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NAVLE > Small Ruminants > Flashcards

Small Ruminants Flashcards

1
Q

What plant can cause “grass staggers” in sheep which lead to rabbit hopping rear limb gait, superexcitability, mustagmus and intentional head tremors (among other neuro/ataxic signs)

A

Canary grasses like folium, cano don and paspalum - genus phalaris

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2
Q

What in sheep can cause similar neuro and ataxic signs you would see if they ingested canary grasses (phalaris)

A

Hypomagnesemia - en happen when sheep graze lush pasture

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3
Q

What primarily causes bloat / rumen acidosis

A

Rich diets like alfalfa or forage , grain overload, those overeating or got into new feedstuffs, or those not adapted to the diet

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4
Q

What causes free gas bloat

A

Grain

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5
Q

What causes frothy bloat

A

Legume forage (alfalfa) more common, grain possible

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6
Q

What is the pathogenesis of rumen acidosis

A

Highly digestible chrbohudates like grain ingested in large amount ferment rapidly which drops the rumen ph, allows bacteria (lactobacillus) to further acidify the rumen which causes communal bacteria to die, osmotic pressure draws fluid into the rumen leading to systemic dehydration and shock - bacterial translocation happens due to damage rumen epithelium

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7
Q

What are clinical signs of bloat / rumen acidosis and when do they occur

A

Usually 6-36 hours after ingestion - colic, anorexia, neuro signs, abdominal distention (left), respiratory distress , toxemia, dehydration, diarrhea, death

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8
Q

How do you treat bloat

A

Orgogastric tube to relieve pressure - can give surfactant/oil, omen trouarization if in severe respiratory distress

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9
Q

How do you treat acidosis

A

Correct fluid/base disturbances and dehydration , NSAIDs for pain, rumen transfaunation, antimicrobials, thiamine supplementation

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10
Q

What clinical signs would you expect to see specific to an acidosis

A

Toxemia, dehydration, diarrhea, death

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11
Q

Define rumen transfaunation

A

Transferring when fluid with microbes + nutrients from a heathy animal to an animal with impaired rumen digestion

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12
Q

Why would thiamine supplementation help treat acidosis

A

Decreased thiamine allows for increased anaerobic metabolism which con worsen lactic acidosis - supplement thiamine to prevent

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13
Q

What comorbidities can occur due to rumen acidosis

A

Secondary polioencephalomalacia, liver abscesses, laminitis

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14
Q

What is polioencephalomalacia and what is often the cause in small ruminants

A

Thiamine deficiency causing bilateral neurologic signs - usually secondary to rumen acidosis and grain overload I can be due to diets that are low roughage high concentrate

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15
Q

How does a lack of thiamine lead to neuro signs (polioencephalomalacia)

A

Thiamine is necessary for ATP in the brain - without it, sodium and water accumulate leading to cerebral edema and necrosis of cerebral gray matter neurons

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16
Q

How does rumen acidosis lead to a thiamine deficiency

A

Thiamine produced by healthy rumen flora - with acidosis, thiamine producing bacteria go down and misfire using bacteria go up leading to deficiency

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17
Q

What are three possible differentials for a thiamine deficiency

A

Rumen acidosis, plant derived thiaminases ingested in bracken fern plants, or coccidia drug treatment with amprolium

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18
Q

What are clinical signs of polioencephalomalacia (a thiamine deficiency)

A

Bilaterally symmetric signs, central blindness, absent menace, intact PLR and palpebrals, opisthotonos, rigidity, nystagmus, head pressing, depression, recumbency

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19
Q

What is your top differential for bilateral neuro disease in small ruminants

A

Polioencephalomalacia - thiamine deficiency

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20
Q

What can help diagnose polioencephalomalacia in small ruminants post Morten

A

Edema and brain tissue that fluoresces under UV light

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21
Q

How do you treat polioercephalomalacia

A

Diane given slow IV or IM, Dexmethasone for edema

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22
Q

Define opisthotonos

A

Spasm of muscles casing backward arching of neck, back, etc

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23
Q

How can you differentiate between polioencephalomalacia and listeriosis in a small ruminant showing neuro signs

A

Polioencephalomalacia causes bilateral neuro signs , listeriosis cause, unilateral signs

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24
Q

What mostly causes listeriosis and when are uw more likely to see this

A

Spoiled or wet feed, improperly fermented silage, spoiled hay bales - most likely to see in winter

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25
Q

What is the pathogenesis of listeriosis in small ruminants

A

Animal ingests listeria monocytogenes through spoiled feed, the bacteria then crosses mucosal surfaces and invades any microabrasions - travels through axons of cranial nerves to CNS causing microabsesses and focal encephalitis

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26
Q

What are clinical signs of listeriosis

A

Unilateral cranial nerve signs / unilateral facial paralysis causing dropped jaw, dysphasia, absent palpebral reflex, drooling , heat tilt, circling , nystagmus, febrile , dehydration, recumbency

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27
Q

How do you treat listeriosis

A

Antimicrobials like oxytetracycline or penicillin, NSAID’s and fluid support

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28
Q

Are you more likely to see a fever with polioercephalomolacia or listeriosis

A

Listeriosis

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29
Q

What is contagious ecthyma in small ruminants

A

Orf/ sore mouth - parapoxvirus causing sores and crusts around the lips or on the mammary gland it from a nursing kid

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30
Q

What is the biggest reason you should remember contagious ecthyma

A

Can be zoonotic and cause painful skin lesions in people

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31
Q

How do you treat contagious ecthyma / orf

A

No treatment - disease is suf limiting and lasts 1-3 weeks, can resist in the herd for years

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32
Q

Orf (contagious ecythma) has a - morbidity and - mortality

A

High morbidity, low mortality

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33
Q

How do you diagnose of / contagious exthyma

A

PCR of crusts

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34
Q

What is caseous lymphadenitis and what is the causative agent

A

Bacterial disease causing subcutaneous abscesses in the head and neck lymph nodes - caused by corneybacterium pseudo tuberculosis (intracellular)

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35
Q

Otitis media causing a head tilt is usually towards

A

The affected side

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36
Q

What happens to saanen goats with papillomas

A

Often become squamous cell carcinomas

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37
Q

Why to outbreaks of cl often occur in sheep flocks

A

Bacteria (c. Pseudotuberculosis) an persist in soil and herds for years, often spread by shearing with infected Clippers

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38
Q

What clinical signs do you see with cl and when

A

2 weeks to 6 months after exposure - enlarged lymph nodes (submandibular, parotid , Supra mammary) filled with caseous material, could see systemic disease due to internal abscesses if severe (respiratory distress weight loss, etc)

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39
Q

How do you diagnose cl

A

Culture and serology

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40
Q

How do you treat cl

A

Lance and drain abscesses (be careful disposing contents - do not just lance in the stall ) / cull affected animals , systemic antibiotics can help prevent secondary infections

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41
Q

Can you vaccinate against cl

A

No - risk of adverse reactions and only decreases severity of disease (does not eliminate from herd)

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42
Q

What is OPP and CAE in sheep and goats

A

Ovine progressive pneumonia and caprine arthritis encephalitis virus - both retroviruses/ RNA viruses causing chronic disease

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43
Q

How do you treat OPP and CAE

A

No treatment - cull affected animals

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44
Q

How are OPP and CAE transmitted

A

Transmitted to lambs and kids through colosseum, then causes lifelong subclinical disease usually

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45
Q

What clinical signs can you see with CAE

A

Poly arthritis in adults, encephalitis in kids , chronic mastitis in adults causing hardbag

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46
Q

What clinical signs could you see with OPP in sheep

A

Pneumonia, poor doers (weight loss, lethargic, mastitis) - affects adults more than lambs

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47
Q

How do you diagnose OPP and CAE

A

Serology - positive antibody means active infection because this is a lifelong disease

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48
Q

When are you likely to see urolitriasis in sheep and goats

A

wethers, Males castrated young (less than 6 months) on high grain diet /rich legume hay that develop the calculi - also if diet has an improper mineral balance, usually at 1-3 years Old

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49
Q

Define urolithiasis

A

Formation of urinary calculi/stones in the urinary system

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50
Q

Describe the treatment and reoccurrence rate of urolithiasis

A

Usually doesn’t work and recurrence happens often - obstruction happens due to size of urethra and number of calculi formed

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51
Q

What are the most common sites of obstruction with urolitiasis

A

Urethral process and sigmoid flexure common

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52
Q

What are the most common calculi types formed with urolithiasis in males

A

Calcium or struvite

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53
Q

What are clinical signs of urolithiasis

A

Stranguria, tail flagging, dribbling urine, teeth grinding, lethargy , anorexia, recumbency

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54
Q

How do you diagnose urolithiasis in small ruminants

A

Azotemia, enlarged bladder on abdominal ultrasound, free abdominal urine on ultras and if bladder ruptured , radiopaque calculi on rads

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55
Q

How do you treat urolithiasis

A

Amputate the urethral process (where they get stuck), tube cystotomy, perineal urethrostomy , urinary acidifies / systemic support

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56
Q

What is a perineal urethrostomy and why would you do it

A

Surgery to make a permanent opening in the urethra for urine outflow - to treat polithiasis in males

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57
Q

Why is parasitism common in small ruminants herds

A

Significant resistance to common dewormers in the US

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58
Q

What ave common internal parasites in small ruminants

A

Coccidia, strongyles (like haemonchus), lungworms

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59
Q

Describe coccidia in young ruminants

A

Causes profuse diarrhea - 3 to 6 months old commonly susceptible

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60
Q

Describe the effect of haemonchus / barber pole worm in small ruminants

A

Severe anemia (pale famancha score ), bottle jaw (head and neck ventral edema), weight loss, diarinea

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61
Q

Describe lungworm infections in small ruminants

A

Causes coughing - diagnose with baermann exam

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62
Q

Describe what parasite control programs for internal parasites should look like in small ruminants and why

A

Should be targeted to avoid anthelmintic overuse - fecal parasite counts done before and after deworming to detect resistance, pasture rotation, routine feces removal, routine famancha scoring

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63
Q

What are common external parasites of small ruminants

A

Lice, mange mites (chorioptic mange)

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64
Q

Describe lice infestations in small ruminants

A

Musty in goats causes pruritis, patchy alopecia, requires multiple rounds of insecticide treatment to kill all life stages

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65
Q

Describe mange mites in small ruminants

A

Mostly in goats - causes alopecia and pruritis

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66
Q

Where do you usually find chorioptic mange mites in small ruminants

A

On legs, rarely ventral abdomen

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67
Q

What is the causative agent of Johne’S disease in small ruminants

A

Mycobacterium avium paratuberculosis

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68
Q

How are small ruminants infected with Johnes disease

A

Through contaminated milk or feces, trans placental if dam infected - either near the bacteria or develop a chronic disease state

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69
Q

What are clinical signs of John’s disease in small ruminants

A

Asymptomatic until 2-7 years old, chronic weight loss, diarrhea

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70
Q

How do you diagnose and treat Johnes in small ruminants

A

Serology ( fecal culture takes awhile ) - no treatment, cull animals and offspring

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71
Q

What is scrapie in small ruminants

A

Transmissible spongiform encephalopathy in sheep mostly causing progressive behavioral and neurologic signs

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72
Q

What is important to remember about scrapie in small ruminants

A

Reportable!

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73
Q

What causes scrapie

A

Prior that is ingested and invades lymphoid tissue then CNS causing spongiform degeneration

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74
Q

What are clinical signs of scrapie

A

Progressive over 6 months, behavior changes, intense pruritis, gait abnormalities, anorexia, weight loss, wool loss

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75
Q

How do you treat scrapie in small ruminants

A

No treatment - cull affected or exposed animals, entire here might be depopulated

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76
Q

What is bighead in sheep

A

Form of malignant edema caused by closhidium novyi type A

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77
Q

What is black disease and what is the causative agent, affecting sheep and cattle

A

Infectious necrotic hepatitis - caused by clostridium novyi type B

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78
Q

Describe the pathogenesis of black disease - what is it similar to?

A

Endosperm are ingested and lodge in the liver , liver dukes in sleep cause damage to the liver which causes the bacteria to release toxins that cause severe liver damage and red blood cell destruction - very similar to redwater disease

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79
Q

What are clinical signs of black disease in sheep

A

Sudden death with no clinica signs usually

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80
Q

How do you diagnose black disease

A

Large areas of damaged tissue in liver that are grey to black with a foul odor - post mortem

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81
Q

How do yo treat and prevent black disease

A

Usually isn’t treated, disease progresses too rapidly - prevent with the 7 way bacteria vaccine (2 doses)

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82
Q

What is the causative agent of overeating disease / pulpy kidney disease

A

Clostridium perfringens type D

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83
Q

What is the causative agent of overeating disease / pulpy kidney disease

A

Clostridium perfringens type D

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84
Q

Why is overeating disease also called pulpy kidney disease

A

Causes rapid carcass decomposition that causes pulpy kidneys on post Mortem

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85
Q

When are you likely to see cases of overeating disease

A

Mostly in sheep and goats under 2 years on a high grain ration or fattening lambs on rich pasture

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86
Q

If clostridium perfringens is a normal inhabitant of the git, why does overeating disease happen

A

Normal fora but causes disease after excessive ingestion of feed or grain

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87
Q

What are clinical signs of overeating disease

A

Decreased appetite, weakness, incoordination, diarrhea, nervous signs, death, can see glucosuria

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88
Q

How do you treat and prevent overeating /pulpy kidney disease

A

Prevent with 7 way bacterin vaccine - no treatment

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89
Q

What clinical signs are seen with yellow lamb syndrome

A

Icterus, weakness, acute death

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90
Q

What is the causative agent of yellow lamb disease

A

Clostridium pertringers type A

91
Q

How do you diagnose yellow lamb syndrome

A

Hemolysis, anemia, hemoglobinuria, icterus, fever

92
Q

You have a pregnant ewe who is ataxic, reluctant to rise, has mild muscle tremors and is anorexic; she also has a high BhB . What is your top differential and how do you treat

A

Pregnancy toxemia - induce partition asap with something like Dexmethasone

93
Q

What is the causative agent caseous lymphadenitis and how do you treat

A

Corneybacterium pseudoteberculosis - cull because it recurs and is not well controlled with antibiotics

94
Q

What vector is required to transport blue tongue virus

A

Culicoides

95
Q

How do you treat acute copper toxicity in sheep

A

D-penicillamine, vitamin E

96
Q

Blue tongue causes widespread -

A

Multisystemic vasculitis causing edema of ears and face, loss of oral mucosa and remarriages in spleen and lymph nodes

97
Q

What might you see that would lead you to suspect a lungworm infection

A

Cough, weight loss, dyspnea, tachypnea

98
Q

What defect will you see with blue tongue virus (lambs from infected ewes)

A

Hydranencephaly

99
Q

Finding acid fast rods on stain from a lymph node indicates what disease process (and causative agent)

A

John’s disease - mycobacterium avian paratuberculosis

100
Q

What is the name and causative agent of hairy shaker disease

A

Border disease, pestivirus similar to bvd and classical swine fever

101
Q

What occurs in pregnant ewes infected with hairy shaker disease /border disease

A

Abortion, fetal resorption, mummification, death

102
Q

What occurs in lambs born from ewes infected with border disease / hairy shaker disease

A

Underweight lambs, muscle tremors, hairy or pigmented fleece, musculoskeletal defects (brachygnathia)

103
Q

Would you expect only one or multiple lambs to be affected by hairy shaker disease

A

Can affect over 50% of lambs when introduced, often endemic

104
Q

What would you see on necropsy of a lamb infected with border disease ( pestivirus)

A

Demyelination of CNS white matter, glial cell hyperplasia, cerebral cavitations

105
Q

What would you see on necropsy of a lamb infected with border disease ( pestivirus)

A

Demyelination of CNS white matter, glial cell hyperplasia, cerebral cavitations

106
Q

How do you treat border disease /hairy shaker disease

A

No effective treatment or vaccines

107
Q

How do you treat border disease /hairy shaker disease

A

No effective treatment or vaccines

108
Q

Describe antibodies for hairy shaker disease

A

High antibody - subsequent immunity
Low antibody - possible persistent infection
Mingle early in breeding season so immunity can develop

109
Q

What TSE - transmissible spongiform encephalopathy affects sheep specifically

A

Scrapie

110
Q

What is the biggest difference in scrapie and BSE if both are TSE

A

There is no evidence of zoonosis with scrapielike there is with BSE /mad cow disease

111
Q

What are clinical signs of scrapie in sheep

A

Intense pruritis, biting, lip smacking incoordination, gait abnormalities , bunny hopping, convulsions I wight loss

112
Q

How is scrapie transmitted and when are you likely to see clinical signs

A

Transplacental - see signs 2-5 years after infection

113
Q

Why does scrapie have no effective treatment

A

Caused by an abnormal protein (prion) is resistant to heat and other sterilization procedures

114
Q

Why does scrapie have no effective treatment

A

Caused by an abnormal protein (prion) is resistant to heat and other sterilization procedures

115
Q

You suspect scrapie in a sheep who is bunny hopping, trembling and has intense pruritis , what is the first thing you do

A

Report to the state vet - reportable!!

116
Q

You suspect scrapie in a sheep who is bunny hopping, trembling and has intense pruritis , what is the first thing you do

A

Report to the state vet - reportable!!

117
Q

How can you diagnose scrapie in sheep

A

Biopsy of the lymphoid tissue in the 3rd eyelid or tonsils

118
Q

What would be seen on histology of the brain of a ewe infected with scrapie

A

Intracytoplasmic vacuolization of neurons

119
Q

Where are uroliths most likely to cause a urethral obstruction in male goats + sheep

A

Urethral process (narrow extension of urethra at tip of penis ), second is the sigmoid flexure

120
Q

What are the most common uroliths causing a urethral obstruction in male goats

A

Calcium or struvite (magnesium ammonium phosphate)

121
Q

What are the most common uroliths causing a urethral obstruction in male goats

A

Calcium or struvite (magnesium ammonium phosphate)

122
Q

What diets are most likely to cause urolithiasis in small ruminants leading to a urethral obstruction

A

Diets high in grain, phosphorous or magnesium or low in roughage

123
Q

A male goat presents with urine dribbling, tail flagging, hematuria and prenuptial swelling, what is your top differential

A

Urolithiasis causing a urethral obstruction

124
Q

What could be a result of urethal obstruction due to urolithiasis

A

Hydronephrosis, bladder rupture, azotemia /uremia leading to a uroabdomen, neuro signs, recumbency, inappetence

125
Q

What are some options for treating urethral obstruction due to urolithiasis

A

Amputate urethral process, perineal urethrostomy, tube cystotomy

126
Q

What is the causative agent of ulcerative posthitis / pizzle rot

A

Corneybacterium renale

127
Q

When are you likely to see a case of pizzle rot

A

Castrated male sheep usually

128
Q

What condition affecting females is similar to ulcerative posthitis and why does it occur

A

Ulcerative vulvitis - happens if the vulva / perineum is not kept clean

129
Q

What factors predispose male sheep to pizzle not / ulcerative posthitis

A

High protein diet (over 16%), ulcerations around the prepuce that become infected with c. Renale , excess hair around the prepuce that traps urine

130
Q

What kind of diet can predispose male sheep to pizzle rot and why

A

High protein (over 16%) - because higher protein increases urea in the urine which is hydrolyzed to ammonia by C. Renale causing irritation to penis and surrounding areas

131
Q

What type of bacteria is C. Renale and what does it cause

A

Gram positive urease producing bacteria causing pizzle rot/ ulcerative posthitus

132
Q

What can be given to treat ulcerative posthitis caused by C. Renale

A

Penicillins and cephalosporins - Beta lactams or topical bacitracin or copper sulfate

133
Q

What clinical signs might you see with pizzle rot

A

Prenuptial swelling and ulceration , urine scald of perineal skin, trouble urinating or breeding

134
Q

What is high on your differential list in goat kids showing acute septicemia and CNS signs

A

Mycoplasma mycoides

135
Q

What is one of the most economically important parasitic diseases in small ruminants

A

Haemonchus contortus

136
Q

What clinical signs would you expect to see from haemonchus contortus infection

A

Failure to thrive, weight loss , decreased appetite, bottle jaw, systemic anemia

137
Q

Why would bottle jaw be a sign of haemonchus contortus infection

A

Intermandibular pitting edema due to a low blood protein level

138
Q

Why is haemonchus contortus such a big problem for small ruminants

A

Becoming more resistant to anthelmintics - due to naturally occuring resistance genes, allowing parasites to survive in the host and the environment

139
Q

Describe the fecundity of H. Contortus

A

Very high - a single worm can produce 5000 eggs perday and goats have an average of 300 worms per goat

140
Q

How many eggs perday are produced in the goat infected with H. Contortsus

A

1.5 million eggs per day

141
Q

What is the current recommendation for treating H. Contortus infections

A

Identity animals with a high worm burden and treat therapeutically before it becomes a disease issue

142
Q

How can you monitor small ruminants for H. Contortus infection

A

Famancha scoring - deworm at 4-5

143
Q

Describe the idea of refugia in terms of treating H. Contortus infections

A

70% of worms occur in 30% of ruminants - only treating those with the high worm burden (the 30%) leaves a population of harm, not exposed to dewormer that are still sensitive to treatment (only treat those who use clinically affected to prevent resistance formation)

144
Q

Can sheep be infected with caprine arthritis encephalitis and vice verse for OPP (ovine progressive pneumonia)

A

Yes - either can be infected

145
Q

How is cae/opp mostly transmitted

A

Vertically from colostrum or horizontal with secretion of mononuclear cells

146
Q

What clinical signs of cae and OPP would you expect to see in adults and kids

A

Adults - large swollen knees, degenerative joint changes, symmetrical firm swelling of mammary gland, inability to maintain weight, Loss of production ability
Kid - encephalitis

147
Q

Describe the current CAE surveillance protocol

A

Annual testing of each animal in the herd - cull clinically affected or sero positive animals ( or have separate housing available for the negatives) I raise kids of the positive animals on preventative program

148
Q

List common viral , bacterial, protozoal and other causes of neonatal diarrhea in kids and lambs

A

Coronavirus, rotavirus, E. Coli, salmonella, cryptosporidium , FPT, colostrum quality

149
Q

List common viral , bacterial, protozoal and other causes of neonatal diarrhea in kids and lambs

A

Coronavirus, rotavirus, E. Coli, salmonella, cryptosporidium , FPT, colostrum quality

150
Q

What is the most common enteric disease leading to diarrhea in small ruminants

A

Johnes disease

151
Q

Describe Johnes direct in adult smalluminants

A

Chronic weight loss with a good appetite, not common to have associated diarrhea but they can - con see clinical disease at a year old

152
Q

Differentiate between Johne’s disease in cattle versus small ruminants

A

In cattle Johnes is mostly associated with very runny diarrhea and though cows are infected at a young age, they often don’t show disease until later (6-7 years old) - in small ruminants, they can show disease at a year old and are not likely to have diarrhea

153
Q

What is important to remember about serologically testing for Johnes disease in small ruminants

A

Can cross react w/ C. Pseudotuberculosis (cause of caseous lymphadenitis)

154
Q

When do goats reach puberty

A

6-8 months

155
Q

Describe the cyclically of goats

A

Short day breeders (October - December) but cycle year round near the equator

156
Q

Do goats have the same estrous cycle as sheep

A

No - goats 21 days, sheep 17 days

157
Q

Describe the proestrus phase in goats.

A

No mating, buck interested in doe, only lasts 1 day

158
Q

Describe estrus in the goat

A

Estradiol increases, vulva swelling , reddenedand moist, tail tagging, lasts 12-36 hours, ovulation occurs at the end of estrus

159
Q

Describe diestrus in goats

A

18 days usually but can be shortened by introducing the buck

160
Q

Will you see hemorrhage during metestrud in goat

A

No

161
Q

Describe scrapie in sheep - are goats affected

A

Goats rarely affected - total progressive neurologic disease in small ruminants (tse) I has a known genetic component in sheep

162
Q

What plays significant role in transmission of scrapie

A

Infected fetal fluids

163
Q

What is the incubation period for scrapie in sheep

A

2-4 years minimum

164
Q

What is the incubation period for scrapie in sheep

A

2-4 years minimum

165
Q

What kind of bacteria is Corneybacterium pseudotuberculosis

A

Facultative anaerobic gram positive colloid rod

166
Q

What Will C. Pseudotuberculosis look like on blood agar

A

Zone of hemolysis around the colony, then dry hockey puck colonies that are easily moveable

167
Q

What is the biggest contributor to transmission of caseous lymphadenitis

A

Environment contamination (persist for weeks ) - bacteria either inhaled, ingested or crosses skin via a break in the epidemic

168
Q

Clinical signs of caseous lymphadenitis masthe consist of

A

Development of abscesses in peripheral lymph nodes - but can cause abscesses in the abdomen and thorax too

169
Q

Which lymph nodes are most commonly affected in caseous lymphadenitis in sheep? Goats?

A

Sheep - more diffuse so parotid, submandibular, prescapular, prefermoral and popliteal
Goats - paroled, submandibular, prescapular

170
Q

What is the incubation time for caseous lymphadenitis .

A

Abscesses develop within 2-6 months

171
Q

How can you test for an active infection of C. Pseudotuberculosis

A

Serology with paired titers done 2 weeks apart - a 4x increase in titers can mean active infection

172
Q

What antibiotics (though not used often) can be used to treat caseous lymphadenitis and why

A

Macrolides (erythromycin), lincosamides (clindamycin) - good abscess penetration

173
Q

Can you vaccinate against C. Pseudotiberculosis

A

Con vaccinate sheep but goats experience localized inflammatory response so not done often

174
Q

What other differential would you consider in a suspected cl case and how could you differentiate

A

Wattle cyst - non encapsulated fluid that is yellow and transparent, low cellularity (no similarity to abscess fluid)

175
Q

What other differential would you consider in a suspected cl case and how could you differentiate

A

Wattle cyst - non encapsulated fluid that is yellow and transparent, low cellularity (no similarity to abscess fluid)

176
Q

Describe ketosis in pregnant ewes

A

Called pregnancy toxemia - occurs in the last 2-4 weeks of gestation when there is increased energy demands by rapidly growing fetuses with inadequate feed intake

177
Q

What clinical signs can you expect to see with pregnancy toxemia/ ketosis

A

Non specific signs - anorexia, weakness, depression

178
Q

How do you treat pregnancy toxemia

A

Induce partition or do a C section I then IV glucose supplementation

179
Q

Ulcerative lesions on the prepuce of a ram on a high protein diet lead you to suspect and why

A

C Renale - splits wea to cause ammonia which causes the painful ulcerations

180
Q

How can you treat C renale infections in Rams

A

Decrease dietary protein , treat with penicillin

181
Q

How can you treat C renale infections in Rams

A

Decrease dietary protein , treat with penicillin

182
Q

What is fly strike

A

When her lay their eggs on an animal, the eggs hatch into maggots and start eating the animals flesh

183
Q

A farmer wants an explanation for a recent outbreak of pillioencephalomalacia in his goat herd - what do yw tell him the likely cause was

A

If goats are being fed grain, that an result in thiaminase producing bacteria that multiply in the rumen 1 destroy thiamine and lead to polio

184
Q

A farmer wants an explanation for a recent outbreak of pillioencephalomalacia in his goat herd - what do yw tell him the likely cause was

A

If goats are being fed grain, that an result in thiaminase producing bacteria that multiply in the rumen 1 destroy thiamine and lead to polio

185
Q

What disease process occurs with malignant caterral fever

A

Fatal lymphocytic vasculitis

186
Q

What disease process occurs with malignant caterral fever

A

Fatal lymphocytic vasculitis

187
Q

What is the causative agent of malignant Catarral fever spread from sheep to cattle

A

Ovine herpes virus 2

188
Q

What is the causative agent of malignant Catarral fever spread from sheep to cattle

A

Ovine herpes virus 2

189
Q

What should a normal whole blood selenium value be

A

0.05ppm se

190
Q

What type of vagal indigestion do Suffolk sheep tend to get

A

Type 4 - abomasal impaction

191
Q

Brucella causes - in male sheep

A

Epididymitis

192
Q

What is the best way to prevent C pseudotuberculosis in a herd and why

A

Vaccinate - very durable organism in the environment so en remain in the soil for years

193
Q

What type of virus is OPP - ovine progressive premonia

A

Retrovirus

194
Q

What clinical signs can you see with OPP

A

Wasting, respiratory distress, secondary bacterial infections causing coughing, depression, fever, hardbag (inductive mastitis) - encephalitic form like ataxia, muscle tremors, circling

195
Q

How do you treat OPP

A

You don’t - serologically test and remove positive animals

196
Q

How does mycoplasma mycoides affect goats

A

Causes meningitis in goat kids

197
Q

How does mycoplasma mycoides affect goats

A

Causes meningitis in goat kids

198
Q

What is bighead and how to sheep become infected

A

Swelling and edema of the face caused by clostridium novyi or sordelli - organism enter u facial wound usually in rams that are fighting/ head butting

199
Q

What is bighead and how to sheep become infected

A

Swelling and edema of the face caused by clostridium novyi or sordelli - organism enter u facial wound usually in rams that are fighting/ head butting

200
Q

How do you treat big head in a ram

A

Penicillin (a clostridial disease)

201
Q

What disease process looks similar to bighead and how can you differentiate

A

Bluetongne (viral disease causing edema of the muzzle, tongue and coronary bands) - blue tongue would usually affect more then one sheep

202
Q

What disease process looks similar to bighead and how can you differentiate

A

Bluetongne (viral disease causing edema of the muzzle, tongue and coronary bands) - blue tongue would usually affect more then one sheep

203
Q

What is the cause of gangrenous mastitis (bacterial and environment

A

Mannheimin and staphylococcus aureus - associated with ewe under nutrition and over vigorous suckling by limbo

204
Q

What is the cause of gangrenous mastitis (bacterial and environment

A

Mannheimin and staphylococcus aureus - associated with ewe under nutrition and over vigorous suckling by limbo

205
Q

How do you treat gangrenous mastitis and why

A

Euthanize at presentation - udder tissue will slough and drain easing superficial bacterial infection, poor growth and poor fleece growth occurs, carcass has to be condemned

206
Q

What part of the brain is affected in un animal with polioencephalomalacia

A

Polio causes destruction of the gray mater in the cerebrum

207
Q

What part of the brain is affected in un animal with polioencephalomalacia

A

Polio causes destruction of the gray mater in the cerebrum

208
Q

Grain overload an often result in

A

Polioencephalomalacia

209
Q

What is the causative agent of overeating disease in lambs

A

Clostridium perfringens type D enterotoxemia - also called pulpy kidney disease due to autolyzation of kidney

210
Q

What is the causative agent of overeating disease in lambs

A

Clostridium perfringens type D enterotoxemia - also called pulpy kidney disease due to autolyzation of kidney

211
Q

What is the causative agent of overeating disease in lambs

A

Clostridium perfringens type D enterotoxemia - also called pulpy kidney disease due to autolyzation of kidney

212
Q

What on necropsy would make you suspect type D clostridial enterotoxemia (overeating disease)

A

Acute mortality, widespread necrosis of small intestines, fetid smelling contents, softening of the brain and kidney

213
Q

Why are whether goats more likely to develop urolithiasis

A

Castration leads to reduced diameter of the urethra

214
Q

Why are whether goats more likely to develop urolithiasis

A

Castration leads to reduced diameter of the urethra

215
Q

What are other names for enterotoxemia

A

Overeating disease or pulpy kidney disease

216
Q

What are other names for enterotoxemia

A

Overeating disease or pulpy kidney disease

217
Q

What are other names for enterotoxemia

A

Overeating disease or pulpy kidney disease

218
Q

What is another name for spider lamb syndrome

A

Ovine hereditary chondrodysplasia

219
Q

What is arthrogyposis and what can cause it

A

Stiffness mania flexion/ extension of limbs - lupine ingestion during gestation can cause it

220
Q

Abortions in healthy ewes with thickened placentas leads you to suspect

A

Coxiella/ Q fever

221
Q

How do you treat haemunchus contortus

A

Ivermectin

222
Q

A sheep with nasal discharge flu of eosinophils and mast cells leads you to suspect - and you should treat with -

A

Oestrus Ovis - treat with ivermectin

223
Q

How do you treat bluetongue

A

Supportive are (soft feed) -no antibiotics unless secondary infection occurs

NAVLE (18 decks)

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