Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 874021, 18 pages http://dx.doi.org/10.1155/2014/874021 Review Article Parasitic Pneumonia and Lung Involvement Attapon Cheepsattayakorn1,2 and Ruangrong Cheepsattayakorn3 1 10th Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand 2 10th Office of Disease Prevention and Control, Department of Disease Control, Ministry of Public Health, Chiang Mai 50100, Thailand 3 Department of Pathology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand Correspondence should be addressed to Attapon Cheepsattayakorn; [email protected] Received 16 February 2014; Revised 15 May 2014; Accepted 20 May 2014; Published 9 June 2014 AcademicEditor:LisaM.Harrison Copyright © 2014 A. Cheepsattayakorn and R. Cheepsattayakorn. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Parasitic infestations demonstrated a decline in the past decade as a result of better hygiene practices and improved socioeconomic conditions. Nevertheless, global immigration, increased numbers of the immunocompromised people, international traveling, global warming, and rapid urbanization of the cities have increased the susceptibility of the world population to parasitic diseases. A number of new human parasites, such as Plasmodium knowlesi, in addition to many potential parasites, have urged the interest of scientific community. A broad spectrum of protozoal parasites frequently affects the respiratory system, particularly the lungs. The diagnosis of parasitic diseases of airway is challenging due to their wide varieties of clinical and roentgenographic presentations. So detailed interrogations of travel history to endemic areas are critical for clinicians or pulmonologists to manage this entity. The migrating adult worms can cause mechanical airway obstruction, while the larvae can cause airway inflammation. Thispaper provides a comprehensive review of both protozoal and helminthic infestations that affect the airway system, particularly the lungs, including clinical and roentgenographic presentations, diagnostic tests, and therapeutic approaches. 1. Introduction Entamoeba histolytica, Paragonimus,andDirofilaria lung involvement are less common [2]. Protozoal and helminthic parasitic pneumonias and lung involvement are common in the tropics [1]withfewexcep- 2. Pulmonary Malaria tions; they most commonly occur in the western world and are diseases of immunocompromised hosts [2]. In USA, The four types of malarial parasites are Plasmodium falci- Toxoplasma gondii pneumonia is observed most frequently parum, Plasmodium malariae, Plasmodium vivax,andPlas- in acquired-immunodeficiency-syndrome (AIDS) patients. modium ovale,andtheprotozoaofthegenusPlasmodium Pulmonary strongyloidiasis is identified in patients with cause Malaria and are primarily transmitted by the bite of chemotherapy or glucocorticoids treatment and is endemic an infected female Anopheles mosquito to infect humans [5]. in the Southeastern USA, whereas Ascaris and hookworm The malaria parasites then infect human hepatocytes in the infestations may be present with eosinophilia and pulmonary forms of sporozoites, schizonts, and merozoites, respectively infiltrates during the larval migration stage2 [ ]. Nevertheless, [6]. This stage is called “human liver stage” which takes protozoal infestations usually do not cause blood and tissue approximately 4.5 days for Plasmodium falciparum [6]. In eosinophilia except helminthic infestations [1]. In 1932, Lof- case of infection with Plasmodium vivax,oneofthetwo fler described the first four cases with minimal respiratory forms (Plasmodium vivax and Plasmodium ovale)ofrelapsing symptoms, peripheral blood eosinophilia, and pulmonary malaria to infect humans, and is the most prevalent in South- infiltrates in the chest roentgenographs3 [ ]. The eosinophilic east Asia and South America, has ability to become dormant lung diseases that are particularly prevalent in the tropics intheliver(“hypnozoite”)andisabletobereactivatedafter are frequently related to parasitic infestations [4], whereas months or years contributing to an attack of intraerythrocytic 2 BioMed Research International stage malaria despite the absence of mosquito bites [6, 7]. distress syndrome) [7]. Recurrent infections with Plasmod- The merozoites then burst out from the hepatocytes and ium falciparum may result in severe anemia [7]. Nephrotic infect human erythrocytes in the form of ring form, tropho- syndrome can result from repeated infections with Plasmod- zoites, schizonts, and merozoites again [6]. This cycle takes ium malariae [7]. Hyperreactive malarial splenomegaly (or approximately 43–48 hours for the Plasmodium falciparum, called “tropical splenomegaly syndrome”) is marked by the andthecycleisabletodevelopclinicalsymptoms[6]. In much enlarged spleen and liver, anemia, abnormal immuno- another cycle, the intraerythrocytic ring form transforms to logical findings, and a susceptibility to other infections and intraerythrocytic gametocyte before infecting the mosquito is attributed to an abnormal immune response to repeated [6]. This stage takes approximately 9 days for Plasmodium malarial infections [7]. Plasmodium falciparum may cause falciparum [6]. Human liver stage and human intraerythro- more severe disease in mother and may lead to premature cytic stage are asexual stages [6]. After mosquito ingestion of delivery or delivery of a low-birth-weight baby [7]. Neuro- the human malaria-infected blood (intraerythrocytic game- logical defects may occasionally persist following cerebral tocytes), the gametocyte transforms to microgametocyte and malaria, particularly in children [7]. On rare occasions, microgametocyte which take approximately 15 minutes and Plasmodium vivax can cause rupture of the spleen [7]. The then transform to diploid zygote in one hour for Plasmodium most common presentations of falciparum malaria in the falciparum, respectively, in the mosquito’s midgut [6]. The study were fever, followed by jaundice, renal involvement, diploidzygotethentransformstoookineteinapproximately cerebral malaria, severe anemia, bleeding manifestation, and 12–36 hours for Plasmodium falciparum before transforming hypoglycemia [10]. The gold standards for the diagnosis of to oocysts and sporozoites in the mosquito’s salivary gland malaria are light microscopic examination of thin and thick before transmission of the sporozoite to humans by mosquito stained blood smears [1, 11]. Additional laboratory findings biting [6]. The malaria parasite stage in the mosquito is may include mild anemia, mild thrombocytopenia, elevation called “mosquito stage or sexual stage” [6]. In most cases, of aminotransferase, and elevation of serum bilirubin [7]. the incubation period varies from 7 to 30 days [7]. The Human urine and saliva PCR detection of Plasmodium shorter incubation periods are demonstrated in Plasmodium falciparum have been introduced [11]. In severe falciparum falciparum, while the longer ones are observed in Plasmod- malaria, the roentgenographic presentations include diffuse ium malariae [7]. Returned travelers should remind their interstitial edema, pulmonary edema, pleural effusion, and healthcare providers of any travel in areas where malaria lobar consolidation [11]. Sanklecha et al. reported three cases occurs during the past 12 months [7]. The main finding of of childhood falciparum malaria in a family and revealed patients with falciparum malaria which is the most deadly that two cases demonstrated bilaterally fluffy pulmonary type of malaria infection is sequestration of erythrocytes infiltrates, whereas the remaining case showed normal chest containing mature forms of Plasmodium falciparum in the roentgenogram [12]. Chest roentgenograms in three cases microvasculature of the organs and is quantified by mea- of malaria with sickle cell anemia also reported that all surement of Plasmodium falciparum specific histidine-rich reported patients demonstrated bilaterally pulmonary infil- protein 2 (PfHRP2) using a quantitative antigen-capture trates [13]. Chest roentgenograms are usually nonspecific, enzyme-linked immunosorbent assay [8]. Gas exchange is but they should be recognized in high endemic areas of significantly impaired in patients with severe malaria9 [ ]. malaria [13]. Chest roentgenogram in a patient with Plas- In patients with uncomplicated malaria, the classical (but modium vivax malaria demonstrated diffuse bilateral alveolar infrequently observed) malaria attack lasts 6–10 hours that opacities which indicated acute respiratory distress syndrome consists of a cold stage (sensation of cold, shivering), a hot [14].ThreecasesofARDSwithPlasmodium vivax malaria stage (fever, headaches, vomiting, and seizures in young were also reported in India and one case was demonstrated children), and a sweating stage (sweats, return to normal tem- with bilateral perihilar infiltrates, one case with bilateral perature, tiredness) [7]. Classically, the attacks occur on every diffuse extensive opacities, and another case with bilateral second day with the “tertian” malaria parasites (Plasmodium basal ground glass opacities on chest roentgenograms [15]. falciparum, Plasmodium vivax,andPlasmodium ovale)and Pulmonary edema is universal finding at autopsy16 [ ]. The on every third day with “quartan” parasite (Plasmodium alveoli