Professional Documents
Culture Documents
Inflammation/infection of lungs
Pneumonia
Bronchospasm
Pulmonary edema
Habitat in Lungs
Trematode : Schistosomes
Nematodes : Hookworms Ascaris Filaria
Strongyloides
Pulmonary amebiasis
Manifestations
Extension of amebic liver abscess fever, chest pain, cough Haemoptysis and anchovy sauce like pus
Diagnosis
Hepatomegaly Plural effusion Active trophozoite in sputum or pleural pus Serology for amebiasis Stool positive for ameba may not relevant
Pulmonary malaria
Pulmonary manifestations
Cough to severe and rapidly fatal pulmonary edema Acute respiratory distress syndrome can occur in vivax malaria.
Diagnosis
Severe falciparum malaria may cause pulmonary edema and pleural effusion
Erythrocytic cycle
Sequestrated of blood vessel between parasite ligand expressed on surface of the infected RBC and the receptor on endothelial cell
CLINICAL DISEASE OF STRONGYLOIDIASIS Pathology in strongyloidiasis varies in both in severity and areas of the body involved. Cutaneous manifestation Pulmonary symptoms Intestinal symptoms Hyperinfection syndrome Reactive arthritis Chronic strongyloidiasis : totally asymptomatic and the only abnormal clinical finding being a peripheral eosinophilia.
Pulmonary strongyloidiasis
Heavy infection or hyperinfection often develop cough, fever, and transient pulmonary infiltrates (Loeffler's Syndrome).
Larval migration through the lungs may stimulate symptoms, depending on host's immune response.
Some patients may be asymptomatic, while others may present with pneumonia.
Cutaneous strongyloidiasis
Initial skin penetration causes very little reaction : pruritus and erythema .
Skin migration or larva migrans : larva curren ("racing larvae") for cases of strongyloidiasis where one or more rapidly progressing linear
Urticarial tracks starting near the anus . These tracks may progress as fast as 10 cm/hour.
Intestinal strongyloidiasis
Mucosa may be severely damaged with sloughing of tissue, although this type of damage is unusual . Symptoms may mimic peptic ulcer with abdominal pain, which may be localized in the right upper quadrant.
In an immunocompetent patient, there is a leukocytosis with a peripheral eosinophilia of 50-75%, while in chronic cases the eosinophilia may be much lower.
Chronic infections have lasted over 30 years as a result of the autoinfective capability of the larvae.
Hyperinfection Syndrome:
Autoinfection is responsible for longterm infections that persist for years
Under immunosuppressed large numbers of larvae produced and found in every tissue of the body.
Other causes of death may include peritonitis, brain damage, or respiratory failure.
LABORATORY DIAGNOSIS
1. Stool examination for rhabditiform larvae. 2. If negative, examination of duodenal contents is recommended (duodenal aspirates, Entero-Test capsule). 3. Various concentrates (Baermann) and cultures (HaradaMori, petri dish, agar plate) can also be used for larval recovery. 4. Eggs are rarely seen in the stool, but may be recovered from duodenal contents. 5. In very heavy infections, eggs (less common), larvae (both types), and adult worms may be recovered in the stool. 6. Serology Antibody detection (ELISA, GAPT).
Free-living adults
TREATMENT Thiabendazole repeated or extended (one week) therapy may be necessary, and the cure rates range from 55 to 100%.
Albendazole is a broad-spectrum anthelmintic variable therapeutic efficacy (cure rate 4555% in strongyloidiasis). Oral dose is 400 mg doses given twice daily for 3 days for uncomplicated strongyloidiasis and for 710 days for hyperinfection.
Ivermectin : become widely used at 200 g/kg/day as a current drug of choice for strongyloidiasis.
Decline in enzyme-linked immunosorbent assay optical density over time from baseline to final post-treatment serologic testing in 40 patients who had received two doses of ivermectin. Indirect evidence of cure
Case study 1
A 47 year old male presented with complaints of severe midepigastric pain, become worse over a period of about a week. He had received prednisone over the course of several years and the dose had been increased two months before. Previous diagnostic testing included an O&P examination, which was reported as "No Parasites Seen." He was treated with supportive care for epigastric pain and developing pneumonia, but failed to improve. He became comatose and died three days later.
Autopsy findings : worms in colon High eosinophilia may or may not be present. In this case, no eosinophils were noted
(eosinopenia can occur in the hyperinfection syndrome = poor prognostic sign)
Case study 2
53 pemphigus vulgaris 1 . intravenous dexamethasone 4 . 8 azathioprine 100 / 3 hypotension ICU acute respiratory distress syndrome ventilatory support. X-ray extensive bilateral bronchopneumonia.
pemphigus vulgaris
Intestinal ascariasis
Mechanical damage in the intestine. Malabsorption of nutrients Intestinal blockage / obstruction.
Pulmonary ascariasis
Ascaris migrates to the lungs via the bloodstream larvae in the lung tissue cause pulmonary eosinophilia, Adult worms release metabolic causing allergic reactions. Asthma, eye pain, and rashes can result from allergic response. Ascaris liberating vasoactive amines and causing the degranulation of intestinal mast cells.
Definition
Hyperresponse to filarial infection. The syndrome includes High eosinophil count Pulmonary symptoms : dyspnea Radiological changes, Fever, and weight loss
Geographic Distribution
Common in southern India, Sri Lanka, Malaysia, and Southeast Asia, Aso occurs in the Caribbean, South America, Africa
Wuchereria
Associated with occult filariasis (amicrofilaremia) and positive serology test. Hypereosinophilia of 3,000 to 50,000 cells/mm and high serum IgE
Lung biopsy showing a pulmonary granuloma with intense eosinophilic inflammatory reaction.
Conclusions
Pneumonia by Protozoa - systemic infection & blood borne caused by infection of visceral organ including lung Pneumonia by Helminths
eosinophilic infiltration Adult in intestine allergic reaction to worm protein (coelomic fluid)