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D. Medinensis aka Guinea worm- taxonomy
Nematoda → Secernentea → Rhabditida → Spirurida → Dracunculus
D. medinensis- general
females up to 120 cm
Vulva rarely seen in gravid females
Live in body cavities- loose connective tissue around peritoneal cavity
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
D. medinensis- epidemiology
SE asia, pockets in NE S america, Iran, Africa
Canines, felines, racoons → animal reservoirs
D. medinensis- transmission
sustained by injestion of infected copepod by humans and contact of infected humans stagnat pools of FRESHwater w/ copepods
WATER WELLS
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
D. medinensis- diagnosis
ID in of worm when blister is seen
D. medinensis- treatment
mechanical/ surgical removal of worm
Metronidazole facilitates removal of worms
D. medinensis- prevention
boidl/filter suspected water
chemical treatment of water
limit human bathing in potential drinking water sources
Soil- transmitted helminth infections in children/adolecents
Ascariasis
Trichuriasis
Hookworm
neglected tropical diseases
cause: Stunted grwoth, anemia, poor cognitive function
Standard practice of soil-transmitted helminth infections in children/adolecents
preventive chemotherapy → mass deworming
questionable benefit of practice
T. trichiuria aka whipworm- taxonomy
Nematoda → Adenophorea → Trichocephalida → trichuris → trichinella
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
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
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
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
What are distinc characterisits of a Trichuriasis infection?
finger and toe clubbing
rectal prolapse
T. trichiuria -diagnosis
presence of characteistic eggs in stool
whipworm dance → ultrasound; lumen of appendix wriggles continuously
T. trichiuria - prevention
limiting fecal oral transmission
naisl kept clean, wash hands
T. trichiuria - treatment
mebendazole and albendazole
Trichuris -egg characteristics
barrel shapped
triple shell in addition to vitelline membrane
bipolar, unstianed intralaminar proccess that look like → mucoid plugs
T. spiralis- taxonomy
nematoda → adenophorea → trichocephalida → trichuris → spiralis
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
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
Trichuris- molecular mediators
tyvelose-bearing glycoproteins
role of excreory/ secretory products →
phosporylcholine bearing molecules
Trichuris- immunity
rapid rejection/ expulsion of L1 in sm. int. —> IgE
IL 10 → limits inital inflammation
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
T. spralis- diseases/presentation
periorbital edema
organ damage: central nervous system, heart, lung
muscle pain
abdominal discomfort
diarrhea
subungual hemorrahges in fingernails
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
T. spralis - treatment
Mebendazole → minimaly effective
T. spralis - prevention
pork/sausage should be cooked at temperatures greater than 70C
meat pigs (scraps) should be sterilized
A. lumbricoides- taxonomy
Nwmatoda -. secernentea Rhabditida → Ascardidia → Ascaris
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
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
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
Ascaris lumbricoides - diseases caused
Pneumonitis
liver granulomas and fibrosis
intestinal discomfort
nutriotonal impairment/ obstruction
abnormal migration of adults to bile ducts, appendix, peritoneum, etc.
In. nematods 3 slide 9 ***
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
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
Ascaris lumbricoides - treatment
w/ mebendazole, peperazine citrate, cyclobendazole
Ascaris lumbricoides - prevention
limit fecal of soil
E. vermicularis aka Pinworm - taxonomy
Nematoda → secernentea → rhabditida → Ascaridia → enterobius
family oxyuroidea
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
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
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
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
Enterobius vermicularis - disease caused
worms may enter female gential tract
perianal itching
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
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
Enterobius vermicularis - treatment
mebendazole
pyrantel pamoate
Enterobius vermicularis - prevention
scrupulous personal hygiene
wash beddings/clothes of infected children → HOT water
Eosinophils and Eosinophilia
express CR3, IgA, IgE receptors
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
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
Anisakis spp. - general
adult stages of Anisakis found in stomach of amrine ammals, dolphins, porpoisses, seals
IH → crusteaceasn, marine fish
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
Anasakis spp. - epidemiology
areas where salt water fish, herring are eaten raew sashimi; → Japan, Scandinavian countries, U.S. both coasts
Anasakis spp. - pathology
caused by inflammatory response
larvae in humans → bore into throat/gastric mucosa
swelling of GI tract walls → cause obstruction/ peritonitis
Anasakis spp. - diagnosis
biospy/endocsopy
biopsy of larvae distinged by large body
moderate thick cuticle, large lateral cords
Anasakis spp. - prevention
infectivity of larvae in infected fish can be reduce if fish kept frozen after catch
prevents parasites from migrating to tissues
Anasakis spp. - treatment
surgical removal of larvae
S. stercoralis aka threadworm - taxonomy
Nematoda → secernentea → rhabitida → rhabditia → rhabditina → strongyloides
Strongyloides stercoralis - general
phasmids
didelphic
protandrogonous females
parthenogenesis:
What is didelphic
2 uteri and oviducts
What is protandrogonous females
male reproductive organs develop fst and then disappear; then female reproductive organs develop
Parthenogenesis
development of an unfertilized egg into an adult
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
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
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
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
S. stercoralis - diseased caused
Pneumonaitis
Abdominal pain
Malabsorption syndrome
Mucosal damage
Doarrhea
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
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
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
S. stercoralis - treatment
albendazole
ivermectin
S. stercoralis - prevention
especially where S. fuelleborni is suspected,
screening of pregnant women/treatment
appropriate disposal of human waste
A. duodenale aka hookworm - taxonomy
Nematoda → secernentea → rhabitida → strongylida → Ancylostoma
N.americanus aka hookworm - taxonomy
Nematoda → secernentea → rhabitida → strongylida → necator
N. americanus/ A. duodenale - general
well developed buccal bearing cutting plates/teetj
males → umbrella shaped burse for mating at post.
life cycle diff.
Ancylostoma spp. - morphology
buccal capsule large ventral cutting teeth
vulva in post. half
Necator spp. - morphology
ventral cutting plates
vulva in ant. half of body
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.
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.
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
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
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
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
What is geophagy
craving to eat soil
from heavy infection from intentinal worm infections
Hookworm disease depends on ….
# of worms
species of hookworm
nutrional condition of infected person
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
N. americanus - pathogenesis
49- 56 days prepatence period
5k - 10k eggs/day/female
percutaneous
PORK
Ascaris effect
Reduced growth rate in ages 5 to15
Trichuris effect
Reduce growth rate, TDA, iron deficiency ages 6 to 18
Ancylostoma/necator effect
iron deficiency/ anemia ages 10 to 50
Ancylostoma/necator spp. - diagnosis
clinical symptoms
characteristic egg in feces- thin walled, transparent shell w/ cleaved embryos
Ancylostoma/necator - treatment
ivermectin
mebendazole
How does medendazole works for Ancylostoma/necator infections
binds helminthic tublin
blocks microtubule assembly, also inhibits glucose uptake in helminths
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
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
Cyclodevelopmental transmission
development in arthropod vector