Parasitology-Lec 3 Nematodes 2

November 9, 2017 | Author: api-3743217 | Category: Medical Specialties, Clinical Medicine, Diseases And Disorders, Medicine, Wellness
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PARASITOLOGY LECTURE 3 - Nematodes Notes from lecture, Zeibig (’97) and Murray (’98) USTMED ’07 Sec C – AsM OUTLINE IN THE STUDY OF PARASITE I. II. III. IV. V. VI. VII. VIII. IX.

Nomenclature and synonyms Geographic distribution Morphology Life cycle Pathology in the host Clinical symptomatology Laboratory diagnosis Treatment Preventive measures

• III.

in the US frequency is greatest in the Appalachian Mountains and surrounding areas in the east, west and south Morphology

Unfertilized Egg

GENERALITIES

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decorticated unfertilized egg

helminths are multicellular and contain internal organ systems nematodes are commonly known as the intestinal roundworms

Morphology and Life Cycle Notes

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members of the class nematoda may assume three basic morphologic forms: egg, larvae, and adult worms eggs vary in size and shape the developing larvae located inside fertilized eggs emerge and continue to mature; they are typically long and slender sexes are separate the adult female worms are usually larger than the adult males the adults are equipped with complete digestive and reproductive systems life cycles of the nematodes are similar yet organism specific infection may be initiated in one of two primary ways: 1. ingestion of the infected eggs 2. by burrowing through the skin of the foot the adult worms reside in the intestine where they concentrate on obtaining nutrition and reproduction adult females lay eggs in the intestine eggs may be passed into the stool; once outside the body, the larvae inside the eggs warm, moist soil and 2-4 weeks to mature

unfertilized egg Fertilized Egg

Laboratory Diagnosis -

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through recovery of eggs, larvae and occasional adult worms the specimens of choice vary by species and include cellophane tape preparations taken around the anal opening, stool, tissue biopsies and infected skin ulcers ELISA is available for the diagnosis of select nematode organisms

very corticated mature egg

mature egg

Pathogenesis and Clinical Symptoms

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the following factors may contribute to the ultimate severity of a nematode infection 1. the number of worms present 2. the length of time the infection persists 3. overall health of the host with one exception, all of the nematodes may cause intestinal infection symptoms at some point during their invasion of the host symptoms include: abdominal pain, diarrhea, nausea, vomiting, fever and eosinophilia other symptoms: skin irritation, formation of blisters, muscle involvement

corticated mature egg Adults

ASCARIS LUMBRICOIDES I.

• • II. • •

Nomenclature and synonyms Ascaris lumbricoides (as’kar-is/lum-bri-koy’deez) Common names: Large Intestinal Roundworm, Roundworm of Man Geographic distribution most common intestinal helminth infection in the world susceptible are warm climates and areas of poor sanitations

adult male

• VI.



adult female IV. Life cycle

1. 2.

infection begins following the ingestion of infected eggs that contain viable larvae inside the small intestine the larvae emerge from the eggs



accompanied by eosinophilia and O2 desaturation a tangled bolus of worms in the intestines may cause obstruction, perforation and occlusion of the appendix Clinical symptomatology Asymptomatic : patients infected with a small number of worms (5-10) will often remain asymptomatic Ascaris/Roundwrom infection : patients who develop symptomatic ascariasis may be infected with as few as a single worm o Intestinal phase



o

VII.

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3.

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the larvae complete a liver-lung migration by first entering the blood via penetration through the intestinal wall 4. first “stop” is the liver 5. continues through the blood stream to second “stop,” the lung 6. once inside the lung, the larvae burrow their way through capillaries into the alveoli 7. migration to bronchioles 8. larvae are transferred through coughing into the pharynx 9. are swallowed and returned to the intestines adult worms take up residence in the small intestine adults multiply and a number of resulting undeveloped eggs (up to 250,000/day) are passed in the feces soil provides the necessary conditions for the eggs to embryonate infective eggs remain viable for years eggs are not easily destroyed by chemicals



Infective stage: embryonated eggs

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V. •

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Pathology in the host a worm can migrate into the bile duct and liver and damage tissue because the worm has a tough, flexible body, it can occasionally perforate the intestine, creating peritonitis with secondary bacterial infection the adult worms do not attach to the intestinal mucosa but depend on constant motion to maintain their position w/in the bowel lumen migration of worms to the lungs can produce pneumonitis resembling an asthmatic attack migration can occur in response to fever, drugs other than those used to treat ascariasis and some anesthetics pulmonary involvement is related to the degree of hypersensitivity induced by previous infections and the intensity of the current exposure and may be

• • IX. • •

may produce tissue damage; secondary bacterial infection may occur following worm perforation  Px infected w/ many worms may exhibit vague abdominal pain, vomiting, fever and distention  Discomfort from adult worms exiting the body through anus, mouth or nose may occur  Protein malnutrition Pulmonary phase  Low-grade fever  Cough  Eosinophilia  Pneumonia  Asthmatic reaction

Laboratory diagnosis specimen of choice for the recovery of Ascaris lumbricoides eggs is stool adult worms may be recovered in several specimen types, depending on the severity of infection, including the small intestine, gall bladder, liver and appendix adult worms may be present in stool, womited, or removed from external nares ELISA is also available Treatment several medications: o mebendazole o pyrantel pamoate o levamisole o peperazine citrate intestinal tract obstruction o combo of drug therapy suction, or surgery pulmonary discomfort o corticosteroids

and

nasogastric

Preventive measures Avoidance of using human feces as fertilizer Proper sanitation and personal hygiene

HOOKWORM NECATOR AMERICANUS/ANCYLOSTOMA DUODENALE GENERALITIES • “hookworm” refers to Necator americanus and Ancyclostoma duodenale • 2 primary differences between the two organisms o geographic distribution o adult worms of each have minor morphologic differences o eggs, larvae stages are indistinguishable I.

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Nomenclature and synonyms Necator americanus (ne-kay’tur/ah’merr”i-kay’nus) Common name: New World Hookworm Ancylostoma duodenale (an”si’los’tuh’muh/dew”o-denay’lee) Common name: Old World Hookworm

II.

Hookworm filariform larva

Geographic distribution/Epidemiology • •

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III.

nearly ¼ of the world population is infected w/ hookworm frequency of hookworm is high in warm areas where the inhabitants practice poor sanitation practices mixed infections w/ any combo of hookworm, Trichuris and Ascaris is possible because all organisms require the same soil conditions Necator is primarily found in North and South America o Also exist in China, India and Africa

Adults

Ancylostoma is a parasite of the Old World o Found in Europe, China, Africa, South America and Caribbean Morphology

Eggs

Necator americanus adult male Hookworm egg 400x

Necator americanus buccal capsule Hookworm egg Rhabditiform Larvae

Ancyclostoma duodenale adult female IV.

Life cycle

Hookworm rhabditiform larva

Hookworm rhabditiform larva 400x close up of buccal cavity Filariform Larvae

short esophagus

1. Pointed tail

humans contract hookworm when third-stage filariform larvae penetrate through the skin, particularly into areas such as unprotected feet

• •

2.



inside the body, the filariform larvae migrate to the lymphatics and blood system 3. blood carries the larvae to the lungs where they penetrate capillaries and enter alveoli 4. migration of larvae continues into the bronchioles where they are coughed into the pharynx, swallowed and deposited into the intestines maturation occurs in the intestine adults live and multiply in the S.I. females lay 10,000 to 20,000 eggs per day eggs are passed into the outside environment via feces first-stage rhabditiform larvae emerge from eggs w/in 24-48 hrs in warm, moist soil larvae continue to develop by molting two times



Infective stage: third-stage filariform larvae

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V.

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• • VI.

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VII. • • • • VIII.

IX.

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for asymptomatic infections : iron replacement and/or other dietary therapy (proteins, iron, vitamins) Preventive measures similar to those of Ascaris proper sanitation, fecal disposal prompt treatment personal protection

STRONGYLOIDES STERCORALIS I.



Pathology in the host human phase of hookworm life cycle is initiated when a filariform (infective form) larva penetrates intact skin egg laying is initiated 4 to 8 weeks after the initial exposure and can persist for 5 years on contact w/ soil, the rhabditiform (noninfective) larva are released from the eggs the rhabditiform larva develop into filariform w/in 2 weeks both species have mouthparts designed for sucking blood from injured intestinal tissue A. duodenale has chitinous teeth

drugs of choice : mebendazole or pyrantel pamoate



Nomenclature and synonyms Strongyloides stercoralis (stron”ji-loy’deez/stur”korray’lis) Common name: Threadworm

II.

Geographic distribution

• III.

found predominantly in tropics and subtropics Morphology

Eggs

N. americanus has shearing chitinous plates Clinical symptomatology Rhabditiform Larvae Asymptomatic Hookworm infection: does not exhibit clinical symptoms Hookworm Disease/Ancylostomiasis/Necatoriasis : patients who are repeatedly infected may develop intense allergic itching at the site of hookworm penetration known as ground itch; other symptoms:  Sore throat  Bloody sputum  Wheezing  Headache  Mild pneumonia w/ cough o Intestinal phase  Symptoms depend on # of worms present  Chronic infections (light worm burden ~500 eggs/g feces) • Vague mild GI symptoms • Slight anemia • Weight loss or weakness  Acute infections (greater than 5000 eggs/g feces) • Diarrhea • Anorexia • Edema • Pain • Enteritis • Epigastric discomfort • Patients may develop a microcytic hypochromic iron deficiency • Weakness • Hypoproteinemia • Mortality due to blood loss

rhabditiform larva 400x

Strongyloides stercoralis rhabditiform larva Strongyloides stercoralis rhabditiform larva, close-up of anterior end showing a typical short buccal cavity Filariform Larvae

Laboratory diagnosis primary means is by recovery of the eggs in stool samples larvae may mature and hatch from the eggs in stool that has been allowed to sit at room temperature w/o additive fixatives recovery and examination of the buccal capsule is necessary to determine the specific hookworm organism reverse enzyme immunoassay for specific IgE Treatment

Strongyloides stercoralis filariform larva Adult

3.

IV. •

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can

be

Life cycle unlike in the hookworm life cycle, where eggs are the primary morphologic form seen in feces, in the threadworm life cycle rhabditiform larvae are usually passed in the feces eggs are only occasionally found the rhabditiform larvae develop directly into the thirdstage infective filariform larvae (in soil) remaining phases of the threadworm life cycle mimic those of the hookworm there are 3 possible routes threadworms may take in their life cycles: o

direct 



  





o

o



intestines and cause autoinfection a free-living, nonparasitic cycle established outside the human host

a skin-penetrating larvae enters the circulation and follows the pulmonary course adults develop in the small intestine adult females burrow into the mucosa of the duodenum, and reproduce parthogenetically @ female produces about 1 dozen eggs/day eggs hatch w/in the mucosa and releaserhabditiform larvae into the lumen of the bowel rhabditiform larvae are distinguished from hookworms by: • short buccal capsule • large genital primordium rhabditiform larvae are passed into the stool and may either: • develop into filariform and continue the direct cycle • develop into free-living adult worms and initiate indirect cycle

indirect  Rhabditiform larvae are passed into the outside environment (soil) and mature into free-living adults that are nonparasitic  Adult females produce eggs that develop into the rhabditiform larvae  Larvae mature and transform into the filariform at w/c time they may either initiate a new indirect cycle or become infective  Several generations of this nonparasitic existence may occur before new larvae become skinpenetrating Autoinfection  Occurs when the rhabditiform larvae develop into the filariform stage inside the intestine of the host  Penetrate the intestinal or perianal skin and follow the course through the circulation and pulmonary structures-coughed-swallowed (become adults)  The larvae may then enter the lymphatics or blood stream  Persist for years and can lead to hyperinfection and massive or disseminated, fatal infection

S. stercoralis differs from the life cycle of hookworms in three aspects: 1. eggs hatch into larvae in the intestine before they are passed in feces 2. larvae can mature into filariform in the

V. •









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VI.

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Pathology in the host Heavy worm loads may involve the biliary and pancreatic ducts, the entire small bowel and colon o Causes inflammation and ulceration leading to epigastric pain and tenderness, vomiting, diarrhea and malabsorption Symptoms mimicking peptic ulcer disease coupled w/ peripheral eosinophilia Individuals w/ chronic strongyloidiasis are at risk of developing severe, life-threatening hyperinfection syndrome if the host-parasite balance is disturbed by any drug or illness that compromises the immune status Hyperinfection syndrome: o Seen in individuals immunocompromised by malignancies and those undergoing corticosteroid therapy o Also observed in Px who have undergone solid organ transplantation and in malnourished people o Intestinal symptoms: diarrhea, malabsorption, and electrolyte abnormalities o Fatal complications: bacterial sepsis, meningitis, peritonitis and endocarditis Loss of cellular immune function may be associated w/ the conversion of rhabditiform larvae to filariform larvae, followed by dissemination of the larvae via the circulation to virtually any organ Extraintestinal infection involves the lung and includes bronchospasm, diffuse infiltrates and cavitation Widespread dissemination that involves the abdominal lymph nodes, liver, spleen, kidneys, pancreas, thyroid, heart, brain and meninges Clinical symptomatology Asymptomatic: patients infected w/ only a light infection often remain asymptomatic o Usually seen in intestinal infections Strongyloidiases/Threadworm infection: o Most common symptoms include diarrhea and abdominal pain o Also exhibit urticaria accompanied by eosinophilia o Additional intestinal symptoms may occur such as vomiting, constipation, weight loss, and variable anemia o Malabsorption syndrome for Px w/ heavy infection o Site of larvae penetration may become itchy and red o Recurring allergic reactions o When larvae migrate to the lungs, Px may develop pulmonary symptoms

o o

Pneumonitis from migrating larvae Immunocompromised persons  Severe autoinfections lead to spread of larvae throughout the body  Increased secondary bacterial infections

 VII. • • •

• • • VIII. • • IX. • •

Death

Laboratory diagnosis diagnostic eggs, often indistinguishable from those of hookworm, may be present in stool samples from patients suffering from severe diarrhea stool concentration with zinc sulfate has successfully recovered these eggs rhabditiform larvae may be recovered in fresh stool samples and duodenal aspirates careful screening of feces is necessary to differentiated rhabditiform larvae of hookworm from Strongyloides Enterotest and ELISA Sputum samples have yielded Strongyloides larvae in patients suffering from disseminated disease Treatment Thiabendazole although not always successful Alternative medications include: albendazole ivermectin

and

Preventive measures same as hookworm proper handling and disposal of fecal material and adequate protection of the skin from contaminated soil

GNATHOSTOMA SPINEGERUM (SPINIGERUM) * can’t find any chapter or topic that discusses this parasite.

The closest was in

reference to the Copepods of the phylum Arthropoda…

GENERALITIES • The arthropods are the largest of the animal phyla • Phylum Arthropoda comprises invertebrate animals w/ a segmented body, several pairs of jointed appendages, bilateral symmetry, and a rigid, chitinous exoskeleton that is molted periodically as the animal grows • Arthropods develop from eg to adult by a process known as metamorphosis • They pass through several distinct morphological stages including egg, larvae, pupa and adult • 5 important classes o Chilopoda o Pentastomida o Crustacea  Copepods  Decapods (crabs, crayfish) o Arachnida o Insecta Copepods • are small, simple aquatic organisms

• •



lack a carapace, have one pair of maxillae, and have 5 pairs of biramous swimming legs are intermediate host in the life cycle of several human parasites including: o Dracunculus medinensis o Diphyllobothrium latum o Gnathostoma spinigerum o Spirometra species Epidemiology o Worldwide distribution o Serve as intermediate hosts for helminthic diseases in the US and Canada o Human infections result from ingesting water contaminated with copepods or from eating the raw or insufficiently cooked flesh of infected fish

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