The Clinical Respiratory Journal ORIGINAL ARTICLE

Pneumocystis pneumonia in non-HIV children: a 10-year

retrospective study
Chen Ling, Suyun Qian, Quan Wang, Jiansheng Zeng, Xinlei Jia, Jun Liu and Zheng Li
Pediatric Intensive Care Unit, Beijing Children’s Hospital affiliated to Capital Medical University, Beijing, China

Abstract Key words

Background: Pneumocytis pneumonia (PCP) is a life-threatening disease in non- CD4/CD8 ratio – non-HIV – pediatric patients
– pneumocystis pneumonia
HIV infected children. However, there have been few studies that have examined
the clinical characteristics associated with PCP and outcomes for these pediatric
Correspondence
patients. Suyun Qian, MD, PhD, PICU, Beijing Children’s
Objectives: A retrospective review was performed over a 10-year period to evaluate Hospital, No. 56, Nan Li Shi Road, Beijing
the clinical characteristics and outcome of non-HIV children diagnosed with PCP 100045, China.
at Beijing Children’s Hospital in China. Tel: 186-010-59616765
Results: A total of 60 non-HIV children diagnosed with PCP were included in the Fax: 186-010-59718726
study. The overall mortality was 41.7% (25/60). Underlying diseases included con- email: syqian@hotmail.com

nective tissue disease (n 5 23; 38.3%), hematological disease (n 5 14; 23.3%),

Received: 10 October 2015
nephrotic disease (n 5 8; 13.3%) and immunodeficiency disease (n 5 10; 16.7%). Revision requested: 29 January 2016
In all, 26/40 (65.0%) children developed PCP after receiving a follow-up large dose Accepted: 08 February 2016
of glucocorticoid because of recurrent disease. Median time from beginning gluco-
corticoid medication to PCP diagnosis was 245.9 days (range: 14–2100 days). The DOI:10.1111/crj.12467
area under the ROC curve of CD4/CD8 T cell levels for the diagnosis of PCP was
0.902 (95% confidence interval, 0.849–0.955). The analysis rendered an optimum Authorship and contributorship
Suyun Qian designed the study, Jiansheng
cut-off value of 0.715 corresponding to 89.2% sensitivity and 80.4% specificity.
Zeng, Xinlei Jia, Jun Liu, Zheng Li were
Using a multivariate logistic regression model, three parameters were identified as involved in data collection. Chen Ling wrote
significantly associated with mortality: LDH level, mechanical ventilation and co- the manuscript and performed the statistical
infection. analysis. Quan Wang edited the manuscript
Conclusion: The outcome of PCP in non-HIV children remains poor. A critical for scientific content.
stage for PCP development is administration of follow-up glucocorticoid without
prophylaxis. CD4/CD8 ratio is a suitable biomarker for predicting PCP and diag- Ethics
This study was approved by Medical Ethics
nostic of PCP in non-HIV children. Poor prognostic factors include LDH level,
Committee of Beijing Children’s Hospital. Due
need for mechanical ventilation and co-infection.
to the retrospective nature of the study,
informed written consent was waived.
Please cite this paper as: Ling C, Qian S, Wang Q, Zeng J, Jia X, Liu J and Li Z. Patients’ information was anonymized and
Pneumocystis pneumonia in non-HIV children: a 10-year retrospective study. Clin de-identified prior to analysis.
Respir J 2016; 00: 000–000. DOI:10.1111/crj.12467.
Conflict of interest
The authors declare that they have no
conflicts of interest.

Introduction result of glucocorticoid therapy and other immuno-

Pneumocystis pneumonia (PCP), caused by Pneumo-
cystis jirovecii, is a major cause of morbidity and mor-
tality in patients with acquired immunodeficiency
syndrome (AIDS) (1). In recent years, the incidence of
PCP in HIV patients has decreased largely due to the
use of routine prophylaxis in susceptible populations
(1–3). However, PCP has been increasingly reported in
non-HIV patients who are immunocompromised as a
suppressive agents, allogeneic hematopoietic stem cell
transplantation, solid organ transplantation and con-
genital immunodeficiency syndromes (4).
In contrast to PCP infection in HIV patients, non-
HIV patients associated with PCP typically presents
with acute and rapid progressive respiratory deteriora-
tion (4–6). In developing countries, PCP-associated
mortality rates among children continue to be 40% or

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PCP in non-HIV children
higher (7). The prognosis of HIV children with PCP
depends on multiple factors, including degree of
hypoxemia at presentation, need for mechanical venti-
lation and access to medical care (4). However, to the
best of our knowledge, few studies have recorded and
analyzed the clinical characteristics and outcome of
PCP in non-HIV children.
Early appropriate prophylaxis for PCP in non-HIV
patients is crucial. Several published studies have
revealed that the most significant risk factor for PCP in
non-HIV patients is the use of glucocorticoid therapy
(8–10). However, practices of PCP prophylaxis in chil-
dren are mostly extrapolated from studies that have
used adult subjects. The appropriate time-point to
start prophylaxis treatment is still being studied, espe-
cially in non-HIV children receiving glucocorticoid.
Although a variety of serum markers have been stud-
ied for evaluation of PCP in non-HIV adult patients,
few serum markers have been examined in non-HIV
children (5, 11). Data suggest that low peripheral
blood CD4 counts may help identify non-HIV patients
at risk for PCP. However, CD4 counts may be inaccu-
rate in neutrophilic states (5, 10, 12, 13). Some
research reported that CD4/CD8 ratio significantly
decreased when PCP developed (14, 15). We specu-
lated that CD4/CD8 ratio may be a serum marker for
PCP in non-HIV children.
The aims of this retrospective study were to (i)
observe the clinical of characteristics and outcome of
PCP in non-HIV children, (ii) assess the utility of
CD4/CD8 as a marker for initiation of PCP prophy-
laxis in non-HIV children and (iii) identify clinical fac-
tors associated with PCP mortality.
Patients and methods
Study population
We retrospectively evaluated data from children (under
15 years old) who were diagnosed with PCP at Beijing
Children’s Hospital, during the period from 1 January
2005 until 31 December 2014. The diagnosis of PCP
was made via immunofluorescence or Giemsa staining
of P. jirovecii cysts in BAL (bronchoalveolar lavage
fluid). BAL fluids were obtained using fiberoptic bron-
choscopy as follows: after examination of tracheobron-
chial tree, normal saline (20–50 mL) was injected and
20–50 mL aliquots were manually aspirated, usually
from middle lobe or lingula airways. PCP-PCR was
not used as a diagnostic tool.
Inclusion criteria
Six inclusion criteria had to be met by each child
included in this study: (i) the presence of relevant pul-
2 The Clinical Respiratory Journal (2016) • ISSN 1752-6981
Ling et al.
monary symptoms (i.e. cough or dyspnea), (ii) pulmo-
nary infiltration observed by chest radiography or
computed tomography, (iii) detection of P. jiroveci cyst
in the BAL samples, (iv) receipt of antimicrobial
therapy for PJP during hospitalization, (v) negative
HIV tests, (vi) only children with primary infections
were included. The study excluded children with
incomplete medical information.
Data collection
Clinical data collected included the following: general
demographic information, underlying diseases, immu-
nosuppressive therapies, clinical symptomatology, lab-
oratory values and hospital mortality.
Demographical and clinical details were retrieved
from the hospital’s computerized record system. For
each patient, clinical symptoms and time from clinical
onset to diagnosis were recorded.
High dose glucocorticoid was defined as 2 mg/kg/
day for at least 14 days or methylprednisolone pulse
therapy for 3–5 days.
CD4%, CD8% and CD4/CD8 were recorded and the
lowest counts in the two weeks preceding diagnosis
were used for analysis.
PCP was considered the cause of mortality when the
treating physician recorded acute respiratory distress
syndrome (ARDS) or ARF (acute respiratory failure)
as cause of death after PCP was diagnosed within one
month.
In order to identify factors affecting PCP outcome,
laboratory data of survivors were compared with non-
survivors.
Co-infections
If children were on the anti-tuberculosis treatment or
tested strong positive in the purified protein derivative
(PPD) test, we considered it as tuberculosis infection.
If children have thrush, we considered it as Candida
albicans infection.
Microbiological investigations performed on BAL
included Gram’s stain, acid-fast stain and cultures for
conventional bacteria, mycobacteria and fungi. Quan-
titative culture of BAL specimens was used for assaying
conventional bacteria, and the threshold value was
104 colony-forming units (CFU)/mL.
Control group
We selected 120 children who underwent BAL for the
diagnosis of PCP during the study period as control
subjects (Table 1). All of them had the presence of pul-
monary symptoms (i.e. cough or dyspnea) and pulmo-
nary infiltration observed by chest radiography or
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Ling et al. PCP in non-HIV children

Table 1. Demographics characteristics of children with PCP and non-PCP

PCP (n 5 60) non-PCP (n 5 120) P value
Demographics
Age, years 8.45 6 4.80 6.27 6 3.98 0.15
Male, gender 37 79 0.34
Clinical presentation
Cough 49 105 0.21
Dyspnea 10 27 0.16
Fever 50 110 0.07
Chest pain 2 7 0.37
Laboratory results
Neu% 73.23 6 18.26 68.15 6 17.34 0.12
Lym% 20.49 6 15.61 25.97 6 14.32 0.34
Hgb g/L 106.30 6 26.79 107.40 6 17.41 0.43
ALB g/L 33.04 6 6.13 35.12 6 4.21 0.56
LDH u/L 730.08 6 452.63 415.98 6 236.78 <0.05
CRP mg/dL 66.36 6 33.96 57.73 6 29.56 0.21
ESR mm/h 29.39 6 20.90 35.39 6 19.26 0.15
CD4 count cells/uL 203.00 (2.00–1560.00) 405 (76.00–1745.00) <0.05
CD4% 21.72 6 12.58 55.17 6 20.98 <0.05
CD8% 41.12 6 16.14 23.25 6 19.64 0.23
CD4/CD8% 0.53 6 0.44 2.20 6 0.67 <0.05

computed tomography. However, BAL results were
negative for PCP. In order to assess the value of CD4/
CD8 to identify PCP from other pneumonia, we
recorded CD4 count, CD4%, CD8% and CD4/CD8
from all subjects with other pneumopathy (including
bacterial pneumonia, tuberculosis pneumonia, fungal
pneumonia, viral pneumonia).
Statistical analysis
The variables in the dataset were described or summar-
ized by using either median and interquartile range or
number and proportion of the total (%). To determine
the association of independent variables with hospital
mortality, continuous variables were compared using
the Student’s two-tailed t test or non-parametric
Mann–Whitney U-test, in case of non-normal distri-
bution. Chi-square test or Fisher’s exact test, in case of
low expected frequencies, was used for comparisons of
categorical variables. We identified variables as signifi-
cant in the univariate analysis, and they were assessed
as predictors of mortality using logistic regression
analysis. To evaluate the sensitivity and specificity
of serum marker, receiver operating characteristic
(ROC) curves were constructed for CD4/CD8. The
areas under the ROC curves were compared in a
non-parametric approach. All statistical tests were two-
sided, and P < 0.05 as considered statistically signifi-
cant. All data were analyzed with SPSS, version 17 for
Windows statistical software package (SPSS Inc., Chi-
cago, IL).
Result
Part 1: Clinical characteristics of the PCP
pediatric patients
From January 2005 to December 2014, we identified
69 PCP-infected children admitted to our hospital.
None of them were receiving prophylaxis at the time of
diagnosis. Four of them were infected with HIV, thus
excluded from the study. Five subjects were excluded
on the basis of incomplete medical history data. We
recorded demographics, clinical characteristics and
underlying diseases of the remaining 60 non-HIV
PCP-infected pediatric patients (Tables 1 and 2).
A total of 45 (75.0%) of the subjects were receiving
immunosuppressants for their underlying diseases.
Glucocorticoid alone was administered in 16 children
(35.6%), chemotherapeutic agents alone were adminis-
tered in 5 children (11.1%) and glucocorticoids com-
bined with immunosuppressive or chemotherapeutic
agents were administered in 24 children (53.3%). PCP
occurred in 23/40 (57.5%) children after they received
an additional high dose of glucocorticoid because of
recurrent disease; 3/40 (7.5%) when receiving initiated
glucocorticoid treatment; 8/40 (20%) during cortico-
steroid tapering; 6/40 (15%) during low dose mainte-
nance of glucocorticoids. The cumulative dose of
corticosteroid when PCP developed was 239.98 mg/kg

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PCP in non-HIV children Ling et al.

Table 2. Underlying diseases at diagnosis of Pneumocystis
pneumonia
Disease
Connective tissue disease
Juvenile idiopathic arthritis
Systemic lupus erythematosus
Juvenile dermatomyositis
Takayasu’s Arteritis
Wegener’s granulomatosis
Hematological diseases
Acute lymphoid leukemia
Immune thrombocytopenic purpura
Acute myeoodi leukemia
Aplastic anemia
Hemophagocytic syndrome
Allogeneic haematopoietic stem
cell transplantation
Nephrotic disease
Nephrotic syndrome
IgA nephropathy
Immunodeficiency disease
X-linked hyperimmunoglobulin M syndrome
severe combined immunodeficiency
Other
Dermatologic disease
Diabetes mellitus
Surgical operation
tively) in all 60 PCP-infected children compared with
120 non-PCP children, while CD8% was increased
Number of (44.38 6 12.93 vs 27.70 6 13.27, P < 0.05).
patients (%) ROC curves were used to assess the potential utility
23 (38.3) of CD4/CD8 ratio detection in children with PCP. The
7 area under the ROC curve of CD4/CD8 levels for the
5 diagnosis of PCP was 0.902 (95% CI, 0.849–0.955).
5 The analysis rendered an optimum cut-off value of
4 0.715 corresponding to 89.2% sensitivity and 80.4%
2
specificity (Fig. 1).
14 (23.3)
7
3
Part 3. PCP treatment and outcome
1 All the PCP-infected children (n 5 60) were treated with
1 TMP/SMZ when PCP was confirmed. In order to define
1
prognosis factors of PCP, 25 children who died were
1
compared with 35 children who survived (Table 3).
8 (13.3) Age; sex; underlying immune defect and immuno-
6 suppressive drug; the duration between the onset of
2 symptoms and initiation of appropriate treatment;
10 (16.7) ALB, Hb, CRP, CD4 counts; and admittance to
6 PICU were not associated with a poor prognosis.
4 Using a multivariate logistic regression model (Table
5 (8.3)
4), the LDH level, need for mechanical ventilation
3
1
and co-infection were associated with a poor prog-
1 nosis of PCP in non-HIV children.

Discussion
(range, 28–1890 mg/kg). The median time from begin-
ning immunosuppressive medication to PCP diagnosis To the best of our knowledge, this is the first study that
was 245.9 days (range: 14–2100 days). examines PCP in non-HIV children. This retrospective
Laboratory data including lactic dehydrogenase
(LDH), C-reactive protein (CRP), neutrophile percent
(neu%), CD4 counts, CD4%, CD8% and CD4/CD8
ratio were available from all 60 children. LDH
(730.08 6 452.63 m/L), Neu% (73.23 6 18.26), CRP
(66.36 6 33.96 mg/L) were increased during the acute
phase, while CD4 count (203.00 cells/mL; range: 2.00–
1560.00 cells/mL) and CD4/CD8 ratio (0.53 6 0.24)
was decreased.
Co-infections were detected in 26/60 (43.3%) chil-
dren. The results were C. albicans (n 5 11), aspergillus
(n 5 5), tuberculosis (n 5 4), Pseudomonas aeruginosa
(n 5 3), Acinetobacter baumannii (n 5 2) and Esche-
richia coli (n 5 1).
Part 2. Evaluation of CD4/CD8 as a biomarker
for PCP in pediatric patients
We collected CD4%, CD8% and CD4/CD8 ratio from
60 PCP-infected children.
We found that CD4% and CD4/CD8 ratio was sig-
nificantly decreased (17.90 6 6.73 vs 36.39 6 10.45, Figure 1. ROC curve analysis for CD4/CD8 as a marker for
0.53 6 0.24 vs 1.65 6 0.67, P < 0.05, P < 0.001, respec- identify PCP with other pneumonia.

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Ling et al. PCP in non-HIV children

Table 3. Prognosis factors

Parameter (number of children) Dead (n 5 25) Living (n 5 35) P
Age, years 7.74 6 4.76 8.83 6 4.44 0.06
Sex, female 8 15 0.39
Underlying immune defect, n
Hematologic disease 5 (20.0%) 9 (25.7%) 0.61
Connective tissue disease 8 (32.0%) 15 (42.9%) 0.39
Renal disease 2 (8.0%) 6 (17.1%) 0.3
Primary immune deficency disease 7 (28.0%) 3 (8.6%) 0.04
Others 3 (12.0%) 2 (5.7%) 0.38
Immunosuppressive drug, 18 27 0.65
Glucocorticoid alone 8 8 0.431
Chemotherapy alone 3 2 0.385
Combined glucocorticoid 1 chemotherapy 7 17 0.109
Time
glucocorticoid begin to PCP developed, days 273.1 6 132.6 199.6 6 24.4 0.059
Time from onset to initial treatment, days 8.48 6 4.20 5.77 6 2.01 <0.001
Lab test
LDH, U/L 938.90 6 270.17 561.87 6 270.17 <0.001
ALB g/L 33.66 6 5.7 32.26 6 6.7 0.4
Hb g/L 114.39 6 25.37 100.76 6 27.08 0.058
CRP mg/L 78.64 6 65.01 53.61 6 53.12 0.128
CD4 count cells/Ul 165 (2–750) 190 (210–1560) 0.09
Critical care
Mechanical ventilation 25 8 <0.001
Pneumothorax 14 2 <0.001
Coinfection 20 6 <0.001

study describes the clinical characteristics and outcome X-linked hyperimmunoglobulin M syndrome, and four
of non-HIV children with PCP at Beijing Children’s subjects with severe combined immunodeficiency dis-
Hospital from January 2005 to December 2014. ease (SCID). Of the 10 children, 7 died, which indicated
Hematologic malignancies and solid tumors are the that the occurrence of PCP in primary immunodefi-
most common underlying diseases in most of the study ciency children may have a poor prognosis. As such,
for non-HIV PCP-infected adults (3, 16, 17). However, appropriate prophylaxis should be considered in chil-
in our study, almost 2/5 of PCP children had inflam- dren with primary immunodeficiency disease.
matory diseases. This is consistent with the report from Glucocorticoid treatment is a well-known risk factor
Matsumura et al. (10). This may be because PCP pro- for PCP in non-HIV patients, and accounts for
phylaxis is common in hematological malignancies, but 55–97% of published cases (8, 9, 13, 18), and 66.7% in
not in inflammatory diseases, and spectrum of disease our study. The mechanism could be a decrease of
is different in adults compared to children. blood CD41 lymphocyte count due to glucocorticoid
Although primary immunodeficiency disease is a therapy (8). It is noteworthy that the duration of corti-
rare cause of PCP in adults, it occurred in 16.7% non- costeroid use prior to diagnosis of PCP was nearly
HIV children in our study. There were six subjects with 8 months in our study, while it was mostly 4–5 months
in adults (5, 13, 16, 19). During that time, children
often received follow-up large dose of glucocorticoid
Table 4. Multivariate analysis of independent factors
or some additional immunosuppressor because of
associated with mortality
underlying disease relapse. Therefore, routine PCP
Variables Odds ratio OR (95% CI) P value prophylaxis should be strongly considered during this
delay treatment 1.08 0.93–1.47 0.18 critical period.
LDH, U/L 2.57 1.23–6.71 0.04 Time from initiation of glucocorticoid medication
mechanical ventilation 0.96 0.77–1.45 0.04 to PCP diagnosis ranged from 14 to 2100 days. A
Coinfection 2.347 0.19–28.44 0.05 10-year-old boy with chronic idiopathic thrombocyto-
Pneumothorax 1.03 1.15–20.52 0.23
penic purpura (ITP) who received intermittent

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PCP in non-HIV children
glucocorticoid for seven years developed PCP after
another large dose of glucocorticoid administration. A
6-year-old boy with SLE developed PCP in 14 days
after receiving methylprednisolone pulse therapy. As it
reported in recent studies (5, 10), there is a wide range
in the dosage and duration of treatment with glucocor-
ticoid in non-HIV before PCP development range.
Therefore, PCP prevention strategies in non-HIV chil-
dren will require considerations that account for indi-
vidual differences.
The identification of biomarkers that can screen for
PCP risk in non-HIV children will be useful for early
detection of this disease. Herein, CD4 counts were rou-
tinely measured in PCP-infected children, with an
average value of 203.00 cells/mL (range: 2.00–1560.00
cells/mL). Pyrgos et al. suggested that CD4 count below
250 cells/mL was a risk factor for PCP in children (4).
However, CD4 counts >250 cells/mL were not rare in
our PCP cohort. Furthermore, we did not find any dif-
ference in CD4 levels in non-survivors and survivors in
our study (P > 0.05). Our study, therefore, suggests
that CD4 counts may not be a suitable diagnostic and
prognostic marker in PCP infected non-HIV children.
In our cohort, we collected CD4%, CD8% and
CD4/CD8 ratio from 60 PCP-infected children. Their
CD4/CD8 ratio was much lower than in non-PCP chil-
dren. We also assessed the possible utility of CD4/CD8
ratio for identification of non-HIV children at a high
risk of developing PCP. CD4/CD8 ratio was available
in 60 non-HIV children, with a median ratio of
0.53 6 0.24. Our results showed that using a cut-off
value of 0.715, the CD4/CD8 enabled PCP to be distin-
guished from other pneumonia with an AUC of 0.902
and an optimized sensitivity of 89.2% and specificity
of 80.4%. We also found CD4/CD8 ratio decreased in
all infants younger than 1 year of age. Thus, the value
of the CD4/CD8 ratio is a suitable marker for predic-
tion and diagnosis of PCP in non-HIV children.
To the best of our knowledge, mortality rate of PCP
in non-HIV children has not been reported. In our
study, the mortality rate was 41.7%, which was similar
to previous studies in non-HIV adults (17, 20–22).
This indicates that PCP is also a life-threatening infec-
tion in non-HIV children and there is a need for more
effective treatment to decrease its mortality. Our analy-
sis determined that mortality was independently asso-
ciated with need for mechanical ventilation, LDH and
co-infection.
Time from onset to initial treatment has previously
been identified as a poor prognostic factor of PCP, and
there is a need for early intervention in order to
improve survival (20, 21). However, when using multi-
variate analysis, our study did not detect any difference
6 The Clinical Respiratory Journal (2016) • ISSN 1752-6981
Ling et al.
in time from onset to initial treatment between non-
survivors and survivors.
Increased LDH level is likely correlated with wide-
spread tissue damage in PCP (11). Wide tissue dam-
age reflects the severity of the illness. As previously
reported, high LDH levels should be regarded as a
predictor of outcome in non-HIV children with PCP
(5, 11).
Co-infection may reflect that children with PCP
infection often have a low immune function caused by
both underlying disease and immunosuppressive med-
ications, which increases their risk for developing a
variety of infections. We observed a high proportion of
subjects had co-infections (43.3%), with the most
common being C. albicans, tuberculosis and aspergillus.
Non-HIV patients with PCP often develop fungal
infections (10, 22). We found 13 non-HIV children
with fungal infections (C. albicans and aspergillus). C.
albicans infection rate reported here was higher than in
other studies in adults (8–10). Co-infection should be
considered when there is a poor treatment response to
PCP therapy in non-HIV children.
The need for mechanical ventilation was a poor
prognostic factor in our study. Compared to HIV
patients with PCP, non-HIV patients are more prone
to ventilator-associated lung injury and the injury is
also more severe (6, 9, 17). In order to correct
hypoxia, ventilator parameters are generally high.
This often leads to ventilator-associated lung injury
(23). In our study, we used high frequency oscilla-
tory ventilation (HFOV) in seven subjects, and
unfortunately, all of them died. Thus, we believe that
mechanical ventilation is a problem in PCP-infected
children. Additional studies are required to improve
protective lung ventilation strategies for this popula-
tion. Pneumothorax is an unsolved problem in PCP
at present. For adults, incidence of pneumothorax
ranges from 4% to 36% (5, 6, 17, 24). In our study,
pneumothorax rate was 26.7%. Nearly all of the
non-HIV children who developed pneumothorax
died. The combination of PCP-related lung injury
and ventilator-associated lung injury may explain
the high occurrence rate in this cohort.
This study has a number of limitations. First, retro-
spective studies, such as this, rely on existing patient
records that were collected for medical reasons other
than research, and when specific information is absent,
it is difficult to resolve. Fortunately, most variables in
our study were the required items in the medical
records. Second, the follow-up beyond 30 days was not
recorded, which does not allow an accurate prediction
of long-term mortality.
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Ling et al.
Conclusion
Our data suggests that PCP in non-HIV children is a
serious illness with high mortality. Routine PCP pro-
phylaxis should be strongly considered in children who
receive additional large doses of glucocorticoid. Our
study suggests that CD4/CD8 ratio may be a suitable
biomarker for the prediction and diagnosis of PCP in
non-HIV children. Poor prognostic features include
increased lactate dehydrogenase levels, the presence of
co-infections and the use of mechanical ventilation.
Acknowledgement
None of the authors have a conflict of interest to dis-
close or a financial relationship with a commercial
entity that has an interest in the subject matter pre-
sented in this manuscript.
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