MAJOR ARTICLE

Tropical Pulmonary Eosinophilia: A Case Series

in a Setting of Nonendemicity
Andrea K. Boggild,1 Jay S. Keystone,1,3 and Kevin C. Kain1,2,3
1
Faculty of Medicine and 2McLaughlin-Rotman Center for Global Health, McLaughlin Center for Molecular Medicine, University of Toronto,
and 3Tropical Disease Unit, Division of Infectious Diseases, Department of Medicine, UHN–Toronto General Hospital, Toronto, Ontario, Canada

Background. Tropical pulmonary eosinophilia (TPE) is a rare but serious manifestation of infection with the
lymphatic filarial parasites Wuchereria bancrofti and Brugia malayi. Although endemicity is limited to the tropical
and subtropical regions of Africa, South America, and Asia, immigration and travel practices have led to the
diagnosis of TPE in areas of nonendemicity.

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Methods. We herein present a case series of all patients with TPE who presented to the Toronto General
Hospital during 1990–2003.
Results. Seventeen individuals presented with TPE during the study period, and all were of South Asian
ancestry. All 17 received an incorrect diagnosis at presentation (median number of consultations before diagnosis,
2), the most frequent of which was asthma (76%). Eosinophil count, serum immunoglobulin E levels, and anti-
filarial antibody titers were elevated in all patients. Ten of 14 patients had an abnormal chest radiograph finding,
and 11 of 12 patients had abnormal results of pulmonary function tests.
Conclusions. TPE is an important diagnostic consideration in patients with eosinophilia, respiratory symptoms,
and history of exposure to this disease. In the untreated individual, TPE can lead to chronic and progressive
respiratory compromise and death. Prompt recognition and treatment with diethylcarbamazine is therefore key
to minimizing morbidity and mortality.

Tropical pulmonary eosinophilia (TPE) is one of a
number of syndromes characterized by pulmonary in-
filtrates and peripheral eosinophilia. TPE is a variant
of filariasis that results from a hypersensitivity response
to the microfilariae of the lymphatic-dwelling parasites,
Wuchereria bancrofti and Brugia malayi [1, 2]. Lym-
phatic filariasis is transmitted by mosquitoes and is
endemic in many of the tropical and subtropical areas
of South America, Africa, Asia, and Oceania [1–3]. Ap-
proximately 70% of infections are concentrated in In-
dia, Nigeria, Bangladesh, and Indonesia, and world-
wide, more than 1 billion people are at risk of acquiring
lymphatic filariasis [4]. The global epidemiological
characteristics of lymphatic filariasis have been altered
by the implementation of the Global Program to Elim-
inate Lymphatic Filariasis, a public-private partnership
Received 9 March 2004; accepted 20 May 2004; electronically published 27
September 2004.
Reprints or correspondence: Dr. Kevin C. Kain, Toronto General Hospital, 200
Elizabeth St., ES-9-412, Toronto, ON M5G 2C4.
Clinical Infectious Diseases 2004; 39:1123–8
 2004 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2004/3908-0004$15.00
initiated in 1998. The regular, mass administration of
ivermectin with diethylcarbamazine or albendazole has
resulted in the treatment of millions of at-risk individ-
uals [4]. In 2002, 80 million residents of 34 countries
were treated, with coverage ranging from !5% (Nigeria,
India, Yemen, and Indonesia) to 195% of at-risk in-
dividuals (Zanzibar, Tanzania, Egypt, Guyana, Cook Is-
lands, French Polynesia, and Samoa) [4].
Although 130 million people are infected with lym-
phatic filariasis worldwide, !0.5% of these infections
manifest as TPE [1, 2]. The predisposing factors for the
development of TPE are not well understood, although
there is evidence that host immune response to a filarial
antigen, g-glutamyl transpeptidase (gGT), confers an
increased risk of developing TPE [5]. Elevated levels
of gGT IgG1 and IgE antibodies are overrepresented
among individuals with TPE, compared with persons
who have other forms of lymphatic filariasis [5]. The
differential antibody response has been postulated to
play a role in the type of pulmonary inflammation that
is characteristic of TPE [5].
Although few cases of TPE are recognized in regions
of nonendemicity [6–9], with increasing global travel
and immigration, TPE is an important diagnosis to

Tropical Pulmonary Eosinophilia • CID 2004:39 (15 October) • 1123

consider in patients with an appropriate clinical presentation
and exposure history. Although TPE typically has a nonspecific
presentation and may mimic a number of conditions, it is most
often misdiagnosed as asthma because of pulmonary manifes-
tations, such as paroxysmal cough and dyspnea [10–13]. Other
commonly reported symptoms include malaise, fever, and
weight loss [10]. Rapid amelioration of signs and symptoms
with diethylcarbamazine treatment is a hallmark of TPE. Al-
though the clinical response to diethylcarbamazine is often
marked, many patients are left with mild residual pulmonary
disease following treatment [14]. Progressive pulmonary fibro-
sis and, ultimately, respiratory failure are the inevitable sequelae
of untreated TPE.
The purpose of this study was to characterize the clinical
presentation and diagnosis of TPE and to identify barriers to
the recognition of this disease in countries in which the disease
is not endemic. We present a series of 17 patients with tropical
pulmonary eosinophilia in Toronto and describe the demo-
graphic characteristics, clinical presentation, and outcome of
this syndrome. The cases we present typify the clinical spectrum
of TPE, including the potential for adverse outcomes in cases
of delayed diagnosis and treatment.
METHODS
The study was a retrospective case series. Charts of all patients
with a diagnosis of TPE who presented to the Tropical Disease
Unit (TDU) at Toronto General Hospital during 1990–2003
were reviewed for prospectively established variables of interest.
The diagnosis of TPE was based on the following clinical and
laboratory criteria: (1) clinical history supportive of exposure
to lymphatic filariasis, (2) peripheral eosinophilia (eosinophil
count, 13 ⫻ 10 9 eosinophils/L), (3) elevated serum IgE levels
(11000 IU/mL; normal range, 0–380 IU/mL), (4) increased
titers of anti-filarial antibodies, (5) peripheral blood specimen
that tested negative for microfilariae, and (6) clinical response
to diethylcarbamazine. Demographic, clinical, and laboratory
data were extracted from the charts onto a standardized data
form and entered into an Excel spreadsheet (Microsoft). De-
scriptive statistics were performed by means of SigmaStat soft-
ware, version 2.03 (SPSS). This study was approved by the
Research Ethics Board of Toronto General Hospital.
Serum specimens were tested for filaria antibodies by the
Laboratory of Parasitic Diseases at the National Institutes of
Health National Institute of Allergy and Infectious Diseases
(Bethesda, MD). During the course of the study period, testing
for anti-filarial antibodies was standardized, and presentation
of data changed from antibody titers (negative titer, !1:32) to
mg/mL of IgG antibodies (as determined by an enzyme im-
munoassay). An anti-filarial antibody concentration 113.0 mg/
mL was considered to be a positive result. A negative titer or
1124 • CID 2004:39 (15 October) • Boggild et al.
concentration of anti-filarial antibody was considered to be
indicative of a low likelihood of filarial infection.
RESULTS
During the study period, 17 patients received a diagnosis of
TPE. We present several illustrative cases that reflect the spec-
trums of the disease and the clinical presentations.
Patient 1. A 29-year-old man from India presented with
a 2-month history of nocturnal cough and occasional wheeze
with dyspnea. He had immigrated to Canada 8 months before
the onset of symptoms. He also reported a 2-kg weight loss
over the preceding 6 months but denied having fever or chills.
At the time of his referral to the TDU, he was receiving an-
tibiotics and inhaled b-agonists for presumed asthma. The past
medical history was otherwise unremarkable. Physical exami-
nation revealed bilateral basilar wheezing.
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Laboratory investigations revealed eosinophilia (eosinophil
count, 20.2 ⫻ 10 9 eosinophils/L) and positive results of filarial
serologic tests (titer, 1:4096). His IgE level was 381 IU/mL.
Results of stool examination were negative for ova and para-
sites, and results of strongyloides serological testing were neg-
ative. Chest radiography detected interstitial markings, and pul-
monary function testing revealed mild lung restriction and
decreased diffusion capacity. The patient was treated with di-
ethylcarbamazine (6 mg/kg per day) for 21 days.
Within 3 days after starting therapy, patient 1 noted a dra-
matic improvement in his symptoms, with complete resolution
by the end of treatment. The eosinophil count decreased to
1.55 ⫻ 10 9 eosinophils/L at the completion of therapy. At the
4-month follow-up visit, patient 1 continued to be asymptom-
atic, and his eosinophil count had further decreased to
0.7 ⫻ 10 9 eosinophils/L. Pulmonary function testing had im-
proved but continued to show borderline restriction and re-
duced diffusion capacity. Seven months after completion of
treatment, patient 1 continued to be asymptomatic, with an
eosinophil count of 0.5 ⫻ 10 9 eosinophils/L. Thirteen months
after the end of treatment, he remained asymptomatic, and the
eosinophil count had normalized to 0.3 ⫻ 10 9 eosinophils/L.
Patient 2. A 56-year-old man, originally from Guyana,
was admitted to the hospital because of shortness of breath.
Patient 2 had immigrated to Canada 3 years before presenta-
tion. He described a 2-year history of dyspnea, wheezing, and
dry cough, with exacerbation at night. He denied having fever,
chills, weight loss, or malaise. During a previous hospital ad-
mission for treatment of shortness of breath, patient 2 was
assessed by 2 respirologists and received a diagnosis of asthma.
Medications included salmeterol, inhaled steroids, terbutaline,
and oral prednisone. The past medical history was notable only
for a remote history of smoking. Findings on multiple chest
radiographs were normal. Pulmonary function testing showed
severe obstruction with gas trapping at residual volumes and
increased airway resistance. Physical examination revealed
wheezes on chest auscultation.
Laboratory investigations at the TDU revealed an eosinophil
count of 10.3 ⫻ 10 9 eosinophils/L, with an IgE level of 8332
IU/mL. Results of a filarial serological test were positive (380.5
mg/mL). Examination of stool specimens did not detect ova or
parasites, and results of a strongyloides serological test were
negative.
Patient 2 completed 21 days of therapy with diethylcarbam-
azine (6 mg/kg per day) and noted marked improvement of
his respiratory symptoms. The eosinophil count 1 month after
the completion of treatment had decreased to 1.7 ⫻ 10 9 eosin-
ophils/L. Pulmonary function testing 6 months following treat-
ment showed moderate airflow limitation with gas trapping
and mild reduction of diffusion capacity. The only respiratory
complaint at the 6-month follow-up visit was mild shortness
of breath with exertion.
months pregnant. Physical examination findings were otherwise
unremarkable.
Laboratory investigations revealed an eosinophil count of
11.0 ⫻ 10 9 eosinophils/L, an elevated serum IgE level, and pos-
itive results of a filarial serologic test (titer, 1:2048). Stool ex-
amination did not detect ova or parasites, and results of a
strongyloides serologic test were negative. Pulmonary function
testing revealed a small reduction in forced vital capacity, a
small concentration of trapped gas, and a small reduction in
diffusion capacity. Although a diagnosis of TPE was made, chest
radiography and treatment with diethylcarbamazine were post-
poned until after delivery.
One month postpartum, patient 3 presented to another hos-
pital with increasing shortness of breath on exertion. Echo-
cardiography showed right axis deviation with right ventricular
hypertrophy, and chest radiography revealed pulmonary edema.
Two-dimensional echocardiogram with Doppler imaging showed

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Patient 3. A 24-year-old woman from Guyana presented
to the hospital with a 5-year history of mild intermittent short-
ness of breath, nocturnal cough, wheezing, and a 4.5-kg weight
loss. Patient 3 had received a diagnosis of asthma several years
before presentation but did receive specific treatment or un-
dergo testing. She did not smoke and had no allergies or other
relevant medical history. She had immigrated to Canada 6 years
earlier. At the time of referral to the TDU, patient 3 was 5
an enlarged right heart with evidence of pulmonary hypertension
and an estimated pulmonary artery systolic pressure of 70 mm
Hg. Cardiac catheterization was performed and demonstrated
the following: estimated pulmonary artery pressure, 70/40/49
mm Hg; pulmonary artery wedge pressure, 8 mm Hg; left ven-
tricular (LV) end-diastolic pressure, 15 mm Hg; right atrial pres-
sure, 12 mm Hg; and cardiac output, 1.4 L/min. An LV angiogram
indicated a grade 2/4 LV (i.e., LV ejection fraction, 40%–60%)

Table 1. Selected characteristics of patients with tropical pulmonary eosinophilia who

presented to the Tropical Diseases Unit (TDU) at Toronto General Hospital between 1990
and 2003.

Duration of
Duration of Canadian No. of
Age, Country symptoms, residence, physicians seen
Patient years Sex of birth months months before TDU
1 39 M India 3 24 2
2 24 F Guyana 60 65 1
3 38 M Guyana 5 24 2
4 24 M India 7 12 2
5 29 M India 2 8 3
6 59 F Guyana 4 8 4
7 24 M Guyana 5 12 2
8 35 F Sri Lanka 4 5 3
9 34 M India 24 24 5
10 20 F Guyana 36 6 2
11 18 F Sri Lanka 9 12 3
12 22 M Guyana 11 132 2
13 52 F India 30 30 4
14 56 M Guyana 36 40 3
15 32 F Guyana 0 84 2
16 6 M Sri Lanka 6 12 2
17 23 M India 0 18 3
Overall,
median value 29 … … 6 18 2

Tropical Pulmonary Eosinophilia • CID 2004:39 (15 October) • 1125

Table 2. Signs and symptoms at presentation to the hospital summarized in table 1. The median age was 29 years, with a
for patients with tropical pulmonary eosinophilia. ratio of male patients to female patients of 1.4:1. All patients
were Canadian residents of South Asian ancestry. The region
n/N (%)
Presenting sign or symptom of patients
of origin was either Guyana (47%) or the Indian subcontinent
(53%). The median interval between immigration to Canada
Cough 15/17 (88)
and presentation to the TDU was 18 months (table 1).
Wheeze 15/17 (88)
Dyspnea 15/17 (88)
The majority of patients presented to the hospital after a
Abnormal chest radiograph findingsa 10/14 (71) chronic course of symptoms (median duration of symptoms
Fever 5/17 (29) before presentation, 6 months) (table 1). Common symptoms
Weight loss 2/17 (12) at presentation were shortness of breath (88%) and nocturnal
Fatigue 1/17 (6) cough (88%), whereas wheezing was the most common sign
Pruritus 1/17 (6) (88% of patients) (table 2). Two patients initially denied res-
a
Documented findings were available for only 14 patients. piratory or constitutional symptoms and were referred for eo-
sinophilia. However, each of these patients had abnormal phys-
with diffuse hypokinesis. A 21-day course of diethylcarbamazine ical examination findings (wheezing) or pulmonary function
(6 mg/kg per day) was started. Five weeks after initiating treat- test results. No patient had clinically detectable hepato-
ment, patient 3 was clinically unchanged. A second transthoracic splenomegaly, lymphadenopathy, or lymphedema.

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echocardiogram showed no improvement. Patient 3 then initi-
ated prednisone (60 mg/kg per day) on a trial basis, with no
improvement in symptoms. Her health continued to deteriorate
despite intervention, and she died 9 months after TPE was first
diagnosed.
All patients. Demographic characteristics of the sample are
All 17 patients had been referred to other specialists for
diagnosis, consulting a median of 2 physicians each, before
being referred to the TDU (table 1). Thirteen patients (76%)
had received a previous diagnosis of asthma. Fifteen patients
(88%) had received some form of pharmacological intervention
for presumed asthma before referral to the TDU, with minimal

Table 3. Laboratory parameters of tropical pulmonary eosinophilia cases.

Total
leukocyte Serum
count, Eosinophil count, IgE level, Anti-filarial Chest radiograph
Patient ⫻109 cells/La ⫻109 eosinophils/Lb IU/mLc antibody titerd findings
1 18.7 11.0 11000 1:16,384 Interstitial infiltrates
2 24.3 11.0 11000 1:2048 …
3 52.9 48.1 7460 1:4096 Normal
4 23.9 16.9 2200 …e Interstitial infiltrates
5 27.4 20.2 381 1:4096 Interstitial infiltrates
6 55.9 45.3 11000 1:32,768 …
7 37.1 27.5 27,100 1:16,384 Interstitial infiltrates
8 35.8 22.6 11000 1:2048 Interstitial infiltrates
9 22.1 11.0 1950 1:2048 Interstitial infiltrates
10 23.0 12.4 1350 1:4096 Interstitial infiltrates
11 37.0 28.0 31,000 1:16,384 Interstitial infiltrates
12 60.6 53.3 2400 1:4096 Normal
13 14.1 5.4 3360 1:1024 Interstitial infiltrates
14 18.0 10.0 8332 …e Normal
15 12.6 5.1 27,689 …e Normal
16 12.5 2.8 775 1:32,768 Interstitial infiltrates
17 39.1 29.7 33,444 1:4096 …
Overall,
median value 24.3 16.9 11,342 … …
a
Normal range, 4.5 ⫻ 109 to 11.0 ⫻ 109 leukocytes/L.
b
Normal range, 0.05 ⫻ 109 to 0.5 ⫻ 109 eosinophils/L.
c
Normal range, 0–380 IU/mL.
d
Normal titer, !1:32.
e
For patients 4, 14, and 15, anti-filarial antibody concentrations were 1172, 1380.5, and 42.4 mg/mL, respectively (normal
concentration, !13.0 mg/mL).

1126 • CID 2004:39 (15 October) • Boggild et al.

or no improvement in symptoms. b-Agonists were the most
prescribed medication (76% of patients), and antibiotics (47%),
prednisone (41%), inhaled steroids (35%), and ipratropium
(12%) were also used.
Chest radiograph findings were documented for 14 patients,
10 (71%) of which were reported as interstitial patterning, and
4 (29%) of which were reported as normal. Pulmonary function
testing was documented for 12 patients (71%), and of these,
results of only 1 test were reported as normal. Pulmonary func-
tion testing revealed an isolated restrictive pattern for 3 patients
(25%), an isolated obstructive pattern for 1 (8%), an isolated
diffusion defect for 2 (16.7%), a combined restrictive pattern
with decreased diffusion capacity for 3 (25%), and combined
airway obstruction and decreased diffusion capacity for 2
(16.7%).
The eosinophil count was elevated in all patients and was
13 ⫻ 10 9 eosinophils/L in 16 patients (94%) at presentation to
the TDU. The median eosinophil count was 16.9 ⫻ 10 9 eosin-
ophils/L (table 3). The median total leukocyte count was
24.3 ⫻ 10 9 leukocytes/L (table 3). IgE levels and filarial titers
were also elevated for all patients. Each patient was treated with
diethylcarbamazine (6 mg/kg per day) for at least 21 days.
Follow-up data were available for 15 patients, with a mean
duration of follow-up of 10.5 months (range, 2–35 months).
All but 1 patient who was treated with diethylcarbamazine re-
sponded and reported resolution of presenting symptoms. Pul-
monary function testing performed after the completion of
treated was reported for 4 patients. Pulmonary function pa-
rameters returned to normal for only 1 patient, who had ini-
tiated a 2-year course of prednisone therapy for his pulmonary
symptoms before the diagnosis of TPE was made.
DISCUSSION
Pulmonary infiltrates with eosinophilia is a broad diagnostic
qualifier encompassing a variety of infectious, inflammatory,
and allergic etiologies [15]. The differential diagnosis of eosin-
ophilic lung disease includes Loeffler syndrome secondary to
helminth infection or drug reaction; allergic bronchopulmon-
ary aspergillosis; chronic eosinophilic pneumonia; vasculitis,
such as Churg-Strauss syndrome, polyarteritis nodosa, and We-
gener granulomatosis; and idiopathic hypereosinophilic syn-
drome [13]. Although all of these diseases share similar clinical
and laboratory features, there are several criteria that must be
met to diagnose TPE, including residence in an area in which
filaria is endemic, peripheral eosinophilia, absence of micro-
filariae in peripheral blood, increased antifilarial antibody titer,
elevated serum IgE level, and a favorable clinical response to
diethylcarbamazine [10, 16]. A history of paroxysmal nocturnal
asthma and radiographic evidence of pulmonary infiltrates are
supportive but not diagnostic. It is important to note that chest
radiograph findings may be normal in up to 20% of TPE cases
[17]. The cases presented above highlight some of the associated
findings in TPE, such as interstitial infiltrates (detected by chest
radiography) and a restrictive pattern of lung disease with su-
perimposed airway obstruction (revealed by pulmonary func-
tion testing), and they reiterate that misdiagnosis is common.
Although the initial presentation may closely resemble that of
asthma, an irreversibility of airflow limitation with conven-
tional therapies, coupled with marked eosinophilia and expo-
sure or travel history, should raise the suspicion of TPE. In
patients with an appropriate exposure history, it is also im-
portant to rule out Loeffler syndrome secondary to Ascaris or
Strongyloides infection by means of stool examination and se-
rological testing, because this form of nonfilarial TPE is re-
fractory to diethylcarbamazine and may be difficult to distin-
guish clinically from true filarial TPE [18].
These cases further underscore the necessity of early inter-
vention, because chronic TPE may result in permanent, irre-
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versible deficits in pulmonary function, despite treatment with
diethylcarbamazine [14]. In fact, it has recently been shown
that pulmonary eosinophils in TPE degranulate and release
toxic oxygen radicals long after treatment with diethylcarbam-
azine [19], increasing damage initiated during the acute stages
of disease. When TPE is recognized and treated early, patients
often have a dramatic and rapid response to diethylcarbama-
zine. As illustrated by the second and third cases (patients 2
and 3, respectively), however, the outcome is often linked to
the chronicity of TPE. To date, a treatment regimen best suited
to patients with chronic TPE has yet to be established. Lung
pathological findings in patients with TPE are directly related
to the immunologic processes involved in microfilarial clear-
ance, thus intimating a role for anti-inflammatory and im-
munomodulatory drugs in TPE treatment. IFN-a may hold
promise because it has been shown to block IgE-dependent
release of eosinophil-derived neurotoxin and IgA-dependent
release of eosinophil cationic protein in vitro [20], both of
which are cytotoxic and helminthotoxic. Furthermore, IFN-a
has clinical use in the treatment of idiopathic hypereosinophilic
syndrome [21, 22]. It is also curious that the only patient in our
series with normal results of follow-up pulmonary function tests
had received a 2-year course of continuous prednisone therapy.
It is clear that there is a need for prospectively designed studies
that evaluate current and novel treatment regimens for TPE.
All of the patients in this case series were of South Asian
ancestry and had immigrated to Canada from regions of lym-
phatic filariasis endemicity, supporting the well-documented
geographic preponderance of lymphatic filariasis [3]. In ad-
dition, our findings are supportive of results in an expanding
body of literature suggesting that disease susceptibility has ge-
netic underpinnings [23]. For instance, immunological hyper-
reactivity to another filarial nematode, Onchocerca volvulus, has
been linked to the Arg110Gln genotypic variant of IL-13 [24],
Tropical Pulmonary Eosinophilia • CID 2004:39 (15 October) • 1127
which also confers an IgE-independent risk for asthma and
atopy. It is postulated that the Arg110Gln variant leads to en-
hanced IL-13 signaling, thus heightening the Th2 response [24].
Racial and ethnic biases within disease spectra are also becom-
ing increasingly recognized and clinically relevant [23]. With
respect to lymphatic filariasis, it is well documented that the
burden of disease is higher in South Asians [10], even in pop-
ulations in which they are a minority [25]. In addition, it has
recently been reported that homozygosity for a variant CHIT1
genotype (encoding chitotriosidase, the putative target for mi-
crofilarial chitin), is overrepresented in South Indians who are
susceptible to filarial infection, compared with individuals who
are not and those who are white or African American [26].
Although the sample in our case series is relatively small, it is
of interest that all patients are of the same racial origin, a fact
that may well be explained by differential genetic susceptibilities
but which requires additional controlled studies.
There are several inherent limitations in the present study.
Although the study is useful in raising awareness about the
diagnosis of TPE in a region of nonendemicity, our ability to
draw conclusions is limited by the small sample size and the
retrospective design. Nevertheless, our data support currently
accepted racial and geographic associations among individuals
with TPE and highlight the need for research initiatives in the
realm of disease susceptibility and treatment.
In summary, TPE is an important diagnostic consideration
in patients with an appropriate clinical and exposure history,
even in an area in which TPE is not endemic. Individuals from
regions in which lymphatic filariasis is endemic who pres-
ent with dyspnea, cough, wheeze, and persistent eosinophilia
should undergoing tests to measure serum IgE and antifilarial
antibody levels, in addition to serological testing for Strongy-
loides stercoralis and stool examination for other helminthes.
Individuals with TPE often receive an incorrect diagnosis of
asthma, despite their poor response to standard treatments for
asthma. Early recognition and treatment of TPE with dieth-
ylcarbamazine is key to minimizing morbidity and mortality,
because chronic untreated TPE may lead to progressive, irre-
versible pulmonary fibrosis.
Acknowledgments
Financial support. Canadian Institutes of Health Research (grant MT-
13721; to K.C.K.) and a Canada Research Chair (to K.C.K.).
Conflict of interest. All authors: No conflict.
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