Parasitic diseases of lung - westermani vivernii paragonimus opisthrochis flukes flatworm

1. Chairperson – Dr. ASHOK G.
Student – Dr. SUMANT BALGANDI

2. INTRODUCTION
 The word parasite comes originally from the Geek word
parasitos.
 Para = alongside of , sitos=food , i.e.one who eats at
another’s table/lives at another’s expense.
 Although the same is true of many bacteria and viruses ,the
designation parasite is reserved ,by convention for helminths
and protozoa.

3.  These organsisms are larger and more complex than
bacteria with a eukaryotic cell structure similar to that
of human host cells.
 Historically this similarity has made it difficult to find
effective antiparasitiic agents that don’t cause
unacceptable toxicity to human cells.
 Intesive research has now provided suitable agents for
the safe and effective treatment of most parasitic
infections.

4. PULMONARY INVOLVEMENT
 Cystic lung lesions
 Consolidation
 Pleural effusion
 Transient pulmonary infiltrates
 Pulmonary nodule,abscess
 Alveolar,interstitial involvement

5. DISEASES PARASITES
NEMATODES
Pulmonary ascariasis Ascaris lumbricoides
Pulmonary ancylostomiasis Ancylostoma duodenale
Necatror americanus
Pulmonary strongyloidiasis Strongyloides stercoralis
Tropical pulmonary eosinophilia Wucheria bancrofti
TREMATODES
Pulmonary schistosomiasis Schistosoma haematobium
Schistosoma japonicum
Pulmonary paragonimiasis Paragonimus westermani
CESTODES
Pulmonary hydatid cyst Echinococcus granulosus
Echinococcus multilocularis

6. DISEASES PARASITES
PROTOZOA
Pulmonary amoebiasis Entamoeba histolytica
Pulmonary leishmaniasis Leishmania donovani
Pulmanary malaria Plasmodium vivax
Plasmodium falciparum
Plasmodium malariae
Plasmodium ovalePlasmodium knowelsi
Pulmonary toxoplasmosis Toxoplasma gondi
Pulmanary babesiosis Babesia microti

7. ASCARIS LUMBRICOIDES
 Human ascariasis results from ingestion of embryonated
A.lumbricoiddes eggs that are contained in the feces contaminated soil.
 Pulmonary symptoms of pneumonia may occur 1-3 weeks after primary
infection.
 Larvae in lung are surrounded by patchy infiltrate of neutophils,
eosinophils
 Alveoli contain serous exudate
 Production of bronchial mucus increased.
 Intensity of the reaction depends on the number of parasite larvae and
previous sensitisation.

8. Pathogenesis
Ingestion of embryonated eggs
Eggs hatch in GIT
Larvae penetrate gutwall
via venous blood reach right heart and lungs
reach trachea and are swallowed
In small intestine develop into adult worms

9. HOOKWORMS AND STRONGYLOIDES
 In immunocompetent subjects, pulmonary disease by
hookworms and strongyloides is minimal as the worm
burden is usually low.
 HYPERINFECTION
In immunosuppressed patients, extensive internal
reinfection takes place leading to increase in the no. of worms
in intestine and lungs
Lung manifestations
 alveolar hemorrhages
 bronchopneumonia,
 chronic bronchitis,
 asthmatic symptoms.

10.  Widespread dissemination of strongyloides is
associated with secondary infection caused by gram
negative bacteria carried along with it from the gut.
 Eosinophilia is absent in strongyloides hyperinfection
syndrome due to defective cell mediated immunity or
use of corticosteroids in many patietnts.
 Mortality in hyperinfection syndrome is around 87%

11. PATHOGENESIS
Infective larvae penetrate the skin
via blood reach lungs
reach alveolar spaces
reach trachea and then swallowed
form adult worms in small intestine

12. LOEFFLER SYNDROME
 Hypersensitivity response leading to respiratory symtoms
including cough,dyspnea,chest pain, fever,hemoptysis.
 Occurs 1-3 week after infection, coincident with larval
migration from pulmonary circulation to alveoli.
 Characterised by transient pulmonary infiltrates and
peripheral eosinoiphilia.
PATHOPHYSIOLOGY
 Damage to respiratory epithelium,
 Increased mucus production

13. Causes
 Ascaris lumbricoides
 Ancylostoma duodenale
 Necator americanus
 Strongyloides stercoralis
 Rare causes-Aspergillus fumigatus,P.carni,NSAIDS.

14. DIAGNOSIS
 Detection of nematodes in Loeffler syndrome is often difficult.
 Stool examination often negative at this point, as adult worms
have not yet reached the small intestine and begun producing
eggs.
 Treatment- symptomatic.
 Specific antihelminthic therapy is ineffective during the
pulmonary stage but can cure the infection once the parasites
reach maturity in small intestine.

15. LAB DIAGNOSIS
 Stool examination-eggs/adult worms
 Demonstration of larvae in sputum
 Serology-Indirect hemgglutination assay
Immunoflorescence antibody test
 Eosinophilia

16. TREATMENT
ASCARIS AND HOOKWORM INFECTIONS
 T. albendazole 400 mg od or
 T.mebendazole 100 mg od for 3 d
STRONGYLOIDES
 T. IVERMECTIN 200µ/kg/d for 2d (longer for autoinfection)
 Repeat after 2 week to ensure eradication.
 Alternatively- T. albendazole 400 mg bd 7d

17. VISCERAL LARVA MIGRANS
 Caused by ingestion of embryonated eggs of nematodes
parasitising animals.
 More common in children.
• Organisms- Toxocara canis (dog roundworm)
Toxoccara cati(cat roundworm)
others-Angiostrongylis
Gnathostoma
Anisakis simplex
 Affect liver,lung,and other organs.

18.  Life cycle is similar to Ascaris lumbricoides, however
they don’t convert to adult worms.
 Tissue injury results from both invasion of different
organs and from hypersensitivity of the host.
 DIAGNOSIS-Serology
 Treatment-albendazole and steroids in severe cases.

19. TROPICAL PULMONARY
EOSINOPHILIA
 It is a distinct syndrome that develops in individiuals
infected with lymphatic dwelling filarial species.
 Common in areas endemic for Wucheria bancrofti and
brugia malayi.
 Its still a poorly defined clinical entity.

20. FEATURES
 h/o residence in filaria endemic areas
 Chronic nocturnal paroxysmal cough
 Marked eosinophilia
 Positive serology
 Therapeutic response to DEC.

21.  Clinical symptoms result from allergic and
inflammatory reactions elicited by the parasites.
 In some patietnts trapping of microfilaria in
reticuloendothelial tissue may cause
hepatosplenomegaly, lymphedenopathy.
 In the absence of treatmet- cause interstitial fibrosis.

22. DIFFERENTIAL DIAGNOSIS
 Asthma
 Loeffler syndrome
 Allergic bronchopulmonary aspergillosis
 Churg-strauss syndrome
 Systemic vasculitis

23. m
DIAGNOSIS-
 Chest xray-normal/miliary lesions
 Spirometry-restrictive patttern in most cases
 Serum IgE –raised
 Antifilarial antibody –raised
 TREATMENT
 DEC- 4-6 mg/kg 14d
 T.Doxycycline 100 mg bd 4-6 week-kills symbiotic
wolbachia bacteria necessary for nutrition and fertility.
 Relapse rate- 12-25% - requires retreatment

24. HYDATID DISEASE
 Caused by cestode Echinococcus granulosus and
multilocularis.
 Dog is the definitive host.
 Humans acquire infection by the ingestion of food
contaminated with feces containing eggs.
 Embryos released migrate to different organs including
liver,lung.
 Forms space occupying lesion HYDATID CYST
 The cyst increases in size by 2-3cm/yr.

25.  The inner lining of these cysts is a germinal layer
capable of producing daughter cysts that may seed other
organs upon spontaneous rupture or surgical
manipulation of the original cyst.
 More common in children
 Cysts in the lungs are usually discovered early in the
course of the disease as radiographic examinations of
the chest are now very common.

26.  Pulmonary cysts are solitary in 60% of cases.
 In 50-80% cases affect only one lobe.
 Cyst is surrounded by the granulomatous reaction eventually
causing calcified solid mass.
 Spontaneous rupture of cysts into bronchus causes expectoration of
scoleces in the sputum,while rupture into mediastinum and pleural
cavity causes secondary implantation and new daughter cysts.
 May be associated with pleural effusion.

27.  Fluid content in the cyst is immunogenic, and leakage
of the cyst fluid can cause anaphylactic reactions.
CLINICAL FEATURES
 Hydatid cysts are usually asymptomatic.
 Cough,
 dyspnea,
 chest pain

30. DIAGNOSIS
 CHEST XRAY- lesions -1-20 cm
atelectasis
pneumonitis
pleural effusion
fluid level-WATER LILY sign
calcification
 Serology
 CT-multiple round cysts
 MRI
 Casoni test - positive in 75% cases
 Weinberg complement fixation test.

31. TREATMENT
 SURGERY is the treatmet of choice for the hydatid disease of the
lung and it will confirm the diagnosis.
 Enucleation of the intact cyst
 Cystotomy
 Removal of the cyst with aspiration
 Lobectomy,segmental resection
 PAIR(Percutaneous aspiration,Injection of cysticidal agent and
Reaspiration are now not recommended now for lung cysts.
 Immediate thoracotomy is recommended for patients who have
rupture of hepatic cyst into pleural space.
 T.albendazole 400 mg bd for 28 days if all the cysts cannot be
removed or when rupture of cyst has occurred.

32. SCHISTOSOMIASIS
 =Blood flukes.
 Man gets infected by the penetration of intact skin by
the free living cercaria.
 Cercaria form schistosomula and via circulation reach
their final habitat.
(pelvic venous plexus-S.hematobium
mesentric plexus-other species)

33.  Some of the schistosome eggs are carried by the
venous plexus to lungs which account for the
pulmonary disease.
 Upon reaching the pulmonary circulation, eggs gather
in small arterioles where they induce formation of
delayed hypersensitivity reactions.

34.  The curtailment of pulmonary vasculature and the
decreased distensibility caused by the perivascular
fibrosis leads to pulmonary htn and cor pulmonale
 PFT shows predominantly restrictive pattern with
decrease in diffusing capacity.

35.  C/F-fever, dyspnea,dry cough
Chronic infection-cor pulmonale
DIAGNSIS
 Detection of schistosoma eggs in stool/urine
 PCR
 Serology

36.  TREATMENT
 T.praziquentel –kills adult worms and stops further
destruction of tissues by ova depostition
 S.hemetobium and S.mansoni- 20mg /kg bd for 1 d
 S.japonicum 20mg/kg tid 1d

38. PARAGONIMIASIS
 =LUNG FLUKES
 Causative organisms-Paragonimus westermani,
P.heterotremus,P.miyazaki,P.kellikotti.
 Prevalent in southeast Asia, Africa,south and central America.
 Infection is maintained in the endemic areas through contamination of
water sources with feces or sputum of infected individuals.
 Definitive host-man,cat,dog etc
 1st intermediate host- freshwater snail
 2nd intermediate host-freshwater crab

40.  The primary site of infection in humans is lungs.
 May also be found in other tissues like brain.
 3 stages of parasite development in lung
 1.Primary infection –granulocytic reaction,charcot leyden
crystals
 2.Encystation
 3.Death-cause collapse of the cyst,fibrosis,calcification.

41. CLINICAL FEATURES
 Incubation period- 2-20 days.
 Cough
 respiratory discomfort mainly upon raising in the morning
 rusty blood tinged sputum containing parasite eggs,necrotic
material,charcoat leyden crystals.
 Frank henmoptysis –confused for TB or malignancy

42. LAB DIAGNOSIS
 Demonstration of eggs- chararcteristic yellow brown
operculated eggs in sputum,feces.
 ELISA
 Intradermal test-using P.westermani antigen
 Biopsy
 Radiology-infiltrates,cavitation,fibrosis,pleural
effusion,pulmonary thickening

43.  PLEURAL FLUID ANALYSIS
1.low glucose <10mg/dl
2.low ph <7.1
3. high LDH (>1000 IU/L)
4.cholesterol crystals –Pseudochylothorax
5.eosinophilia in pleural fluid
6.elevated IL-5 in pleural fluid
 TREATMENT
T.Praziquentel 25mg/kg tid 2d

46. ENTAMOEBA HYSTOLYTICA
 It is a protozoan infection occurring as a result of contamination of food and
water .
 Infection can also be acquired by the ano-genital or orogenital sexual contact
among heterosexual males.
 Quadrinucleate cyst –infective form.
 Amoebic pulmonary disease occurs as the result of concomitant liver abscess.
 Liver abscess may produce diaphragmatic irritation and can cause sympathetic
pleural effusion .
 Liver abscess may rupture through the diaphragm into the pleural space
causing respiratory distress, empyema lung abscess.

47.  Pleural fluid is described as ANCHOVY
PASTE/CHOCOLATE SAUCE.
 Pleural fluid does not contain purulent material rather
it is a mixture of blood, cytolysed liver tissue,small
solid particles of liver parenchyma that have resisted
dissolution..

48.  Many patients with extraintestinal amoebiasis may not
have symptomatic intestinal disease, so the absence of
preceding gastrointestinal symptoms does not exclude
the diagnosis.
 So the diagnosis of amoebiasis should be considered in
all patients with right sided pleural effusion for which
no other explaination is obvious.

49. DIAGNOSIS
 Stool examination-cysts, trophozites
 Stool antigen detection –ELISA
 SEROLOGY-sensitivity of antibody testing in
extraintestinal amoebiasis -95%
 PCR

53. TREATMENT
 T. Metronidazole 500-750 mg tid for 10 d.
 Patients with transdiaphragmatic rupture should undergo
percutaneous drainage of both the liver abscess and the
collection of material in pleural space.

54. REFERENCES
 FISHMAN’S PULMONARY DISEASES AND
DISORDERS 5TH EDITION
 PLEURAL DISEASES by W.LIGHT 6TH EDITION
 HARRISON’S PRINCIPLES OF INTERNAL MEDICINE
 TEXTBOOK OF PARASITOLOGY BY BHAVEJA 5TH
EDITION
 SRB’S MANUAL OF SURGERY 4TH EDITION

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