Parasiology Exam 4- nematodes Kima UF

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171 Terms

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D. Medinensis aka Guinea worm- taxonomy

Nematoda → Secernentea → Rhabditida → Spirurida → Dracunculus

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D. medinensis- general

  • females up to 120 cm

  • Vulva rarely seen in gravid females

  • Live in body cavities- loose connective tissue around peritoneal cavity

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D. medinensis- life cycle

  • L3 larvae penetrate gut → adults reside in cavities → gravid females migrate to subcutaneous site → Rhhabitiform larvae (L1) released into water → copepod ingest larvae where they metamorphose → ingestion of infected copepod

  • blister from worm soaks in water for relief → work burts, releasing hundreds of thousands of L1 larvae →water fleas injest the larvae → larvae become mature L3, 2 wks → someone drinks water w/ contaminated fleas → larvae released in stomahc → migrate to sm int. penetrate int wall into body cavity → grow and mate → fertilized females migrate to connective tissue usually lower limbs → yr later larvae ingested form blister near surface for eruption → blister bursts exposing worm soaking in water for relief

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D. medinensis- epidemiology

  • SE asia, pockets in NE S america, Iran, Africa

  • Canines, felines, racoons → animal reservoirs

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D. medinensis- transmission

  • sustained by injestion of infected copepod by humans and contact of infected humans stagnat pools of FRESHwater w/ copepods

  • WATER WELLS

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D. medinensis- pathogenesis

  • effects worm mostly associated w/ migrating adultss- may cause eosinophilia, naseua, astham indeuces by worm products

  • most significant pathology → cutaneous ulcer formaed by female worm

  • dead worm elicit vigorus host response → chronic arthrisits when near joints

  • secondary bactrial infection of lesion may occur

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D. medinensis- diagnosis

  • ID in of worm when blister is seen

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D. medinensis- treatment

  • mechanical/ surgical removal of worm

  • Metronidazole facilitates removal of worms

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D. medinensis- prevention

  • boidl/filter suspected water

  • chemical treatment of water

  • limit human bathing in potential drinking water sources

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Soil- transmitted helminth infections in children/adolecents

  • Ascariasis

  • Trichuriasis

  • Hookworm

  • neglected tropical diseases

  • cause: Stunted grwoth, anemia, poor cognitive function

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Standard practice of soil-transmitted helminth infections in children/adolecents

  • preventive chemotherapy → mass deworming

    • questionable benefit of practice

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T. trichiuria aka whipworm- taxonomy

Nematoda → Adenophorea → Trichocephalida → trichuris → trichinella

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Trichinella spp.- general

  • lack excretory sytem

  • mouth simple opening w/o lips

  • capillary like esophagus, thin walled containg glands -→ STICHOCYTES

  • NO phasmids

  • monodelphic

  • eggs require mosit soil conditions to complete development → 21 days for egg development

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T. trichiuria - epidemiology

  • WW —> mainly TROPICS

  • second most prevalent nematode

  • prevalence up to 20-25% in small children some areas

  • aquire infection by ingesting parasite egg in food/water/soil

  • children → most infected

  • whipworm of pigs/monkeys similar

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T. trichiuria - life cycle

  • Unembryonated eggs passed in feces →2-cell stage → advanced cleave → L3, embroynated eggs are injested → larvae hatch in Sm. int → adults travel in cecum → released in feces

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T. trichiuria - pathogenesis

  • asymptomatic

  • immaturre t. worms penetrate deep into int walls → worms that penetrat walls of large int most likely to survive

  • ant. end o mature worm -. buried in colon sub musocas → post. end exposed in in lumen

  • chronically infected: whipworm dysentery, mild anemia, finger/tow clubbing, growth retardation

  • heavy infections: found in distal end of colon

  • mucosa becomes edematosu → anal sphinter tone lost → rectum tends to PROLAPSE

  • secondary bacterial infections

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What are distinc characterisits of a Trichuriasis infection?

  • finger and toe clubbing

  • rectal prolapse

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T. trichiuria -diagnosis

  • presence of characteistic eggs in stool

  • whipworm dance → ultrasound; lumen of appendix wriggles continuously

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T. trichiuria - prevention

  • limiting fecal oral transmission

  • naisl kept clean, wash hands

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T. trichiuria - treatment

  • mebendazole and albendazole

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Trichuris -egg characteristics

  • barrel shapped

  • triple shell in addition to vitelline membrane

  • bipolar, unstianed intralaminar proccess that look like → mucoid plugs

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T. spiralis- taxonomy

nematoda → adenophorea → trichocephalida → trichuris → spiralis

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T. spiralis - epidemiology

  • WW

  • strain diff in geographically distinct regions

  • parasite maintained by human-pig-tate cycles (domestic)

  • wild carnivores- prey cycles (sylvatic)

  • aquire thru eating minimally cooked infected meat, pork, sausage

  • Europe → game widely consumed

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T. spiralis - life cycle

  • injestion of undercooked infected meat → larvae released in sm. inte → adults migrate to sm int -. larvea deposited in mucosa → encysted larva in striated muscle, systemactic circulation → expuslion of adults a few wks after primary infetion, dead end infection,

  • females in messenteric LN

  • larva intracellular parasite

  • muscle de-differentiaties → metaplasia

  • Nurse cell → multi-nuc, fformed

  • capsule forms around nurse cell -. derived from host muscle/inflammatroy cells

  • larva - developmental arrest

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Trichuris- molecular mediators

  • tyvelose-bearing glycoproteins

  • role of excreory/ secretory products →

  • phosporylcholine bearing molecules

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Trichuris- immunity

  • rapid rejection/ expulsion of L1 in sm. int. —> IgE

  • IL 10 → limits inital inflammation

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T. spiralis - pathogenesis

  • marked eosinophilia

  • early symptoms: w/in 2 days of larva ingestion → nausea, fever, profuse perspiration, facial edema, secondary bacterial infection

  • parasites move into tissue → pneumonia, encephalitis, myocarditis

  • parasites in muscles/nervous tissue

  • infections → lethal

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T. spralis- diseases/presentation

  • periorbital edema

  • organ damage: central nervous system, heart, lung

  • muscle pain

  • abdominal discomfort

  • diarrhea

  • subungual hemorrahges in fingernails

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T. spralis- diagnosis

  • serological/ skin tests

  • negative results -→ early infections

  • intradermal injection of larval suspension should result in appearance ofa wheel

  • detection of live larevae in biopsy

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T. spralis - treatment

  • Mebendazole → minimaly effective

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T. spralis - prevention

  • pork/sausage should be cooked at temperatures greater than 70C

  • meat pigs (scraps) should be sterilized

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A. lumbricoides- taxonomy

Nwmatoda -. secernentea Rhabditida → Ascardidia → Ascaris

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Ascaris lumbricoides - general

  • largest of common nematode parasites

  • females up to 45 cm

  • didelphic w/ vulva towards ant end of body

  • cylindrical esophagus, well developed lips

  • prolific egg producers → 200k/day

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Ascaris lumbricoidea- epidemiology

  • WW → prevalent in tropics

  • maintained by favorable qualites of soil, frequent fecal contamination of soil

  • eggs killed by prolonged dry conditions → NEED MOIST

  • ingested by eating dirt-eating ages 5-9 children,

  • eating raw vegetables where eggs lodge

  • disperesed by animals/beetles that eat human feces → eggs passes trhu animals unchanged

  • PIGS → Ascaris Suum; suseptible to human ascaria, vice versa w/ humans

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Ascaris lumbricoides- life cycle

  • adults in sm int. → passed thru feces→ unfertilized eggs will not undergo further development→ embryonated egg w/ L3 larvae ingested → hatched larvae enter circulation and migrate to lungs → larvare cough up/swallowed, reentering GI → maturation proceeds in Sm. int.

  • pre patent period → 8 to 9 wks

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Ascaris lumbricoides - diseases caused

  • Pneumonitis

  • liver granulomas and fibrosis

  • intestinal discomfort

  • nutriotonal impairment/ obstruction

  • abnormal migration of adults to bile ducts, appendix, peritoneum, etc.

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In. nematods 3 slide 9 ***

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Ascaris lumbricoides - Pathogenesis"***

  • adult worms cause obstructive appendicitis/ lodge in bile duct, liver

  • fevers tend to induce worm migration, worms are passed through mouth/anus

  • host reaction to larvae, especially in lungs can cause Ascaris pneumonitis →Loeffler’s pneumonia

  • WANDERING WORMS**

  • mechanical effects of adults worms

  • immmune rxn of host

  • milder infection may cause loss of appetite, colickly cramps

  • effect adult worms on host nutrition

  • growth may be impaired; periodic deworming encouraged

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Ascaris lumbricoides - Diagnosis

  • ID eggs in feces

  • fertlized eggs broadly ovoidal, thick transparent middle layer

  • unfertilized eggs → elongateed w/ relativley thin middle layer

  • both egs bile stianed

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Ascaris lumbricoides - treatment

  • w/ mebendazole, peperazine citrate, cyclobendazole

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Ascaris lumbricoides - prevention

limit fecal of soil

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E. vermicularis aka Pinworm - taxonomy

Nematoda → secernentea → rhabditida → Ascaridia → enterobius

  • family oxyuroidea

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Enterobius vermicularis - general

  • primarliy inhabit ileocecal region, spread to adjacent areas of sm./lg. int,

  • males 1-4 mm lomng —> SINGLE spicule

  • females 8-13 mm; post end extends into long slender pt.

  • Alae- wind like extensions at ant. end

  • didelphic worms

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Enterobius vermicularis - epidemiology

  • most common nematode

  • cosmopolitan distribution, WW → temperate regions

  • infrequent b athing habits in temperate climates -. may cause high prevalence

  • eggs been found on seats, armrests in public places

  • more common in chilren → daycares, institutions and in families

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Enterobius vermicularis aka PINWORM Tape on asshole atnight- life cycle

  • eggs on perianal folds → larvae inside the eggs mature w/in 4-6 hrs -. embryonated eggs ingested → larvae hatch in sm. int. _. adults in lumen of cecum → gravid female migrates to perianal region at night to lay eggs

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Enterobius vermicularis - modes of transmission

  • self infection when infected person reinfected by hand to mouth

  • cross-infection, when infective eggs are ingested from fingers that been in contact with contaminated surface

  • inhalation/ airborne eggs

  • retro-infection → parasite hatches and migrates back to cecum → minimal evidence

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Enterobius vermicularis - disease caused

  • worms may enter female gential tract

  • perianal itching

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Enterobius vermicularis - pathogenesis

  • minimal effects

  • perineall/perianal itching

  • excessive scratching → scarification

  • girls: owrms migrate to vagina, heavy infection mucoid vaginal discharge observed, rare cases → migrate up to fallopian tubes, get trapped, granuloma formation ensues

  • worms found in the urinary tract, peritoneum cause abdominal/urinary tract infections in girls as well as older women

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Enterobius vermicularis - diagnosis

  • detection of adult worms in perianal area/eggs

  • eggs elongate-ovoidal, flattened on 1 side

  • shell thick/colorless

  • eggs recovered by cellophane technique → eggs stick to tape

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Enterobius vermicularis - treatment

  • mebendazole

  • pyrantel pamoate

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Enterobius vermicularis - prevention

  • scrupulous personal hygiene

  • wash beddings/clothes of infected children → HOT water

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Eosinophils and Eosinophilia

express CR3, IgA, IgE receptors

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Toxocara spp. - visceral larval migrans

  • infection w/ nematodes of animals

  • paasites of genus toxocara → T. canis/cati (OLM) that infect dogs/puppies and cats (materlan-fetal transmission

  • high infection rate in puppies

  • ingestion of eggs harbouring L2 larvae, migrate thru human tissue, liver,

  • host rxn _. inflmmation

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Angiostrongylus

  • infect humans

  • parasites of wild rates → rat lung worms

  • utlize crustaceans/ mollusks as Ih

  • humans aquire thru eating L3 larvae in crustaceans/mollusks; migrate to brian

  • SE asai, C/S America

  • may cause meningoencephalitis

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Anisakis spp. - general

  • adult stages of Anisakis found in stomach of amrine ammals, dolphins, porpoisses, seals

  • IH → crusteaceasn, marine fish

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Anasakis spp. - life cycle

  • eating contaminated fish → larvae enter int. tissue, cause eoxinophilic granuloma → fish eaten by marine mamals → L3/4 larvae migrate thru tissue back to int. → adult males/female in int of marine mammals -. eggs in water → larvae hatches from egg → larvae enter euphauslids and reaches hemoccoel → euphausids eaten by fish, larvae penetrate int. tissue and enter abdominal caivty, larvae kie on surface of rogamn, in messenteries or musculature -. then eaten by marien animal

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Anasakis spp. - epidemiology

  • areas where salt water fish, herring are eaten raew sashimi; → Japan, Scandinavian countries, U.S. both coasts

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Anasakis spp. - pathology

  • caused by inflammatory response

  • larvae in humans → bore into throat/gastric mucosa

  • swelling of GI tract walls → cause obstruction/ peritonitis

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Anasakis spp. - diagnosis

  • biospy/endocsopy

  • biopsy of larvae distinged by large body

  • moderate thick cuticle, large lateral cords

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Anasakis spp. - prevention

  • infectivity of larvae in infected fish can be reduce if fish kept frozen after catch

  • prevents parasites from migrating to tissues

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Anasakis spp. - treatment

  • surgical removal of larvae

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S. stercoralis aka threadworm - taxonomy

Nematoda → secernentea → rhabitida → rhabditia → rhabditina → strongyloides

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Strongyloides stercoralis - general

  • phasmids

  • didelphic

  • protandrogonous females

  • parthenogenesis:

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What is didelphic

2 uteri and oviducts

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What is protandrogonous females

male reproductive organs develop fst and then disappear; then female reproductive organs develop

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Parthenogenesis

development of an unfertilized egg into an adult

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S. stercoralis - morphology

  • parasitic females longer and have an esophagus that extends 1/3 the length of the body

    • vulva at posterior end

  • free-living female is wider

    • vulva at mid section

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S. stercoralis - epidemiology

  • eggs seldom seen in feces

  • dogs/cats infected w/ strains indistinguisbable from those that infect humans

  • zoonosis

  • WW

  • high incidence in mental institutions → adults are more often infected that children

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S. fuelleborni - epidemiology

  • infection of monekys

  • sub-saharan africa

  • Papua-new guinea

  • affects children more

  • EGGS in FECES

  • acquired from mothers milk

  • swollen belly syndrome

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S. stercoralis - life cycle

  • Rhabditiform L1 larvae in int excreded in stool → development into free-living adult worms → eggs are produced by fertilized femaleworms → rhabditiform larvae hatch from embryonated eggs → rhabditiform larvae develop into filariform larvae L# → infective filariformlarvae penetrate intacts skin of DH → filariform larvae migrate by various pathways to small int. where they become adults → parasitic adult female in sm. int. → eggs deposited in int. mucosa rhabditiform larvae hatch and migrate to int. lumen → autoinfection: rhabditiform larvae in lg int. become filarifrom, penertrate int. mucosa or perianal skin and migrate to other organs

  • prepatent period: 25-30 days

  • L3 larvae migrate via bloodstream/ lymphatics to lungs → coughed up and swallowed → L3 larvae appear capable of migrating to int. via alt routes, thru abdomincal viscera/connective tissue → in sm. int. larvae molt TWICE and become adult female worms

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S. stercoralis - diseased caused

  • Pneumonaitis

  • Abdominal pain

  • Malabsorption syndrome

  • Mucosal damage

  • Doarrhea

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S. stercoralis - autoinfection

  • development of 1st stage to infective larvae on hosts intestine

  • linear skin lesions → perianal origin

  • Disseminated infection → stomach, colon, lungs, CNS, liver, etc.

  • Bacteremia

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S. stercoralis - pathogenesis

  • cutaneous phase - swelling/ intense itching at sites transversed by infective filariform larvae ground itch, host response may slow parasite migration thru skin → creeping eruption

  • secondary infection

  • pulmonary phase - migration thru lung induces host cellular rxn, parasites develop maturity in lung if passage blocked, larvae may also seen in sputum

  • Intestinal infection: significant in heavy infections, abdominal pain, vomiting/ intermittent dirrhea, sysentery, weight loss in chronic infections

  • problemtic in immunocompromised

  • heavy strongyloids infections can be fatal

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S. stercoralis - Diagnosis

  • IDing of rhabditifrom larvae in feces, sometimes flarifrom larvae

  • Strongyloides fuellebornie eggs → passed in feces

  • sputum maybe contain larvae

  • Serological test (ELISA ) → definitive diagnosis

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S. stercoralis - treatment

  • albendazole

  • ivermectin

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S. stercoralis - prevention

  • especially where S. fuelleborni is suspected,

  • screening of pregnant women/treatment

  • appropriate disposal of human waste

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A. duodenale aka hookworm - taxonomy

Nematoda → secernentea → rhabitida → strongylida → Ancylostoma

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N.americanus aka hookworm - taxonomy

Nematoda → secernentea → rhabitida → strongylida → necator

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N. americanus/ A. duodenale - general

  • well developed buccal bearing cutting plates/teetj

  • males → umbrella shaped burse for mating at post.

  • life cycle diff.

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Ancylostoma spp. - morphology

  • buccal capsule large ventral cutting teeth

  • vulva in post. half

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Necator spp. - morphology

  • ventral cutting plates

  • vulva in ant. half of body

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Ancylostoma spp. - epidemiology

  • old world countires

  • Southern europe, SE asia, China, Africa

  • New world

    • US, Caribbean

  • mostly humans infected

  • zoonotic

  • use night soil for fertilization of crops in ag

  • mines

  • affected by temperature

  • dung beetles appear to make soil suitable for hookworm devel.

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Necator spp. - epidemiology

  • most prevelant in US

  • C/S america

  • Africa, china

  • infects dogs

  • zoonotic

  • areas that use night soil for fertilization of crops in ag

  • mines

  • affected by temperatures

  • dung beetles appear to make soil suitable for hookworm devel.

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N. americanus - lifecycle

  • L3 on vegetation, can survie for 3-4 wks → L3 penetratae skin/enter bloodstream →L3 reach heart, entre pulmonary vasculature, cross into alveolae, → L3 ascend trachea, swallowed, entre GI tract → larvae lot twice L5, mature in sm. int. →eggs passed in feces → larvae hatcha dn develop in soil L1→ L3 → L3 on veg.

  • molt twice before reaching sm. int

  • no passage thru lungs

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Ancylostoma spp. - life cycle

  • Egg in feces → rhabditiform L1 larvae hatches → devel to filariform L3 larvae in envrio. →L3 larvae penetrate skin → larvae become developmentally arrests and domant tissues, re-activated larvae may entr sm. int. → larvae exist circulation inlungs, coughed up and swallowed → adults in sm. int.

  • aquired trhu contact or ingestion of L3/filariform from soil

  • molt twice in Gi tract

  • No passage thru lungs

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Arrested developemnt - ancylostoma

  • parasites ability to halt life cycle as L3 in host tissues, adaption to favorable conditions, later reactivate, causing prolonged/sudden infections

  • triggers: pregnancy/lactation

  • host immune status

  • removal of adult worm

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N. americanus/ A. duodenale - pathogenesis

  • cutaneou, pulmonary, intestinal phases

  • most serious → intestinal infection

  • worms burrow in int. wall

  • salivary secretions have anticoagulants

  • molecules target factor Xa and tissue factor VIIa → platelet inhibitor

  • iron deficiency anemia infections

  • protein energy deficiency

  • blood loss

  • heavliy infected individuals ahve craving to eat soil geophagy

  • pulmonary infection

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What is geophagy

  • craving to eat soil

  • from heavy infection from intentinal worm infections

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Hookworm disease depends on ….

  1. # of worms

  2. species of hookworm

  3. nutrional condition of infected person

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A. duodenale - pathogenesis

  • 53 days prepatence period

  • 10k-25k eggs/day/female

  • 20-27 C

  • oral route, percutaneous route

  • transplacental route

  • arrested development

  • Lamb, beef, pork

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N. americanus - pathogenesis

  • 49- 56 days prepatence period

  • 5k - 10k eggs/day/female

  • percutaneous

  • PORK

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Ascaris effect

  • Reduced growth rate in ages 5 to15

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Trichuris effect

  • Reduce growth rate, TDA, iron deficiency ages 6 to 18

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Ancylostoma/necator effect

  • iron deficiency/ anemia ages 10 to 50

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Ancylostoma/necator spp. - diagnosis

  • clinical symptoms

  • characteristic egg in feces- thin walled, transparent shell w/ cleaved embryos

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Ancylostoma/necator - treatment

  • ivermectin

  • mebendazole

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How does medendazole works for Ancylostoma/necator infections

  • binds helminthic tublin

  • blocks microtubule assembly, also inhibits glucose uptake in helminths

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Cutaneous larval migrans - general

  • CREEPING ERUPTIONS

  • zoonotic

  • Ancylostoma caninum → dogs

  • A. brazillinesis found in SE USA

  • passage thru skin results in skin eruptions

  • ground itch

  • feet/arm most common sites

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Filarial - general

  • adults live in tissues/ body cavities of vertebrae host

  • females produce microfilariae that circulate

  • microfilariae less differentiated than L1 larvae of other nematodes

  • undergo devel., transmitted by arthropod vectors → cyclodevelopmental transmission

  • infected w/ rickettsial bacteria → specificallu Wolbachia

    • affect bacteria reproduction of worms/ host reponse to worms

    • some dont harbor wolbachia

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Cyclodevelopmental transmission

  • development in arthropod vector