blood cells. Because of these toxicities, most physicians use IV pentamidine
only in the worst cases, and only after first trying TMP-SMX.
In recent years, trimetrexate has emerged
as a third-line IV therapy for PCP. The drug must be administered with
a second drug, leucovorin, to counter its toxic side effects. In an ACTG-sponsored
study comparing trimetrexate plus leucovorin to TMP-SMX in patients with
moderate to severe PCP, trimetrexate was better tolerated but less effective;
the trimetrexate group had a significantly higher death rate. The high
cost of trimetrexate-leucovorin is another disadvantage.
In moderate to severe cases, using a short
course of corticosteroids such as prednisone along with antibiotic therapy
has been shown to reduce the chances of respiratory failure and death.
These regimens do not affect P. carinii directly; rather, they apparently
decrease the body's inflammatory response to the organism, thereby alleviating
breathing difficulties.
Several options are now available for people
who cannot tolerate TMP-SMX but do not need IV therapy. The first fallback
option is usually dapsone-trimethoprim or clindamycin-primaquine. Dapsone-trimethoprim,
Leoung notes, is simple to administer and generally easier to tolerate
than clindamycin, but some physicians prefer clindamycin-primaquine. In
a recent 91-patient Canadian study, clindamycin-primaquine worked roughly
as well as TMP-SMX, with fewer serious side effects but greater incidence
of rash.
A more recent entry among the oral drugs
is atovaquone (Mepron). Manufacturer Burroughs Wellcome (now Glaxo-Wellcome)
took offense when Baker listed atovaquone as the fourth-line therapy 3
years ago (BETA, pp 18-19, March 1993). Data obtained since then, as well
as a new formulation, have only somewhat boosted the drug's position.
Atovaquone's strongest positive attribute is its low level of side effects.
In studies comparing it to either TMP-SMX or pentamidine, atovaquone generally
was less active against PCP but better tolerated--enough so that significantly
more patients completed therapy without having to switch drugs.
A new, better-absorbed liquid formulation
could improve atovaquone's efficacy, but the new formulation came with
new labeling reducing the dosing from 3 to 2 times a day--producing approximately
the same blood levels of the drug. To get new labeling, the company will
need to do further research on the new formulation; in the meantime, doctors
are not sure how best to use the drug. Leoung comments that "people
have always had a little concern about using atovaquone alone. Most doctors
who've had experience with atovaquone say, 'Well, I wouldn't give it to
somebody who's really sick.' We don't know yet."
As with all areas of HIV/AIDS care, optimal
prevention and treatment of pneumonia are facilitated when patients take
an active role in their care. Persons who carefully note and report symptoms
and side effects to their health care providers and who ask questions
when they are unsure about tests or treatments improve their chances for
successful care. In the present cost-conscious managed-care environment,
doctors can be under tremendous pressure to do things as quickly and inexpensively
as possible. "Be proactive," Leoung advises, "Speak up."
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Bruce Mirken is a freelance
writer based in San Francisco.
Page last updated 23 July 1996
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