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68 Cards in this Set
- Front
- Back
Parasitic gastroenteritis (PGE) accounts for ____% of all digestive tract disease reports in sheep. |
53% |
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Parasitic Gastroenteritis (PGE) |
Term for disease caused by parasitic nematodes in GIT. * Disease of grazing livestock * Predominantly in young stock; adults generally acquire immunity * Often caused by mixed parasitic infection |
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What are the top three most important disease syndromes caused by sheep GI nematodes in the UK? |
1. Parasitic gastroenteritis (PGE) - Ostertagia Teladorsagia (equivalent of ostertagi in cattle) 2. Nematodirus battus - significant with lamb populations 3. Haemonchosis |
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Major contributing factors to the increasing trends of PGE, nematodirus & haemonchus contortus infections of ovine in the UK? |
1. Anthelmintic resistance - Most resistance Benzimidazole > Levamisole > Ivermectins (macrocyclic lactones) 2. Climate change |
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What are the three main parasites of the ovine abomasum? |
1. Ostertagia teladorsagia 2. Haemonchus 3. Trichostrongylus
* All from TRICHOSTRONGYLOIDEA superfamily.
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What are the three main parasites of the ovine small intestine? |
1. Cooperia 2. Nematodirus 3. Trichostrongylus ^ TRICHOSTRONGYLOIDEA superfamily ^
Others: Bunostomum & Strongyloides |
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What is the most important superfamily of nematode pathogens in grazing ruminant? |
TRICHOSTRONGYLOIDEA |
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Typical life cycle of trichostrongyloidea? Infective stage? PPP? |
LIFE CYCLE: Direct INFECTIVE STAGE: L3 PPP: Short, ~21 days |
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What is the equivalent of ostertagia ostertagi of cattle found in ovine? |
TELADORSAGIA CIRCUMCINCTA * Similar life cycle, PPP, infective stage & hypobiosis of L4 |
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Life cycle of Teladorsagai circumcincta? |
Similar to that of ostertagia ostertagi (in cattle): - Adults in abomasum reproduce & eggs released in feces - Eggs hatch in feces & moult to the infective L3 stage - Once ingested penetrate the abomasal gland & moult to L4 stage - L4s may either enter hypobiosis (arrested state in tissue) or become reproductive adults in abomasum (~d18) & perpetuate the cycle. |
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Of the two types of ostertagiosis in ovine, which is most common? |
Type I Ostertagiosis - MOST COMMON; buildup of larvae in the Summer, which are ingested by newborn lambs & disease signs are seen in the Autumn
Type II = NOT COMMON |
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Clinical signs of Ovine ostertagiosis (teladorsagiosis)? |
1. Weight loss/failure to gain weight 2. Intermittent diarrhea (less dramatic than in cattle) 3. Appetite loss |
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Pathology of teladorsagia circumcincta (ovine ostertagiosis)? |
1. Rupture of intracellular junctions of abomasum 2. Destruction of parietal cells = reduced HCl production 3. Increased abomasal pH (2 ->7) = elevated plasma pepsinogen (inability to convert to pepsin due to lower pH 4. Bacterial overgrowth |
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Diagnosis of teladorsagia circumcincta? |
1. Observation of clinical signs (predominantly in lambs) 2. Monitoring time of year (grazing & anthelmintic history) 3. FEC 4. PM |
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Epidemiology of teladorsagia circumcincta? |
TYPE I = Sept - Nov infections very high due to Spring born lambs feeding on highly contaminated Summer pasture |
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Worm burdens and FEC low in adult ewes, except during ____________________________. |
PERIPARTURIENT PERIOD - Approx 2 weeks before to 6 weeks after lambing |
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Higher worm burdens in ewes during periparturient period (2 wks before to 6 wks after lambing) is due to: |
1. Increased establishment of overwintered larvae acquired from pasture 2. Inhibited L4s within tissue reactivating & developing to adults 3. Female worms have increased fecundity due to plumpness of pregnant ewes |
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What is the main difference in epidemiology between bovine and ovine ostertagiosis? |
Ewes are the main source of egg contamination to pasture, shedding large amounts during their periparturient period (Spring months: Feb-April) - Lambs are then exposed to these freshly excreted eggs along with overwintered larvae during Summer months, resulting in large amounts of infective L3 on pasture from about late-July to Oct |
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Control methods of ovine ostertagiosis (teladorsagia circumcincta)? |
1. NOT GRAZING HEAVILY-INFESTED PASTURE with susceptible lambs * Rotate pastures 2. Anthelmintic treatment of ewes & lambs! * Resistance is a major problem |
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What is the largest parasite in the abomasum of the sheep? |
HAEMONCHUS CONTORTUS "Barber's pole worm"
Blood sucking worm, which causes haemorrhagic anemia (>5000 adult worms can have very serious if not fatal effects) |
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Extremely pathogenic nematode (poor immunity) that is of major concern in tropical climates, but causes only sporadic disease in temperate climates. - Anthelmintic resistance common - "Model parasite" for research |
HAEMONCHUS CONTORTUS |
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Life cycle of Haemonchus contortus? |
Typical trichostrongylid: - Within feces, eggs moult to infective L3 stage (2-12 weeks depending on climate) - Infective L3s ingested from contaminated pasture into host (ruminants) - Continue development within host to adults who live within the abomasum, suck blood & reproduce |
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Sheep may develop complete immunity to Haemonchus contortus.
True or False? |
FALSE - Ewes remain susceptible to disease |
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Pathogenesis of ovine haemonchosis can be broken into three different categories. What are they & list clinical signs? |
1. Hyperacute Haemonchosis (up to 30,000 adults) - Sudden death due to severe haemorrhagic gastritis 2. Acute Haemonchosis (2,000-20,000 adults) - Clinical signs seen ~2 weeks post-infection - Regenerative anemia followed by non-regenerative if not treated - Submandibular edema, ascites (fluid build-up) dark feces (blood loss), dropping wool, inappetance 3. Chronic Haemonchosis (several hundred) - Weight loss, weakness & inappetance - Anemia absent or slight |
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Bottle jaw is a clinical sign of nematodes that effect the abomasum.
True or False? |
TRUE = submandibular edema! |
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Diagnosis of Haemonchosis? |
1. Observation of clinical signs - Anemia = pale mucous membranes - Ewes & lambs both affected - Predominantly, dense lowland flocks 2. FEC (Fecal egg counts); very fecund! - Typical trichostrongyle egg - 1,000-20,000 epg 3. Post-mortem - Large, 2-3cm worms on lumenal surface of abomasum; appear dark brown |
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FAMACHA? |
System for assessing clinical anemia, based on conjunctiva color of the eye. - Used to decide which animals in a flock to treat - Increasingly used in tropical countries - Five different levels: 1-2 (no dose), 3 (borderline), 4-5 (dose!) |
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Epidemiology of haemonchus contortus? |
Best adapted to warm climates, as larval development in environment requires high temps & humidity. Epidemiology varies depending on region: 1. Tropical with little/no dry season (E. Africa) - High burden year round = year round anthelmintic usage - High worm fecundity - # of L3s on pasture dependent on rainfall 2. Tropical with severe dry season (AU, Brazil) - L3 don't survive dry season - High levels of inhibited larval development; parasite survives predominantly in host - Disease outbreaks at start of wet season due to reactivation of inhibited L4s & rapid inc in pasture L3s 3. Temperate (UK, W Europe) - Inhibited L4s reactivate in Spring, leading to pasture contamination of infective L3s in Summer (May-Aug) - Lambs ingest these Summer L3s & lead to outbreaks in Autumn (Sept-Nov) - Almost 100% of larvae ingested in October-on will become arrested in tissue until following Spring. |
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Nematodes of sheep small intestine? |
Trichostrongyloidea (superfamily): 1. Nematodirus 2. Trichostrongylus 3. Cooperia
Strongyloidea Bunostomum |
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"Cotton wool worm" - Major cause of specific syndrome in lambs in the UK - Epidemiology different to other causes of PGE (Spring) |
NEMATODIRUS BATTUS |
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Life cycle of NEMATODIRUS BATTUS? |
Similar to that of other trichostonglyoidea species as far as egg excretion in feces & ingestion of infective L3s from pasture. BUT MAJOR DIFFERENCE: - L1-L3 development within the environment occurs WITHIN THE EGG, then larvae remains inactive while overwintering for 8-9 months before hatching in the SPRING and being ingested. |
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Describe the very specific hatching requirements of nematodirus battus, which make this trichostrongyliodea parasite life cycle different from the rest. |
Requires prolonged period of chill followed by a mean day/night temperature of 10C |
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Lambs more than _______ of age are non-permissive hosts of nematodirus battus. |
>3 months of age
* Ewes very resistant to infection; no periparturient rise unlike in telodarsagia circumcincta * Resistance is physiological & not due to acquired immunity |
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Lambs between the age of ____________________ are susceptible to nematodirus battus. |
between 3 weeks - 3 months * Lambs don't graze significantly during first few weeks of life & after 3 months have acquired physiological resistance. * For disease to occur emergence of L3s must coincide with presence of susceptible lambs |
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Pre-Patent Period (PPP) of nematidorus battus? |
TWO WEEKS (very short) |
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During what time of the year are nematodirosis diagnoses highest in the UK? |
Summer months * Scotland = May-July * Wales/SW England = April-July |
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Ewes play little role in epidemiology of nematodirus battus.
True or False? |
FALSE - Ewes develop age resistance; "lamb-to-lamb" disease * Large #s of L3s hatch in Spring from eggs passed onto pasture from last years lambs * Unlike, telodarsagia circumcincta where ewes experience periparturient rise in fecal egg release, contributing massively to epidemiology. |
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Risk of outbreaks of nematodirus battus varies from year to year on particular farms depending on __________ & ______________. |
CLIMATE & LAMBING PERIOD |
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______________ are permissive hosts of Nematodirus battus. |
CATTLE - particularly young calves; disease occasionally occurs in calves * Consideration in rotational grazing |
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Pathogenesis of nematodirus battus? |
- Pathology largely due to larval stages, which cause severe disruption of SI mucosa - Most damage = 10-12d post-infection (L4-adult moult * Can be severe if L4s reactivated at same time as newly acquired L3s moult. - Results in enteritis & villus atrophy |
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Clinical signs of nematodirus battus? |
RAPID ONSET (10-12 days) - Profuse diarrhea - Dehydration (increased thirst) - Lambs severely affected & can die quite rapidly if arrested L4s reactivated at same time as newly acquired moulting L3s.
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Diagnosis of nematodirus battus? |
1. Grazing history 2. Clinical signs (profuse diarrhea, dehydration, inc thirst) 3. PM - cotton wool worms in SI * Fecal egg counts not reliable since pathology often due to larvae |
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Control of nematodirus battus? |
ROTATIONAL GRAZING - Avoid grazing ewes & lambs on pasture used for lambs the previous year (ideally previous two years) |
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What is distinctive of the nematodirus battus egg compared to the teladorsagia & other trichostrongyloidea species? |
Distinctive parallel sides with several blastomeres observed within. - LARGER |
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What are the three main trichostrongylus species of parasites found in ovine SI? |
TRICHOSTRONGYLUS: 1. vitrinus (black scour worms) = sheep & goats 2. capricola = sheep & goats 3. colubriformis = all ruminants |
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Commonly contributes to PGE in lambs in Autumn/early Winter, resulting in dark, foul smelling, mucousy feces. - Causes chronic wasting disease in hoggs & ewes in early Winter - Poor skeletal growth & wool quality |
Trichostrongylosis |
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Epidemiology of trichostrongylus vitrinus is similar to that of T. circumcinta, except tends to occur _________ in grazing season. |
LATER (Sept-Dec/Jan) |
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Pathology of Trichostrongylosis? |
Larvae & adults burrow beneath the surface epithelium resulting in: - Enteritis - Mucous & mucousal hypertrophy - Lamina propria infiltrated with inflammatory cells - Villi shortened/atrophy - Lesions become more localized as resistance develops = "finger-print" lesions |
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Cooperia curticei infects the ___________ of sheep, is not very pathogenic, but is a _______________ species, meaning it requires increased amounts of anthelmintics & underdosing can commonly lead to resistance. |
SMALL INTESTINES
DOSE-LIMITING SPECIES |
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Life cycle of cooperia curticei? |
Typical trichostrongyloidea life cycle! - Eggs shed in feces - Moult to infective L3 stage - Ingested by host - Moult to adults in host & reproduce |
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Small intestinal parasite with large bursa that grow to be ~1 cm and have "watch spring" appearance. - Not very pathogenic - Dose-limiting species
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COOPERIA CURTICEI |
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Sheep & goat hookworm found in the SI - Superfamily Strongyloidea - Adults 1-3 cm w/ hooked anterior end & cutting plates which bite off chunks of tissue & feed on blood - PPP = 1-2 months |
BUNOSTOMUM TRIGONOCEPHALUM |
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Life cycle of BUNOSTOMUM TRIGONOCEPHALUM? |
Typical hookworm life cycle: - Eggs released in feces - Infective L3s picked up either percutaneous route with pulmonary migration or orally (ingested) |
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Nematodes of the sheep LI? |
STRONGYLOIDEAs: 1. Chabertia ovina = large-mouthed bowel worm 2. Oesophagostomum spp TRICHUROIDEA: 1. Trichuris ovis |
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Large-mouthed bowel worm of LI -1.5-2cm with large buccal capsule - No cutting plates, but removes chunks of mucosa - Common in temperate regions, but disease important during warmer, Winter rainfall areas (AU & S. Africa) - Low levels of infection - Contributes to PGE |
CHABERTIA OVINA (Strongyloidea) |
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Life cycle of Chabertia ovina? |
1. Adults in colon release eggs into feces 2. Eggs moult to infective L3 stage 3. L3s ingested & enter SI or LI mucosa 4. Moult to L4 at ~1 week 5. L4s may either emerge & migrate to cecum and eventually colon or arrest until environmental conditions are ideal |
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Pathogenesis of chabertia ovina? |
CONTRIBUTES TO PGE (parasitic gastroenteritis)! - Mucosal damage - Hemorrhage - Protein losing enteropathy - Diarrhea - +/- anemia * 200-300 worms cause disease! |
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What are the oesophagostomum species commonly found in sheep? |
1. Oesophagostomum columbianum = nodule formation 2. O. venulosum = no nodule formation |
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Large bowel worm whose L3 migrates into the tissue triggering an immune response by the host & causing nodules. |
Oesophagostomum columbianum |
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Clinical signs associated with oesophagostomum species? |
Diarrhea & weight loss * Clinical signs unusual in UK. |
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What are the top three ovine PGE contributors in the UK? |
1. Telodorsagia circumcincta = Abomasum 2. Trichostrongylus vitrinus = abomasum & SI 3. Nematodirus battus = SI of Spring lambs! |
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__________ intestine ovine parasites are typically present in small numbers. |
LARGE intestine parasites present in small numbers. |
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Goats generally have problems with the same parasites that infect sheep, but goats are _______ susceptible. Why? |
MORE - Because goats are naturally browsing animals, which are often forced to graze. So less adapted/immune than sheep to grazing parasites. |
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How does anthelmintic treatment for goats differ from that of sheep? |
Control more difficult for goats - Anthelmintics used on ALL AGE GROUPS & often MOST OF THE YEAR. - Pharmacokinetics differ; Goats require 2X the dosage (underdosing common) - Resistance develops much more quickly. |
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Fecal egg counts and adult worm burdens have a linear relationship.
True or False? |
FALSE - NOT LINEAR; too many varying factors per individual, such as: - # of adult parasites present - level of host immunity - age - species of parasite - stage of infection - consistency of feces |
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Give two examples of disease syndromes which are caused by pre-patent parasites (before eggs are present in feces): |
1. Type II Ostertagiosis in Cattle 2. Nematodrus battus |
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What are two major guidelines for accurate FEC samplings? |
1. Sample sufficient number of animals per group - At least 10 animals for large groups - All in small groups 2. Sample from a mixture of severely affected, moderately affected & clinically normal animals. |
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FEC general rules of thumb for diagnosis for: 1. Teladorsagia/ostertagia 2. Haemonchosis 3. Nematodirus |
1. Teladorsagia: - 200 epg = burden to sufficient - 200-1000 epg = mild/moderate clinical signs - >1000 epg = HEAVY BURDEN 2. Haemonchosis - 1000-2000 epg often seen 3. Nematodirus - FEC often low or even -ve with significant worm burdens |