Lecture Quiz 3 - Exam 1 - Nematodes - Trichostrongyloidea

Front 1

Describe males of Trichostrongylus axei

Back 1

Bursate with short, stout spicules

Buccal cavity small or absent

Front 2

What is the life cycle of Trichostrongyloids?

Back 2

Adults in stomach or small intestine (Dictyocaulus = respiratory tract)

Direct life cycle:
1. Develop from egg --> L1 --> L2 --> L3 in environment
2. Infection by ingestion of L3
3. Can undergo hypobiosis

Front 3

What is the prepatent period for Trichostrongyles?

Back 3

2-3 weeks

Front 4

What are the superfamilies (Genus') of Trichostrongyloidea?

Back 4

1. Trichostrongylus
2. Cooperia
3. Ostertagia
4. Haemonchus
5. Nematodirus
6. Dictyocaulus
7. Marshallagia

5-7 don't produce typical strongylid or strongyle-type eggs

Front 5

What is special about Haemonchus contortus eggs?

Back 5

Haemonchus eggs bind fluoroscein-labelled peanut agglutinin. (Glow in the dark) Eggs of other strongylids in ruminants do not.

Front 6

What is the most pathogenic species for cattle?

Back 6

Ostertagia ostertagi

Front 7

What is the most pathogenic species for sheep/goats?

Back 7

Haemonchus contortus

Front 8

What are environmental influences from eggs --> L3?

Back 8

1. Temperature
2. Moisture
3. Rate of development
4. Ability to survive environmental extremes varies with species
5. Dispersal and availability of L3
6. "Conditioning" of L3 for hypobiosis

Front 9

When does hypobiosis occur?

Back 9

Ingested L3 enter gut mucosa and suspend further development at L3/L4 stage: development resumes when environmental conditions are favorable for survival of free-living stages

Become hypobiotic during winter in Northern states and during midsummer in Southern states.

Front 10

What happens during the spring regarding strongylid eggs?

Back 10

There is an increase in numbers in host feces due to the emergence and maturation of hypobiotic larvae in the spring

Front 11

What is periparturient rise?

Back 11

Increased shedding of strongylid eggs in host feces around time of parturition:
1. Due to decreased immunity in pregnant females
2. Occurs ~2 weeks before to 8 weeks after parturition
3. Can occur at any time of the year
4. Often superimposed on spring rise

Front 12

What is premunition?

Back 12

A state of resistance to infection which is established after an acute infection has become chronic and lasts as long as the infecting organisms remain in the body

Front 13

What is the fate of strongylid L3 ingested by hosts with premunition?

Back 13

1. Expelled from host
2. Become hypobiotic
3. Replace existing adult population

Front 14

What is the "Self-cure" response?

Back 14

Develops in lambs after repeated exposure to infective larvae as immune system matures.
1. Response localized to gut
2. Results in expulsion of all adult worms in affected gut

Front 15

What are the abomasal (stomach) worms? [HOTT]

Back 15

1. Haemochus
2. Osteragia
3. Telodorsagia
4. Trichostrongylus axei

Front 16

What are the Haemonchus spp?

Back 16

1. Haemonchus contortus: most important parasite of sheep and goats; can also infect cattle and camelids

2. Haemonchus placei: primarily in cattle worldwide, but can infect sheep (not significant problem)

Front 17

What is the Haemonchus structure?

Back 17

1. Large of stomach worms (1/2 to 1 inch)

2. Fresh worms (females): white ovaries and red intestinal tract twist around one another (barber pole) and may have a large flap of cuticle over vulva

3. Males: red when fresh and large bursa

Front 18

What is on anterior end of Haemonchus contortus?

Back 18

1. Both sexes are blood suckers

2. Small buccal capsule with "lancet" used to lacerate mucosa and obtain blood

Front 19

What is the Haemonchus life cycle?

Back 19

Direct: infection by ingestion of L3

L3 ex-sheathed in abomasum and enter mucosa. Penetrate between gastric epithelial cells where they emerge as L4 and mature to adults

Front 20

What are the prepatent periods of H. contortus and H. placei?

Back 20

1. H. contortus: 15 days
2. H. placei: 25-28 days

Front 21

What are some factors in pathogenicity for Haemonchus?

Back 21

1. Short pre-patent period

2. Females are prolific egg layers: produce 5,000 - 6,000 eggs/day, typical strongyle (trichostrongyle) eggs, increases pasture contamination and likelihood of infection

3. Voracious blood feeders

Front 22

What are the clinical signs of H. contortus?

Back 22

Anemia

Can see blood in feces at 6-12 days PI

Diarrhea is NOT a feature unless animal is also infected with other strongylids

Front 23

What is peracute/hyperacute hemonchosis?

Back 23

1. Occurs with massive infection of highly susceptible animal - uncommon

2. Sudden death - often with no other signs
Bleed to death in <7 days
No eggs in feces
Pale animal with melena in feces

Front 24

How do you diagnose peracute/hyperacute hemonchosis?

Back 24

Signalment, clinical signs suggestive

Necropsy findings:
Severe hemorrhagic gastritis
Very pale organs
Dark, bloody GI contents
1,000s of worms (L4)

Front 25

Describe acute hemonchosis.

Back 25

1. Pale mucous membranes
2. Dependent edema
3. Weakness, lethargy, shortness of breath
4. Melena
5. Agalactia in ewes --> lambs starve

Front 26

What is the pathogenesis of acute hemonchosis?

Back 26

1. Anemia from blood loss due to: parasites sucking blood and blood lost via feces and iron stores depleted by compensatory erythropoiesis +/- inadequate diet

2. Hypoproteinemia: loss of blood protein

3. Dependent edema: hypoproteinemia results in decreased oncotic pressure (submandibular, facial and ventral abdominal edema)

Front 27

What is the diagnosis of acute hemonchosis?

Back 27

Clinical signs suggestive

Fecal exam-many trichostrongylid eggs

Definitive ante-mortem diagnosis: fecal culture and Baermann to ID; specific binding of lectin to eggs of H. contortus

Front 28

What necropsy findings are there for acute hemonchosis?

Back 28

Pale watery carcass
Thin watery blood
Abomasal mucosa: edematous with many petechial hemorrhages, many Haemonchus present, and erythropoietic response in bone marrow

Front 29

Describe chronic hemonchosis.

Back 29

1. Most common
2. Chronic infection with lower number of parasites
3. Chronic insidious blood loss
4. Erythropoiesis

Front 30

What are clinical signs of chronic hemonchosis?

Back 30

1. Anorexia, progressive weight loss and emaciation
2. Weakness and lethargy
3. Adult sheep: wool-breaks, "wool-peeling"
4. NO OBVIOUS ANEMIA OR EDEMA.

Front 31

What are lab findings and necropsy findings of chronic hemonchosis?

Back 31

1. Lab findings: PCV, RBC count, hemoglobin levels at low end of normal range

2. Necropsy: emaciated carcass, poor fleece quality, low number of worms, increased red marrow in long bones

Front 32

What is the diagnosis of chronic hemonchosis?

Back 32

1. Poor-doing animals with low grade or borderline anemia
2. Fecal exam: moderate to high number of strongylid eggs

Front 33

Treatment of Haemonchosis

Back 33

1. Depends on economic value
2. Therapeutic anthelmintic treatment and supportive care
3. Salvage slaughter

Front 34

How do you select animals for treatment using the FAMACHA card?

Back 34

1. Examine in sunlight
2. Open for a short time only
3. Look at color inside lower eyelid
4. Score according to card
5. Treat those with score greater than or = to 4 or 3

Front 35

Describe and name the Ostertagia spp.

Back 35

Ostertagia ostertagi - cattle
Telodorsagia circumcincta - sheep/goats/camelids

All morphologically similar:
1. Brown when fresh
2. Small, slender worms
3. Males: prominent bursa; 2 short brown spicules
4. Females: vulvar flap

Front 36

What is the life cycle of Ostertagia ostertagi?

Back 36

Adults in abomasal lumen (females produce 200-400 eggs/day)

Eggs --> L1 -->--> L3 in environment (moist, cool conditions favorable); L3 ingested on forage; L5 in gastric glands --> mature to adults, mate, lay eggs, etc....

Front 37

Why does Ostertagia ostertagi have an uninterrupted life cycle?

Back 37

Ingested L3 ex-sheath, penetrate GASTRIC GLANDS OF ABOMASUM

Front 38

What is the prepatent period of O. ostertagi?

Back 38

3 weeks and no hypobiosis

Front 39

What is the Phase I pathogenesis of ostertagiosis?

Back 39

Phase I: Days 1-17 PI
1. L3 enter gastric glands, develop to L4
2. Larval activity damages gastric gland cells: zymogen, parietal (chief) and mucous secreting cells
3. Consequences of parietal (chief) cells death: loss of HCl production --> abomasal pH increases from 2.5 to 5-7, bacteria proliferate, profuse diarrhea, pepsinogen not converted to pepsin (protein not utilized) and increased plasma pepsinogen levels result from increased permeability of damaged gastric mucosa

Front 40

What is Phase II of the pathogenesis of ostertagiosis?

Back 40

Phase II: Days 18-35 PI
1. L5s exit gastric glands and destroy cells of glands
2. Smooth muscle compression and capillary disruption
3. Decreased mucus production
4. Hyperemia and edema
5. Undifferentiated cells replace specialized cells = hyperplastic, non-functional gastric mucosa (2-3 mm nodules)

Front 41

What is Phase III of the pathogenesis of ostertagiosis?

Back 41

Phase III: days 35-70
1. Gradual death and expulsion of adults
2. Gradual repair of gastric mucosa and return to normal function

Front 42

What are the overall effects of clinical infection of ostertagiosis?

Back 42

1. Reduced weaning weights of calves
2. Reduced milk production
3. Reduced breeding efficiency

Front 43

What are the clinical signs of ostertagiosis?

Back 43

2 clinical syndromes recognized:

1. Type I (summer) ostertagiosis: life cycle without hypobiosis

2. Type II (winter) ostertagiosis: life cycle with hypobiosis

Front 44

Describe Type 1 (summer) ostertagiosis.

Back 44

1. Large number of L3s is acquired in a short period of time

2. Usually affects young animals during first grazing season (late summer, early fall in MW)

3. High morbidity rate

4. Profuse continuous diarrhea (usually bright green)

5. Rapid weight loss and decreased body condition

6. Fecal exam: many trichostrongyle eggs

7. Lab findings: elevated plasma pepsinogen levels, hyoalbuminemia, possible mild anemia

8. Necropsy findings: abomasal pH more than 4.5 (nodules), hyperplastic, edematous abomasal folds, and mainly adult Ostertagia present

Front 45

What is Pre-type II ostertagiasis?

Back 45

1. Sub-clinical state: occurs while larvae are hypobiotic (fall to spring in North and from spring to fall in South)

2. Thousands of L4 may be present in gastric glands

3. Animals show no overt clinical signs, but appear to be in poor condition

Front 46

Describe Type II (winter) ostertagiosis.

Back 46

1. Mass emergence of hypobiotic L4 from gastric glands in short period of time = results in sudden mass destruction of gastric glands

2. Clinical disease can be protracted if larvae mature and emerge more gradually

Front 47

What is the epidemiology of ostertagiosis?

Back 47

1. Calves and yearlings are most susceptible to clinical disease
2. Adults develop immunity with repeated exposure
3. Parasites over-winter as:
A few adults in abomasum
Inhibited L4 in gastric glands
L3 on pastures

Front 48

What are clinical signs of Type II ostertagiosis?

Back 48

1. Profuse diarrhea
2. Anorexia
3. Weight loss, loss of condition
4. Abomasal lesion more severe than Type I
5. Carries poorer prognosis than Type I

Front 49

Describe Trichostrongylus axei.

Back 49

1. Stomach hair worm: smallest ruminant abomasal nematode
2. Life cycle similar to Ostertagia: L3 mucosal migration between gastric glands not in gastric glands; causes less damage to gastric glands

Front 50

Describe the clinical disease of Trichostrongylus axei.

Back 50

1. Usually a secondary problem in ruminants
2. Can occur with high dose of L3 in an immature or non-resistant animals
3. Diarrhea-watery, dark green, stains rear quarters
4. Anorexia, weight loss, etc...

Front 51

Describe the gastric gland epithelium from Trichostrongylus axei.

Back 51

Erosion of gastric gland epithelium
1. Ulceration +/- hemorrhage, necrosis
2. Replaced by undifferentiated gastric gland cells
3. Increased abomasal pH
4. Increased permeability of mucosa

Ruminants: white, circular plaques on abomasal mucosa; nodular lesions as in ostertagiosis

Horse: hyperemic gastritis; thickened glandular stomach

Front 52

Diagnosis of Trichostrongylus axei.

Back 52

1. Strongylid eggs: can ID L3 from fecal culture

Horses: history of grazing with or after ruminants plus sudden weight loss suggestive

Front 53

What are the small intestinal nematodes?

Back 53

1. Trichostrongylus
2. Cooperia
3. Nematodirus

Front 54

What is different in Nematodirus life cycle from other small intestinal nematodes?

Back 54

1. L3 develops within egg
2. Egg with L3 and hatched L3 both infective
3. Hatching stimulated by egg exposure to cold followed by warm temperatures

Front 55

Which species are small intestinal nematodes primary pathogens?

Back 55

1. Trichostrongylus colubriformis - sheep
2. Cooperia - calves
3. Nematodirus - mainly calves

Front 56

Define Nematodirus battus.

Back 56

1. Found in sheep
2. Clinical problem mainly in Europe: up to 30% mortality in lambs < 10 weeks old
3. Signs occur as larvae emerge from mucosa: acute onset diarrhea; begins black-green and becomes yellowish

Front 57

Name the Dictyocaulus spp.

Back 57

1. Superfamily Trichostrongyloidea
Only lungworm not in Metastrongyloidea

2. Dictyocaulus viviparous: cattle, bison, camelids, wild ruminants

3. D. filariae: sheep, goats, +/- wild ruminants

4. D. arnfieldi: donkey, horse

Front 58

Structure of D. viviparous

Back 58

4-8 cm
Eggs: ~35 um x 87 um and contain an L1

Front 59

Structure of D. filariae

Back 59

Adults and eggs are slightly bigger than D. viviparous

Front 60

What is the life cycle of Dictyocaulus?

Back 60

L3 ingested on forage migrate to lungs

Gut --> lymphatics --> blood --> heart --> lung capillaries --> alveoli --> bronchioles and bronchi

Adults in bronchi + bronchioles lay eggs --> L1 hatch in airways --> coughed up, swallowed and passed in feces; L1 --> L3 in 5-7 days in environment (don't molt or feed)

Front 61

What are the prepatent periods for Dictyocaulus spp?

Back 61

1. D. viviparus: 4-10 weeks
2. D. filariae: 4-6 weeks in goats/8 weeks in sheep
3. D. arnfieldi: 4-5 weeks

Front 62

What is special about the larvae of Dictyocaulus

Back 62

1. Rely on mechanical dispersion fromfecal pat
2. Rain, feet, fungal spores of Pilobolus - sporangium explodes and disperses and disperse

Front 63

Epidemiology of Dictyocaulus.

Back 63

1. Most common in Sept-Oct in MW: usually after period of cool, wet weather; build up of L3 numbers on fall pasture

2. Over winter survival of parasite: some L3 survive on pasture; some adults survive in host

Front 64

What are the phases of Dictyocaulosis?

Back 64

1. Penetration phase: days 1-7 PI; usually asymptomatic: L3 migrate from gut to lungs

2. Prepatent phase: days 7-25 PI; larvae mature and migrate from alveoli --> bronchioles; bronchioles blocked with eosinophilic exudate; mild cough +/- labored breathing; massive infection can cause death

Paten phase: days 25-55 PI; adults in upper airways --> severe bronchitis, epithelial damage; airways blocked by worms + frothy mucus + cellular exudate; secondary infection and pneumonia common; marked coughing and dyspnea

Post-patents phase: 55-70 DPI; adult lungworms expelled; most animals slowly recover; pulmonary function remains impaired in some individuals (chronic bronchiectasis, pneumonia and poor-doer)

Front 65

What is the diagnosis of dictyocaulosis?

Back 65

1. Coughing, rapid breathing, dyspnea, bronchitis
"hoose" or "husk", cough with head extended, tongue protruding

2. Herd problem affecting younger animals on pasture: high morbidity, low mortality

3. Detect L1 in fresh feces or sputum

Front 66

How do you control Dictyocaulosis in ruminants?

Back 66

1. Good management practices: nutritoin, pasture management and anthelmintic treatment

2. Natural infection induces immunity: re-infection can results in clinical signs without shedding of L1 in feces

3. Europe: vaccine (irradiated L3): decreased use + reliance on anthelmintics --> poor immunity and clinical disease in adults

Front 67

Describe Dictyocaulus arnfieldi.

Back 67

1. Natural host = donkey
2. Best in areas with mild temperatures and adequate moisture
3. Adults live in bronchi and bronchioles

Front 68

What is the life cycle of D. arnfieldi

Back 68

1. Adults mate and lay eggs in bronchi
2. Eggs coughed up and swallowed: hatch to L1 in GI tract or within a few hours in environment
3. L1 to L3 within 1 week
4. L3 ingested by host, migrate to bronchi via lymphatics
5. Prepatent period: 4-5 weeks

Front 69

What are the clinical signs of D. arnfieldi?

Back 69

1. Donkeys are asymptomatic
2. Clinical signs most likely in young hosts:
Infection often prolonged
Secondary bacterial pneumonia possible
Possible persistent dry cough

Front 70

Diagnosis of Dictyocaulus spp.

Back 70

1. Detection L1 in feces or bronchial washings: use fresh feces from rectal collection

2. ID of L1 contains food granules; tail has punctiform transparent progjection

NOTE: infection often not patent in horses and ponies

Front 71

Prevention and control of D. arnfieldi.

Back 71

1. Keep donkeys and horses separated
2. Quarantine new animals and treat as needed
3. Deworm horses 2x yearly with effective anthelmintic

Front 72

Describe Hyostrongylus rubidus.

Back 72

1. Superfamily Trichostrongyloidea: small stomach worm or red stomach worm

2. Adults: small (1/2 in); red when fresh

3. Eggs: typical trichostrongyl type

4. Fairly common in MW: 50% prevalence in WI

Front 73

What is the life cycle of Hyostrongylus rubidus?

Back 73

1. Adults in stomach lumen: suck blood and lay eggs passed non-embryonated in feces

2. L1 develops within egg in environment: hatches and develops to infective L3; L3 ingested

3. L3 undergoes brief mucosal migration in gastric glands; emerge into lumen and develop to adutls

Prepatent period ~ 20-25 days

Front 74

What are the clinical signs and lesions of Hyostrongylus?

Back 74

1. Severity depends on number of worms
2. Usually asymptomatic
3. Can cause chronic catarrhal gastritis: untrhiftyness, possible diarrhea, possible intermittent gastric hemorrhage (melena)
4. Lesions - stomach mucosa with cobblestone appearance

Front 75

Describe Ollulanus tricuspis.

Back 75

1. Adults are less than 1 mm long
2. Anterior coiled
3. Males bursate
4. Tail of female has more than 3 cusps
5. Often burrow into stomach mucosa
6. Potential cause of gastritis, vomiting, weight loss in cats

Front 76

What is the life cycle of Ollulanus tricuspis?

Back 76

1. Viviparous female gives birth to L3
2. Development from L3 to adult can occur in the same host
3. Transmission to new host by ingestion of L3 in vomitus

Front 77

Describe Libyostrongylus douglassi.

Back 77

1. Proventricular wire worm of ostriches
2. A trichostrongylid
3. Causes "rotten stomach"
4. Introduced with imported ostriches and now well established in US
5. Also in proventriculus

Front 78

Name the worm and sex.

Name the letters.

Back 78

Trichostrongylus axei - male

A = Bursa
B = Spicules
C = Head

Front 79

Name worm and sex

Name red and white parts and circled area

Back 79

Haemonchus contortus - female

Red = intestine
White = reproduction
Circled area = vulvar flap

Front 80

Name this species and what is at the anterior end.

Back 80

Haemonchus contortus - small buccal capsule with lancet used to lacerate mucosa and obtain blood

Front 81

Name the letters.

Back 81

A = adult male Ostertagia ostertagi
B = arrested L4 Ostertagia ostertagi

Front 82

Name this species and label letters.

Back 82

Cooperia curticei - female

A = Head
B = Uterus with eggs
C = Vulva
D = Uterus with eggs
E = Tail

Front 83

Name this species.

Back 83

Dictyocaulus showing mouth opening surrounded by lips

Front 84

Name this species.

Back 84

Dictyocaulus viviparus L1

Front 85

Name this species.

Back 85

Dictyocaulus filaria L1

Front 86

Name this species.

Back 86

Adult male and female Ollulanus tricuspis