PARASITOLOGY - Bovine Nematodes

Question 1

What is the pre-patent period (PPP)?

Answer 1

The pre-patent period (PPP) is the time taken between initial infection of a helminth and the production of eggs by the adult worms

Question 2

What is parasitic gastroenteritis (PGE)?

Answer 2

Parasitic gastroenteritis (PGE) is the condition caused by co-infection of gastrointestinal nematodes which reside in the gastrointestinal tract of ruminant hosts

Question 3

What is the typical signalement for parasitic gastroenteritis (PGE)?

Answer 3

Young cattle in their first grazing season during summer/autumn

Summer/autumn is the second half of the grazing season where pasture larval challenge increases

Question 4

What are the two most significant nematodes which cause parasitic gastroenteritis (PGE) in cattle?

Answer 4

Ostertagia ostertagi
Cooperia oncophora

Question 5

Where is ostertagia ostertagi found within the bovine gastrointestinal tract?

Answer 5

Ostertagia ostertagi is found within the abomasum

Question 6

What is the lifecycle of ostertagia ostertagi?

Answer 6

1. Adult worms breed and the female worms produce eggs
2. Eggs are excreted in the host faeces into the environment
3. Eggs develop into L3 larvae on pasture within the L2 cuticle
4. L3 are ingested by cattle on pasture
5. L3 exsheath and penetrate the abomasal glands and develop into L4 larvae
6. L4 larvae rupture the abomasal glands and emerge into the abomasal lumen and develop into adult worms

Question 7

What is hypobiosis?

Answer 7

Infective ostertagia ostertagi larvae ingested towards the end of the grazing season will develop into L4 and undergo a period of hypobiosis in the abomasal glands. This occurs if the environmental conditions become unfavorable to accommodate larval development in the environment. These larvae typically resume development in late winter and become adult worms (the mechanism for resumed development is unknown)

Question 8

Describe the pathogenesis of ostertagia ostertagi

Answer 8

Parasitised abomasal glands become undifferentiated, hyperplastic and dysfunctional. This results in decreased HCl production due to damage to the parietal cells, resulting in an increased abomasal pH. This prevents the conversion of pepsinogen to pepsin (as it requires an acidic pH), which is the enzyme which breaks down protein. Increasing abomasal pH also triggers gastrin secretion to try and stimulate HCl production and secretion. Hypergastrinaemia will result in appetite suppression and decreased feed intake which contributes to reduced growth rate

Question 9

What is type I ostertagiosis?

Answer 9

Type I ostertagiosis is infection of ostertagia ostertagi typically seen late summer/early autumn and caused by the ingestion of and maturation of infective larvae by susceptible calves or yearlings

Question 10

What is type II ostertagiosis?

Answer 10

Type II ostertagiosis is infection of ostertagia ostertagi caused by the ingestion of infective larvae near the end of the grazing season. The larvae will go into hypobiosis in the abomasal mucosa and then emerge in the late winter months and cause disease (which can be severe clinical disease due to the emergence of large numbers of L4 larvae)

Question 11

How can type II ostertagiosis be prevented?

Answer 11

Type II ostertagiosis can be prevented with routine macrocyclic lactone treatment at housing during late autumn/early winter. However, it could be beneficial to test (i.e. blood pepsinogen) and assess if anthelmintics are actually indicated as the risk can vary from year to year

Question 12

Which important history question should you ask when trying to determine the cause of scour in housed calves and yearlings?

Answer 12

It is important to ask the farmer if the calves and yearlings were treated with anthelmintics at housing during late autumn/winter. If no, then this puts type II ostertagiosis further up your differential diagnosis list. It is also important to determine if the animals were on pasture during grazing season

Question 13

What are the clinical signs of clinical ostertagia ostertagi?

Answer 13

Reduced feed intake
Poor growth rate/Ill thrift
Profuse, green, watery scour

Question 14

(T/F) Subclinical parasitic gastroenteritis (PGE) is much more common compared to clinical parasitic gastroenteritis (PGE)

Answer 14

TRUE. Though clinical parasitic gastroenteritis is not uncommon in young cattle, by far the most common expression is subclinical infections

Question 15

What are the consequences of subclinical parasitic gastroenteritis (PGE) in first season grazing calves?

Answer 15

Subclinical parasitic gastroenteritis (PGE) in first season grazing calves results in decreased growth rates, decreased daily liveweight gain and decreased feed conversion ratio, mainly due to a reduction in feed intake. This all results in poor productivity

Be aware that not all animals are going to have the same parasite burden, resulting in uneven growth rates and productivity

Question 16

What are the consequences of subclinical parasitic gastroenteritis (PGE) in second grazing season cattle (yearlings)?

Answer 16

Subclinical parasitic gastroenteritis (PGE) in second season grazing calves results in decreased growth rates, decreased daily liveweight gain, reduced feed conversion ratio, decreased carcase yield and quality and decreased fertility. This all results in poor productivity

Be aware that not all animals are going to have the same parasite burden, resulting in uneven growth rates and productivity

Question 17

What are the consequences of subclinical parasitic gastroenteritis (PGE) in adult beef cattle?

Answer 17

Subclinical parasitic gastroenteritis can result is reduced fertility and milk yield in adult beef cattle. This reduced milk yield is also reflected in reduced weaning weights in beef suckler calves

This can happen is animals that haven’t developed a good immunity

Question 18

What are the consequences of subclinical parasitic gastroenteritis (PGE) in adult dairy cattle?

Answer 18

Subclinical parasitic gastroenteritis can result is reduced fertility and milk yield in adult dairy cattle

This can happen is animals that haven’t developed a good immunity

Question 19

When do cattle develop immunity to gastrointestinal nematodes?

Answer 19

It takes exposure to larvae over one grazing season for cattle to develop immunity to cooperia oncophora and exposure to larvae over two grazing seasons for cattle to develop immunity to ostertagia ostertagi

Question 20

What are the features of bovine host immunity to gastrointestinal nematodes?

Answer 20

Decreased fecundity (decreased egg production)
Stunting nematode growth
Expulsion of adult nematodes
Limits establishment of infective larvae in the gastrointestinal tract

Question 21

(T/F) When cattle develop immunity against gastrointestinal nematodes, nematode eggs are no longer excreted in the faeces

Answer 21

FALSE. When cattle develop immunity against gastrointestinal nematodes, they DO NOT develop sterile immunity, and thus they still excrete eggs in their faeces however there will be reduced fecundity

Question 22

How do environmental factors influence gastrointestinal nematode larval challenge on pasture?

Answer 22

The development time of gastrointestinal nematodes from egg to L3 larvae on pasture can range from three weeks to three days with increasing temperatures. Moisture (rain) is also required for the dispersal of L3 larvae across the pasture, as if the weather is dry, the host faeces will dry up and form a crust which traps the larvae. Furthermore, any other factors which can disturb the faeces and distribute the larvae - such as harrowing - will increase the larval challenge on pasture

Question 23

How long do gastrointestinal nematode larvae survive on pasture?

Answer 23

Gastrointestinal nematode larvae typically survive for 12 months on pasture, but some can live up to 24 months and act as a reservoir (over-wintering larvae)

Question 24

What is a typical grazing season?

Answer 24

A typical grazing season is from April to October

Question 25

Describe the epidemiology of parasitic gastroenteritis (PGE) in weaned dairy cows in their first grazing season

Answer 25

Weaned dairy cows are highly susceptible to parasitic gastroenteritis (PGE) during their first grazing season, as they have limited immunity to parasitic infections. Weaned dairy calves are put out to pasture around April, where they will ingest overwintered larvae immediately once they start to graze. Following the pre-patent period of three weeks, the eggs are continually excreted in the faeces, where they develop into infective larvae. Given the temperature dependence of egg hatching and larval development, it follows that eggs deposited early in the spring take considerably longer to develop than those deposited later, when ambient temperatures increase as summer approaches. This results in a concertina effect with calf egg output and pasture larval challenge peaking around July to September where there will be increased infection pressure and risk of poor growth rates *(however be aware that as this is an early marker of parasitic challenge it is seen as early as may)* and clinical disease ## Footnote Be aware this is epidemiology on set pasture in absence of anthelmintic treatment

Question 26

Describe the epidemiology of parasitic gastroenteritis (PGE) in beef suckler cows in their first grazing season

Answer 26

Beef suckler calves rarely suffer from clinical parasitic gastroenteritis (PGE) before weaning due to a relative lack of exposure to infective larvae. When beef suckler calves are first put out to pasture, their diet will consist of milk from the dams, limiting the intake of infective larvae from the pasture until they begin to graze. Even when the calves begin to graze and grass becomes a significant component of their diet, there will be reduced larval challenge compared to weaned dairy calves as though the dams will still be excreting eggs, their faecal egg counts will be low due to their acquired immunity. As the grazing season continues, the calf egg output will begin to increase as the calves will augment the faecal egg output, increasing pasture larval challenge. When beef calves are weaned, they are at increased risk of clinical disease

Question 27

Which techniques can be used to monitor and diagnose parasitic gastroenteritis (PGE) in cattle?

Answer 27

Monitor daily liveweight gain Faecal egg counts Serum pepsinogen Post mortem (PM)

Question 28

What are the benefits and limitations of monitoring daily liveweight gain to monitor for parasitic gastroenteritis (PGE)?

Answer 28

Monitoring daily liveweight gain is a very sensitive and the most rapid test for parasitic gastroenteritis (PGE), however, it is not very specific as poor growth can be caused by multiple other factors

Question 29

What the benefits of faecal egg counts for parasitic gastroenteritis (PGE)?

Answer 29

Cheap (can be pooled) Easy Good indicator of pasture contamination FECRT to demonstrate anthelmintic efficacy Can be used to determine pattern of infection on individual farms ## Footnote Need at least 15 samples to pool for it to be representative

Question 30

What are the limitations of faecal egg counts for parasitic gastroenteritis (PGE)?

Answer 30

Requires training Not representative of total worm burden Faecal egg counts do not correlate to clinical disease Faecal egg counts should not be used as a threshold for treatment in individual animals *(however can be useful at a group level)*

Question 31

Describe how faecal egg counts can be used to guide anthelmintic treatment at a group level

Answer 31

You can do regular faecal worm egg counts *(i.e. every month)* during the grazing season to continuously indicate the degree of pasture contamination and if anthelmintic treatment is necessary. It may not be required until later in the grazing season where the pasture contamination will increase - this helps to reduce unnecessary anthelmintic use

Question 32

What are the limitations of measuring serum pepsinogen levels?

Answer 32

Expensive Delayed results as has to be sent to the lab

Question 33

What is the aim of integrated parasite control?

Answer 33

The aim of integrated parasite control is to reduce the use of and reliance on anthelmintic treatment to control parasites

Question 34

How is integrated parasite control achieved?

Answer 34

Integrated parasite control is achieved by incorporating diagnostic testing for parasites before treating, monitoring the herd, grazing management, appropriate use of anthelmintics and approriate vaccination use. This will have to be tailored to each farm and consider the farmer's objectives, and altered from year to year to be effective

Question 35

What is the main objective for the control of parasitic gastroenteritis (PGE)?

Answer 35

The main objective for the control of parasitic gastroenteritis (PGE) is to reduce the larval challenge to a level that does not cause clinical disease and permits good productive performance

Question 36

Which grazing management methods can be used to control parasitic gastroenteritis (PGE)?

Answer 36

Graze on newly sown grass fields Graze on silage/hay aftermath Mixed livestock grazing Multispecies swards Rotational grazing Deferred grazing

Question 37

What are the benefits of mixed livestock grazing for controlling parasitic gastroenteritis (PGE)?

Answer 37

Mixed livestock grazing, such as co-grazing cows and sheep can reduce the larval challenge for each species as they do not share the same gastrointestinal nematodes (however remember the both share liver fluke)

Question 38

What are multispecies swards?

Answer 38

Multispecies swards is pasture consisting of multiple plant species. Chicory contains tannins which have a deworming effect

Question 39

What would be seen as low risk pasture for parasitic gastroenteritis (PGE)?

Answer 39

Newly sown pasture Silage/hay aftermath Pasture that hasn't been grazed in a year *(as most larvae die off in 12 months)* Pasture that has been grazed by adult cattle or another species

Question 40

What would be seen as high risk pasture for parasitic gastroenteritis (PGE)?

Answer 40

Permanent pasture that has been grazed by youngstock cattle within the last year

Question 41

What are the three groups of anthelmintics available for parasitic gastroenteritis (PGE) in cattle?

Answer 41

White drenches (Benzimidazoles) Yellow drenches (Levamisole) Clear drenches (Macrocyclic lactones)

Question 42

Why are clear drenches (Macrocyclic lactones) most commonly used on farms?

Answer 42

Clear drenches have high levels of efficacy against a broad spectrum of nematodes and arthropods, persistent activity and ease of administration *(are available as pour on)*

Question 43

What is the main disadvantage of clear drenches (Macrocyclic lactones) on farms?

Answer 43

Macrocyclic lactones have persistent activity which increases the risk of anthelmintic resistance

Question 44

What should you always do before advising farmers on which anthelmintic treatment to use?

Answer 44

There are many different formulations of anthelmintics with varying withdrawal periods, duration of action etc. so it is very important to check the data sheet. Furthermore, you should always check if the anthelmintic protocol is compatible with the lungworm vaccination

Question 45

What is targeted selective treatment (TST) with anthelmintics?

Answer 45

Targeted selective treatment (TST) is treatment of individual animals with anthelmintics when monitoring daily liveweight gain (measured monthly) indicates subclinical infection and loss of performance

Question 46

When is targeted selective treatment (TST) indicated?

Answer 46

Targeted selective treatment (TST) is indicated if the daily liveweight gain is less than 750g per day | As this is the minimum required for cows to calf at 24 months old

Question 47

What is strategic anthelmintic treatment?

Answer 47

Strategic anthelmintic treatment is the treatment of groups of animals early in the grazing season and at housing to limit pasture contamination with eggs and hence reduce the risk of parasitism *(this is more routine treatments which we are trying to limit)*

Question 48

What is tactical anthelmintic treatment?

Answer 48

Tactical anthelmintic treatment is the treatment of groups of animals in anticipation of a decline in immunity and performance

Question 49

What is therapeutic anthelmintic treatment?

Answer 49

Therapeutic anthelmintic treatment is anthelmintic treatment of individual animals exhibiting clinical disease

Question 50

How do you manage housing anthelmintic treatments?

Answer 50

Farmers will often carry out routine anthelmintic treatment at housing to reduce the risk of type II ostertagiosis and reduces the pasture contamination during turnout the following year *(as the hypobiosis larvae will have been killed off with the treatment)*. However, this is not always necessary if there is a low parasite challenge and this is where measuring blood pepsinogen at housing is useful to establish if anthelmintics are necessary ## Footnote Be aware that macrocyclic lactone treatments are also useful for ectoparasites at housing, however if the only indicator for this is ectoparasites, use an ectoparasitide drug instead to reduce macrocyclic lactone use

Question 51

What is the most significant lung worm found in cattle?

Answer 51

Dictyocaulus viviparus

Question 52

What is the other name used to describe dictyocaulus viviparus?

Answer 52

Husk

Question 53

Describe the lifecycle of dictyocaulus viviparus

Answer 53

1. L3 larvae are ingested by host 2. L3 larvae penetrate the intestinal mucosa and travel to the mesenteric lymph nodes where they moult into L4 larvae 3. L4 larvae travel via the blood and lymphatics to the bronchioles where they moult into young adults 4. Young adults migrate to the bronchi where they moult into mature adults and produce eggs 5. L1 larvae hatch from the eggs and migrate to the lungs and up the trachea where they are coughed up and swallowed 6. L1 are shed in the faeces 7. L2 and L3 develop in the faeces

Question 54

Which signalement is typically affected by dictyocaulus viviparus?

Answer 54

Dictyocaulus viviparus typically has a clinical effect on first season grazing calves during summer/autumn ## Footnote Summer/autumn is the second half of the grazing season where pasture larval challenge increases

Question 55

What are the clinical signs of dictyocaulus viviparus?

Answer 55

Frequent coughing Tachypnoea Depression

Question 56

What are the effects of subclinical dictyocaulus viviparus?

Answer 56

Poor perfromance and growth rates Provides carrier animals *(which can be animals of any age)*

Question 57

What are the sources of infective dictyocaulus viviparus larvae at turnout to pasture?

Answer 57

Overwintered larvae Adult carrier animals

Question 58

How do environmental factors influence dictyocaulus viviparus larval challenge on pasture?

Answer 58

The development time of dictyocaulus larvae from L1 to L3 larvae on pasture can range from weeks to days with increasing temperaures. Moisture (rain) is also required for the dispersal of L3 larvae across the pasture, as if the weather is dry, the host faeces will dry up and form a curst which traps the larvae. Furthermore, pilibolus fungi which grow on faeces can distribute the larvae

Question 59

What is the first line of acquired immunity against dictyocaulus viviparus?

Answer 59

In an immune animal, when the larvae penetrate the mesenteric lymph nodes, an immune response is initiated which destroys most of the larvae in situ and prevents them from reaching the respiratory tract

Question 60

How is the first line of immunity against dictyocaulus viviparus acquired?

Answer 60

The first line of immunity against dictyocaulus viviparus is acquired within two weeks of a primary, natural infection with dictyocaulus viviparus, or induced by vaccination

Question 61

How long does the first line of immunity agaisnt dictyocaulus viviparus last?

Answer 61

The first line of immunity agaisnt dictyocaulus viviparus is short lasting so without re-exposure to the parasite, this first line defence will be lost after 6 months

Question 62

What is the second line of acquired immunity against dictyocaulus viviparus?

Answer 62

Larvae that have not been incapacitaed by the host immune response in the mesenteric lymph nodes - either because the animal is naive to infection or because the immunity from previous exposure has waned - complete migration to the respiratory tract. Here an immune response is invoked which results in the destruction and elimination of dictyocaulus viviparus from the lungs

Question 63

How long does the second line of immunity agaisnt dictyocaulus viviparus last?

Answer 63

Unlike the host response in the mesenteric lymph nodes, the response to dictyocaulus viviparus in the lungs invokes an immune memory and protection persists for at least 24 months, even in the absence of parasitic challenge

Question 64

What is re-infection syndrome?

Answer 64

Re-infection syndrome occurs in cattle that have been previously exposed to dictyocaulus viviparus and have acquired immunity, however following a lack of exposure to the parasite lasting 6 months or more, the host immune response in the mesenteric lymph nodes is ineffectual and hence the L4 can travel to the respiratory tract. This will trigger the second line of immune defence (which remains functional even in the absence of parasite challenge), resulting in immunopathological changes in the respiratory tract which can present similarly to clinical dictyocaulus viviparus

Question 65

What causes dictyocaulosis in adult cattle?

Answer 65

Primary infection occurs when older cattle that have never been vaccinated or exposed to natural dictyocaulus viviparus are put onto pasture with high larval populations to graze. Adult cattle can also experience re-infection syndrome if they have been previously vaccinated or exposed to natural infection, but have not been exposed to infection for 6 months or more and encounter larval challenge at pasture

Question 66

How can you monitor and diagnose dictyocaulus viviparus?

Answer 66

Monitor young cattle for clinical signs Monitor daily liveweight gain Faecal larval counts Bronchoalveolar lavage (BAL) Post mortem (PM)

Question 67

What is a contraindication to bronchoalveolar lavage (BAL) to diagnose dictyocaulus viviparus?

Answer 67

If the animal is in respiratory distress, bronchoalveolar lavage (BAL) is contraindicated as it involves the infiltration of fluid into the lungs which will further impair gaseous exchange

Question 68

Which methods can be used to control dictyocaulus viviparus?

Answer 68

Anthelmintics Grazing management Vaccination

Question 69

What is the recommended vaccination protocol for dictyocaulus viviparus?

Answer 69

The recommended schedule is to vaccine calves equal to or more than 8 weeks old with two doses, administered 4 weeks apart. Animals should not be turned out to pasture until 2 weeks after the second vaccination

Question 70

Why is it important for animals vaccinated against dictycaulus viviparus graze lightly infected pasture?

Answer 70

Vaccinated animals should be exposed to low grade levels of dictyocaulus viviparus infected pasture in order to maintain the first line immune response against the larvae

Question 71

Why should you avoid anthelmintic treatment when vaccinating against dictyocaulus viviparus?

Answer 71

Avoid the use of anthelmintics from 8 weeks before the first vaccine dose until 2 weeks after the second vaccine dose as the dictyocaulus vaccination is an irradiated larval vaccine and if you treat with anthelmintics it will kill the larvae within the vaccine and render it useless