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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
what toxins do C novyi produce
α & β
26
what are the clinical features of Braxy
Rapidly fatal abomasitis
27
what sheep does Braxy commonly affect
Sudden death of young non-immune sheep eating frosted forage ## Footnote Usually store lambs and ewe lambs
28
what are the clinical signs of Braxy if the lambs are alive
Sudden onset of illness with weakness, anorexia Inability to keep up with groups May be fevered (to 42ºC)
29
what is the pathogenesis of C septicum 3
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
30
what toxins does C septicum produce
Toxins produced α, β, γ, δ
31
how is c septicum diagnosed
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
what is the pathology of C septicum
Abomasitis Abomasal, duodenal walls thickened edematous, hemorrhage and necrosis (mucosa intensely inflamed or blackened) Excess turbid peritoneal fluid Some epicardial petechiae
33
where is C sordellii found
Primary pathogen of sheep intestine
34
what age of lambs does C sordellii affect
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
what is the pathology for C sordellii
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
what is shown here
C sordellii enteritis in sheep jejunum
37
how are clostridial diseases treated
Sensitive to penicillin (44, 000 IU/kg) Treatment for blackleg (penicillin) and black disease (fluke control)
38
how are clostridial diseases prevented
Vaccination! Introducing to rich feed gradually Remove affected groups to pasture, housing to prevent access to frosted grass?
39
when should ewes be vaccinated with clostridial vaccines
booster 4-6 weeks pre lambing to provide protective colostrum
40
how long to maternal clostridial antibodies last
up to 10 weeks
41
when should lambs be vaccinated for clostridial disease
10 weeks old booster 4-6 weeks later
42
when should lambs of non immune ewes be vaccinated for clostridium diseases
2 weeks booster 4-6 weeks later
43
what is the pathogen that causes septicemic pasteurellosis
mannheimia hemolyica
44
what age does septicemic pasteurellosis affect lambs
sudden death in lambs up to 12 weeks old best lambs of group
45
how do septicemic pasteurellosis lambs present
Depressed Febrile (\>41ºC) Toxic mucous membranes Dyspnea
46
what causes systemic pasteurellosis
Pasteurella trehalosi
47
when does Pasteurella trehalosi affect lambs
sudden death in recently weaned lambs
48
when does systemic pasteurellosis appear
stress conditions
49
how does systemic pasteurellosis present
Depressed Febrile (\>41ºC) Toxic mucous membranes Dyspnea
50
how is septicemic and systemic pasteurellosis diagnosed
1. history 2. clincal signs 3. pm
51
what is the gross pathology of septicemic and systemic pasteurellosis
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
what is the histology of septicemic and systemic pasteurellosis
Widespread bacterial emboli in arterioles Multifocal necrotizing hepatitis Pulmonary congestion and edema
53
how is Systemic and septicemic pasteurellosis treated
oxytetracyline?
54
how is Systemic and septicemic pasteurellosis prevented
With clostridial vaccine (Ovivac and Heptavac P plus) Ovipast plus
55
what causes acidosis
Sudden and unaccustomed intake of high quantities of rapidly fermentable carbohydrate (grain overload)
56
when does acidocis occur
Sheep (lambs) turned to graze on grain stubble with high quantities spilled grains Sudden introduction of concentrates
57
what are the two types of acidosis
rumenal and metabolic (L and D-lactate)
58
what are the clinical signs of acidosis
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
how is acidosis diagnosed
History Clinical signs (if alive) PM
60
what can be found in PM exam with acidosis
Rumen contents milky grey (porridge like) Rancid odour Rumen epithelium sloughing off Rumen pH \<5.5
61
how is acidosis prevented
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
how is acidosis treated
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
what age is polioencephalomalacia seen in
adult sheep and weaned lambs
64
what is polioencephalomalacia preceded by
dietary change (concentrates) disruption to normal feeding in prev 2 weeks (anthelmintic treatment?)
65
what is polioencephalomalacia caused by
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
what are clinical signs of polioencephaomalacia (CCN)
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
what are some ddx of polioencephaomalacia
Pregnancy toxemia Listeriosis Focal symmetrical encephalomalacia Acute coenurosis
68
how is polioencephaomalacia diagnosed
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
what is seen on PM with polioencephaomalacia
Fluorescence of cerebral cortex under UV light Histology: bilateral laminar necrosis
70
how is POLIOENCEPHALOMALACIA treated
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
when is obstructive urolithiasis seen
Male animals on high concentrate diets Tups & fattening lambs
72
what are causes of obstructive urolithiasis
Low calcium high phosphate/magnesium
73
what are the crystals seen obstructive urolithiasis
struvite crystals
74
what are clinical signs of obstructive urolithiasis
Hematuria Dribbling urine Abdominal pain Tail flicking End stages * Depression * Possibly prepucal swelling

Module 18: Ruminant Production (25 decks)

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