ORIGINAL PAPERS

ORIGINAL PAPERS
Adv Clin Exp Med 2009, 18, 5, 487–492
ISSN 1230−025X
© Copyright by Wroclaw Medical University
BEATA MĄCZYŃSKA1, ALEKSANDRA SKRZYPEK2, URSZULA KASPRZYKOWSKA1,
MONIKA MORAWSKA−KOCHMAN2, MARIA ZALESSKA−KRĘCICKA2, ADRIANA JANCZURA1,
ADAM JUNKA1, MARZENNA BARTOSZEWICZ1
Investigation of Mycoplasma pneumoniae
in the Upper Respiratory Tracts
of Children Operated for Adenoid Hypertrophy
Badanie występowania Mycoplasma pneumoniae
w górnych drogach oddechowych u dzieci operowanych
z powodu przerostu migdałka gardłowego
1
2
Department of Microbiology, Wrocław Medical University, Poland
Department of Otolaryngology, Wrocław Medical University, Poland
Abstract
Background. Mycoplasma pneumoniae is responsible for 18–25% of atypical pneumonia. It is considered to cause
acute and chronic upper respiratory tract infections, otitis media, and sinusitis, but there are few literature reports
on this subject.
Objectives. Determination of the possible role of M. pneumoniae in the pathogenesis of adenoid hypertrophy in
children, antibody dynamics in serum during Mycoplasma infection development, and the most useful methods to
detect the pathogen for the routine diagnostics of M. pneumoniae.
Material and Methods. The study group included 40 children in two age groups (3–6 and 7–14 years old) with
clinically proven adenoid hypertrophy. Adenoid tissue to determine M. pneumoniae antigen, pharyngeal swab to
determine carrier status, and blood serum to determine IgG and IgM specific antibodies were collected. PCR was
used to detect specific M. pneumoniae DNA fragments and enzymatic immunoassay to determine IgG and IgM
antibodies.
Results. There was no Mycoplasma DNA in the adenoid tissues and swabs of the patients. Serological tests were
98% negative. IgG antibodies were found in 3 cases and IgM in 1.
Conclusions. M. pneumoniae is not a pathogenic factor of adenoid hypertrophy. PCR analysis together with
immunological tests makes M. pneumoniae diagnostics more sensitive (Adv Clin Exp Med 2009, 18, 5, 487–492).
Key words: adenoid hypertrophy, Mycoplasma pneumoniae, PCR, enzymatic immunoassay.
Streszczenie
Wprowadzenie. Mycoplasma pneumoniae jest odpowiedzialna za 18–25% zapaleń płuc, które określa się mianem
atypowych. Uznaje się udział Mycoplasma pneumoniae także w ostrych i przewlekłych nieżytach górnych dróg od−
dechowych, zapaleniu ucha środkowego i zatok obocznych nosa, doniesień na ten temat jest jednak niewiele.
Cel pracy. Określenie możliwej roli Mycoplasma pneumoniae w przeroście migdałka gardłowego u dzieci, zbada−
nie dynamiki przeciwciał powstających w surowicy w czasie rozwoju zakażeń mikoplazmowych oraz określenie
metod wykrywania patogenu najbardziej przydatnych w rutynowej diagnostyce Mycoplasma pneumoniae.
Materiał i metody. Badanie przeprowadzono na 40 dzieciach w dwóch grupach wiekowych: 3–6−latków oraz
7–14−latków, u których stwierdzono przerost migdałka gardłowego. Pobrano następujące materiały diagnostyczne:
tkankę migdałka (określenie występowania antygenu M pneumoniae), wymaz z gardła (określenie nosicielstwa),
osocze krwi (określenie występowania swoistych przeciwciał klas IgG oraz IgM). Użyto następujących metod:
PCR (wykrycie swoistych fragmentów DNA M. pneumoniae) oraz metody immunoenzymatycznej (oszacowanie
występowania swoistych przeciwciał klasy IgG oraz IgM).
Wyniki. Badanie obecności DNA Mycoplasma pneumoniae metodą PCR w grupie badanej dało we wszystkich
przypadkach wynik negatywny. W przypadku oznaczeń serologicznych (98% badanych) otrzymano wyniki ujem−
ne w obydwu klasach przeciwciał. Przeciwciała klasy IgG wykryto u 3 pacjentów, a klasy IgM u jednego.
488
B. MĄCZYŃSKA et al.
Wnioski. M. pneumoniae nie jest czynnikiem chorobotwórczym w przeroście migdałka gardłowego u dzieci. Po−
łączenie testu PCR z badaniami immunologicznymi w diagnostyce M. pneumoniae skutkuje jej zwiększoną czu−
łością (Adv Clin Exp Med 2009, 18, 5, 487–492).
Słowa kluczowe: przerost migdałka gardłowego, M. pneumoniae, PCR, metoda immunoenzymatyczna.
Trials conducted at the different centers
demonstrated that Mycoplasma pneumoniae is
responsible for 18–25% of atypical pneumonias [3].
M. pneumoniae can also be responsible for acute
infections of the upper respiratory tract, otitis
media, and sinusitis, although there are only a few
reports about this [11]. M. pneumoniae infection is
characterized by a great diversity of clinical mani−
festations, from poorly symptomatic diseases of
the upper respiratory tract (pharyngitis, laryngitis,
and tracheitis), to bronchitis and bronchiolitis, to
severe pneumonia. About 20% of infections
caused by M. pneumoniae progress asymptomati−
cally, possibly as reinfections [4, 5]. The begin−
ning of the infection is gradual and the casual
symptoms are body temperature subfebrile or
around 38°C, dry cough, headache, sore throat,
general weakness, and poor disposition [4].
Complications such as meningitis, myocarditis
with associated hemolytic anemia, liver and spleen
enlargement, increased bilirubin level, and a sig−
nificant decrease in hemoglobin level and red cell
count occur in ca. 25% of patients [18]. Symptoms
other than pulmonary are connected with joints,
the digestive tract, skin, and kidneys [5].
The presence and possibility of M. pneumoniae
colonization of the nasal−pharyngeal cavity and
subsequently high IgG antibody titer is still open
to question. Some authors suggest a possible role
of M. pneumoniae antigens in pharyngeal adenoid
lymphocyte activation. The diverse clinical picture
of the infection, the specific character of M. pneu−
moniae bacteria, and difficulties interpreting sero−
logical tests often lead to misrecognition of the eti−
ological factor of disease. The main aim of this
study was to investigate the possible role of
M. pneumoniae in adenoid hyperthrophy in children,
determine antibody dynamics in serum during the
development of Mycoplasma infection, and assess
the most useful methods of detecting the pathogen
for the routine diagnostics of M. pneumoniae.
Material and Methods
The study included 40 children in two age
groups (3–6 and 7–14 years old) with clinically
proven pathological hypertrophy and who under−
went adenoidectomy. The diagnostic materials col−
lected were adenoid tissue to determine M. pneu−
moniae antigen, pharyngeal swabs to determine
carrier status, and blood serum to determine spe−
cific IgG and IgM antibodies. A control group con−
sisting of 22 ambulatory patients with chronic
cough and upper respiratory tract infections was
tested at the Microbiological Laboratory of the
Department of Microbiology, Wroclaw Medical
University, using blood serum (for specific IgG
and IgM antibodies) and pharyngeal swabs (for
M. pneumoniae antigen).
The first stage of the study used polymerase
chain reaction (PCR) to determine the frequency
of M. pneumoniae antigen in the adenoid tissue
and pharyngeal swabs taken from the children who
had had adenoidectomy and the control group
(swabs only). The second stage used enzymatic
immunoassay to detect antibodies in blood serum
from both groups directed against M. pneumoniae
IgG and IgM. Genetic material was obtained from
the adenoid tissue using a QIAamp DNA Mini Kit
(Qiagen, Germany) and from the pharyngeal
swabs using a SWAB isolation kit (A&A Bio−
technology, Poland). The genetic material was
amplified in a PTC−200 termocycler (MJ Research)
using a commercial PCR test (Venor®Mp, Minerva−
Biolabs) according to the producer’s instructions.
The sensitivity and specificity of this test had been
validated in an earlier study on a group of children
with diagnosed atypical pneumonia [14]. The
amplification products were analyzed by agarose
electrophoresis (2%, TAE, 96 V, 1 h). IgG and IgM
antibodies from both groups of patients were
detected directly by commercial tests (Platelia®
Mycoplasma pneumoniae IgM TMB, Platelia®
Mycoplasma pneumoniae IgG TMB) according to
the producer’s instructions (BIO−RAD, Poland).
Results
No M. pneumoniae antigen was detected by
PCR in the study group or M. pneumoniae DNA in
the adenoid tissue samples or pharyngeal swabs
from the group of children who had had ade−
noidectomy. Negative results were also obtained
for both classes of antibodies in the serological
tests. The level of IgG antibodies was medium in
one sample and low in two others, which showed
only a trace of past infection. IgM antibodies were
detected in only one sample, but PCR did not
detect M. pneumoniae DNA presence.
489
Mycoplasma pneumoniae and Adenoid Hypertrophy
Because of the negative results in the samples
from the patients with removed adenoid, a parallel
analysis was performed in the control group to
verify the Minerva−Biolabs PCR test and to deter−
mine antigen and antibody occurrence in these
patients with upper respiratory tract infections. In
one case, a positive PCR result was obtained with
concurrent positive serological results for IgG and
IgM antibodies. In this example, M. pneumoniae
was considered a cause of the upper respiratory
tract infection in this patient (Figs. 1, 2). In rest of
the control patients, no M. pneumoniae DNA was
detected in the pharyngeal swabs. The serological
tests detected a high titer of IgG antibodies in one
patient with concurrent IgM antibody presence,
but no antigen was detected by PCR. In 13 other
patients, only IgG antibodies were detected (with
no IgM antigen) and their level was estimated to
be medium or low (Fig. 3).
3%
8%
89%
brak przeciwcia³
œrednie miano
niskie miano
Fig. 2. Percentage of positive results for IgG antibod−
ies in the children who had had adenoidectomy
Ryc. 2. Odsetek próbek dodatnich w kierunku przeci−
wciał IgG w grupie dzieci po adenotomii
5%
Discussion
95%
Children’s respiratory tract infections are
mainly caused by viruses and bacteria. Six bacter−
ial pathogens are considered to cause 90% of doc−
umented bacterial pneumonias, these being Strep−
tococcus pneumoniae, Haemophilus influenzae,
1
2
3
4
5
6
obecnoϾ DNA M. pneumoniae
brak DNA M. pneumoniae
Fig. 3. Percentage of positive PCR results for
Mycoplasma pneumoniae DNA in the control group
Ryc. 3. Procent wyników dodatnich w kierunku DNA
Mycoplasma pneumoniae otrzymanych metodą PCR
w grupie kontrolnej
9%
5%
28%
58%
Fig. 1. Electrophoretic discrimination of DNA amplifi−
cation products of patients of the control group. Lanes:
1 – molecular mass marker pBR322 Dna/AluI Marker,
20 Fermentas, 2–4 – negative results, 5 – positive
result (product size: 270 bp), 6 – positive control
Ryc. 1. Elektroforetyczny rozdział produktów ampli−
fikacji DNA pacjentów grupy kontrolnej. Ścieżki:
1 – marker wagowy pBR322 Dna/AluI Marker, 20
Fermentas, 2–4 – próby ujemne, 5 – próbka dodatnia
(produkt 207 pz), 6 – badanie kontrolne dodatnie
Staphylococcus aureus, and, causing atypical
pneumonia, Mycoplasma pneumoniae, Chlamydia
pneumoniae, and Legionella pneumophila. M. pneu−
brak przeciwcia³
œrednie miano
niskie miano
wysokie miano
Fig. 4. Percentage of positive results for IgG antibod−
ies in the control group
Ryc. 4. Procent próbek dodatnich w kierunku przeciw−
ciał IgG w grupie kontrolnej
moniae is responsible for upper respiratory tract
infection and pneumonia. These infections involve
children more than adults. The role of this
pathogen in bronchitis and upper respiratory tract
infection is still weakly documented. It is known
that M. pneumoniae takes part in bronchiolitis, tra−
cheitis, pharyngitis, otitis, and sinusitis, but very
little is known about the frequency of such infec−
490
tions. This is because of the very diverse clinical
picture, difficulties in isolating the pathogen, and
interpretation of the serological results, which
often leads to discontinuing microbiological tests
and misrecognition of the etiological factor. The
best confirmation of current infection is isolation
of the pathogen, but the specific character of this
bacterium and its special culture requirements
result in obtaining results too late to be useful in
diagnostics and medical treatment. Infections
caused by M. pneumoniae are currently diagnosed
mostly with serological tests such as ELISA or
indirect fluorescent antibody tests and molecular
biological techniques based on PCR. Because of
the wide spectrum of infection caused by M. pneu−
moniae and because of reports suggesting a prob−
able role of Mycoplasma antigens in the in vitro
activation of lymphocytes from the adenoid [6, 8],
determining the role of Mycoplasma in pathologi−
cal adenoid hypertrophy of children appeared
interesting; thus this attempt, never conducted in
Poland before, to detect Mycoplasma DNA in
removed (because of the clinical indications)
hypertrophied adenoids.
The adenoid is an element of the Waldeyer
ring, a cluster of lymphoid tissue on the border
between the ectodermal and endodermal parts of
the respiratory and alimentary tracts. Because of
its location, the tissue is in constant contact with
the external environment. Different kinds of anti−
gens can penetrate to this tissue, gradually activat−
ing lympho−epithelial organs and shaping resis−
tance mechanisms. Different factors, such as rein−
fection, can affect the growth of the adenoid.
Pathological adenoid hypertrophy can cause
impairment or obstruction of the Eustachian tubes,
disturbing middle ear ventilation, which is a factor
predisposing to exudative otitis which can result in
recurrent pharyngitis and lower respiratory tract
infections. Literature reports emphasize a probable
role of Mycoplasma antigens in lymphocyte acti−
vation. Trials by Morgesen et al. showed that lym−
phocytes obtained from the pharyngeal adenoid
and the blood of children with current or recent
M. pneumoniae infection incorporate thymidine at
a significantly higher level than analogous lym−
phocytes of children from a control group and sug−
gested that infection is expressed mainly in lym−
phocytes obtained from the adenoid [15]. Huminer
et al., investigating the presence of Mycoplasma
and Chlamydia in children after adenoidectomy
and tonsillectomy, confirmed the presence of
Mycoplasma bacteria in patients with relapsing
infections of the palatine tonsil and adenoid [9].
That is why further investigations on the presence
of Mycoplasma in the adenoid should proceed.
Biberfeld et al. indicated an activating influence of
B. MĄCZYŃSKA et al.
M. fermentas on lymphocytes from the peripheral
blood, adenoid, and spleen [2]. Moreover, lym−
phocytic subpopulations were activated in differ−
ent ways. Other experiments of this group showed
a stimulating influence of M. pneumoniae on
human lymphocyte subpopulations (mainly B lym−
phocytes from the adenoid) [1].
Investigations of M. pneumoniae presence in
the adenoid seem to be crucial because of reports
suggesting a role of this pathogen in coronary
heart disease, arthritis in children and youth, peri−
carditis, myocarditis, and hemolytic anemia [3].
Therefore the possibility of adenoid colonization
by M. pneumoniae was analyzed to find possible
correlation between its presence and increased
adenoid lymphocyte activation. However, the tri−
als did not confirm this hypothesis. There was no
M. pneumoniae DNA in any of the patients’ ade−
noid tissue obtained from adenoidectomy. Of
course, this does not exclude the possibility of
M. pneumoniae adenoid infection or the need for
continuing such trials.
The patients were a relatively small group (the
number of samples was limited by the number of
adenoidectomies performed). This pathogen was
probably not the main and direct cause of the ade−
noid hypertrophy typical in many children. Open
to question is also the colonization of the nasal−
pharyngeal cave by M. pneumoniae and the pres−
ence of a high titer of IgG antibodies in the serum.
Therefore a pharyngeal swab was taken from all
the children who had had adenoidectomy to isolate
M. pneumoniae DNA using PCR. The lack of pos−
itive PCR results suggested creating the control
group to verify the method. In just one sample
from this group was the PCR result positive,
which confirmed the reliability of the commercial
test, especially in that the antibody tests showed
very high titers of both classes of antibodies,
which suggests active infection rather than carrier
status.
In the literature there are several studies con−
cerning pneumonias caused by M. pneumoniae,
but there are only a few publications concerning
infections of the upper respiratory tract. Layani−
Milon et al. carried out nose swab tests for five
successive years in the winter in 3897 patients
with acute respiratory infection (ARI). They
obtained positive results in 7.3% of the patients.
The differences in the detection of M. pneumoniae
in individual years fluctuated between 10 and 2%
[10], which is the result of epidemic waves every
4–5 years. Similar trials were conducted by
Dorego−Zetsma et al. in 1172 patients with ARI.
Swabs from the throat and nose were investigated
with the use of PCR. M. pneumoniae was con−
firmed in only 39 (3.3%) patients [7]. Both studies
Mycoplasma pneumoniae and Adenoid Hypertrophy
were performed to determine carrier status fre−
quency in humans. According to the definition,
a carrier is an individual without clinical symp−
toms who, after symptomatic or asymptomatic
infection, possibly because of the specific compo−
sition of his bacterial flora, constantly or periodi−
cally excretes pathogenic microorganisms, which
leads to the infection of other individuals. Patients
in both groups suffered from respiratory tract
infections. It is hard to describe patients with
M. pneumoniae presence as carriers with total cer−
tainty, which is why the results of these studies are
not fully reliable, in contrast to those of Palma et
al. [17], in which a trial was conducted in a group
of 185 healthy children to estimate the level of
M. pneumoniae carrier status. Pharyngeal swabs
were used and the children were divided into two
age groups. M. pneumoniae was detected in 2/105
of examples in the age group of 1–4 years (1.9%)
and 2/80 of examples in the group of 5–14 (2.5%).
Together, carrier status was detected in 2.16% of
the samples [17]. One can therefore regard
M. pneumoniae carrier status as rather sporadic.
Trials conducted in subsequent studies fully
confirmed these results. In the pharyngeal swabs
of the group of 40 children of the present study
who had had adenoidectomy there was no example
of M. pneumoniae antigen presence which would
give evidence of carrier status. In the control
group, ambulatory patients with acute upper respi−
ratory tract infections, the percentage of positive
results was 4.5% (1 sample). Of course, this group
was too small to treat this result as reliable, but it
confirms investigations of the earlier mentioned
researchers and indicates that M. pneumoniae is
not often an etiological factor of upper respiratory
tract infections, in the contrast to pneumonia
occurring outside the hospital, where the frequen−
cy of this pathogen is high [6, 7, 10, 12, 17].
A distinct problem is serological tests, which
can be difficult to use in the case of Mycoplasma
infection. Serology is the most often used method
in the diagnostics of infections caused by M. pneu−
moniae. Many authors note differences in detect−
ing anti−M. pneumoniae antibodies when different
serological enzymatic immunoassays are used
[13, 20]. The reliability of these tests depends to
a large degree on the antigen used, the number of
controls, and the calibrators [13, 14]. Against this
background, the Platelia test seems to display high
specificity and sensitivity, although its results are
also sometimes ambiguous. When interpreting the
test, many factors, such as disease stage, time
since the appearance of clinical symptoms, patient
age, and associated diseases, should be evaluated.
Using ELISA to determine at least two classes of
antibodies (IgM and IgG) allows the detection of
491
Mycoplasma infection during the time of the ill−
ness, with no necessity of repeating the serological
test upon recovery. However, with low antibody
titers, testing serum is necessary after two weeks.
The problem of M. pneumonia diagnostics is
crucial in the case of pneumonia in small children
because of the need for immediate, directed treat−
ment. Waris et al. stated that during acute infec−
tion, a combination of PCR, which detects the
presence of M. pneumoniae DNA isolated from
pharyngeal swabs, and serological ELISA increas−
es the sensitivity of diagnostics to 95%. At the
same time, these authors considered the determi−
nation of specific IgM antibodies using ELISA the
most valuable of the uncoupled tests. A combina−
tion of serological tests with PCR for antigen pres−
ence also allows an interpretation of the intensity
and stage of infection, so this combination can be
treated as a “gold standard” of M. pneumoniae
diagnostics. The results of the present study also
indicated this. In the group of 40 children, pres−
ence of IgM antibodies was detected with simulta−
neous lack of M. pneumoniae DNA in the clinical
materials (pharyngeal swabs, adenoid tissue).
The presence of IgM antibodies as a marker of
current Mycoplasma infection in children is
proven and emphasized in many publications [8,
13, 16], although there is the opinion that IgM
antibodies can be detected in patients’ blood
serum for a very long time, which can be treated as
a limitation of serological diagnostics. The result
could then be treated as a current M. pneumoniae
infection, which is denied by the lack of antigen
presence in PCR. In the tested group there was no
example of a significant titer of IgG antibodies,
but in 4 samples the titer was estimated as medium
or low. Presence of IgG antibodies against
M. pneumoniae can be detected for many months
in a convalescent’s blood serum, so it cannot be
treated as a marker of current infection and is use−
ful rather for epidemiological purposes. However,
in clinical diagnostics, results are often hard to
interpret. In the present study, concurrent testing
of pharyngeal swabs and adenoid tissue with the
use of PCR (where negative results were obtained)
permits omitting a second serum test and allows
a more certain interpretation. There was a similar
situation in the control group; in one sample a pos−
itive PCR result was obtained and for this patient
significant titers of both antibodies were also
detected. In that case, the interpretation was rather
unambiguous. In the patients with negative PCR
results and concurrent lack of IgM antibodies, the
presence of IgG antibodies was confirmed in
13 examples as of a low or medium level, which
suggests past infection or reinfection, similarly to
the tested group. In any event, the results confirm
492
B. MĄCZYŃSKA et al.
the thesis that the PCR result makes the serolog−
ical test and the clinical diagnostics of patients
easier.
These results indicate that pathologically
hypertrophied adenoid seems to have no correla−
tion with M. pneumonie infection, but the results
are still not decisive because of the small number
of samples and the lack of analogous experiments
conducted by other researchers. The adenoids are
a unique material obtained by an invasive surgical
method. Obtaining 40 pathologically hypertro−
phied adenoids in such a short time was not easy.
To exclude possible Mycoplasma infection from
the etiopathogenesis of adenoid hypertrophy, fur−
ther research on a larger number of patients should
be conducted.
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Address for correspondence:
Beata Mączyńska
Sielska 19a
54−144 Wrocław
Poland
Tel.: +48 71 784 13 01
E−mail: [email protected]
Conflict of interest: None declared
Received: 13.01.2009
Revised: 5.08.2009
Accepted: 29.09.2009