Tropical Pulmonary Eosinophilia.

Based on- Indian Journal of Medical Research (IJMR)

Presented by:

Dr. Sayat Quayum

MD- Phase A
Internal Medicine
What is tropical pulmonary
eosinophilia ?
Tropical pulmonary eosinophilia (TPE) is a
syndrome of:
wheezing
fever
eosinophilia

It is seen predominantly in the Indian

subcontinent and some other tropical areas.
Its etiological link with Wuchereria bancrofti
and Brugia malayi has been well established.
 Epidemiology
TPE is endemic in areas with filarial endemicity.
It is most commonly found in regions of
Indian subcontinent,
South East Asia,
South America and
Africa.
It is also found in some non-endemic countries like:
Japan
Netherlands
United Kingdom
Australia.

Probably as a result of travel to or immigration from

endemic areas. In fact, persons travelling to endemic areas
may be more prone as they lack natural immunity to filarial
antigens.
Historical background

First described in 1940 and labelled as

pseudotuberculosis with eosinophilia, the term
tropical pulmonary eosinophilia (TPE) was first coined
by Weingarten in 1943.

TPE was initially thought to be a benign self-limiting

condition. It is now an accepted fact that though TPE
does not end fatally, it does and can scar the lung
badly.
 Pathology
The pathogenesis is due to an exaggerated
immune response to the filarial antigens which
includes type I, type III and type IV reactions
with eosinophils playing a pivotal role.

The histopathological reactions observed were

mainly classified into:
Acute eosinophilic infiltration
Mixed cell type of infiltrate (i.e. eosinophils and
histiocytes) with generally well-marked fibrous tissue
formation between six months to two years.
Histiocytic infiltration and fibrosis beyond two years in
the natural history of the disease.
Correlation of the clinical features with
the lung functions and histopathology

Earliest cough
histopathological
breathlessness
response is a histiocytic
infiltrate in the lung wheezing
parenchyma an increased peripheral
eosinophil count.

Acute eosinophilic
exudate within the symptom is
lungs unchanged
Correlation of the clinical features with the
lung functions and histopathology (Contd)

Mixed cell reaction

Lung function shows
(histiocytes,
more restriction and
epitheloid cells,
less obstruction.
lymphocytes and
Six months to two years.
eosinophils)

More histiocytes and Breathlessness on exertion is

lymphocytes and
eosinophils along
with fibrous bands.
the dominant feature.
At 2-5 years from onset,
untreated patients show
well-marked pulmonary
fibrosis.
Clinical features
Systemic symptoms Extra-pulmonary
include: manifestations include:
fever lymphadenopathy
weight loss Hepatosplenomegaly
Fatigue
malaise.
There may be Chest pain
The respiratory symptoms due to rib fractures caused
are: by excessive vigorous
Cough coughing.
Breathlessness
wheezing
chest pain.
Symptoms are mostly nocturnal but may also
occur during the day. Sputum is scanty, viscous
and mucoid.
Investigations

Serology:
CBC: Striking eosinophilia >3000/m and
may rise as high as 80,000/m

ESR: High
Investigations

High serum levels of IgE and filarial-

specific IgE and IgG are found.
Wb E34 penicillinase and W. bancrofti
microfilarial excretory secretory (Wb mf
ES) antigen detect filarial antibody in 35
per cent of cases of TPE (which rises to
almost 81% in the presence of
microfilaraemia)
Investigations

Chest Imaging:
Chest x-Ray:
Usually normal
The main radiological features include reticulo-
nodular shadows more in the mid to lower zones and
miliary mottling .
CT Chest:
Features of bronchiectasis, air trapping,
lymphadenopathy, cavitation, consolidation or
pleural effusions in addition to the miliary mottling
and interstitial shadows
Investigations
Chest x-Ray of TPE CT scan of chest
 Investigations
Spirometry

Mixed restrictive and obstruction which may be mild to

moderate in degree

BAL
BAL from acute untreated TPE revealed a striking
eosinophilic alveolitis.
Differential diagnosis

Eosinophilia in tropical countries is mostly caused

by a hypersensitivity reaction to helminthes. While
TPE due to hypersensitivity to filarial antigen is
commonest, eosinophilia may also be due to
roundworm, Toxocara, strongyloides and
hookworm.

Non-infectious causes mainly include bronchial

asthma, allergic bronchopulmonary aspergillosis,
acute and chronic eosinophilic pneumonia,
Churg-Strauss syndrome, idiopathic
hypereosinophilic syndrome, and drug reactions.
 Management
No universal TREATMENT
guidelines have been
established for TPE.

DEC (Di-ethyle carbamazine) 5

mg/kg/day is the drug of
choice.(7-10 or 21 days
regimen)

Many patients may not

respond to DEC due to already
established fibrosis.

Steroids have been shown to

have beneficial effects. But the
exact dose and duration in
combination with DEC is yet to
be determined by randomize
control trials.
Relapse

In the only follow up study of patients for five

years, the relapse rate was found to be
almost 20 per cent after DEC therapy. As a
result, monthly courses at 2-3 month intervals
for 1-2 years have been suggested.
-Ref- Udwadia FE. Herzog H, editor. Tropical eosinophilia. Pulmonary
eosinophilia: progress in pulmonary research. 1975;VII:35155. Basel: S Karger

.
Prevention

The World Health Assembly aims to eliminate

lymphatic filariasis as a public health
problem by 2020. The WHO strategy aims at
preventing transmission of microfilaria
through mosquito bites.
For prevention, once yearly combination of
DEC (6 mg/kg) and albendazole (400 mg)
for 4-6 years need to be given.
Ref-
Gyapong JO, Kumaraswami V, Biswas G, Ottesen EA. Treatment strategies
underpinning the global programme to eliminate lymphatic filariasis. Expert Opin
Pharmacother. 2005;6:179200. [PubMed]
Ottesen EA. Lymphatic filariasis: treatment,control and elimination. Adv Parasitol.
2006;61:395441. [PubMed]

.
Tropical pulmonary eosinophilia
(TPE) is a syndrome of wheezing,
fever and eosiniphilia seen
predominantly in the Indian
subcontinent.

Type I, type III and type IV

hypersensitivity reaction.

Peripheral blood eosiniphilia is

present.

Both pulmonary and extra

pulmonary features are present.

DEC (Di-ethyle carbamazine) is

the drug of choice.

Sometimes steroid is given to the

patients.
Any Questions??