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Selected GI disease Flashcards

1
Q

What type of virus is BVD?

A
  • Pestivirus
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2
Q

How are biotypes determined?

A

In vitro designations

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3
Q

Non-cytopathic BVD

A
  • Do not destroy cells
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4
Q

What is the predominant biotype?

A
  • Non-cytopathic

- Persists in cattle populations

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5
Q

Reservoir for non-cytopathic BVD

A
  • PI animals
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6
Q

How does cytopathic BVD happen?

A
  • Via mutation of non-cytopathic
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7
Q

What is BVD mucosal disease?

A
  • Co-infection of homologous NCP and CP
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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

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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

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10
Q

Type I species of BVD

A
  • many subspecies
  • NCP and CP
  • Worldwide now
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11
Q

WHat is the outstanding feature of Type II BVD?

A
  • Thrombocytopenic strains
  • Causes some more damage too
  • NCP and CP
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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
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13
Q

BVD Type I and Type II - disease syndrome differences

A
  • They are similar
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14
Q

Seroprevalence of BVD

A
  • 60-85%
  • It’s widespread
  • 60-80% of cattle >1 year have seroconverted
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15
Q

Source of infection for BVD

A
  • Persistently infected animals!!

- They are responsible for persistence in herds

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16
Q

How common are PI calves?

A
  • ~2% of general cattle population

- 10-50% of US herds have at least 1

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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
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18
Q

Transmission source of BVD

A
  • PI or TI animals

- shedding it everywhere

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19
Q

How long does BVD last in environment?

A
  • <2 weeks in environment

- Can persist in the environment

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20
Q

Transmission of PI vs TI

A
  • TI shed fewer, shed for a shorter period of time compared to PI
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21
Q

Where is BVD secreted?

A
  • Most body secretions
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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)
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23
Q

BVD in pigs and wild ruminants and pigs

A
  • Isolated from many domestic and wild ruminants and pigs
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24
Q

Clinical sign variability in BVD

A
  • Subclinical to death

- Hugely variable

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25
Q

What determines BVD variability?

A
  • Immunotolerant vs immunonaive
  • Immune status (exposure, vaccines, etc.)
  • Stressed animals are worse off
  • Pregnancy status
  • Gestational age
  • Environmental stress
  • Genetic diversity of virus
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26
Q

When are PI calves infected during gestation?

A
  • 30-150d (<125 d in utero)
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27
Q

PI calf pathophys

A
  • Fetus is immunotolerant

- NCP virus persists, no effective immune response

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28
Q

Clinical appearance of BVD

A
  • Clinically normal

- Weak, poor do’er, immunosuppressed

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29
Q

Which biotype of BVD infects PI calves?

A
  • Non-cytopathic
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30
Q

Who are we most worried about protecting during gestation for BVD?

A
  • Pregnant cow!
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31
Q

<60 d BVD infection signs

A
  • Abortion, early embryonic death, congenital defects
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32
Q

60-120 day BVD infection signs

A
  • PI calf
  • Commonly die young but may rarely live to produce more PI calves
  • Always shedding large amounts of BVD
  • Immunosuppression
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33
Q

100-150 days signs BVD infection

A
  • Congenital defects
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34
Q

> 120 days clinical signs BVD infection

A
  • Calf born with antibodies to BVDV, may be normal or stunted
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35
Q

Significance of PI cows that are at repro age

A
  • may need to test more than just calves

- Cows can do it too

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36
Q

What is the most common manifestation of BVD?

A
  • Acute BVD (TI)
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37
Q

When do cows experience acute BVD most often?

A
  • 80% in 1st year life
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38
Q

Who gets acute BVD?

A
  • Immunocompetent but naive animals or fetuses >150-180 days
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39
Q

Acute BVD morbidity and mortality

A
  • Most inapparent***

- High morbidity, low mortality

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40
Q

How long are most cows infected with BVD if acutely infected?

A
  • Several weeks, but short lived viremia (2-3 weeks)

- Seroconvert but virus negative with time

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41
Q

Clinical signs of Acute BVD (TI)

A

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
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42
Q

BVD and Bovine Respiratory Disease Complex

A
  • Remember that BVD sets you up for BRD***
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43
Q

Ulcerative lesions and BVD

A
  • Around the coronet, nose, any mucosal surface
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44
Q

Most common signs of acute BVD***

A
  • Inapparent!!!
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45
Q

Papillae in the mouth with BVD***

A
  • They are blunted
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46
Q

Thrombocytopenic/hemorrhage syndrome BVD - which type of BVD?

A
  • Acute, type II, NCP, BVD
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47
Q

Mortality of Thrombocytopenic/hemorrhage syndrome BVD

A
  • Higher mortality and more severe signs
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48
Q

Mechanism of Thrombocytopenic/hemorrhage syndrome BVD

A
  • Unknown

- Virus associated with platelets, megarkaryoctes, and platelet function is altered

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49
Q

Clinical signs of Thrombocytopenic/hemorrhage syndrome BVD

A
  • Severe GIT bleeding, epistaxis, hyphema, bleeding from injection sites, etc.
  • Ecchymoses of heart and lungs (you will find on necropsy)
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50
Q

Who gets mucosal BVD?

A
  • PI animals ONLY***

- Following fetal infection <125 days with NCP virus

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51
Q

Clinical signs of mucosal BVD

A
  • Fever, lethargy, dehydration, diarrhea, mucosal erosions, neutropenia, lymphopenia, respiratory disease, acute death
  • MOST OFTEN DIE
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52
Q

Severe acute BVD and Mucosal disease

A
  • Clinically indistinguishable from severe acute BVD

- They almost always go on to die!

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53
Q

Chronic MD

A
  • RARE
  • Occasional
  • Can survive up to 18 months
  • Intermittent diarrhea
  • Poor appetite, weight loss, bloat
  • Interdigital erosions, lameness
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54
Q

How does mucosal disease occur (MOST COMMON)?

A
  • Combined infection of antigenically homologous NCP (persistent) and CP virus)
  • Spontaneous mutation from NCP to CP (MOST COMMONLY)
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55
Q

Antigenic similarity of NCP and CP in mucosal disease

A

-They are antigenically homologous

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56
Q

Vaccination and Mucosal disease

A
  • 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
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57
Q

What cells does BVD target for immunosuppression?

A
  • Lymphocytes and macrophages
  • Decreases CD4+, CD8+, and B lymphocytes as well as neutrophils
  • Also decreases neutrophilic bactericidal activity
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58
Q

Immunomodulatory agents impacted by BVD

A
  • IFN, IL-1, IL-2, and TNF-alpha

- These are the early indicators

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59
Q

Consequences of immunosuppression of BVD

A
  • Much lower capacity to fight off disease
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60
Q

Congenital defects of BVD (100-170 d)

A
  • Cerebellar hypoplasia
  • Hydranencephaly/hydrocephalus
  • Eye problems (microphthlamia, retinal atrophy, cataracts, optic neuritis)
  • Pulmonary hypoplasia (small lungs; die after death)
  • Skeletal defects
  • Thymic hypoplasia
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61
Q

Infected during 1st trimester BVD outcome (0-110d)

A
  • Abortion, congenital damage, PI calves
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62
Q

During which trimester can BVD calves be born?

A
  • 1st and 2nd trimester overlap
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63
Q

Infected during 2nd trimester BVD outcome (111-180d)

A
  • Congenital damage, fetal loss
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64
Q

Infected during 3rd trimester BVD outcome

A
  • Fetus immunocompetent and mounts a response
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65
Q

Other syndromes with BVD

A
  • Repro failure, infertility, repat breeders

- Abortion, mummies (infected <100 d)

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66
Q

When are mummies infected?

A
  • <100 d
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67
Q

Leukogram for BVD

A
  • Leukopenia
  • Lymphopenia
  • Neutropenia (severe, no left shift; helps differentiate from Salmonella which will normally have a left shift )
  • Thrombocytopenia
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68
Q

Thrombocytopenia in BVD

A
  • < 100,000/µL
  • Can bottom out <10,000/µl
  • Acute type II, NCP BVDV
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69
Q

Dfdx for BVD WITHOUT oral erosions in adults

A
  • Salmonella (has a left shift)
  • Winter dysentery
  • Johne’s
  • Copper deficiency
  • Ostertagiasis
  • Coccidiosis
  • Grain overload
  • Renal amyloidosis
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70
Q

Dfdx for BVD WITH oral erosions in adults

A
  • Vesicular stomatitis
  • MCF
  • BT/EHDV
  • FMD
  • Papular stomatitis
  • Rinderpest
  • BVD
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71
Q

Suspicion of BVD signs

A
  • Herd records (decreased production, poor repro performance, signs of immunosuppression)
  • Signalment and history
  • Clinical signs and CBC
  • Pathology and histopathology (necropsy super helpful)
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72
Q

Herd records of BVD herds

A
  • Decreased production
  • Poor repro performance
  • Signs of immunosuppression
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73
Q

Peyer’s patch in BVD

A
  • CAN be hemorrhagic in BVD
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74
Q

VI for BVD sample

A
  • Blood, feces, nasal swab, tissue
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75
Q

VI for BVD - when to use?

A
  • 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
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76
Q

BVDV Ag ELISA sample

A
  • buffy coat or serum or ear notch
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77
Q

BVDV Ag ELIA when to use?

A
  • 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
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78
Q

BVDV IHC - what sample?

A
  • Ear notch
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79
Q

BVDV ICH when to do?

A
  • Ear notch
  • They can take those and pool them and test that way or individually
  • IHC can be done at WADDL for PIs
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80
Q

Serology for BVDV

A
  • 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
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81
Q

Issues with serology for BVDV

A
  • Cross reacts with vaccines

- Kind of a pain

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82
Q

PCR for BVDV which sample?

A
  • Ear notch
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83
Q

PCR for BVDV when to use?

A
  • 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
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84
Q

Treatment for MD BVDV

A
  • None
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85
Q

Treatment for acute BVD

A
  • Support
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86
Q

Treatment for hemorrhagic syndrome

A
  • May need transfusion
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87
Q

Main principle of control for BVD

A
  • Eliminate PI animals
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88
Q

Testing for BVDV with new animals

A
  • Test all incoming (ELISA or PCR)

- Quarantine all incoming for 1 month

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89
Q

What to do for BVD testing if herd tests have not been performed in the past

A
  • Test all open cows or cows that lost calves
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90
Q

Vaccination of BVDV - will it eliminate disease?

A
  • NO
  • May mask clinical signs
  • Still see repro problems and PI calves
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91
Q

WADDL recommendations for testing - who to test?

A
  • Test ALL calves

- Test all bulls and replacement heifers that have not been tested (cows lost calves)

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92
Q

WADDL recommendations for testing - what to test?

A
  • Ear notch test (pooled PCR of 36 animals)

- Individual test with Ag ELISA if positive (PI)

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93
Q

WADDL recommendations for testing - what to do with positive animals?

A
  • Quarantine

- Retest in 2-3 weeks (2% false positives)

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94
Q

What to do with PI animals?

A
  • Euthanize, slaughter, BVD feedlot (???)

- Don’t sell your problem

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95
Q

<12 samples for BVD Ear Notch testing

A
  • No pooling

- Just do Ag-ELISA

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96
Q

At 36+ samples BVD Ear notch testing

A
  • Do the PCR pool up to 36 and then Ag-ELISA per head if needed
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97
Q

Which BVDV tests go for antibody?

A
  • Serology

- Also use to determine type I and type II

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98
Q

Which BVDV tests go for antigen?

A
  • VI
  • PCR
  • Ag ELISA
  • Ag IHC
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99
Q

Which test for export testing?

A
  • Viral isolation

- 5-9 days for results

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100
Q

Can PCR differentiate PI and TI?

A
  • No

- Too sensitive

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101
Q

Can Ag ELISA differentiate PI and TI?

A
  • Yes
  • Only detects high levels of antigen
  • Good for herd screening
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102
Q

WHich are screening tests for BVDV?

A
  • Ag ELISA
  • PCR
  • Ag IHC
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103
Q

Cow vax recommendations for BVD

A
  • 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
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104
Q

Calf vax recommendations

A
  • Protect against systemic infection
  • +/- branding (MAY be too young though!)
  • 3-4 weeks before weaning
  • 3 times the first year
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105
Q

Which products for BVDV vaccinations?

A
  • Killed vs MLV

- Brand

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106
Q

Which type of vaccine for BVDV in a cow that didn’t receive vaccines prior to breeding?

A
  • Have to use killed
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107
Q

Brand of BVDV vaccine

A
  • He recommends using the same vaccine throughout life
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108
Q

What causes and influences coccidiosis?

A
  • Caused and influenced by MANAGEMENT
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109
Q

Etiology of Coccidiosis

A
  • Eimeria and Isospora
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110
Q

Can Eimeria in cattle infect sheep/goats and vice versa?

A
  • No, unless immune compromised
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111
Q

PPP of Coccidiosis

A
  • Variable with species
  • They don’t shed until at least 17 days
  • Don’t have clinical signs until shedding
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112
Q

Where is coccidiosis normally found?

A

“Normal” inhabitant of adult GIT

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113
Q

Who gets Salmonellosis?

A
  • All species
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114
Q

Prevalence of Salmonellosis?

A
  • CA dairy herds up to 75%
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115
Q

Is Salmonella host specific?

A
  • No, most serotypes are non-host specific
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116
Q

Make sure you go back and make notecards for the one lecture you missed on 3/7

A

:)

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117
Q

Carriers and Salmonellosis

A
  • Host adapted Salmonella, which increases chance for carriers
  • They can make a carrier state
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118
Q

Subclinical infections of Salmonella

A
  • If you have clinically affected, there are probably a great many more that are subclinically affected
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119
Q

Age groups for Salmonella

A
  • From the day they are born on

- It can impact a 1 day old calf or a 15 year old calf

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120
Q

Main etiologies for calf diarrhea in the first few days of life

A
  • E. coli
  • Salmonella
  • Also Campylobacter and Clostridia, but the others are the main two
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121
Q

How can Salmonella invade?

A
  • Ocular, nasal, oral, GIT mucous membranes

- S. dublin via ingestion of milk from intramammary infection

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122
Q

Stress and Salmonella

A
  • Stress can lead to a recrudescence of of Salmonella

- Shed via feces or milk

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123
Q

What age group of animal can get Salmonella and which types of serotypes?

A
  • Any age animal

- Only invasive serotypes

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124
Q

What are the three mechanisms of diarrhea for Salmonella?

A
    1. Inflammation and necrosis
    1. Increased fluid secretion
      1. Decreased absorption and digestion
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125
Q

How does inflammation and necrosis occur with Salmonella?

A
  • Salmonella attacks the villi and invades to lamina propria
  • Macrophage response destroys organism and/or tissues
  • PMN response (inflammatory edema)
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126
Q

How does Salmonella increase fluid secretion (hypothesis)?

A
  • Locally induced PG production stimulates adenylate cyclase –> increased fluid secretion
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127
Q

How does Salmonella decrease absorption/maldigestion?

A
  • 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)
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128
Q

Clinical presentations for Salmonella

A
  1. Peracute septicemia
  2. Acute enteritis
  3. Chronic enteritis
    - All three can be concurrent in a herd
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129
Q

What 3 things determine individual Salmonella disease?

A
  • Virulence of serotype, pathogen concentration, and immune status of host
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130
Q

Who typically gets septicemia from Salmonella?

A
  • Calves and lambs 10 days to 3 months
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131
Q

Which serotypes cause Salmonella septicemia?

A
  • S. typhimurium, S. dublin
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132
Q

Clinical signs of septicemia/endotoxemia

A
  • Scleral injection
  • Petechiation (pinna)
  • Toxic (gum) line
  • Recumbent, dead
  • Can be found dead with minimal signs
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133
Q

Course of Salmonella

A
  • Hours to 1-2 days
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134
Q

Neurologic form of Salmonella signs

A
  • Opisthotonus, convulsions
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135
Q

Enteric form fo Salmonella septicemia signs

A
  • Diarrhea, colic, etc.
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136
Q

Typical hemogram with septicemia

A
  • Leukopenia (profound)
  • Hyperfibrinogenemia
  • Left shift (severe)***
  • Metabolic acidosis (+/- diarrhea, dehydration)
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137
Q

Sequela for Salmonella septicemia

A
  • Polyarthritis, fibrinous pneumonia
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138
Q

Predisposing factors for Salmonella

A
  • Failure of Passive trasnsfer

- You would want to check your program if you have an increase in Salmonella

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139
Q

What is the predominant form of Salmonella?

A
  • Acute enteritis
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140
Q

Clinical signs of acute enteritis with S. typhimurium, S. newport

A
  • Fever, enteritis, anorexia, depression, dehydration
  • Diarrhea later
  • Watery at first
  • FOllowed by mucosal shreds, casts, blood, foul odor
  • Dehydration worsens, hypothermia, etc.
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141
Q

S. dublin clinical signs with acute enteritis

A
  • Fever, anorexia, depression
  • Calves can die without diarrhea***
  • More likely to see meningitis, polyarthritis, osteomyelitis, pneumonia
  • Adults can get abortion
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142
Q

Can calves die without diarrhea with S. dublin?

A
  • YES
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143
Q

Hemogram for acute enteritis

A
  • Initial leukopenia
  • Later (3-4 d) - leukocytosis, left shift
  • Hyperfibrinogenemia
  • Metabolic acidosis
  • Hyponatremia
  • Hypokalemia (whole body)
  • Hypoproteinemia in the face of an elevated PCV
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144
Q

Mortality of acute enteritis with Salmonella and what determines it?

A
  • 0-75%

- Depends on the health of the group of calves, how naive they are, and the virulence of the strain

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145
Q

Postmortem signs with Salmonella

A
  • Enteritis (If they’ve been dead longer than 6-12 hours you can’t see this regardless)
  • Erosions of small and large bowel
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146
Q

Who gets chronic Salmonella enteritis?

A
  • Older calves (6-8 weeks)
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147
Q

Clinical signs of Salmonella chronic enteritis?

A
  • “Failure to thrive”
  • Scruffy
  • Loose stool (not diarrheic)
  • No mucosal shreds, blood, casts

-

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148
Q

Postmortem signs of Salmonella chronic enteritis

A
  • Localized necrosis of cecum/colon
  • button ulcers
  • Pseudomembranes (yellow/gray)
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149
Q

S. dublin - where can it exist?

A
  • Endemic in certain farms (adapted strain)

- Can persist in mammary glands, source of chronic mastitis

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150
Q

S. typhimurium signs

A
  • Isolated cases in adults
  • Outbreaks in calves
  • Affected cows often present with signs of abdominal discomfort, pain and colic
151
Q

S. typhimurium and RDA

A
  • They can look like an RDA
  • If they have diarrhea, sample the diarrhea
    Time: 8:38 AM
152
Q

Which strain of Salmonella is most associated with consumption of raw milk in immunocompromised hosts?

153
Q

Which strain of Salmonella is most associated with ground beef, pork, and poultry products?

A
  • S. typhimurium
154
Q

Which strain of Salmonella is most associated with turkey products?

A
  • Most commonly associated with turkey products

- Some strains with multiple antibiotic resistance plasmids

155
Q

Potential infection routes for Salmonella - which is the main?

A
  • ORAL (main)***
  • Ocular
  • nasal
  • Streak canal
  • Rectal? (may want to use new sleeves in an infected herd)
156
Q

Excretion routes of Salmonella - which is the main?

A
  • MANURE**
  • Oronasal secretions
  • Milk
  • Urine
157
Q

Diagnosis of Salmonella

A
  • History (endemic disease)
  • Clinical signs
  • Neutropenia with left shift
  • Serology usually positive within about 2 weeks of infection
  • Bacteriology
158
Q

What is the definitive test for Salmonella?

A
  • Bacteriology
159
Q

Sample for Salmonella bacteriology testing

A
  • 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
Q

What % of bacteriology for Salmonella is positive with one culture?

161
Q

Salmonella treatment for carriers and chronic cases

A
  • Ineffective
162
Q

Antibiotics for Salmonella - key principles

A
  • Won’t generally improve diarrhea (may make it worse by depressing normal flora!)
  • Best to do C&S
  • Use early in systemic animals
163
Q

Should you use antibiotics in a cow with just diarrhea?

A
  • No, likely just fluid therapy
164
Q

Antibiotics for Salmonella - when to do?

A
  • In a systemically ill animal
165
Q

Antibiotics for systemic Salmonella when monogastrics

166
Q

At what age can you give TMS?

A
  • They say about first 3 weeks of life you can get away with this monogastrics
167
Q

Cephalosporins for systemic Salmonella

A
  • Safe, effective, ELDU
168
Q

Aminoglycosides for systemic Salmonella

A
  • 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
Q

Fluoroquinolones for systemic Salmonella

A
  • Only if respiratory disease (shouldn’t use)

- (probably shouldn’t be using it)

170
Q

Other medications for systemic Salmonella

A
  • Florfenicol

- Ampicillin

171
Q

What’s the best way to try and select the correct antibiotic?

172
Q

What should fluids contain for Salmonella treatment? Routes

A
  • Sodium, bicarbonate, glucose
  • IV if in circulatory shock
  • PO if ambulatory
173
Q

Summary of treatments for Salmonella

A
  • Antibiotics based on C&S (IF they are systemic)
  • Fluids with sodium, bicarbonate, and glucose
  • NSAIDs
  • Plasma/antiserum if very expensive
174
Q

Control and prevention with host adapted strains of Salmonella (i.e. S. dublin)

A
  • Minimize stresses
  • Biosecurity (environmental hygiene; test incoming animals/purchase from free herd)
  • ID carriers (test animals >6 months; ELISA, fecal cultures, milk cultures)
175
Q

What should you do with positive carrier animals?

176
Q

Control and prevention for non-host adapted and host adapted strains

A
  • 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
Q

Salmonella survival times in the environment

A
  • Quite variable

- reality is that it can last a long time in the environment, which makes it difficult to get rid of

178
Q

How can Salmonella get into and be maintained in a herd (general, just list some ways)?

A
  • Wildlife reservoirs
  • Animal importation
  • Farm livestock
  • Slaughter houses
  • Pet animals
  • imported food
  • Imported animal and vegetable protein
179
Q

Replication cycles of Salmonella in cattle intestinal tracts

A
  • 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
Q

What are animals can act as reservoirs for Salmonella?

Which of these seems to be the most significant?

A
  • Rodents
  • Flies***
  • Feral dogs and cats
  • Birds
  • Domestic pets
  • Wild mammals
  • Humans
181
Q

What changes should be made to management to reduce Salmonella contamination? (3 major points)?

A
  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
Q

How can you reduce fecal contamination of feed and water?

A
  • 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
Q

Vaccination for Salmonella

A
  • 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
Q

Is the SRP vaccine effective?

185
Q

What are some issues with killed whole cell bacterin vaccines?

A
  • 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
Q

How to manage herds to reduce risk of Salmonella?

A
  • 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
Q

Isolation protocols to reduce Salmonella-

A
  • 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
Q

Disinfection and cleaning strategies to reduce risk of Salmonella

A
  • 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
Q

Equipment and feed handling for prevention of Salmonella

A
  • 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
Q

Colostrum handling to reduce Salmonella

A
  • 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
Q

Review: how is Salmonella primarily transmitted?

A
  • Fecal-oral route
192
Q

What are three things that determine Salmonella infection and disease?

A
  • Innate resistance of the host
  • Infectious dose
  • Strain infectivity and virulence characteristics
193
Q

What does Salmonella infect?

A
  • Anything that has an intestinal tract
194
Q

Are majority of Salmonella cases clinical or not?

A
  • Subclinical mostly
195
Q

Where is Salmonella shed?

A
  • Oral and nasal secretions, urine, and milk
196
Q

What can kill Salmonella in functional rumens?

Implications for management?

A
  • Exposure to the volatile fatty acids produced by fully functioning normal rumens
  • IMportant to feed good rations
197
Q

What type of environment will allow Salmonella to survive for a long time?

A
  • Dairy farm environmental conditions

- Replicates in moist, warm environments

198
Q

What can be seen in the GIT on necropsy of animals with Salmonella that might clue you in?

A
  • Fibrin casts
  • Mucosal hemorrhage and petechiation (this is why you must do it quickly)
  • Ulceration
199
Q

What additional findings can be seen with Salmonella dublin?

A
  • Respiratory disease and joint infection
  • Enlarged pale spleen on the left
  • Not just diarrhea, but other signs seen first often
200
Q

Timeline of winter dysentery?

201
Q

Is winter dysentery contagious?

A
  • Yes, rapid spread
202
Q

When does winter dysentery occur?

203
Q

Disease course of winter dysentery

A
  • Usually runs its course in 1 week
204
Q

Age of animals affected by winter dysentery

A
  • Primarily adults, calves >4 months
205
Q

Morbidity and mortality of winter dysentery

A
  • Morbidity high, mortality low
206
Q

Etiology of winter dysentery

A
  • Not Vibrio

- Thought to be coronavirus more likely (seen on EM of feces and elevated titers after outbreaks)

207
Q

Clinical signs of winter dysentery

A
  • 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
Q

Clinical pathology findings of winter dysentery

A
  • Unremarkable

- Anemia if persistent dysentery

209
Q

Pathophysiology of winter dysentery

A
  • 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
Q

Diagnosis of winter dysentery

A
  • Clinical signs and low mortality
  • Usually diagnoses based on ruling out other diseases
  • Ag capture ELISA or PCR on feces
  • EM possibly too
211
Q

Dfdx for winter dysentery

A
  • BVD/MD
  • Salmonellosis
  • Coccidiosis
  • Exotic causes
  • Indigestion (big rule out for a lot of animals having a problem)
212
Q

Winter dysentery treatment

A
  • None for most
  • Symptomatic (fresh feed, water, salt, rest)
  • Doubtful value (oral antibiotics, oral fluids, antihistamines)
213
Q

Prevention of winter dysentery

A
  • Appropriate biosecurity (same as with Salmonella)

- Herds are usually resistant for several years after outbreaks

214
Q

How long are herds usually resistant after outbreaks of winter dysentery?

A
  • Several years
215
Q

How long does winter dysentery take usually to run its course?

A
  • A week or two
216
Q

Paratuberculosis other name

A
  • Johne’s disease
217
Q

Paratuberculosis - who gets it?

A
  • Sheep, goats, llamas, wild ruminants
218
Q

Time frame of paratuberculosis

A
  • Insidious and chronic
219
Q

Etiology of paratuberculosis

A
  • Mycobacterium avium subspecies paratuberculosis (Map)
220
Q

What is Johne’s disease vs paratuberculosis?

A
  • Johne’s: clinical syndrome of weight loss and diarrhea

- Paratuberculosis: animals infected but not necessarily clinical

221
Q

Prevalence of Johne’s in dairy HERDS

A
  • 68% up from 22% (HERD prevalence)
  • 2-10% of dairy cattle
  • up to 60% of cows subclinical in infected herds
222
Q

Beef herd prevalence of Johne’s

A
  • 8% up from 1-2%
223
Q

What are the two types of losses due to paratuberculosis (general categories)?

A
  • visible losses

- Hidden losses

224
Q

Visible losses of paratuberculosis - what are they and what %?

A
  • Death and clinical disease

- 1-6%

225
Q

Hidden losses of paratuberculosis - what are they and what %?

A
  • Subclinical carriers and silent infections

- Hard to put #s on but account for anywhere from 30%-85%

226
Q

Economic losses of paratuberculosis

A
  • 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
Q

Death loss associated with paratuberculosis

A
  • Overall low at any one time
228
Q

What is onset of Johne’s clinical signs usually associated with?

229
Q

When are cattle usually infected with Johne’s?

A
  • As calves

- Adult infection is much less likely

230
Q

Route of transmission for Johne’s

A
  • Fecal/oral
  • Colostrum/milk
  • Transplacental
231
Q

What determines how early signs show up with Johne’s?

A
  • Increased infectious dose
232
Q

How long before signs are cattle with Johne’s shedding?

A
  • Years before signs
233
Q

Where and how long does Map/Johne’s persist?

A
  • Persists on pasture, soil, and in water

- 12 + months

234
Q

Major source of infection for Johne’s**

A
  • Fecal/oral**
235
Q

How else besides fecal/oral can Johne’s be transmitted?

A
  • Colostrum and milk from both symptomatic and asymptomatic cows
  • Transplacental transmission possible
  • Sexual transmission from semen and embryos
236
Q

What % of calves are born infected with Map if born from clinical cows?

A
  • 20-40%

- Also possible to have infection from asymptomatic cows but overall less likely

237
Q

For every clinical case of Johne’s, what % of the herd is probably infected?

238
Q

What is our overall sensitivity for Johne’s detection?

A
  • Likely only 35-50% of these with current technique
239
Q

At what % of clinical cases with Johne’s is everyone likely infected?

A
  • 25-30% infected
240
Q

Incubation of paratuberculosis

A
  • 2-10 years
241
Q

When are animals clinical with paratuberculosis?

A
  • 2-6 years on average
242
Q

Clinical signs with paratuberculosis

A
  • 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
Q

What can lead to bottle jaw with paratuberculosis?

A
  • Lack of protein usually

- They are starving because they can’t absorb anything from the GIT

244
Q

Clinical pathology in early stages of Johne’s

245
Q

Clinical pathology in later stages of Johne’s

A
  • Hypoproteinemia (albumin and globulins)
  • Hypocalcemia
  • Hyponatremia
  • Hypokalemia
  • Anemia
  • Hyperphosphatemia
246
Q

What are the four stages of paratuberculosis?

A
  • Stage I
  • Stage II
  • Stage III
  • Stage IV
247
Q

Stage I of paratuberculosis

  • What is it?
  • Who gets it?
  • Clinical signs?
  • Histopath and culture results
A
  • Silent infection
  • Infection of calves primarily
  • No diarrhea
  • Usually not seen on histology and unlikely to culture
248
Q

Stage II of paratuberculosis

  • What is it?
  • Clinical signs?
  • Histopath and culture results
  • Can they contaminate the environment?
A
  • 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
Q

Stage III of paratuberculosis

  • What is it?
  • Clinical signs?
  • Histopath and culture results
A
  • Clinical disease
  • weight loss, diarrhea, normal appetite, increased thirst
  • Decreased production
    • fecal culture (most)
    • antibody (ELISA, AGID)
  • Usually fecal PCR positive
250
Q

Stage IV of paratuberculosis

  • What is it?
  • Clinical signs?
  • What causes death?
A
  • Advanced clinical disease
  • Weak or emaciated with pipestream diarrhea
  • Intermandibular edema and can deteriorate rapidly
  • Death due to dehydration and cachexia
251
Q

Where does Map usually proliferate?

A
  • Ileal mucosa and regional lymph nodes
252
Q

What are the two arms of testing for Map?

A
  1. Detect Map or one of its parts (Antigen)

2. Detect immune response to Map

253
Q

Which tests detect Map or one of its parts (Ag)?

A
  • Culture
  • PCR
  • Culture/PCR combo
254
Q

Which tests detect the immune response to Map?

A
  • Antibodies (ELISA, AGID, CF, etc.)

- Cell mediated immunity (gamma interferon, others)

255
Q

Spectrum of immune responses to Map

KNOW THIS*

A
  • 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
Q

Why can’t you detect an antibody response to Map early in the course of disease?

A
  • No antibodies early on
257
Q

Why can’t you use CMI to test for Map?

A
  • Many false positives, which would be a bad things
258
Q

AGID

  • when to use?
  • Sensitivity and specificity?
A
  • Animal with clinical signs

- Sensitivity is 80% and specificity is >95% (which means 5% of false positives)

259
Q

ELISA

  • when to use?
  • Sensitivity and specificity?
  • Cost?
A
  • 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
Q

Complement fixation

  • Sensitivity and specificity?
A
  • Not a very good test

- Low sensitivity and specificity

261
Q

Sensitivity of ELISA for clinical disease

262
Q

Sensitivity of ELISA for subclinical disease?

263
Q

Sensitivity of ELISA for early stage II disease

264
Q

Again, what is ELISA most useful for with Johne’s?

A
  • Most helpful for herd screening

- Antibody levels jump up and down quite a bit even in infected animals

265
Q

What is the gold standard test for Johne’s?

A
  • Fecal culture

- Supposedly CAN detect 1-4 years prior to clinical signs

266
Q

Sensitivity and specificity of fecal culture for Johne’s

A
  • In clinical animals, 85% sensitivity
  • In subclinical animals, <50% sensitivity
  • In clinical animals 99% specificity
267
Q

Cost of fecal culture

A
  • $50 approximately from WADDL
268
Q

What are the drawbacks of fecal culture?

A
  • Time consuming (up to 6 months)
  • Labor intensive
  • Prone to contaminants
  • Expensive
269
Q

How much do bacterial load levels vary with fecal culture?

A
  • They also go up and down
270
Q

Where can you get DNA fragments of Map to sample for PCR?

A
  • Feces*
  • Blood
  • Milk
  • Tissues (liver, lymph nodes, etc.)
271
Q

What is PCR sometimes combined with for Map?

272
Q

Advantages of PCR

A
  • High sensitivity
  • High specificity
  • Automation
273
Q

Problems with PCR

A
  • Inhibitors
  • Contaminants
  • Test availability
  • Cost ($40-55 per head or pool)
274
Q

Intradermal or IV Johnin test sensitivity and specificity

A
  • Poor for both
275
Q

What can you biopsy for Map?

  • How feasible is this really?
A
  • ileocecal junction and lymph node

- High sensitivity and specificity

276
Q

Cell mediated immunity test (Gamma interferon) - sensitivity and specificity?

A
  • Good sensitivity but low specificity

- Many false positives

277
Q

Where is Map taken up by the immune system?

A
  • M cells and antigen presenting cells of the intestines
278
Q

How does Map evade the immune system?

A
  • 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
Q

Compare the efficacy of CMI vs humoral immunity with Map

A
  • 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
Q

Why is Johne’s difficult to control?

A
  • 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
Q

Treatment for paratuberculosis

A
  • None practical

- Some compounds for high value animals to emliorate clinical signs

282
Q

Which drugs could be used for paratuberculosis, and what is the caveat of these?

A
  • Isoniazid, rifampin, clofazimine

- None are approved for FA

283
Q

Post mortem findings with Johne’s

A
  • Emaciation, cachexia
  • Terminal SI, cecum, colon (thickened or corrugated)
  • Mesenteric and ileocecal LNs are enlarged and edematous
284
Q

Control strategy for Johne’s

A
  • 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
Q

What are the two arms of controlling Johne’s?

A
  1. Prevent new infections (biosecurity, “Certified free” herds, and minimize exposure to animals in the herd)
  2. Test and cull infected animals
286
Q

Vaccination for Johne’s - what does it do?

How does it impact tests?

  • Health risks?
A
  • 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
Q

Johne’s - is it zoonotic?

A
  • 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
Q

What virus is behind malignant catarrhal fever?

A
  • Ovine herpes virus 2
289
Q

Who gets Malignant catarrhal fever?

Who is most susceptible?

A
  • Bison**
  • Cattle
  • Water buffalo
  • Pigs
290
Q

What is almost always in the history with bison or cattle that have MCF?

A
  • Exposure to young sheep
291
Q

Clinical signs of MCF

A
  • Fever
  • Inappetence
  • Ocular and nasal discharge
  • Mucosal lesions
  • Diarrhea
  • Depression
  • Death (almost all that get it will die)
292
Q

Post mortem signs with MCF

A
  • Petechial hemorrhages in the mucosa, GI, respiratory tract, urinary bladder
  • raised pale foci on the surface of the kidney
  • General LN enlargement
293
Q

Morbidity and mortality of MCF

A
  • Usually sporadic morbidity, but almost 100% with bison

- 100% mortality (of those that get it, almost all will die)

294
Q

Transmission of MCF

A
  • Aerosol or contact*
  • Incubation can be 2-12 weeks or longer***
  • It can be a long time after sheep are removed
295
Q

Diagnosis of MCF

A
  • Histopath, PCR, ELISA, immunofluorescence Ab

- LN, spleen – lung, kidney, and intestines

296
Q

Treatment for MCF

A
  • None

- SUpportive care, but most die

297
Q

Prevention of MCF

A
  • Separate cattle and bison from high risk shedders
  • Lambs and goat kids 6-9 months
  • Don’t allow grazing right after sheep
298
Q

Signs of MCF in lambs and kids?

A
  • Basically asymptomatic
299
Q

What are the two types of copper deficiency?

A
  • Primary and secondary
300
Q

Primary copper deficiency?

A
  • Straight up deficiency of copper
301
Q

Secondary copper deficiency?

A
  • Excess Mo, S, Fe, Zn, Ca, Cd

- This is what they see the most

302
Q

Clinical signs of copper deficiency

Which are most typical in 2° Cu deficiency?

A
  • 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
Q

Pathophysiology for Copper deficiency

A
  • 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
Q

Diagnosis of Cu deficiency

  • Which sample type is better for mild deficiencies?
A
  • Serum Cu; good at detecting very big deficiencies

- Liver Cu (site of body reserves; better for mild deficiencies)

305
Q

How many serum samples do you typically get for Copper deficiency?

A
  • 8-10 samples
306
Q

Treatment of copper deficiency

A
  • Injectable, oral copper

- Also copper oxide needles

307
Q

Prognosis for copper deficiency if showing signs or have diarrhea

A
  • Guarded to poor
308
Q

What do you need to be careful about if sheep are diagnosed with a copper deficiency?

A
  • They are susceptible to copper toxicity

- If they’re using bovine trace mineral supplements, you’ll see this

309
Q

Prevention of copper deficiency

A
  • 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
Q

What pigment changes do you see with Copper deficiency?

A
  • Graying of black cattle
  • Blonding of Herefords
  • Blonding or turning red of black cattle can be just the sun
311
Q

What is the most common cause of chronic diarrhea in the US (although arguably so in the PNW)?

312
Q

What is the major clinical sign and loss with parasites?

A
  • Decreased feed efficiency
313
Q

Clinical signs with parasites

A
  • **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
Q

Common history with parasites

A
  • Crowded conditions, dirty environment, poor deworming history
315
Q

Diagnosis of parasites

A
  • A lot can be diagnosed on a simple fecal sample
316
Q

When does Pre-Type II Ostertagiasis happen in the Northern US and the Southern US?

A
  • Northern US: Fall

- Southern US: Spring

317
Q

What is the underlying pathophysiology of Pre-Type II Ostertagiasis?

A
  • 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
Q

When does Type II Ostertagiasis occur in the Northern and Southern US?

A
  • Northern US: Spring

- Southern US: fall

319
Q

Pathophysiology of Type II Ostertagiasis?

A
  • Larvae emerge to abomasal lumen
  • Severe damage during emergence
  • Damage can persist for months
320
Q

How commonly does CVCT occur?

321
Q

Pathophysiology of CVCT?

A
  • Liver abscess usually post-rumenitis

- Too many carbohydrates kill off the good rumen bugs, bacteria get through the rumen wall and translocate

322
Q

Possible sequellae with CVCT?

A
  • 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
Q

How can CVCT syndrome lead to diarrhea?

A
  • Ascites and portal hypertension
324
Q

Clinical signs of portal hypertension (2° to CVCT)?

A
  • Abdominal distension
  • Congested superficial epigastric veins
  • Diarrhea
325
Q

Clin path findings of CVCT?

A
  • Increased GGT/SDH/AST
  • Hyperglobulinemia due to chronic infection
  • Anemia due to chronic infection
326
Q

What usually happens with CVCT?

A
  • Typically go on to exsanguinate or develop metastatic pneumonia
327
Q

Amyloidosis Pathogenesis

A
  • Sporadic, previous or concurrent inflammatory disease

- Chronic antigen stimulation –> amyloid deposits in kidney, liver, etc.

328
Q

Pathophys of diarrhea and amyloidosis

A
  • Proteinuria –> hypoproteinemia –> decreased plasma oncotic pressure –> diarrhea
329
Q

Findings on PE with amyloidosis

A
  • Palpate enlarged, firm kidney
330
Q

Which breeds get fat necrosis?

A
  • Channel Island Breeds (Guernsey, Jersey)
331
Q

Which individuals tend to get fat necrosis?

A
  • Herds in good-fat condition
  • Other breeds it’s cattle being fattened or fed long chain saturated FA
  • Usually mature animals
332
Q

What plant has been associated with fat necrosis?

A
  • Tall fescue pasture (acremonium coenophealum)
333
Q

Clinical signs of fat necrosis

A
  • 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
Q

Diagnosis of fat necrosis

A
  • Rectal or laparotomy
335
Q

What can cause peritonitis?

A
  • Traumatic
  • Visceral rupture
  • Abscess rupture
  • Iatrogenic
  • Miscellaneous
336
Q

Acute peritonitis signs

A
  • Pain, anorexia, ileus, septicemia, abdominal distention, decreased fecal output, etc.
337
Q

Chronic peritonitis signs

A
  • Tendency for chronic diarrhea*

- Typically had earlier signs of acute peritonitis

338
Q

What can cause diarrhea with chronic peritonitis?

A
  • Adhesions I think
339
Q

Which age group gets coccidiosis most often?

A
  • Growing (<1 year old) ruminants
340
Q

Clinical signs with coccidiosis

A
  • Diarrhea, ill thrift

- Mild infections most common

341
Q

Immunity with coccidiosis

A
  • Host is essentially immune after infection
342
Q

Bovine coccidiosis life cycle

A
  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
Q

How long does it take for an oocyst to sporulate?

A
  • As little as 1 week or as long as 1 year
344
Q

Which stage (sexual or asexual) causes most of the damage with bovine coccidiosis?

A
  • Asexual reproduction
345
Q

What damages the host intestinal cells with coccidiosis?

A
  • 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
Q

What determines the amount of damage with coccidiosis?

A
  • 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
Q

How long does coccidia survive in the environment?

A
  • Up to 2 years
348
Q

What do coccidia require to sporulate?

A
  • Warmth and humidity
349
Q

Can coccidia over-winter?

350
Q

What don’t coccidia survive?

A
  • Drought and high temperatures
351
Q

Clinical signs in most cases of coccidiosis

352
Q

Who tends to get acute coccidiosis?

A
  • Youngest group of animals
353
Q

Coccidiosis: acute disease signs

A
  • Profuse diarrhea with mucus and blood
  • Fibrin casts, tenesmus, rectal prolapse
  • Anemia, anorexia
  • Can die before showing overt signs
354
Q

General mortality with coccidiosis?

355
Q

Does coccidiosis occur before 3 weeks of age?

356
Q

Coccidiosis chronic disease

A
  • Common in kids, lambs, crias
  • Diarrhea without blood, wasting, stunted
  • Weight loss, cachexia
  • Poor growth, decreased feed efficiency
357
Q

How long can it take post-coccidiosis for the gut to return to normal function?

A
  • Weeks if ever

- There is a decreased appetite during this time as well

358
Q

Nervous coccidiosis signs

A
  • Tremors, muscle fasciculations, convulsions, blindness
359
Q

Mortality with nervous coccidiosis

A
  • > 80% mortality
360
Q

Pathophysiology of nervous coccidiosis

A
  • Unknown
  • Maybe lesions that block Ca and Mg
  • Unknown neurotoxin
  • Look like polioencephalomalacia so often given thiamine
361
Q

Coccidiosis fecal results

A
  • Baseline shedding in immune animals and non-immune animals without signs
  • BUT affected animals usually shed large numbers of oocysts
362
Q

When does Dr. Allen usually treat coccidiosis based on fecal egg count?

A
  • Usually 300 and above and showing signs
363
Q

Postmortem findings with coccidiosis

A
  • Hemorrhagic enteritis
  • Villous blunting
  • Acute to chronic inflammatory bowel disease
  • Organisms on H&E sections
  • No organisms found in CNS in nervous coccidiosis
364
Q

Treatment options for coccidiosis

A
  • Sulfadimethoxine
  • Amprolium
  • Ionophores
365
Q

Adverse effects seen with sulfadimethoxine

A
  • Crystalluria, CNS toxicity, marrow depression
366
Q

Adverse effects seen with Amrpolium

A
  • Competes with thiamine

- Risk of polioencephalomalacia

367
Q

Ionophores side effects

A
  • Some toxic in high doses

- Not for horses

368
Q

Treatment overview for coccidiosis

A
  • Fluid replacement
  • Support (nutrition, increase comfort, decrease other stresses)
  • Antibiotics
  • Sulfadimethoxine, amprolium, or ionophores as coccidiostat
369
Q

Coccidiostats for prevention of coccidiosis

A
  • Amprolium, Lasalocid, monensin, decoquinate

- Can put it in creep feeds

370
Q

Limitations of anti-coccidial medications as preventatives?

A
  • 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
Q

Which environments would have a problem with coccidiosis?

A
  • Muddy, crowded conditions
  • Younger animals primarily
  • Feed on the ground
372
Q

Do range cattle tend to have a problem with coccidia?

A
  • Not as much
373
Q

Other management practices that can reduce coccidiosis?

A
  • Removal of feces
  • Decrease stocking densities
  • Proper feeders (movable, above ground)
  • Rotating animals previous to calving, lambing, kidding
  • Good drainage

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