ruminant GI parasites Flashcards
list abomasl worms
- ostertagia ostertagi
- teladorsagia (ostertagia) circumcincta
- haemonchus contortusn
outline the lifecycle nof ostertagia ostertagi
inside the cow:
- L3s migrate through the fore-stomach to the abomasum where they moult into L4s inside the gastric glands
- immature adults (L5s) emerge from the gastric glands (cause of pathology)
- adults produce eggs which begin a new life cycle all over again
what is type 1 ostertagiasis
occurs in calves/yearlings (younger animals) and is caused byOstertagia ostertagiresults from the ingestion of large numbers of L3larvae from herbage.
how will climatic factors influence the outcome of type 1 ostertagiasis
- long and cold winter will decrease the larvae on pasture resulting in less infection rate
- warm and moist spring will enhance the survivial of larvae on pasture, leading to more animals being infected
what is type 2 ostertagiasis
occurs in animals which are old enough to have arrested larvae from previous grazing season
what is the effect of ostertagia ostertagi on the gastric gland
- damage parietal cells = HCl not produced (pH may change from 2.5 to over 5)
- high pH = prevents conversion of pepsinogen to pepsin (protein digestion significantly affected)
- pepsinogen and gastrin detected in increased levels in blood (increased abomasal pH stimulates production of gastrin)
- blood proteins (albumin) increase in abomasum and in some tissues
- bacterial overgrowth in the abomasum also occurs due to alkaline pH
what is the pathology ostertagia ostertagi
- diarrhea may be severe
- rapid weight loss
- sub mandibular edema
- cobblestone lesions as gastric glands are destroyed
discuss immunity to O. ostertagi
- first immune response does not protect against re-infection with L3 (hence repeated re-infection occurs)
- delays larval development, increases the number of inhibited worms (immune-induced hypobiosis) stunts adults, reduce fecundity/less egg production by the worms
- immunity is beleived to be IgA-mediated
- second immune response may take up to 2 years
- reduces number of L3s infecting cattle
- sterile immunity is never observed thus even immune naimals will produce low numbers of nematode eggs
- eosinophils and mast cells increase in intestine (suggests Th2 driven response)
- a stereotypical worm induced Th2 response has not been reported with studies reporting both Th1 and Th2 cytokines
discuss control measures against O. ostertagi
- type 1 (calves): frequent drenching may be required during the first grazing season, especially for animals raised on pasture on which calves have been grazed in the previous season
- type 2 (cows): difficult to treat hypobiosis but drugs such as ivermectin can kill the hypobiotic L4s. in some cases, drenching may be required around calving
- lower stocking density
- separate calves and adults
- rotate onto fresh pasture if possible
haemonchus contotus is also known as
baber’s pole
outline the lifecycle of H. contortus
The life cycle ofHaemonchusis simple. Infective L3 larvae, ingested by the host on pasture, develop into adults in the abomasum and produce eggs (10,000 eggs per gram) that are passed in the feces. The eggs hatch in the feces and undergo two molts, becoming L3 larvae that can migrate up blades of grass in drops of moisture. In proper conditions, it takes only 3-4 days for an egg deposited in feces to develop to the L3 stage. Depending on temperature and moisture, L3 larvae can survive on pasture up to 6 months. Adult worms only survive several months in the host. The prepatent period forH. contortusis 15-21 days in sheep, and peracute infections can result in death before eggs are present in the feces.
what happens inside the sheep in a H. contortus infection
- anemia sue to feeding worms can be very severe
- if the worm burden is very high, the removal of blood may overtake eythropoesis and this may cause death
- diarrhea, loss of body condition (weight gain in lambs) and wool quality
- TH2 immunity = increased eosinophils, mast cells, IgA, IgE, IgG, IL-4, IL-5 and IL-13
how is haemonchiasis and ostertagiasis diagnosed
- McMaster slide is used to count eggs
- Famacha chart (and/or PCV) may be used to assess extent of anemia in lambs infected with haemonchus
- adults on necropsy
- condition of abomasum (cobblestone effect for ostertagia, red haemorrhagic surface may be seen in sheep infected with haemonchus)
list common species of nematodirus spp.
- N. battus (sheep and calves)
- N. fillicolis (sheep)
- N. spathiger (sheep)
- N. helvetianus (cattle)
outline the nematodiris lifecycle
what makes N. Battus a unique trichostrongyle
- pre-parasitic phase (L1-L3) occurs within egg shell
- eggs extremely tough and resistant to freezing and drought, viable up to 2 years on pasture
- hatching is stimulated by cold period followed by a mean day/night temp of 10 degrees but L3 are susceptible to climcate and need to be ingested quickly. thus this is usually the first species to peak on pasture in spring
- large number of larvae simultaneously burrowing into the gut cause the pathology (disease is caused by larvae and not adult)
Is N. battus hatching only occur from eggs excreted in previous year?
No, some eggs deposited in spring can hatch in autumn of the same year causing contamination of pasture at this time.
why is N. battus of special significance to lambs in the UK
- acute onset in young recently weaned lambs (6weeks to 4 months)
- rapid weight loss, watery diarrhea and dehydration
- sudden death (disease usually first reported in may/june
discuss immunity to N. battus
- strong age related immunity (immunity occurs after about 3-4 months of age)
- increased eosinphils and mast cells at site of infection
- nematode specific IgA and serum IgG
- villus shedding is important rejection mechanism when infected with species which are closely associated with villi
outline the life cycle of oesophagostomum
discuss O. radiatum infection
- in young calves: cause severe disease. adult worms can cause anorexia, anemia and edema. very dark diarrhea, weight loss (death. immunity quickly built up
- in older animals: strong protective immunity causes nodule formation. nodules (granulomas) calcify and in very severe infections may cause intestinal intussusception which may lead to stenosis
