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Nematodes > Ancylostoma > Flashcards

Ancylostoma Flashcards

1
Q

Ancylostoma bursate or non bursate?

A

bursate

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2
Q

Strongyles bursate or non bursate?

A

bursate

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3
Q

Ancylostoma with 3pr Cutting teeth

A

Ancylostoma caninum

Ancylostoma tubaeforme

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4
Q

Ancylostoma with 1 pr cutting teeth

A

Ancylostoma braziliense

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5
Q

Ancylostoma with cutting plates?

A

Uncinaria stenocephala

Bunostomum spp.

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6
Q

Hookworms

A

Ancylostoma

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7
Q

Site of infection for hookworms?

A

mucosal tissue in small intestine

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8
Q

Clinical signs of hookworms

A
  • Hemorrhagic enteritis: dark, tarry or bloody feces
  • Anemia
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9
Q

most pathogenic hookworm

A

A. caninum

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10
Q

Ancylostoma caninum host

A

dogs, wild canids

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11
Q

Life Cycle of Ancylostoma caninum

A

Direct

  1. Skin penetration of free L3
    * Environment
  2. Ingestion of free L3
    * Environment
  3. Transmammary of L3
    * Ingestion

Indirect- ingestion of paratenic host infected with L3 (rodent)

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12
Q

A. caninum transmammary or transplacental transmission?

A

transmammary

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13
Q

A. caninum PPP

A

2 weeks after ingestion

4 weeks after penetration

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14
Q

most voracious eater of the hookworms

A

A. caninum

50-100 worms can be fatal in pups

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15
Q

Dermatitis- what does the dog have?

A

Dermatitis:

•Chronic dermatitis of lower limbs and feet

  • Older dogs exposed to larvae in environment
  • Swollen, painful footpads; hyperkeratosis

A. caninum

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16
Q

A. caninum- clinical forms

A
  1. Peracute- neonatal pups- need blood transfusion
  2. Acute- Sudden exposure of older susceptible pups (& occasionally mature dogs) to large numbers of 3rd-stage juveniles, anemia
  3. Chronic(compensated)- subclincal carriers- eggs in feces
  4. chronic(decompensated)- old, malnourished dog with profound anemia, secondary cause of death
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17
Q

Cat hookworm

A

Ancylostoma tubaeforme

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18
Q

Direct infection of Ancylostoma tubaeforme

A
  • Ingestion of free L3s from environment
  • Cutaneous penetration of free L3s from environment
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19
Q

Ancylostoma tubaeforme- transmammary or transplacental transmission?

A

•No transmammary transmission

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20
Q

Indirect Infection of Ancylostoma tubaeforme

A

•Ingestion of infected paratenic hosts (rodents)

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21
Q

Ancylostoma braziliense host:

A

dogs and cats

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22
Q

Ancylostoma braziliense distribution

A

•Tropical Atlantic and Gulf Coast areas; Caribbean

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23
Q

Infective routes of Ancylostoma braziliense

A
  • Skin penetration of free L3s
  • Ingestion of free L3s from environment
  • Zoonotic (human cutaneous larva migrans)
24
Q

Uncinaria stenocephala infective route

A

•Ingestion of free L3 from environment only

25
Q

Uncinaria stenocephala host

A

dogs and cats

26
Q

Uncinaria stenocephala distribution

A

“northern hookworm”

cold adapted species

27
Q

Bunostomum host

A

•Ruminants, camelids

28
Q

Bunostomum distribution

A
  • Less common in North America
  • Occasionally found in southeastern US, Gulf Coast states
29
Q

Bunostomum infective route

A
  • ingestion of free L3 from the environment
  • skin penetration of L3 in ruminants exposed to larvae
    • causes pruritis and foot stomping
30
Q

Diagnosis of hookworms

A

clinical signs of anemia

in newborns deworm as early as possible

deworm pregnant dogs due to larval leak

31
Q

CLM

A

cutaneous larva migrans

A. braziliense

•Hypersensitivity reaction when larvae invade skin of humans

Area of body in contact with ground (feet, buttocks, hands)

32
Q

identify

A

strongyle egg

33
Q

Small stronglyes

A

Cyanthostomins

34
Q

Large strongyles

A

strongylus spp.

35
Q

Nodular worm

A

Oesophagostomum spp.

36
Q

Small strongyles- cyanthostomum spp. host

A

horses

37
Q

Site of infection of small strongyles

A

adults in colon and cecum

juveniles in mucosa of colon and cecum

38
Q

All horses are infected with

A

small strongyles cyathostomum

39
Q

Small Strongyles Pathogenesis

A

•Larval emergence responsible for disease

  • Damages mucosa
  • Usually sub-clinical alteration of GI function, mild inflammatory enteropathy
  • Mild in well-nourished, unstressed individuals
  • Slight production loss (feed efficiency and preformance decrease)
40
Q

synchronous emergence of a huge number of larvae

A

Larval cyathostomiasis

41
Q

Small strongyle Diagnosis of adults in colon/cecum

A

•Fecal flotation

  • Strongyle eggs
  • High fecal egg counts
42
Q

Large strongyles

A
  • Adults in colon and cecum (lumen)
  • Juveniles migrate extensively outside of intestinal tract
43
Q

Most pathogenic of the strongyles

A

large strongyles- strongylus vulgaris

44
Q

Maintainence of small strongyles

A

In a given herd, ~20% of animals are responsible for 80% environmental contamination (high egg shedders)

  • Fecal egg counting monitoring/selective deworming to reduce pasture contamination
  • Anthelmintic resistance
45
Q

Identify

A

strongyle egg

46
Q

Oesophagostomum spp.

A

nodular worm

47
Q

Oesophagostomum spp. host

A

ruminants and swine

48
Q

Oesophagostomum spp. pathogenesis

A

In ruminants

  • Diarrhea, weakness, emaciation
  • Calcification

In swine:

  • Enteritis
  • Diarrhea with mucous
49
Q

Oesophagostomum spp. site of infection

A

•Adults in cecum and colon (lumen)

50
Q

Oesophagostomum spp. PPP

A

6 weeks

51
Q

Strongylus vulgaris pathogenesis

A

•Thickening of cranial mesenteric artery

  • Migrating larvae
  • Compromise blood flow to intestine à colic
  • Fever, anorexia, weight loss, depression
52
Q
  • Larvae migrate extensively within horse
  • S. vulgaris
  • S. edentatus
  • S. equinus
A
  • S. vulgaris: cranial mesenteric artery
  • S. edentatus: liver, abdominal cavity
  • S. equinus: liver, abdominal cavity
53
Q

Large strongyle species in horses

A
  • S. vulgaris- most important need to know
  • S. edentatus
  • S. equinus
54
Q

Resistance to dewormers?

A

some small strongyle populations

55
Q

S. vulgaris PPP

A

7 months

56
Q

oesophagostomum spp. why nodular worm?

A

Areas infected become nodules and aspect

Nematodes (5 decks)

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