Selected GI disease Flashcards
1
Q
What type of virus is BVD?
A
- Pestivirus
2
Q
How are biotypes determined?
A
In vitro designations
3
Q
Non-cytopathic BVD
A
- Do not destroy cells
4
Q
What is the predominant biotype?
A
- Non-cytopathic
- Persists in cattle populations
5
Q
Reservoir for non-cytopathic BVD
A
- PI animals
6
Q
How does cytopathic BVD happen?
A
- Via mutation of non-cytopathic
7
Q
What is BVD mucosal disease?
A
- Co-infection of homologous NCP and CP
8
Q
Which versions of BVD cause clinical infection and disease? Which is not found as a cause of PI animals?
A
- Both cause clinical infection and disease
- CP is not found as a cause of PI animals
9
Q
Significance of species BVD
A
- There are Type I and Type II with a bunch of subspecies
- Might be an explanation for why vaccines don’t work as well
10
Q
Type I species of BVD
A
- many subspecies
- NCP and CP
- Worldwide now
11
Q
WHat is the outstanding feature of Type II BVD?
A
- Thrombocytopenic strains
- Causes some more damage too
- NCP and CP
12
Q
BVD Type I and Type II Antigenic and genetic similarity?
A
- They are DISSIMILAR with regards to both antigen and genetics
- Means that antibodies likely aren’t cross-protective, and may be why some vaccine companies are putting multiple strains
13
Q
BVD Type I and Type II - disease syndrome differences
A
- They are similar
14
Q
Seroprevalence of BVD
A
- 60-85%
- It’s widespread
- 60-80% of cattle >1 year have seroconverted
15
Q
Source of infection for BVD
A
- Persistently infected animals!!
- They are responsible for persistence in herds
16
Q
How common are PI calves?
A
- ~2% of general cattle population
- 10-50% of US herds have at least 1
17
Q
Transiently infected calves
A
- They get it and may get affected a little but usually get through it
- 1-2 weeks, seroconvert, and become part of the group that has had it
18
Q
Transmission source of BVD
A
- PI or TI animals
- shedding it everywhere
19
Q
How long does BVD last in environment?
A
- <2 weeks in environment
- Can persist in the environment
20
Q
Transmission of PI vs TI
A
- TI shed fewer, shed for a shorter period of time compared to PI
21
Q
Where is BVD secreted?
A
- Most body secretions
22
Q
Transmission of BVD mode
A
- Direct contact (ignestion, inhalation, etc.)
- Vectors (insects and inanimate)
- Transplacental (virtually 100%)
- Semen (AI are tested previous to using them)
23
Q
BVD in pigs and wild ruminants and pigs
A
- Isolated from many domestic and wild ruminants and pigs
24
Q
Clinical sign variability in BVD
A
- Subclinical to death
- Hugely variable
25
What determines BVD variability?
- Immunotolerant vs immunonaive
- Immune status (exposure, vaccines, etc.)
- Stressed animals are worse off
- Pregnancy status
- Gestational age
- Environmental stress
- Genetic diversity of virus
26
When are PI calves infected during gestation?
- 30-150d (<125 d in utero)
27
PI calf pathophys
- Fetus is immunotolerant
| - NCP virus persists, no effective immune response
28
Clinical appearance of BVD
- Clinically normal
| - Weak, poor do'er, immunosuppressed
29
Which biotype of BVD infects PI calves?
- Non-cytopathic
30
Who are we most worried about protecting during gestation for BVD?
- Pregnant cow!
31
<60 d BVD infection signs
- Abortion, early embryonic death, congenital defects
32
60-120 day BVD infection signs
- PI calf
- Commonly die young but may rarely live to produce more PI calves
- Always shedding large amounts of BVD
- Immunosuppression
33
100-150 days signs BVD infection
- Congenital defects
34
>120 days clinical signs BVD infection
- Calf born with antibodies to BVDV, may be normal or stunted
35
Significance of PI cows that are at repro age
- may need to test more than just calves
| - Cows can do it too
36
What is the most common manifestation of BVD?
- Acute BVD (TI)
37
When do cows experience acute BVD most often?
- 80% in 1st year life
38
Who gets acute BVD?
- Immunocompetent but naive animals or fetuses >150-180 days
39
Acute BVD morbidity and mortality
- Most inapparent***
| - High morbidity, low mortality
40
How long are most cows infected with BVD if acutely infected?
- Several weeks, but short lived viremia (2-3 weeks)
| - Seroconvert but virus negative with time
41
Clinical signs of Acute BVD (TI)
Fever, lethargy, nasal/ocular discharge
- Diarrhea/enteritis
- Mucosal erosion***
- Neutropenia
- Respiratory disease**
- Profuse diarrhea and agalactia in adult dairy cattle
- Virus damages epithelium of GIT, integument, and respiratory systems
42
BVD and Bovine Respiratory Disease Complex
- Remember that BVD sets you up for BRD***
43
Ulcerative lesions and BVD
- Around the coronet, nose, any mucosal surface
44
Most common signs of acute BVD***
- Inapparent!!!
45
Papillae in the mouth with BVD***
- They are blunted
46
Thrombocytopenic/hemorrhage syndrome BVD - which type of BVD?
- Acute, type II, NCP, BVD
47
Mortality of Thrombocytopenic/hemorrhage syndrome BVD
- Higher mortality and more severe signs
48
Mechanism of Thrombocytopenic/hemorrhage syndrome BVD
- Unknown
| - Virus associated with platelets, megarkaryoctes, and platelet function is altered
49
Clinical signs of Thrombocytopenic/hemorrhage syndrome BVD
- Severe GIT bleeding, epistaxis, hyphema, bleeding from injection sites, etc.
- Ecchymoses of heart and lungs (you will find on necropsy)
50
Who gets mucosal BVD?
- PI animals ONLY***
| - Following fetal infection <125 days with NCP virus
51
Clinical signs of mucosal BVD
- Fever, lethargy, dehydration, diarrhea, mucosal erosions, neutropenia, lymphopenia, respiratory disease, acute death
- MOST OFTEN DIE
52
Severe acute BVD and Mucosal disease
- Clinically indistinguishable from severe acute BVD
| - They almost always go on to die!
53
Chronic MD
- RARE
- Occasional
- Can survive up to 18 months
- Intermittent diarrhea
- Poor appetite, weight loss, bloat
- Interdigital erosions, lameness
54
How does mucosal disease occur (MOST COMMON)?
- Combined infection of antigenically homologous NCP (persistent) and CP virus)
- Spontaneous mutation from NCP to CP (MOST COMMONLY)
55
Antigenic similarity of NCP and CP in mucosal disease
-They are antigenically homologous
56
Vaccination and Mucosal disease
- Combined infection of antigenically homologous NCP (persistent) and CP virus
- Natural or iatrogenic (MLV vaccine) infection
- Rare, but they're already PI so need to be out of the herd anyways
57
What cells does BVD target for immunosuppression?
- Lymphocytes and macrophages
- Decreases CD4+, CD8+, and B lymphocytes as well as neutrophils
- Also decreases neutrophilic bactericidal activity
58
Immunomodulatory agents impacted by BVD
- IFN, IL-1, IL-2, and TNF-alpha
| - These are the early indicators
59
Consequences of immunosuppression of BVD
- Much lower capacity to fight off disease
60
Congenital defects of BVD (100-170 d)
- Cerebellar hypoplasia
- Hydranencephaly/hydrocephalus
- Eye problems (microphthlamia, retinal atrophy, cataracts, optic neuritis)
- Pulmonary hypoplasia (small lungs; die after death)
- Skeletal defects
- Thymic hypoplasia
61
Infected during 1st trimester BVD outcome (0-110d)
- Abortion, congenital damage, PI calves
62
During which trimester can BVD calves be born?
- 1st and 2nd trimester overlap
63
Infected during 2nd trimester BVD outcome (111-180d)
- Congenital damage, fetal loss
64
Infected during 3rd trimester BVD outcome
- Fetus immunocompetent and mounts a response
65
Other syndromes with BVD
- Repro failure, infertility, repat breeders
| - Abortion, mummies (infected <100 d)
66
When are mummies infected?
- <100 d
67
Leukogram for BVD
- Leukopenia
- Lymphopenia
- Neutropenia (severe, no left shift; helps differentiate from Salmonella which will normally have a left shift )
- Thrombocytopenia
68
Thrombocytopenia in BVD
- < 100,000/µL
- Can bottom out <10,000/µl
- Acute type II, NCP BVDV
69
Dfdx for BVD WITHOUT oral erosions in adults
- Salmonella (has a left shift)
- Winter dysentery
- Johne's
- Copper deficiency
- Ostertagiasis
- Coccidiosis
- Grain overload
- Renal amyloidosis
70
Dfdx for BVD WITH oral erosions in adults
- Vesicular stomatitis
- MCF
- BT/EHDV
- FMD
- Papular stomatitis
- Rinderpest
- BVD
71
Suspicion of BVD signs
- Herd records (decreased production, poor repro performance, signs of immunosuppression)
- Signalment and history
- Clinical signs and CBC
- Pathology and histopathology (necropsy super helpful)
72
Herd records of BVD herds
- Decreased production
- Poor repro performance
- Signs of immunosuppression
73
Peyer's patch in BVD
- CAN be hemorrhagic in BVD
74
VI for BVD sample
- Blood, feces, nasal swab, tissue
75
VI for BVD - when to use?
- Not used that often
- Used when you don't know what's going on exactly
- Used when you're pretty certain it's a virus but not sure what type
76
BVDV Ag ELISA sample
- buffy coat or serum or ear notch
77
BVDV Ag ELIA when to use?
- This is a very common test to define the PI calf
- The reason it's useful is that it's not that sensitive for BVD
- Less likely to detect a transiently infected animal at all
- This is how you determine a PI calf
78
BVDV IHC - what sample?
- Ear notch
79
BVDV ICH when to do?
- Ear notch
- They can take those and pool them and test that way or individually
- IHC can be done at WADDL for PIs
80
Serology for BVDV
- Negative titers suggest PI animals (normally 80% animals are +), definite if VI+
- 4x rise suggests clinical BVD
- Precolostral titers positive suggests exposure (but a pain to do)
- Much less frequently used
- Cross reacts with vaccines
- Sometimes used to determine if an abortion outbreak
- Compare a group of 10 cows that did abort and 10 that didn't
- Then measure again 3 weeks later
- His preference is every aborted fetus, placenta, and serum from the cow
81
Issues with serology for BVDV
- Cross reacts with vaccines
| - Kind of a pain
82
PCR for BVDV which sample?
- Ear notch
83
PCR for BVDV when to use?
- This is the test that almost everyone has gone to for detecting PI
- They will follow this up with BVDV Ag ELISA to determine that it's PI and not TI
- PCR is super sensitive
84
Treatment for MD BVDV
- None
85
Treatment for acute BVD
- Support
86
Treatment for hemorrhagic syndrome
- May need transfusion
87
Main principle of control for BVD
- Eliminate PI animals
88
Testing for BVDV with new animals
- Test all incoming (ELISA or PCR)
| - Quarantine all incoming for 1 month
89
What to do for BVD testing if herd tests have not been performed in the past
- Test all open cows or cows that lost calves
90
Vaccination of BVDV - will it eliminate disease?
- NO
- May mask clinical signs
- Still see repro problems and PI calves
91
WADDL recommendations for testing - who to test?
- Test ALL calves
| - Test all bulls and replacement heifers that have not been tested (cows lost calves)
92
WADDL recommendations for testing - what to test?
- Ear notch test (pooled PCR of 36 animals)
| - Individual test with Ag ELISA if positive (PI)
93
WADDL recommendations for testing - what to do with positive animals?
- Quarantine
| - Retest in 2-3 weeks (2% false positives)
94
What to do with PI animals?
- Euthanize, slaughter, BVD feedlot (???)
| - Don't sell your problem
95
<12 samples for BVD Ear Notch testing
- No pooling
| - Just do Ag-ELISA
96
At 36+ samples BVD Ear notch testing
- Do the PCR pool up to 36 and then Ag-ELISA per head if needed
97
Which BVDV tests go for antibody?
- Serology
| - Also use to determine type I and type II
98
Which BVDV tests go for antigen?
- VI
- PCR
- Ag ELISA
- Ag IHC
99
Which test for export testing?
- Viral isolation
| - 5-9 days for results
100
Can PCR differentiate PI and TI?
- No
| - Too sensitive
101
Can Ag ELISA differentiate PI and TI?
- Yes
- Only detects high levels of antigen
- Good for herd screening
102
WHich are screening tests for BVDV?
- Ag ELISA
- PCR
- Ag IHC
103
Cow vax recommendations for BVD
- Prevent fetal infection
- 2 weeks to 2 months befor ebreeding
- Revaccinated annually (if they're set up young though it's usually okay)
- Need to start young
104
Calf vax recommendations
- Protect against systemic infection
- +/- branding (MAY be too young though!)
- 3-4 weeks before weaning
- 3 times the first year
105
Which products for BVDV vaccinations?
- Killed vs MLV
| - Brand
106
Which type of vaccine for BVDV in a cow that didn't receive vaccines prior to breeding?
- Have to use killed
107
Brand of BVDV vaccine
- He recommends using the same vaccine throughout life
108
What causes and influences coccidiosis?
- Caused and influenced by MANAGEMENT
109
Etiology of Coccidiosis
- Eimeria and Isospora
110
Can Eimeria in cattle infect sheep/goats and vice versa?
- No, unless immune compromised
111
PPP of Coccidiosis
- Variable with species
- They don't shed until at least 17 days
- Don't have clinical signs until shedding
112
Where is coccidiosis normally found?
"Normal" inhabitant of adult GIT
113
Who gets Salmonellosis?
- All species
114
Prevalence of Salmonellosis?
- CA dairy herds up to 75%
115
Is Salmonella host specific?
- No, most serotypes are non-host specific
116
Make sure you go back and make notecards for the one lecture you missed on 3/7
:)
117
Carriers and Salmonellosis
- Host adapted Salmonella, which increases chance for carriers
- They can make a carrier state
118
Subclinical infections of Salmonella
- If you have clinically affected, there are probably a great many more that are subclinically affected
119
Age groups for Salmonella
- From the day they are born on
| - It can impact a 1 day old calf or a 15 year old calf
120
Main etiologies for calf diarrhea in the first few days of life
- E. coli
- Salmonella
- Also Campylobacter and Clostridia, but the others are the main two
121
How can Salmonella invade?
- Ocular, nasal, oral, GIT mucous membranes
| - S. dublin via ingestion of milk from intramammary infection
122
Stress and Salmonella
- Stress can lead to a recrudescence of of Salmonella
| - Shed via feces or milk
123
What age group of animal can get Salmonella and which types of serotypes?
- Any age animal
| - Only invasive serotypes
124
What are the three mechanisms of diarrhea for Salmonella?
- 1. Inflammation and necrosis
- 2. Increased fluid secretion
3. Decreased absorption and digestion
125
How does inflammation and necrosis occur with Salmonella?
- Salmonella attacks the villi and invades to lamina propria
- Macrophage response destroys organism and/or tissues
- PMN response (inflammatory edema)
126
How does Salmonella increase fluid secretion (hypothesis)?
- Locally induced PG production stimulates adenylate cyclase --> increased fluid secretion
127
How does Salmonella decrease absorption/maldigestion?
- Damage to intestinal villi (decreased digestive enzyme production)
- Blockage of lymph and blood flow (impede nutrient and fluid uptake which leads to an osmotic type diarrhea)
- Fusion of villi (secondary to healing; decreased absorptive surface area)
128
Clinical presentations for Salmonella
1. Peracute septicemia
2. Acute enteritis
3. Chronic enteritis
- All three can be concurrent in a herd
129
What 3 things determine individual Salmonella disease?
- Virulence of serotype, pathogen concentration, and immune status of host
130
Who typically gets septicemia from Salmonella?
- Calves and lambs 10 days to 3 months
131
Which serotypes cause Salmonella septicemia?
- S. typhimurium, S. dublin
132
Clinical signs of septicemia/endotoxemia
- Scleral injection
- Petechiation (pinna)
- Toxic (gum) line
- Recumbent, dead
- Can be found dead with minimal signs
133
Course of Salmonella
- Hours to 1-2 days
134
Neurologic form of Salmonella signs
- Opisthotonus, convulsions
135
Enteric form fo Salmonella septicemia signs
- Diarrhea, colic, etc.
136
Typical hemogram with septicemia
- Leukopenia (profound)
- Hyperfibrinogenemia
- Left shift (severe)***
- Metabolic acidosis (+/- diarrhea, dehydration)
137
Sequela for Salmonella septicemia
- Polyarthritis, fibrinous pneumonia
138
Predisposing factors for Salmonella
- Failure of Passive trasnsfer
| - You would want to check your program if you have an increase in Salmonella
139
What is the predominant form of Salmonella?
- Acute enteritis
140
Clinical signs of acute enteritis with S. typhimurium, S. newport
- Fever, enteritis, anorexia, depression, dehydration
- Diarrhea later
- Watery at first
- FOllowed by mucosal shreds, casts, blood, foul odor
- Dehydration worsens, hypothermia, etc.
141
S. dublin clinical signs with acute enteritis
- Fever, anorexia, depression
- Calves can die without diarrhea***
- More likely to see meningitis, polyarthritis, osteomyelitis, pneumonia
- Adults can get abortion
142
Can calves die without diarrhea with S. dublin?
- YES
143
Hemogram for acute enteritis
- Initial leukopenia
- Later (3-4 d) - leukocytosis, left shift
- Hyperfibrinogenemia
- Metabolic acidosis
- Hyponatremia
- Hypokalemia (whole body)
- Hypoproteinemia in the face of an elevated PCV
144
Mortality of acute enteritis with Salmonella and what determines it?
- 0-75%
| - Depends on the health of the group of calves, how naive they are, and the virulence of the strain
145
Postmortem signs with Salmonella
- Enteritis (If they've been dead longer than 6-12 hours you can't see this regardless)
- Erosions of small and large bowel
146
Who gets chronic Salmonella enteritis?
- Older calves (6-8 weeks)
147
Clinical signs of Salmonella chronic enteritis?
- "Failure to thrive"
- Scruffy
- Loose stool (not diarrheic)
- No mucosal shreds, blood, casts
-
148
Postmortem signs of Salmonella chronic enteritis
- Localized necrosis of cecum/colon
- button ulcers
- Pseudomembranes (yellow/gray)
149
S. dublin - where can it exist?
- Endemic in certain farms (adapted strain)
| - Can persist in mammary glands, source of chronic mastitis
150
S. typhimurium signs
- Isolated cases in adults
- Outbreaks in calves
- Affected cows often present with signs of abdominal discomfort, pain and colic
151
S. typhimurium and RDA
- They can look like an RDA
- If they have diarrhea, sample the diarrhea
Time: 8:38 AM
152
Which strain of Salmonella is most associated with consumption of raw milk in immunocompromised hosts?
- S. dublin
153
Which strain of Salmonella is most associated with ground beef, pork, and poultry products?
- S. typhimurium
154
Which strain of Salmonella is most associated with turkey products?
- Most commonly associated with turkey products
| - Some strains with multiple antibiotic resistance plasmids
155
Potential infection routes for Salmonella - which is the main?
- ORAL (main)***
- Ocular
- nasal
- Streak canal
- Rectal? (may want to use new sleeves in an infected herd)
156
Excretion routes of Salmonella - which is the main?
- MANURE****
- Oronasal secretions
- Milk
- Urine
157
Diagnosis of Salmonella
- History (endemic disease)
- Clinical signs
- Neutropenia with left shift
- Serology usually positive within about 2 weeks of infection
- Bacteriology
158
What is the definitive test for Salmonella?
- Bacteriology
159
Sample for Salmonella bacteriology testing
- Feces, blood, tissues
- but they don't shed every day
- Usually recommended to get five straight days of fecal testing to say that they are or aren't
- You can't confirm that they are Salmonella negative without five negative fecal exams
160
What % of bacteriology for Salmonella is positive with one culture?
- 50%
161
Salmonella treatment for carriers and chronic cases
- Ineffective
162
Antibiotics for Salmonella - key principles
- Won't generally improve diarrhea (may make it worse by depressing normal flora!)
- Best to do C&S
- Use early in systemic animals
163
Should you use antibiotics in a cow with just diarrhea?
- No, likely just fluid therapy
164
Antibiotics for Salmonella - when to do?
- In a systemically ill animal
165
Antibiotics for systemic Salmonella when monogastrics
- TMS
166
At what age can you give TMS?
- They say about first 3 weeks of life you can get away with this monogastrics
167
Cephalosporins for systemic Salmonella
- Safe, effective, ELDU
168
Aminoglycosides for systemic Salmonella
- Withdrawals?
- These are often effective and show up on C&S
- However, gentamicin can last up to 6 months in the kidneys of these animals
- Usually a big no-no
169
Fluoroquinolones for systemic Salmonella
- Only if respiratory disease (shouldn't use)
| - (probably shouldn't be using it)
170
Other medications for systemic Salmonella
- Florfenicol
| - Ampicillin
171
What's the best way to try and select the correct antibiotic?
- C&S
172
What should fluids contain for Salmonella treatment? Routes
- Sodium, bicarbonate, glucose
- IV if in circulatory shock
- PO if ambulatory
173
Summary of treatments for Salmonella
- Antibiotics based on C&S (IF they are systemic)
- Fluids with sodium, bicarbonate, and glucose
- NSAIDs
- Plasma/antiserum if very expensive
174
Control and prevention with host adapted strains of Salmonella (i.e. S. dublin)
- Minimize stresses
- Biosecurity (environmental hygiene; test incoming animals/purchase from free herd)
- ID carriers (test animals >6 months; ELISA, fecal cultures, milk cultures)
175
What should you do with positive carrier animals?
- Cull
176
Control and prevention for non-host adapted and host adapted strains
- Isolate and treat affected calves (<6 months)
- Decontaminate environment
- All in - all out
- Environmental monitoring (evaluates sanitation and disinfecting procedures)
- Critical control points
- test feed stuffs
- Rodent control
- Animal handling
177
Salmonella survival times in the environment
- Quite variable
| - reality is that it can last a long time in the environment, which makes it difficult to get rid of
178
How can Salmonella get into and be maintained in a herd (general, just list some ways)?
- Wildlife reservoirs
- Animal importation
- Farm livestock
- Slaughter houses
- Pet animals
- imported food
- Imported animal and vegetable protein
179
Replication cycles of Salmonella in cattle intestinal tracts
- Typically youngstock make it to adulthood with Salmonella
- It can be maintained in the cow herd or they transmit it
- Cow herd maintains it, gets diarrhea, gets over it, and passes it to the calves
180
What are animals can act as reservoirs for Salmonella?
Which of these seems to be the most significant?
- Rodents
- Flies***
- Feral dogs and cats
- Birds
- Domestic pets
- Wild mammals
- Humans
181
What changes should be made to management to reduce Salmonella contamination? (3 major points)?
1. Minimize animal movement between groups of animals (don't hold back poor-doing animals)
2. Control vermin (flies and rodents) and feral animals!
3. Reduce fecal contamination of feed and water
182
How can you reduce fecal contamination of feed and water?
- Secure stored commodities by eliminating bird roosting sites, rodent hiding sites, and feral animal dunging
- Prevent fecal contamination of feed delivery areas
- Put guards over water tanks to prevent fecal contamination
- Use piped potable water instead of ground water
183
Vaccination for Salmonella
- Vaccinating dams with killed bacterins - protect calves <3 weeks via PT
- Vaccinating to boost nonspecific immunity (J5 vaccines to reduce the severity of disease)
- SRP vaccine (never shown to be effective)
184
Is the SRP vaccine effective?
- No
185
What are some issues with killed whole cell bacterin vaccines?
- Adverse reactions related to endotoxin
- These stem from genetic sensitivity
- lack efficacy (bad combo, e.g. things that give bad reactions and don't work)
186
How to manage herds to reduce risk of Salmonella?
- Adopt an all in-all out system in calf and heifer raising facilities
- Maintain a closed herd or make purchases from low risk herds (crucial)*
- Manage new additions to minimize stress and infection of residents (keep them off site for a month)*
- Minimize stress by feeding good rations, providing adequate time and space for transitions, and maintain clean, uncrowded maternity pens*
187
Isolation protocols to reduce Salmonella-
- Manage new additions to minimize stress and infection of residents*
- Use different facilities for calving cows and sick cows
- Avoid adult to calf contact and isolate heifers from lactating herd
- Isolate the entire group in which affected cows comingle
- Segregate Salmonella test-positive cows at calving
- Do not use colostrum or milk from test positive cattle
188
Disinfection and cleaning strategies to reduce risk of Salmonella
- Scrape manure, remove organic debris, disinfect clean, non-porous surfaces and expose to sun or UV light
- Minimize fecal contamination of feedstuffs, feeding surfaces, water troughs and equipment
- Drain and level areas that collect water
- Allow no access to pond water or feeding areas cohabited by birds and waterfowl
- Isolate the entire group in which affected cows comingle
- No shared bunk spaces, water source, feeding or handling equipment
189
Equipment and feed handling for prevention of Salmonella
- No shared bunk spaces, water source, feeding or manure handling equipment
- Leftover TMR from the cows should not be fed to the heifers
- Manure handling equipment is not used to handle feed, and it is kept out of feed lanes or food storage areas
- Make certain that feed delivery vehicles do not travel through manure or across manure-scraping lanes
- Control rodents, birds, and feral cat populations
190
Colostrum handling to reduce Salmonella
- Pasteurization of waste milk and colostrum; even refrigeration will contain growth of salmonellae in contaminated colostrum and waste milk
- Do not use colostrum or milk from test positive cattle
- Salmonella dublin can be transmitted through milk
191
Review: how is Salmonella primarily transmitted?
- Fecal-oral route
192
What are three things that determine Salmonella infection and disease?
- Innate resistance of the host
- Infectious dose
- Strain infectivity and virulence characteristics
193
What does Salmonella infect?
- Anything that has an intestinal tract
194
Are majority of Salmonella cases clinical or not?
- Subclinical mostly
195
Where is Salmonella shed?
- Oral and nasal secretions, urine, and milk
196
What can kill Salmonella in functional rumens?
Implications for management?
- Exposure to the volatile fatty acids produced by fully functioning normal rumens
- IMportant to feed good rations
197
What type of environment will allow Salmonella to survive for a long time?
- Dairy farm environmental conditions
| - Replicates in moist, warm environments
198
What can be seen in the GIT on necropsy of animals with Salmonella that might clue you in?
- Fibrin casts
- Mucosal hemorrhage and petechiation (this is why you must do it quickly)
- Ulceration
199
What additional findings can be seen with Salmonella dublin?
- Respiratory disease and joint infection
- Enlarged pale spleen on the left
- Not just diarrhea, but other signs seen first often
200
Timeline of winter dysentery?
- Acute
201
Is winter dysentery contagious?
- Yes, rapid spread
202
When does winter dysentery occur?
- WInter!
203
Disease course of winter dysentery
- Usually runs its course in 1 week
204
Age of animals affected by winter dysentery
- Primarily adults, calves >4 months
205
Morbidity and mortality of winter dysentery
- Morbidity high, mortality low
206
Etiology of winter dysentery
- Not Vibrio
| - Thought to be coronavirus more likely (seen on EM of feces and elevated titers after outbreaks)
207
Clinical signs of winter dysentery
- Explosive diarrhea (rapid spread, +/- blood, mucus, casts; musty, fetid, sweet, nasty; dehydration if persistent)
- Milk production (precipitous drop)
- Anorexia, depression
- Decreased rumen activity
- Increased small intestinal activity (dilated bowel on rectal)
- Weight loss due to decreased rumen fill
- +/- fever
- +/- cough (corona can cause respiratory diseases)
- Affected herds usually don't have outbreaks for several years (immunity???)
208
Clinical pathology findings of winter dysentery
- Unremarkable
| - Anemia if persistent dysentery
209
Pathophysiology of winter dysentery
- If coronavirus, should have typical lesions
- See lesions of colonic mucosa and hemorrhage of distal SI
- However, most usually don't die so no postmortems are done
210
Diagnosis of winter dysentery
- Clinical signs and low mortality
- Usually diagnoses based on ruling out other diseases
- Ag capture ELISA or PCR on feces
- EM possibly too
211
Dfdx for winter dysentery
- BVD/MD
- Salmonellosis
- Coccidiosis
- Exotic causes
- Indigestion (big rule out for a lot of animals having a problem)
212
Winter dysentery treatment
- None for most
- Symptomatic (fresh feed, water, salt, rest)
- Doubtful value (oral antibiotics, oral fluids, antihistamines)
213
Prevention of winter dysentery
- Appropriate biosecurity (same as with Salmonella)
| - Herds are usually resistant for several years after outbreaks
214
How long are herds usually resistant after outbreaks of winter dysentery?
- Several years
215
How long does winter dysentery take usually to run its course?
- A week or two
216
Paratuberculosis other name
- Johne's disease
217
Paratuberculosis - who gets it?
- Sheep, goats, llamas, wild ruminants
218
Time frame of paratuberculosis
- Insidious and chronic
219
Etiology of paratuberculosis
- Mycobacterium avium subspecies paratuberculosis (Map)
220
What is Johne's disease vs paratuberculosis?
- Johne's: clinical syndrome of weight loss and diarrhea
| - Paratuberculosis: animals infected but not necessarily clinical
221
Prevalence of Johne's in dairy HERDS
- 68% up from 22% (HERD prevalence)
- 2-10% of dairy cattle
- up to 60% of cows subclinical in infected herds
222
Beef herd prevalence of Johne's
- 8% up from 1-2%
223
What are the two types of losses due to paratuberculosis (general categories)?
- visible losses
| - Hidden losses
224
Visible losses of paratuberculosis - what are they and what %?
- Death and clinical disease
| - 1-6%
225
Hidden losses of paratuberculosis - what are they and what %?
- Subclinical carriers and silent infections
| - Hard to put #s on but account for anywhere from 30%-85%
226
Economic losses of paratuberculosis
- Decreased milk production (est at 1840 lb/milk lost and increase in calving interval by 2 months)
- Increased susceptibility
- Decreased genetic potential
- Loss of exports
- Increased medical costs
- Decreased slaughter weight
- Poor feed conversion
- Increased calving interval
- Premature culling
- sale yard losses with cattle exposed to Johne's
227
Death loss associated with paratuberculosis
- Overall low at any one time
228
What is onset of Johne's clinical signs usually associated with?
- Stress
229
When are cattle usually infected with Johne's?
- As calves
| - Adult infection is much less likely
230
Route of transmission for Johne's
- Fecal/oral
- Colostrum/milk
- Transplacental
231
What determines how early signs show up with Johne's?
- Increased infectious dose
232
How long before signs are cattle with Johne's shedding?
- Years before signs
233
Where and how long does Map/Johne's persist?
- Persists on pasture, soil, and in water
| - 12 + months
234
Major source of infection for Johne's****
- Fecal/oral**
235
How else besides fecal/oral can Johne's be transmitted?
- Colostrum and milk from both symptomatic and asymptomatic cows
- Transplacental transmission possible
- Sexual transmission from semen and embryos
236
What % of calves are born infected with Map if born from clinical cows?
- 20-40%
| - Also possible to have infection from asymptomatic cows but overall less likely
237
For every clinical case of Johne's, what % of the herd is probably infected?
- 15-25%
238
What is our overall sensitivity for Johne's detection?
- Likely only 35-50% of these with current technique
239
At what % of clinical cases with Johne's is everyone likely infected?
- 25-30% infected
240
Incubation of paratuberculosis
- 2-10 years
241
When are animals clinical with paratuberculosis?
- 2-6 years on average
242
Clinical signs with paratuberculosis
- Pipestream diarrhea that usually increases over several weeks
- Can appear suddenly
- No tenesmus, blood, or mucus
- Gradual weight loss, increased appetite (lethargic, emaciated, bottle jaw)***
243
What can lead to bottle jaw with paratuberculosis?
- Lack of protein usually
| - They are starving because they can't absorb anything from the GIT
244
Clinical pathology in early stages of Johne's
- NOTHING
245
Clinical pathology in later stages of Johne's
- Hypoproteinemia (albumin and globulins)
- Hypocalcemia
- Hyponatremia
- Hypokalemia
- Anemia
- Hyperphosphatemia
246
What are the four stages of paratuberculosis?
- Stage I
- Stage II
- Stage III
- Stage IV
247
Stage I of paratuberculosis
- What is it?
- Who gets it?
- Clinical signs?
- Histopath and culture results
- Silent infection
- Infection of calves primarily
- No diarrhea
- Usually not seen on histology and unlikely to culture
248
Stage II of paratuberculosis
- What is it?
- Clinical signs?
- Histopath and culture results
- Can they contaminate the environment?
- Inapparent carriers
- No diarrhea but may be prone to other diseases
- Start to become antibody positive
- Usually negative on fecal culture
- Can contaminate the environment
249
Stage III of paratuberculosis
- What is it?
- Clinical signs?
- Histopath and culture results
- Clinical disease
- weight loss, diarrhea, normal appetite, increased thirst
- Decreased production
- + fecal culture (most)
- + antibody (ELISA, AGID)
- Usually fecal PCR positive
250
Stage IV of paratuberculosis
- What is it?
- Clinical signs?
- What causes death?
- Advanced clinical disease
- Weak or emaciated with pipestream diarrhea
- Intermandibular edema and can deteriorate rapidly
- Death due to dehydration and cachexia
251
Where does Map usually proliferate?
- Ileal mucosa and regional lymph nodes
252
What are the two arms of testing for Map?
1. Detect Map or one of its parts (Antigen)
| 2. Detect immune response to Map
253
Which tests detect Map or one of its parts (Ag)?
- Culture
- PCR
- Culture/PCR combo
254
Which tests detect the immune response to Map?
- Antibodies (ELISA, AGID, CF, etc.)
| - Cell mediated immunity (gamma interferon, others)
255
Spectrum of immune responses to Map
***KNOW THIS****
- Know that early on you have a rise in cellular immunity, followed by a dip
- As the cellular immune response drops, the bacterial load will take off
- Humoral response increases when the bacterial load takes off
- This is why we can't just detect early on in the life of the animal
- See the graph
256
Why can't you detect an antibody response to Map early in the course of disease?
- No antibodies early on
257
Why can't you use CMI to test for Map?
- Many false positives, which would be a bad things
258
AGID
- when to use?
- Sensitivity and specificity?
- Animal with clinical signs
| - Sensitivity is 80% and specificity is >95% (which means 5% of false positives)
259
ELISA
- when to use?
- Sensitivity and specificity?
- Cost?
- Not good for individuals!
- Sensitivity only ~40% (but highest of all the serum antibody tests)
- Specificity is 90+%
- good screening for herds and groups
- Usually pretty accurate for advanced clinical disease in individuals
- Lower cost, higher through-put
260
Complement fixation
- Sensitivity and specificity?
- Not a very good test
| - Low sensitivity and specificity
261
Sensitivity of ELISA for clinical disease
- 92%
262
Sensitivity of ELISA for subclinical disease?
- ~40%
263
Sensitivity of ELISA for early stage II disease
- ~15%
264
Again, what is ELISA most useful for with Johne's?
- Most helpful for herd screening
| - Antibody levels jump up and down quite a bit even in infected animals
265
What is the gold standard test for Johne's?
- Fecal culture
| - Supposedly CAN detect 1-4 years prior to clinical signs
266
Sensitivity and specificity of fecal culture for Johne's
- In clinical animals, 85% sensitivity
- In subclinical animals, <50% sensitivity
- In clinical animals 99% specificity
267
Cost of fecal culture
- $50 approximately from WADDL
268
What are the drawbacks of fecal culture?
- Time consuming (up to 6 months)
- Labor intensive
- Prone to contaminants
- Expensive
269
How much do bacterial load levels vary with fecal culture?
- They also go up and down
270
Where can you get DNA fragments of Map to sample for PCR?
- Feces*
- Blood
- Milk
- Tissues (liver, lymph nodes, etc.)
271
What is PCR sometimes combined with for Map?
- Culture
272
Advantages of PCR
- High sensitivity
- High specificity
- Automation
273
Problems with PCR
- Inhibitors
- Contaminants
- Test availability
- Cost ($40-55 per head or pool)
274
Intradermal or IV Johnin test sensitivity and specificity
- Poor for both
275
What can you biopsy for Map?
- How feasible is this really?
- ileocecal junction and lymph node
| - High sensitivity and specificity
276
Cell mediated immunity test (Gamma interferon) - sensitivity and specificity?
- Good sensitivity but low specificity
| - Many false positives
277
Where is Map taken up by the immune system?
- M cells and antigen presenting cells of the intestines
278
How does Map evade the immune system?
- Survives within the antigen presenting cells avoiding lysosomal degradation
- Infection spreads through mucosa and regional lymph nodes
- Accumulating mycobacteria-laden macrophages interfere with intestinal absorption
279
Compare the efficacy of CMI vs humoral immunity with Map
- Immunity to Map depends on CMI
- Humoral immunity appears to have little or no protective value
- For effective killing of Map, macrophages require IFN-Gamma and TNF-alpha
- CD4+ T cells are the major contributor
- Towards the end of the sub-clinical phase, CMI response transitions to a humoral response and disease progresses
- CD4+ T cells decrease, and gamma delta T cells increase
- Up regulation of IL-10 and TGF-Beta with clinical disease
280
Why is Johne's difficult to control?
- SLow growing
- Usually no clinical signs until 2-5 years of age
- Shedding organism throughout subclinical phase
- Persistence of organism in the environment 55 weeks
- Diagnostic tests perform poorly on sub-clinical cows
- Available vaccines are of marginal efficacy
281
Treatment for paratuberculosis
- None practical
| - Some compounds for high value animals to emliorate clinical signs
282
Which drugs could be used for paratuberculosis, and what is the caveat of these?
- Isoniazid, rifampin, clofazimine
| - None are approved for FA
283
Post mortem findings with Johne's
- Emaciation, cachexia
- Terminal SI, cecum, colon (thickened or corrugated)
- Mesenteric and ileocecal LNs are enlarged and edematous
284
Control strategy for Johne's
- Must be individually tailored to each herd
- No quick fix - herd owner must be committed long term
- Management practices must be implemented to minimize or eliminate exposure of susceptible animals
285
What are the two arms of controlling Johne's?
1. Prevent new infections (biosecurity, "Certified free" herds, and minimize exposure to animals in the herd)
2. Test and cull infected animals
286
Vaccination for Johne's - what does it do?
How does it impact tests?
- Health risks?
- Used in control programs in the past
- Decreases clinical signs and shedding but not infection
- Prevents use of serologic tests (Not DIVA)
- Health risk to veterinarians
- Not to use in the USA
287
Johne's - is it zoonotic?
- Summary is that he thinks it's not zoonotic, but immunodeficient people or those genetically susceptible may get it
- He doesn't think it can infect that many people but could be the trigger for IBD
288
What virus is behind malignant catarrhal fever?
- Ovine herpes virus 2
289
Who gets Malignant catarrhal fever?
Who is most susceptible?
- Bison****
- Cattle
- Water buffalo
- Pigs
290
What is almost always in the history with bison or cattle that have MCF?
- Exposure to young sheep
291
Clinical signs of MCF
- Fever
- Inappetence
- Ocular and nasal discharge
- Mucosal lesions
- Diarrhea
- Depression
- Death (almost all that get it will die)
292
Post mortem signs with MCF
- Petechial hemorrhages in the mucosa, GI, respiratory tract, urinary bladder
- raised pale foci on the surface of the kidney
- General LN enlargement
293
Morbidity and mortality of MCF
- Usually sporadic morbidity, but almost 100% with bison
| - 100% mortality (of those that get it, almost all will die)
294
Transmission of MCF
- Aerosol or contact*
- Incubation can be 2-12 weeks or longer***
- It can be a long time after sheep are removed
295
Diagnosis of MCF
- Histopath, PCR, ELISA, immunofluorescence Ab
| - LN, spleen -- lung, kidney, and intestines
296
Treatment for MCF
- None
| - SUpportive care, but most die
297
Prevention of MCF
- Separate cattle and bison from high risk shedders
- Lambs and goat kids 6-9 months
- Don't allow grazing right after sheep
298
Signs of MCF in lambs and kids?
- Basically asymptomatic
299
What are the two types of copper deficiency?
- Primary and secondary
300
Primary copper deficiency?
- Straight up deficiency of copper
301
Secondary copper deficiency?
- Excess Mo, S, Fe, Zn, Ca, Cd
| - This is what they see the most
302
Clinical signs of copper deficiency
Which are most typical in 2° Cu deficiency?
- Diarrhea***
- Unthrifty appearance**
- Decreased weight gain
- Anemia
- Depigmentation
- Immunosuppression
- Myocardial fibrosis
- Spontaneous fractures
- Neonatal ataxia
*** = most typical in 2° Cu deficiency
One sign most typically dominates in a herd
303
Pathophysiology for Copper deficiency
- Unknown for most syndromes
- Essential element for many enzymes (superoxide dysmutase, cytochrome oxidase, lysyl oxidase, ascorbic acid oxidase, ceruloplasmin)
- Probable role in preventing cellular oxidative damage and Fe and S metabolism
- Lots of respiratory problems or diarrhea going on in the background
304
Diagnosis of Cu deficiency
- Which sample type is better for mild deficiencies?
- Serum Cu; good at detecting very big deficiencies
| - Liver Cu (site of body reserves; better for mild deficiencies)
305
How many serum samples do you typically get for Copper deficiency?
- 8-10 samples
306
Treatment of copper deficiency
- Injectable, oral copper
| - Also copper oxide needles
307
Prognosis for copper deficiency if showing signs or have diarrhea
- Guarded to poor
308
What do you need to be careful about if sheep are diagnosed with a copper deficiency?
- They are susceptible to copper toxicity
| - If they're using bovine trace mineral supplements, you'll see this
309
Prevention of copper deficiency
- Inorganic or organic copper in loose trace mineral (best), lick, block, injectable
- Copper boluses (in the Scablands they find they need this; should last 6 months to a year but retest)
- Follow up copper levels (key)***
310
What pigment changes do you see with Copper deficiency?
- Graying of black cattle
- Blonding of Herefords
- Blonding or turning red of black cattle can be just the sun
311
What is the most common cause of chronic diarrhea in the US (although arguably so in the PNW)?
- Parasites
312
What is the major clinical sign and loss with parasites?
- Decreased feed efficiency
313
Clinical signs with parasites
- **decreased feed efficiency
- Unthrifty, weight loss, anemia, diarrhea, edema
- If you see a pot belly with long hair and a bottle jaw, you should pull a fecal
314
Common history with parasites
- Crowded conditions, dirty environment, poor deworming history
315
Diagnosis of parasites
- A lot can be diagnosed on a simple fecal sample
316
When does Pre-Type II Ostertagiasis happen in the Northern US and the Southern US?
- Northern US: Fall
| - Southern US: Spring
317
What is the underlying pathophysiology of Pre-Type II Ostertagiasis?
- Larvae (4th stage) encyst in the abomasal wall
- Destroy parietal cells and increase abomasal pH (>5)
- This prevents the conversion from pepsinogen to pepsin and impairs protein digestion
318
When does Type II Ostertagiasis occur in the Northern and Southern US?
- Northern US: Spring
| - Southern US: fall
319
Pathophysiology of Type II Ostertagiasis?
- Larvae emerge to abomasal lumen
- Severe damage during emergence
- Damage can persist for months
320
How commonly does CVCT occur?
- Sporadic
321
Pathophysiology of CVCT?
- Liver abscess usually post-rumenitis
| - Too many carbohydrates kill off the good rumen bugs, bacteria get through the rumen wall and translocate
322
Possible sequellae with CVCT?
- Sudden death via anaphylaxis after rupture
- Metastatic pneumonia (severe dyspnea)
- Epistaxis/hemoptysis via pulmonary thromboembolism and ruptured aneurysm
- Ascites and portal hypertension leading to diarrhea
323
How can CVCT syndrome lead to diarrhea?
- Ascites and portal hypertension
324
Clinical signs of portal hypertension (2° to CVCT)?
- Abdominal distension
- Congested superficial epigastric veins
- Diarrhea
325
Clin path findings of CVCT?
- Increased GGT/SDH/AST
- Hyperglobulinemia due to chronic infection
- Anemia due to chronic infection
326
What usually happens with CVCT?
- Typically go on to exsanguinate or develop metastatic pneumonia
327
Amyloidosis Pathogenesis
- Sporadic, previous or concurrent inflammatory disease
| - Chronic antigen stimulation --> amyloid deposits in kidney, liver, etc.
328
Pathophys of diarrhea and amyloidosis
- Proteinuria --> hypoproteinemia --> decreased plasma oncotic pressure --> diarrhea
329
Findings on PE with amyloidosis
- Palpate enlarged, firm kidney
330
Which breeds get fat necrosis?
- Channel Island Breeds (Guernsey, Jersey)
331
Which individuals tend to get fat necrosis?
- Herds in good-fat condition
- Other breeds it's cattle being fattened or fed long chain saturated FA
- Usually mature animals
332
What plant has been associated with fat necrosis?
- Tall fescue pasture (acremonium coenophealum)
333
Clinical signs of fat necrosis
- Depend on size and location of mass
- Progressively obstructive masses
- Weight loss, anorexia, abdominal enlargement, diarrhea (due to restriction of the intestinal lumen), bloody stool, discomfort, etc.
334
Diagnosis of fat necrosis
- Rectal or laparotomy
335
What can cause peritonitis?
- Traumatic
- Visceral rupture
- Abscess rupture
- Iatrogenic
- Miscellaneous
336
Acute peritonitis signs
- Pain, anorexia, ileus, septicemia, abdominal distention, decreased fecal output, etc.
337
Chronic peritonitis signs
- Tendency for chronic diarrhea*
| - Typically had earlier signs of acute peritonitis
338
What can cause diarrhea with chronic peritonitis?
- Adhesions I think
339
Which age group gets coccidiosis most often?
- Growing (<1 year old) ruminants
340
Clinical signs with coccidiosis
- Diarrhea, ill thrift
| - Mild infections most common
341
Immunity with coccidiosis
- Host is essentially immune after infection
342
Bovine coccidiosis life cycle
1. Calf ingests infective sporocyst, which releases sporozoites into the gut cells. These develop and multiply asexually to produce merozoites.
2. First generation merozoites are released from ruptured gut cells and invade neighboring cells, then multiply further. Most damage from asexual reproduction.
3. Second generation merozoites differentiate into male and female gametes. The male fertilizes the female to form the zygote, or oocyst which is shed through the feces.
4. Under the correct climatic conditions (heat, humidity, oxygen), the oocyst sporulates and becomes infective.
343
How long does it take for an oocyst to sporulate?
- As little as 1 week or as long as 1 year
344
Which stage (sexual or asexual) causes most of the damage with bovine coccidiosis?
- Asexual reproduction
345
What damages the host intestinal cells with coccidiosis?
- Invasion and release of various stages of organism damages host intestinal cells.
- As cells rupture, damage results in loss of blood, fluid, albumin, and electrolytes
346
What determines the amount of damage with coccidiosis?
- Amount of damage is PROPORTIONAL to dose of oocysts
- Dose of oocysts is PROPORTIONAL to environmental contamintion
- Environmental contamination is a REFLECTION of management decisions
347
How long does coccidia survive in the environment?
- Up to 2 years
348
What do coccidia require to sporulate?
- Warmth and humidity
349
Can coccidia over-winter?
- Yes
350
What don't coccidia survive?
- Drought and high temperatures
351
Clinical signs in most cases of coccidiosis
- NONE
352
Who tends to get acute coccidiosis?
- Youngest group of animals
353
Coccidiosis: acute disease signs
- Profuse diarrhea with mucus and blood
- Fibrin casts, tenesmus, rectal prolapse
- Anemia, anorexia
- Can die before showing overt signs
354
General mortality with coccidiosis?
- Low
355
Does coccidiosis occur before 3 weeks of age?
- NO
356
Coccidiosis chronic disease
- Common in kids, lambs, crias
- Diarrhea without blood, wasting, stunted
- Weight loss, cachexia
- Poor growth, decreased feed efficiency
357
How long can it take post-coccidiosis for the gut to return to normal function?
- Weeks if ever
| - There is a decreased appetite during this time as well
358
Nervous coccidiosis signs
- Tremors, muscle fasciculations, convulsions, blindness
359
Mortality with nervous coccidiosis
- >80% mortality
360
Pathophysiology of nervous coccidiosis
- Unknown
- Maybe lesions that block Ca and Mg
- Unknown neurotoxin
- Look like polioencephalomalacia so often given thiamine
361
Coccidiosis fecal results
- Baseline shedding in immune animals and non-immune animals without signs
- BUT affected animals usually shed large numbers of oocysts
362
When does Dr. Allen usually treat coccidiosis based on fecal egg count?
- Usually 300 and above and showing signs
363
Postmortem findings with coccidiosis
- Hemorrhagic enteritis
- Villous blunting
- Acute to chronic inflammatory bowel disease
- Organisms on H&E sections
- No organisms found in CNS in nervous coccidiosis
364
Treatment options for coccidiosis
- Sulfadimethoxine
- Amprolium
- Ionophores
365
Adverse effects seen with sulfadimethoxine
- Crystalluria, CNS toxicity, marrow depression
366
Adverse effects seen with Amrpolium
- Competes with thiamine
| - Risk of polioencephalomalacia
367
Ionophores side effects
- Some toxic in high doses
| - Not for horses
368
Treatment overview for coccidiosis
- Fluid replacement
- Support (nutrition, increase comfort, decrease other stresses)
- Antibiotics
- Sulfadimethoxine, amprolium, or ionophores as coccidiostat
369
Coccidiostats for prevention of coccidiosis
- Amprolium, Lasalocid, monensin, decoquinate
| - Can put it in creep feeds
370
Limitations of anti-coccidial medications as preventatives?
- Treatment in contaminated environment may not prevent subsequent outbreaks
- Treatment with "stats" may allow resumption of disease after withdrawal
- Partial efficacy if underdosed
- May not be ingested by sick animals (he recommends individual drenching)
- Only effective against later developmental stages
371
Which environments would have a problem with coccidiosis?
- Muddy, crowded conditions
- Younger animals primarily
- Feed on the ground
372
Do range cattle tend to have a problem with coccidia?
- Not as much
373
Other management practices that can reduce coccidiosis?
- Removal of feces
- Decrease stocking densities
- Proper feeders (movable, above ground)
- Rotating animals previous to calving, lambing, kidding
- Good drainage
