Gi Nematodes In Domestic Livestock

Front 1

Describe parasitic gastroenteritis (PGE).

Back 1

Disease caused by parasitic nematodes in GI tract.

- Predominantly a disease of young, grazing stock; adults generally have strong acquired immunity by 2 years.

- Often caused by mixed species of parasitic nematodes.

- Much more common in sheep then cattle!

Front 2

What is the most important nematode superfamily with regard to bovine GI tract disease?

Back 2

TRICHOSTRONGYLOIDEA

- Ostertagia

- Haemonchus

- Cooperia

- Nematodirus

- Trichostrongylus

Front 3

Trichostrongyloidea life cycle? Infective stage? PPP?

Back 3

DIRECT LIFE CYCLES = no IMH

L3 = INFECTIVE STAGE

PPP = 21 days (short!)

Front 4

Life cycle of ostertagi ostertagi?

Back 4

Adults in abomasum reproduce

- Eggs passed in feces, hatch, & moult to L3 infective stage

- L3s ingested by animal & penetrate abomasal gland

- Moult into mature adults (L4) that will then either:

1) Enter hypobiosis - rest in tissues until environmental conditions are ideal

2) Reproduce in abomasum

Front 5

Swollen glands containing developing L4 ostertagi ostertagi may develop within the SI __________ days post infection.

Back 5

7-10 days!

Front 6

Ostertagi ostertagi larvae begin emerging from gastric glands into the abomasum by _____ days.

Back 6

18

Front 7

Pathogenesis of ostertagi ostertagi?

Back 7

1. HYPOPROTEINAEMIA - parasitized gastric glands lead to rupturing of intercellular junctions and leakage of plasma proteins into the lumen

2. Elevated plasma pepsinogen - parasites destroy parietal cells (HCl producers) & replace with undifferentiated cells, resulting in an increase in pH => failure to activate pepsinogen to pepsin => leakage of pepsinogen into blood

3. Bacterial overgrowth - due to increased pH

4. Hyperplasia of abomasal mucosa

5. Edematous - regional lymph nodes

6. Morrocan leather appearance

Front 8

What are the two clinical forms of ostertagiosis?

Back 8

TYPE I

- Grazing calves (usually first season)

- July-October

- Due to larvae acquired from pasture 2-3 weeks previously

TYPE II (much less common)

- Yearlings

- March-May

- Due to reactivation/maturation of inhibited larvae acquired from pasture during previous autumn.

Front 9

Clinical signs of Type I Ostertagiosis?

Back 9

1. Profuse watery diarrhea (typically bright green)

2. Weight loss

3. Submandibular edema (occasionally)

4. Morbidity is high; mortality is low

(many animals presenting, but survive if treated)

Front 10

Clinical signs of Type II Ostertagiosis?

Back 10

1. Intermittent diarrhea (not always present)

2. Submandibular edema = hypoalbuminaemia (COMMON)

3. Weight loss

4. +/- Moderate anemia

5. Anorexia & increased thirst

6. Morbidity low; mortality high

Front 11

Diagnosis of ostertagiosis?

Back 11

1. Clinical picture & grazing history for herd (not individual basis)

2. Diagnostic aids:

- FECs = fecal egg counts

- Serum pepsinogen (high with infection)

- Serum antibody

- Post mortem (PM)

Front 12

Describe the McMaster method of fecal egg counting (FEC).

Back 12

Eggs are separated from fecal debris by floatation in saturated salt solution

- Nematode eggs float in liquid of specific gravity 1.1-1.2

Front 13

How is serum pepsinogen tested for when diagnosing ostertagiosis?

Back 13

Measuring hydrolyzing activity of serum on albumin

- Serum incubated with BSA at pH 2.5 at 37C for 24 hours

- Amount of TYROSINE released then measured by OD at 680nm following addition of Folin's reagent

- Normal = 1 U tyr (micromoles of T released/L of serum/minute

- Parasitized = 3-5 U tyr

- Useful in calves, but not so in older animals (often have low burdens due to immunity)

Front 14

At which times of the year do TYPE I Ostertagiosis outbreaks occur? TYPE II?

Back 14

TYPE I = Aug - Nov

TYPE II = February

Front 15

How long does immunity to ostertagia take to develop?

Back 15

~ 2 years

* Immune animals still carry low burdens

Front 16

What triggers Ostertagi ostertagi L4s to become hypobiosis?

Back 16

Exposure during free living stages (L1 & L2) to low temperatures on pasture triggers them to be stored in the abomasal glands until conditions are more ideal

Front 17

Type II Ostertagiosis occurs due to reactivation of inhibited larvae. When does this typically occur?

Back 17

FEBRUARY

Front 18

"Classic" Type II Ostertagiosis predisposing factors?

Back 18

Ingestion of large numbers of L3 delayed to autumn, which is caused by:

1. Poor Grazing Management - moving animals to contaminated pasture late in grazing season.

2. Climate - dry Summers delay emergence of larvae from fecal pats

Front 19

Ostertagiosis is uncommon in:

1) Spring calving herds

2) Autumn calvin herds?

Back 19

SPRING CALVING HERDS (uncommon)

- Because calves aren't weaned until Autumn (over-wintered larvae now dead)

Ostertagiosis is COMMON in AUTUMN CALVING HERDS

- Calves weaned in Spring & exposed to over-wintered larvae.

Front 20

Atypical forms of bovine ostertagiosis?

Back 20

1. Early season type I ostertagiosis

2. Ostertagiosis in adult cattle

Front 21

Treatments for Ostertagiosis?

Back 21

TYPE I Disease:

- Currently available anthelmentics

- Move to clean pasture

TYPE II Disease:

- Modern benzimidazoles

- Macrocyclic lactones

- Pro-benzimidazoles (higher dosage rate)

Front 22

Control of Ostertagi ostertagi?

Back 22

1. Grazing management/prophylactic medication

- avoid grazing contaminated pasture at peak season ('dose & move')

- limited exposure okay to 'safe pasture' to gain immunity

2. Monitoring

- FEC/growth - only worm when necessary

3. Worm at housing

- Stock susceptible to type II disease

Front 23

Predilection site for trichostrongylus axei? Hosts?

Back 23

ABOMASUM

HOSTS: Ruminants & Horses

Front 24

Pathology of trichstrongylus axei?

Back 24

- Haemorrhages/edema/enteritis in the abomasum

- Flattened nodules (dinstinctive!)

- Sub-epithelial tunnels

Front 25

Trichostrongylus axei is rarely a primary pathogen in the UK.

True or False?

Back 25

TRUE - More so in Sub-tropics

* In UK, often contributes to clinical signs of PGE (parasitic gastroenteritis) as part of a mixed infection.

Front 26

Trichostrongylus axei L3 are particularly resistant to cold & dessication.

True or false?

Back 26

TRUE

- Occasionally over-winter L3s can cause clinical problems in Spring.

Front 27

What species of haemonchus is more important in the UK: Placei/contortus?

Back 27

Haemonchus contortus - important with sheep in the UK

Front 28

"Barber's Pole Worm"

Back 28

HAEMONCHUS - white ovaries/ blood-filled intestines

Front 29

Pathogenesis of haemonchus?

Back 29

SEVERE ANEMIA - blood sucking worms that feed on mucosal vessels of abomasum; punctures through epithelium & feeds off the blood that pours out

Front 30

When does the lancet develop in the haemonchus?

Back 30

Before the final moult

Front 31

When are bovine haemonchosis outbreaks most common in the tropics?

Back 31

RAINY SEASON - remains in ALD until rain comes

Front 32

When does immunity typically develop in cattle against bovine haemonchosis?

Back 32

>2 years (longer in sheep)

Front 33

Immunity can be broken down during drought.

True or False?

Back 33

TRUE - Due to poor nutrition/heavier challenge

Front 34

What are the three types of cooperia species found commonly affecting cattle?

Back 34

C. oncophora - temperate areas (UK)

C. punctata - sub-tropical/tropical

C. pectinata - sub-tropical/tropical

Front 35

Cooperia oncophora often contributes to PGE as part of a mixed infection & can sometimes be the predominant parasite.

True or False?

Back 35

TRUE

Front 36

What is the predilection site for cooperia?

Back 36

SI

Front 37

Cooperia oncophora is a _____________ species for anthelmintics.

Back 37

DOSE-LIMITING - requires increased amounts in heavier infections.

Front 38

Cooperia oncophora is the cattle parasite most commonly implicated in anthelmintic resistance.

True or False?

Back 38

TRUE

Front 39

Trichostrongylus colubriformis predilection site? Hosts? Life cycle?

Back 39

SMALL INTESTINES

HOSTS: Ruminants

Life cycle: Direct ingestion of larvae

Front 40

Trichostrongylus colubriformis is commonly a primary pathogen in the UK.

True or False?

Back 40

FALSE - Rarely a primary pathogen.

Often contributes to PGE, but not primary pathogen.

Front 41

What are the two nematodirus species in cattle which contribute to PGE (parasitic gastroenteritis) as part of a mixed infection?

Back 41

NEMATODIRUS BATTUS & SPATHIGER

* Occur in cattle but much more common in sheep & further discussed in sheep lecture.

Front 42

Bunostomum phlebotomum superfamily? Type of worm? Predilection site? Appearance?

Back 42

SUPERFAMILY: Strongyloidea

TYPE: Hookworm (sucks blood)

PREDILECTION SITE: SI

APPEARANCE: 1-3cm with hooked anterior end

Front 43

What is the life cycle of bunostomum phlebotomum? PPP?

Back 43

Similar to that of dog/cat hookworm:

- Percutaneous transmission from ground & pulmonary migration

- Orally

PPP: ~6 weeks

Front 44

Where is bunostomum phlebotomum mainly a problem?

Back 44

TROPICS - at the end of a dry season (HYPOBIOTIC LARVAE)C

Front 45

Clinical signs of bunostomum phlebotomum?

Back 45

- Anemia (blood-sucker)

- Hypoalbuminaemia

- Weight loss

- Sometimes diarrhea

- Pedal dermatitis - foot stamping/ itching/ penetration of infective larvae

Front 46

Control of bunostomum phlebotomum?

Back 46

Improved indoor hygiene (manure disposal)

Front 47

Largest intestinal nematode parasite of cattle?

Back 47

TOXOCARA VITULORUM = 30cm

Front 48

Who is more susceptible to toxocara vitulorum: calf or adult?

Back 48

Young calves most susceptible

- L3 Transmammary infections!

Front 49

What are the two cattle worms that reside in the large intestine?

Back 49

Oesophagostomum radiatum & Trichuris

Front 50

Nodules formed on serosal surface of LI in cattle commonly related to . . .

Back 50

Oesophagostomum radiatum

Front 51

Whipworm

Back 51

Trichuris globulosa

Front 52

What are the most common contributing species to Parasitic GastroEnteritis (PGE) in cattle in the UK?

Back 52

1. Ostertagia ostertagi (Abomasum)

2. Cooperia oncophora (SI)

*KNOW IN DETAIL!*