parasitic infestion in respiratory

8/12/2019 Parasitic Infestion in Respiratory

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Lung lesion

1. Focal lung lesion

a. cystic lung lesion

b. coin lesionc. consolidation/pleural effusion

2. Diffuse lung disease

a. transient pulmonary infiltratesb. alveolar/interstitial lung changes.



Cystic Lung Lesion

Causes : larvae of Echinococcus sp

Definite hosts : Canidae family (dogs andfoxes).

Distribution (Echinococcus granulosus) :

South America, countries surrounding theMediterranean, the Middle East, some

sub-Saharan African countries, Russia

and China

Hydatidosis



Patogenitas

The eggs travel to the liver or lungs and

slowly develop into hydatid cysts over a

period of several months or years.

Although most cysts form in the liver,

20 –30% form in the lung.

Occasionally, lung cysts form after

transdiaphragmatic spread of parasites

following the rupture of liver cysts.



Clinical presentation

Primary infection : asymptomatic for years,

may be discovered incidentally on a chest x-

ray.

Symptoms : chest pain, cough, haemoptysisor pneumothorax.

Antigenic material from the cyst :

hypersensitivity reaction with fever, wheeze

and urticaria and, rarely, anaphylaxis.

Secondarily infection : empyema or lung

abscess formation.



Chest x-ray showing a hydatid cyst in the left

lower lobe with a collapsed hydatid cyst

exhibiting the 'lily pad' sign lying above it.



CT scan of the thorax showing a

ruptured hydatid cyst in the left

upper lobe of the lung.



Laboratory Diagnosis

Eosinophilia

Serological tests

Percutaneous aspiration of liver

cysts under ultrasound guidance :

protoscolices or hooklets

notgenerally recommended



Management

Small cases resolve spontaneously.

Surgical excision of cysts with a view topreserve as much lung parenchyma as

possible, albendazole as adjunctivetherapy once the cyst has been removed

Medical treatment with albendazole with or

without praziquantel Aspiration followed by injection of a

scolicidal agent



Coin Lesions

Causes : Dirofilaria immitis (dog

heartworm)

Habitat : Adult worms live in the right

ventricle

Definite hosts : Canidae family

Vector : mosquito species

Distribution : Japan, Australia, the USA

and Italy (D repens).

Dirofilariasis



Patogenitas

Adult worms live in the right ventricle of

Canidae family and produce circulating

microfilaria which can be transmitted by a

variety of mosquito species to humans. Inhumans the worms pass through the right

ventricle but fail to mature and are swept

away to peripheral pulmonary arteries.



Clinical Presentation

Most patients are asymptomatic

Symptoms : chest pain, cough,haemoptysis, wheezing, fever, chills and

malaise Radiography : coin lesion usually 1 –3 cm

in diameter and sharply defined, central

necrotic area is surrounded by agranulomatous reaction and fibrous wall,dead worms may calcify.




Eosinophilia, no reliable serologicaltests, biopsy specimens after

thoracatomy

Management

Chemotherapy is ineffective. The onlytreatment is surgical excision if

indicated.



Consolidation/Pleural Effusion

Causes : Paragonimus westermani (lungflukes)

Distribution : south east Asia, central Africa and South America.

Habitat : the adult worms : pulmonary

cysts, usually in pairs. Eggs : sputum orfaeces.

Second intermediate host: fresh watercrab or crayfish

Paragonimiasis



Patogenitas

Humans are usually infected by eating the

second intermediate host, fresh water crab

or crayfish, if raw or lightly cooked. After

ingestion the larvae penetrate theintestinal wall and migrate to the lung

parenchyma. They mature in a fibrous

host-derived capsule, usually in the upperzones of the lung.




Symptoms : pleuritic chest pain,haemoptysis, chronic cough and fever.

If pulmonary cysts erode into adjacent

bronchi, patients may suffer life-threateninghaemoptysis

Radiography : patchy air space consolidation,

cystic changes and ring shadows. Pleural

effusions and pneumothoraces may occur.

Paragonimiasis is often misdiagnosed as

tuberculosis or malignant disease




Eosinophilia

Total serum IgE may be raised.

The identification of the characteristicoperculated eggs in faeces, sputum or

bronchoalveolar lavage fluid confirms thediagnosis.

Management Medical treatment : praziquantel.

Surgery for persistent pneumothorax,pleural effusion or empyema.



Amoebiasis

Causes: Entamoeba histolytica

E histolytica is endemic in regions with poor

sanitation and poor socioeconomicconditions.

Cysts are passed in the faeces and are highly

resistant to environmental conditions,facilitating faecal-oral transmission. Ingested

cysts are transformed into trophozoites.



Patogenitas

In a subset of cases the Ehistolytica trophozoites bind to intestinalepithelial cells, leads to lysis of the

epithelial cells and invasive amoebiasisresulting in colitis. Blood-borne spread ofthe parasite may lead to the formation ofan amoebic liver abscess

Amoebic pleuropulmonary disease is themost common complication of amoebicliver abscess




cough, pleuritic pain and dyspnoea

Intrathoracic complications include rupture

of an amoebic liver abscess into thepleural cavity with empyema formation

hepatobronchial fistula Rarely, a

bronchobiliary fistula



Chest x-ray showing right basal

consolidation and pleural effusion secondary

to amoebic liver abscess



Eosinophilia is not a feature of amoebic

infections.

freshly passed stools should be examinedfor amoebic trophozoites. Trophozoites

are seldom found in sputum, pleural fluid

or abscess aspirates.The E histolytica adhesin may be detected

in faecal specimens by ELISA.

Laboratory Investigations



Management

Medical treatment : tinidazole ormetronidazole to kill trophozoites in tissue,followed by diloxanide furoate or

paromomycin to eliminate cysts from theintestinal lumen

Surgical treatment of pulmonaryamoebiasis may be required when there isdirect pulmonary involvement or spread topleura.



Transient Pulmonary Infiltrates

Causes : Ascaris lumbricoides

Distribution : worldwide in areas with poorsanitation where there is faecalcontamination of soil or food.

Ascariasis




During the second week of infection, as thelarvae invade the lung tissue, a smallproportion of patients become symptomatic.

Loeffler's syndrome : larval migration into thealveoli which triggers an allergic responseleading to respiratory symptoms

cough, wheeze, dyspnoea, chest pain, feverand haemoptysis.

The illness usually resolves spontaneouslyafter several weeks.



Radiography : transient nodular or diffuse

pulmonary infiltrates

Laboratory Diagnosis : leucocytosis and

peripheral blood eosinophilia and total

serum IgE may be elevated. Ascaris eggs

in the stool on microscopy

Management : A single dose of

albendazole is the treatment of choice.

Mebendazole, piperazine and pyrantelpamoate are alternatives.



Hookworm Infections

Causes : Ancylostoma

duodenale and Necator americanus)

Distribution : A duodenale is also found in

the Middle East and southern Europe; N

americanus is found sporadically in the

southeastern USA.

Poor sanitation and the absence of

footwear favour transmission.



Patogenitas

Hookworm eggs are passed in faeces and

develop in soil into filariform larvae able to

penetrate the skin of the human host.

The larvae penetrate blood vessels and

undergo heart –lung migration before

breaking out into the alveoli and ascending

to the pharynx from where they areswallowed.




Pulmonary manifestations are usually

mild. Loeffler's syndrome including dry

cough, wheeze, dyspnoea and fever.

Radiography : changes are consistent with

Loeffler's syndrome]




Eosinophilia

Finding eggs in the stool

Serological tests are not useful in view ofmany cross-reactions with otherhelminthic infections.

Management

a single dose of albendazole.Mebendazole and pyrantel pamoate arealternatives.



Patogenitas

The disease primarily affects children, who

acquire the infection through contact with

soil contaminated with embryonated eggs.

Fresh animal faeces are not infectious as theeggs require 2 –3 weeks to embryonate in the

soil.

Ingested eggs hatch in the stomach. Larvae

penetrate the mucosa of the gut and enter

the mesenteric vessels from where they

migrate to the lungs and other organs.




Most infections occur in children and mostare asymptomatic.

Cough, dyspnoea and wheeze which may

present as asthma or bronchitis. Hepatomegaly, splenomegaly and ocular

lesions.

Radiography : transient localised changesor widespread patchy areas ofconsolidation.



Laboratory Diagnos is

Toxocara larvae do not develop into adults inthe human host, so eggs are not passed inhuman faeces.Visceral larva migrans is characterised bypersistent peripheral eosinophilia andleucocytosis.

Management

Ocular disease : local or systemic steroidsby ophthalmologist.

Anthelminthics are not usually given.Visceral larva migrans is treated withalbendazole.

Corticosteroids may be required .



Alveolar/Interstitial Changes

Causes : Schis tosoma manson i

, Schistosoma haemato-

b ium and Schistosoma japonicum . Distribution : worldwide distribution,

endemic throughout the tropics

Habitat : The adult trematode worms are

found in the vesical plexus (S haematob ium )or in the mesenteric veins (S manson i and S

japon icum ). Their eggs are excreted in urineor faeces respectively.

Schistosomiasis



Patogenitas

Humans are infected by cercariaeduring contact with fresh water.

The worms releasing eggs 4 –6 weeks

after skin penetration. The initial release of eggs may give rise

to acute schistosomiasis which occurspredominantly in non-immune hosts.

Eggs that are not passed into thebladder or intestinal lumen are the maincause of chronic disease, causinggranulomatous reactions and fibrosis.



Patogenitas

In severe longstanding S mansoni and S

japonicum infections, the development of

hepatosplenomegaly and portal

hypertension may lead to diversion ofeggs to the lung vasculature. This results

in obliterative arteritis which may cause

pulmonary hypertension.




Acute schistosomiasis (Katayama fever) :

fever, cough, dyspnoea, rash and arthralgias.

Acute symptoms are usually self-limiting.

Heavy infections : pneumonitis, Loeffler-likesyndrome, dyspnoea, reduced exercise

tolerance and chest pain.

Clinical signs of severe hypoxaemia such as

digital clubbing may be seen.

Pulmonary arteriovenous fistulas.



Chest x-ray showing

widespread pulmonary nodules



Laboratory d iagnos is

E osinophilia

Eggs may be found in faeces, urine andsputum or bronchoalveolar lavage 6weeks after infection. Eggs of Shaematobium are most likely to be foundin late morning urine samples. Terminalurine specimens maximise sensitivity.

IgG antibodies to Sch is tosoma eggantigen are detectable 6 –12 weeksfollowing infection and can be measuredby ELISA. Schistosomal serology may benegative, especially in Katayama fever



Management

In acute schistosomiasis (Katayamafever) praziquantel is administeredunder steroid cover. A second course

of praziquantel may need to be given3 –6 months later to eradicate anyschistosomes that may have survived

the first course of treatment.Treatment is less beneficial inadvanced chronic disease.



Patogenitas

Filariform larvae penetrate the skin, enterblood vessels and undergo heart and lungmigration. They migrate into alveoli andsubsequently ascend to the trachea.

Larvae are swallowed and develop in thesmall intestine into adult worms whichproduce eggs. These are deposited in theintestinal mucosa where they hatch into

rhabditiform larvae which are excreted infaeces.

Filariform larvae may penetrate the bowelwall or the perianal skin to initiate a new

cycle (autoinfection).




Often asymptomatic, but mild symptoms mayoccur in the initial stages of lung migration.

In the immunocompromised patient ahyperinfection syndrome can result in severe

disseminated infection Respiratory symptoms may be non-specific

and, apart from gastrointestinal complaints,symptoms of asthma might be the onlyfeature.

Adult respiratory distress syndrome may beseen.

Extensive intra-alveolar haemorrhage





eosinophilia, may absent in thehyperinfection syndrome in immuno

compromised patientsRhabditiform larvae in stool, sputum orduodenal aspirates. Filariform larvae mayalso be seen.

Antibody assays, cross-reactions occur withother helminth infections and antibody levelsmay be low in immunocompromisedpatients.

Management

Ivermectin is usually effective.

Hyperinfection : repeated treatments



Radiolography : pulmonary infiltrates

Radiographic changes may include miliarynodules, reticular opacities and airspace

opacities ranging from multifocal to lobar

distribution. These are thought to be due

to secondary infection, haemorrhage,inflammatory pneumonitis and bacterial

abscess formation



Tropical Pulmonary Eosinophilia

Causes : Wuchereria bancrofti and Brugia

malayi

Distribution : south east Asia, India, China

and Africa.




slow onset over several months, respiratory symptoms including cough,

dyspnoea and wheeze which may be worseat night.

Systemic features including fever, malaiseand weight loss may occur.

Radiological Findings : Bilateral fine nodularor reticulonodular shadowing, CT scan of thethorax might be more sensitive to detectreticulonodular pulmonary opacities andmediastinal lymphadenopathy.



Laboratory Investigations

High titres of antifilarial antibodies

peripheral blood eosinophilia

The extensive immune response rapid

clearance of microfilariae from the blood

no microfilariae can be found in the

peripheral blood.

Total serum filarial-specific IgE and IgG

antibody levels are raised.

parasitic infestion in respiratory

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