Teguh Wahju Sardjono Sudjari Aswin Djoko Baskoro 2010-2011.

Teguh Wahju SardjonoSudjari

Aswin Djoko Baskoro2010-2011

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• 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.

• Classification ( topics which will be discussed right here)– Helminthic Pneumonia (egg, larval and adult stage) 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 Pneumonia1. Nematodes : Larvae

Loeffler’s syndrome Occult filariasis

2. Cestodes : Hydatid cyst

3. Trematodes : rare cases Egg : Schistosoma/ BilharziasisPathogenesis :

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.

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

Ascaris lumbricoides

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 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 syndromeDuring 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 (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

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: 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 = EchinococcosisIntermediate 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 5 × 6 cm circular lesion located in the apex of the right lung at X-ray.

A round partially filled cystic opacity of >8cm diameter in

right lower zone.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 wallAt the opposite of the operculum

Broncho-Pulmonary Bilharziasis (Schistosomiasis) This includes:

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.

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

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.

Pulmonary amebiasis

Type of extra intestinal Amoebiasis

Pulmonary amebiasisAmebic pulmonary disease can develop in several ways Rupture of an amebic hepatic abscess through the diaphragm, which is the most commonLymphatic spread from the liver through the diaphragmHematogenous 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 diseaseFever, 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 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 hemi-diaphragm or obliteration of the costo-phrenic angle by pleural effusion.

Medical Treatment Antibiotics in lung abscess Anaerobic organisms:

First choice - Clindamycin (Cleocin 3) Alternative - Penicillin Oral therapy - Clindamycin, metronidazole (Flagyl), amoxicillin

(Amoxil) Gram-negative organisms

First choices - Cephalosporins, aminoglycosides, quinolones Alternatives - Penicillins and cephalexin (Biocef) Oral therapy - Trimethoprim/sulfamethoxazole (Septra)

Pseudomonal organisms: First choices include aminoglycosides, quinolones, and

cephalosporin. Gram-positive organisms

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 m 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.