Diagnosis

The treatment aims to eradicate intestinal colonization responsible for recurrent respiratory

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

a roundworm of dog and cat can infect human, who is an intermediate host, and determine

Severe respiratory syndromes (ARDS) have rarely been observed (Bartelink AK et *al*., 1983), while asthma-like symptoms are currently reported among pulmonary manifestations.

Defects in neutrophil function have been reported in children with visceral larva migrans. This defect should be explained by the neutrophilic adherence to larvae illustrated else‐

Exacerbations of inflammatory reactions during antihelminthic treatment emphasize the

The causative agent is Strongyloides stercoralis, endemic in the tropics and subtropics. Eggs containing larvae ready to hatch, are the contaminating form after penetrating the skin; they then disseminate in all tissues via venous or lymphatic route in immunodeficient host

Autoinfestation is a common feature of this parasite, meaning the penetration of filariform larvae in the perianal skin of the infected subject without leaving the host. This phenomenon

Lung invasion result from larvae carried by the blood stream to the right heart and then to the lung. Larvae can pierce the pulmonary capillaries and reach the alveoli through the al‐ veolo-capillary membrane, inducing non cardiogenic edema and hemoptyses. After their migration through the bronchi and superior respiratory tree, some larvae can be swallowed in the intestine. Hyperinfection syndrome is related to severity of symptoms in the lung and the intestine, which are common sites of the parasitic life cycle, while disseminated disease represent the invasion of other organs not generally involved in the growth of the parasite

The skin penetration by the larva determines an hypersensitivity reaction as the result of a strong cell mediated immunity reaction in immunocompetent host preventing the tissue in‐ vasion (Neva FA, 1986). Marked autoinfection and subsequent hyperinfection are the main determinants of tissue dissemination in immunosuppressed subjects such as AIDS patients

can determine the persistence of infection even many years after (Scowden EB, 1978).

a Loeffler's like syndrome caused by larva migrans as with Ascaris.

where in animal models (Martin Huwer, 1989).

146 Oncogenesis, Inflammatory and Parasitic Tropical Diseases of the Lung

need of combination with corticosteroids.

(Cook, 1987; Longworth and Weller, 1986).

(Longoworth DL, and Weller PF, 1986).

Pathophysiology

2.2.1.3. Pulmonary strongyloidiasis

episodes.

of ascariasis.

2.2.1.2. Toxocariasis

Lung strongyloidiasis is commonly asymptomatic in immunocompetant individuals, or present with mild symptoms.

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‐ logic malignancies being at higher risk for the latter.

Eosinophilic pleural effusion have been reported among pulmonary manifestations of strongyloidiasis; and rare cases of acute respiratory failure due to respiratory muscle paraly‐ sis have been observed (da Silva OA, 1981).

The hyperinfection syndrome with Strongyloides stercoralis can worsen asthma or COPD exacerbations in some patients (Sen P, 1995; Ossorio MA, 1990).

Peripheral blood eosinophilia, anemia, and hypoalbuminemaia are current laboratory findings.

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

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

Serology is also interesting for detection of specific antibodies.

Treatment

Thiabendazole (25 mg/kg, twice a day for two days), Albendazole (400 mg, twice a day/5 days), Ivermectine (200 microgr/kg for one or two days) are recommended.

2.2.1.4. Pulmonary ancylostomiasis

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

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‐* *odenale* can reach the mammary glands and be transmitted to the child by maternal breastfeeding (Yu Sen-Hai, 1995).

Respiratory manifestations are frequently associated with systemic symptoms such as: fever,

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The diagnosis should be evoked after exclusion of other causes of pulmonary eosinophilia

Leucocytosis is common in TPE, with marked peripheral blood eosinophilia; and elevated

Serological examinations may reveal high level of specific IgG or IgE antibodies to microfi‐

Diethylcarbamazine (6 mg/kg/day for 3 weeks), a current treatment of filariasis, has been

This is a zoonosis caused by Dirofilaria immitis and repens. The nematode is a vascular par‐ asite, with the human as accidental host. The parasite is transmitted by mosquito. The vas‐ cular location induce embolism of pulmonary artery, with subsequent pathophysiological

Thoracic imaging (TTDM) shows well delimited nodule neigbouring an arterial branch.

Histopathological analysis of pulmonary biopsies is strongly contributive for the diagnosis

The larvae grow in striated muscles after invading the bloodstream. Man is infected after in‐ gesting partially or cooked or raw meat, and the larvae develop in the gut into adult worms. Pulmonary symptoms include: dyspnoea due partially to the involvement of diaphragm,

Peripheral blood eosinophilia and elevated IgE level are depending on Th-2 cytokines re‐ leased by TCD4 cells recruited by parasitic antigens. Elevated LDH enzyme suggest muscle

Stool examination is very important to determine co-infection with other helminths. The chest radiograph may show miliairy nodules mimicking miliairy tuberculosis.

Histopathological analysis of lung biopsies may illustrate microfilariae

Steroids have shown additional improvement of symptoms in TPE patients.

manifestations such as: hemoptyses, chest pain, dyspnoea …

The food-borne disease is caused by *Trichinella spiralis* in the man.

weight loss, and fatigue.

Laboratory findings

lariae.

Treatment

as other helmintic diseases, or drug use.

erythrocyte sedimentation rate is often reported.

successfully indicated In patients with TPE.

2.2.1.6. Pulmonary dirofilariasis

The disease is mainly asymptomatic

of this disease lacking specific treatment.

2.2.1.7. Pulmonary Trichinellosis

and cough.

involvement.

#### Pathophysiology

The lung migration can elicit blood eosinophilia as for other larva migrans. Larvae release low molecular weight proteins with anticoagulant properties (Cappello M, 1993), favoring blood loss during the intestinal capillaries destruction. Anemia with iron deficiency is often associated with this infection.

Local prurit and erythema follow skin penetration. Clinical, immunological and radiologi‐ cal manifestations of Loeffler's syndrome can be observed during larval migration through the lung.

#### Diagnosis

Gastrointestinal symptoms associated with respiratory asthma-like symptoms in an exposed individual are suggestive of parasitic lung infections

## Laboratory findings

Stool examination may demonstrate the presence of eggs, blood samples may identify eosi‐ nophilia and iron deficient anemia.

#### Treatment

Mebendazole and Albendazole have equivalent efficacy.

Ivermectine has been reported as an alternative.

2.2.1.5. Tropical Pulmonary Eosinophilia (TPE)

This syndrome is an immunological response of the host to filarial parasites invasion, main‐ ly Wuchereria bancrofti and Brugia malayi, affecting only 1% of patients with filariasis (Johnson S, 1994).

The filarial etiology has been suggested by the prevalent occurrence of the syndrome in the world regions with reported high filarialsis prevalence (South-East Asia), as well as the re‐ covery after antifilarial drug administration.

#### Pathophysiology

The hypersensitivity reaction to filarial antigens induce a strong eosinophilic inflammatory response in the lungs. The microfilariae in lymphatics invade the pulmonary circulation and parenchyma with further granulomatous and fibrosing pattern. The concentration of eosino‐ phils in the lung has been shown to be more significant than in the peripheral blood sug‐ gesting the compartimentalisation, and a prominent role of these cells in the pulmonary involvement and clinical manifestations (Pinkstori P, 1987).

#### Diagnosis

Epidemiological data state a male predominance in TPE (sex ratio M/F; 4:1), a disease of children and young adult (15-40 yrs).

Respiratory manifestations are frequently associated with systemic symptoms such as: fever, weight loss, and fatigue.

The diagnosis should be evoked after exclusion of other causes of pulmonary eosinophilia as other helmintic diseases, or drug use.

Laboratory findings

*odenale* can reach the mammary glands and be transmitted to the child by maternal breast-

The lung migration can elicit blood eosinophilia as for other larva migrans. Larvae release low molecular weight proteins with anticoagulant properties (Cappello M, 1993), favoring blood loss during the intestinal capillaries destruction. Anemia with iron deficiency is often

Local prurit and erythema follow skin penetration. Clinical, immunological and radiologi‐ cal manifestations of Loeffler's syndrome can be observed during larval migration

Gastrointestinal symptoms associated with respiratory asthma-like symptoms in an exposed

Stool examination may demonstrate the presence of eggs, blood samples may identify eosi‐

This syndrome is an immunological response of the host to filarial parasites invasion, main‐ ly Wuchereria bancrofti and Brugia malayi, affecting only 1% of patients with filariasis

The filarial etiology has been suggested by the prevalent occurrence of the syndrome in the world regions with reported high filarialsis prevalence (South-East Asia), as well as the re‐

The hypersensitivity reaction to filarial antigens induce a strong eosinophilic inflammatory response in the lungs. The microfilariae in lymphatics invade the pulmonary circulation and parenchyma with further granulomatous and fibrosing pattern. The concentration of eosino‐ phils in the lung has been shown to be more significant than in the peripheral blood sug‐ gesting the compartimentalisation, and a prominent role of these cells in the pulmonary

Epidemiological data state a male predominance in TPE (sex ratio M/F; 4:1), a disease of

feeding (Yu Sen-Hai, 1995).

associated with this infection.

individual are suggestive of parasitic lung infections

148 Oncogenesis, Inflammatory and Parasitic Tropical Diseases of the Lung

Mebendazole and Albendazole have equivalent efficacy.

involvement and clinical manifestations (Pinkstori P, 1987).

Ivermectine has been reported as an alternative. 2.2.1.5. Tropical Pulmonary Eosinophilia (TPE)

covery after antifilarial drug administration.

children and young adult (15-40 yrs).

Pathophysiology

through the lung.

Laboratory findings

(Johnson S, 1994).

Pathophysiology

Diagnosis

nophilia and iron deficient anemia.

Diagnosis

Treatment

Leucocytosis is common in TPE, with marked peripheral blood eosinophilia; and elevated erythrocyte sedimentation rate is often reported.

Serological examinations may reveal high level of specific IgG or IgE antibodies to microfi‐ lariae.

Stool examination is very important to determine co-infection with other helminths.

The chest radiograph may show miliairy nodules mimicking miliairy tuberculosis.

Histopathological analysis of lung biopsies may illustrate microfilariae

Treatment

Diethylcarbamazine (6 mg/kg/day for 3 weeks), a current treatment of filariasis, has been successfully indicated In patients with TPE.

Steroids have shown additional improvement of symptoms in TPE patients.

2.2.1.6. Pulmonary dirofilariasis

This is a zoonosis caused by Dirofilaria immitis and repens. The nematode is a vascular par‐ asite, with the human as accidental host. The parasite is transmitted by mosquito. The vas‐ cular location induce embolism of pulmonary artery, with subsequent pathophysiological manifestations such as: hemoptyses, chest pain, dyspnoea …

The disease is mainly asymptomatic

Thoracic imaging (TTDM) shows well delimited nodule neigbouring an arterial branch.

Histopathological analysis of pulmonary biopsies is strongly contributive for the diagnosis of this disease lacking specific treatment.

2.2.1.7. Pulmonary Trichinellosis

The food-borne disease is caused by *Trichinella spiralis* in the man.

The larvae grow in striated muscles after invading the bloodstream. Man is infected after in‐ gesting partially or cooked or raw meat, and the larvae develop in the gut into adult worms.

Pulmonary symptoms include: dyspnoea due partially to the involvement of diaphragm, and cough.

Peripheral blood eosinophilia and elevated IgE level are depending on Th-2 cytokines re‐ leased by TCD4 cells recruited by parasitic antigens. Elevated LDH enzyme suggest muscle involvement.

Larvae may be also identified in striated muscle biopsies.

#### Treatment

Mebendazole (for almost 2 weeks), associated to analgesics and corticosteroids is recom‐ mended.

named Katayama syndrome. Pulmonary acute manifestations mimic Loffler's syndrome or

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Chronic manifestations result from mechanical action of eggs or adult worm on the tissues. Pulmonary hypertension, haemoptysis, cor pulmonale could be observed. Pulmonary embo‐ lism is the consequence of small blood vessels obstruction by foreign bodies surrounded by various cells (eosinophils, neutrophils, lymphocytes, giant multinucleated cells (Wyler and Postlehwaite WE, 1983); Granuloma formation is the end-stage of the maintained inflamma‐

Optic microscopical identification of eggs in urine or stools is mandatory for the diagnosis.

Extrapulmonary manifestations include hepatosplenomegaly due to portal hypertension.

Cortcosteroides are indicate during acute phase and praziquantel (10-15 mg/kg, each 12 hours, one day). Artemether has shown effectiveness on juvenile forms of schistosomes.

The food-borne zoonosis is more frequent in Asia, affecting± 20 million people (Schwartz E, 2002); Subacute or chronic lung manifestations are described. The agent Paragonimus west‐ ermani lives in the lung, and eggs are eliminated in the sputum or faeces. Miracidiae devel‐ op into cercariae in the snail before infecting the second intermediate host, the crabs. The

Clinical manifestations are not specific, and chest radiograph may demonstrate cavitations as in tuberculosis. Pleural effusion or pneumothorax are frequently seen in paragonimiasis.

Lung involvement is mainly linked to extension of amoebic liver abscess; hematogenous

During intestinal transit and mutations, Trophozoites released after the cysts digestion by digestive secretions, may reach the muscularis mucosa and erode the lymphatics or the walls of mesenteric venules to invade the portal system of the liver. The parasitic embols

Rectal or bladder's mucosal biopsies could help demonstrating eggs of Schistosoma.

Asthma-like syndrome (Walt F., 1954).

tory response to schistosomal antigens.

Treatment

Treatment

Pulmonary Paragonimiasis

**2.3. Protozoal lung diseases**

*2.3.1. Pulmonary amoebiasis*

Schistosomiasis is an infectious cause of liver cirrhosis.

Peripheral blood eosinophilia and high IgE level are frequent.

man get infection after eating partially cooked or raw crabs.

Praziquantel is the first choice for treatment of this helminthic disease.

*Entamoeba histolytica* is the pathogenic form of infectious agent for the man.

spread and aspiration have rarely been reported (Shamsuzzaman SM et *al*, 2002).

## 2.2.1.8. CESTODES and the lung

Lung disease due to cestodes are caused by *Echinococcus granulosis* and *Echinococcus multilo‐ cularis* in the man. The lung and the liver are the main sites of cysts formation. Dogs are de‐ finitive hosts and eggs excreted in their faeces contaminate human when ingested with food or water.

Pulmonary symptoms are non specific and resemble asthma manifestations. Mechanical compression by hydatid cysts may influence clinical features. Rupture of Cysts in the bron‐ chi could explain haemoptysis or excretion of cyst fluid, and may lead to anaphylaxis. Pneu‐ mothorax, pleural effusion, and emphysema are possible lung presentation.

Blood laboratory findings extend from eosinophilia to IgE production.

Serodiagnosis is helpful by detection of specific antibodies.

Chest radiograph manifestations may consist in multiple nodules mimicking lung tumors.

#### Treatment

Surgical resection of the lesion is the most relevant approach. Mebendazole, Albendazole and praziquantel are indicated, mainly in recurrent disease.

2.2.1.9. Trematodes and the lung

This group include pulmonary scistosomiasis and paragonimiasis.

Pulmonary Shistosomiasis

*Schistosoma haematobium, mansoni*, and *japonicum* are the major pathogenic species for hu‐ man. *Shistosoma intercalatum* and *Shistosoma mekongi* are rarely encountered. Eggs excreted in urine or faeces of the infected patient contaminate water and infect the snail, intermediate host. The eggs then evolve in cercariae wich can penetrate the skin or be ingested by man. The adult worm stay in the bladder (*haematobium*), or in the gut (*S. mansoni, S. japonicum*).

#### Pathophysiology

Local inflammation occurs at the penetration site, while the onset of pulmonary manifesta‐ tions may be acute or chronic.

Pulmonary inflammatory reaction may induce a cytotoxic reaction to migrating agents, and facilitate the secretions of chimiotactic mediators for eosinophils, involved in the *schistosoma* immunity (Schwartz E et *al*, 2000).

Acute manifestations result from immunologic hypersensitivity reactions, and consist of systemic complaints such as fever, myalgia, chills, diarrhea, abdominal pain, urticaria, named Katayama syndrome. Pulmonary acute manifestations mimic Loffler's syndrome or Asthma-like syndrome (Walt F., 1954).

Chronic manifestations result from mechanical action of eggs or adult worm on the tissues. Pulmonary hypertension, haemoptysis, cor pulmonale could be observed. Pulmonary embo‐ lism is the consequence of small blood vessels obstruction by foreign bodies surrounded by various cells (eosinophils, neutrophils, lymphocytes, giant multinucleated cells (Wyler and Postlehwaite WE, 1983); Granuloma formation is the end-stage of the maintained inflamma‐ tory response to schistosomal antigens.

Optic microscopical identification of eggs in urine or stools is mandatory for the diagnosis. Rectal or bladder's mucosal biopsies could help demonstrating eggs of Schistosoma.

Extrapulmonary manifestations include hepatosplenomegaly due to portal hypertension. Schistosomiasis is an infectious cause of liver cirrhosis.

Peripheral blood eosinophilia and high IgE level are frequent.

Treatment

Larvae may be also identified in striated muscle biopsies.

150 Oncogenesis, Inflammatory and Parasitic Tropical Diseases of the Lung

Mebendazole (for almost 2 weeks), associated to analgesics and corticosteroids is recom‐

Lung disease due to cestodes are caused by *Echinococcus granulosis* and *Echinococcus multilo‐ cularis* in the man. The lung and the liver are the main sites of cysts formation. Dogs are de‐ finitive hosts and eggs excreted in their faeces contaminate human when ingested with food

Pulmonary symptoms are non specific and resemble asthma manifestations. Mechanical compression by hydatid cysts may influence clinical features. Rupture of Cysts in the bron‐ chi could explain haemoptysis or excretion of cyst fluid, and may lead to anaphylaxis. Pneu‐

Chest radiograph manifestations may consist in multiple nodules mimicking lung tumors.

Surgical resection of the lesion is the most relevant approach. Mebendazole, Albendazole

*Schistosoma haematobium, mansoni*, and *japonicum* are the major pathogenic species for hu‐ man. *Shistosoma intercalatum* and *Shistosoma mekongi* are rarely encountered. Eggs excreted in urine or faeces of the infected patient contaminate water and infect the snail, intermediate host. The eggs then evolve in cercariae wich can penetrate the skin or be ingested by man. The adult worm stay in the bladder (*haematobium*), or in the gut (*S. mansoni, S. japonicum*).

Local inflammation occurs at the penetration site, while the onset of pulmonary manifesta‐

Pulmonary inflammatory reaction may induce a cytotoxic reaction to migrating agents, and facilitate the secretions of chimiotactic mediators for eosinophils, involved in the *schistosoma*

Acute manifestations result from immunologic hypersensitivity reactions, and consist of systemic complaints such as fever, myalgia, chills, diarrhea, abdominal pain, urticaria,

mothorax, pleural effusion, and emphysema are possible lung presentation.

Blood laboratory findings extend from eosinophilia to IgE production.

Serodiagnosis is helpful by detection of specific antibodies.

and praziquantel are indicated, mainly in recurrent disease.

This group include pulmonary scistosomiasis and paragonimiasis.

Treatment

mended.

or water.

Treatment

2.2.1.8. CESTODES and the lung

2.2.1.9. Trematodes and the lung

Pulmonary Shistosomiasis

tions may be acute or chronic.

immunity (Schwartz E et *al*, 2000).

Pathophysiology

Cortcosteroides are indicate during acute phase and praziquantel (10-15 mg/kg, each 12 hours, one day). Artemether has shown effectiveness on juvenile forms of schistosomes.

#### Pulmonary Paragonimiasis

The food-borne zoonosis is more frequent in Asia, affecting± 20 million people (Schwartz E, 2002); Subacute or chronic lung manifestations are described. The agent Paragonimus west‐ ermani lives in the lung, and eggs are eliminated in the sputum or faeces. Miracidiae devel‐ op into cercariae in the snail before infecting the second intermediate host, the crabs. The man get infection after eating partially cooked or raw crabs.

Clinical manifestations are not specific, and chest radiograph may demonstrate cavitations as in tuberculosis. Pleural effusion or pneumothorax are frequently seen in paragonimiasis.

Treatment

Praziquantel is the first choice for treatment of this helminthic disease.

## **2.3. Protozoal lung diseases**

#### *2.3.1. Pulmonary amoebiasis*

*Entamoeba histolytica* is the pathogenic form of infectious agent for the man.

Lung involvement is mainly linked to extension of amoebic liver abscess; hematogenous spread and aspiration have rarely been reported (Shamsuzzaman SM et *al*, 2002).

During intestinal transit and mutations, Trophozoites released after the cysts digestion by digestive secretions, may reach the muscularis mucosa and erode the lymphatics or the walls of mesenteric venules to invade the portal system of the liver. The parasitic embols then obstruct the bloodstream and lead to abscess development with necrosis. The lung is the most frequent site of extra-intestinal invasion.

in Indonesia has reported occurrence of ARDS in uncomplicated and severe malaria, in pa‐ tients within the first 5 days after the start of the treatment, while peripheral parasitemia was decreased. The authors hypothesize that lung injury could then be related to an inflam‐ matory response following treatment (Louis Schofield, Georges E. Grau, 2005). Their work suggest that impaired lung function is not exclusively the fact of microvascular obstruction by parasitized red cells, but include also white blood cells, contributing to impairment of gas

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Pulmonary edema follows increased alveolar capillary permeability with extravasation of

Systemic symptoms of malaria are: fever, myalgia, headache, loss of appetite, nausea, vomit‐ ing. Severe respiratory symptoms may be observed, following the onset of edema and respi‐

Thick and thin stained blood smears are the routine laboratory examination to identify the

Serodiagnosis and PCR of *plasmodium* in urine or saliva, may be contributive where available.

Chest radiograph demonstrates variable patterns such as lobar consolidation, pleural effu‐

Parenteral quinine is the drug of 1st choice for the treatment of severe malaria. Artemisinine derivatives are an alternative in case of contra-indications. Adjunctive therapy with clinda‐

Antivectorial eradication, using insecticide treated bed-nets is widely utilized in endemic re‐

The disease caused by the Protozoan parasite, *Toxoplasma gondii* infects the man, after inges‐

Immunocompromised individuals are at higher risk of developing toxoplasmosis with the

Toxoplasma infection is asymptomatic in most immunocompetent humans. The pathogen is then destroyed by strong antibody dependent reactions or delayed type hypersensitivity mechanism. A strong Th1 cytokine profile is elicited by cells of innate immunity for efficient protection, and pathogen could be destroyed also by monocytes- derived mediators such as nitric oxide, which inhibits the parasite growth in different organs, mainly the lung and the

sion, alveolar infiltrates suggesting pulmonary edema, or hemorrhages.

mycine or doxycycline has been proposed in complicated malaria.

General resuscitation measures could be indicated in life threatening cases.

central nervous system involvement as the most common complication.

transfer, subsequent to ventilation and perfusion mismatch (Anstey NM et *al*, 2002).

capillary content into the alveoli (Mohan Alladi et *al*, 2008)

Diagnosis

Treatment

gions.

ratory distress syndrome.

*2.3.3. Pulmonary Toxoplasmosis*

tion of cyst-contaminated food.

central nervous system, as prominent targets.

plasmodium species.

Clinical symptoms are related to the hepatic and intrathoracic implications. General symp‐ toms including fever, right upper quadrant pain, cough, chest pain are frequent in the lung amoebiasis. Pleural effusion could develop, following hepatobronchial fistula. The paren‐ chymal disease can present as pulmonary abscess with characteristic chocolate pus and air‐ space consolidation at chest radiograph. Elevation of right hemidiaphragm is an earlier radiographical feature in liver abscess.

*E histolytica* may be identified in sputum, in stools specimen or pleural pus.

The accuracy of serodiagnosis is established in the tissue amoebiasis, mainly in non endemic populations. PCR should also be more contributive, even not routinely performed in many institutions.

#### Treatment

Metronidazole is widely used, with established effectiveness. Lactoferrin and lactoferricins combined to low metronidazole doses has been proposed as an alternate therapeutic option.

#### *2.3.2. Pulmonary malaria*

Malaria is a public health problem in tropical and subtropical areas. With the increasing population travelling, mosquitos which transmit the disease can be carried out of the natural frontiers and cause illness in naïve, non exposed patients. Four species of *Plasmodium* are identified (*P falciparum, P. ovale, P. malariae, P. vivax*). *Plasmodium falciparum*, *vivax*, and *ovale* can cause acute lung injury, or acute respiratory distress syndrome (Mohan A et *al*, 2008).

#### Pathophysiology

The pathogen lives in the erythrocytes and could impair their functions. Impaired red cells motility, favored by exaggerated cytoadherence to the capillaries endothelium (Corbett CE et *al*, 1989), induce sequestration of the red and white blood cells in different organs, with subsequent deprivation in oxygen delivery, endothelial dysfunction, and enhancement of anaerobic metabolism. Multiple organ dysfunctions (MODS) is the condition leading to death. Red cells sequestration and destruction enhances the release of parasites and erythro‐ cyte material in the bloodstream, inducing a vigorous inflammatory response

Pulmonary involvement extend from cough and dyspnoea, to fatal ARDS, non cardiogenic pulmonary edema, and intra-alveolar hemorrhages. Parenchymal disease due to plasmodial infections has not yet been clearly evidenced, due to numerous viral or bacterial co-infec‐ tions, mainly in child under 5 years.

ARDS in malaria is more common in adults than in children, as well as in pregnant women and non immune individuals

The pathogenesis of ARDS in severe malaria is poorly understood. Sequestration of parasi‐ tized red cells in small vessels seems not to be the only underlying mechanism. Recent study in Indonesia has reported occurrence of ARDS in uncomplicated and severe malaria, in pa‐ tients within the first 5 days after the start of the treatment, while peripheral parasitemia was decreased. The authors hypothesize that lung injury could then be related to an inflam‐ matory response following treatment (Louis Schofield, Georges E. Grau, 2005). Their work suggest that impaired lung function is not exclusively the fact of microvascular obstruction by parasitized red cells, but include also white blood cells, contributing to impairment of gas transfer, subsequent to ventilation and perfusion mismatch (Anstey NM et *al*, 2002).

Pulmonary edema follows increased alveolar capillary permeability with extravasation of capillary content into the alveoli (Mohan Alladi et *al*, 2008)
