NEMATODES -2-

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NEMATODES NEMATODES -2- -2- Doç.Dr.Hrisi BAHAR Doç.Dr.Hrisi BAHAR

description

NEMATODES -2-. Doç.Dr.Hrisi BAHAR. Hookworms of medical importance & Trichinella spiralis Filarial worms W.bancroftii. Doç.Dr.Hrisi BAHAR. Ancylostoma and Necator (Hookworms ). Causative agents of ancylostomosis and necatorosis (hookworm infection) Ancylostoma duodenale - PowerPoint PPT Presentation

Transcript of NEMATODES -2-

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NEMATODESNEMATODES

-2--2-

Doç.Dr.Hrisi BAHARDoç.Dr.Hrisi BAHAR

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HookwormsHookworms of medical importance of medical importance

&&Trichinella spiralisTrichinella spiralis

Filarial wormsFilarial worms W.bancroftiiW.bancroftii

Doç.Dr.Hrisi BAHARDoç.Dr.Hrisi BAHAR

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Ancylostoma and Necator (Hookworms))

Causative agents of ancylostomosis and necatorosis (hookworm infection)

Ancylostoma duodenaleAncylostoma duodenale Necator americanusNecator americanus

are common parasites of the human small intestine, causing enteritis and anemia.

Infection is mainly by the percutaneous

route.

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms)(Hookworms)

Occurrence.Occurrence.●Human hookworm infections are mostfrequent in the subtropics and tropicsarea in southern Europe, Africa, Asia,SouthernUS, Central and South America.

● In central Europe, hookworm infectionsare seen in travelers returning from thetropics or in guest workers from southerncountries.

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms)(Hookworms)

MorphologyThe hookworms

that

parasitize humans

are 0.7–1.8 cm long

with the anterior

end bent dorsally in

a hooklike shape

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms)(Hookworms)

AncylostomaAncylostoma

The entrance

to the large buccal capsule is armed with

toothlike structures

Ancylostoma duodenale

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms)(Hookworms)

NecatorNecator

The entrance

to the large buccal capsule is armed with

cutting plates

Necator americanus

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms)(Hookworms)

● The thin-shelled, oval eggs (about 60µm long)containing only a small number of blastomeres are shed with feces. In one to two days the first-stage larvae leave the egg molt twice, and develop into infective third-stage larvae.

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms)(Hookworms)

● Since the shed second-stage cuticle is not entirely removed, the third-stage larva is covered by a special sheath.

● Larvae in this stage are sensitive to dryness.

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms(Hookworms

In moist soil or water they remain viable for about one month.

Higher temperatures (optimum:

20–30 8C) and sufficient moisture is favor for the development of the parasite stages outside of a host.

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Life Cycles of HookwormsLife Cycles of Hookworms

● Humans are infected mainly by the percutaneous route.

● Factors favoring infection include working in rice paddies, walking barefoot on contaminated soil.

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Life Cycles of HookwormsLife Cycles of Hookworms

1-In favorable conditions of moisture, temperature, and oxygen, eggs develop in the soil and hatch when they reach maturity.

2-They release a rhabditiform larva which feeds for a short time and molts twice before becoming an infective filariform larva.

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Life Cycles of HookwormsLife Cycles of Hookworms

Filariform larva enters the host either by being swallowed or through hair follicles.

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Life Cycles of HookwormsLife Cycles of Hookworms

3-While penetrating the skin, the larvae shed their sheaths and migrate into lymphatic and blood vessels.

2-Once in the bloodstream, they migrate via

the right ventricle of the heart and by tracheal

migration into the small intestine, where they

develop to sexual maturity.

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Life cycle of hookworm

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● Following oral infection, immediate development in the intestine is probably possible , without the otherwise necessary migration through various organs.

● The parasites can survive in the human gut for one to 15 years.

Life Cycles of HookwormsLife Cycles of Hookworms

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms(Hookworms

Clinical manifestation● Hookworms are bloodsuckers. The

buccal capsule damages the mucosa and induces inflammatory reactions.

● The intestinal tissue damage results in diarrhea with bloody admixtures, steatorrhea, loss of appetite, nausea, flatulence, and abdominal pains.

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms(Hookworms

General symptoms

1-Iron deficiency anemia due to constant blood loss

2-Edemas caused by albumin losses

3-Weight loss due to reduced food uptake and malabsorption.

4-Blood eosinophilia is often present.

Mild infections cause little of clinical note.

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms(Hookworms

Diagnosis.●Diagnosis relies on finding of eggs in stool

samples.

● The eggs are thin-shelled and oval

● When fresh they contain only two to eight

blastomeres

● The eggs in older stool samples have already

developed a larger number of blastomeres

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Eggs of HookwormsEggs of Hookworms

Hookworm eggs

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Ancylostoma and Necator Ancylostoma and Necator (Hookworms(Hookworms

Therapy and controlDrugs effective against hookworms are

pyrantel, mebendazole,and albendazole. Practicable preventive and control measuresinclude mass chemotherapy of the population

in endemic regions, reduction of disseminationof hookworm eggs by

adequate disposal of fecal matter and reduction of percutaneous infection by

use of properly protectiv footwear

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Nematodal Infections of Tissues and Nematodal Infections of Tissues and the Vascular Systemthe Vascular System

Filarial nematodesTrichinella

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FilariaeFilariae The nematode genera of the superfamily

Filarioidea will be here under the collective term filariaefilariae, and the diseases they cause are designated as FilariosesFilarioses. .

In the life cycle of filariae infecting humans,insects (mosquitoes, blackflies, flies etc.)insects (mosquitoes, blackflies, flies etc.)

function as intermediate hosts and vectors. function as intermediate hosts and vectors.

Filarioses are endemic in subtropical andtropical regions; in other regions they areobserved as occasional imported cases.

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FilariaeFilariae

The most important filariosis is onchocercosis,the causative agents is Onchocerca volvulus,istransmitted by blackflies.

Microfilariae of this species can cause severe skinlesions and eye damage, even blindness.

Diagnosis of onchocercosis is based on clinicalsymptoms,detection of microfilariae in the skinand eyes, as well as on serum antibody detection.

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FilariaeFilariae

Other forms of filarioses includelymphatic filariosis .The causativeagent is Wuchereria bancrofti, Brugiaspecies and Loaosis that thecausative agent is Loa loa. Dirofilariaspecies from animals can cause lungand skin lesions in humans

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FilariaeFilariae

● Filariae are threadlike nematodes.● The length of the adult stages of the species

that infect humans varies between 2–50 cm whereby the females are larger than the males.

● The females release embryonated eggs or larvae called microfilariae.

● The eggs are about 0.2–0.3 mm long,surrounded by an extended eggshell● They can be detected in the skin or in blood

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FilariaeFilariae

● Based on the periodic appearance of microfilariae in peripheral blood, periodic filaria species are differentiated from the nonperiodic ones showing continuous presence.

● The periodic species produce maximum microfilaria densities either at night (nocturnal periodic) or during the day (diurnal periodic).

● Different insect species, active during the day or night, function as intermediate hosts accordingly to match these changing levels of microfilaremia.

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Life Cycle of FilariaeLife Cycle of Filariae

Insect: Ingestion of microfilaria with a blood meal

development in thoracic musculature with two

moltings to become infective larva

migration to mouth parts and tranmission into skin of a new host through puncture wound

during thenext blood meal.

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Life Cycle of FilariaeLife Cycle of Filariae

Human

Migration to definitive localizations and

further development with two more

moltings to reach sexual maturity.

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Wuchereria bancroftiWuchereria bancroftiCausative agents of lymphatic filariosisCausative agents of lymphatic filariosis

About 120 million people in 80 countries suffer from lymphatic filariosis caused by Wuchereria Wuchereria bancroftiibancroftii or Brugia species

(One-third each in India and Africa, the rest in southern Asia, Pacific

region,and South America),

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Wuchereria bancroftiWuchereria bancrofti

Life cycle and epidemiology

●Humans are the only natural final hosts of

W. bancrofti.

●The intermediate hosts of W. bancrofti are

various diurnal or nocturnal mosquito

genera.

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Wuchereria bancroftiWuchereria bancrofti

● The development of infective larvae in

the insects is only possible at high

environmental temperatures and humidity

levels;

● In Wuchereria bancrofti the process takes about 12 days at 28 ºC.

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Wuchereria bancroftiWuchereria bancrofti

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Wuchereria bancroftiWuchereria bancrofti

● Following a primary human infection,the filariae migrate into lymphatic vessels where they develop to sexual maturity.

● Microfilariae appear in the blood after seven to eight months.

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Wuchereria bancroftiWuchereria bancrofti

● Pathogenesis and clinical manifestations.

The initial symptoms can appear as early as

1 month , although in most cases the incubation

period is 5 to 12 months or much longer.

Asymptomatic infection,is with

microfilaremia that can persist for years.

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Wuchereria bancroftiWuchereria bancrofti

Acute symptomatic infection:

Inflammatory and allergic reactions in the lymphatic system caused by filariae

Swelling of lymph nodes, lymphangitis, general malaise, swellings

onegs, arms, scrotum, orchitis.

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Wuchereria bancroftiWuchereria bancrofti

Chronic symptomatic infection

Chronic obstructive changes in the lymphatic system hindrance or blockage of the flow of lymph and dilatation of thelymphatic vessels (“lymphatic varices”)

Indurated swellings caused by connective tissue proliferation inlymph nodes, extremities (especially the legs, “elephantiasis”),the scrotum. thickened skin ,lymphuria, when lymph vesselsrupture.

This clinical picture develops gradually in indigenous inhabitantsover a period of 10–15 years after the acute phase, in immigrantsusually faster.

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Wuchereria bancroftiWuchereria bancrofti

Tropical, pulmonary eosinophilia

Syndrome with coughing, asthmatic

pulmonary symptoms, high-level blood

eosinophilia, lymph node swelling and high

concentrations of serum antibodies

(including IgE) to filarial antigens.(including IgE) to filarial antigens.

No microfilariae are detectable in blood, but

sometimes in the lymph nodes and lungs.

This is an allergic reaction to filarial antigens

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Wuchereria bancroftiWuchereria bancrofti

1-A diagnosis can be based on clinical symptoms (frequent eosinophilia)

2-Finding of microfilariae in blood (sampling at night for nocturnal periodic species).

3-Microfilariae of the various species can be differentiated morphologically in stained blood smears and byDNA analysis.

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Wuchereria bancroftiWuchereria bancrofti

4-Detection by ultrasonography, particularly in the male scrotal area.

5-Detection of serum antibodies (group-specific antibodies, specific IgE and IgG subclasses) and circulating antigens

6-The recent development of a specific ELISA and a simple quick test (the ICT filariosis card test ıs usefull for serology.

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Wuchereria bancroftiWuchereria bancrofti

Therapy. Both albendazole and diethylcarbamazine have been shown to be at least partially effective against adult filarial stages.

However, optimal treatment regimens still need to be defined.

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Wuchereria bancroftiWuchereria bancrofti

● In 1997, the WHO initiated a program to

eradicate lymphatic filariosis.The control

measure is mass treatment of populations in

endemic areas with microfilaricides.

● Concurrent single doses of albendazole with

either ivermectin or diethylcarbamazineare

99% effective in removing microfilariae from

the blood for 1 year after treatment with

measure of mosquito bites.

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● Humans can acquire an infection with larvae of various Trichinella species by ingesting raw meat (from pigs, wild boars, horses, and other species).

● Adult stages develop from the larvae and inhabit the small intestine, where the females produce larvae that migrate through the lymphatics and bloodstream into skeletal musculature, penetrate into muscle cells and encyst.

TrichinellaTrichinellaCausative agent of trichinellosisCausative agent of trichinellosis

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TrichinellaTrichinella

OccurenceOccurence

Eight Trichinella species and several

strains have been described to date based

on typical enzyme patterns, DNA

sequences,and biological characteristics.

The most widespread and most important species is Trichinella spiralis.

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TrichinellaTrichinella

Male Trichinella spiralisTrichinella spiralis are approximately1–2mm long, the females 2–4mm.

The larvae are released following exposure to thedigestive juices,whereupon they invade epithelial cellsin the small intestine.

Reaching sexual maturity within a few days after fourmoltings. The males soon die after copulation, thefemales live for about four to six weeks.

Each female produces about 200–1500 larvae (eacharound100 lm long), which penetrate into the laminapropria.

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TrichinellaTrichinella

The larva penetrates into organs and body tissues by lymphogenous and hematogenous migration.Development occurs only in striated muscle cells that they reach five to seven days

The larvae penetrate into muscle fibers, which are normally not destroyed.

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TrichinellaTrichinella

The muscle cell begins to encapsulate the parasite.

Encapsulation is completed after four to six weeks.

The capsules are about 0.2–0.9mmlong with an oval form resembling alemon.

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TrichinellaTrichinella

The encapsulated Trichinella remain viable for years in the host

The developmental cycle is completed when infectious muscle Trichinella are ingested by a new host.

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