706 THE PEDIATRIC INFECTIOUS DISEASE JOURNAL
8, August, 2000
16. Varteresian-Karanfil L, Josephson A, Fikrig S, Kaufman S,
Steiner P. Pulmonary infection and cavity formation caused
by Mycobacterium tuberculosis in a child with AIDS. N Engl
J Med 1988;319:1018 –9.
17. Lindegren ML, Thomas P, Fleming P, Schulte J, Valappil T,
Ward J. M. tuberculosis among children reported with HIV/
AIDS, US [Abstract I-48]. In: 36th Interscience Conference on
Antimicrobial Agents and Chemotherapy, New Orleans, Sep-
tember 15 to 18, 1996. Washington, DC: American Society for
Microbiology, 1996.
18. Caldwell MB, et al. Biologic foster, and adoptive parents:
Caregivers of children exposed perinatally to human immu-
nodeficiency virus in the United States. Pediatrics 1992;90:
603–7.
19. Centers for Disease Control. 1994 revised classification sys-
tem for human immunodeficiency virus infection in children
less than 13 years of age. MMWR 1994;43(RR-12):1–7.
20. New York City Department of Health. Information summary,
Bureau of Tuberculosis Control, New York City, 1995.
21. Frieden TR, Sterling T, Pablos-Mendez A, et al. The emer-
gence of drug-resistant tuberculosis in New York City.
N Engl J Med 1993;328:521– 6.
22. Agrons GA, Markowitz RI, Kramer SS. Pulmonary tubercu-
losis in children. Semin Roentgenol 1993;28:158 –72.
23. Nolan RJ. Childhood tuberculosis in North Carolina: a study
Pediatr Infect Dis J, 2000;19:706–10
Copyright © 2000 by Lippincott Williams & Wilkins, Inc.
Reduced lung diffusion capacity after
Mycoplasma pneumoniae pneumonia
ELIZABETH MARC, MD, MICHÈLE CHAUSSAIN, MD, FLORENCE MOULIN, MD, JEAN-LUC INIGUEZ, MD, GABRIEL
KALIFA, MD, JOSETTE RAYMOND, MD AND DOMINIQUE GENDREL, MD
Background. Mycoplasma pneumoniae is a fre-
quent but underdiagnosed cause of community-
acquired pneumonia (CAP) in children, and ap-
propriate macrolide treatment is often given
late. The aim of this work was to estimate the
frequency of pulmonary involvement in children
6 months after a clinical episode of Mycoplasma
CAP.
Accepted for publication May 3, 2000.
From the Departments of Pediatrics (EM, FM, JLI, DG),
Physiology (MC), Radiology (GK) and Bacteriology (JR), Hôpital
Saint Vincent de Paul, Paris, France.
Presented at the 38th Interscience Conference on Antimicro-
bial Agents and Chemotherapy, San Francisco, September 26 to
29, 1999.21
Key words: Mycoplasma pneumoniae, community-acquired
pneumonia, carbon monoxide diffusion capacity, pulmonary se-
quelae.
Address for reprints: Professor Dominique Gendrel, Hôpital
Saint Vincent de Paul, 82 Av Denfert-Rochereau, 75014 Paris,
France. Fax 33 1 4048 8386; E-mail dominique.gendrel@svp.ap-
hop-paris.fr.
Vol. 19, No.
of the opportunities for intervention in the transmission of
tuberculosis to children. Am J Public Health 1986;75:26 –30.
24. Starke JR, Correa AG. Management of mycobacterial infec-
tion and disease in children. Pediatr Infect Dis J 1995;14:
455–70.
25. Brudney K, Dobkin J. resurgent tuberculosis in New York
City: human immunodeficiency virus, homelessness, and the
decline of tuberculosis control programs. Am Rev Respir Dis
1991;144:745–9.
26. Costello AM de L, Rook G. Tuberculosis in children. Curr
Opin Pediatr 1995;7:6 –12.
27. Drucker E, Alcabes P, Bosworth W, Sekell B. Childhood tuber-
culosis in the Bronx, New York. Lancet 1994;343:1482–5.
28. New York City Office of AIDS Surveillance. AIDS surveil-
lance update, second quarter 1995. New York: New York City
Department of Health, 1995.
29. Jereb J, Kelly GD, Porterfield DS. The epidemiology of
tuberculosis in children. Semin Pediatr Infect Dis 1993;4:
220 –31.
30. Jacobs RF, Eisenach KD. Childhood tuberculosis. Adv Pedi-
atr Infect Dis 1993;8:23–51.
31. CDC. Essential components of a tuberculosis prevention
and control program: recommendations of the Advisory
Council for the Elimination of Tuberculosis. MMWR 1995;
44(RR-11).
Vol. 19, No. 8
Printed in U.S.A.
Methods. We measured carbon monoxide diffu-
sion capacity (TLCO) and conducted spirometric
tests in 35 children without asthma or chronic
lung disease (ages 4.5 to 15 years), 6 months and
1 year after acute CAP caused by M. pneumoniae
(23 children), pneumococci (5 children) or vi-
ruses (7 children). Only 11 of 23 patients with M.
pneumoniae CAP required hospitalization,
whereas all the patients with pneumococcal or
viral pneumonia were admitted to hospital.
Results. Lung volumes and spirometric tests
were normal for all children. TLCO was normal 6
months after pneumococcal or viral pneumonia
(87 to 112% of expected values for height and
sex). After acute M. pneumoniae CAP, 11 of 23
patients (48%) had TLCO values <80% of the
expected value. The extent of change in lung
diffusion capacity was correlated with the delay
to diagnosis and treatment: TLCO was low in 8 of
11 patients given macrolide treatment 10 days or
Vol. 19, No. 8, August, 2000 THE PEDIATRIC INFECTIOUS DISEASE JOURNAL
more after the onset of acute symptoms vs. only 3
of 10 patients given appropriate treatment in the
first 10 days. TLCO was low in 7 of 7 who received
macrolide therapy for <2 weeks. TLCO had in-
creased slightly after 1 year in the 5 patients
retested after a new course of macrolide treat-
ment. TLCO reached the lower normal range in 2
patients controlled after 3 years.
Conclusions. The abnormal TLCO values sug-
gest that some children with Mycoplasma pneu-
monia have reduced pulmonary gas diffusion
after recovery from the illness. The reduction is
related to delay and short macrolide therapy.
INTRODUCTION
Childhood respiratory infections are generally
thought to predispose to some of the chronic pulmonary
diseases that affect adults.1–3 Pneumonia is a frequent
and serious illness in children, but few studies have
evaluated the long term outcome of children with
community-acquired pneumonia. The difficulty in di-
agnosing rapidly the cause of the illness in cases of
community-acquired pneumonia often delays specific
treatment. This is particularly true for Mycoplasma
pneumoniae pneumonia, in which the clinical and ra-
diologic signs lack specificity, often resulting in delay
or absence of specific and effective therapy. It is un-
known whether delay in treatment results in sequelae.
Some studies have shown that asthma-type bron-
chial illnesses may begin in the years after an episode
of Mycoplasma pneumonia in childhood.4, 5 Many
adults who had pneumonia in childhood can present
⬎20 years later with a restrictive or obstructive syn-
drome.6 However, the series reported tested only pul-
monary volumes and flow as a means of looking for
asthma-like diseases and abnormalities in pulmonary
development. No study has assessed diffusion of gases
in children after pneumonia as a marker of interstitial
damage.
The aim of this study was to evaluate pulmonary
function in children 6 months and 1 year after acute
episodes of community-acquired pneumonia caused by
Streptococcus pneumoniae, viruses or M. pneumoniae.
We used spirometric tests and evaluated gaseous dif-
fusion across the pulmonary parenchyma, by measur-
ing carbon monoxide diffusion (TLCO) after the pneu-
monia had been cured.
PATIENTS AND METHODS
Thirty-five patients with acute pneumonia and who
were examined at Saint Vincent de Paul Hospital
between March, 1992, and October, 1999, were in-
cluded in the study. We excluded from the study all
patients who had had a chronic disease, respiratory or
otherwise, before the acute episode of pneumonia. We
excluded in particular those children who were known
707
to be asthmatic. Age was used as a selection criterion
so that respiratory tests could be performed reproduc-
ibly. Thus only children older than 5 years were in-
cluded. The other selection criterion was the identifi-
cation of the pathogen by blood culture for pneumococci
and by direct immunofluorescence or serologic testing
(increase in serum concentration of specific antibodies
at ⬎3 dilutions for 2 successive samples) for viruses. M.
pneumoniae infection was diagnosed by specific sero-
logic tests, with positive tests for IgM and an increase
in serum concentration of antibodies at more than 3
dilutions at 10-day intervals (Pasteur-Diagnostics-Bio-
Rad Co., Paris, France).
The respiratory tests were conducted 6 to 7 months
after the initial episode by techniques previously re-
ported and validated in children.7–9 Nine patients with
Mycoplasma pneumonia had further evaluation 1 year
after the acute episode and two others were seen after
3 years.
Vital capacity (VC) was determined by spirometry,
and functional residual capacity (FRC) was measured
with the use of helium dilution. TLCO was measured
by a steady state method in which the alveolar gas was
sampled and used for carbon monoxide alveolar pres-
sure determination. Results are expressed as a per-
centage of the normal value for sex and height,
matched to control values previously reported.7–9 The
lower limit for TLCO in our laboratory was set at 80%
of the expected value, as reported by the European
Group for Standardization of Lung Function Tests in
Paediatrics.7 The method was reproducible, with the
differences between two TLCO measurements on suc-
cessive days being ⬍5% of the expected values.
RESULTS
The patients included 13 girls and 22 boys ages 4.5 to
15 years (mean, 7.4 years). All had febrile community-
acquired pneumonia with consolidation on radiograph
or, in 4 cases, localized alveolar infiltrates. Five pa-
tients had positive blood cultures for S. pneumoniae
and 7 patients had parainfluenza III (3 cases), influ-
enza A (2 cases), parainfluenza I (1 patient) and ade-
novirus (1 patient). All 12 of these patients were
hospitalized because of high fever and respiratory
symptoms including 7 cases of hypoxia.
Twenty-three patients had Mycoplasma pneumonia,
but the wide range of severity of the clinical symptoms
often resulted in these patients being treated on an
ambulatory basis.10 Eleven patients were hospitalized,
2 of whom had hypoxia. All 23 patients were treated
with macrolides when the diagnosis of Mycoplasma
infection, which was from 3 to 28 days after the onset of
fever and coughing.10
PNEUMOCOCCAL AND VIRAL PNEUMONIA
For patients with pneumococcal or viral pneumonia,
pulmonary function was normal 6 months after the
708 THE PEDIATRIC INFECTIOUS DISEASE JOURNAL
initial episode. The mean vital capacity was 104%, and
the mean FRC was 105% of the expected value. All
forced expiratory volume in 1 s (FEV1):VC ratios were
⬎90%. TLCO (Fig. 1) was between 83 and 116% of the
expected value.
MYCOPLASMA PNEUMONIA
Spirometric tests provided no evidence of restrictive
syndrome. Mean vital capacity was 102% of the ex-
pected value (range, 85 to 121%). Mean FRC was 109%
of the expected value and four patients had an FRC of
120 to 140% of the expected value. Only 2 of the 23
children had FEV1:VC ratios lower than 80% (76 and
78%, respectively). None of the patients was known to
have had an episode of asthma after the acute pneu-
monia.
TLCO was low, below 80% of the expected value for
sex and height, in 11 of the 23 patients (48%), with
extremes of 39 to 125% (Fig. 1), Ten of these patients
had TLCO ⬍70% of the expected value. Chest radio-
graphs were normal at the time of TLCO measurement
except in 4 cases in which there was a slight blurring of
pulmonary vasculature with no major interstitial syn-
drome. The decrease in TLCO was independent of the
severity of the initial pneumonia and ages and was
found in both ambulatory and hospitalized patients.
The decrease in TLCO appeared to be associated
with a delay in prescribing macrolide therapy and in a
shorter duration of treatment (Table 1). The patients
were treated with macrolides commercially available in
France at the time of examination: josamycin (11
patients); spiramycin (9 patients); erythromycin (2 pa-
tients); and roxithromycin (1 patient). Twelve patients
received macrolides after the clinical failure of beta-
lactam treatment, 2 to 9 days after the onset of fever: 3
of 12 (25%) had a TLCO of ⬍80%. The other 11 patients
were treated late, 11 to 28 days after the onset of fever
and coughing; 8 of 11 (72%) had a TLCO ⬍80% (P ⬍
0.05, chi square with Yates correction).
FIG. 1. Results of TLCO 6 months after acute community-
acquired pneumonia.
Vol. 19, No. 8, August, 2000
TABLE 1. Results of TLCO 6 months after Mycoplasma
pneumonia related to macrolide treatment
Macrolide Treatment
Delay after onset of Total course of
fever treatment
⬎10 ⬎15
⬍10 days ⬍15 days
days days
TLCO ⬎80% 9 3 0 7
TLCO ⬍80% 3 8 7 2
Chi square analysis P ⬍ 0.05 P ⬍ 0.01
For 16 children it was possible to estimate the
duration of macrolide treatment with precision (Table
1). Seven children received macrolide treatment for 7 to
14 days, and in 5 of these children the cough started
again at the end of treatment. All 7 patients had TLCO
⬍80%. In the other 9 children the treatment was taken
for ⬎2 weeks. Only 2 of these 9 children had low TLCO
values (P ⬍ 0.01, chi square with Yates correction). The
type of macrolide used did not seem to affect the result.
The patients with low TLCO were assumed to have
persistent or chronic Mycoplasma infection and were
treated with another course of macrolides 6 months
after the initial episode. Five underwent checkups 6
months later, 1 year after the initial episode. All
showed a partial improvement in TLCO. In two cases
complete normalization above the cutoff value of 80%
did not occur until three years after the initial episode.
Four other patients whose TLCO was normal after 6
months were retested 6 months later, 1 year after the
initial episode. In one case (Patient 2) TLCO had fallen
from 90% to 71% of the expected value.
DISCUSSION
This study shows that 6 months after an acute
community-acquired pneumonia caused by M. pneu-
moniae, one in two patients had abnormal pulmonary
gaseous diffusion as shown by measurement of the
diffusion of carbon monoxide. This decrease in pulmo-
nary diffusion was not associated with any clinical
signs and with minor abnormalities on standard radio-
graphs in rare cases. This decrease in diffusion was the
only abnormality found; neither the flow nor the vol-
ume was affected. No decrease in diffusion was ob-
served in cases of pneumonia of pneumococcal or viral
origin, even if they were severe and resulted in hospi-
talization. The decrease in TLCO was associated only
with delay to macrolide treatment and the short dura-
tion of such treatment.
The transfer of carbon monoxide between alveolar
gas and hemoglobin in lung capillaries is the result of
several processes including diffusion across alveolar
capillary membranes and chemical reactions in capil-
lary blood. The effective interface for gaseous diffusion
is bounded on one side by the alveoli, which are
Vol. 19, No. 8, August, 2000 THE PEDIATRIC INFECTIOUS DISEASE JOURNAL
ventilated, and on the other by the capillary mem-
brane. Hemosiderosis, sarcoidosis, hypersensitivity
pneumonitis, histiocytosis X and malignancies with
interstitial pneumonia are the main causes of intersti-
tial lung diseases in children. In these cases TLCO is
severely affected, with evidence of pulmonary fibrosis
on chest radiographs, small lung volumes and low
arterial oxygen pressure in a high proportion of these
patients. TLCO is low during the acute phases of
Schonlein-Henoch purpura and IgA nephropathy, with
no evidence of interstitial pulmonary involvement and
only minor signs on chest radiographs, possibly result-
ing from the deposition of immune complexes on the
vascular side of the alveolar-capillary membrane.8, 9
In this study we can only speculate on the reasons for
the decrease in TLCO. It was significantly correlated
with a delay and shorter duration of macrolide therapy
which, unlike beta-lactams, are active against Myco-
plasma. There have been several reports in adults of
Mycoplasma pneumonia leading to pulmonary fibrosis.
The patient reported by Tablan and Reyes11 had pul-
monary fibrosis and low TLCO; another patient re-
ported by Koletsky and Weinstein12 had extensive
pulmonary fibrosis. In the series reported by Hallal et
al.13 and Rollins et al.,14 six patients were found to
have pulmonary fibrosis after severe Mycoplasma
pneumonia. Experimental protocols have shown that
in mice, a phase of acute Mycoplasma pneumonia may
lead to a chronic infection.15 Many scientists believe
that Mycoplasma might persist in the respiratory tract
after treatment.16 However, the children in this series
with low TLCO after 6 months showed gradual normal-
ization after a new course of macrolide treatment.
Although presence of immune complexes known in
Mycoplasma infections cannot be excluded, we specu-
late that the delay in treatment and the short duration
of macrolide treatment leads to pulmonary lesions
resulting in the persistence in the alveoli of Myco-
plasma, preventing normal scar tissue formation. Con-
versely in cases of infection with pneumococci and
viruses, even if severe, the pulmonary lesions are
extensive at the start of the illness but heal completely
because of the complete disappearance of the microor-
ganism responsible.
A report by Mok et al.4 showed that respiratory
function sequelae may follow respiratory infections
caused by Mycoplasma. However, the series was het-
erogeneous, including cases of pneumonia and bron-
chial infections and not excluding patients who were
asthmatic before the Mycoplasma infection. Only the
known asthmatics showed bronchial hyperreactivity,
and certain children who were not previously asth-
matic had lower FEV1:forced vital capacity (FVC) ra-
tios on effort. In the study of Sabato et al.5 some
children had, 3 years after Mycoplasma infection, bron-
709
chitis or pneumonia and a low FEV1, and others had
wheezing during the acute infection. In our series two
nonasthmatic children also had slightly lower FEV1:
FVC ratios. However, in these series gaseous diffusion
was not studied. Another major study6 measured pul-
monary function in adults older than 20 years old who
had suffered pneumonia in childhood. Patients who
had had pneumonia in childhood had a lower mean
FVC and FEV1, but with no reduction in the FEV1:FVC
ratio. Thus these patients had a restrictive pulmonary
syndrome without true asthma. The precise cause of
pneumonia for these patients, who were children
younger than the age of 7 years at the time, is not
known but Mycoplasma was probably at the origin of a
certain number. A restrictive syndrome is generally
found in patients with pulmonary fibrosis. Thus it is
possible that Mycoplasma infections are involved in the
genesis of late sequelae. There have been several
reports of isolated clinical cases of major sequelae after
childhood Mycoplasma infection, pulmonary necrosis
and bronchiolitis obliterans in particular, but in these
cases the infection was severe.11, 12, 17–19 Few studies
have focused on the follow-up of apparently banal cases
of Mycoplasma pneumonia, as in our series. A recent
Korean study20 showed that in the years following
Mycoplasma pneumonia, one-third of children had
signs on high resolution computerized tomography
scans including bronchiectasis, mosaic perfusion and
air trapping on expiration.
New studies and longer follow-up are required to
investigate whether Mycoplasma pneumonia in child-
hood can lead to alter pulmonary function in older
children and adults. However, the results of this study
show that late and insufficient treatment with macro-
lides may possibly lead to abnormalities in pulmonary
gaseous diffusion in children with Mycoplasma pneu-
monia. This is particularly important for the manage-
ment of pneumonia in children, which remains largely
empiric in emergency cases because there is currently
no method of rapid diagnosis for reliably identifying
the cause of the illness.
ACKNOWLEDGMENT
This work was supported in part by a scientific grant from
Aventis.
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Copyright © 2000 by Lippincott Williams & Wilkins, Inc.
Absence of a significant interaction between a
Haemophilus influenzae conjugate vaccine
combined with a diphtheria toxoid, tetanus
toxoid and acellular pertussis vaccine in the
same syringe and inactivated polio vaccine
ROBERT S. DAUM, MD, CAROL E. ZENKO, PHD, GILBERT Z. GIVEN, MD, GERARD A. BALLANCO, MD,
HEMENDRA PARIKH, MD, EMMANUEL VIDOR, MD AND XILING LIU, MS
Background. We compared the antibody re-
sponse to Haemophilus influenzae type b capsu-
lar polysaccharide (PRP) after three doses of a
diphtheria toxoid, tetanus toxoid and acellular
Accepted for publication May 3, 2000.
From the Departments of Pediatric Infectious Diseases (RSD,
CEZ, GZG) and Health Studies (XL), The University of Chicago,
Chicago, IL; Department of Pediatrics, Louisiana State Univer-
sity, New Orleans, LA (GAB); Suniti Medical Corp., Merrillville,
IN (HP); and Aventis Pasteur, Swiftwater, PA (EV).
Key words: Combination vaccine, Haemophilus influenzae type
b vaccine, polio vaccine, pertussis vaccine.
Reprints not available.
Vol. 19, No. 8, August, 2000
14. Rollin S, Colby T, Clayton F. Open lung biopsy in Myco-
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capacity after Mycoplasma pneumoniae pneumonia [Abstract
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ogy, 1999.
Vol. 19, No. 8
Printed in U.S.A.
pertussis vaccine (DTaP) combined with a PRP-
tetanus conjugate (PRP-T) in infants randomized
to receive oral polio vaccine (OPV) or inactivated
polio vaccine (IPV). The polio vaccine was given
separately at the same visit.
Methods. Three hundred fifty-six infants from
pediatric practices in suburban Chicago and
New Orleans were randomized into two groups.
Group A received OPV at 2 and 4 months of age;
Group B received IPV at 2 and 4 months of age.
Both groups received DTaP/PRP-T at 2, 4 and 6
months of age and hepatitis B vaccine at 2 and 4
months of age. A serum sample was obtained