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Parasitology > Nematodes Part 2 > Flashcards

Nematodes Part 2 Flashcards

1
Q

what nematode parasites are common in ruminants

A

Trichostrongyles

HOTC = Haemonchus, Ostertagia, Trichostrongylus, Cooperia

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2
Q

Describe morphological characteristics of HOTC parasites

A

Family Trichostrongyloidea

  1. small
  2. bursate
  3. males have copulatory bursa with spiracles
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3
Q

Trichostrongyle habitat

A

abomasum and small intestines of ruminants

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4
Q

Trichostrongyle distribution

A

generally throughout N. America but some more common in certain regions

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5
Q

Name two examples of Trichostrongyles - scientific name and common name

A

Ostertagia ostertagi = brown stomach worm, bankrupt worm

Haemonchus contortus = Barberpole Worm

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6
Q

describe how the eggs of the two examples of trichostrongyles differ

A

Haemonchus contortus = more roung
Ostertagia ostertagi = more egg shaped
Note that there is overlap
EGGS NON LARVATED

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7
Q

What is the food source of both Trichostrongyle examples

A

blood - both are blood feeders although Haemonchus is known to be more of an avid blood feeder

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8
Q

In the Trichostrongyloid life cycle what is the infective stage?

A

L3

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9
Q

Describe the Trichostrongyloid life cycle

-What is the prepatent period?

A
  1. Eggs shed in feces
  2. L1-L3 in feces - feed on fecal bacteria
  3. L3 ingested while DH (ruminant) grazing – exsheath in rumen
  4. enter wall of abomasum or SI – develop into L4
  5. develop to lumen-dwelling adult in muscosa of predilection site

NO MIGRATION OCCURS
Prepatent period = 3 weeks

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10
Q

Define hypobiosis and the process

*Clinically speaking, why is this significant

A

larval inhibition, arrest development/go dormant during unfavorable conditions
occurs as L4 in abomasum
* less susceptible to anthelminthics at this stage

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11
Q

What is PGE

A

Parasitic Gastroenteritis caused by a complex of mainly Trichostrongyloid nematodes

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12
Q

Clinical signs of PGE in cattle (8)

A

rough coat
weight loss
diarrhea
anemia – more common in sheep and goats
submandibular edema = bottle jaw
high fecal count
adult worms at necropsy – lesions specific to certain species (ie Ostertagia ostertagi moroccan leather)

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13
Q

What animals are more susceptible to acquiring PGE?

A

weanlings

adults = good immunity but if experiencing stress/ starvation this immunity can go down

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14
Q

What males prevention of PGE difficult?

A
  1. management of dz is labor intensive
  2. high egg numbers and survival of L3 = total eradication is unlikely
  3. resistance to preventative dewormers
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15
Q

What is the Brown Stomach Worm

A

Ostertagia ostertagi - Family Trichostrongyloidea - Phylum Nematoda

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16
Q

Discuss the pathogenesis of the Brown Stomach Worm

A

as developing, larvae destroys gastric glands - cell tight jxn rupture
damages HCL-producing parietal cells = pH becomes neutral = can no longer digest proteins = bacterial overgrowth

adult = some blood sucking –> anemia

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17
Q

Type 1 Ostertagiasis

who is affected/infected, effect of infection

A

young cattle - suckling, dairy heifers, stocker

damage during exodus of gastric glands = moroccan leather = pebbled appearance of abomasal mucosa

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18
Q

Type 1 Ostertagiasis pathology

A

large # larvae in pasture, daily ingestion

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19
Q

Type 1 Ostertagiasis Dx

Prognosis

A
  1. high egg counts in FF
  2. incremental to rapid onset of clinical signs
    diarrhea, weightloss, bottle jaw, anemia, rough coat, death

Prognosis - good w/ tx, move to safe pasture

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20
Q

What is Pre-type II Ostertagiasis

A

ingestion of L3 that go into hypobiosis once in gastric gland – can last 3-4 months, no clinical dz seen

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21
Q

What is Type II Ostertagiasis

-Clinical signs

A

stimulated hypobiotic larvae acquired 3-6m prior
larvae resume developement - emerge from gastric glands
-gradual destruction of abomasum
-seen more in yearlings, calf replacement heifers and older stock
-signs of PGE
-high egg count

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22
Q

What is the Barberpole Worm?

A

Haemonchus contortus
Family Trichostrongyloidea
Phylum Nematoda

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23
Q

Barberpole Worm

  1. hosts
  2. habit and severity of effects
A

major cause of PGE in goats/sheep

pathogenic bloodsucker, most impt parasite in small ruminants except in cold climates

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24
Q

What are the signs of PGE in small ruminants?

A 
weight loss
rough hair/wool breaks 
anemia 
diarrhea - general PGE 
hypoproteinemia
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25
Q

Why is H. contortus such a problem? (5)

A
  1. year round transmission in Fl
  2. sheep and goat acquire little to no immunity
  3. deadly blood sucker
  4. very fecund
  5. resistant to most antihelmintics
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26
Q

Why are sheep and goats so susceptible to worms?

A
  • never evolved ability to acquire strong immunity to worms – originally from dry/deserts or cold mountains \
  • browse by preference avoiding grass
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27
Q

What is Periparturient Rise?

A

massive outpouring of worm eggs by ewes and does while lactating

PRL suppresses immunity to worms
condition begins near parturition
ceases w/in few days of weaning

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28
Q

What are the 3 sources of Periparturient Rise?

A
  1. Hypobiotic larvae resume development, ewe/doe has reduced immunity at this point
  2. ingestion of larvae overwintered on pasture –mature in large numbers
  3. increased egg output from an existing adult population
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29
Q

What is the final outcome of Periparturient Rise?

A
  • worm burdens maintained rather than expelled
  • worms free to produce many eggs
  • massive past L3 contamination develops
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30
Q

Name management principles

A

good nutrition
don’t overstock or overgraze
segregate classes of animals whenever possible
use mixed species/alternate grazing wherever possible – horses/cattle

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31
Q

Name the member of Family Strongyloidea learned

scientific and common name

A

Ancylostoma Caninum - 3 teeth
Hookworm of dogs

A. tubaeformae = cats - 3 teeth
A. braziliense = dogs and cats - 2 teeth

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32
Q

What kind of eggs do hookworms have?

A

non-embryonated/larvated eggs

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33
Q

What is the infective stage of hookworms?

A

Ancylostoma Caninum

L3 stage

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34
Q

Habitat for adult hookworm?

A

small intestine

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35
Q

Life cycle of Ancylostoma Caninum

A
  1. hookworm adult attached to small intestine of DH
  2. non-larvated eggs leave DH via feces
  3. eggs embryonate in environment - moist
  4. L1 develops in egg in 24 hrs and hatched
  5. L1 molts to L2 then matures to L3 but remains ensheathed (doesnt molt) NOW INFECTIVE
  6. infects DH
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36
Q

Name the 5 possible ways Ancylostoma Caninum can infect the DH

A

as ensheathed L3

  1. oral ingestion
  2. skin penetration
  3. prenatal/transplacental
  4. lactogenic infection
  5. ingestion of paratenic host
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37
Q

What is characteristic about oral ingestion of Ancyclostoma Caninum L3 larvae?

A

rarely occurs in nature
no larval migration, adult matures in small intestine
prepatent period = 15-18 days

38
Q

What is characteristic about skin penetration of Ancyclostoma Caninum infective L3 larvae in dogs <3m old?

A

extensive migration = blood vessels/lympathic vessels –> heart –> lungs –> alveoli –> migrate to bronchioles/bronchi –> swallowed –> mature in small intestine

39
Q

What is characteristic about skin penetration of Ancyclostoma Caninum infective L3 larvae in dogs >3m old?

A

extensive migration but follow more somatic route from blood vessels/lymphatic vessels

  • **become hypobiotic – encyst in muscle = pool of infection
    • mammary gland population at onset of lactation
    • repopulate adult worms in SI if eliminated
40
Q

What is characteristic about prenatal/transplacental infection of Ancyclostoma caninum infective L3 larvae?

A

rare
L3 enters blood stream, pass to placenta to fetus
source = hypobiotic larva in mom, infection occurs during pregnancy

41
Q

What is characteristic about lactogenic infection of Ancyclostoma caninum infective L3 larvae?

A

L3s recovered from milk up to 20d after whelping
source = hypobiotic larvae migrate to mammary glands
adult mature in SI, no migration occurs in puppies

42
Q

What is characteristic about paratenic host ingestion infection of Ancyclostoma caninum infective L3 larvae?

A

ingest rodent host w/ hypobiotic L3s

adults now mature in SI of DH no migration occurs

43
Q

What is the pathogenicity of Ancyclostoma caninum

A
  • anemia - site of attachment continues to bleed
  • severity depends on age of host, # worms, overall health
  • adults can have acquired immunity
  • puppies most susceptible b/c no aquired immunity and low iron reserves
44
Q

What are the clinical signs of an Ancyclostoma caninum infection?

A
  • bloody diarrhea, mucus, black/tarry
  • decreased appetite
  • weakness
  • poor growth/hair coat
  • pale mucus membranes
  • hemorrhagic pneumonitis -migrating larvae
  • most eczema - skin penetration
45
Q

Name the condition and specifics of the zoonotic hookworm discussed in class

A

Ancyclostoma braziliense causes Cutaneous Larval Migrans (CLM)

  • L3 skin penetration marked by elevated, red and winding pruritic lesions
  • rarely enter SI and mature to adults
  • also called sand worms, plumbers itch, creeping eruption
46
Q

What is the scientific name and family of the large equine pinworm discussed?

A

Oxyuris equi

Family: Oxyruoidea = pinworms

47
Q

What is the habitat of the large equine pin worm?

A

large intestine

48
Q

What is the morphology of the adult Oxyuris equi?

eggs?

A

adults = whitish, thick bodies, club shaped/double bulbed esophagus

eggs - asymmetrical, operculated, unembryonated

49
Q

Life cycle of Oxyuris equi

A
  1. oviparous female deposits egg in perianal region
  2. eggs embryonate
  3. eggs fall into bedding, food, water
  4. eggs ingested and hatch in SI
  5. larval development in crypts of SI
  6. larvae enter lumen, move to large intestine and develop into adults
50
Q

What is “Pruritis Ani” / “Seat Itch” ?

A

pathology of Oxyuris equi

  • rubbing leads to hairloss and secondary bacterial infection
  • skin thick, scaly, rat tailed appearance
51
Q

How is Oxyuris equi dx?

A

eggs at perineum or feces

“scotch tape” test

52
Q

Name the member of Ascaroidea discussed?

What is its DH

A

Phylum Nematoda
Toxacara canis

DH = dogs, in small intestine

53
Q

What morphological characteristic helps ID species of Ascarids?

A

alae modifications

54
Q

What is unique about the Toxicara Canis life cycle?

A

eggs with L2 is infective to new DH = larva is inside egg

55
Q

Describe the Toxicara Canis life cycle

A
  1. adults in SI of DH
  2. non-embryonated eggs leave via feces
  3. eggs embryonate L1-L2 in environment
  4. egg with L2 larvae is infective to DH
  5. enters DH via several routes
56
Q

Name the 4 possible routes Toxicara canis can enter the DH

A
  1. ingestion = direct transmission
  2. prenatal/transuterine trasmission
  3. colostral/lactogenic transmission
  4. ingestion of paratenic host
57
Q

Discuss direct transmission of Toxocara canis to dogs <3 months

A

ingest L2 larvea infective stage

Tracheal migration = penetrate intestine, mesenteric lymph nodes, liver, heart, pulmonary arteries, lungs MOLTS TO L3 - then alveoli, bronchioles, trachea, coughed and swallowed to stomach

molts to L4/L5 in small intestine and mature to adult

prepatent period = 3-4 wks

58
Q

Discuss direct transmission of Toxocara canis to dogs >3 months

A

ingest L2 larvea infective stage

somatic migration = hatch, penetrate intestine, enters system circulation
L2 larvae encysts becomes hypobiotic, maturation occurs

59
Q

Discuss prenatal/transuterine trasmission of Toxocara canis

A

Hypobitoic L2 larvae migrate to fetus
L3 mold in fetal liver
L3 in lungs at birth, migrate to stomach
L4/L5 in stomach - mature to adult

Eggs found in puppy feces by 23-40 days old

60
Q

Discuss colostral/lactogenic trasmission of Toxocara canis

A

Hypobiotic L2 larvae in mammary tissues passed via colostrum
L2 directly to stomach - SI
NO MIGRATION

61
Q

Discuss the paratinic host form of Toxocara canis transmission

A

Ingestion of encysted L2 in rodents
L2 directly to SI
No migration

62
Q

Discuss the pathogenicity of Toxocara canis

A 
More problematic in younger puppies 
Signs with heavy infections = 
Pneumonia due to migrations 
Vomiting, diarrhea 
Pot-belled appearance 
Focal lesions in CNS - migrations to wrong location = neuro disorders
63
Q

What zoonotic dz is associated with Toxocara canis – discuss pathogenicity

A

Visceral Larval Margins

  • chronic granulomatous lesions due to larval migrations
  • humans = paratenic host , more often children
64
Q

What is the species name of the example worm from the family Trichoroidea

A

Trichinella spiralis

Phylum Nematoda

65
Q

What are the hosts of the Trichina worm?

A

Trichinella spiralis
Adult parasite in = SI
Larval parasite = in striated muscles

Possible hosts = pigs, rats, bears, wild boar, humans, horse, other mammals

66
Q

What type reproductive method does Trichinella Spiralis female have?

A

Larviparous = eggs in uterus, gives birth to live larva

67
Q

Discuss the epidemiology of Trichinella spiralis

A

Sylvanic and urban cycles, human. Infection usually due to ingestion of undercooked meat

68
Q

What is unique regarding the life cycle of Trichella spiralis?

A

Nurse cells – parasite encysts as L1 and uses host tissue to protect themselves

Therefor the host acts as the DH and the IH = parasite is born in and encysted in the same host until eaten again

69
Q

Discuss the life cycle of Trichinella spiralis

A
  1. Female deposits larvae into intestinal wall
  2. Larvae enter lymphatics
  3. Migrations to thoracic duct, heart, lungs, heart
  4. Enter systemic circulation
  5. Larvae encyst (encapsulate) in striated muscle
  6. Larvae excuse in SI when ingested by different host
  7. Mature to adults in SI
70
Q

What are the pathological phases of Trichinella spiralis?

A

Clinical signs rarely seen in swine

2 phases in other hosts =

  1. Intestinal infection with adults - occurs in intestines 1-2 after ingested
  2. Skeletal muscle invasion by L1 - 2 week, larvae invade many cell types but only encapsulate in skeletal muscle
71
Q

How do you dx Trichinella spiralis?

A

Muscle biopsy
Serum samples -skin sensitive test, elisa
Slaughterhouse inspection

72
Q

How do you control Trichinella spiralis

A

Prevention cannibalism
Cook meath thoroughly
Freezing - some can resist freezing however

73
Q

Name the example of Filaroidea

What is the habitat of the adult worm?

A

Dirofilaria immitis

Right ventricle, pulmonary arteries of dogs, cats, ferrets, sea lions, seals and others

74
Q

Describe the prelarval stage of Dirofilaria immitis?

What is the vector/IH of Dirofilaria immitis?

A

Found in circulating blood

Tapered anterior end, may be straight or hooked

Mosquitoes - many species can transmit the parasite

75
Q

What is the significance of Acanthocheilonema reconditum?

A

On blood smear can be confused for microfilaria of Dirofilaria immitis.

Appearance is different in that it is more curved and has a blunt head in comparison with Dirofilaria immitis

76
Q

What are the characteristics of an occult Dirofilaria immitis infection?

A

Hidden infections characterized by
-single sex infection, adults are either strictly
female or strictly male
-low numbers

Mff not detectable in peripheral blood at this stage
Best dx with antigen tests to find mature adults

77
Q

What is the microfilarial periodicity of Dirofilaria immits?

A

Nocturnal periodicity - Mff present in blood during evening hours

And

Incomplete periodicity - Mff never disappear completely from peripheral blood during 24 hour period

78
Q

What is the prevalence and frequency of Dirofilaria immits?

A

Determined by signalment and habits - more common in males, outdoor dogs, between 3-15 yrs, larger breeds

79
Q

Describe the Diofilaria immitis lifecycle

A
  1. Mff released by female worm into circulation
  2. Mosquito takes up Mff from blood
  3. Mff molt to infective L3
  4. infective L3 enters DH after mosquito bite
  5. Larvae migrates to heart and lungs and undergo L3-L5 molts
  6. Adult worms mature in heart and produce Mff after mating
80
Q

What is the pre-patent period of Dirofilaria immitis?

A

5.5-7 m

81
Q

Discuss the IH of Dirofilaria immitis

A

Mosquito vectors = 23 species can transmit dz
Distribution of species vary, feeding habits vary, and breeding sites vary

Carry infective L3 to DH

82
Q

When does a dog become antigen-positive?

A

Without prophylaxis earliest 5 months but most at 7 months after infection

With macrocyclic lactose doses missed -earliest 9 months after infection

83
Q

What is possible to occur of a macrocyclic lectins prevention dose is missed?

A

Delayed HW maturation and patient conversion to antigen positive status

84
Q

When does a dog become Mff positive

A

No prophylaxis = earliest 6.5 months after infection

Pets receiving macrocyclic lactose may never develop nuff or they may appear only transiently in small numbers but adults will still be present if doses are missed

85
Q

What is the gold standard for HW antigen test

A

DiroChek HW Ag test

86
Q

What are 6 reasons why a pet may be Antigen positive but Microflilaria test negative?

A
  1. Maturing infection, Mff not in circulation
  2. Use of prevention w/o removing adult worms
  3. Use of microfilaricide w/o remove of adult worms
  4. Unisex female infections, no male present
  5. Dog is true immune-mediated occult - rare but some dogs can destroy Mff
  6. . failure to use Mff concentration test
87
Q

What are 4 reasons why a pet would be Ag test negative but Mff test positive

A
  1. Jeff are those of another species- usually in lower numbers
  2. Mff acquired transplacentally - few numbers and seen in young dogs
  3. Adult worms were removed for have died but Mff persist
  4. Contamination of test materials
88
Q

For what reason would hw Ag test be variable and Mff negative or positive

A

Fluctuation Ag levels due to # of female worms, ages of worms, quality of samples

-older worms not as fecund

89
Q

Discuss the Pathogenicity/Clinical signs of Dirofilaria immtis

A

Dz in adult - right ventricular and pulmonary artery obstruction

Vilous endarteritis = inflamed vessels 
Vascular resistance = increased cardiac workload due to inflammation 
Decreased cardiac output 
Exercise intolerance 
Coughing 
Hemoptysis =blood in sputum 
Vena cava syndrome

Some dogs can be asymptomatic

90
Q

7 ways feline hw infection differs from canine infection

1 similarity

A
  1. Cats less susceptible
  2. Few worms can cause dz 1-2 in cats whereas caine dz depends on dog size and number of worms
  3. Worms short lived in cats, long lived in dogs
  4. Worms in cats dont usually produce Mff
  5. Lungs most often affected in cats, vs heart and lungs in dogs
  6. Diagnosis usually requires more steps that dogs
  7. No treatment, can only treat symptoms

1 there are preventative available

91
Q

What is the tx for Hw dz that has the greatest efficacy, what is its limitation

A

Melarsomine dihydrichloride

Kills adult worms, no activity against worms <4 months

92
Q

What is “Slow Kill”

A

Continuous monthly use of preventative in conjunction with antibiotics
Current macrocyclic lactones are not approved for this use
Requires client compliance
Takes a long time to work

SHOULD ONLY BE USED WHEN IMMITICIDE CANNOT BE

Parasitology (4 decks)

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