12144861
Description
Flashcards by Louise Mason, updated more than 1 year ago
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Created by Louise Mason
over 6 years ago
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| Question | Answer |
| What are some key features of the body structure of a bursate nematode? | mouth and tubular gut stoma at head end chitinous body wall tubular digestive tract |
| What are the key features of female bursate nematodes? | tail annules (ring around base of tail) anus |
| What are the key features of a male bursate nematode? | copulatory bursa three-pronged spicules |
| What is characteristic of the Trichostrongyloidea superfamily? | small buccal capsule direct life cycle |
| Of what animals are the Trichostrongyloidea parasites most important? | ruminants |
| Where in the body are Trichostrongyloidea mostly parasitic? | in the gut |
| What roundworm and member of the Trichostrongyloidea superfamily is most common in cows? | Ostertagia ostertagi |
| In adults, where is Ostertagia ostertagi found? | within the surface abomasal mucosa |
| What is the appearance of Ostertagia ostertagi? | slender red-brown about 1 cm long |
| What type of life cycle does Ostertagia ostertagi have? | direct life cycle |
| What is the definitive host in the Ostertagia Ostertagi life cycle? | adult cows |
| Describe the life cycle of Ostertagia Ostertagi | eggs shed in faeces hatch and develop to L3 L3 migrate onto grass L3 ingested by host with feeding L3 exsheaths in rumen and develops to adult in abomasal gland adults emerges after 18 days |
| What is the pathogenesis of Ostertagia ostertagi with regards to the gastric gland? | reduction in gastric gland mass replacement of parietal cells with rapidly proliferating and poorly differentiated cells |
| What is the pathogenesis of Ostertagia ostertagi with regards to pH? | HCl production is reduced pH rises pepsinogen not cleaved to pepsin protein not digested bacteria not killed |
| What is the pathogenesis of Ostertagia ostertagi with regards to gastric mucosa? | mucosa becomes thickened and hyperplastic cell junctions do not fully form protein moves from blood to lumen pepsinogen moves from lumen to blood |
| How are the cell junctions described under Ostertagia ostertagi pathogenesis? | 'leaky' cell junctions (movement of proteins out of cells) |
| What are the clinical signs of an infection with Ostertagia ostertagi? | diarrhoea anorexia weight loss submandibular oedema death |
| What is the cause of the majority of clinical signs associated with Ostertagia ostertagi? | the loss of protein from cells into the lumen |
| What are low levels of parasitic infection characterised by? | sub-clinical disease (poor weight gain and production loss) |
| How is Ostertagia ostertagi diagnosed? | clinical and sub-clinical signs season and grazing history faecal egg counts plasma pepsinogen |
| What is hypobiosis? | arrested development of larvae at early L4 stage |
| Why do some parasites undergo hypobiosis? | useful life cycle adaptation to ensure persistence through colder winter months |
| When do larvae emerge from hypobiosis? | late winter/early spring |
| Why is hypobiosis such a problem? | causes acute onset of severe disease |
| What type of infection does hypobiosis cause with regards to Ostertagia ostertagi? | type 2 ostertagiosis |
| What causes hypobiosis with Ostertagia ostertagi? | immunity of calves cold conditions of L3 photperiod? innate arrest? |
| What is the treatment for an Ostertagia ostertagi infection? | anthelmintic treatment |
| What should be done to control parasitic infections? | prevention encourage herd immunity reduce opportunity for build up of high burdens |
| What stages of Ostertagia ostertagi occur in the host? | L4 larvae adult |
| What stages of Ostertagia ostertagi occur in the faeces? | embryonated eggs L1, L2 |
| What stage of Ostertagia ostertagi occurs on pasture? | L3 |
| How does Ostertagiosis epidemiology affect infection? | larvae build up on pasture over winter ingested at spring turnout infections cycle |
| When is Ostertagiosis most commonly seen and why? | late summer as the pathology is related to burden and so the burden gradually increase over spring and summer grazing |
| What is Type 1 Ostertagiosis? | affects calves in first grazing season ingestion of large number of infective L3 increasing burden disease from mid-July in UK |
| What is Type 2 Ostertagiosis? | affects yearlings late winter/spring following first grazing maturation of larvae from hypobiosis year before |
| What is the pathogenesis of Type 1 Ostertagiosis? | high morbidity low mortality diarrhoea poor weight gain high egg counts |
| What is the pathogenesis of Type 2 Ostertagiosis? | low morbidity high mortality hypoalbuminaemia anaemia and weight loss low egg counts |
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