Transcript Tropical Pulmonary Eosinophilia

RESPIRATORY TRACT
PARASITIC INFECTION
(PARASITIC PNEUMONIA)
Teguh Wahju Sardjono
Sudjari
Aswin Djoko Baskoro
2010-2011
Learning Objectives
After getting this lecture, student has ability to :
- Describe the kind, biology and life cycle of
parasites which infect respiratory tract
- Explain the pathogenesis, clinical manifestation,
treatment, prevention and rehabilitation of
pulmonary diseases caused by parasites
Introduction
The Anatomy of Lung
Parasitic Pneumonia
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Definition
– Parasitic pneumonia is an infection of the lungs by parasites.
It is a rare cause of pneumonia, occurring almost exclusively
in immuno-compromised persons.
– This is a respiratory infection that may or may not be serious.
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Classification ( topics which will be discussed right here)
– Helminthic Pneumonia (egg, larval and adult stage)
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Nematodes
 Loeffler Syndrome
 Occult Filariasis
 Cestodes (Hydatid cyst).
 Trematodes (Bronchopulmonary bilharziasis i.e. Schistosomiasis,
paragonimiasis).
•
- Protozoal Pneumonia
– Amoebic Lung Absces
– Pneumocystic Pneumonia
– Toxoplasmic Pneumonia
Helminthic Pneumonia
1. Nematodes : Larvae
 Loeffler’s syndrome
 Occult filariasis
2. Cestodes : Hydatid cyst
3. Trematodes : rare cases
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Egg : Schistosoma/ Bilharziasis
Pathogenesis :
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Verminous pneumonitis i.e. focal pneumonia caused by the
worms of bilharziasis when reaching the lungs.
Bilharzial granuloma or bilharzial tubercles that represent a
distinctive reaction around the ovum after it penetrates the vessel
wall
Adult : Paragonimiasis
Loeffler’s Syndrome
(Löffler's syndrome)
 Is a disease in which a certain type of white blood cell
(eosinophil) accumulates in the lung in response to a
parasitic infection.
 It was first described in 1932 by Wilhelm Löffler in cases
of eosinophilic pneumonia caused by the parasites
 Ascaris lumbricoides,
 Strongyloides stercoralis
 Hookworms : Ancylostoma duodenale and Necator americanus.
 Many authors give the term "Löffler's syndrome" to any
form of acute onset pulmonary eosinophilia no matter
what the underlying cause.
Ascaris lumbricoides
 common name : “human round worm”
 the largest of the intestinal nematodes parasitizing humans.
 worldwide in distribution
 most prevalent through out the tropics, sub-tropics
 more prevalent in the countryside than in the city
 Infection initiated by swalowing infective stage of eggs 
hatch in the intestine  blood stream  lung migration 
pathologic effects
Hookworms
 There are 2 species that infect
human :
1. Ancylostoma duodenale
2. Necator americanus
 Adult stage parasitizes
intestinal tract  produce eggs
 Eggs hatched on the soil to be
rhabditiform  filariform larva
 Larvae penetrate the skin 
blood stream  migrates
through lungs (lung migration)
 pathologic effects
Strongyloides stercoralis
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Adult: Parasitizes intestinal tract 
produces eggs, hatched to be larvae
Larvae : Penetrates skin  Migrates
through lungs
Asymptomatic - most
Acute infection
 Migrating larvae in lungs
(Loeffler’s)
 Migration through intestinal tract 
abdominal pain and diarrhea
 Heavy infection  malabsorption,
steatorrhea, weight loss and
edema
 Eosinophilia - not constant finding
The blood-lung migration phase of
the larvae  Löffler's syndrome
During the migration through the lungs
- the larvae may cause a pneumonia.
- The symptoms/Clinical manifestation of the pneumonia are:
- low fever,
- cough,
- blood-tinged sputum,
- asthma.
- Large numbers of worms may give rise to allergic symptoms.
- Eosinophilia is generally present.
.
Occult Filariasis
 Occult Filariasis is commonly used to designate filarial infections in
which microfilaria (mf) are not found in the peripheral blood although
they may be seen in tissues. However, it has now been shown that in
some cases with occult filariasis, mf may actually be found after more
careful blood examination despite their low density.
 Occult filariasis is believed to result from a hypersensitivity reaction
to filarial antigens derived from microfilariae. Only a very small
proportion of individuals in a community where filariasis is endemic
develop occult forms of the disease.
 Caused by the larvae of :
- Wuchereria bancrofti
- Brugia malayi
- Brugia timori
The clinical manifestations of Occult
filariasis
 Tropical Pulmonary Eosinophilia
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(TPE)
Glomerulopathies
(Granulonephritis)
Endomyocardial fibrosis
Filarial Arthritis
Filarial granulomas in the breast
Tropical Pulmonary Eosinophilia(TPE)
 was first described by Frimodty Moller and Barton in 1940.
 Its main clinical symptoms are:
 Severe Cough and wheezing (specially at night)
 Frequent weight loss and fatigue but with minimal or no fever.
 Restrictive or obstructive lung abnormalities.
 Abnormal chest radiographs that frequently show diffuse
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mottled pulmonary interstitial infiltrate.
Peripheral blood eosinophilia > 3000 cell/µl
Extreme elevation of immunoglobin (IgE)
Extreme elevation of anti-filarial antibodies
caused by an immune hyperresponsiveness to microfilariae
trapped in the lungs
typically seen in young males.
Tropical Pulmonary Eosinophilia
(TPE)
 Detection:
Using IFAT(Indirect Flourescent Antibody Test)
filarial antibodies are detected.
 Treatment:
Dramatic clinical improvement in response to
specific anti-filarial chemotherapy with DEC
GLOMERULOPATHIES (GLOMERULONEPHRITIS)
 Glomerulonephritis is associated with lymphatic filariasis.
 Filarial antibodies have been detected in 2 of 5 children with
filariasis and acute glomerulonephritis.
 Renal biopsy showed diffuse messangial proliferative
glomerulonephritis with C3 deposition on the basement
membrane.
 The condition responds well to DEC therapy.
Filarial granulomas in the breast
• particularly prevalent in India and Srilanka where
W.bancrofti is the predominant species.
• Filarial granulomas present as hard breast lumps
attached to the overlying skin
• difficult to distinguish from malignant tumours.
• Histological examination an eosinophilic
granulomatous reation around the filarial parasites
which are in varying stages of degeneration.
• Both adult worms and mf have been found in the
granulomas.
• Filarial antibodies have been demonstrated in
these patients and the condition responds to DEC
therapy which, in many instances, can lead to
complete disappearance of the lump.
Pulmonary Hydatid cyst
 Hydatid disease is a parasitic infestation by a tapeworm of the genus
Echinococcus
 Human echinococcosis is a zoonotic infection caused by the
tapeworm of the genus Echinococcus.
 Of the 4 known species of Echinococcus, 3 are of medical importance
in humans:
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Echinococcus granulosus, causing cystic echinococcosis (CE);
Echinococcus multilocularis, causing alveolar echinococcosis (AE);
Echinococcus vogeli.
 E granulosus is the most common of the three. E multilocularis is rare
but is the most virulent
 Pulmonary hydatid diseases are less prevalent rather than hepatic
hydatid disease
Life cycle and pathogenesis
Definitive host: dogs and other canidae  adult worm = Echinococcosis
Intermediate host : (sheep, goat, swine and also human) got infection by
ingestion of embryonated eggs  larvae invade and live inside several
organs eg. Liver (the most prevalent) lung, brain heart etc)
Hydatid cyst
 Clinical picture of the ruptured cyst:
 30% of pulmonary cysts rupture, especially those with a diameter
greater than 7 cm. Rupture may occur spontaneously or as a
result of coughing, sneezing, muscular effort, trauma to the chest
or infection.
 A communication with the bronchial tree allows air to leak into
the potential space between the pericyst and the laminar layer.
The air localizes at the superior aspect of the cyst, giving rise to
the meniscus radiological sign (air cap or operculum) i.e. halo
appearance.
 Rupture of a cyst produces an abrupt cough with expectoration
and fever; hemoptysis is common.
Diagnosis:
 A high index of suspicion is invaluable, rural residence
and contact with dogs are suggestive.
 Diagnosis is established radiologically and
serologically.
 The complement fixation test (Casoni test). It is
positive in 66% cases.
 The indirect hemagglutinin test. It is positive in about
70% of cases.
Treatment :Surgical excision is the best.
Radiological Diagnosis
A round partially filled cystic
opacity of >8cm diameter in
right lower zone.
A 5 × 6 cm circular lesion
located in the apex of the
right lung at X-ray.
A case with bilateral hydatid
cysts at lower zone of thorax.
Microscopic features of
hydatid cyst.
C.
Adult form : Paragonimiasis
 caused by Paragonimus westermani
 Geographic Distribution:
Mostly in Far East, some species
also found in Southeast Asia
(Thailand, Cambodya etc)
 Habitat of adult worm
 Can migrate to other organ esp
brain and striataed muscle
 Infection in human may as long as
20 years.
 Cat, dog and pig can be the host
Clinical symptoms
 Acute phase (invasion and migration):
 Pulmonary disturbance, diare, abdominal pain, fever, cough,
urticaria, hepatosplenomegaly.
 Chronic phase, lung symptoms eg cough, hemoptisis (bloody cough)
 abnormal radiological appearance
Lesion in other organs  more severe (eg : brain)
Laboratory Diagnosis
 By finding the eggs in stool or sputum examination
(2-3 months after infection)
Treatment
- Praziquantel (drug of choice).
- Bithionol
Oval shape, brown colour,
(85 µm x 53 µm) with operculum
On one side and thickening of the wall
At the opposite of the operculum
Broncho-Pulmonary Bilharziasis
(Schistosomiasis)
 This includes:
 Verminous pneumonitis i.e. focal pneumonia caused by the
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worms of bilharziasis when reaching the lungs.
Bilharzial granuloma or bilharzial tubercles that represent a
distinctive reaction around the ovum after it penetrates the
vessel wall.
Pleural effusion is reported secondary to hypoproteinemia or
after administration of anti-bilharzial treatment.
Demonstration of bilharzial ova in the sputum was also reported.
Bronchospasm simulating an asthmatic attack can also occur
early in the course of the disease or during anti-bilharzial
treatment.
Hemoptysis can occur during the larva through the lung.
Interstitial fibrosis can also occur.
Transient pulmonary infiltration with oesinophils.
Diagnosis
Adults of Schistosoma spp. in lung tissue, stained with H&E.
Images courtesy of Harvard Medical School, Cambridge, MA
Pulmonary amebiasis
 The protozoa causing human
amebiasis, Entamoeba
histolytica, is not primarily a
respiratory tract parasite.
However, pleuropulmonary
involvement may arise as a
complication of amebic intestinal
or extraintestinal disease.
 infection of the lung by amebae;
usually indicates extension of
Entamoeba histolytica infection
from abscess of liver, penetrating
through the diaphragm into the
lung.
Type of extra intestinal Amoebiasis
Pulmonary
amebiasis
Amebic pulmonary disease can
develop in several ways
Rupture of an amebic hepatic abscess
through the diaphragm, which is the
most common
Lymphatic spread from the liver
through the diaphragm
Hematogenous embolic spread from
the liver or colon, an unusual disorder
that should be suspected when there is
pulmonary amebiasis without hepatic
disease or noncontiguous pulmonary
and hepatic disease
Fever, enlarged tender liver, weight
loss, pain in the lower chest and
shoulder may be found. Leucocytosis,
mild anemia and raised sedimentation
rate are also present.
 Pleuropulmonary amebiasis is a very rare complication of
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amebiasis infection
Direct pulmonary involvement is exceptional.
The clinical diagnosis is difficult without any intestinal
or extraintestinal manifestations.
Extension of infection through the diaphragm may result
in fibrinosis pleurisy, pleural effusion or basal pneumonia.
Radiologically, there may be elevation of the right hemidiaphragm or obliteration of the costo-phrenic angle by
pleural effusion.
Medical Treatment
Antibiotics in lung abscess
 Anaerobic organisms:
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Gram-negative organisms
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First choices - Cephalosporins, aminoglycosides, quinolones
Alternatives - Penicillins and cephalexin (Biocef)
Oral therapy - Trimethoprim/sulfamethoxazole (Septra)
Pseudomonal organisms:
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First choice - Clindamycin (Cleocin 3)
Alternative - Penicillin
Oral therapy - Clindamycin, metronidazole (Flagyl), amoxicillin (Amoxil)
First choices include aminoglycosides, quinolones, and cephalosporin.
Gram-positive organisms
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First choices - Oxacillin (Bactocill), clindamycin, cephalexin, nafcillin (Nafcil), and
amoxicillin
Alternatives - Cefuroxime (Ceftin) and clindamycin
Oral therapy - Vancomycin (Lyphocin)
Synthetic Emetine
 Dehydroemetine, a synthetic product, introduced into therapeutics
in 1961, replaces Emetine :  six times more active than Emetine,
half as toxic and of being eliminated twice as rapidly. Some time
later, it is produced in the form of sugar-coated pills, which simplifies
its administration.
The derivatives of nitroimidazole
 Metronidazole, had been used since 1966 revolutionizes the
treatment of all forms of Amoebiasis and leads gradually to the
disappearance of all the other medicines. It is easily administered,
well-tolerated and effective on the vegetative forms and cysts. This
medicine is a complete amebicide.
Surgery : irigation abscess fluid using water sealed drainage (WSD)
Pulmonary toxoplasmosis
 Toxoplasmosis is an infection due to the parasite Toxoplasma gondii.
 The disease can affect the brain, lung, heart, eyes, or liver, but most
primary infections produce no symptoms. The time between
exposure to the infection and symptom development is 1 - 2 weeks.
 Pulmonary Toxoplasmosis should be considered in patients with HIV
receiving Aerosolized Pentamidine, who have fever and pulmonary
disease but do not respond to IV Pentamidine, especially if CPK, LDH
and IgG to T. gondii are elevated.
 The diagnosis of Pulmonary Toxoplasmosis in HIV disease may be
delayed or overlooked, leading to death from a treatable infection.
 Medications to treat the infection include an antimalarial drug and
antibiotics. AIDS patients should continue treatment for as long as
their immune system is weak to prevent the disease from
reactivating.
Pneumocystis Carinii
 This organism appears as minute oval bodies or cysts 5-10 mm in
length and is probably related to the protozoa. It causes pneumonia
in infants of a few months of age and in adults who are
immunosuppressed.
 Breathlessness and tachypnea are the main features, other physical
signs are rarely helpful.
 Gas exchange becomes progressively impaired with progressive fall
in the transfer factor and ultimately cyanosis.
 The X-ray shows widespread mottling which is slowly progressive.
 The diagnosis may be confirmed by lung biopsy (usually
transbronchial biopsy) or broncho-alveolar lavage.