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Parasitology > Exam 3 > Flashcards

Exam 3 Flashcards

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1
Q

Ascaris suum Basics

A
  • Pig ascarid
  • small intestine 

  • Eggs can live in soil for years 

  • Young pigs are most susceptible and contribute most to environmental contamination
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2
Q

Ascaris suum Life Cycle

A
  • 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
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3
Q

Ascaris suum Pathologic Effects

A 
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

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4
Q

Ascaris suum Public Health & Diagnosis

A

Public Health
• Zoonotic
• Undergoes same lifecycle in humans

Diagnosis
• History
• Fecal float for “fluffy” egg
• Necropsy – milk spot liver, pneumonia, adults in intestine

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5
Q

Ascaris suum Prevention/Control & Treatment

A

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
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6
Q

Basics of Stongyloides ransomi

A
  • 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
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7
Q

Stongyloides ransomi Life Cycle

A
  • 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
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8
Q

Stongyloides ransomi Pathology/Clinical Signs

A

• 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

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9
Q

Stongyloides ransomi Diagnosis

A

Antemortem
o Fecal float for larvated egg
o 50 mm, FRESH sample

Postmortem

o Small intestine scraping,
o adult worms, 1-2 mm

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10
Q

Stongyloides ransomi Treatment & Control

A

Prevent transmammary transmission
o Treat sows 1wk before parturition w/ Ivermectin

Treat 1wk old piglets
o Ivermectin

Reduce moist areas

Rotate out older sows

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11
Q

Physocephalus & Ascarops

A
  • 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
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12
Q

Hyostrongylus rubidis Basics

A
  • Thin, red pig stomach worm
  • Strongyle, <1 cm long
  • Clinically significant

  • Pasture operations in midwest and S
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13
Q

Hyostrongylus rubidis Life Cycle

A
  • 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
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14
Q

Hyostrongylus rubidis Pathology, Diagnosis, Treatment

A

Pathology
• Adult pigs at pasture
• Inappetance
• Gastritis, ulcers, melena, anemia

Diagnosis
• 65-75 micrometer strongyle eggs
• postmortem exam

Treatment
• Fenbendazole, ivermectin

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15
Q

Oesophagostomum Basics

A
  • Nodular worm
  • Strongyle
  • Pig large intestine as adult
  • L4 can insist in intestinal mucosa
  • Pasture & poor management operations
  • Affects feeder pigs
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16
Q

Oesophagostomum Life Cycle

A
  • 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
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17
Q

Oesophagostomum Clinical Signs & Pathology

A
  • 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!
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18
Q

Oesophagostomum Diagnosis & Treatment

A

Diagnosis
• Postmortem
• Presumptively based on history

Treatment
• Fenbendazole (resistance reported)
• Pyrantel
(resistance reported)
• Ivermectin

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19
Q

Trichuris suis Basics

A
  • 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
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20
Q

Trichuris suis Life Cycle

A
  • Adult in large intestine produces egg ->
  • Pig ingests larvated egg ->
  • adult in Large I & cecum
  • PPP = 6 weeks
  • affects growers and adults
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21
Q

Trichuris suis Pathology/Clinical SIgns

A
  • Head embeds in mucosa and damages intestinal epithelium
  • Most severe damage in pigs 10-16 wks old
  • Anemia
  • Bloody D
  • Rectal prolapse
  • Stunted growth
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22
Q

Trichuris suis Diagnosis & Treatment/Control

A

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
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23
Q

Globocephalus, Gonglyonema, & Macracanthorrhynchus hirudinaceous

A

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 


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24
Q

Metastrongylus Basics

A
  • 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
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25
Metastrongylus Life Cycle
* Adult in lung -> * egg coughed up and swallowed -> * larvated egg in feces -> * earthworm ingests larvated egg -> * pig ingests earthworm
26
Metastrongylus Pathology & Clinical Signs
* Migrating larvae -> irritation, inflammation -> cough & secondary infections * Chronic adult infection - lung consolidation, cough, secondary infections * Modest clinical and economic significance
27
Metastrongylus Diagnosis & Treatment
Diagnosis • Fecal float- larvated eggs, 55 x 40 um • Adults are deep in airways Treatment • Fenbendazole • Ivermectin
28
Stephanurus dentatus Basics
* Swine kidney worm * Strongyle * Usually in SE * Likes warmth & humidity
29
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
30
Stephanurus dentatus Pathology
* Due to L4 * Hemorrhage, necrosis, fibrosis of liver * Stunting * Meat destruction due to migration * Aberrant migration to spinal cord = necrosis & inflammation
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
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!
39
Taenia solium Basics
* Pork tapeworm of humans * Humans get cysticercus & adult * Pigs only get cysticercus (pork measles) * Causes neurocysticercosis in humans
40
Taenia solium Life Cycle
* Adult in human SI
-> * egg in human feces -> * pig ingests -> * cysticercus in pig muscle -> * human ingests -> * develops into adult tapeworm
41
How do humans get cysticercus?
* Ingestion of eggs from human feces | * Potentially retroperistalsis
42
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
43
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 

44
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
45
Cysticercus Diagnosis in Humans & Pigs
Humans • CT or MRI • Serology for Abs • Eosinophilia Pigs • Cysticerci visible at slaughter • Condemn carcass • Reportable in US
46
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
47
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
48
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
49
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
50
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
51
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
52
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
53
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
54
Trichomonas & Giardia in Pigs
Trichomonas • Flagellated parasite • Insignificant in pigs • Lives in nasal turbinates & large bowel Giardia • flagellated protozoa • Rare cause of diarrhea
55
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
56
Zoonotic Swine Parasites
* Trichinella spiralis * Taenia solium * Toxoplasma gondii * Ascaris suum – possible, but not common
57
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
58
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
59
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 ```
60
Gasterophilus Clinical Signs & Diagnosis
Clinical Signs • Usually asymptomatic • Ulcers at site of attachment ``` Diagnosis • Assumed • Endoscopy • Eggs on fur • Larvae in mouth ```
61
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
62
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
63
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
64
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
65
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
66
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
67
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
68
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
69
Parascaris equorum Treatment
• Fenbendazole at 2 & 4 months Heavy infections • ½ dose pyrantel • + full dose few days later • OR full dose Fenbendazole
70
Strongyloides westeri Basics
o Threadworm in horse small intestine o Not a strongyle o Most important in foals o PPP 1-2 weeks
71
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
72
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)
73
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 ```
74
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
75
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
76
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
77
Strongylus vulgaris Prevention
* Stocking rates (horses/acre) - most important management factor! * Pasture cleaning (remove poo) * Rotational grazing
78
Strongylus vulgaris Treatment
Adults • Fenbendazole • Ivermectin • Pyrantel Migrating larvae • Ivermectin • Fenbendazole (5-day course)
79
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
80
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
81
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 ```
82
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

83
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
84
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
85
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 ```
86
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
87
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
88
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 ```
89
Dictocalus arnfieldi Diagnosis & Treatment
Diagnosis • Difficult • No larvae in feces of horses Treatment • Fenbendazole • Ivermectin
90
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
91
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
92
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
93
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
94
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
95
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
96
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
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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
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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
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Eimeria leuckarti
o Only coccidia in horses | o Not a concern
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Trypanosoma equiperdum
o Sexually transmitted in horses o Eradicated form US o Horses tested for import
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Equine Protozoal Myeloencephalitis Basics
o Neuro dz caused by different species of protozoans o sarcocystis neurona o Opossum- definitive host for S. neurona 

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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)
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Equine Protozoal Myeloencephalitis Pathogenesis & Clinical Signs
* Replicates in spinal cord & brain * Depression 
 * Head tilt 
 * Facialparalysis 
 * Leaning 
 * Ataxia 
 * Lethargy 
 * Muscle atrophy (often 1 side) 
 * Weakness 

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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!

Parasitology (4 decks)

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