Final Exam Flashcards

1
Q

HOT Complex Basics & Life Cycle

A
o	Infect all ruminant species
o	HOT complex
o	Haemonchus – small ruminants mostly
o	Ostertagia – mosty cattle
o	Trichostrongylus – ALL

Life Cycle
• Short PPP
• Inhibited development (can encyst in tissue)
• Induced by environmental cues

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2
Q

Periparturient / Spring Rise of HOT complex

A
  • Increase in egg output in the spring
  • Especially periparturient ewes
  • Mostly due to maturation of mucosal-inhibited L4 into adults
  • Seeds the pasture with eggs → L3 → lambs, kids, calves
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3
Q

Haemonchus contortus Basics & Life Cycle

A
  • Sheep
  • Most important parasite in small ruminants
  • Tropical & high humidity
  • Feed on blood
  • LOTS of eggs
  • Rapid drug resistance
Life Cycle
•	Adults in abomasum produce eggs ->
•	Molt on pasture from egg to L3 ->
•	L3 ingested by host ->
•	L4 in mucosa ->
•	adult 
•	Inhibited L4's survive winter in host  
•	Low survival of L3's in hot/dry or cold
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4
Q

Haemonchus contortus Clinical Signs

A

Anemia
o Acute & rapid -> death
o Chronic compensated
o Chronic decompensated -> clin dz

Bottle jaw (edema)

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5
Q

Haemonchus contortus Pathology, DIagnosis, Treatment

A

Pathologic Effects
• Immunity- incomplete, develops after 6 months
• Acute disease usually in young

• Chronic disease in older animals

Diagnosis
• Strongyle eggs if fecal float
• Post mortem adults in abomasum

Treatment
• Ivermectin or fenbendazole
• Move to clean pasture

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6
Q

Haemonchus contortus; Control & FAMCHA / Selective Deworming

A

Control
• Treat ewes at parturition
• Treat lambs at weaning, move to clean pasture
• Treat all adult animals in spring to kill adult worms
• Treat all adult animals in fall to kill adults and inhibited larvae
• Tactical treatments as needed

• Increasing protein content in ewe feed in spring helps prevent spring rise
• Do FECRT to monitor drug resistance
• Vaccine available in Australia & SA

FAMCHA & Selective Deworming
• Reduce number of animals treated
• Must evaluate every animal

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7
Q

Ostertagia Basics & Life Cycle

A
  • Brown stomach worm of cattle
  • Most important GI nematode of cattle
  • May have antithelmentic resistance
  • L4s survive in gastric glands
  • L3s survive on pasture
  • Irrigation improves survival
Life Cycle
•	Adults in abomasum produce eggs ->
•	pasture L1, 2, 3 ->
•	ingested by host ->
•	migrate to mucosa & L4s survive in gastric glands ->
•	adult 
•	PPP ~3 weeks 

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8
Q

Ostertagiosis Type I Basics, Diagnosis, Treatment

A
  • Adult worms cause diarrhea and reduced weight gain
  • “Summer ostertagiosis”
  • Most important for young pastured cattle
  • Adult cattle develop modest levels of immunity

Diagnosis
o Scours in cattle less than 2 years old

o Strongyle eggs in high 100’s to low 1,000’s

Treatment
o Fenbendazole (can use in dairy)
o Ivermectin
o Moxidectin (can use in dairy)

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9
Q

Ostertagiosis Type II Basics, Cinical Signs, Diagnosis, Treatment

A
  • Inhibited L4 in gastric glands cause severe abomasitis
  • “Winter ostertagiosis”
  • young adults & calves
Clinical signs
o	Emaciation
o	Profuse watery Ds
o	Chronic anemia
o	Protein-losing enteropathy (bottle jaw)

Diagnosis
o difficult
o Clinical signs and history

o Strongyle eggs- usually low (still L4s)
o Necropsy shows nodules on mucosa of abomasum = “Morocco leather appearance”
o Can identify tissue L4 on Mucosal scrape
o Histology of the abomasum shows larvae in gastric glands

Treatment
o Albendazole
o Ivermectin
o Moxidectin

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10
Q

Ostertagiosis Type II Pathogenesis

A

o L4 in gastric glands ->
o damage parietal cells ->
o decrease in HCl production & rise in pH ->
o no conversion of pepsinogen to pepsin ->
o severe digestive problems, diarrhea, wasting

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11
Q

Ostertagia Prevention & Control

A
  • Treat spring & fall
  • Treat calves w/ 400-500+ eggs
  • Treat cows w/ 200 eggs
  • Focus on cows <2yo (older have some immunity)
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12
Q

Trichostrongylus axei Basics, winter survival, & Life Cycle

A
  • Stomach hairworm of ruminants (and horses)
  • L3s survive winter on pasture
Life Cycle
•	Adults in abomasum produce eggs ->
•	pasture L1, 2, 3 ->
•	L3 enter host & migrate to mucosa ->
•	L4 -> adult 
•	PPP ~3 weeks
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13
Q

Trichostrongylus axei Clinical Signs & Treatment

A

Clinical Signs
• Mild gastritis & reduced growth of young

Treatment
• Fenbendazole (can use in dairy)
• Ivermectin
• Moxidectin (can use in dairy)

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14
Q

Treating for Strongyles on Cow-Calf Operations

A

• Treat spring and fall

High Risk Pastures
• Heavily stocked (> 1-2 cows/acre) 

• Irrigated 

• Constantly grazed 


High – Risk Cattle
• Weaned calves 

• First and Second-season grazing cattle

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15
Q

Treating for Strongyles on Feedlots & Dairies

A

Feedlot Operations
• Weaned cattle dewormed upon arrival
• Feedlot environment uninhabitable for strongyles

Dairy
• Weaned calves require deworming
• Adults don’t need nematode treatment
• Pastured adults - unsure

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16
Q

Trichostrongylus sp. Basics, Clin Signs, Diagnosis

A

o Nematode
o Intestinal trichostrongylus are species specific

Clinical Signs
•	Often asymptomatic
•	Protracted watery Ds
•	Wasting / emaciation
•	Late summer

Diagnosis
• Strongyle egg on fecal float
• Watery Ds in late summer
• Adult worms visible on necropsy

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17
Q

Trichostrongylus colubriformis

A
  • Type of trichostrongylid
  • Black scour worm or bankrupt worm
  • 6mm long
  • small intestine of small ruminants
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18
Q

Cooperia

A
  • Type of trichostrongylid
  • 1cm long
  • in small intestine of cows
  • not usually primary cause of dz
  • most prevelant parasite in cow/calf ops
  • resistance to ivermectin
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19
Q

Nematodirus sp. Basics & Life Cycle

A
  • Type of Trichostrongylid
  • 2.5 cm
  • small intestine
  • Immunity often develops after 1st year of exposure
Life Cycle
•	L1, L2, and L3 develop in eggs ->
•	Eggs very cold-resistant & hatching highly dependent on weather conditions ->
•	Synchronized hatching of L3s ->
•	Outbreaks in late spring
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20
Q

Nematodirus sp. Clin Signs, Diagnosis, Treatment

A

Clinical Signs
• Often asymptomatic
• N. battus in lambs = unthrifty, severe Ds, high mortality

Diagnosis
• HUGE eggs (150-200microns)
• Heavy infection = low hundreds/gram

Treatmet
• Fenbendazole

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21
Q

Bunostomum Basics, Clin Signs, Diagnosis, Treatment

A

o Ruminat hookworm
o 2cm long
o small intestine

Clinical Signs
• Anemia
• Death in calves/lambs

Diagnosis
• Adults on necropsy

Treatment
• Ivermectin
• Fenbendazole

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22
Q

Strongyloides papillosus Life Cycle & Clin Signs

A
Life Cycle
•	PPP 1-2wks
•	Adult female in the small intestine ->
•	larvated egg shed on  ground ->
•	hatches and molts L2, L3  ->
•	to host via ingestion or skin penetration ->
•	can go to *mammary gland* 
Clinical Signs
•	If high numbers present
•	Ds in young
•	Goats more susceptible
•	Skin lesions
•	Sudden death syndrome in older calves
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23
Q

Capillaria

A

o Adults in small intestine of ruminants

o Unimportant

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24
Q

Oesophagostomum Basics & Life Cycle

A

o Nodular worm
o Strongyle
o Large intestine

Life Cycle
•	Host ingests L3  ->
•	L3 burrows into mucosa of intestine & becomes L4 ->
•	adult in lumen of L Int ->
•	strongyle egg in poop ->
•	molts L1 to L3 on pasture
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25
Q

Oesophagostomum Clin Signs & Diagnosis

A

Clinical Signs
• Granulomas around encysted L4 larvae
• chronic fetid diarrhea
• Ds also predispose sheep to blowfly strike

Diagnosis
• No eggs in fecal float during dz (encysted larvae)
• Strongyle egg in fecal float
• Nodules & adults in large intestine on necropsy

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26
Q

Chabertia ovina

A
o	Sheep
o	Strongyle
o	Feeds on blood
o	Causes anemia
o	uncommon
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27
Q

Trichuris ovis Basics, Clin Signs, Treatment

A

o Whipworm of ruminants & camelids
o Common
o Eggs environmentally resistant

Clinical signs
• Poor growth
• bloody Ds

Treatment
• Fenbendazole
• Regular deworming every few months

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28
Q

Gonglyonema

A

o Esophageal worm

o Ruminants

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29
Q

Dictyocaulas Basics & Life Cycle

A

o Lungworm in Cattle
o Direct life cycle
o Sterilizing immunity develops and protects against disease

Life Cycle
•	Adult in bronchi ->
•	larvated egg coughed up and swallowed ->
•	hatches in intestinal tract ->
•	L1 in feces & L2, L3 on pasture ->
•	L3 ingested by host ->
•	enter lymphatics ->
•	lung as L4 ->
•	molt to adult in airways 
•	PPP 4 weeks
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30
Q

Dictyocaulas Clin Signs, Treatment, Prevention

A
Clinical Signs
•	Acute lungworm disease- 
•	mostly calves
•	Disease severity depends on number of worms present
•	Obstruct air passages 
•	Cough 
•	Tachypnea

Treatment
• Ivermectin, fenbendazole, or albendazole

• Move cattle off the contaminated pasture for at least several weeks, L3 do not live long

Prevention
• General nematode control program works
• Treat when suspected or necessary
• Vaccine in Britain- irradiated L3


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31
Q

Dictyocaulas Diagnosis

A

Early infections
• difficult to diagnose

• L4s are causing damage = no L1 in feces
• History, clinical signs
• Necropsy - look for larval worms in airways

Later stages of infections

• Fecal Baermann apparatus to isolate L1

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32
Q

Muellerius Basics & Life Cycle

A
o	Common and difficult to control 
o	Lungworm of goats
o	Requires snail intermediate host 
o	Adults deeply embedded in parenchyma form nodules or raised areas 
o	Usually nonpathogenic

Life Cycle
•	Adult in lungs ->
•	larvated egg coughed up and swallowed ->
•	hatches in intestinal tract ->
•	L1 in feces molts to L2, ->
•	Molts to L3 in snail ->
•	ingested by host ->
•	enter lymphatics ->
•	lung, L4 ->
•	airways molt to adult 
•	PPP 4 weeks
33
Q

Muellerius Diagnosis & Treatment

A

Diagnosis
• Baermann to identify L1


Treatment
• FBZ , Ivermectin, ABZ
• requires several treatments

34
Q

Protostrongylus rufescens Basics & Life Cycle

A

o Domestic sheep -uncommon
o Wild sheep- very common
o Requires snail intermediate host

o Adults in small airways and alveoli (hard to find)

Life Cycle
•	Adult in lungs ->
•	larvated egg coughed up and swallowed ->
•	hatches in intestinal tract ->
•	L1 in feces molts to L2, ->
•	Molts to L3 in snail ->
•	ingested by host ->
•	enter lymphatics ->
•	lung, molt L4 ->
•	airways adult 
•	PPP = 4 weeks
35
Q

Protostrongylus rufescens Diagnosis & Treatment

A

Diagnosis
• Baermann for L1

Treatment
• FBZ , Ivermectin, ABZ
• requires several treatments

36
Q

Parelaphostrongylus tenuis Basics

A
o	Meningeal worm
o	Natural host is white-tailed deer 
o	Camelids and other accidental hosts- migration in CNS can cause serious CNS damage and death 
o	Found east of the Missouri River 
o	Present in W & SW US
37
Q

Parelaphostrongylus tenuis Diagnosis,Treatment, Prevention

A

Diagnosis
• Accidental hosts do not pass L1 in feces
• CSF analysis: eosinophils may be helpful

Treatment
• Prognosis is poor
• Can try Fenbendazole or IVM + doxycycline


Prevention
• Preventive treatments of ivermectin (30 days) or doramectin (45 days) when snails are abundant and where P. tenuis is endemic


38
Q

Elaeophora schneideri Basics

A
o	Filarial nematode
o	the “arterial worm” of wild cervids and sheep
o	8-10 cm in carotid artery 
o	Microfilaria in skin of forehead 
o	Tabanid flies are vectors
39
Q

Elaeophora schneideri Clinical Signs

A

Endothelial damage from the presence of adult arterial worms
• Multisystemic ischemic lesions- CNS, ears, and muzzle
• Blindness
• Sudden death

Sheep- microfilariae cause hypersensitivity
• “Sore head”- uncontrolled rubbing and itching 

• Diagnose by detecting microfilariae in skin from head

40
Q

Stephanofilaria stilesi

A

o Brisket filarial worm of cows

o Hornfly is vector

41
Q

Onchocerca

A

o Filarial worm in connective tissue
o Intermediate hosts (vectors)- Simulium, Culicoides
o Nuchal ligament, abdominal fascia
o Microfilariae in skin

42
Q

Setaria cervi

A

o abdominal filarid worm,
o aka necropsy worm, Surgeon’s glove worm
o Intermediate host- mosquitoes

43
Q

Thelazia

A

o Filarid worm of eye
o Transmitted by face flys
o Treated w/ ivermectin

44
Q

Fasciola hepatica Basics

A

o Common liver fluke
o Adult fluke can live in bile ducts for many years 

o Uses snail as intermediate host
o Infective stage metacercariae encysts on aquatic plants in late spring, summer, fall 

o Killed by freezing and dry conditions 

o 1 cycle per year in northwest- use anthelmintics in the fall 

o 2 cycles + per year gulf states

45
Q

Fasciola hepatica Life Cycle

A
  • Adult lays egg in bile ducts ->
  • egg gets pooped out ->
  • miracidium hatches and penetrates snail ->
  • undergoes asexual amplification ->
  • motile cercariae develop and leave snail ->
  • metacercariae encyst on vegetation
46
Q

Fasciola hepatica Acute Clinical Signs

A
  • due to ingestion of large numbers of metacercariae over a short period of time
  • Migration of immature flukes in parenchyma causes significant liver damage
  • Sheep and goats are most sensitive

  • Can see high mortality with heavy infections
  • Can predispose animals to Clostridial infections
  • Hemorrhagic, traumatic hepatitis

  • Elevated serum liver enzymes
  • fulminant liver failure
47
Q

Fasciola hepatica Chronic Clinical Signs

A
  • due to adult flukes in bile ducts when animals ingest more modest numbers over a longer period of time
  • Often asymptomatic
  • If clinical disease does develop- usually manifests in fall and winter
  • Chronic poor doer
 & decreased weight gains
  • Poor milk production & reproductive success
  • Anemia, bottle jaw, and elevated liver enzymes
48
Q

Fasciola hepatica Diagnosis, Treatment, Prevention

A
Diagnosis
•	History
•	Fecal sedimentation
•	ELISA serum test in Europe
•	Adult or larval flukes found on necropsy
•	Bile duct fibrosis on necropsy
•	fluke exhaust

Treatment
• Anthelmintics not effective against immature stages
• Clorsulon & albendazole (no use in dairy)
• Treat in fall for adults
• Maybe treat in spring

Prevention
• Fence off access to snail habitat
• Routine treatment to prevent eggs

49
Q

Fascioloides magna Basics & Life Cycle

A

o Giant liver fluke of white tailed deer & elk
o Flukes develop into adults in cattle livers but eggs never find their way into the bile ducts
o Flukes do not fully mature in small ruminant livers

Life Cycle
• Adult lays egg in bile ducts ->
• egg gets pooped out ->
• miracidium hatches and penetrates snail ->
• undergoes asexual amplification ->
• motile cercariae develop and leave snail ->
• metacercariae encyst on vegetation

50
Q

Fascioloides magna Pathology/Clinical Signs in Cows, Sheep, Goats

A

Cattle
• Adult flukes encapsulate in large cysts in liver parenchyma
• chronic liver disease
• No eggs in feces

Sheep & Goats
• Flukes never fully mature

• Immature flukes migrate aimlessly and cause massive liver damage
• One fluke can cause death
• Rapid onset anorexia, lethargy, depression

51
Q

Fascioloides magna Diagnosis & Treatment

A

Diagnosis
• Elevated liver enzymes
• No eggs in feces for cows, sheeps, goats
• Fecal sedimentation for elk & deer
• Immature flukes in sheep/goat liver on necropsy
• Encapsulated adults in cow liver on necropsy

Treatment
• Difficult to treat

52
Q

Dicroelium dendriticum

A

o “Lancet liver fluke” of ruminants
o common in NE
o Lives in bile ducts

o Small fluke produces small eggs

53
Q

Paramphistomum

A

o Rumen fluke
o Non pathogenic
o Not common

54
Q

T. solium Vs T. saginata

A

T. solium
• Hooks on scolex
• 5-10 lateral uterine branches
• From pork

T. saginata
• No hooks on scolex
• Highly branched uterus
• From beef

55
Q

Moniezia Basics & Life Cycle

A
o	Anoplocephalid tapeworm
o	over 4 meters long

o	Pasture mites serve as the reservoir 
o	Young ruminants have highest infections 
o	Concern for producers 
Life Cycle
•	Adult in small intestine ->
•	proglottids and eggs in feces ->
•	pasture mite ingests ->
•	becomes cysticercoid ->
•	mite ingested by ruminant
56
Q

Moniezia Clin Signs, Diagnosis, Treatment

A

Clinical Signs
• Usually non-pathogenic
• Heavy infections in young = Ds

Diagnosis
• Proglottids in manure of live animals
• Fecal float- geometric square eggs
• Adults at necropsy

Treatment
• Fenbendazole
• Albendazole

57
Q

Thysanosoma Basics & Life Cycle

A

o Adult in bile
o tapeworm in all ruminants except cattle

Life Cyle
•	Proglottids in feces ->
•	Eggs ingested by pasture lice ->
•	Lice infected by cysticercoid ->
•	Ruminant eats lice
58
Q

Taenia Saginata Life Cycle, Clin Signs, Diagnosis

A

o Cysticercus is only stage in cows

Life Cycle
•	Adult in human SI
->
•	egg in human feces ->
•	cow ingest egg off of ground ->
•	cysticercus in beef muscle ->
•	human 

Clinical Signs
• Mostly non-pathogenic
• Occasional myocarditis

Diagnosis
• Meat inspection

59
Q

Taenia hydatigena, ovis, multiceps

A

Taenia hydatigena
o Cysticerci in sheep viscera

Taenia ovis
o Cysticerci in sheep muscle

Taenia multiceps
o Coenurus in sheep brain

60
Q

Echinococcus Life Cycle

A
  • Egg from dog can infect humans and ruminants with larval hydatid cyst 

  • Dog consumes hydatid cyst to become infected with adult tapeworm 

61
Q

Eimeria Basics & Life Cycle

A

o Young animals most likely affected (cows < 6mo)
o Many animals are carriers
o Stress is an important factor in development or recrudescence of clinical coccidiosis
o Immunity develops and protects against disease > 1-2 years old

Life Cycle
• Ppp = 3wks
• Cow eats infective oocyst ->
• Asexual replication ->
• Sexual replication & production of oocyst ->
• Oocyst sporulates in environment to infective form

62
Q

Eimeria Clinical Signs

A

• All result in economic losses

Acute
• often results in death

• Rapid onset diarrhea, dehydration
• Bloody Ds in cattle; not bloody in small ruminants 

• CNS signs “nervous coccidiosis”- poorly understood, but tends to happen in cold regions 


Subacute
• poor growth, some deaths
• Diarrhea
• Predispose to fly strike- mostly in sheep


Chronic
• constant low-level cycle in intestine
• Malabsorption, poor feed conversion


63
Q

Eimeria Diagnosis Prevention Treatment

A

Diagnosis
• Diarrhea
• lots of oocysts in fecal flotation

• hemorrhagic enteritis on necropsy

Prevention
•	Amprolium in feed or water 
•	Rigorous sanitation
•	Separate animals w/ Ds
•	Reduce stress

Treatment
• Amprolium
• Doesn’t work well

64
Q

Eimeria macusaniensis Basics, Treatment, Management

A

o Camelid coccidiosis
o Low number of oocysts may accompany clinical disease
o Necrotizing and hemorrhagic enteritis
o Ds may precede oocyst appearance in feces
o Oocysts can be hard to float (needs high specific gravity flotation media

Treatment
• Amprolium, sulfadimethoxine

Management
• prevent overcrowding

65
Q

Cryptosporidium parvum Basics, Zoonosis, Diagnosis

A

o Type of coccidian in young ruminants
o dairy/confinement operations as a cause of 
neonatal scours 

o Direct life cycle 

o PPP is very short: 2-7 days 

o Effective immunity generally develops following primary exposure 

o No effective treatment 


Zoonosis
• Ds in healthy people
• Severe clin dz & death in immunocompromised
• Immunity after infection

Diagnosis
• Fecal float
• Fecal PCR

66
Q

Sarcocystis Basics, Life Cycle, Diagnosis, Control

A

o Protozoal infection of ruminants
o cysts develop in muscle cells
o Usually completely asymptomatic
o High level infections = ill-thrift, Weight loss, Hair loss around eyes and tail

Life Cycle
• Sexual rep and productionof oocysts in dogs, cats, humans
• Asexual rep in ruminants

Diagnosis
• Muscle biopsy

Control
• Don’t feed uncooked carcasses to dogs, cats

• Prevent access of dogs and cats to pasture and feed

67
Q

Neospora caninum Basics & Life Cycle

A

o Toxoplasma like organism
o Dogs are definitive host
o Causes abortions in dairy cattle

Life Cycle
• Dog definitive host ->
• produces oocysts that contaminate ruminant feed/water ->
• Cattle tissue cysts ->
• Cattle can transmit transplacentally to calves ->
• Abortion OR persistent infection of calf

68
Q

Neospora caninum Transmission, Diagnosis, Prevention

A

Transmission
• Ingestion of oocyst
• Transplacental infection

Diagnosis
• Serology shows exposure
• Must also look at histo lesions of aborted calves

Prevention
• Cull infected cows to avoid vertical transmission
• Do not feed carcass or placenta to dogs

69
Q

Epidemic Vs Endemic Abortion Due to Neospora caninum

A

Epidemic
• Ingestion of contaminated food or water ->
• Abortion storm

Endemic
• Recrudescence of infection during pregnancy
• Mom is a persistently infected animal

70
Q

Toxoplasma gondii Basics, Life Cycle, Diagnosis

A

o Cause of abortion in small ruminats

Life Cycle
• Cat definitive host ->
• produces oocysts that contaminate ruminant feed/water ->
• tissue cyst

Diagnosis
• Convalescent serum serology w/ four fold increase in IgG is diagnostic
• Histo of fetal tissue

71
Q

Tritrichomonas foetus “Trich”; Baiscs, Life Cycle, Transmission

A

o Flagellated protozoan in reproductive organs of cattle
o Reduces reproductive success, Early embryonic death, Metritis in cows

Life Cycle
• Simple
• 1 trophozoite divides to 2 trophozoites

Transmission
• Bull is the source and carrier
• located in preputial folds
• Bulls > 4 years most likely to have infection
• Transfers from cow to cow by bull
• Cows typically have transient infections
• Immunity is not complete

72
Q

Tritrichomonas foetus “Trich”; Pathology & Clinical Signs

A

• Usually mild

Cow
• Vaginitis, metritis, pyometra
• Abortion first trimester 


Bull
• None

Herd
•	High numbers of repeat breeders

•	Increases in nonpregnant and late-bred cows
•	Decreased calving rates

•	Increases in fetal death rates 

73
Q

Tritrichomonas foetus “Trich”; Diagnosis, Prevention, Control

A

Diagnosis
• Definitive – find organism in bull by PCR of preputial scraping of bull
• Requires clinician performing the sampling to be trained, certified, and registered with WSDA 

• Very specific protocols for collecting and submitting samples
• PCR is the standard in WA
• Highly regulated transport between states

Prevention & Control
• Rigid culling of infected bulls
• Replace with young, virgin bulls

• Replace after 90 days of sexual rest to allow cows to clear infection
• Use AI for breeding with good biosecurity protocols
• No treatments for bulls

• Vx can decrease shedding rates

74
Q

Trypanosoma

A

o Flagellated protozoans transmitted by biting flies

o Nonpathogenic trypanosomes in cattle, sheep, and deer in the US

75
Q

Giardia (in ruminants); Basics, Diagnosis, Treatment, Prevention

A

o Common commensal, occasional parasite
o Most commonly isolated from dairy calves 1-3 mo old
o Calves w/ chronic diarrhea that does not respond to antibiotics, electrolytes, or anti-coccidials

Diagnosis
• Fecal float w/ cysts
• Fecal smear for protozoa

Treatment
• No drug licensed for treatment in ruminats
• Fenbendazole
• Albendazole

Prevention
• Clean and dry areas thoroughly

76
Q

Babesia bigemina Basics & Clinical SIgns

A

o Bovine babesiosis or Texas fever
o Infects erythrocytes of adult cattle
o Rhiphicephalus sp. (one host) ticks are vectors
o Eradicated from the US & REPORTABLE

Clinical Signs
•	High-grade fever

•	Anemia

•	Icterus

•	Hemoglobinuria

•	Cerebral babesiosis

•	Death can occur rapidly 
•	Calves are not susceptible to disease
77
Q

Babesia bigemina Diagnosis, Control, Treatment

A

Diagnosis
• Blood smear for pyriform in RBCs

Control
• Surveillance of imported cattle

Treatment
• Only used in endemic countries
• Diminazene
• Imidocarb

78
Q

Theileria parva Basics, Clinical Signs, Control

A

o East Coast Fever
o Infects cattle lymphocytes and erythrocytes
o Africa and the Southern mediterranean

Clinical signs

• Up to 100% mortality in susceptible cattle
• Pulmonary edema and respiratory failure
• Profound lymphadenomegaly

Control
• tick control

• Live vaccine with concurrent oxytetracycline treatment
• Can treat clinical cases with oxytetracycline early