Ancylostoma Flashcards

(56 cards)

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
Uncinaria stenocephala host
dogs and cats
26
Uncinaria stenocephala distribution
"northern hookworm" cold adapted species
27
Bunostomum host
•Ruminants, camelids
28
Bunostomum distribution
* Less common in North America * Occasionally found in southeastern US, Gulf Coast states
29
Bunostomum infective route
* ingestion of free L3 from the environment * skin penetration of L3 in ruminants exposed to larvae * causes pruritis and foot stomping
30
Diagnosis of hookworms
clinical signs of anemia in newborns deworm as early as possible deworm pregnant dogs due to larval leak
31
CLM
cutaneous larva migrans A. braziliense •Hypersensitivity reaction when larvae invade skin of humans Area of body in contact with ground (feet, buttocks, hands)
32
identify
strongyle egg
33
Small stronglyes
Cyanthostomins
34
Large strongyles
strongylus spp.
35
Nodular worm
Oesophagostomum spp.
36
Small strongyles- cyanthostomum spp. host
horses
37
Site of infection of small strongyles
adults in colon and cecum juveniles in mucosa of colon and cecum
38
All horses are infected with
small strongyles cyathostomum
39
Small Strongyles Pathogenesis
•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
synchronous emergence of a huge number of larvae
Larval cyathostomiasis
41
Small strongyle Diagnosis of adults in colon/cecum
•Fecal flotation * Strongyle eggs * High fecal egg counts
42
Large strongyles
* Adults in colon and cecum (lumen) * Juveniles migrate extensively outside of intestinal tract
43
Most pathogenic of the strongyles
large strongyles- strongylus vulgaris
44
Maintainence of small strongyles
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
Identify
strongyle egg
46
Oesophagostomum spp.
nodular worm
47
Oesophagostomum spp. host
ruminants and swine
48
Oesophagostomum spp. pathogenesis
In ruminants * Diarrhea, weakness, emaciation * Calcification In swine: * Enteritis * Diarrhea with mucous
49
Oesophagostomum spp. site of infection
•Adults in cecum and colon (lumen)
50
Oesophagostomum spp. PPP
6 weeks
51
Strongylus vulgaris pathogenesis
•Thickening of cranial mesenteric artery * Migrating larvae * Compromise blood flow to intestine à colic * Fever, anorexia, weight loss, depression
52
* Larvae migrate extensively within horse * S. vulgaris * S. edentatus * S. equinus
* S. vulgaris: cranial mesenteric artery * S. edentatus: liver, abdominal cavity * S. equinus: liver, abdominal cavity
53
Large strongyle species in horses
* S. vulgaris- most important need to know * S. edentatus * S. equinus
54
Resistance to dewormers?
some small strongyle populations
55
S. vulgaris PPP
7 months
56
oesophagostomum spp. why nodular worm?
Areas infected become nodules and aspect