Small Ruminant Parasitology - Text PDF

Small Ruminant Parasitology - Text Sunday, November 17, 2024 6:51 PM Tail up = Goat Tail down = Sheep Parasitic Gastrointestinal Disease of Small Ruminants Objectives After this lecture, students enrolled in VCS 861, will be able to: 1. Employ the best strategies to deworm small ruminants 2. Su...

Small Ruminant Parasitology - Text Sunday, November 17, 2024 6:51 PM Tail up = Goat Tail down = Sheep Parasitic Gastrointestinal Disease of Small Ruminants Objectives After this lecture, students enrolled in VCS 861, will be able to: 1. Employ the best strategies to deworm small ruminants 2. Summarize pathology associated with most common gastrointestinal parasites 3. Develop an appropriate diagnostic and treatment plan for gastrointestinal parasites Gastrointestinal Nematodes of Small Ruminants Haemonchus contortus Telodorsagia circumcinta Trichostrongylus axei Nematodirus spp Cooperia spp Abomasal Nematodes Abomasal worms are most pathogenic: Haemonchus contortus (haemonchosis) Telodorsagia circumcincta (formerly Ostertagia) Gastrointestinal Nematode Infections Most susceptible: Young Periparturient ○ Fecal egg counts often go up during last month of gestation Immuno-compromised Resistance Veterinarians and producers must customize and implement integrative deworming programs to control exposure to infection and reduce the use of anthelmintics. Life Cycle Pre-patent Period: 3 weeks (ingestion of larvae – fecal excretion of eggs) Egg → Larvae: Summer: 4-10 days Winter: 1-2 months ○ Can survive for longer until environment is more favorable Epizootiology Life cycle of each GIN has 4 phases: 1. Symbiotic/Parasitic 2. Contamination 3. Free-living 4. Infection 1. Symbiotic/Parasitic Phase Organism must survive within host Host defense: ○ Immune system Immune system dependent upon: ○ Age  ○ Nutritional status ○ Stress Hypobiosis: ○ Arrested development 2. Contamination Hallmark: ○ Eggs passed in feces Factors affecting the magnitude of contamination: ○ Stocking rate  Primary factor that leads to contamination ○ Age ○ Periparturient*  Elevated egg count ○ Season ○ Hypobiosis 3. Free-Living Phase Larval development & survival L1 ➔ L2 ➔ L3 occurs in fecal mass L1 & L2 unprotected: ○ Need O2 ○ Need moisture L3 have protective shell: ○ Moisture resistant ○ Temperature adversely affects growth Haemonchus contortus (Haemonchosis) “Barber pole” worm ○ Coiling of white ovaries around blood-filled intestine ○ Can consume 0.05mL of blood a day ○ At peak infection can consume 1/5 of an animals blood volume a day  Susceptible species: ○ ALL ruminants ○ goat > sheep > cow H. contortus - Pathogenesis / Infestation Adults and L4 attach to abomasal mucosa ○ Consume a blood meal Pathogenic effect from: ○ Blood loss – anemia ○ Abomasitis (mild) – impaired nutrient digestion H. contortus Clinical Signs 1° reflect anemia: ○ Lethargy ○ Peripheral edema  Under jaw ○ Pale mucous membranes  At arrow extremely pale  ○ Diarrhea????  Do not rule out if no diarrhea Ostertagia / Telodorsagia Species: Cattle, South American Camelids ○ Ostertagia ostertagi: cattle, South American Camelids Sheep & Goats: ○ Telodorsagia circumcincta ○ Ostertagia trifurcata Abomasal worm Pathogenic effect ----> SEVERE abomasitis Impaired nutrient digestion Sheep and Goats Pathogenesis Two types – I & II Type 1: ANOREXIA  ○ BOTTOM LINE - Type 1 characterized by the parasite completing entire life cycle, with diseased animal showing heavy fecal egg counts ○ “Moroccan Leather” Nodular Abomasitis Type II ○ Identical to Type I until L4 enters parietal cell  Receive “Hold-Up” signal from environment □ Northern US/Canada: Late fall early winter □ Southern US/Tropics: Summer  Improved weather = L4 emergence from hypobiosis □ Northern US/Canada: Spring □ Southern US/Tropics: Fall ○ Pathology = ABOMASITIS ○ Pathogenesis  Type II – Simultaneous emergence of large numbers of hypobiotic L4’s ○ BOTTOM LINE - Abomasitis occurs before egg production by adult worms…NO EGGS in fecal. Clinical signs: Neg fecal, High  serum pepsinogen, Abomasal pH alkaline Important Intestinal Nematodes Just here for reference CANOT or NO CAT Cooperia Ascaris sp Nematodirus Oesophagostomum Trichuris Important Intestinal Worms Cooperia: Most common intestinal worm of cattle. Erosive mucosal lesions within small intestine Ascaris: “Traveling worm” Intestine -> Liver -> Lungs -> Intestine. Focal scarring in liver “white spots”. 2nd bronchitis and bacterial pneumonia Nematodirus: Common in confined camelids. Resistant to ivermectin Oesophagostomum: Large intestine. Nodular abscess formation within large intestinal wall Trichuris: Whipworms. Bloody diarrhea ddx swine dysentery. Emaciation. Pigs on dirt lots Nematodes: Basics of Treatment Anthelmintic therapy Blood or plasma transfusion Iron/B-vitamin supplementation TLC: Low competition environment High quality nutrition Class MOA Other Info Here for Reference Imidazothiazole / tetrahydropyrimidine ○ Levamisole ○ Morantel, Pyrantel ○ Neuromuscular depolarization and paralysis of the parasite ○ Only dewormer that worms can re-gain sensitivity if discontinued for several years ○ Cholinergic agonists ○ Not effective against larval stages Macrocyclic Lactones ○ Avermectins / Milbemycins ○ Ivermectin ○ Doramectin ○ Moxidectin ○ Increase permeability of parasite cell membranes to CL- ○ Ineffective against flukes and tapes Benzimidazoles ○ Fenbendazole ○ Albendazole ○ Oxbendazole ○ Impair worm carbohydrate metabolism ○ Inhibit fumarate reductase ○ BROADSPECTRUM ○ Fenbendazole - can increase dosage 2-3X up to 10X for hypobiotic  larvae ○ Albendazole - DO NOT give during 1st 1/3 gestation Why Don’t Dewormers Work? 1. Resistance 2. Inappropriate dose ○ Very few products that have small ruminant dose ○ Small ruminants metabolize drugs much faster than other species 3. Treating the wrong parasite Four Types of Dewormers Who to Deworm? Principles for Anthelmintic Use Ensure that the correct dose is being used ○ Goats metabolize drugs differently and require higher doses Use oral anthelmintics Withhold feed for 12-24 ○ Benzimidazoles and/or ivermectin ○ Increases contact time due to decreased GI transit time Use a combination of anthelmintics Avoid long acting dewormers (Longrange) DO NOT treat all animals Recommendations from Dr. Lisa Williamson (full article “Choosing the right drug for worm control” can be found on small ruminant parasite consortium website) FAMACHA System System of identifying anemic animals, scoring the anemia and treating based on severity of disease ○ More pallor = greater worm burden NOTE: ○ Only appropriate for adult animals ○ Significantly increases amount of labor ○ Effective for identification of H. contortus ○ Does not account for other causes of anemia  ○ 1, 2 - do not deworm ○ 3 - questionable ○ 4,5 - deworm ○ 5 - potentially culled Important factor affecting RATE of resistance within a herd: ○ # of treated worms: # of un-treated worms ○ Goal is NOT to have 0 worms https://docs.wixstatic.com/ugd/6ef604 _c5fb241d19d3421686b8b25e4f4cc3a0.pdf Combination Deworming Strategy Dewormers should be used in combination at the same time How Combination Deworming Works: 1. Additive effect of each drug = Increased efficacy 2. Increased drug efficacy = fewer resistant worms (great dilution of resistant worms) Rotational Deworming Example 90% efficacy: Will leave 10% of resistant worms Combination Deworming Example Drug #1 = 90% efficacy Drug #2 = 90% efficacy Drug #1 will kill 90% of worms Drug #2 will kill 90% of the 10% of worms that did not respond to Drug # 1 (90% + (90% (10%)) = 99% efficacy 60% effective (i.e. will kill 60% of worms) - (10 worms)(0.6) = 4 worms 75% effective (i.e. will kill 75% of remaining worms) - (4 worms)(0.75) = 3 worms (0.6) + (0.75)(0.40) = 0.9 or 90% Anthelmintic Resistance - Detection Fecal egg count reduction test (FECRT) 10-15 animals at the same time Collect feces directly from the animal ○ Immediately prior ○ 10-14 days after Calculate difference in egg # Animals must have min of 150-200 epg before treatment Use oral form of dewormers Alternative Treatments Copper wire particles Parasite inhibiting plants  ○ Condensed tannins (sericea lespedeza) Nematophagus fungi ○ (Duddingtonia flagrans) Pasture management Alternate species Good nutrition Genetic improvement Copper Oxide Wire Particles (COWP) Mechanism of action: Lodge within abomasum Insoluble at pH >3.2 ○ Allows them to not dissolve in rumen Cause cuticle defect in adult worms Effect occurs within 12 h post administration Duration of effect = 21 days Duddingtonia flagrans D. flagrans Worm eating fungi Fed to animals and kills worms in feces 68% reduction in pasture contamination in sheep Unique Properties of D. flagrans (as advertised on www.BioWorma.com) Kills multiple worms Effective in multiple species (horses, cattle, goats, alpacas, sheep) Safe to other good “worms” found on pasture Not very pallatable Special Considerations D. flagrans Should not be used as sole worm control method Will not reduce current worm burden Temperature and environmental conditions determine efficacy Take Home Message Treat only animals that need to be dewormed Administer an appropriate dose Develop relationship with clients (VPCR) for extra label drug use  Use smart drenching techniques Coccidiosis VERY common disease of juvenile livestock NOT worms…anthelmintic don’t work! Species: ○ Eimeria ○ Isospora Disease of the minority and subclinical disease of the majority Coccidiosis - Pathogenesis Fecal oral transmission Oocytes infect enterocytes ○ 1 oocyst can destroy ~1 million enterocytes Rupture of enterocytes results in intestinal inflammation, mucosal cell loss Oocysts passed in feces Outside host oocysts sporulate to become infective 2-5 days Coccidiosis - C/S 1–6-month-old kids Diarrhea ○ +/- hematochezia Anorexia Dehydration Weight loss ○ Hair is dull and puffy Treatment Supportive Care ○ Intravenous fluids ○ Vitamin B complex ○ Blood transfusion Anti-coccidial Drugs ○ Coccidiostat  Ionophores  Decoquinate ○ Coccidiocidal   Amprolim □ (50 mg/kg, PO 5 days) □ Can NOT treat water like in cattle since so much higher dose  Triazinones NO DRUGS APPROVED FOR TREATMENT OF COCCIDOSIS IN GOATS Coccidia - Determinants of Disease ○ Dose  Proportional to fecal contamination of environment ○ Host stress  Weaning  Processing  Weather  Shipping  Co-mingling  Feed changes  Confinement  Concurrent Infections ○ Virulence Coccidia – Clinical Signs Diarrhea ○ Bloody Dull rough hair coat Anemia Tenesmus ○ Significant proctitis ○ Secondary rectal prolapse Nervous coccidiosis Subclinical ○ – poor weight gains, failure to thrive Coccidia - Treatment Clinical Coccidiosis ○ Sulfonamide antibiotics: sulfamethazine, sulfdimethoxine ○ Blood transfusion ○ Oral or IV fluids ○ B Vitamins, transfaunation, supportive care  Coccidia - Control ○ Separate feed and water from feces ○ Manage maternal source of oocyst  Crutching ○ Adequate bedding changes ○ Coccidiostatic drugs  Decoquinate  Amprolium ○ Ionophor antibiotics – coccidiocidal  Monensin  Lasalocid