Mode of contamination

**1.2. Specific defense mechanisms**

immunity) (Kohlmeter JE, Woodland DL, 2006).

144 Oncogenesis, Inflammatory and Parasitic Tropical Diseases of the Lung

**2. Tropical parasitic lung diseases**

pertension). (Santiago M et *al*., 2005).

**2.2. Helminthic parasites**

*2.2.1. Nematodes and the lung*

2.2.1.1. Pulmonary ascariasis

**2.1. Overview**

reactions

Adaptive immunity relays on the interaction between antigen-presenting cells (macrophag‐ es, dendritic cells, neutrophils) with specific T-lymphocytes in the context of cell mediated immunity, as well as, on the antibodies production by activated B-lymphocytes (humoral

Protozoa and helminthes can affect the lung as a primary site, or a complication. Some para‐ sites have a migration cycle through the lung (larva migrans), inducing blood and tissue eo‐ sinophilia. Tissue and peripheral blood eosinophilia are elicited by chimiotactic activity of released inflammatory mediators, such as cytokines (IL-3, IL-5), which play a key role in ac‐ tivation and differentiation of eosinophils. Eosinophils secrete various substances, some with antiparasitis properties, others favoring tissue damage in targeted organs. Elevated IgE level observed in these conditions relay on the Th2-lymphocytes, stimulating antibodies

Clinical manifestations of the lung involvement could be acute: asthma –like syndrome, or Loeffler's syndrome, with dyspnea, wheezing, cough (Ford RM, 1996); or chronic such as he‐ moptysis or right heart failure signs. Acute manifestations depend on immunological reac‐ tion (hypersensitivity), and chronic feature relay on the mechanical action of pathogen on the vessels and tissues. (vg: schistosoma eggs in the pulmonary artery and pulmonary hy‐

Löeffler's syndrome represent transient clinical, immunological and radiological manifesta‐ tions due to parasites whose life cycle elicit a transit through the lung or not, and to drug

Hypereosinophilia observed in this syndrome is antigen –induced, and circulating IL-5, is

The three classes of helminths (Cestoidea, Trematoda, and Nematoda) can affect the lung.

This group include: ascariasis, strongyloidiasis,ancylostomiasis, tropical pulmonary eosino‐

Ascariasis is a round worm infection caused by Ascaris lumbricoides. This nematode dis‐ ease affects ± 25% of the world population whose 95% are in Africa (Crompton, 1999).

the key mechanism for the recruitment and differentiation of the eosinophils.

philia, pulmonary dirofilariasis, and pulmonary trichinellosis.

production by B-lymphocytes (Om P Sharma, 1991; VijayanVK, 2008).

The starting point is the survival of eggs able to contaminate ingesta by the new host. Poor sanitation, fecal contamination of food or water, are the main risk factors of dissemination. Embryonated eggs (2-4 weeks), when ingested are dissolved in the stomach juice and then release rabdoid larvae in the duodenum, before migration through the intestine. Larvae then enter the portal system via capillaries and lymphatics, after penetrating the wall of the intes‐ tine. The involvement of the hepatic circulation allow the right heart and lung invasion. The eggs reach the alveolar space after crossing the capillary walls and can be swallowed and then reach again the small intestine to mute in adult forms. This pilgrimage can take 14 days after ingestion (Sarinas PS, Chitkara RK, 1997).

#### Pathophysiology

Adult worms or migrating larvae exert a mechanical pressure on lung structures inducing inflammatory responses, leading to granuloma formation with eosinophils, neutrophils and macrophages. Activated cells release cytokines such as IL-3 and IL-5 involved in the recruit‐ ment and differenciation of eosinophils, explaining the blood and tissue eosinophilia report‐ ed. TH2 Lymphocytes are responsible for the high IgE (Yazicioglia, 1996) and IgG4 levels (Santra A, 2001) described.

Hypersensitivity reaction inducing peribronchial inflammation, mucus production, and sometimes bronchospasm is responsible for the clinical manifestations.

#### Diagnosis

Abdominal manifestations are currently reported: gastric pain, vomiting, diarrhea, abdomi‐ nal discomfort. In some complicated cases pancreatitis or obstruction of biliary duct or small intestine can occur, caused by adult worms.

Respiratory symptoms due to larval migration in the lungs, consist in mild cough or Loef‐ fler's syndrome (Ford RM, 1996). This syndrome associates respiratory symptoms (dry cough, wheezing, dyspnoea) with blood and lung eosinophilia, and chest radiograph with fleeting infiltrates. General symptoms such as fever, loss of appetite, myalgia can be ob‐ served.

Pneumonia is a more rare condition with ascariasis infection

Laboratory findings

Stool examination may show eggs or adult worms.

Larvae may be found in respiratory secretions

Serological approach (specific IgG4 antibodies) could be helpful (Santra A *et al*., 2001; Bhat‐ tacharya T, 2001).

Blood hypereosinophilia and high IgE level are common.

Chest radiograph may show migrating inhomogenous alveolar infiltrates.

Treatment

The treatment aims to eradicate intestinal colonization responsible for recurrent respiratory episodes.

(Lessman KD, 1993), individuals on long term corticosteroid therapy, or with malnutrition,

Tropical Lung Diseases

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http://dx.doi.org/10.5772/52371

Mechanical action by the adult worms and host reaction are responsible for digestive mani‐

Secondary gram negative bacterial infection by gram- pathogen is frequent, bacteria being carried by larvae during the crossing of the intestinal wall. The migration through the lung can determine bronchopneumonia,alveolar hemorrhages, and pulmonary abscess and hae‐

Lung strongyloidiasis is commonly asymptomatic in immunocompetant individuals, or

Gastrointestinal manifestations, cough, dyspnoea, wheezing and haemoptysis are frequent during lung involvement. Hyperinfection and disseminated disease are commonly fatal, which elderly individuals and those on long term corticosteroid therapy, or having hemato‐

Eosinophilic pleural effusion have been reported among pulmonary manifestations of strongyloidiasis; and rare cases of acute respiratory failure due to respiratory muscle paraly‐

The hyperinfection syndrome with Strongyloides stercoralis can worsen asthma or COPD

Peripheral blood eosinophilia, anemia, and hypoalbuminemaia are current laboratory

Larva may be observed in repeted stool specimen examination due to the low parasitic load

Thiabendazole (25 mg/kg, twice a day for two days), Albendazole (400 mg, twice a day/5

Eggs eliminated with the feces continue the maturation in the soil, where larvae will pene‐ trate the intact skin to infect the man, which is the only definitive host. The oral route of in‐ fection is possible for *Ancylostoma duodenale*. Migrant larvae reach the lung structures has illustrate for other helminths, inducing a Loeffler's syndrome. The larvae of *Ancylostoma du‐*

Pulmonary secretions, duodenal juice, may be contributive for parasite identification.

days), Ivermectine (200 microgr/kg for one or two days) are recommended.

*Ancylostoma duodenale* and *Necator americanus* are the two helminths in this group.

lymphomas etc..(Casati A, 1996; Genta RM, 1989).

logic malignancies being at higher risk for the latter.

exacerbations in some patients (Sen P, 1995; Ossorio MA, 1990).

Serology is also interesting for detection of specific antibodies.

sis have been observed (da Silva OA, 1981).

in immunocompetent individuals.

2.2.1.4. Pulmonary ancylostomiasis

festations.

moptyses.

Diagnosis

findings.

Treatment

present with mild symptoms.

Mebendazole (100 mg twice a day for three days, or 500mg one day) and Albendazole (400mg, single dose) are the drugs of choice. Pyrantel Pamoate, Levamisole, and Piperazine are alternative choices. Ivermectine, an antifilarial drug has shown efficacy in the treatment of ascariasis.
