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Module 18: Ruminant Production > Sudden Death in Lambs > Flashcards

Sudden Death in Lambs Flashcards

1
Q

what are reasons for sudden death in growing lambs

A

Clostridial diseases

Pasteurellosis —> septicaemia (M. hemolytica, P. Multocida), systemic (Pasteurella trehalosi)

Acidosis (grain overload) vs cerebrocortical necrosis (CCN)

Acute liver fluke

Others

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2
Q

what are clostridial diseases and the bacteria that cause them (7)

A
  1. lamb dysentery (clostridium perfringens type B)
  2. pulpy kidney (cl. perfringens type D)
  3. black leg (cl. chauvoei)
  4. tetanus (cl. tetani)
  5. black disease (cl. novyi type B)
  6. braxy (cl. septicum)
  7. abomasitis (cl. sordellii)
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3
Q

what are the clinical features of pulpy kidney

A

Enterotoxemia

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4
Q

what does pulpy kidney cause

A

Sudden death in non-immune lambs

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5
Q

what age of lamb does pulpy kidney commonly affect

A

4 weeks to 8 month old lambs

Often the bigger, better lambs

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6
Q

what could be seen in pulpy kidney if the lambs are alive

A

Severe depression

Abdominal pain

Grinding teeth

Neurological signs (seizures, opisthotonus)

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7
Q

describe the pathogenesis of pulpy kidney 12

A
  1. organism is present in gut
  2. reaches high # in presence of undigested CHO (high milk intake or excess food in weaned)
  3. in presence of trypsin and absence of antibody the protoxin is cleaved to the active ε toxin
  4. ε is 3rd most lethal C toxin
  5. ε produced and enters bood
  6. increased intestinal permeability
  7. toxin absorbed and fixes to cells in liver, kidney and brain
  8. in brain causes liquefactive necrosis, perivascular edema and hemorrhage (focal symmetrical encephalomalacia)
  9. in brain the cell tight junctions degenerate, increased permeability with fluid loss followed by elevated intracranial pressure
  10. mobilization of hepatic glycogen stores
  11. hyperglycemia, glycosuria, nervous changes
  12. death
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8
Q

how is pulpy kidney diagnosed

A

history of recent move to rich feeding

PM

C. perfringens type D in smears by gram stain, by culture and toxin gene PCR

toxin detectable in ELISA

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9
Q

what is the pathology of pulpy kidney

A

Good condition, some fecal staining

No gross lesions, clear fluid in body cavities

Small petechial hemorrhages on lungs and epicardium

Pulpy kidneys and glycosuria

Small intestinal contents in fluid

Focal symmetrical hemorrhages in basal ganglia of brain and later focal symmetrical encephalomalacia

C. perfringens type D and its toxin in small intestinal contents

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10
Q

what pathology is shown here

A

pulpy kidney

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11
Q

how does clostridium chauvoei enter

A

via skin wounds

ex. shearing, castration

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12
Q

what does blackleg affect

A

skeletal and cardiac muscle

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13
Q

how do blackleg lambs present

A

sudden death

or

if alive

dullness

febrile (<41C)

toxic mucous membranes

severe lameness with edema and emphysema

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14
Q

what toxins does c chauvoei produce

A

α, β, γ, δ

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15
Q

where are C tetani spores found

A

ubiquitous in soil

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16
Q

when is c tetani commonly associated

A

docking

castration wounds

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17
Q

what is responsible for the clinical signs in C tetani

A

production of potent neurotoxin tetanospasmin

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18
Q

what are the clinical signs of C tetani

A

generalized stiffness

rigidity of limbs

unable to swallow or eructate

progress to convulsions

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19
Q

how are early cases of C tetani treated

A

tetanus antitoxin

penicillin

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20
Q

what age does black disease affect

A

sheep of all ages

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21
Q

what does black disease affect

A

liver

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22
Q

what is C novyi associated with

A

migration of immature liver fluke in the liver

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23
Q

when is C novyi commonly seen

A

late autumn/winter

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24
Q

what does C novyi cause

A

sudden death

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25
Q

what toxins do C novyi produce

A

α & β

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26
Q

what are the clinical features of Braxy

A

Rapidly fatal abomasitis

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27
Q

what sheep does Braxy commonly affect

A

Sudden death of young non-immune sheep eating frosted forage

Usually store lambs and ewe lambs

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28
Q

what are the clinical signs of Braxy if the lambs are alive

A

Sudden onset of illness with weakness, anorexia

Inability to keep up with groups

May be fevered (to 42ºC)

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29
Q

what is the pathogenesis of C septicum 3

A
  1. Frosted kale, grass or other forage damages the abomasal wall
  2. Infection of the wall of the abomasum, invasion by C. septicum which produces α toxin to cause local and systemic effects
  3. α toxin of C. septicum is a pore forming toxin — inserts into cells and lyses them resulting in cell death — causes release of cell potassium and hemoglobin
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30
Q

what toxins does C septicum produce

A

Toxins produced α, β, γ, δ

31
Q

how is c septicum diagnosed

A
  1. History of frost and absence of vaccination
  2. PM
  3. Presence of C. septicum in profuse culture — direct detection by gram stain of mucosal lesions and heart blood
  4. Detection by immunohistochemistry in tissue
  5. Demonstration of its toxin in tissue or body cavity fluids
32
Q

what is the pathology of C septicum

A

Abomasitis

Abomasal, duodenal walls thickened edematous, hemorrhage and necrosis (mucosa intensely inflamed or blackened)

Excess turbid peritoneal fluid

Some epicardial petechiae

33
Q

where is C sordellii found

A

Primary pathogen of sheep intestine

34
Q

what age of lambs does C sordellii affect

A
  1. Acute abomasitis young lambs 3-10 weeks
  2. Sudden death and abomasitis in finishing 6-12 months
  3. Rotten lambs post vaginal prolapse in pregnant ewes?
35
Q

what is the pathology for C sordellii

A

C. sordellii morphologically distinctive (hairpin cells)

Distinct colonial morphology

Two toxins, hemolysin and lethal toxin — antigenically similar to C. difficile toxins A and B

Lesions include single abomasal ulcers which ruptures or diffuse enteritis which may be necrotic or emphysematous

36
Q

what is shown here

A

C sordellii enteritis in sheep jejunum

37
Q

how are clostridial diseases treated

A

Sensitive to penicillin (44, 000 IU/kg)

Treatment for blackleg (penicillin) and black disease (fluke control)

38
Q

how are clostridial diseases prevented

A

Vaccination!

Introducing to rich feed gradually

Remove affected groups to pasture, housing to prevent access to frosted grass?

39
Q

when should ewes be vaccinated with clostridial vaccines

A

booster 4-6 weeks pre lambing to provide protective colostrum

40
Q

how long to maternal clostridial antibodies last

A

up to 10 weeks

41
Q

when should lambs be vaccinated for clostridial disease

A

10 weeks old

booster 4-6 weeks later

42
Q

when should lambs of non immune ewes be vaccinated for clostridium diseases

A

2 weeks

booster 4-6 weeks later

43
Q

what is the pathogen that causes septicemic pasteurellosis

A

mannheimia hemolyica

44
Q

what age does septicemic pasteurellosis affect lambs

A

sudden death in lambs up to 12 weeks old

best lambs of group

45
Q

how do septicemic pasteurellosis lambs present

A

Depressed

Febrile (>41ºC)

Toxic mucous membranes

Dyspnea

46
Q

what causes systemic pasteurellosis

A

Pasteurella trehalosi

47
Q

when does Pasteurella trehalosi affect lambs

A

sudden death in recently weaned lambs

48
Q

when does systemic pasteurellosis appear

A

stress conditions

49
Q

how does systemic pasteurellosis present

A

Depressed

Febrile (>41ºC)

Toxic mucous membranes

Dyspnea

50
Q

how is septicemic and systemic pasteurellosis diagnosed

A
  1. history
  2. clincal signs
  3. pm
51
Q

what is the gross pathology of septicemic and systemic pasteurellosis

A

Lungs edematous and congested

Enlarged, hemorrhagic lymph nodes

Widespread petechiae, serosal surfaces, epicardium, kidneys

Focal necrotizing hepatitis

Upper alimentary tract erosions

Pleurisy and pericarditis

52
Q

what is the histology of septicemic and systemic pasteurellosis

A

Widespread bacterial emboli in arterioles

Multifocal necrotizing hepatitis

Pulmonary congestion and edema

53
Q

how is Systemic and septicemic pasteurellosis treated

A

oxytetracyline?

54
Q

how is Systemic and septicemic pasteurellosis prevented

A

With clostridial vaccine (Ovivac and Heptavac P plus)

Ovipast plus

55
Q

what causes acidosis

A

Sudden and unaccustomed intake of high quantities of rapidly fermentable carbohydrate (grain overload)

56
Q

when does acidocis occur

A

Sheep (lambs) turned to graze on grain stubble with high quantities spilled grains

Sudden introduction of concentrates

57
Q

what are the two types of acidosis

A

rumenal and metabolic (L and D-lactate)

58
Q

what are the clinical signs of acidosis

A

Sudden death

  • Within 24 hours from sudden introduction

Anorexia and bruxism

Distended abdomen and ruminal stasis

Severe metabolic acidosis

  • Tachypnea
  • Hyperpnea

Diarrhea

Dehydration and toxic mucous membranes

59
Q

how is acidosis diagnosed

A

History

Clinical signs (if alive)

PM

60
Q

what can be found in PM exam with acidosis

A

Rumen contents milky grey (porridge like)

Rancid odour

Rumen epithelium sloughing off

Rumen pH <5.5

61
Q

how is acidosis prevented

A

Gradually introduce to grain concentrate feeding over 3 weeks before ad-lib 100g/day per lamb recommended (as introduction)

Good quality roughage available

Closed feed storage

62
Q

how is acidosis treated

A

In severe emergency consider rumenectomy

Correct ruminal and metabolic acidosis and dehydration (sodium bicarbonate per os and IV)

Encourage feeding on forage

Rumen function stimulants (Pro-rumen)

Transfer of rumen contents from healthy sheep

63
Q

what age is polioencephalomalacia seen in

A

adult sheep and weaned lambs

64
Q

what is polioencephalomalacia preceded by

A

dietary change (concentrates)

disruption to normal feeding in prev 2 weeks (anthelmintic treatment?)

65
Q

what is polioencephalomalacia caused by

A

Caused by induced thiamine (vit B12) deficiency (ex. by overgrowth of thiaminase-producing bacteria in rumen —> altered glucose metabolism —> necrosis superficial cerebral grey matter —> generalized cerebral edema)

Occasional outbreaks also associated with high levels of dietary sulphur

66
Q

what are clinical signs of polioencephaomalacia (CCN)

A

Typical of diffuse cerebral lesion:

  • Blind, wandering, “stargazing”
  • High stepping gait
  • Head pressing
  • Dorso-medial strabismus in some cases
  • Progression to recumbency, backwards flexion of neck
  • Hyperaesthesia
  • Convulsions
67
Q

what are some ddx of polioencephaomalacia

A

Pregnancy toxemia

Listeriosis

Focal symmetrical encephalomalacia

Acute coenurosis

68
Q

how is polioencephaomalacia diagnosed

A

Decrease erythrocyte transketolase and increase thiaminase activity in feces, rumen fluid, blood (rarely used)

Usually based on clinical signs and response to treatment

PM

69
Q

what is seen on PM with polioencephaomalacia

A

Fluorescence of cerebral cortex under UV light

Histology: bilateral laminar necrosis

70
Q

how is POLIOENCEPHALOMALACIA treated

A

Early cases most likely to respond

  • IV vitamin B1 (10-20mg/kg) and dexamethasone (1mg/kg)
  • Continue vit B1 IM BID for 3 days
  • Check adequate levels of thiamine in ‘multivitamin’ injectables
  • Usually improve within 24 hours
  • May remain blind for 2-3 weeks
71
Q

when is obstructive urolithiasis seen

A

Male animals on high concentrate diets

Tups & fattening lambs

72
Q

what are causes of obstructive urolithiasis

A

Low calcium high phosphate/magnesium

73
Q

what are the crystals seen obstructive urolithiasis

A

struvite crystals

74
Q

what are clinical signs of obstructive urolithiasis

A

Hematuria

Dribbling urine

Abdominal pain

Tail flicking

End stages

  • Depression
  • Possibly prepucal swelling

Module 18: Ruminant Production (25 decks)

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