Final Exam Flashcards

(78 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Haemonchus contortus Clinical Signs

A

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

Bottle jaw (edema)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Trichostrongylus colubriformis

A
  • Type of trichostrongylid
  • Black scour worm or bankrupt worm
  • 6mm long
  • small intestine of small ruminants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Capillaria

A

o Adults in small intestine of ruminants

o Unimportant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Oesophagostomum Clin Signs & Diagnosis
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
26
Chabertia ovina
``` o Sheep o Strongyle o Feeds on blood o Causes anemia o uncommon ```
27
Trichuris ovis Basics, Clin Signs, Treatment
o Whipworm of ruminants & camelids o Common o Eggs environmentally resistant Clinical signs • Poor growth • bloody Ds Treatment • Fenbendazole • Regular deworming every few months
28
Gonglyonema
o Esophageal worm | o Ruminants
29
Dictyocaulas Basics & Life Cycle
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 ```
30
Dictyocaulas Clin Signs, Treatment, Prevention
``` 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

31
Dictyocaulas Diagnosis
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
32
Muellerius Basics & Life Cycle
``` 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
Muellerius Diagnosis & Treatment
Diagnosis • Baermann to identify L1
 Treatment • FBZ , Ivermectin, ABZ • requires several treatments
34
Protostrongylus rufescens Basics & Life Cycle
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
Protostrongylus rufescens Diagnosis & Treatment
Diagnosis • Baermann for L1 Treatment • FBZ , Ivermectin, ABZ • requires several treatments
36
Parelaphostrongylus tenuis Basics
``` 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
Parelaphostrongylus tenuis Diagnosis,Treatment, Prevention
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
Elaeophora schneideri Basics
``` 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
Elaeophora schneideri Clinical Signs
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
Stephanofilaria stilesi
o Brisket filarial worm of cows | o Hornfly is vector
41
Onchocerca
o Filarial worm in connective tissue o Intermediate hosts (vectors)- Simulium, Culicoides o Nuchal ligament, abdominal fascia o Microfilariae in skin
42
Setaria cervi
o abdominal filarid worm, o aka necropsy worm, Surgeon’s glove worm o Intermediate host- mosquitoes
43
Thelazia
o Filarid worm of eye o Transmitted by face flys o Treated w/ ivermectin
44
Fasciola hepatica Basics
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
Fasciola hepatica 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
46
Fasciola hepatica Acute Clinical Signs
* 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
Fasciola hepatica Chronic Clinical Signs
* 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
Fasciola hepatica Diagnosis, Treatment, Prevention
``` 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
Fascioloides magna Basics & Life Cycle
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
Fascioloides magna Pathology/Clinical Signs in Cows, Sheep, Goats
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
Fascioloides magna Diagnosis & Treatment
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
Dicroelium dendriticum
o “Lancet liver fluke” of ruminants o common in NE o Lives in bile ducts
 o Small fluke produces small eggs
53
Paramphistomum
o Rumen fluke o Non pathogenic o Not common
54
T. solium Vs T. saginata
T. solium • Hooks on scolex • 5-10 lateral uterine branches • From pork T. saginata • No hooks on scolex • Highly branched uterus • From beef
55
Moniezia Basics & Life Cycle
``` 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
Moniezia Clin Signs, Diagnosis, Treatment
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
Thysanosoma Basics & Life Cycle
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
Taenia Saginata Life Cycle, Clin Signs, Diagnosis
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
Taenia hydatigena, ovis, multiceps
Taenia hydatigena o Cysticerci in sheep viscera Taenia ovis o Cysticerci in sheep muscle Taenia multiceps o Coenurus in sheep brain
60
Echinococcus Life Cycle
* Egg from dog can infect humans and ruminants with larval hydatid cyst 
 * Dog consumes hydatid cyst to become infected with adult tapeworm 

61
Eimeria Basics & Life Cycle
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
Eimeria Clinical Signs
• 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
Eimeria Diagnosis Prevention Treatment
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
Eimeria macusaniensis Basics, Treatment, Management
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
Cryptosporidium parvum Basics, Zoonosis, Diagnosis
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
Sarcocystis Basics, Life Cycle, Diagnosis, Control
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
Neospora caninum Basics & Life Cycle
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
Neospora caninum Transmission, Diagnosis, Prevention
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
Epidemic Vs Endemic Abortion Due to Neospora caninum
Epidemic • Ingestion of contaminated food or water -> • Abortion storm Endemic • Recrudescence of infection during pregnancy • Mom is a persistently infected animal
70
Toxoplasma gondii Basics, Life Cycle, Diagnosis
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
Tritrichomonas foetus “Trich”; Baiscs, Life Cycle, Transmission
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
Tritrichomonas foetus “Trich”; Pathology & Clinical Signs
• 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
Tritrichomonas foetus “Trich”; Diagnosis, Prevention, Control
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
Trypanosoma
o Flagellated protozoans transmitted by biting flies | o Nonpathogenic trypanosomes in cattle, sheep, and deer in the US
75
Giardia (in ruminants); Basics, Diagnosis, Treatment, Prevention
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
Babesia bigemina Basics & Clinical SIgns
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
Babesia bigemina Diagnosis, Control, Treatment
Diagnosis • Blood smear for pyriform in RBCs Control • Surveillance of imported cattle Treatment • Only used in endemic countries • Diminazene • Imidocarb
78
Theileria parva Basics, Clinical Signs, Control
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