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Parasites Affecting the Respiratory Tract

Victoria Basa-Dalay,MD, MScCTM Department of Microbiology and Parasitology August 18, 2011 Parasites Mainly Affecting the Respiratory System Paragonimus westermani Pneumocystis jirovecii (carinii) Parasites that May Affect the Respiratory System Ascaris lumbricoides Necator americanus Strongyloides stercorales Enterobius vermicularis Filarial Worms: Wuchereria and Brugia Objectives: 1. List down the parasites affecting the respiratory tract 2. Given the parasites affecting the respiratory system, discuss the following: a. Taxonomy,morphology and its stages b. Life cycle of the parasite c. Pathology and symptomatology d. Diagnosis and treatment e. Prevention and control 3. Briefly discuss the taxonomic classification parasites affecting the respiratory tract

PARAGONIMIASIS Given a case with recurrent cough and hemoptysis.

Questions 1. 2. 3. 4. 5. 6. What is the diagnosis? What caused the disease? What is the burden of this disease? How to diagnose it? What treatment should be given? How to prevent and control transmission of this infection?

Paragonimiasis Synonyms: Endemic Hemoptysis / / Parasitic hemoptysis/ Manson hemoptysis. Oriental lung fluke disease/ Lung distoma/ Pulmonary distomiasis or distomatosis Etiologic Agent:Paragonimus westermani Common name: Lung Fluke; Oriental Lung Fluke Habitat: Lungs Clinical features: Symptoms mimics TB History of P. westermani 1877 - first identified in Bengal tigers in Amsterdam zoo Named after the zoo keeper,Westerman 1879, Ringer discovered the first case of human paragonimiasis when he found a lung fluke while performing an autopsy on a Portuguese patient in Formosa (Taiwan). In 1880, Manson acquired some sputa from Japanese patients who had hemoptysis and showed that the "endemic hemoptysis" of Formosa and Tokyo was caused by the same parasite. Uneventful symbiotic relationship occurred, hence, often left undiagnosed

Taxonomic Classification Kingdom: Animalia Phylum: Platyhelminthes Class: Trematoda Subclass: Digenea Order: Plagiorchiata Family: Pleuroceridae Genus: Paragonimus Epidemiology 30 species of Paragonimus but only about 10 species affect human beings The most common and wide-spread species is Paragonimus westermani Human infections with this species are reported mostly from Asian and African countries: Japan, Korea, Formosa, China, Manchuria, the Philippine Islands and India. in tropical West Africa, from the Congo and Nigeria, especially from the Southern Cameron Zoonotic infections in cats, dogs, pigs and a large number of other animals occur Life cycle of Paragonimus westermani Indirect life cycle Definitive host: Man & Other domestic/ wild animals First Intermediate Host: Operculated snails Thiara, Melanoides, Hua, Semisulcospira, Syncera Brotia asperata Second Intermediate Host: Freshwater Crab or crayfish Sundathelpusa philippina, Potamon, Sesarma, Parathelpusa Paratenic Host: Wild bore and rats, Dogs Mode of Transmission 1. Ingestion of raw and insufficiently cooked a. freshwater crabs or crayfish b. meat of paratenic and reservoir host 2. Drinking contaminated water with metacercariae (rare) 3. Accidental ingestion of metacercariae from contaminated kitchen utensils

Pathology and Symptomatology 1. DUE TO EGGS- minor histologic changes a. Leukocytic infiltration around the eggs 2. DUE TO ADULT OR ABBERANT WORMS a. Provoke a granulomatous reaction within a fibrous tissue capsule in the lungs b. Develops into a localized to diffuse cirrhosis, cystic dilatation of bronchi & tubercle -like abscesses c. Abscess formation in the abdominal cavity d. Indolent ulcer in muscular tissues Clinical Features Incubation Period: 2 - 20 days

Early Stage: insidious onset with non-specific signs and symptoms Clinical features: depends on the organ/s involved Pulmonary Paragonimiasis y mimics tuberculosis y Persistent or chronic cough and hemoptysis y distressing pulmonary pain y viscous sputum flecked with dark golden brown eggs and at times with blood y symptoms more severe after physical exertion y chest pain and night sweats may be present Extrapulmonary Paragonimiasis a. Abdominal- less definite symptoms i. may include palpable masses ii. dull abdominal pains w/ tenderness & rigidity on deep palpation; diarrhea b. Glandular/cutaneous- rare usually associated with aberrant immature flukes i. abscesses with or without indolent ulcer ii. creeping tumors or migratory swelling in the inguinal or lower abdominal region c. Spinal involvement though very rare may produce monoplegia, paraplegia, lower extremity paresthesias, or sensory loss; . Most of the lesions are epidural and in the thoracic region, and consist of dark brown cysts, single or multiple, 1 to 2 cm or more across. d. Renal involvement :Hematuria may be observed and eggs may sometimes be detected in the urine e. Scrotal paragonimiasis may mimic epididymitis or an incarcerated hernia f. Cerebral Paragonimiasis i. BRAIN is the most important extrapulmonary site 1. by migration through the soft tissues of the neck along the sheaths of the jugular veins, internal carotid arteries, or nerve trunks ii. Occurs 1%- 24% of symptomatic patients iii. This form of the disease is particularly common in children or juveniles < 15 years old esp Asians iv. Early symptoms can resemble meningo-encephalitis v. Signs of cerebral paragonimiasis include facial palsy, hemiplegia, and paraplegia vi. Ocular signs include impaired visual acuity because of optic atrophy, papilledema, and hemianopsia vii. May persist 1-2 months viii. Chronic phase symptoms include headache, vomiting, seizures, or weakness ix. MRI shows a conglomerate of multiple ring-shaped cluster in the right lower temporal-occipital lobe of a chronic cerebral paragonimiasis patient 1. A computerized tomography shows multiple calcified density in the right frontal and temporal areas of chronic 2. cerebral paragonimiasis patient Diagnosis 1. History & P.E. a. travel in endemic place b. eating raw crustaceans c. S/Sx: rusty sputum, non-specific Sx 2. Microscopy: medium sized operculated eggs/ ova in sputum and feces Ova a. from sputum and feces b. golden brown in color c. Asymetrical with thick shell d. oval shape with flattened large opercular end and thickened but smaller abopercular rim e. medium sized: 85 x 55 u f. unembryonated when oviposited 1. Medical Significance: Diagnostic Stage 3. Chest X-ray

a. May show patchy migrating infiltrations, cavitations, fibrosis and preliminary thickening b. Characteristic pictures are ring shadows in the X-ray known as Corona effect (worm cyst) c. Lateral chest radiograph shows a worm migration tract identified by the meandering linear opacity d. Chest radiograph may also shows aggregated, uniform-sized, thin-walled cysts with a soap-bubble appearance in the left upper lobe. e. Other Chest radiograph shows various findings, including 1. nodules (white arrow), 2. ring shadow (black solid arrow), and 3. patchy air-space consolidation (open arrow), representing worm cysts without airway communication, with communication, and pneumonic consolidation surrounding worm cysts, respectively f. 10 to 20% of cases X-ray does not show abnormality Morphology of the other stages of the Parasite Metacercariae Developed from cercariae Encyst in the gills, body muscles, legs, viscera of crabs or crayfish Golden brown in color Round- shaped Size: 250 x 500 u Medical Significance: Infective Stage Adult y Ovoid, thick worm (preserved) y Fleshy,resembles a spoon (active, alive) y 8-12 mm by 4-6 mm in size y Spinous cuticle y OS = VS (middle in anterior third of the body) y Simple intestinal ceca y Densely distributed lateral vitellaria y 6-lobed ovary y 2 irregularly lobed testes Treatment 1. Specific Treatment Praziquantel drug of choice Dose: 25 mg/Kg 3 times a day for 3 days Bithionol alternative drug Triclabendazole 5 mg/kg 3 times daily, 10 mg/kg 2 times daily and 10 mg/kg in a single dose, were all effective in treating cases. 2. Nonspecific Treatment Symptomatic and supportive management Control and Prevention 1. 2. 3. 4. 5. Early diagnosis and treatment of cases Health Education Thorough cooking of crabs, crayfish, and crustaceans Good sanitary and hygienic practices Drinking potable water

Pneumocystosis Pneumonia
Synonym: Interstitial Plasma Cell Pneumonia- an opportunistic infection among premature infants and AIDS cases. It is the leading cause of mortality among AIDS cases Etiologic agent: Pneumocystis jirovecii Classification: Controversial Protozoan: Morphology and Fungus: RNA and DNA sequences Kingdom: Phylum: Class: Order: Family: Genus: Species: Fungi Ascomycota Pneumocystidomycetes Pneumocystidales Pneumocystidaceae Pneumocystis P. jirovecii

History of Pneumocystis Classification a. 1909- Carlos Chagas discovered it in experimental animals but confused it with part of the life-cycle of Trypanosoma cruzi (causal agent of Chagas Disease) and later called both organisms 'Schizotrypanum cruzi' a form of trypanosome infecting humans. b. 1910 rediscovery of Pneumocystis cysts was reported by Antonio Carini c. 1912 - discovered in by Delano and Delano this time at the Pasteur Institute in Paris, France who found it in rats and who proposed the genus and species name Pneumocystis carinii after Carini. d. 1952 - Otto Jirovec who described Pneumocystis pneumonia in humans e. 1976, - The name P. jirovecii, to distinguish the organism found in humans from physiological variants of Pneumocystis found in other animals, was first proposed f. History of Pneumocystis Classification g. 1999 - After DNA analysis showed significant differences in the human variant, the proposal was made again in and has come into common use i. P. carinii still describes the species found in rats and that name is typified by an isolate from rats. ii. The International Code of Botanical Nomenclature(ICBN) requires that the name to be spelled jirovecii rather than jiroveci. 1. Fungus Protozoan h. 2005 - A change in the ICBN in now recognizes the validity of the 1976 publication, making the 1999 proposal redundant. The name P. jirovecii is typified by samples from human autopsies dating from the 1960s. i. Stages of the Parasite Trophozoite or trophic forms the vegetative form most numerous stage unicellular, pleiomorphic, 1-5 um Cyst spherical , 4-6 um

has thick or thin walls mature thick-walled cyst contains 6- 8 intracystic bodies Life Cycle of P. jirovecii

Mode of Transmission Inhalation of the organism tranplacental transfer (?) Infective stage: Unknown Source of the organism environment (?) found in healthy human lungs but cause disease only among IC cases Epidemiology Most healthy children are exposed at an early age More common in premature and debilitated children and immunocompromised adults Severity of the disease is due to the susceptibility of the host to this organism Predisposing factors: Immunocompromised status 1. AIDS cases 2. Premature and debilitated infants 3. Patients undergoing chemoTx and prolonged steroid 4. Protein malnutrition Clinical features: 1. 2. 3. 4. Incubation period: 4 -8 weeks Prodromal Sx: nonspecific S/sx Pulmonary: rapid respirations, dyspnea, non-productive cough and cyanosis Extrapulmonary: any organ may be involved

Pathology and Symptomatology: 1. Initiated by attachment of the trophic stage to pneumocyte type 1 2. maintains extracellular existence 3. leads to proliferation of the organism until they fill-up the alveolar spaces 4. causes hyaline membrane formation, interstitial fibrosis and edema 5. Pneumocystis jirovecii (carinii)

6. maintains an extracellular existence 7. proliferation of the organism may fill alveolar lumen producing foamy, eosinophilic alveolar exudation with plasma cells Diagnosis A.Lung biopsy - best specimen 50-90% P. jirovecii found in induced sputum and fiberoptic endoscopy 1. Giemsa stains the cysts nuclei and not the wall a. Cysts in bronchoalveolar material, Giemsa stain b. Three (3) rounded cysts (size 4 to 7 m) contain 6 to 8 intracystic bodies, i. nuclei are stained by Giemsa ii. the walls of the cysts are not stained c. Note: the presence of several smaller, isolated trophozoites. 2. Methenamine silver, or toluodine blue O to stain cyst wall a. Cysts in lung tissue, silver stain i. the walls of the cysts are stained black thus shows the irregular, saucer shape of the cysts. ii. the intracystic bodies are not visible with this stain 3. Immunofluorescence-most sensitive B. Serology: of little help C. Chest X-ray of patient with dyspnea, hypoxia and HIV infection showing diffuse interstitial infiltrates Treatment I. Prophylactic Treatment

Indications: 1. Prior episode of PCP 2. CD4+ count <200 cells/mm3 3. HIV associated thrush 4. Unexplained fevers of greater than 100oF for more 2 weeks DOC: Trimetoprim -Sulfamethoxazole II. Therapeutic treatment Specific: DOC: Trimetoprim sulfamethoxazole Intravenous pentamidine Dapsone Atovaquone Nonspecific: Symptomatic and supportive measures

Parasites that MAY affect the Respiratory Tract

I. Loeffler s Syndrome y a transient respiratory illness associated with blood eosinophilia and radiographic shadowing (Loeffler, 1932). y With larval infection of Ascaris lumbricoides as its most common cause, but can be caused by other parasites (Crofton, 1952) y However, other parasitic infections and acute hypersensitivity reactions to drugs are included as etiologies for simple pulmonary eosinophilia.


helminthiases associated with Lffler syndrome are distributed worldwide; however, they are more prevalent in tropical climates, especially in communities with poor sanitary conditions. young children are exposed to contaminated soil and exhibit hand-to-mouth behavior more often than adults No deaths due to Lffler syndrome have been reported Symptoms usually subside within 3-4 weeks Pathophysiology of Loeffler s Syndrome y Related to the transit of parasitic organisms through the lungs during their life cycle in the human host. y In these situations, accumulation of eosinophils in the lungs is likely secondary to immunologic hyperresponsiveness. The exact immunopathogenic mechanism for this reaction remains unknown. y development of pulmonary eosinophilia is T cell dependent y Production of cytokines such as circulating interleukin-5 (IL-5) is necessary for development of pulmonary eosinophilia. Loeffler s Syndrome can be caused by other soil transmitted parasites, such as y Necator americanus y Ancylostoma duodenale, y Strongyloides stercoralis i. have a similar cycle to Ascaris, with passage of larval forms through the alveolar walls ii. these parasites are not orally ingested but they directly enter the human host through the skin Clinical features a. Symptoms are usually mild or absent b. Spontaneously resolve after several days (2-3 weeks) c. Cough is the most common symptom among symptomatic patients. It is usually dry and unproductive but may be associated with production of small amounts of mucoid sputum. Parasitic infection Symptoms appear 10-16 days after ingestion of Ascaris eggs. A similar timeframe has been described for Lffler syndrome associated with N americanus, A duodenale, or S stercoralis infection. Fever, malaise, cough, wheezing, and dyspnea are the most common symptoms. Less commonly, the patient may present with myalgia, anorexia, and urticaria. Usually on PE, no abnormalities are found Occasionally, crackles or wheezes may be heard on lung auscultation. Diagnosis : a.Parasites and ova can be found in the stool 6-12 weeks after the initial parasitic infection. b.CX-ray

Tropical Pulmonary Eosinophilia

Disease: results from immunologic hyperresponsiveness to filarial parasites Etiologic agents: Filarial worms (Wuchereria bancrofti and Brugia malayi) Epidemiology: Occurs mostly in men Clinical Features: characterized by persistent cough and wheezing of insidious onset associated with a striking eosinophilia and elevated antifilarial IgE . The cough is often worse at night with nonproductive sputum. Physical examination reveals minimal pulmonary findings, hepatosplenomegaly, and generalized lymphadenopathy.

Diagnosis: 1. Radiography shows increased bronchovascular markings and diffuse coarse interstitial infiltrates a. may be normal in up to 30% of cases. b. may be multiple, diffuse, tiny nodules 2-3 mm in size. miliary nodulation with patchy opacification c. may be quite variable, with transient shifting opacities 2. Pulmonary function testing reveals a predominant restrictive pattern with mild reversible airway obstruction in the majority of patients. 3. Blood Examination: The absolute eosinophil count often exceeds 4,000/mm3 with elevation in serum IgE levels (> 1,000 U/mL) and erythrocyte sedimentation rate. 4. Bronchoalveolar Lavage often reveals an intense eosinophilic alveolitis and striking elevation of antifilarial IgE. Filarial antibodies are typically detected, microfilaria cannot be found in the peripheral blood. 5. Low-grade alveolitis persists in almost half of such treated patients and may be the cause of progressive pulmonary fibrosis seen in many inadequately treated patients. Treatment: 1. 2. 3. Therapy with diethylcarbamazine is effective . Relapses can occur and are treated with repeat courses of the same drug. Corticosteroids may be helpful in treating the chronic forms of TPE, Low-grade alveolitis persists in almost half of such treated patients and may be the cause of progressive pulmonary fibrosis seen in many inadequately treated patients.