MEDICINE TROPICAL FOR THE
PULMONOLOGIST(MALARIA,HYDATID
DISEASE,AMOEBIASIS,LEPTOSPIROSIS)
DR.AMIT RAODEO
MALARIA
1
INTRODUCTION
Malaria remains a major public health problem in endemic
Malaria
areas.
Responsible for 1.5 to 2.7 million deaths each year worldwide.
Responsible
Tropical African countries are estimated to contribute >90% of
Tropical
the total malaria incidence and great majority of malarial
deaths.
Respiratory tract involvement ranging from upper respiratory
Respiratory
symptoms to ARDS is seen in 3-10% cases.
3Incidence of pulmonary edema was around 1per 1000 cases in
Incidence
a large study from vietnam.
vietnam.
SEVERE MALARIA
Definition:Presence of P.falciparum asexual parasitaemia and no other
obvious cause of their symptoms,the presence of one or more of the
following clinical/laboratory features is classified as severe malaria
malaria
CLINICAL:
CLINICAL:
a)
b)
c)
d)
e)
f)
g)
g)
h)
i)
Prostration
Impaired consciousness
Respiratory
distress(acidotic breathing)
Multiple convulsions
Circulatory collapse
Pulmonary edema
Abnormal bleeding
Jaundice
Hemoglobinuria
a)
b)
c)
d)
e)
f)
LAB:
LAB:
Severe anaemia
Hypoglycemia
Acidosis
Renal impairment
Hyperlactataemia
hyperparasitaemia
2
COMPARISON BETWEEN
LEPTOSPIROSIS,MALARIA AND DENGUE
Clinical
difference
Leptospirosis
Malaria
dengue
Splenomegaly
+
++
+ or -
Subconjunctival
hemorrhage
Classically present
Can be present
Rare
Can be present
Myalgia
Classically present
Usually
present
Can be present
Hemoptysis
Common
Uncommon
Uncommon
Encephalopathy
Uncommon
Common
Uncommon
Abdominal pain
Common
Uncommon
Uncommon
Arthralgia
Less common
Uncommon
common
COMPARISON BETWEEN LEPTOSPIROSIS,MALARIA AND DENGUE
Lab difference
Leptospirosis
Malaria
Dengue
Hemoglobin
Normal unless bleeding
Anemia
Elevated/normal unless
bleeding
TLC
Leucocytosis
Usually
normal,leucocytosis can be
present
Increased TLC bad
prognostic sign
Normal/leucopenia
Potassium levels
Hypokalemia common
common
Hyperkalemia poor
prognostic
Hyperkalemia(IV
hemolysis/ ARF)
hemolysis/
/hypokalemia
Normal/raised/reduced
DIC
Uncommon
Common
Common
P.S
Left shift
Malarial parasite
Atypical lymphocyte
Hypoglycemia
Uncommon
Common
Uncommon
Pulmonary involvement
Pulmonary hemorrhage
ARDS
Pnuemonia
Diffuse nodular shadows
Cardiogenic pulmonary
edema
ARDS
Fluid overload
Pulmonary sequestration
due to parasite
Less common ALI/ARDS
ABG
Normal anion gap,acidosis
more common
High anion gap metabolic
acidosis(lactic)
acidosis(lactic)
Lactic acidosis less common
Ascites / bilateral pleural
effusion
Absent
Absent
Present
Myocarditis
Common
Less common
Less common
3
HOW COMMON IS MALARIA AS CAUSE OF ARDS?
PATHOGENESIS OF ALI/ARDS IN MALARIA
4
PATHOGENESIS OF ARDS AND PULMONARY EDEMA
IN MALARIA
DIFFERENTIAL DIAGNOSIS OF HYPOXEMIA IN
MALARIA
1)
2)
3)
4)
5)
ARDS
Fluid overload
Aspiration pneumonia
Gram negative bacteremia
Sequestration of parasitised RBCs in pulmonary
vasculature
5
BACTERIAL SUPERINFECTION IN MALARIA
Both community acquired as well as nosocomial infections
Both
are common.
Mechanism:
Mechanism:
1)Transient immunosuppression.
1)Transient immunosuppression.
2)Impaired splanchnic perfusion-translocation of gut
2)Impaired
perfusionbacteria.
Most common infection is aspiration pneumonia.
Most
Recommendation:-Empirical antibiotics in severely ill
Recommendation:patients without delay.
COMMUNITY ACQUIRED BACTERIAL INFECTIONS IN
SEVERE MALARIA
PARAMETER
SEVERE
MALARIA(n=93)
MALARIA(n=93)
LESS SEVERE
MALARIA
Number of episodes
13(14%)
6(6%)
Number of patients
13(14%)
6(6%)
Site of infection
17
6
Pneumonia
6
1
Bacteremia
5
1
Urinary tract infection
3
1
Miscellaneous
3
3
6
LAB DIAGNOSIS OF MALARIA
METHOD
ADVANTAGE
1) Thick blood film
DISADVANTAGE
Sensitive(0.001% parasitemia)
parasitemia)
Species specific.
Inexpensive.
Requires experience.
Underestimates true count.
Rapid
Species specific.
Provides prognostic information
in severe malaria.
Insensitive (>0.05%
parasitemia).
parasitemia).
Uneven distribution of P.vivax.
P.vivax.
Rapid
Sensitivity similar to or slightly
less than thick film (>0.001%
parasitemia).
parasitemia).
Detects only P.falci.
P.falci.
Remains +ve after weeks of
+ve
infection.
Does not give quantitative
analysis.
4) Plasmodium LDH dipstick or
card test
Rapid
Sensitivity similar to
PFHRP2dipstick.
Less sensitive diagnosis for
P.vivax,malarie and ovale.
ovale.
Slightly more difficult than
PFHRP2.
Miss low levels of parasitemia
with other malarias.
Does not provide quantitative
analysis.
5)Membrane concentration
methods with acridine orange
staining
Sensitivity similar or superior to
that of thick films (~ 0.001%
parasitemia).
parasitemia).
Ideal for processing large no. of
samples rapidly.
Does not specify or quantitate.
quantitate.
Requires fluorescence
microscopy.
2)Thin blood film
3)PFHRP2 dipstick or card test
PROGNOSTIC MARKERS IN MALARIA
PARAMETER
SURVIVORS
(n=83)
NONSURVIVORS
(n=10)
P VALUE
Unrousable
coma,n(%)
coma,n(%)
25(30)
9(90)
<0.001
Severe anaemia,n(%) 7(8)
anaemia,n(%)
1(10)
1
Renal failure,n(%)
failure,n(%)
40(48)
7(70)
0.3
Pulmonary
edema,n(%)
edema,n(%)
5(6)
5(50)
<0.001
Hypoglycemia,n(%)
Hypoglycemia,n(%)
3(4)
0
1
Shock,n(%)
Shock,n(%)
12(15)
8(80)
<0.001
Bleeding/DIC,n(%)
Bleeding/DIC,n(%)
19(23)
3(30)
0.7
Seizures,n(%)
Seizures,n(%)
2(2)
0
1
Acidosis,n(%)
Acidosis,n(%)
11(13)
8(80)
<0.001
Coma and
acidosis,n(%)
acidosis,n(%)
2(2)
8(80)
<0.001
Coma and
shock,n(%)
shock,n(%)
3(4)
8(80)
<0.001
Parasitemia of more
than 5%,n(%)
32/79(41)
7/9(78)
0.07
7
TREATMENT OF SEVERE FALCIPARUM MALARIA
Trial
No. of
patients
(SEAQUAMAT)
(SEAQUAMAT)
1461
Wellcome Trust
Clinical Research
560
Unit
Faculty of Tropical
Medicine, Mahidol
University
131
Faculty of Tropical
Faculty
Medicine, Mahidol
University
102
Drugs
Results
Reference
Artes(730)
Vs.
Quin(731)
34.7%
absolute
mortality
Lancet 2005; 366:
71725
717
Artem(284)
Vs.
Quin(276)
Faster
Parasite
clearance
N Engl J Med. 1996
Jul 11;335(2):76-83.
11;335(2):76-
Faster
Parasite
clearance,
mortality
Clin Infect Dis. 2003
Clin
Jul 1;37(1):7-16
1;37(1):7-
Faster
Parasite
clearance,
mortality
Trans R Soc Trop
Med Hyg. 1995 NovHyg.
Nov-
Artes
Vs.
Quin
Artem(50)
Vs.
Quin(52)
Dec;89(6):668-71.
Dec;89(6):668-
CURRENT RECOMMENDATION
Artimisinin derivatives like artisunate , artimether are drug of
Artimisinin
choice for severe malaria.
Artisunate has the advantage of being water soluble and can be
Artisunate
given I.V.
8
CURRENT RECOMMENDATION FOR
EXCHANGE BLOOD TRANSFUSION
Currently there are no randomized control trials to show any
Currently
benefits of exchange blood transfusion over conventional
therapy.
Procedure is hazardous and availability of blood is a limiting
Procedure
factor.
Currently WHO does not recommend exchange blood
Currently
transfusion in the management of severe malaria.
OTHER ADJUVANT THERAPY
Corticosteroids
Corticosteroids
No survival benefit
No
GI bleed
GI
Anticonvulsants
Anticonvulsants
Phenobarb
Phenobarb
Others
Others
Adrenaline
Adrenaline
Heparin
Heparin
Prostacyclin
Prostacyclin
Pentoxyfylline - No established role
Pentoxyfylline
Cyclosporin A
Cyclosporin
Iron chelators
Iron
Anti TNF
Anti
9
ROLE OF aPC IN MALARIA/LEPTOSPIROSIS
Report
Clinical
scenario
Inference
Reference
Drotrecogin alfa
(activated) in severe
falciparum malaria
severe falciparum
malaria
parasitaemia levels
of 40%
MODS
aPC for 96 hrs f/b
gradual
improvement
Anaesthesia, 2006,
Anaesthesia,
61, pages 899902
899
Case series of 10
patients with
tropical infections
Includes 4 cases of
falciparum and I
leptospirosis
1 out 4 died
Intensive care Med
(2006) 32:1281
32:1281
1282
LEPTOSPIROSIS
10
INTRODUCTION
Zoonotic disease.
Zoonotic
Transmitted by contact with infected urine and rarely
Transmitted
blood of infected rodent.
Penetration recurs through intact mucous membrane
Penetration
or abraded skin.
PATHOGENESIS
Septicemic phase vascular injury
Septicemic
Immune phase immune complex deposition
Immune
11
PATHOGENESIS OF LUNG INJURY
In contrast to liver and kidney, isolation of leptospires is
In
uncommon from lung tissue.
Antigenic debris is also less common in lungs.
Antigenic
Widespread but subtle inflammatory process.
Widespread
Presence of antibody along the septal wall in infected guinea
Presence
pigs may suggest an autoimmune response similar to
Goodpastures disease (Abs to type IV collagen).But renal
tissue did not reveal glomerulonephritis characteristic of
Goodpasture disease.
The exact mechanism is largely unknown.
The
CLASSICAL FEATURES OF LEPTOSPIROSIS
CLASSICAL
Biphasic illness -1)Septicemic phase
Biphasic
2)Brief afebrile period
3)Immune phase
(liver and kidney)
Diagnosis in early phase is commonly missed.
Diagnosis
Hence Faine proposed a clinical scoring system which has
Hence
good sensitivity (81.8%) and specicity(72.9%).
Usually helpful in excluding diagnosis because of high
Usually
negative predictive value.
J Postgraduate Med.2005 Sept.51(3),169
Post
12
LUNG INVOLVEMENT
Ist publication of lung involvement in leptospirosis is
Ist
attributable to Moeschlin in 1943.
Varies between 20%-70% in all cases in various studies.
Varies
20%Pulmonary examination ranges from normal to extensive
Pulmonary
alveolar hemorrhage and respiratory failure.
Patients with severe alveolar hemorrhage can die within 24
Patients
hrs.
BAL examination in patients with leptospirosis by D u couedic
BAL
and colleagues found that alveolar hemmorrhage was present
in all patients with sign /symptom of respiratory involvement
and 7/10 patients in asymptomatic patients.
Med Trop.1992,25:21-30
Trop.1992,25:21-
13
LUNG INVOLVEMENT (CONTD)
There is absence of significant inflammation in areas of
There
hemorrhage.
Usually associated with hepato-renal involvement but can
Usually
hepatooccur in the absence of these.
J.Infect.Disease.1998;178;1457-63
J.Infect.Disease.1998;178;1457-
LAB DIAGNOSIS OF LEPTOSPIROSIS
TEST
ADVANTAGE
DISADVANTAGE
DGM
Convenient
Lacks sensitivity and
specificity.
Immunofluoroscent
staining
Can be done on blood,
urine or rarely CSF.
10,000 leptospira/ml for
leptospira/ml
visualization is necessary.
Immunoperoxidase
staining
Can be done on blood,
urine or rarely CSF.
10,000 leptospira/ml for
leptospira/ml
visualization is necessary.
A)MICROSCOPY
14
LAB DIAGNOSIS OF LEPTOSPIROSIS
TEST
ADVANTAGE
DISADVANTAGE
B) SEROLOGY
MAT
Complex
Gold standard
Requires maintaining strains
Highly sensitive
Detects group specific Abs. for preparation of Ag.
IgM ELISA
Most widely used
( sensitivity 100% and
specificity 93%)
IgG ELISA
High rate of false positive.
Indirect Fluorescent Rapidity
Antibody test
Microscopic slide
agglutination
High sensitivity and
specificity
CIEP
LAB DIAGNOSIS OF LEPTOSPIROSIS
LAB
TEST
ADVANTAGE
DISADVANTAGE
C) Culture
Gives confirmed diagnosis
Low sensitivity
Cumbersome
Requires atleast 1 month before
can be declared negative
D) Molecular diagnosis
1)Dot blotting
2)In situ hybridization
3)PCR
Useful for DNA detection in
serum and urine.
Useful when other tests fail to
establish diagnosis.
Used for post mortem
diagnosis.
Inability to identify serovar.
serovar.
Cost and availability.
15
PROGNOSTIC MARKERS
Multivariate revealed analysis three variables associated
Multivariate
with mortality
VARIABLE
ODDS RATIO
P VALUE
Hemodynamic
disturbance
6 (CI 0.9-38.5)
0.9-
0.005
Serum
10.6 (0.9-123.9)
(0.9creatinine>265.2um
creatinine>265.2um
ol/l
0.02
Serum potassium>4 19.9 (1.2-342)
(1.2-
0.009
TREATMENT OF LEPTOSPIROSIS
Ceftriaxone was found effective in severe
Ceftriaxone
leptospirosis in a study by Raptis et al .
23 patients were given ceftriaxone out of which 21
23
survived.No significant ADR noted.
Int J Antimicrobial Agent 2006 Sept,28(3);259-61
Sept,28(3);259-
16
TREATMENT OF LEPTOSPIROSIS
A prospective,open label, randomized trial in
prospective,open
Thialand was conducted in 2000-2001,where they
compared ceftriaxone(1 gm/day for 7 days) with
sodium penicillin G (1.5 MU 6 hrly for 7 days).
Both were found equally effective with median
Both
duration of fever was 3 days and equal number of
deaths (5) were found in each group.
ROLE OF STEROIDS IN LEPTOSPIROSIS
17
AMOEBIASIS
INTRODUCTION
Protozoan infection caused by Entamoeba histolytica.
Protozoan
histolytica.
Third most common cause of death from parasitic diseases
Third
after malaria and schistosomiasis worldwide.
Extraintestinal manifestations are the most comon cause of
Extraintestinal
death.
18
EXTRAINTESTINAL SITES INVOLVED
1)
2)
3)
4)
5)
Amoebic liver abscess-most common.
abscessPleuro-pulmonary second most common.
PleuroPericardial.
Brain.
Genitourinary tract.
RISK FACTORS FOR AMOEBIASIS
5)
Lower socio-economic class
Poor hygiene
Lack of safe drinking water
Male homosexuals
Travellers
6)
Prisoners
1)
2)
3)
4)
19
RISK FACTORS FOR PULMONARY
AMOEBIASIS
1)
2)
2)
3)
Malnutrition
Alcoholism
ASD with left to right shunt
MODES OF PULMONARY INVOLVEMENT
Primary - Very rare
Primary
- Inhalation of dust containing cysts.
- Aspiration of cysts or triphozoites of
amoeba.
Secondary- Infrequent.
Secondary- Hematogenous spread from colon.
Tertiary - Most common. Extension of amoebic liver abscess
Tertiary
20
ROUTES OF INVOLVEMENT
Routes of involvement
1) Abcess extending from
liver
2) Bronchohepatic
3) Empyema extending from
liver
4) Hematogenous spread
without liver involvement
5) Hematogenous lung abcess
and independent liver abcess
Percent
37.2
19.6
17.6
14.3
10.4
TYPES OF LUNG INVOLVEMENT
Types of lung involvement
1) Heptobronchial fistula
2) Pleural effusion and
empyema
3) Lung abscess
4) Consolidation
Percent
47
19
14
10
21
CLINICAL FEATURES
Fever of weeks duration and right upper abdominal and right
Fever
pleuritic type of chest pain.
Dramatic presentation of severe pain,respiratory distress and
Dramatic
shock.
Hepatomegaly in 50% cases.
Hepatomegaly
Hemoptysis is common followed by expectoration of
Hemoptysis
ancchovy sauce like pus.
Bile in sputum is important clue toward hepatic origin.
Bile
DIAGNOSIS
When to suspect amoebiasisWhen
amoebiasis1)Elevated hemidiaphragm.
hemidiaphragm.
2)Hepatomegaly.
3)Pleural effusion.
4)Basal pulmonary involvement in patient from endemic area >3
years age.
22
DIAGNOSIS
1)
2)
3)
4)
5)
Lateral radiograph: Lateral
Upward hump like prominance which can be anterior,
middle or posterior.Anterior hump is more common.
Consolidation which may have cavitation.
cavitation.
Pleural effusion.
Hydropneumothorax-bronchopleural fistula.
HydropneumothoraxCavity with air fluid level in case of bronchial
communication.
DIAGNOSIS
DIAGNOSIS
Stool examionation :Limited value.
Limited
Only positive in 15-33% cases of extraintestinal amoebiasis.
Only
15amoebiasis.
Pathogenic and nonpathogenic amoeba can be differentiated
Pathogenic
by zymodeme analysis,ELISA,RFLP.
analysis,ELISA,RFLP.
Sputum examination ::Usually sterile and paucicellular unless superinfected.
Usually
superinfected.
23
ROLE OF ULTRASONOGRAPHY
Monitoring response to therapy.
Monitoring
To detect small pleural effusion.
To
To look for subpulmonic collection.
To
To differentiate from bacterial empyemas loculations and
To
septations are rare in amoebic empyemas.
empyemas.
WHAT IS ROLE OF CT SCAN?
Can detect intrapleural fluid anywhere in the thorax example
Can
beneath scapula or within fissure which is usually missed by
USG.
Guide interventional procedure.
Guide
To differentiate empyema with bronchopleural fistula from
To
lung abscess.
24
IMMUNOLOGICAL TESTS IN AMOEBIASIS
A)ConventionalA)Conventional1)IHA
2)ELISA
for IgG and IgM , IgM is more specific
3) IFAT
B)NewerB)Newer1) Gal or GalNAC inhibitable - Potential role in extraintestinal
adherence lectin IgM
amoebiasis.
amoebiasis.
2) Gal-GalNAC Ag by ELISA- >90% sensitivity before
Gal
ELISA
treatment.
3) E.histolytica Ag detection kit- useful for sputum and pleural
kitfluid.
4) DNA by PCR- most sensitive method of detection of pleuropulmonary
PCRamoebiasis.
amoebiasis.
DIFFERENTIAL DIAGNOSIS OF AMOEBIASIS
Lung carcinoma
Lung
Pulmonary tuberculosis
Pulmonary
Lung abscess
Lung
Sarcoidosis
Sarcoidosis
Hydatidosis
Hydatidosis
Presence of palpable liver can be mistaken as secondary.
Presence
Anterior basal segment of right lower lobe involvement is
Anterior
characteristic of amoebic origin.
25
TREATMENT OF AMOEBIASIS
Oral or parentral metronidazole 800 mg (35-50 mg/kg/day)
Oral
(35three times daily for 5-10 days is the treatment of choice.
5Chloroquin and emetine are other alternatives but should be
Chloroquin
avoided because of potential cardiovascular side effects.
PULMONARY HYDATID
26
INTRODUCTION
Hydatidosis is one of the most geographically
Hydatidosis
widespread zoonoses in the world.
Four species of Echinococcus are recognised.
Four
EPIDEMIOLOGY OF HYDATID DISEASE
Species Geographical Definitive Intermediate Transmission
distribution Host
Host
E.granulos Mediterrean
region,eastern
us
Dogs
Sheeps
Feco-oral route
Feco-
Rodents
Ingestion
Europe,Africa,South
america middle
east,China,Australia,
New Zealand
E.multiloc Arctic,Asia,Wester Foxes,
ularis
n central europe
Wolves
E.Vogeli
South America
---
---
E.oligarthia South America
---
---
27
LUNG INVOVLEMENT IN HYDATID
Through transdiaphragmatic thoracic involvement- most
Through
involvementcommon.
Hematogenous dissemination.
Hematogenous
Lymphatic dissemination.
Lymphatic
LUNG INVOLVEMENT IN HYDATID
Sometimes lesions develop in area of lung remote from
Sometimes
diaphragmdiaphragm1)Hematogenous spread.
2)Transbronchial spread.
3)Rupture of liver abscess into inferior vena cava and
thromboembolic disease which may progress to pulmonary
hypertension and cor pulmonale.
pulmonale.
28
PLEURO-PULMONARY MANIFESTATIONS OF
HYDATID
HYDATID CYST
RUPTURE
PLEURAL SPACE
BRONCHUS
ASYMPTOMATIC
PRESSURE EFFECT
COUGH
DYSPNOEA
PNUEMOTHORAX
PERSISTENT PNUEMONIA
PLEURAL EFFUSION
RECURRENT HEMOPTYSIS
EMPYEMA
CHEST PAIN
VOMIT LIKE CYSTIC FLUID
ALLERGIC OR ANAPHYLACTIC REACTION
DIAGNOSIS OF HYDATID DISEASE
1) Specific serum antibodies.
2) Chest X-ray
XSolitary lesions- 60% cases.
Solitary lesionsMultiple unilateral/bilateral lesions in 25-50%.
Multiple
25Ruptured cyst-Consolidation surrounding area.
Ruptured cystIt communicates with bronchus-air fluid level.
bronchusMiniscus sign or crescent sign.
Miniscus
Cumbos sign (onion peel sign).
Cumbo
Water lily sign.
Water
Mass within a cavity.
Mass
Newer signs
Rim sign.
Rim
Inverse crescent sign.
Inverse
29
TREATMENT OF PULMONARY HYDATID
Surgery is the mainstay of the therapy as complete
Surgery
elimination of parasite can only lead to cure.
The principle is to preserve as much lung tissue as possible.
The
Akin et al observed that radical resection is too aggressive and
Akin
often not necessary.
Paraenchyma around a hydatid cyst is often affected by lesion
Paraenchyma
and may show chronic
congestion,hemorrhage,bronchopneumonia or interstitial
pneumonia.
These changes often resolve after surgery, hence parenchymal
These
resection is rarely indicated.
TREATMENT OF PULMONARY HYDATID (CONTD)
Conservative surgery are preferred.
1)Enucleation.
2)Pericystectomy.
3)Simple cystectomy.
cystectomy.
4)Cystectomy with cappitonage.
cappitonage.
Spillage of daughter cyst is to be avoided.
Spillage
Recurrence can occur but fresh infection is also reported in
Recurrence
person living in endemic area.
Bilateral pulmonary hydatid :One stage/two stage surgery.
One
Larger cyst/ruptured cyst area treated first.
Larger
30
RECENT ADVANCES N THE TREATMENT OF
PULMONARY HYDATID
Thoracophrenotomy is less invasive & preferred method of
Thoracophrenotomy
surgery in cases of combined lung & liver hydatid
Br.J.surg.2005;92(6);729-33
Br.J.surg.2005;92(6);729-
Recent reports have described VATS in pulmonary hydatid.
Recent
CAN J SURG.2004;47,380-381
SURG.2004;47,380-
TREATMENT OF PULMONARY HYDATID (CONTD)
Medical therapy:Medical
Advocated by few authors.
Advocated
Mebendazole/Albendazole.
Mebendazole/Albendazole.
68-70% of patients with pulmonary hydatid show some degree
68of response.
25-34% cure rates have been documented.
25Considering high risk of complications, hydatidosis patients
Considering
should be followed closely.
PARASITOL.INT.2005;54;135-138
PARASITOL.INT.2005;54;135-
31
DRAWBACKS OF MEDICAL THERAPY
Poor compliance and ADR due to long course of treatment.
Poor
Poor follow up most patients are from rural areas.
Poor
Poor cure rates.
Poor
High risk of complications.
High
CONSENSUS
Lung hydatids produce more complications than liver,hence all
Lung
patients of pulmonary hydatid irrespective of size or
presence/absence of complications are to be surgically treated.
Medical therapy should be used to prevent recurrence.
Medical
Recommended regimen mebendazole 1 month preoperative
Recommended
& 3 interrupted courses postoperatively
32
TROPICAL PULMONARY
EOSINOPHILIA (FILARIASIS IN
LUNG)
INTRODUCTION
One of the many syndromes with pulmonary infiltrates and
One
peripheral blood eosinophilia.
eosinophilia.
Originally described in India in 1940.
Originally
ILD thought to be due to immunological hyperresponsiveness
ILD
to human lymphatic dwelling filarial parasites-W.bancrofti and
parasitesB.malayi.
B.malayi.
33
DIAGNOSTIC CRITERIA FOR TPE
Cough worse at night.
Cough
count >3300/cube mm.
count
Clinical Residence in filarial endemic areas.
Clinical
Eosinophil and hematological response to DEC.
Eosinophil
Filarial antibody test has little value.
RESP. MED. 1999;93;655-659
1999;93;655-
PATHOGENESIS
Out of 90 million people infected worldwide,<1%
Out
manifest symptoms of TPE.
Exact reason is not known.
Exact
Intense inflammation of lung parenchyma to trapped
Intense
microfilaria which are released into circulation by
adult worms residing in lymphatic system.
Microfilaria are always absent in peripheral blood
Microfilaria
smear.
Sometimes detected in lung biopsy specimens.
Sometimes
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PATHOGENESIS (CONTD)
BAL of affected individuals reveal that polyclonal IgE and
BAL
filarial specific IgM,IgG and IgE accumulate in the lung.
Eosinophilic alveolitis.
Eosinophilic alveolitis.
Profound dysregulation in otherwise tightly regulated IgE Ab
Profound
response.
Limited evidence to suggest underlying genetic basis.
Limited
Usually complete resolution after therapy with DEC but in
Usually
some cases some degree of irreversible interstitial fibrosis
occurs.
Pathogenesis in some aspects analogues to atopic asthma
Pathogenesis
- obstructive ventilatory picture.
- partial reversibility with beta2 agonists.
- high levels of serum IgE.
IgE.
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