Download A Possible Pathologic Link Between Chronic

under anaerobic conditions), only one anaerobic bacterium was
isolated in this study, leading to the conclusion that anaerobic
bacteria were not likely to be involved in these infections and that
antibiotics effective against anaerobic bacteria may not be useful
as empiric treatment in these situations. However, it is well
known that the concentration of anaerobic bacteria in the
oropharynx is higher than that of aerobic bacteria. These bacteria
colonizing the oropharynx are responsible for nosocomial pneumonia. Thus the inability to isolate anaerobic bacteria in this
study is surprising. Using specific transport and culture conditions, we could isolate a high percentage of anaerobic strains from
protected brush specimens (PSB) in patients with ventilatoracquired pneumonia (VAP).2 These striking differences between
the results of Marik and Careau and ours may be related to
technical differences in the laboratory procedures used to recover anaerobic bacteria from PSB. First, we used freshly
prepared meat yeast VL agar medium (Sanofi Pasteur; Marnes La
Coquette, France) for anaerobic culture. This medium is prepared twice each week and is complemented with 8% sheep
blood, menadione, and gentamicin, making this medium selective
for anaerobes. Secondly, the anaerobic atmosphere was obtained
in an oxoid jar with the Anaerogen Oxoid system (Oxoid;
Basingstoke, England), which gives us better results than other
tested systems (unpublished data). Finally, 2 of the 20 technicians
in our laboratory are specifically assigned to the anaerobic
bacteria department because of their skill in studying these
bacteria.
Nevertheless, the potential interest of using antibiotics effective against anaerobic bacteria in patients with nosocomial pneumonia remains controversial.3 We recently reported that patients
with VAP receiving well-adapted empiric antibiotherapy against
anaerobic bacteria had a better outcome at D10.4 Furthermore,
in a recent large study comparing the efficacy of ceftazidime vs
piperacillin-tazobactam in ICU patients with VAP, mortality was
lower in patients receiving piperacillin-tazobactam than in those
receiving ceftazidime.5 Although anaerobic bacteria were not
specifically investigated in this study, we can speculate that the
mortality difference might be explained in part by a better activity
of piperacillin-tazobactam than ceftazidime on anaerobes, which
could have been associated with aerobic bacteria in patients with
VAP.
In conclusion, because anaerobic bacteria are numerous in the
oropharynx, and because colonized oropharyngeal content leads
to nosocomial pneumonia, anaerobes associated with aerobic
bacteria should be isolated in patients with VAP or aspiration
pneumonia. Furthermore several arguments suggest taking into
account these bacteria in the choice of empiric antibiotic therapy
in patients with VAP.
René Robert, MD
Ghislaine Grollier, MD
Michel Hira, MD
Pierre Doré, MD
Service de Réanimation Médicale et de Microbiologie A,
CHU La Milèterie
Poitiers cedex, France
Correspondence to: René Robert, MD, Service de Réanimation
Médicale, CHU La Milèterie, 86021 Poitiers cedex, France; e-mail
[email protected]
References
1 Marik PE, Careau P. The role of anaerobes in patients with
ventilator-associated pneumonia and aspiration pneumonia.
Chest 1999; 115:178 –183
2 Doré P, Robert R, Grollier G, et al. Incidence of anaerobes in
ventilator-associated pneumonia with use of a protected
specimen brush. Am J Respir Crit Care Med 1996; 153:1292–
1298
3 Kollef MH. Antimicrobial therapy of ventilator-associated
pneumonia: how to select an appropriate drug regimen. Chest
1999; 115:8 –11
4 Robert R, Grollier G, Dore P, et al. Nosocomial pneumonia
with isolation of anaerobic bacteria in ICU patients: therapeutic considerations and outcome. J Crit Care 1999;
14:114 –119
5 Brun-Buisson C, Sollet JP, Schweich H, et al. Treatment of
ventilator-associated pneumonia with piperacillin-tazobactam/amikacin versus ceftazidime/amikacin: a multicenter,
randomized controlled trial. VAP Study Group. Clin Infect
Dis 1998; 26:346 –354
A Possible Pathologic Link Between
Chronic Cough and Sleep Apnea
Syndrome Through
Gastroesophageal Reflux Disease in
Older People
To the Editor:
In a recent issue of CHEST (August 1999), Palombini and
colleagues1 reported that asthma, postnasal drip syndrome
(PNDS), and gastroesophageal reflux disease (GERD), alone or
in combination, were responsible for ⬎ 90% of the causes of
chronic cough. They proposed that asthma, PNDS, and GERD
should be called a pathologic triad in chronic cough.1 Because
cough is the most common symptom for which adult patients
seek medical attention from primary care physicians, and because
cough is associated with deterioration in patients’ quality of life,2
the study of Palombini et al is very important, not only for
assessing chronic cough, but also for determining therapeutic
strategies for patients with chronic cough.1–3
However, in older patients, the causes of chronic cough may be
more complicated. Age-related changes in cough reflex may
affect the causes and therapeutic efficacy of chronic cough.4 – 6
Further, the protective role of cough as the defense mechanism
of aspiration is very important for the pathogenesis of chronic
cough in older patients.7–9 We have recently reported that
gastroesophageal reflux (GER) is frequently found in obstructive
sleep apnea syndrome (OSAS) in the elderly.10 Indeed, many
patients with OSAS complain of sleep-related heartburn and
regurgitation of gastric contents into the pharynx.11 It has been
reported that treatment with nasal continuous positive airway
pressure at night can correct the sleep apnea-related GER in
patients with OSAS.12 We have also reported that the swallowing
reflex is impaired in patients with OSAS,13 suggesting that OSAS
may perturb the inspiratory-expiratory transition during deglutition in the patients. Because OSAS and GER may aggravate
bronchial asthma, it is more difficult to control asthma in such
patients.14,15 In these patients, treatment with nasal continuous
positive airway pressure at night is sometimes reported to
improve control of asthma.14,15 These observations indicate that
OSAS may be a cause of chronic cough through GERD in the
elderly. Because GERD manifests a spectrum of conditions,
including asthma, posterior laryngitis, and chronic coughing, the
cause of GERD is not always simply determined in older people.
Owing to the explosive growth of the older population, we are
seeing many more elderly patients with pulmonary disease. Because
the incidence of OSAS increases with age, a possible pathologic link
CHEST / 117 / 4 / APRIL, 2000
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between chronic cough and sleep apnea syndrome through GERD
should be carefully considered in the treatment of elderly patients.
Shinji Teramoto, MD, FCCP
Yasuyoshi Ouchi, MD
Department of Geriatric Medicine
Tokyo University Hospital
Tokyo, Japan
Correspondence to: Shinji Teramoto, MD, FCCP, Department of
Geriatric Medicine, Tokyo University Hospital, 7-3-1 Hongo
Bunkyo-ku, Tokyo, Japan 113-8655; e-mail: [email protected]
References
1. Palombini BC, Villanova CAC, Araujo E, et al. A pathologic
triad in chronic cough: asthma, postnasal drip syndrome, and
gastroesophageal reflux disease. Chest 1999; 116:279 –284
2. French CL, Irwin RS, Curley FJ, et al. Impact of chronic cough
on quality of life. Arch Intern Med 1998; 158:1657–1661
3. Irwin RS, Boulet LP, Cloutier MM, et al. Managing cough as
a defense mechanism and as a symptom. Chest 1998;
114:133S–181S
4. Pontopiddan H, Beecher HK. Progressive loss of protective
reflexes in the airway with the advancing age. JAMA 1960;
174:2209 –2013
5. Sekizawa K, Ujiie Y, Itabashi S, et al. Lack of cough reflex in
patients with aspiration pneumonia [letter]. Lancet 1990;
335:1228 –1229
6. Teramoto S, Matsuse T, Ouchi Y. Clinical significance of
cough as a defence mechanism or a symptom in elderly
patients with aspiration and diffuse aspiration bronchiolitis
[letter]. Chest 1999; 115:602– 603
7. Kobayashi H, Sekizawa K, Sasaki H. Aging effects on swallowing reflex [letter]. Chest 1997; 111:1466
8. Matsuse T, Oka T, Kida K, et al. Importance of diffuse
aspiration bronchiolitis caused by chronic occult aspiration in
the elderly. Chest 1996; 110:1289 –1293
9. Teramoto S, Matsuse T, Ouchi Y. Foreign body aspiration
into the lower airways may not be unusual in older adults
[letter]. Chest 1998; 113:1733–1734
10. Teramoto S, Ohga E, Matsui H, et al. Obstructive sleep apnea
syndrome may be a significant cause of gastroesophageal reflux
disease in older people. J Am Geriatr Soc 1999; 47:1273–1274
11. Samelson CF. Gastroesophageal reflux and obstructive sleep
apnea. Sleep 1989; 12:475– 476
12. Kerr P, Shoenut JP, Miller T, et al. Nasal CPAP reduces
gastroesophageal reflux in obstructive sleep apnea syndrome.
Chest 1992; 101:1539 –1544
13. Teramoto S, Sudo E, Ohga E, et al. Impaired swallowing
reflex in patients with obstructive sleep apnea syndrome.
Chest 1999; 116:17–21
14. Stein MR. Advances in the approach to gastroesophageal
reflux (GER) and asthma. J Asthma 1999; 36:309 –314
15. Bruno G, Graf U, Andreozzi P. Gastric asthma: an unrecognized disease with an unsuspected frequency. J Asthma 1999;
36:315–325
bacteria usually colonize the oropharynx while Pseudomonads
favor the lower respiratory tract.
The statement that the gastric flora is not a major cause of
pneumonia has been indirectly confirmed by Cook et al,3 who
found that the use of sucralfate instead of H2-antagonists for
stress ulcer prophylaxis had no benefit either in decreasing
mortality or in the incidence of ventilator-associated pneumonia.
Also several unsuccessful trials with selective digestive decontamination (SDD) with the use of nonabsorbable antibiotics4,5
argue against theories that consider the stomach an important
source of nosocomial pneumonia in patients on mechanical
ventilation. We hope that the article by Cendrero and colleagues
might convince physicians who still believe in the SDD concept
that there is no evidence for using SDD for the prevention of
ventilator-associated pneumonia, in particular because of its risk
for induction of local antibiotic resistance.5
Stijn Blot, RN, MA
Koenraad Vandewoude, MD
Eric Hoste, MD
Francis Colardyn, MD
University Hospital Gent
Gent, Belgium
Correspondence to: Stijn Blot, RN, MA, Department of Intensive
Care, University Hospital Gent, De Pintelaan 185, B-9000 Gent,
Belgiou; e-mail: [email protected]
References
1 Cendrero JAC, Solé-Violán J, Benı́tez AB, et al. Role of
different routes of tracheal colonization in the development
of pneumonia in patients receiving mechanical ventilation.
Chest 1999; 116:462– 470
2 Geddes DM. Infection vs colonization. Intensive Care Med
1990; 6:201–205
3 Cook D, Guyatt G, Marshall J, et al. A comparison of
sucralfate and ranitidine for the prevention of upper gastrointestinal bleeding in patients requiring mechanical ventilation. N Engl J Med 1998; 338:791–797
4 Kollef MH. The role of selective digestive tract decontamination on mortality and respiratory tract infections: a metaanalysis. Chest 1994; 105:1101–1108
5 Colardyn F, Decruyenaere J, Verschraegen G, et al. Failure
of selective digestive decontamination (SDD) to control an
epidemic of colonization by extended spectrum B-lactamaseproducing Klebsiella pneumoniae (CAZ) [abstract no. IM-9].
In: Abstracts of the 37th Interscience Conference on Antimicrobial Agents and Chemotherapy. Toronto, Canada: American Society for Microbiology, 1997:365
Infants Exposed to Maternal Smoking
and With a Family History of Asthma
To the Editor:
Tracheal Colonization in Pneumonia
To the Editor:
Based on their prospective study (CHEST; August 1999),
Cendrero and colleagues1 state that bacteria colonizing the gut
are often responsible for tracheal colonization but are rarely the
cause of nosocomial pneumonia. Indeed, different types of
bacteria causing upper vs lower respiratory tract infections have
been demonstrated before.2 Independent patterns of colonization may be found in the oropharyngeal and tracheal secretions
from the same patient. For example, enteric Gram-negative
We read with special interest the article by Sheikh et al
(CHEST; July 1999),1 who studied infants using the rapid
compression technique. They found an increase in forced expiratory flow (FEF) at 25% of the remaining tidal volume (Vt)
following the administration of albuterol in infants with a family
history of asthma. The authors concluded that this was due to
reversible bronchospasm, which seemed absent in infants who
were exposed to maternal smoking and did not show such
improvement, and they suggested that this technique could be
used in recognizing different phenotypes of wheezy infants. If
this interpretation is correct, this would have important practical
implications.
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Communications to the Editor