Flashcards in non-diarrheal invasive infestations Deck (58):
giant intestinal roundworm, "the wanderer"
adult female: 30 cm long, 5mm diameter
male: shorter, narrower, curved posterior with pair of copulatory spicules -yikes!
Ascaris adults live in the ?? where they do not ?? but rather ??
don't hatch, but constantly move agains peristalsis
Ascaris female produces how many eggs/day
eggs are ??? until they are deposited in soil with poop
embryonization can take place in ?? or longer if unfav. conditions
fertilized, not embryonated
when ingested, Ascaris larvae hatch in the ?? penetrate the ??and are carried via blood to ??
lamina propria, carried to the liver, heart, then lungs
in the lungs, Ascaris larvae lodge in the ?? and break out into the ??
from there the larvae actively migrate ???
up the bronchi into the trachea, across the epiglottis
are SWALLOWED, reaching the lumen of the small intestine
Ascaris lumbricoides larvae do what in the small intestine
grow and reach sexual maturity
cycle then begins again
whole Ascaris cycle takes ??
how long to the worms live ??
Ascaris occurs where ??
S and SE US (need warm embryonation in soil)
humans are sole host/reservoir, 1-4 mill affected
Africa, Latin America, East Asia
light Ascaris infections are
asymptomatic (typ. of parasites: host-parasite homeostasis)
most intense reactions with Ascaris are caused by ??
what type of reaction occurs ??
migrating larvae, esp. if high numbers
Type 1 hypersensitivity rxn: cough, wheezing, urticaria, fever
other complications of Ascaris larvae migration
lung damage, vermis pneumonitis
if moderately infected with Ascaris adult worms...
vague abd pain, acute colicky pain (heavier infections)
Ascaris aka "the wanderer" may pass spontaneously via
vomiting, thru nares when adult worms wander up there
young kids with large Ascaris burden may ??
be malnourished or have nutr. deficiencies, stunted growth
Ascaris adult worm infection complications
perforation of intestine
blockage of bile duct
-others related to aberrant adult migration
this may irritate Ascaris adult worm and cause migration
tx for other nematode infections
migrating larvae, vermis pneumonitis
*eosinophilia, Charcot-Leyden crystals* NO anemia
worms in stool, other sites
ova in stool (easily found due to so many produced)
how to prevent Ascaris
sanitary disposal of feces
educating at risk pop
washing raw fruit/veggies in clean water
this 2 hookworms are very similar
but differ in ??
crazy estimate !!
New World hookworm
-tropical and subtropical regions of Africa, Asia, Central and South America
-US: S/SE (2-15% prevalence)
estimated 1/6th of world infected!
Old World hookworm
distribution overlaps Necator americanus
N. americanus morphology
female adults: 1 cm, males a bit shorter
buccal cavity has 2 cutting plates
ova: thin-shelled, early cleavage stage found in feces
larvae: Rhabditiform (non-inf) and Filariform (infective)
N. americanus adults live in ?? where the feed on ??
the small intestine, feed on the intestinal villi by their cutting plates (Necator) or teeth (Ancylostoma)
N. american eggs are embryonated ?? after pooped out and deposited in soil
the ?? will hatch w.in 48 hrs of deposition and will grow/dev. in soil into ??
the N. american filariform larvae will seek out ?? in order to ??
a tall blade of grass, etc. to contact human skin
then actively penetrate subcutaneous tissue (hair follicle) and carried via blood
N. american filariform larvae are carried via blood to ??
where they ??
similar to ???
break out of alveolar capillaries, cruel up bronchi and trachea over the epiglottis and into pharynx and swallowed
Ascaris "the wanderer"
N. american larvae develop into adult worm in the ??
N. americanus symps caused by ??
penetration of larvae
ground or dew itch (allergic reaction): intense itching, burning erythema, edema, papular lesions-->vesicular if sensitized
N. american symps not typically caused by ??
larval migration thru lung (inapparent)
unless heavy worm infestation-->vermis pneumonitis
N. american sypms from adults in sm. intestine
depends on ?? and ??
loss of blood
worm burden (need 200+)
host nutritional status (related to host Fe++ loss and replacement)
light N. american infection typically
no recog. symptoms
acute/heavy N. american infection
heartburn, flatulence, diarrhea, wl, +/- eosinophilia
GI symps disappear if become chronic
chronic N. american infection resembles ??
bad symps in kiddos?
iron deficiency anemia
fatigue, ha, numbness, tingling, dyspnea, anorexia, hd/ft edema, sexual dysfunction, pallor, tachy, enlarged heart
physical, mental dev. may be arrested
N. armerican dx
clinical suspicion +
labs: ova in feces, quant. counts for worm burden, CBC looks like infection/iron deficiency (hypochromic RBC, eosinophilia)
N. american tx
N. american prevention
improve sanitary facilities, only poop in toilets!
don't use night soil
occurs in warms climates like hookworms (N. americanus)
also spread sporadically in temperate climates
signif reservoir of Strong ster
Strong ster has both a ??
free living phase and parasitic cycle
Strong free-living phase: larvae are ??
form of larvae ?? will ??
pooped out and deposited in soil (unlike hookworms)
rhabditiform larvae will grow and dev. into free-living adult worms
Strong free-living phase is
diecious, adults mate and female produces embryonated eggs that hatch and undergo similar cycle
if poor conditions, the Strong filariform larvae will ??
penetrate skin of host and begin parasitic infection
initial part of Strong parasitic life cycle:
similar to hookworms and Ascaris (spread to lungs, swallowed)
larvae develop into *female* adults in small intestine
Strong female adult is ?? and can live ??
weird brief appearance of ??
2 mm (small), lives w.in and among columnar epi cells of sm. intestine
male sex organs-->self-fertilization-->involution of male gonads
*no parasitic male per se*
Strong embryonated eggs hatch in ?? and proceed to ??
where they develop to ?? and are ??
rhabditiform larvae, pooped into soil
if host is constipated, Strong rhabditiform larvae will ??
develop into filariform larvae and directly re-infect host by penetrating colon mucosa or perianal area
Strong ster: common?
found where ??
less prevalent than hookworm
SE USA, rural areas (0.4-4%)
mental institutions (40%)
Strong ster symptoms due to penetration
little reaction observed in direct cycle, if auto infected may see creeping eruption at perianal region
Strong ster sypms from larval migration thru lungs..
few unless large infestation: pneumonitis, peripheral eosinophilia
Strong intestinal symps
invasion of mucosa, enteritis, tissue damage
manifestation of Strong ster infection
moderate: pain in epigastric region, diarrhea w. alternating constipation
autoinfections of Strong ster may lead to
sev. systemic infections, gen. abd pain, shock, fever, G- sepsis
Strong steer may cause ?? in immunocompromised host
Strong ster dx
most difficult roundworm to dx
eosinophilia in 50-80%
look for larvae in feces (vs. ova in feces for hookworm)
serum IgG by ELISA
larvae in sputum: agar test, look for worm tracks
Strong ster tx
Strong ster prevention
same as hookworm:
improve sanitary facilities, only poop in toilets!
don't use night soil