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86 Cards in this Set

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  • Back
Describe males of Trichostrongylus axei
Bursate with short, stout spicules

Buccal cavity small or absent
What is the life cycle of Trichostrongyloids?
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
What is the prepatent period for Trichostrongyles?
2-3 weeks
What are the superfamilies (Genus') of Trichostrongyloidea?
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
What is special about Haemonchus contortus eggs?
Haemonchus eggs bind fluoroscein-labelled peanut agglutinin. (Glow in the dark) Eggs of other strongylids in ruminants do not.
What is the most pathogenic species for cattle?
Ostertagia ostertagi
What is the most pathogenic species for sheep/goats?
Haemonchus contortus
What are environmental influences from eggs --> L3?
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
When does hypobiosis occur?
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.
What happens during the spring regarding strongylid eggs?
There is an increase in numbers in host feces due to the emergence and maturation of hypobiotic larvae in the spring
What is periparturient rise?
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
What is premunition?
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
What is the fate of strongylid L3 ingested by hosts with premunition?
1. Expelled from host
2. Become hypobiotic
3. Replace existing adult population
What is the "Self-cure" response?
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
What are the abomasal (stomach) worms? [HOTT]
1. Haemochus
2. Osteragia
3. Telodorsagia
4. Trichostrongylus axei
What are the Haemonchus spp?
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)
What is the Haemonchus structure?
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
What is on anterior end of Haemonchus contortus?
1. Both sexes are blood suckers

2. Small buccal capsule with "lancet" used to lacerate mucosa and obtain blood
What is the Haemonchus life cycle?
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
What are the prepatent periods of H. contortus and H. placei?
1. H. contortus: 15 days
2. H. placei: 25-28 days
What are some factors in pathogenicity for Haemonchus?
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
What are the clinical signs of H. contortus?

Can see blood in feces at 6-12 days PI

Diarrhea is NOT a feature unless animal is also infected with other strongylids
What is peracute/hyperacute hemonchosis?
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
How do you diagnose peracute/hyperacute hemonchosis?
Signalment, clinical signs suggestive

Necropsy findings:
Severe hemorrhagic gastritis
Very pale organs
Dark, bloody GI contents
1,000s of worms (L4)
Describe acute hemonchosis.
1. Pale mucous membranes
2. Dependent edema
3. Weakness, lethargy, shortness of breath
4. Melena
5. Agalactia in ewes --> lambs starve
What is the pathogenesis of acute hemonchosis?
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)
What is the diagnosis of acute hemonchosis?
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
What necropsy findings are there for acute hemonchosis?
Pale watery carcass
Thin watery blood
Abomasal mucosa: edematous with many petechial hemorrhages, many Haemonchus present, and erythropoietic response in bone marrow
Describe chronic hemonchosis.
1. Most common
2. Chronic infection with lower number of parasites
3. Chronic insidious blood loss
4. Erythropoiesis
What are clinical signs of chronic hemonchosis?
1. Anorexia, progressive weight loss and emaciation
2. Weakness and lethargy
3. Adult sheep: wool-breaks, "wool-peeling"
What are lab findings and necropsy findings of chronic hemonchosis?
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
What is the diagnosis of chronic hemonchosis?
1. Poor-doing animals with low grade or borderline anemia
2. Fecal exam: moderate to high number of strongylid eggs
Treatment of Haemonchosis
1. Depends on economic value
2. Therapeutic anthelmintic treatment and supportive care
3. Salvage slaughter
How do you select animals for treatment using the FAMACHA card?
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
Describe and name the Ostertagia spp.
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
What is the life cycle of Ostertagia ostertagi?
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....
Why does Ostertagia ostertagi have an uninterrupted life cycle?
Ingested L3 ex-sheath, penetrate GASTRIC GLANDS OF ABOMASUM
What is the prepatent period of O. ostertagi?
3 weeks and no hypobiosis
What is the Phase I pathogenesis of ostertagiosis?
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
What is Phase II of the pathogenesis of ostertagiosis?
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)
What is Phase III of the pathogenesis of ostertagiosis?
Phase III: days 35-70
1. Gradual death and expulsion of adults
2. Gradual repair of gastric mucosa and return to normal function
What are the overall effects of clinical infection of ostertagiosis?
1. Reduced weaning weights of calves
2. Reduced milk production
3. Reduced breeding efficiency
What are the clinical signs of ostertagiosis?
2 clinical syndromes recognized:

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

2. Type II (winter) ostertagiosis: life cycle with hypobiosis
Describe Type 1 (summer) ostertagiosis.
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
What is Pre-type II ostertagiasis?
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
Describe Type II (winter) ostertagiosis.
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
What is the epidemiology of ostertagiosis?
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
What are clinical signs of Type II ostertagiosis?
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
Describe Trichostrongylus axei.
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
Describe the clinical disease of Trichostrongylus axei.
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...
Describe the gastric gland epithelium from Trichostrongylus axei.
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
Diagnosis of Trichostrongylus axei.
1. Strongylid eggs: can ID L3 from fecal culture

Horses: history of grazing with or after ruminants plus sudden weight loss suggestive
What are the small intestinal nematodes?
1. Trichostrongylus
2. Cooperia
3. Nematodirus
What is different in Nematodirus life cycle from other small intestinal nematodes?
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
Which species are small intestinal nematodes primary pathogens?
1. Trichostrongylus colubriformis - sheep
2. Cooperia - calves
3. Nematodirus - mainly calves
Define Nematodirus battus.
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
Name the Dictyocaulus spp.
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
Structure of D. viviparous
4-8 cm
Eggs: ~35 um x 87 um and contain an L1
Structure of D. filariae
Adults and eggs are slightly bigger than D. viviparous
What is the life cycle of Dictyocaulus?
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)
What are the prepatent periods for Dictyocaulus spp?
1. D. viviparus: 4-10 weeks
2. D. filariae: 4-6 weeks in goats/8 weeks in sheep
3. D. arnfieldi: 4-5 weeks
What is special about the larvae of Dictyocaulus
1. Rely on mechanical dispersion fromfecal pat
2. Rain, feet, fungal spores of Pilobolus - sporangium explodes and disperses and disperse
Epidemiology of Dictyocaulus.
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
What are the phases of Dictyocaulosis?
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)
What is the diagnosis of dictyocaulosis?
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
How do you control Dictyocaulosis in ruminants?
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
Describe Dictyocaulus arnfieldi.
1. Natural host = donkey
2. Best in areas with mild temperatures and adequate moisture
3. Adults live in bronchi and bronchioles
What is the life cycle of D. arnfieldi
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
What are the clinical signs of D. arnfieldi?
1. Donkeys are asymptomatic
2. Clinical signs most likely in young hosts:
Infection often prolonged
Secondary bacterial pneumonia possible
Possible persistent dry cough
Diagnosis of Dictyocaulus spp.
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
Prevention and control of D. arnfieldi.
1. Keep donkeys and horses separated
2. Quarantine new animals and treat as needed
3. Deworm horses 2x yearly with effective anthelmintic
Describe Hyostrongylus rubidus.
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
What is the life cycle of Hyostrongylus rubidus?
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
What are the clinical signs and lesions of Hyostrongylus?
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
Describe Ollulanus tricuspis.
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
What is the life cycle of Ollulanus tricuspis?
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
Describe Libyostrongylus douglassi.
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
Name the worm and sex.

Name the letters.
Trichostrongylus axei - male

A = Bursa
B = Spicules
C = Head
Name worm and sex

Name red and white parts and circled area
Haemonchus contortus - female

Red = intestine
White = reproduction
Circled area = vulvar flap
Name this species and what is at the anterior end.
Haemonchus contortus - small buccal capsule with lancet used to lacerate mucosa and obtain blood
Name the letters.
A = adult male Ostertagia ostertagi
B = arrested L4 Ostertagia ostertagi
Name this species and label letters.
Cooperia curticei - female

A = Head
B = Uterus with eggs
C = Vulva
D = Uterus with eggs
E = Tail
Name this species.
Dictyocaulus showing mouth opening surrounded by lips
Name this species.
Dictyocaulus viviparus L1
Name this species.
Dictyocaulus filaria L1
Name this species.
Adult male and female Ollulanus tricuspis