hookworms Flashcards
hookworm morphology
small, stout worms (10-16mm)
dioecious, sexually dimorphic, females larger
-males w copulatory bursa
anterior end curved dorsoventrally
buccal cavity w 3 pairs teeth
esophagus club-shaped (very muscular and powerful pump)
-voracious blood suckers!
develop into infective stage in environment
occupy small intestine of host
ancylostoma caninum
canine hookworm
ancylostoma caninum life cycle
direct
-eggs passed
-larvae develop in environment 7-14 days
ancylostoma caninum host infection
skin penetration
oral ingestion
tracheal migration through somatic tissues
adults in small intestine, 17-21 days following infection
-lifespan 12-18 months in absence of reinfection
ancylostoma caninum arrested larvae via lactogenic route
most important!
larvae do not appear to migrate
mature in small intestine following attachment
clinical signs of anemia 8 days post infection
peak blood loss between 15-18th day
nursing puppies may pass eggs as early as 10-12 days after birth
sources of infective larvae L3 for oral infection
environmental (pet park)
paratenic host
hookworm pathogenesis
cause disease bc voracious blood suckers!
severity depends on:
-intensity of infection
-age of host
-nutritional status
-degree of iron reserves
-presence of acquired immunity
peracute infection
signifigant blood loss
-rapid progression to hypochromic anemia within hours of days as worms feed @ 8 days post infection
-pale mucous membranes
-diarrhea w black tarry stools
large # worms in short time
naiive immune status
deficient nutrition-insufficient iron reserves
acute infection
exposure of older puppies and adults
acuired from environment over short period of time
cumulative process w prolonged exposure and progressive acquisition of additional worms
chronic compensated infection
presence of infection w/o overt clinical signs
measurable reductions in PCV, erythocyte count
secondary decompensated infection
older dogs w other primary health issues
malnourished animals
diagnosis peracute disease
neonatal puppies showing profound anemia
pale mucous membranes
hematocrit or PCV <20%
weakness, listless, anorexia
bloody diarrhea
FECAL MAY BE NEG
diagnosis acute disease
older animals (>3-4 months-adult)
PCV<25%
listless w pale mucous membranes
diarrhea w black-tarry stools
low BCS
poor hair coat
dermatitis on feet
thin shelled eggs on fecal
diagnosis chronic compensated disease
older animals
PCV on low end
low weight for age/ low BCS
poor hair coat
dermatitis on feet
thin shelled eggs on fecal
diagnosis secondary decompensated disease
older animals
PCV below normal
emaciated w low BCS
poor hair coat
dermatitis on feet
eggs on fecal
parasitic disease secondary to underlying!
treatment peracute
immediate anthelmintic treatment
assessment based on age, clinical presentation, hematocrit
supportive care (fluids, electrolytes) important to keep alive for treatment to be effective
pyrantel is drug of choice, fast acting and peak serum levels quickly
-safe to use in young animals bc pass quickly through gi
treatment of animal w/o signs
target is removal of egg laying adult worms from S.I
-pyrantel pamoate
-fenbendazole & albendazole
-heartworm prophylaxis regimens (adequate for control, not prevention)
prevent perinatal infections
daily administration fenbendazole
-40th day gestation through 14th day lactation
-attacks reactivated larvae in moms tissue and prevents infection of pups
ivermectin
-4-9 days prior to whelping and 10 days post
treat puppies at 2 week intervals for 4 treatments (pyrantel)
arrested development
vacant gut is repopulated by worms in arrested development
-frustrating to vets and clients, explain lifecycle
rationale for post-treatment confirmation of treatment efficiency
-evaluate 7-10 days following treatment
ancylostoma tubaforme
feline hookworm
morphologically similar to A. caninum, eggs on fecal smaller
ancylostoma tubaforme life cycle
eggs passed
larvae develop in environment
L3 or paratenic host ingested
tracheal migration
adults in S.I
-rodent paratenic host play sig role bc predator-prey interaction
Ancylostoma braziliense
endemic in southern US
more prevalent in cats than dogs
identification of infection status and clinical correlation not possible
Ancylostoma braziliense morphology
adult worms smaller than A. caninum, female still larger
buccal capsule w 2 teeth
eggs on fecal slightly smaller
Ancylostoma braziliense lifecycle
eggs passed in feces
larval development prefers warmer conditions
no vertical transmission!
uncinaria stenocephala
dog, cat, fox
-cats appear to be largely refractory to infection
endemic to temperate climates
uncinaria stenocephala morphology
size comparable to other hookworms
cutting plates rather than teeth in buccal capsule
eggs on fecal exam large
uncinaria stenocephala lifecycle
eggs passed in feces
larvae develop in cooler climates
no vertical transmission in dogs/cats
uncinaria stenocephala treatment
ivermectin- only 1/2 effective against
cutaneous larval migrans
skin penetration by infective L3
-inflammation under skin of host
common in SE U.S
all hookworms may be implicated in CLM
-histologic differentiation difficult
visceral larval migrans
larval stage hookworms penetrate deep and reach pulmonary circulation
non-specific respiratory illness, dry cough, dyspnea
diffuse pulmonary infiltrates on radiograph
hookworm associated gastroenteritis
successful colonization of human S.I
-adult of advanced L4 stage
transmission by cutaneous or oral route
prevent by feces removal in backyard
