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Parasitology > Unit 3 - Nematodes > Flashcards

Unit 3 - Nematodes Flashcards

1
Q

Physaloptera spp. affects what species?

A

felids, canids

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2
Q

stomach worm

A

Physaloptera

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3
Q

What is the US distribution of physaloptera?

A

most common in midwest

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4
Q

DH of Physaloptera:

A

canids and felids (also variety of wild carnivorous mammals, including coyotes and foxes)

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5
Q

PPP of Physaloptera:

A

~44-83 days; different species

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6
Q

What stage of Physaloptera is in feces?

A

larvated eggs

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7
Q

What is the infective stage of Physaloptera?

A

L3

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8
Q

Where does L3 of Physaloptera attach?

A

to the stomach

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9
Q

Where are the adult Physaloptera located in the host?

A

stomach

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10
Q

What is the IH for Physaloptera?

A

beetles, cockroaches, crickets

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11
Q

What is the PH for Physaloptera spp?

A

amphibians, reptiles, mammals (have to ingest IH first)

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12
Q

How do DH become infected with Physaloptera?

A

ingestion of PH/IH with L3

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13
Q

List the pathogenesis seen with Physaloptera adults?

A
  • attach to mucosa
  • feed on blood and mucosa
  • ulceration
  • hemorrhage
  • catarrhal gastritis
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14
Q

Physaloptera spp. clinical signs:

A

usually asymptomatic

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15
Q

What is the primary way to differentiate between ascarids and Physaloptera?

A

ascarids are found free in the stomach while physaloptera are attached to the mucosa

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16
Q

While Phylasoptera eggs are not usually found on fecal flotation, instead you should use:

A

fecal sedimentation (easy to miss)

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17
Q

Effective treatment for Physaloptera is difficult and often involves these three things:

A
  • limit exposure
  • removal of nematodes via endoscopy
  • repeated tx of antihelmintics
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18
Q

Dracunculus insignis affects what species:

A

raccoons, mink, canids (felids are rare)

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19
Q

Dracunculus insignis can be found across North America, but infections are:

A

rare

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20
Q

PPP for D. insignis:

A

~200 days

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21
Q

DH for D. insignis:

A

racoons, minks, canids (felids - rare)

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22
Q

Which stage of D. insignis is released into the water?

A

L1

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23
Q

How do DH become infected with D. insignis?

A

ingestion of PH/IH with infective L3 in water

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24
Q

L3 for D. insignis goes to the:

A

thoracic and abdominal muscles

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25
Q

Once D. insignis matures to its adult stage, the females move to the:

A

SubQ extremities

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26
Q

IH for D. insignis:

A

copepods (water fleas)

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27
Q

PH for D. insignis:

A

frogs

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28
Q

D. insignis pathology and clinical signs:

A
  • pyogranulomatous inflammation

- chronic nodules or abscesses (~ 2 in. on limb and abd)

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29
Q

D. insignis diagnosis:

A

removal of adult from nodules

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30
Q

Which nematode species affect equids?

A

Draschia & Habronema spp

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31
Q

IH for Draschia and Habronema spp.:

A 
Musca domestica (house flies)
Stomoxys calcitrans (stable flies)
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32
Q

Which is the most important IH for Draschia and Habronema (in US)?

A

house fly

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33
Q

Which stage of the Draschia and Habronema spp. are in equid feces?

A

L1

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34
Q

Which stage of D & H is transferred to the DH?

A

L3 (infective stage)

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35
Q

All stages of D & H spp. are in the stomach except the eggs which:

A

hatch in the GI tract

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36
Q

How do flies get infected with D & H species?

A

ingest L1 from DH feces

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37
Q

How do flies transfer D & H L3 to DH?

A

Fly feeds on horse; horses ingests fly or licks and ingests L3

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38
Q

Draschia and Habronema spp. pathogenesis:

A
  • tumor like lesions near margo plicatus

- fibrous nodules filled with pus-like material in which the worms live

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39
Q

Draschia adults are found:

A

in tumors close to margo plicatus

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40
Q

Habronema adults are found in:

A

glandular portion of stomach

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41
Q

Draschia and Habronema clinical signs associated with adults:

A
  • usually asymptomatic
  • gastritis
  • perforation
  • peritonitis
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42
Q

Draschia and habronema clinical signs associated with larvae:

A
  • granulomatous lesions
  • cutaneous (summer sores)
  • both D & H species
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43
Q

D&H diagnosis:

A
  • eggs: PCR
  • Larvae: lesions
  • Adults: necropsy
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44
Q

esophageal worm

A

Spirocerca lupi

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45
Q

What species does Spirocerca lupi affect?

A

domestic and wild canids, wild felids (rare in domestic cats)

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46
Q

PPP for Spirocerca lupi:

A

4-6 months

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47
Q

What stage of Spirocerca lupi can be found in DH (cats, dogs) feces?

A

larvated eggs

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48
Q

How do DH become infected with Spirocerca lupi?

A

ingests PH/IH with infective L3

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49
Q

What does L3 of Spirocerca lupi do once it is ingested by the DH?

A
  • penetrates gastric wall

- L3 walls of gastroepiploic & gastric artery –> celiac artery –> thoracic aorta –> L4 –> adults

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50
Q

Where do the adult Spirocerca lupi migrate to?

A
  • connective tissue

- found in nodules in esophageal wall, stomach

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51
Q

What is the IH for Spirocerca lupi?

A
  • coprophagous beetles (dung beetles)
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52
Q

What is the PH for Spirocerca lupi?

A

mammals, birds, lizards, toads

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53
Q

Spirocerca lupi pathogenesis:

A
  • aortic aneurysms, thrombosis

- granulmoas/sarcomas in esophagus

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54
Q

Spirocerca lupi clinical signs (5):

A
  • esophageal dysphagia
  • vomiting
  • esophogeal neoplasia
  • aortic aneurysm or rupture
  • thickening of long bones (hyptertrophic osteopathy)
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55
Q

Idenitification of spirocerca eggs can be done via:

A
  • fecal flotation

- vomitus

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56
Q

Identification of Spirocerca lupi adults can be done via:

A
  • vomitus

- necropsy

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57
Q

Oxyuris equi affects what species:

A

equids

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58
Q

pinworms

A

Oxyuris equi

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59
Q

PPP for Oxyuris equi:

A

4-5 mos

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60
Q

Infective stage of Oxyuris equi:

A

L3 in egg

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61
Q

Only the female moves to the anus of the equids. Why?

A

lay eggs in gelatinous substance (“cement”) under tail

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62
Q

Which adult stage of Oxyuris equi is of primary importance in pathology?

A

egg-laying females (inflammation of colon and rectum)

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63
Q

Oxyuris equi diagnosis:

A
  • presumptive: clinical signs

- definitive: “scotch tape method”

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64
Q

Filarids in the order Spirurida have what type of life cycle?

A

indirect

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65
Q

What is the intermediate host for filarids?

A

blood sucking arthropods

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66
Q

Ochocerca cervicalis infects what species?

A

equids

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67
Q

What is the IH for Onchocerca cervicalis?

A

generally culicoides spp (ie biting midges)

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68
Q

PPP for Onchocerca cervicalis:

A

~16 months

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69
Q

How do L3 infect the DH?

A

next blood meal of IH

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70
Q

L3 for Ochocerca travels to the:

A

nuchal ligament (also L4 and adults)

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71
Q

What causes Onchocercal dermatitis?

A

antigen released from dying microfilaria (causes pathogenesis)

72
Q

To diagnose Onchocerca cervicalis, you must:

A

perform a full-thickness skin biopsy (> 6 mm)

73
Q

What is a differential for Onchocerca cervicalis?

A

hypersensitivity reaction to biting flies

74
Q

What is used to treat Onchocerca cervicalis?

A
  • NO TX for adults

- ivermectin efficacious against microfilariae

75
Q

Onchocerca lupi affects:

A

canids

76
Q

DH for Onchocerca lupi:

A

dogs, cats

77
Q

Canine onchocercosis is associated with pathogenesis in/around the:

A

eye

78
Q

DH for Acanthocheilonema reconditum?

A

Dogs

79
Q

Life cycle for A. reconditum:

A

indirect

80
Q

PPP for Acanthocheilonema reconditum?

A

2-3 mos

81
Q

IH for A. reconditum:

A

fleas (C. felis, C. canis, P. irritans)

82
Q

A. reconditum clinical signs?

A

generally nonpathogenic

83
Q

Since A. reconditum is nonpathogenic, why is it important?

A

differentiating its microfilaria from D. immitis (heartworms)

84
Q

DH for dirofilaria immitis:

A

domestic dog, domestic cat (much lower prevalence)

85
Q

IH for Dirofilaria immitis:

A

mosquitoes

86
Q

No larval development of D. immitis occurs in the temperature is below:

A

14 C

87
Q

Late stage pathogenesis for HWs:

A
  • heart may enlarge and become weakened

- CHF

88
Q

Where do nearly all heartworms reside?

A

in lower caudal pulmonary arteries

89
Q

What medicines are effective against L3 and L4 and the elimination of microfilariae on Dirofilaria immitis?

A

macrocyclic lactones (ivermectin, milbemycin, etc.)

90
Q

Caval syndrome is an acute disease/clinical emergency characterized by:

A
  • large number of worms

- increased venous pressure in liver

91
Q

Caval syndrome clinical signs:

A
  • acute weakness/anorexia
  • dyspnea
  • collapse
  • pale mucous membranes
  • bilirubinemia
  • bilirubinuria
  • hemoglobinuria
92
Q

PPP of heartworms in cats?

A

7-8 months

93
Q

Where are heartworms located in cats?

A

pulmonary artieries and right heart

94
Q

When adult heartworms die in cats,it can lead to:

A
  • inflammation
  • thromboemboli
  • infarction
  • respiratory failure possible
95
Q

With heartworms, cats are:

A

rarely microfilaremic

- also rare to find any circulating

96
Q

Intracellular gram-negative bacteria:

A

Wolbachia pipientis

97
Q

Why do we need to know about Wolbachia pipientis?

A

Necessary for Dirofilaria immitis to reproduce/thrive

98
Q

Primary tx for heartworms:

A

doxy

99
Q

What is a periparturient rise?

A
  • relaxation of immunity due too increases in prolactin

- rise in nematode egg counts in the feces of lactating ewes or does at weaning

100
Q

What are three important characteristics of Trichostrongyles?

A
  • common
  • high significance
  • primarily ruminants
101
Q

Parasitic Gastroenteritis (PGE) of ruminants has dramatic production (and thus economic) losses when disease is:

A

subclinical

102
Q

What are some common symptoms of subclinical PGE?

A
  • watery, green diarrhea

- submandibular edema

103
Q

What are some causes for arrested larval development (ALD)?

A
  • seasons
  • climate
  • immune response
  • overcrowding
104
Q

A susceptible parasite gene pool not exposed to a particular control measure (escapes selection for resistance)

A

Refuge

105
Q

What are some integrated pest management protocols for controlling ruminant strongyles?

A
  • pasture rest/rotation

- multi-species grazing

106
Q

Ostertagia ostertagi host:

A

cattle

107
Q

Ostertagia ostertagi adult site:

A

abomasum

108
Q

O. ostertagi PPP:

A

18-21 days

109
Q

Where does the L3 (infective stage) of Ostertagia ostertagi go?

A

burrows into gastric glands in pyloric and fundic regions of abomasum

110
Q

Of major importance in cattle:

A

O. ostertagi

111
Q

When and where can O. ostertagi arrest?

A

L4; abomasal glands

112
Q

Ostertagiosis pathogenesis is associated with _______ _______and __________ NOT feeding behavior.

A

larval growth and development

113
Q

What is the name of the lesion seen in the abomasum in association with Ostertagiosis?

A

cobblestone lesions

114
Q

What are the clinical signs of Ostertagiosis (4)?

A
  • diarrhea
  • weight loss (emaciation)
  • dehydration (thirst)
  • submandibular edema (hypoproteinemia)
115
Q

Teladorsagia circumcincta host?

A

sheep/goats

116
Q

Teladorsagia circumcincta adult site?

A

abomasum

117
Q

Which ruminant strongyle is a contributor to PGE via diarrhea and weight loss?

A

Teladorsagia circumcinta (goats, sheep only)

118
Q

Haemonchus placei host:

A

cattle

119
Q

Haemonchus placei adult site:

A

abomasum

120
Q

Haemonchus placei PPP:

A

23-32 days

121
Q

Haemonchus contortus host:

A

sheep, goats

122
Q

Haemonchus contortus adult site:

A

abomasum

123
Q

Haemonchus contortus PPP:

A

18-21 days

124
Q

Haemonchus spp. can:

A

arrest

125
Q

L3, L4, and adults of Haemonchus spp. feed on:

A

blood

126
Q

Where do the L3 of Haemonchus go?

A

exsheath in rumen and move to abomasum near glands

127
Q

Because Haemonchus species are blood feeders, what are some common clinical signs for hyperacute, acute, and chronic Haemonchosis?

A

anemia, skin pallor, pale mucus membranes

128
Q

What are some GENERAL clinical signs for Haemonchosis?

A
  • bottle jaw
  • dark feces
  • death (before patency possible)
129
Q

Trichostrongylus axei host location:

A
  • abomasum in ruminants

- stomach in horses

130
Q

Trichostrongylus axei host:

A

horses, cattle

131
Q

Trichostrongylus axei PPP:

A

14-21 days

132
Q

T. colubriformis host:

A

ruminants

133
Q

T. colubriformis location in host:

A

small intestine

134
Q

T. colubriformis PPP:

A

18-20 days

135
Q

Often asymptomatic contributor to PGE; ALD:

A

Trichostrongylus spp.

136
Q

Trichostrongylus species can have massive infections known as:

A

“black scours”

137
Q

Cooperia spp. that affect cattle:

A
  • onchophora
  • punctata
  • pectinata
  • sumabada
138
Q

Cooperia spp. that affect sheep:

A
  • sumabada

- curticei

139
Q

Cooperia spp. that affect goats:

A

curticei

140
Q

All Cooperia spp. adults go to the:

A

small intestine

141
Q

Cooperia spp. PPP:

A

13-19 days

142
Q

Oesophagostomum radiatum host:

A

cattle**

143
Q

Oesophagostomum columbianum host:

A

sheep and goats

144
Q

Oesophagostomum spp. adult site:

A

large intestine

145
Q

Oesophagostomum spp. PPP:

A

28-41 days

146
Q

Oesophagostomum pathology/signs:

A
  • hemorrhagic/purulent nodules
  • mucus
  • leakage of blood and plasma proteins
147
Q

Diagnosis of ruminant strongyles can really only be done through:

A
  • culture and identification of L3

- identification of adults at necropsy

148
Q

Nematodirus spp. adult site:

A

small intestine

149
Q

Nematodirus spp in cattle:

A

helvetianus

150
Q

Nematodirus spp in sheep:

A
  • battus
  • filicolis
  • spathiger
151
Q

What’s important about the pasture larvae of Nematodirus spp?

A

resistant to drying and freezing

152
Q

Equine strongyles are broken into two groups:

A
  1. Strongylinae (large)

2. Cyathostominae (small)

153
Q

Has ear shaped teeth and can be up to 2.4 cm long:

A

Strongylus vulgaris

154
Q

Has one large tooth and two smaller teeth

A

Strongylus equinus

155
Q

Has no teeth but can be as long as 4.5 cm

A

Strongylus edentatus

156
Q

Host for Strongylus vulgaris:

A

horses, donkeys, mules, zebra

157
Q

Where does the L4 of Strongylus vulgaris migrate to in the body?

A

cranial mesenteric artery

158
Q

What is the infective stage of Strongylus vulgaris?

A

L3

159
Q

PPP for Strongylus vulgaris:

A

6-7 months

160
Q

Strongylus vulgaris migrating larvae can cause what pathology?

A
  • arteritis**
  • thrombi
  • emboli
  • intestinal nodules (adults emerge from these)
161
Q

Primary clinical sign associated with S. vulgaris regardless of age:

A

anemia

162
Q

S. vulgaris acute syndrome:

A
  • infarction and necrosis of intestine
  • damage to smooth endothelial surfaces
  • inflamed/thickened arterial walls
  • thromboemboli (cranial mesenteric)
163
Q

Strongylus equinus host:

A

horses, donkeys, mules, zebras

164
Q

Where do the L4 of strongylus equinus go?

A

liver, pancreas (3-4 months)

165
Q

Strongylus equinus PPP:

A

~9 months

166
Q

S. equinus pathology:

A
  • mainly due to larvae*
  • hemorrhagic nodules in intestines
  • nodules, fibrotic tracts in liver
  • nodules in pancreas
167
Q

Strongylus edentatus host:

A

horses, donkeys, mules, zebras

168
Q

Where does the L4 of S. edentatus travel to?

A

liver, hepatic ligament, parietal peritoneum; right flank

169
Q

PPP for S. edentatus:

A

~6-11 months

170
Q

Describe the pathology caused by Strongylus edentatus:

A
  • Mainly due to larvae**
  • perivascular thickening
  • subperitoneal cysts
  • nodules and fibrous tissues
171
Q

Specific signs for S. vulgaris:

A
  • high fever
  • inappetence
  • colic (intussesception, cranial mesenteric artery)
172
Q

Diagnosis of large strongyle infections:

A

fecal float and detection of strongyle-type eggs

173
Q

Which stage of small strongyles (cyathostomes) can arrest? Where?

A

L3; Crypts of Leiberkuhn

174
Q

Small strongyle pathology:

A
  • larval cyathostomes in colon wall

- hemorrhagic nodule formation

175
Q

What is the most pathological event of small strongyles?

A

L4s emerging from tissues

176
Q

What are small strongyles in comparison with large strongyles?

A

less severe

Parasitology (13 decks)

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