Exam 3 Flashcards
Ascaris suum Basics
- Pig ascarid
- small intestine
- Eggs can live in soil for years
- Young pigs are most susceptible and contribute most to environmental contamination
Ascaris suum Life Cycle
- Larvated egg ingested orally ->
- L3 hatches in intestine->
- migrates to liver ->
- lung ->
- trachea ->
- coughed up and swallowed ->
- Small intestine (L4, adult) ->
- Egg in feces
- Prepatent period is 8 weeks
- No in utero or transmammary transmission
Ascaris suum Pathologic Effects
Adult worms o In intestine o Malnutrition o Occlude lumen o Obstruct bile/pancreatic duct o Can cause perforation o Decrease weight gain & production
Migrating larva
o Liver fibrosis – milk spot (Not clinically relevant)
o Inflammation & secondary infections of lungs
Ascaris suum Public Health & Diagnosis
Public Health
• Zoonotic
• Undergoes same lifecycle in humans
Diagnosis
• History
• Fecal float for “fluffy” egg
• Necropsy – milk spot liver, pneumonia, adults in intestine
Ascaris suum Prevention/Control & Treatment
Prevention/Control
• Drugs alone not successful
• Prevent accumulation of eggs
• Treat sows 2 weeks before and on the day of transport to farrowing crates
• Clean sows with soap and warm water before farrowing
• Treat piglets again at weaning
Treatment • Piperazine • Pyrantel (approved to kill larvae) • Heavy Infections o ½ dose dewormer o full dose few days later
Basics of Stongyloides ransomi
- small intestine threadworm of pigs
- Parasitic and free-living life cycles
- Up to 50% mortality in infected baby pigs
- Can strike first weeks of life
Stongyloides ransomi Life Cycle
- Adult female in the small intestine ->
- larvated egg (L1) shed in environment & hatches ->
- L2, L3 enter host via ingestion or skin penetration ->
- can go to mammary gland (important transmission)
OR
- L3 from free-living cycle can infect host
- Pre-patant period – 5 days oral, 12 days skin
Stongyloides ransomi Pathology/Clinical Signs
• Usually asymptomatic
Acute disease
o Very young pigs- first few weeks of life
o Acute enteritis with bloody diarrhea
o Rapid emaciation and growth stunting
Chronic
o older pigs
o Tend to store up larvae in mammary glands rather than develop adults
Larvae tissue migration
o Lung symptoms
Skin penetration
o inflammation, sensitization, mange-like
Stongyloides ransomi Diagnosis
Antemortem
o Fecal float for larvated egg
o 50 mm, FRESH sample
Postmortem
o Small intestine scraping,
o adult worms, 1-2 mm
Stongyloides ransomi Treatment & Control
Prevent transmammary transmission
o Treat sows 1wk before parturition w/ Ivermectin
Treat 1wk old piglets
o Ivermectin
Reduce moist areas
Rotate out older sows
Physocephalus & Ascarops
- thick, white pig stomach worms
- 1-2 cm long- easy to see on necropsy
- Distinctive eggs in fecal floats
- Elongate (40 um long), thick-walled, larvated egg
- Use beetles as intermediate hosts
- Clinically insignificant and not typically treated
Hyostrongylus rubidis Basics
- Thin, red pig stomach worm
- Strongyle, <1 cm long
- Clinically significant
- Pasture operations in midwest and S
Hyostrongylus rubidis Life Cycle
- Adult in stomach ->
- strongyle egg ->
- motls from L1, L2, L3 on ground ->
- pig ingests L3 ->
- embeds in stomach mucosa ->
- L4 ->
- adult emerges in lumen of stomach
Hyostrongylus rubidis Pathology, Diagnosis, Treatment
Pathology
• Adult pigs at pasture
• Inappetance
• Gastritis, ulcers, melena, anemia
Diagnosis
• 65-75 micrometer strongyle eggs
• postmortem exam
Treatment
• Fenbendazole, ivermectin
Oesophagostomum Basics
- Nodular worm
- Strongyle
- Pig large intestine as adult
- L4 can insist in intestinal mucosa
- Pasture & poor management operations
- Affects feeder pigs
Oesophagostomum Life Cycle
- Adult in large intestine ->
- strongyle egg pooped onto ground ->
- molts L1, L2, L3 ->
- pig ingests L3 ->
- L4 encysts in intestinal wall ->
- adult in lumen of large intestine
Oesophagostomum Clinical Signs & Pathology
- Clinical disease is usually due to L4 encysted in intestinal wall
- Nodule formation
- Granuloma formation in large intestine
- Nodules with inflammation -> chronic diarrhea
- May not detect eggs in feces during clinical disease
- Encysted larvae don’t produce eggs!
Oesophagostomum Diagnosis & Treatment
Diagnosis
• Postmortem
• Presumptively based on history
Treatment
• Fenbendazole (resistance reported)
• Pyrantel
(resistance reported)
• Ivermectin
Trichuris suis Basics
- Whipworm- in cecum & large intestine
- Common in all ages > 6 weeks old
- Produces fewer eggs than Ascaris suum
- Eggs survive years in the environment
- Reinfection is common
Trichuris suis Life Cycle
- Adult in large intestine produces egg ->
- Pig ingests larvated egg ->
- adult in Large I & cecum
- PPP = 6 weeks
- affects growers and adults
Trichuris suis Pathology/Clinical SIgns
- Head embeds in mucosa and damages intestinal epithelium
- Most severe damage in pigs 10-16 wks old
- Anemia
- Bloody D
- Rectal prolapse
- Stunted growth
Trichuris suis Diagnosis & Treatment/Control
Diagnosis
• Fecal float- “fecal jewel” egg
• Adult- whip-like – attached to mucosa
Treatment/Control o Hygiene! eggs persist in environment o Routine treatments o Relocate operation due to envir contamination o Fenbendazole
Globocephalus, Gonglyonema, & Macracanthorrhynchus hirudinaceous
Globocephalus
• hookworms in small intestine of pig
• strongyle type egg
• rare
Gonglyonema
• Pig Esophageal worm
• Clinically insignificant
• Requires beetle intermediate host
Macracanthorrhynchus hirudinaceous
• Acanthocephalan- “spiny headed worm”
• Requires beetle intermediate host
Metastrongylus Basics
- Swine lungworm
- 8.5 cm long and thin
- Most common in MW & S
- Earthworm intermediate host is a reservoir for transmission
- Clinical signs occur relatively late
Metastrongylus Life Cycle
- Adult in lung ->
- egg coughed up and swallowed ->
- larvated egg in feces ->
- earthworm ingests larvated egg ->
- pig ingests earthworm
Metastrongylus Pathology & Clinical Signs
- Migrating larvae -> irritation, inflammation -> cough & secondary infections
- Chronic adult infection - lung consolidation, cough, secondary infections
- Modest clinical and economic significance
Metastrongylus Diagnosis & Treatment
Diagnosis
• Fecal float- larvated eggs, 55 x 40 um
• Adults are deep in airways
Treatment
• Fenbendazole
• Ivermectin
Stephanurus dentatus Basics
- Swine kidney worm
- Strongyle
- Usually in SE
- Likes warmth & humidity
Stephanurus dentatus Life Cycle
- Adult in perirenal area lays eggs in ureter ->
- ground via urine ->
- L3 into host via oral or skin penetration ->
- L4 migrates to liver & stays 4-9 months = liver damage ->
- Migrates thru retroperitoneal tissue
- Earthworms are paratenic hosts (reservoir) Facultative intermediate hosts- NOT required for development
- PPP = 9-16mo
Stephanurus dentatus Pathology
- Due to L4
- Hemorrhage, necrosis, fibrosis of liver
- Stunting
- Meat destruction due to migration
- Aberrant migration to spinal cord = necrosis & inflammation
Stephanurus dentatus Diagnosis
Problematic young pigs
o No adult worm in young pigs
o Past clinical history
Postmortem diagnosis
o Livers with necrosis and fibrosis and worms
o Adult worms around kidney
Adult swine
o Strongyle eggs in urine
Stephanurus dentatus Treatment & Control
Treatment
• Doramectin
• Fenbendazole
• Kills adults
Control
• Due to long PPP if you breed very young gilts you can eliminate worm in pop
Trichinella spiralis Basics
o Trichinellosis or Trichinosis
o Larvae (L1) in muscle, and adults in intestine of infected mammals
o Infects essentially all mammals
o 10,000 people infected every year & Serious disease and death in people
o Transmitted in undercooked meat
o Pork, (horse) in domestic cycle
o Wild pigs, bear, seal, walrus, cougar in sylvatic cycle
o Typically occurs as outbreaks
o Economic importance
Trichinella spiralis Life Cycle
- L1 ingested from pig muscle ->
- Excyst in small intestine ->
- Embed in mucosa ->
- Molts L2, L3, L4, adult in 5 days ->
- Produce more L1 ->
- L1 enters lymphatics then blood stream ->
- Enters tissue then muscle cell ->
- Muscle induces cyst form ->
- Chronic infection (months to years)
- Entire life cycle in one host
- No stages in feces
Trichinella spiralis Sources of Infection
- Backyard operations or poorly managed swine operations- dead pigs, cannibalism, tail biting, rodents
- Hunted wild animal meat products
- Unusual sources- horse meat
Trichinella spiralis Pathology in Humans
• Dose dependent
Intestinal Phase
• 1 week after infection may get clinical signs
• Nausea
• Vomiting
Migration Phase • 2-3 weeks PI; acute trichinellosis • Severe inflammation in skeletal muscle- diaphragm, tongue, periorbital • Heart (myocarditis), cause of death • Lungs, liver • CNS (encephalitis, meningitis)
Muscle Phase- Chronic
• Mild to severe inflammation, tissue dysfunction
Trichinella spiralis Diagnosis in Pigs
Muscle digestion in acid
• Pepsin and HCl
Microscopic inspection of muscle
• Tissue squash, histology
ELISA serology
• Antibodies develop after ~ 40 days
• Mostly used for surveys
Trichinella spiralis Diagnosis in Humans & Prevention
Diagnosis • Eosinophilia, muscle pain, periorbital edema, gastroenteritis, pruritis and skin eruption • Biopsy • ELISA serology • Outbreaks • History
Prevention
• Education on proper food prep
• Good rodent management on pig farms
• Cook your meat!
Taenia solium Basics
- Pork tapeworm of humans
- Humans get cysticercus & adult
- Pigs only get cysticercus (pork measles)
- Causes neurocysticercosis in humans
Taenia solium Life Cycle
- Adult in human SI ->
- egg in human feces ->
- pig ingests ->
- cysticercus in pig muscle ->
- human ingests ->
- develops into adult tapeworm
How do humans get cysticercus?
- Ingestion of eggs from human feces
* Potentially retroperistalsis
Taenia solium Pathology
- Infection in pigs is not a major clinical concern
- economic and public health importance
Cysticerci in people
o pea sized parasitic cysts in Brain, eyes, muscle
o CNS signs - epilepsy
o Inflammation upon death of cysticercus
Adult tapeworm in humans
o Intestinal discomfort
o Source of eggs
4 Zoonotic Tapeworms
Dipylidium caninum
• 2 genital pores
Diphyllobothrium latum
• 1 central genital pore
Taenia solium- pork
• 1 lateral genital pore
Taenia saginata- beef
• 1 lateral genital pore
Differentiating T solium & T. saginata
o T. solium and T. saginata eggs cannot be differentiated
T. solium
• Hooks on scolex
• 5-10 lateral uterine branches
• From pork
T. saginata
• No hooks on scolex
• Highly branched uterus
• From beef
Cysticercus Diagnosis in Humans & Pigs
Humans
• CT or MRI
• Serology for Abs
• Eosinophilia
Pigs
• Cysticerci visible at slaughter
• Condemn carcass
• Reportable in US
Taenia solium Prevention & Treatment for Humans
o Identify source of infection
o Cook pork to 145F
o Freeze to kill cysticerci
Human treatment
• Albendazole for adult
• Praziquantel & anti-inflammatories for cysticercus
Coccidiosis in Pigs (Cystoisospura suis & Eimeria) Life Cycle
- Pig eats infective oocyst ->
- Extracellular asexual replication ->
- Intracellular sexual replication & fusion of gmaetes ->
- Poop out oocyst ->
- Sporulates in infective form in environment
Clinical Signs of Coccidiosis in Pigs
Diarrhea- first two weeks of life
• Watery, greasy, yellowish, foul-smelling diarrhea
• Often bloody due to epithelial cell destruction
- Dehydration
- Growth stunting
- Death
- Immunity develops with exposure
- some chronic shedding of oocysts happens
- Clinical signs uncommon in weaners and adults
Diagnosis of Coccidiosis in Pigs
- Fecal float- oocyst 20-40 um long
- Clinical disease can precede oocysts
- Hemorrhagic enteritis
- Microscopy to find epithelial stages
- Mucosal scrape or histopathology
Prevention & Treatment of Coccidiosis in Pigs
• Sows are carriers
Rigorous sanitation of farrowing areas is the most effective control!!
• Steam clean farrowing crates
• Wet down crates with ammonia or phenol-based detergent and let stand overnight
• Steam clean next day
Treatment with coccidiostats
• Coccidiostat treatment of acute disease in baby piglets is usually futile
• Coccidiostats in farrowing sows- often used, unreliable
Cryptosporidium Life Cycle
- Pig eats infective oocyst ->
- Extracellular asexual replication ->
- Intracellular sexual replication & fusion of gametes ->
- Poop out INFECTIVE oocyst ->
- Zoonotic
- Can be fond on fecal float
Balantidium coli Basics, Life Cycle, Diagnosis, Treatment
- Normal intestinal fauna in pigs
- Commonly seen but usually not problem
- Ciliated protozoan Located in the large intestine & can be invasive- possible ulcerative enteritis and diarrhea
Life cycle:
• Trophozoite -> Cyst (infective stage)
Diagnosis
• Cysts in fecal float
• Trophozoites in fecal smear
Treatment
• Treat only if pig has clinical disease
• Tetracycline
Toxoplasma gondii in Pigs; Basics & Control
- Public health importance - undercooked pork is source for humans
- Abortions and clinical disease in piglets
Control in Swine Operations
• Keep cats out of barns, feed, and water
• Remove dead pigs immediately to prevent cannibalism
• Eliminate access to wildlife, including rodent control
• Never feed uncooked garbage to pigs
• Washboots
Trichomonas & Giardia in Pigs
Trichomonas
• Flagellated parasite
• Insignificant in pigs
• Lives in nasal turbinates & large bowel
Giardia
• flagellated protozoa
• Rare cause of diarrhea
Entamoeba & Mycoplasma suis in Pigs
Entamoeba sp.
• an amoeba
• Appear in feces in normal animals
• significance??
Mycoplasma suis
• rickettsia bacteria
• Transmitted by the hog louse Haematopinus suis
Zoonotic Swine Parasites
- Trichinella spiralis
- Taenia solium
- Toxoplasma gondii
- Ascaris suum – possible, but not common
Prevention for Parasites Generally in Well Managed Operation
Maybe treat at 9-10 weeks for Ascaris
• Piperazine, pyrantel, fenbendazole
• Ivermectin- also efficacious against lice and mites
• Fenbendazole for whipworms
- Maybe treat at 16 weeks with FBZ
- Evaluate the need for treating adult pigs- fecal floats
Coccidia control
• clean farrowing areas, coccidiostats
Prevention for Parasites on Heavily Contaminated Farms
- Pyrantel more regular basis for Ascaris control in feeder pigs
- FBZ every few months for whipworms
Coccidia control
• clean farrowing areas, coccidiostats
- Consider Pre-partum ivermectin for sows - Strongyloides, Ascaris
- Use gilts for breeding- Strongyloides, Stephanurus
Gasterophilus Basics & Life Cycle
o Horse bot fly
o Lives in stomach, small intestine, rectum
o Some have one cycle per year some cycle continuously
Life Cycle • Eggs laid on hair are licked -> • hatch in and around mouth -> • larvae in oral cavity swallowed into stomach -> • molt to 3rd stage larva -> • in spring feces to ground and pupate -> • hatch to adult fly -> • adults die after frost
Gasterophilus Clinical Signs & Diagnosis
Clinical Signs
• Usually asymptomatic
• Ulcers at site of attachment
Diagnosis • Assumed • Endoscopy • Eggs on fur • Larvae in mouth
Gasterophilus Prevention & Control
Eliminate eggs on horse
• Bot block, fine comb, scissors
• Water at 104-118o F (+ 0.06% coumaphos)
Treat horse
• Most effective after first heavy frost in November
• ivermectin, moxidectin
Couple with treatments for strongyles
Habronema / Draschia Basics & Life Cycle
o Adult nematode is nonpathogenic in stomach
o Aberrant larval infection due to fly laying eggs in open wounds = cutaneous habronemiasis
Life Cycle
• Adult worm in stomach lay eggs ->
• hatch on ground ->
• fly maggots ingest the larvae ->
• L3 develops in adult fly mouth parts ->
• fly lands on mouth and L3 ingested by the horse ->
• stomach
OR
• Worm larva deposited on conjunctiva or wound ->
• Cutaneous habronemiasis
Cutaneous Habronemiasis Basics, Diagnosis, Treatment
- Summer sores
- Habronema or Draschia L3 in sore or eye
Diagnosis
• Wound- hard to definitively diagnose- biopsy
• fecal float to find larvated egg
Treatment
• Adults Oral ivermectin, or moxidectin
• Larva are hard to kill- lesions are often removed surgically
Trichostrongylus axei Basics, symptoms, diagnosis, treatment
o < 7 mm long stomach strongyle
of horses
o Can also infect ruminants
Symptoms
• Gastritis
• mostly asymptomatic
Diagnosis
• Produces strongyle eggs
• Many other horse strongyle eggs complicate fecal diagnosis
Treatment
• ivermectin, fenbendazol, pyrantel
Parascaris equorum Basics
o Roundworm
o Most common parasite in young horses
o Huge worms - up to 2 feet long in small intestine
o High reproductive capacity ~500,000 eggs per day
o Environmentally resistant eggs
o Young horses acquire some immunity with exposure
Parascaris equorum Life Cycle
- Larvated egg ingested orally ->
- L3 hatches in intestine & migrates to liver, lung (L3,L4), trachea ->
- coughed up and swallowed ->
- Small intestine (L4, adult) ->
- Unembryonated egg
Parascaris equorum Pathology
- Most severe in young horses
- No in utero or transmammary transmission
Liver
• inflammation, fibrosis (less common)
Lungs
• inflammation, secondary infections
• due to larval migration
Intestine
• Colic
• Undernourishment
• Heavy loads = occluded lumen, bile duct migration, rare perforation and peritonitis
Parascaris equorum Diagnosis, Prevention
Diagnosis
• Eggs on fecal float
• Adults in manure after deworming
• Adults in small intestine and pathological damage in lung or liver on necropsy
Prevention
• Clean up manure in areas where young horses are maintained
• Thorough cleaning of stalls with pressure washer or steamer
• Clean mare’s udders and teats before foaling
Parascaris equorum Treatment
• Fenbendazole at 2 & 4 months
Heavy infections
• ½ dose pyrantel
• + full dose few days later
• OR full dose Fenbendazole
Strongyloides westeri Basics
o Threadworm in horse small intestine
o Not a strongyle
o Most important in foals
o PPP 1-2 weeks
Strongyloides westeri Transmission & Clinical Signs
Transmission
• Transmammary
• Skin from ground
• Oral from ground
Clinical signs
• Diarrhea in young horses 10-14 days old
• Associated with “foal-heat diarrhea”
• Skin lesions from larvae penetration
Strongyloides westeri Diagnosis, Treatment, Prevention
Diagnosis-
• Fecal float for eggs requires very fresh sample
• Mucosal scraping postmortem for adult
Treatment
• Ivermectin
Prevention
• Treat mares at foaling with ivermectin (not usually necessary)
Basics of Large Strongyles in Horses
o Bloodworms o Long life cycle o Large & red o Anterior w/ large buccal cavity o Strongylus vulgaris, edentates, equinus
Strongylus vulgaris Life Cycle
- Adult in Large Intestine ->
- egg laid on pasture & molts L1, L2, L3 ->
- L3 ingested by horse ->
- penetrate wall of Large I and molt ->
- L4 penetrate arterioles -> large arteries ->
- Cranial Mesenteric Artery for ~4 mos.->
- arteries and arterioles ->
- Large I, Adult
Strongylus vulgaris Pathology
L4 arterial migration • endothelial damage • Aneurisms • Thrombo-embolisms • Rupture of vessels • lameness • Infarction of artery & intestinal necrosis (rare)
Chronic infection
• mineralization in arteries & permanent damage
Intestinal Damage
• L4 migration through wall of LI -> hemorrhage
• Adults feed on blood -> anemia, ill-thrift
Strongylus vulgaris Diagnosis
Fecal float
• cannot differentiate by eggs (strongyle eggs)
Fecal egg culture to identify L3
• Incubate feces 2wks
• Baermann isolation of L3
• Large strongyles have >16 cells
Rectal exam to feel arterial thickening
Necropsy to see Adults, Enlarged mineralized CMA, L4s in arteries
Strongylus vulgaris Prevention
- Stocking rates (horses/acre) - most important management factor!
- Pasture cleaning (remove poo)
- Rotational grazing
Strongylus vulgaris Treatment
Adults
• Fenbendazole
• Ivermectin
• Pyrantel
Migrating larvae
• Ivermectin
• Fenbendazole (5-day course)
Horse Parasite Treatment Strategy
2mo
• fenbendazole for P. equorum
4mo
• fecal float
• fenbendazole for P. equorum
8mo & 12mo
• ivermectin for strongyles
Year 2-4
• March – ivermectin for strongyles
• May –ivermectin for strongyles (maybe not needed in NW)
• Nov - ivermectin for strongyles
Year 4 & onward
• May –ivermectin for strongyles (fecal float to see if needed)
• Nov - ivermectin for strongyles
Quantitative Fecal Float
o Quantifies the number of eggs per gram of feces
o Determine level of infection of strongyle eggs in horse or ruminant
o Estimates pasture contamination rates
o Deworm when shedding is high and delay treatment when shedding is low
o Deworm horses that shed >200 epg
o May or may not estimate the degree of clinical illness
Small Strongyle Basics
o Cyathostomes o At least 50 species o Small white worms o Can insist in large intestine mucosa for up to 2yrs o PPP = 40 days
Small Strongyle Life Cycle
- Adult in Lareg I ->
- Strongyle egg molts to L3 on pasture ->
- ingested by horse ->
- encyst in cecum and large intestinal mucosa as L3, ->
- L4 emerge into lumen ->
- adult
Small Strongyle Pathology
- Most damage is caused by larval stages
- Chronic mild granulomatous typhlitis and colitis
Larval cyathostomiasis • mass emergence of larva • Catarrhal and hemorrhagic colitis • Severe colic, diarrhea, Rapid emaciation • 50% fatal • rare
Adult worms
• Low numbers: nonpathogenic
• Moderate to high numbers: ill-thrift, diarrhea, some anemia
Small Strongyle Diagnosis
Fecal float
• cannot differentiate by eggs- strongyle eggs
• accounts for >90% of strongyle egg output
• Encysted larvae do not produce eggs
• cannot detect clinical larval cyathostomiasis
Fecal culture
• <10 intestinal cells
Blood chemistry
• Hypoproteinemia during larval cyathostomiasis
Detect in feces after deworming
Necropsy
• Adults or granulomas in the Large I wall with larvae coiled in mucosa
Small Strongyle Treatment & Control
Treatment
• Encysted larval stages are difficult to treat
• Moxidectin is efficacious against some encysted larva
• 5-day course of fenbendazole effective but resistance is starting
• Widespread anthelmintic resistance in small strongyles (fenbendazole, pyrantel etc)
Control • Pasture management & stocking rates • Don’t underdose • Deworm new horses • Individualize treatments based on fecal egg counts
Oxyuris equi Basics, Clinical Signs, Diagnosis, Treatment
o Horse pinworm in large intestine
o All ages
o PPP = 5mo
Clinical Signs
• Prurtis, irritation, & rubbing
• Damage to tail & hair
Diagnosis
• Scotch tape around anus
• Adults white, translucent, w/ long pointed tail
Treatment
• Pyrantel, ivermectin
Oxyuris equi Life Cycle
- Female adult repeatedly migrates out of rectum ->
- lays eggs around anus ->
- irritation, horse rubs, & eggs contaminate environment ->
- egg is eaten ->
- adult in large intestine
Dictocalus arnfieldi Basics & Life Cycle
o Lungworm primarily of donkeys
o Can cause severe dz in horses
o Lives in large airways
Life Cycle in donkeys • Adults in lungs lay eggs -> • egg coughed up and swallowed -> • hatches in intestines -> • L1 in feces -> • L3 on pasture is ingested -> • L3 enters circulation & goes to lungs
Dictocalus arnfieldi Diagnosis & Treatment
Diagnosis
• Difficult
• No larvae in feces of horses
Treatment
• Fenbendazole
• Ivermectin
Setaria
o Filarial worm transmitted to horses by mosquitoes
o in peritoneal cavity,
o incidental finding
o AKA Necropsy worm, surgeon’s glove worm, peritoneal worm
Thelazia; basics, treatment, prevention
o Eye worm of horses o Often hidden in conjunctival and lacrimal sacs o Transmitted by face flies o Usually nonpathogenic o Can cause conjunctivitis
Treatment
• Manual removal
• Systemic ivermectin
Prevention
• Fly control
Halicephalobus gingivalis; Basics & Clinical Signs
o Very rare and creepy
o Environmental soil nematode
o opportunistic infection
o in nasal sinus, but can migrate into brain
Clinical Signs
• Lack of condition
• Nonspecific neurologic signs
Anoplocephala Life Cycle & Clinical Signs
Life Cycle • Eggs in feces on ground -> • cysticercoid in pasture mite -> • ingested by horse -> • tapeworm in small intestine or at ileocecal junction
Clinical Signs
• Nonpathogenic in low numbers
• Colic, diarrhea
• A. perfoliata may cause intussusception of the ileocecal valve = severe colic
Anoplocephala Diagnosis, Treatment, Prevention
Diagnosis
• Flotation to detect eggs (false negatives are common)
• Serology indicates exposure
Treatment
• Praziquantel
Prevention
• Treat once per year in fall
Equine Piroplasmosis Basics & Import Rules
o Babesia caballi
o Theileria equi
o Reportable
For import, horses are tested serologically, and if positive
• Treat -> if becomes seronegative -> imported
• Treat -> Remain seropositive -> no import to USA
Equine Piroplasmosis Life Cycle & Tick Vector
Life Cycle
• Sporozoites in tick saliva infect horse RBCs after tick bite ->
• merozoites in RBCs can infect other new RBCs ->
• RBCs w/ merozoites ingested by tick ->
• sexual replication
Tick Vector
• Mostly Dermacentor sp.- 1 host tick
• Also Amblyomma sp.- 3 host tick
Equine Piroplasmosis Clinical Signs
- High fever, anorexia, depression, peripheral edema
- Hemolysis, anemia, hemoglobinuria, icterus
Acute
• Rapid onset of clinical disease & death
Chronic
• Recovery from acute
• carrier state for years
usually with no clinical signs
• If stressed or immunosuppressedre-emergence of clinical disease
Equine Piroplasmosis Diagnosis
Acute phase • Blood smears • B. caballi = 2 merozoites • T. equi = 4 merozoites • PCR
Chronic phase
• difficult to diagnose by blood smears
• Serological ELISA tests for determining carrier status
Eimeria leuckarti
o Only coccidia in horses
o Not a concern
Trypanosoma equiperdum
o Sexually transmitted in horses
o Eradicated form US
o Horses tested for import
Equine Protozoal Myeloencephalitis Basics
o Neuro dz caused by different species of protozoans
o sarcocystis neurona
o Opossum- definitive host for S. neurona
S. neurona Life Cycle
• Opossums shed oocysts in feces ->
• contaminate food/water ->
• skunks, cats, armadillos, raccoons (intermediate host) ingest and develop asexual stages in muscles ->
• eaten by opossums
OR
• Horse eats opossum feces (dead end host)
Equine Protozoal Myeloencephalitis Pathogenesis & Clinical Signs
- Replicates in spinal cord & brain
- Depression
- Head tilt
- Facialparalysis
- Leaning
- Ataxia
- Lethargy
- Muscle atrophy (often 1 side)
- Weakness
Equine Protozoal Myeloencephalitis Diagnosis & Treatment & Prevention
Diagnosis
• Clinical signs + Serology for Abs
• Histopath of CNS tissue
Treatment • Ponazuril • Diclazuril • Anti-inflammatories • Immune stims • Vit E • Relapse common, some don’t respond to therapy, only 10% full recovery
Prevention
• No contact w/ opossum feces!
