PARASITOLOGY - Bovine Nematodes Flashcards
What is the pre-patent period (PPP)?
The pre-patent period (PPP) is the time taken between initial infection of a helminth and the production of eggs by the adult worms
What is parasitic gastroenteritis (PGE)?
Parasitic gastroenteritis (PGE) is the condition caused by co-infection of gastrointestinal nematodes which reside in the gastrointestinal tract of ruminant hosts
What is the typical signalement for parasitic gastroenteritis (PGE)?
Young cattle in their first grazing season
What are the two most significant nematodes which cause parasitic gastroenteritis (PGE) in cattle?
Ostertagia ostertagi
Cooperia oncophora
Where is ostertagia ostertagi found within the ovine gastrointestinal tract?
Ostertagia ostertagi is found within the abomasum
What is the lifecycle of ostertagia ostertagi?
- Adult worms breed and the female worms produce eggs
- Eggs are excreted in the host faeces into the environment
- Eggs develop into L3 larvae on pasture within the L2 cuticle
- L3 are ingested by cattle on pasture
- L3 exsheath and penetrate the abomasal glands and develop into L4 larvae
- L4 larvae rupture the abomasal glands and emerge into the abomasal lumen and develop into adult worms
What is hypobiosis?
Infective ostertagia ostertagi larvae ingested towards the end of the gazing 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)
Describe the pathogenesis of ostertagia ostertagi
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
What is type I ostertagiosis?
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
What is type II ostertagiosis?
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)
How can type II ostertagiosis be prevented?
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
Which important history question should you ask when trying to determine the cause of scour in housed calves and yearlings?
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
What are the clinical signs of clinical ostertagia ostertagi?
Reduced feed intake
Poor growth rate
Ill thrift
Profuse, green, watery scour
(T/F) Subclinical parasitic gastroenteritis (PGE) is much more common compared to clinical parasitic gastroenteritis (PGE)
TRUE. Though clinical parasitic gastroenteritis is not uncommon in young cattle, by far the most common expression is subclinical infections
What are the consequences of subclinical parasitic gastroenteritis (PGE) in first season grazing calves?
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
What are the consequences of subclinical parasitic gastroenteritis (PGE) in second grazing season cattle (yearlings)?
Subclinical parasitic gastroenteritis (PGE) in yearlings 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
What are the consequences of subclinical parasitic gastroenteritis (PGE) in adult beef cattle?
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 beed suckler calves
What are the consequences of subclinical parasitic gastroenteritis (PGE) in adult dairy cattle?
Subclinical parasitic gastroenteritis can result is reduced fertility and milk yield in adult dairy cattle
When do cattle develop immunity to gastrointestinal nematodes?
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
What are the features of bovine host immunity to gastrointestinal nematodes?
Decreased fecundity (decreased egg production)
Stunting nematode growth
Expulsion of adult nematodes
Limits establishment of infective larvae in the gastrointestinal tract
(T/F) When cattle develop immunity against gastrointestinal nematodes, nematode eggs are no longer excreted in the faeces
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
How do environmental factors influence gastrointestinal nematode larval challenge on pasture?
The development time of gastrointestinal nematodes from egg to L3 larvae on pasture can range from three weeks to three 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, any other factors which can disturb the faeces and distribute the larvae - such as harrowing - will increase the larval challenge on pasture
How long do gastrointestinal nematode larvae survive on pasture?
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)
What is a typical grazing season?
A typical grazing season is from April to October
Describe the epidemiology of parasitic gastroenteritis (PGE) in weaned dairy cows in their first grazing season
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, were they will ingest overwintered larvae immediately once they start to graze. Following this 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 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 larvae challenge peaking around July to September
Describe the epidemiology of parasitic gastroenteritis (PGE) in beef suckler cows in their first grazing season
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 gass becomes a significant part 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 developed immunity. As the grazing season continues, the calf egg output will begin to increase, increasing pasture larval challenge
Which techniques can be used to monitor and diagnose parasitic gastroenteritis (PGE) in cattle?
Monitor daily liveweight gain
Faecal egg counts
Serum pepsinogen
Post mortem (PM)
What are the benefits and limitations of monitoring daily liveweight gain to monitor for parasitic gastroenteritis (PGE)?
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
What the benefits of faecal egg counts for parasitic gastroenteritis (PGE)?
Cheap
Easy
Good indicator of pasture contamination
Can be used to demonstrate anthelmintic efficacy
Can be used to determine pattern of infection on individual farms
Faecal egg count reduction tests (FECRT)
What are the limitations of faecal egg counts for parasitic gastroenteritis (PGE)?
Requires training
Not representative of total worm burden
What are the limitations of measuring serum pepsinogen levels?
Expensive
Delayed results as has to be sent to the lab
What is the aim of integrated parasite control?
The aim of integrated parasite control is to reduce the use of and reliance on anthelmintic treatment to control parasites
How is integrated parasite control achieved?
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
What is the main objective for the control of parasitic gastroenteritis (PGE)?
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
Which grazing management methods can be used to control parasitic gastroenteritis (PGE)?
Graze on newly sown grass fields
Graze on silage/hay aftermath
Mixed livestock grazing
Multispecies swards
Rotational grazing
Deferred grazing
What are the benefits of mixed livestock grazing for controlling parasitic gastroenteritis (PGE)?
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)
What are multispecies swards?
Multispecies swards is pasture consisting of multiple plant species
What are the three groups of anthelmintics available for parasitic gastroenteritis (PGE) in cattle?
White drenches (Benzimidazoles)
Yellow drenches (Levamisole)
Clear drenches (Macrocyclic lactones)
Why are clear drenches (Macrocyclic lactones) most commonly used on farms?
Clear drenches have high levels of efficacy against a broad spectrum of nematodes and arthropods, persistent activity and ease of administration
What is the main disadvantage of clear drenches (Macrocyclic lactones) on farms?
Macrocyclic lactones have persistent activity which increases the risk of anthelmintic resistance
What should you always do before advising farmers on which anthelmintic treatment to use?
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
What is targeted selective treatment (TST) with anthelmintics?
Targeted selective treatment (TST) is treatment of individual animals with anthelmintics when monitoring daily liveweight gain indicates subclinical infection and loss of performance
When is targeted selective treatment (TST) indicated?
Targeted selective treatment (TST) is indicated if the daily liveweight gain is less than 0.75kg per day
What is strategic anthelmintic treatment
Strategic anthelmintic treatment is the treatment of groups of animals during housing or early in the grazing season to limit pasture contamination with eggs and hence reduce the risk of parasitism
What is tactical anthelmintic treatment?
Tactical anthelmintic treatment is the treatment of groups of animals in anticipation of a decline in performance
What is therapeutic anthelmintic treatment?
Therapeutic anthelmintic treatment is anthelmintic treatment of individual, clinically affected animals
What is the most significant lung worm found in cattle?
Dictyocaulus viviparus
What is the other name used to describe dictyocaulus viviparus?
Husk
Describe the lifecycle of dictyocaulus viviparus
- L3 larvae are ingested by host
- L3 larvae penetrate the intestinal mucosa and travel to the mesenteric lymph nodes where they moult into L4 larvae
- L4 larvae travel via the blood and lymphatics to the bronchioles where they moult into young adults
- Young adults migrate to the bronchi where they moult into mature adults and produce eggs
- L1 larvae hatch from the eggs and migrate to the lungs and up the trachea where they are coughed up and swallowed
- L1 are shed in the faeces
- L2 and L3 develop in the faeces
Which signalement is typically affected by dictyocaulus viviparus?
Dictyocaulus viviparus typically has a clinical effect on first grazing season weaned calves
What are the clinical signs of dictyocaulus viviparus?
Frequent coughing
Tachypnoea
Depression
What are the effects of subclinical dictyocaulius viviparus?
Poor perfromance and growth rates
Provides carrier animals
What are the sources of infective dictyocaulus viviparus larvae at turnout to pasture?
Overwintered larvae
Adult carrier animals
How do environmental factors influence dictyocaulus viviparus larval challenge on pasture?
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
What is the first line of acquired immunity against dictyocaulus viviparus?
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
How is the first line of immunity against dictyocaulus viviparus acquired?
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
How long does the first line of immunity agaisnt dictyocaulus viviparus last?
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
What is the second line of acquired immunity against dictyocaulus viviparus?
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
How long does the second line of immunity agaisnt dictyocaulus viviparus last?
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
What is re-infection syndrome?
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 immuniopathological changes in the respiratory tract which can present similarly to clinical dictyocaulus viviparus
What causes dictyocaulosis in adult cattle?
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
How can you monitor and diagnose dictyocaulus viviparus?
Monitor young cattle for clinical signs
Monitor daily liveweight gain
Faecal larval counts
Bronchoalveolar lavage (BAL)
Post mortem (PM)
What is a contraindication to bronchoalveolar lavage (BAL) to diagnose dictyocaulus viviparus?
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
Which methods can be used to control dictyocaulus viviparus?
Anthelmintics
Grazing management
Vaccination
What is the recommended vaccination protocol for dictyocaulus viviparus?
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
Why is it important to animals vaccinated against dictycaulus viviparus graze lightly infected pasture?
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
Why should you avoid anthelmintic treatment when vaccinating against dictyocaulus viviparus?
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
