Pulmonary Manifestations of Parasitic Diseases




Respiratory diseases are important causes of morbidity and mortality among children throughout the world. Although diseases attributed to parasitic infection are uncommon for many physicians in temperate climates, these infections remain important conditions that must be addressed. Because of the influx of immigrants from developing countries and the volume of global travel, including children, physicians should have a basic understanding of respiratory illnesses attributed to parasitic infections.


The spectrum of syndromes related to parasitic respiratory infection is quite large. Diagnosis of a parasitic infection should be classified through the recognition of identifiable host characteristics, underlying medical conditions, and specific clinical manifestations. The etiology of acute respiratory infections caused by parasitic agents can be suggested, however, through knowledge of the specific geographic locale of the ill child or the location from which the child has arrived ( Table 13-1 ). Clinical presentations, findings on imaging studies, or individual laboratory results can differentiate infection among particular parasitic organisms. Underlying immunodeficiency should suggest infection with certain organisms, such as Strongyloides stercoralis or Toxoplasma gondii. In patients from appropriate geographic locations with respiratory symptoms and elevated peripheral eosinophil counts, infection with Ascaris lumbricoides, hookworm, S. stercoralis, or Toxocara species should be considered. This chapter reviews parasitic diseases that have pulmonary manifestations.



Table 13-1

Etiologies of Pulmonary Infiltrates Based on Geographic Distribution of Infecting Parasite































































































































































GEOGRAPHIC DISTRIBUTION
ORGANISM AF AM AS E OC WS
Helminthic
Ascariasis X
Capillariasis hepatica X X X X
Dirofilariasis X
Echinococcosis X X X X X
Filariasis X X X
Gnathostomiasis X *
Hookworm X
Paragonimiasis X X X X X
Schistosomiasis X X X
Strongyloidiasis X
Toxocariasis X
Trichinellosis ( Trichinella spiralis ) X
Protozoan
Amebiasis X
Cryptosporidiosis X
Malaria ( Plasmodium falciparum ) X X X X X
Toxoplasmosis X

AF, Africa; AM, Americas; AS, Asia; E, Europe; OC, Oceania; WS, widespread.Modified from Martin G: Approach to the patient in the tropics with pulmonary disease. In Guerrant RL, ed: Tropical Infectious Diseases, vol 2, 2nd ed. Philadelphia, WB Saunders, 2006, pp 1544–1553.

* Rare in other geographic locales.


Infiltrate early in disease, Katayama disease.



Protozoa


Malaria


Epidemiology


Malaria is endemic throughout the tropical areas of the world; one half of the world’s population lives in areas where malaria occurs. From a global perspective, there are approximately 300 to 500 million infections per year, resulting in approximately 1 million deaths ( Fig. 13-1 ). Most of these deaths occur in children.




Figure 13-1


Geographic distribution of malaria ( dots ). The infection is distributed widely in many tropical and subtropical climates. Plasmodium vivax is the most prevalent WORLDWIDE type of malaria. Plasmodium ovale is especially prevalent in tropical West Africa. Infection with Plasmodium falciparum has the highest mortality rate.

(Adapted from Martinez S, et al. Thoracic manifestations of tropical parasitic infections: a pictorial review. Radiographics 25:135–155, 2005.)


Etiology


The Anopheles mosquito transmits the parasite ( Fig. 13-2 ). Various Plasmodium species— Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae —are responsible for human malaria. Of these four, only P. falciparum causes pulmonary disease. The disease onset is almost always within 1 year of exposure.




Figure 13-2


Life cycle of Plasmodium species ( P. falciparum, P. vivax, P. ovale, and P. malariae ). ARDS, acute respiratory distress syndrome.

(Adapted from Martinez S, et al. Thoracic manifestations of tropical parasitic diseases: a pictorial review. Radiographics 25:135–155, 2005.)


Clinical Manifestations


Shortness of breath and cough are the main respiratory symptoms in conscious patients; some also report chest tightness. Dyspnea often starts abruptly and progresses rapidly over a few hours, causing life-threatening hypoxia in patients with falciparum malaria.


Pathogenesis


The pathogenesis of malarial lung disease is attributed to a diffuse alveolar injury resulting in a capillary leak syndrome and acute pulmonary edema. This noncardiogenic pulmonary edema is associated with normal or low capillary wedge pressures without evidence of left ventricular dysfunction. Hypoalbuminemia and high-level parasitemia are risk factors associated with the development of pulmonary disease. Pathologic findings may include features of acute respiratory distress syndrome in some individuals; this is thought to be secondary to sequestered malaria parasites in the lung, inducing an inflammatory cascade. This mechanism mainly involves cytokines, neutrophils, and endothelial adhesion molecules. Substantial evidence implicates the neutrophil as central to the pathogenesis of microvascular lung injury, which results in increased capillary permeability and subsequent pulmonary edema.


Diagnosis


Radiographic and computed tomography (CT) findings may suggest noncardiogenic pulmonary edema. Pleural effusion, diffuse interstitial edema, and lobar consolidation may be seen. Laboratory assessments may show anemia and leukocytosis. A peripheral thick blood smear has high sensitivity for detecting parasitemia. A peripheral thin blood smear is better for species differentiation and staging of parasite development in P. falciparum .


Treatment


Effective treatment strategies for falciparum malaria depend on the pattern of parasite drug resistance in the geographic area where the infection is acquired and the severity of disease ( Table 13-2 ). The website for the Centers for Disease Control and Prevention should be reviewed to identify areas of chloroquine resistance. Severe malaria, such as that complicated by pulmonary disease, warrants therapy with parenteral medications. In addition to patient management in a critical care unit, the mortality rate is high. For physicians in nonmalarial areas, malaria always should be considered in the differential diagnosis of a sick patient who has traveled to a malaria-endemic area.



Table 13-2

Drugs to Treat Parasitic Lung Infections













































































































































































































































































































































INFECTION DRUG PEDIATRIC DOSE ADULT DOSE
Malaria ( Plasmodium falciparum —in areas of chloroquine resistance)
Oral ( only in uncomplicated or mild disease)
Drugs of choice Atovaquone/proguanil <5 kg: not indicated 2 adult tabs bid or
5–8 kg: 2 pediatric tabs once daily × 3 days 4 adult tabs once daily × 3 days
9–10 kg: 3 pediatric tabs once daily × 3 days
11–20 kg: 1 adult tab once daily × 3 days
21–30 kg: 2 adult tabs once daily × 3 days
31–40 kg: 3 adult tabs once daily × 3 days
40 kg: 4 adult tabs once daily × 3 days
or
Quinine sulfate 30 mg/kg/day in 3 doses × 3–7 days 650 mg q8h × 3–7 days
plus
Doxycycline 4 mg/kg/day in 2 doses × 7 days 100 mg bid × 7 days
or plus
Tetracycline 6.25 mg/kg qid × 7 days 250 mg qid × 7 days
or plus
Clindamycin 20 mg/kg/day in 3 doses × 7 days 20 mg/kg/day in 3 doses × 7 days
Alternatives Mefloquine 15 mg/kg followed 12 hr later by 10 mg/kg 750 mg followed 12 hr later by 500 mg
Artesunate 4 mg/kg/day × 3 days 4 mg/kg/day × 3 days
plus
Mefloquine 15 mg/kg followed 12 hr later by 10 mg/kg 750 mg followed 12 hr later by 500 mg
Malaria ( P. falciparum— chloroquine-susceptible)
Oral
Drug of choice Chloroquine phosphate 10 mg base/kg (maximum 600 mg base), then 5 mg base/kg at 24 hr and 48 hr 1 g (600 mg base), then 500 mg (300 mg base) 6 hr later, then 500 mg (300 mg base) at 24 hr and 48 hr
Parenteral (all Plasmodium )
Drugs of choice Quinidine gluconate 10 mg/kg loading dose (maximum 600 mg) in normal saline over 1–2 hr, followed by continuous infusion of 0.02 mg/kg/min until PO therapy can be started 10 mg/kg loading dose (maximum 600 mg) in normal saline over 1–2 hr, followed by continuous infusion of 0.02 mg/kg/min until PO therapy can be started
or
Quinine dihydrochloride 20 mg/kg loading dose in 5% dextrose over 4 hr, followed by 10 mg/kg over 2–4 hr q8h (maximum 1800 mg/day) until PO therapy can be started 20 mg/kg loading dose in 5% dextrose over 4 hr, followed by 10 mg/kg over 2–4 hr q8h (maximum 1800 mg/day) until PO therapy can be started
Alternative Artemether 3.2 mg/kg IM, then 1.6 mg/kg daily × 5–7 days 3.2 mg/kg IM, then 1.6 mg/kg daily × 5–7 days
Ascariasis ( Ascaris lumbricoides —roundworm)
Drug of choice Albendazole 400 mg once 400 mg once
or
Mebendazole 100 mg bid × 3 days or 500 mg once 100 mg bid × 3 days or 500 mg once
or
Ivermectin 150–200 μg/kg once 150–200 μg/kg once
Hookworm ( Ancylostoma duodenale, Necator americanus )
Drug of choice Albendazole 400 mg once 400 mg once
or
Mebendazole 100 mg bid × 3 days or 500 mg once 100 mg bid × 3 days or 500 mg once
or
Pyrantel pamoate 11 mg/kg/day(maximum 1 g) × 3 days 11 mg/kg/day (maximum 1 g) × 3 days
Strongyloidiasis ( Strongyloides stercoralis )
Drug of choice Ivermectin 200 μg/kg/day × 2 days 200 μg/kg/day × 2 days
Alternatives Albendazole 400 mg bid × 7 days 400 mg bid × 7 days
or
Thiabendazole 50 mg/kg/day in 2 doses × 2 days (maximum 3 g/day) 50 mg/kg/day in 2 doses × 2 days (maximum 3 g/day)
Amebiasis ( Entamoeba histolytica )
Severe intestinal or extraintestinal disease Metronidazole 30–50 mg/kg/day in 3 doses × 7–10 days 750 mg tid × 7–10 days
or
Tinidazole 50 mg/kg/day (maximum 2 g) × 5 days 2 g once daily × 5 days
In treating extraintestinal disease follow with Iodoquinol 30–40 mg/kg/day (maximum 2 g) in 3 doses × 20 days 650 mg tid × 20 days
or
Paromomycin 25–35 mg/kg/day in 3 doses × 7 days 25–35 mg/kg/day in 3 doses × 7 days
Alternative Diloxanide furoate 20 mg/kg/day in 3 doses × 10 days 500 mg tid × 10 days
Toxocariasis (visceral larva migrans)
Drug of choice Albendazole 400 mg bid × 5 days 400 mg bid × 5 days
or
Mebendazole 100–200 mg bid × 5 days 100–200 mg bid × 5 days
Echinococcosis ( Echinococcus granulosus —hydatid cyst)
Drug of choice Albendazole 15 mg/kg/day (maximum 800 mg) × 1–6 mo 400 mg bid × 1–6 mo
Patients may benefit from surgical resection or percutaneous drainage of cysts
Echinococcosis ( Echinococcus multilocularis ) Surgical excision is only available means of cure for this infection. In nonresectable cases, treatment with albendazole or mebendazole is recommended
Paragonomiasis ( Paragonimus westermani —lung fluke)
Drug of choice Praziquantel 75 mg/kg/day in 3 doses × 2 days 75 mg/kg/day in 3 doses × 2 days
Alternative Bithionol 30–50 mg/kg on alternate days × 10–15 doses 30–50 mg/kg on alternate days × 10–15 doses

Modified from Drugs for parasitic infections. Med Lett Drugs Ther 1–12, August 2004.


Amebiasis


Etiology and Epidemiology


Approximately 1% of the world’s population is infected with Entamoeba histolytica. After malaria and schistosomiasis, amebiasis is the third most common cause of mortality from parasitic diseases. Although pleuropulmonary disease in E. histolytica infection is uncommon, it can occur in 15% of individuals with an amebic liver abscess.


Pathogenesis


After a host ingests cysts in contaminated food or drink, pathogenic amebic trophozoites invade the colonic wall and disseminate hematogenously to the liver ( Fig. 13-3 ). Less commonly, infection may occur after aspiration. Disease onset may be either acute or chronic. Diarrhea is frequently absent. As an amebic liver abscess enlarges, adhesions may develop between the liver surface and the diaphragm. A sterile sympathetic pleural effusion may develop above the abscess. Alternatively, infection may spread through lymphatics or via the bloodstream and extend through the diaphragm after abscess rupture with empyema formation. The rupture frequently evokes severe pain in the right chest, back, or shoulder. Fever, hypoxemia, and circulatory collapse may follow. Classic “anchovy paste” can be obtained from an amebic hepatic abscess or from expectorate that has traveled through a hepatobronchial fistula.


May 20, 2019 | Posted by in GENERAL RADIOLOGY | Comments Off on Pulmonary Manifestations of Parasitic Diseases
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