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FAMS Exam 2 Flashcards

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1
Q

What is the term for the disease caused by Trichophyton verrucosum?

A

(Ringworm/dermatophycosis)

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2
Q

What is the most common causative agent of ringworm?

A

(Trichophyton verrucosum)

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3
Q

Why is it important to know that Trichophyton verrucosum is spore forming?

A

(This is the causative agent for ringworm, spore forming indicates that it will live in the environment for a long time)

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4
Q

(T/F) You cannot write a health certificate for an animal with ringworm.

A

(T, both transmissible and zoonotic)

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5
Q

Why do ringworm lesions typically pop up on the head and neck in cattle?

A

(Bc they communicate with each other and the world with their heads → rub on stuff, lick stuff, etc.)

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6
Q

Are ringworm lesions typically pruritic?

A

(No)

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7
Q

What should you assess in a cow with extensive ringworm lesions?

A

(Immune function, could indicate there is immune compromise such as BVDV PI, chronic lymphoma, etc.)

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8
Q

(T/F) Ringworm is not associated with any production losses in cattle.

A

(T)

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9
Q

Using topical clotrimazole is an option for treatment of ringworm in cattle, what is the meat withdrawal period?

A

(24 hours/1 day)

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10
Q

What will indicate if a ringworm lesion is no longer infected and is healing?

A

(When hair is growing back in the middle of the lesion)

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11
Q

What is the pathophysiology behind primary photosensitization?

A

(Animal obtains a photodynamic agent (from ingestion, injection, or absorption) which then reacts to UV light in the skin, free radicals are released which damage cell and lysosomal membranes of skin cells causing ulceration, necrosis, and edema)

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12
Q

Why does primary photosensitization only affect the non-pigmented skin of cattle?

A

(Because pigmented skin contains melanin which is protective against the UV light needed to react with the photodynamic agents)

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13
Q

Photosensitization is more likely to affect dairy/beef (choose) cattle and why.

A

(Beef, they are out on pasture and exposed to the sun)

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14
Q

What two forages primarily cause primary photosensitization?

A

(Legumes and Brassica)

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15
Q

What antibiotic does Dr. Guynn suggest for use in cases of primary photosensitization that she usually doesn’t use in beef cattle?

A

(Excede → works on skin lesions and lasts a long time)

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16
Q

Why is the prognosis poor for secondary photosensitization when it is good for primary photosensitization?

A

(Because secondary is associated with liver damage, not a lot to do to fix the liver in cattle)

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17
Q

Why is bovine ulcerative mammilitis associated with cold weather?

A

(Because the virus that causes it (bovine herpes virus II and IV) replicates at lower temperatures)

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18
Q

The use of what type of PPE is important for preventing the spread of pseudocowpox from cattle to humans?

A

(Gloves)

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19
Q

What are cow related risk factors for teat-end hyperkeratosis?

A

(Teat conformation (long and pointy is no good), age (older), being later in lactation, longer milking time (higher production or slow milker), and questionably genetics)

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20
Q

What are the two etiologies of the impaired blood and lymph circulation that leads to udder edema?

A

(Pressure from the fetus and/or the decrease in protein oncotic pressure as IgG is being diverted to the udder)

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21
Q

Why should you perform a skin scrape on udder cleft dermatitis lesions?

A

(They have an associated with sarcoptic mange)

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22
Q

What are the three causes of polioencephalomalacia?

A

(1- Ingestion of plants containing thiaminases; 2 - rumen acidosis from eating too much high starch grain with secondary lack of production of thiamine (rare cause); 3 - eating a lot of corn gluten or distillers grain which will contain more that 0.4% sulfur)

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23
Q

What are the main clinical signs of polioencephalomalacia in cattle?

A

(Blindness, staggering, down, and seizures)

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24
Q

A deficiency in what vitamin reduces the energy available for sodium/water transport mechanisms in the cells of the brain which leads to PEM?

A

(Thiamine → cofactor for enzymes associated with energy production in the brain)

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25
Q

How does the response to thiamine supplementation for the treatment of PEM differ between if the PEM is non-sulfur or sulfur induced?

A

(Non-sulfur → up and running around in 15 minutes after giving thiamine versus sulfur induced → you look for 50% improvement in the first 24 hours after starting tx, takes days for 100% improvement and there is a good chance for relapse if thiamine tx is stopped too early)

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26
Q

What is the number one source of lead poisoning in cattle?

A

(Batteries, have you ever put your tongue on a 9v battery just to feel alive?)

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27
Q

Lead intoxication is acute/chronic (choose).

A

(Tricky me, cattle may develop signs of lead intoxication from ingestion of a single dose of lead (400-800 mg/kg) or low levels of lead (6 mg/kg) for longer periods of time)

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28
Q

What is the best treatment for lead intoxication?

A

(Calcium EDTA at various doses → binds lead)

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29
Q

Why is it controversial to treat lead intoxication?

A

(Hard to establish an appropriate withdrawal time and there is a possibility for future release of lead from the rumen, Dr. Currin usually goes with a 12 month minimum slaughter withdrawal)

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30
Q

Thrombotic meningoencephalitis (TME) is a fulminant neurological disease of cattle caused by what bacteria?

A

(Histophilus somni)

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31
Q

What is the causative agent of sleeping sickness in cattle?

A

(Histophilus somni, sleeping sickness is a trade name for thrombotic meningoencephalitis)

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32
Q

What is the antibiotic of choice for treatment of TME?

A

(Florfenicol → good penetration into brain tissue)

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33
Q

What is the most common way that listeria is obtained in cattle?

A

(Ingesting poorly ensiled feed → pH > 4.5 or moldy edges)

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34
Q

Listeria unilaterally affects which cranial nerve in cattle?

A

(The trigeminal nerve)

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35
Q

What are the four things that are needed to make appropriately ensiled feed?

A

(Moisture, anaerobic environment, bacteria, and a substrate for the bacteria to eat (usually starches))

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36
Q

Why should you not allow water deprived cattle to drink as much water as they want?

A

(Because salt has been packed away into the cells of the brain making them hyperosmolar and when they ingest a bunch of water, that water rushes into the cells and causing them to swell → brain edema, increased ICP, encephalopathy)

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37
Q

A sodium value of what or greater on a chemistry panel indicates salt intoxication?

A

(> 160 mEq/L)

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38
Q

At what rate should water be reintroduced to water deprived cattle?

A

(1-3 gallons every 6 hours for 24 hours)

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39
Q

What are the clinical signs associated with radial nerve paralysis?

A

(Dropped elbow and inability to extend the affected leg)

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40
Q

Radial nerve paralysis occurs secondarily to what issue?

A

(Prolonged lateral recumbency → why you usually limit time in tilted chutes to 30 minutes especially for larger cattle)

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41
Q

What is a cattle specific rabies clinical sign?

A

(Tenesmus)

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42
Q

How long does it take Trichostrongylus spp. to develop once eggs are passed in the manure?

A

(5-7 days to get to L3, if its cooler it will take longer)

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43
Q

Once L3 Trichostrongyles become adults in their hosts, how long does it take them to start laying eggs?

A

(3 weeks)

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44
Q

What are the two main important Trichostrongylus spp. that affect cattle?

A

(Ostertagia and Cooperia, there are other species present that contribute to parasitic gastroenteritis but rarely are the primary pathogens)

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45
Q

(T/F) Most strongylid eggs in the manure of young cattle are Cooperia spp.

A

(T)

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46
Q

The macrocyclic lactone dose for the treatment of Cooperia spp. in cattle is higher/lower (choose) than that needed to treat Ostertagia.

A

(Higher)

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47
Q

Why are Trichostrongyle infections greatest in younger cattle?

A

(Bc immunity develops over several years)

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48
Q

What results from subclinical Trichstrongyle infections?

A

(Decreased weight gain and growth from anorexia and gastric disturbance)

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49
Q

Trichostrongylus spp. infections typically are subclinical but when they become clinical, what signs do you typically see?

A

(Diarrhea, weight loss, unthriftiness, and hypoproteinemia)

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50
Q

What dewormer drug class is available in pour on formulas?

A

(Macrocyclic lactones → ivermectin, doramectin, eprinomectin, and moxidectin all have pour on formulas (as well as injectable))

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51
Q

What dewormer drug classes are available in oral formulas?

A

(Benzimidazoles (fenbendazole, albendazole, oxfendazole) and nicotinics (levamisole, morantel))

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52
Q

Parasite impact is higher on dairy/beef (choose) productions.

A

(Beef)

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53
Q

Anthelmintic resistance is an issue for all three of the major drug classes but is particularly bad for which drug class?

A

(Macrocyclic lactones → it is heavily used d/t pour on convenience and low cost)

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54
Q

How is anthelmintic resistance tested for in cattle?

A

(Fecal egg count reduction test → looking for drug efficacy over 90%)

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55
Q

How long should you wait before taking your comparison fecal egg count reduction test sample when testing a macrocyclic lactone? What about a benzimidazole?

A

(ML → 14-17 days (moxidectin 17-21), BZD → 10-14 days)

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56
Q

If your reduction in fecal egg count is 90% after using an anthelmintic, would you say that drug has:
A - Full efficacy
B - Possible resistance
C - Likely resistance
D - Highly likely resistance

A

(B, 95% and above is full efficacy, 90-95% is possible resistance, 80-90% is likely resistance, and <80% is highly likely resistance)

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57
Q

What is the main way producers are getting around anthelmintic resistance in their cattle?

A

(Combination treatment with two different drug classes)

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58
Q

(T/F) Oral administration is the most effective treatment route for intestinal parasites.

A

(T)

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59
Q

What practices can be put in place to minimize resistance to extended release eprinomectin?

A

(Do not use year after year as a sole method, consider combination treatment, leave a refugia, and use other methods of parasite control such as pasture management)

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60
Q

What is the main strategy used to maintain refugia in cattle?

A

(Selective non-treatment → leave 10-20% of the animals untreated; cannot easily ID animals that need tx bc fecal egg counts are not predictive and neither are using their weights)

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61
Q

Haemaphysalis longicornis is the vector for which disease?

A

(Theileria orientalis)

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62
Q

When is Haemaphysalis longicornis active during the year?

A

(March-November)

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63
Q

How does Haemaphysalis longicornis reproduce?

A

(Parthenogenetically)

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64
Q

What are the three locations that an esophageal obstruction is likely to occur in cattle?

A

(Thoracic inlet, right after the pharynx, and base of the heart)

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65
Q

Why would a cow with an esophageal obstruction have an increased lactate?

A

(Bc she is unable to swallow her saliva which contains sodium bicarb, could also be d/t dehydration)

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66
Q

Why would a cow with an esophageal obstruction be hypokalemic and hypophosphatemic?

A

(Hypokalemia → not eating but still losing potassium, hypophosphatemia → not swallowing her saliva which contains phosphorus)

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67
Q

What can you do to aid in your decision to treat potential aspiration pneumonia after an esophageal obstruction case?

A

(Listen to the lungs, if sounds are harsh go ahead and treat, if not tell producer to keep an eye on them)

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68
Q

Esophageal obstruction is more likely to occur in what time period after you clear the initial obstruction?

A

(Within 24 hours)

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69
Q

When checking the pH of rumen fluid, you should make sure it is definitely rumen fluid and not what other substance that can throw off your pH results?

A

(Saliva)

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70
Q

Why should you auscultate the lungs in a bloat case?

A

(If there is pneumonia and subsequent swelling of the bronchial lnn, they could be pushing on the esophagus and preventing eructation, there could also be aspiration pneumonia after bloating)

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71
Q

You should especially palpate the esophagus of calves if they bloated, why is that?

A

(Checking for a thymoma)

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72
Q

What are your treatment options for frothy bloat? 4 answers.

A

(Poloxalene, mineral oil, dish washing soap, or a permanent trocar)

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73
Q

Optimally after administering a surfactant in a case of frothy bloat, you would tube the gas out of her rumen instead of depending on her to eructate on her own, why is that?

A

(Bc she is less likely to eructate on her own due to the distension)

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74
Q

You are called about a cow/heifer with a prolapse of unknown origin coming out the back end, what are your prolapse location options?

A

(Rectal, vaginal, uterine → uterine is an emergency)

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75
Q

When you receive a call about a potential prolapse in a cow/heifer, what is a primary question you should ask?

A

(Is she pregnant or has she calved recently?)

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76
Q

You have established that a cow/heifer has a prolapse coming from her vagina and she has recently calved, what do you need to know next?

A

(If it is long (uterus) or short (vagina) and smooth (vagina) or bumpy (uterus))

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77
Q

What are risk factors for rectal prolapses? 8 answers :).

A

(Straining d/t tenesmus or dysuria, neuropathy (tail docking, alcohol epidural, spinal lymphoma), chronic coughing, genetics, neoplasia, diet (estrogenic feedstuff), obesity, and hormone treatments)

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78
Q

(T/F) Rectal prolapses are an emergency.

A

(F, urgent rather than an emergency, see it the next day if call overnight)

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79
Q

How can you gauge the prognosis of a rectal prolapse?

A

(By grading it (read grades in powerpoint), grade I and II good prognosis with prompt treatment, grade III and IV associated with risk for severe vascular injury to descending colon, requires surgical resection, poor prognosis)

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80
Q

What can be performed if you are attempting to fix a rectal prolapse but the animal is continuing to strain?

A

(An epidural, caudal in cattle and lumbosacral in other species)

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81
Q

What does it mean that an alcohol epidural is a salvage procedure?

A

(You are just trying to get them to slaughter at this point)

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82
Q

What does injecting lidocaine or oxytet around the rectum cause to aid in preventing rectal prolapses?

A

(Adhesions)

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83
Q

What are the complications associated with amputating a rectal prolapse if replacement is not an option?

A

(Strictures, peritonitis, and abscesses)

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84
Q

One of the risk factors for vaginal prolapses is advanced stage pregnancy d/t increased abdominal pressure, this is especially true for what species in what time of gestation?

A

(Multiparous ewes in the last 3 weeks of gestation)

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85
Q

Why should you increase concentrate consumption and reduce hay consumption in late gestation ewes with vaginal prolapses?

A

(That will decrease abdominal filling and hopefully decrease abdominal pressure)

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86
Q

A caslick’s procedure is best performed in what animals for treatment of Grade I vaginal prolapses?

A

(Non-pregnant animals that experience Grade I eversion during estrus → embryo donors)

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87
Q

Of your short-term retention techniques for vaginal prolapse, which is better for advanced grade and chronic prolapses?

A

(Buhner stitch, must untie at parturition)

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88
Q

Uterine prolapses are associated with which stage of labor?

A

(3rd stage, placental expulsion)

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89
Q

What are the risk factors for uterine prolapse? 5 answers.

A

(Multiparous animals, exposure to estrogenic substances, extreme weather changes and pasture composition changing mineral availability, uterine inertia/hypocalcemia/recumbency, and dystocia/retained fetal membranes/uterine tears)

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90
Q

Why are uterine prolapses an emergency? Be specific.

A

(Risk of middle uterine artery rupture)

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91
Q

(T/F) Uterine prolapses are not associated with a genetic risk.

A

(T)

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92
Q

What should you tell a producer to do if you suspect they are calling about a uterine prolapse?

A

(Do not transport that animal, restrain her, and place a bag over the uterus)

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93
Q

Why might you not reach for sugar in the case of a uterine prolapse?

A

(It can be irritating and could potentially affect her future fertility, can try glycerol or chlorhexidine ointment with a pressure bandage instead)

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94
Q

You should begin a uterine prolapse reduction with the non-gravid/gravid (choose) horn.

A

(Non-gravid)

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95
Q

Why should you ensure that the uterine horns are fully inverted when reducing a uterine prolapse?

A

(The animal will want to keep straining if they are not)

96
Q

What is the disadvantage to a closed approach uterine amputation in response to a uterine prolapse that has severe ischemic necrosis and/or lacerations?

A

(Other viscera, such as the bladder, could be unintentionally trapped and amputated with the uterus which is fatal)

97
Q

What are some of the benefits of choosing local anesthesia over general anesthesia?

A

(Ruminants are poor candidates for general anesthesia, general anesthesia is expensive, and there is a lower risk of toxic effects if you pursue local anesthesia)

98
Q

Why are ruminants poor candidates for general anesthesia?

A

(Regurg, bloat, muscle damage/compartment syndrome)

99
Q

What is the duration of action for lidocaine?

A

(1-3 hours)

100
Q

What is the duration of action of bupivacaine?

A

(Up to 6 hours)

101
Q

What are the toxic doses for lidocaine in cattle versus small ruminants?

A

(Cattle → 10 mg/kg, small ruminants → 5mg/kg)

102
Q

The potency and duration of activity of local anesthetic can be increased by adding what drug?

A

(Epinephrine)

103
Q

What is the mechanism of action of lidocaine?

A

(Lidocaine blocks the fast voltage-gated sodium channels in neuronal cell membranes and with enough blockage, those sodium channels will not open and an action potential will not be generated)

104
Q

What needle size and length should be used for an inverted L block?

A

(18g, 1.5 inch, may need longer for fat cattle)

105
Q

Why are inverted L blocks not a first choice in small ruminants?

A

(You need a lot of lidocaine, can be hard to do with their lower toxic dose)

106
Q

What nerves are being targeted with a distal paravertebral block?

A

(T13, L1, and L2)

107
Q

What vertebrae are used as landmarks in a distal paravertebral block?

A

(L1, L2, and L4)

108
Q

How much lidocaine should be placed in each site for a distal paravertebral block in cattle?

A

(10-20mls, will end up being 60-120 mls of lidocaine total)

109
Q

What vertebrae are used as landmarks in a proximal paravertebral block?

A

(L1, L2, and L3, need should enter at the cranial edge of each vertebrae and you are targeting where the nerve root emerge from the intervertebral foramen)

110
Q

What spine space are you aiming for in a caudal epidural?

A

(S5-C1)

111
Q

Explain the hang and drop technique that is useful for caudal epidural anesthesia in cattle.

A

(If you are in the right spot with your needle, if you place a drop of lidocaine in the hub it will be drawn into the needle, then you can attach your syringe and anesthetic can be pushed easily)

112
Q

High volume caudal epidurals are a replacement for what other block that is used for abdominal, udder, urogenital surgeries, and c-sections?

A

(Lumbosacral block → still used in small ruminants and swine since high volume caudal epidurals are not successful in those species but good for cattle)

113
Q

How do you find the site of injection for a lumbosacral epidural?

A

(You go just caudal to the spinous process of L6 in swine or draw a line between the wings of the ileum and go just caudal to that line)

114
Q

What needle size and length is used for retrobulbar eye blocks?

A

(18 g 6 inch spinal needle)

115
Q

What nerves are blocked when using a Peterson eye block?

A

(Oculomotor, trochlear, abducens, and trigeminal)

116
Q

What are your two block options for teat anesthesia?

A

(Ring or V-block)

117
Q

What electrolyte change would you expect to see on bloodwork of a cow with simple indigestion?

A

(Hypocalcemia → d/t not eating)

118
Q

If mastitis is on your list of differentials, how can you rule it out?

A

(Palpate the udder (should be hard and swollen) and CMT (should be >1mil for clinical))

119
Q

What are the different levels and associated somatic cell count for the california mastitis test?

A

(Negative - 0, trace - 300k, CMT 1 - 900k, CMT 2 - 2.7mil, CMT 3 - 8.1mil)

120
Q

The BHB comes back as 3.3mmol/L on a cow you tested, would you consider her subclinical/clinical/severe (choose)?

A

(Severe, >3 mmol/L is severe; subclinical is 1.1-1.4 mmol/L)

121
Q

What are some causes of a displaced abomasum?

A

(Anything that causes atony of the abomasum → ketosis, hypocalcemia, increased VFAs, endotoxemia)

122
Q

Whether a DA goes to the left or right depends on what other structure and what characteristic of that structure?

A

(Rumen, if its large/full → RDA, if small/empty → LDA)

123
Q

RTAs are a counterclockwise/clockwise rotation of a DA (when viewing the cow from the rear).

A

(Counterclockwise)

124
Q

How do you determine where you are going to place your tacks for a roll and tack fix of a displaced abomasum?

A

(A hand’s breadth lateral to midline and a hand’s breadth caudal to the sternum)

125
Q

How can you confirm that you have punched into the abomasum in a roll and tack?

A

(Test with litmus paper, will be greenish to pink)

126
Q

What are the pros and cons of a roll and tack?

A

(Pros → cheap, quick, less invasive; cons → entrapment of other stuff, can displace again)

127
Q

What are the pros and cons of a right side omentopexy?

A

(Pros → you know its back in place, relatively easy, can check for fatty liver; cons → omental tears in fat cows, risk of peritonitis and wall abscess (can mitigate with abx), and cannot break down adhesions or observe tears/ulcers)

128
Q

(T/F) A right sided omentopexy can be used to fix a left or right side DA.

A

(T)

129
Q

(T/F) Left sided abomasopexy can only fix LDAs.

A

(T)

130
Q

(T/F) A right sided paramedian approach can be used to correct both an RDA and LDA.

A

(T)

131
Q

If a weaning calf presents for pain in the lower right anterior quadrant of their abdomen, what is likely the issue?

A

(Abomasal ulcer)

132
Q

What is the purpose of giving a calf with an abomasal ulcer aluminum hydroxide and magnesium oxide?

A

(Will neutralize acid)

133
Q

What is the typical clinical manifestation of a sheep with an abomasal emptying defect?

A

(Anorexia and weight loss)

134
Q

What do you expect to see on bloodwork of a sheep with an abomasal emptying defect?

A

(Hypochloremia, hypokalemia, and metabolic alkalosis)

135
Q

What is the purpose of administering erythromycin to a sheep with an abomasal emptying defect?

A

(It is an abomasal stimulant, can also try cathartics and laxatives but nothing is super useful)

136
Q

A study showed that palpation at what day of gestation has been associated with atresia ani in cattle?

A

(42)

137
Q

How do females affected by atresia ani, recti, or coli compensate?

A

(Form a rectovaginal fistula → can go on and live life, just cannot be bred but still good for slaughter)

138
Q

What are the treatments for atresia ani, recti, and coli?

A

(Ani → create an anus, recti and coli → euthanasia)

139
Q

Why is oral and IM penicillin administered in cases of hemorrhagic bowel syndrome?

A

(It is thought to be caused by clostridium perfringens type A)

140
Q

Why is hemorrhagic bowel syndrome typically seen within the first 100 days in milk?

A

(Bc that is when the most stress occurs and when they are eating the most → sets up the perfect spot for Clostridium perfringens type A)

141
Q

What are the clinical manifestations of hemorrhage bowel syndrome?

A

(Off feed, depressed, increase heart and resp rate, progressive abdominal distention, low pitched pings in lower right abdomen (d/t gas in GI tract))

142
Q

What do you expect to find per rectal palpation in a cow with hemorrhagic bowel syndrome?

A

(Blood clots/bloody feces and distended small bowel loops)

143
Q

How do cattle with a cecal dilation/retroflexion/torsion present clinically?

A

(Anorexic, drop in milk, scant feces (d/t being blocked), and signs of colic (bruxism, looking at flank, and shifting weight))

144
Q

How is cecal dilation/retroflexion/torsion prevented?

A

(Increase forage and decrease grain)

145
Q

What in the clinical presentation of a cow with a suspect cecal pathology will allow you to determine if the cecum is just dilated versus torsed?

A

(Heart rate → will be much higher with a torsion)

146
Q

What clinical signs are associated with intussusception in ruminants?

A

(Colic, depressed, anorexic, abdomen swells over a couple of days, dehydration)

147
Q

Why is surgery not a great option for correction of intussusceptions?

A

(It is difficult to get good surgical access to the small intestines → will self correct but prognosis is poor)

148
Q

What is the clinical manifestation of small intestinal volvulus in cattle and is it usually an acute or chronic progression?

A

(Clinical manifestation → increased heart and resp rate, painful, and swollen abdomen; acute onset with rapid progression)

149
Q

What are the landmarks for an inverted L or 7 block?

A

(Just caudal to the last rib and under the transverse process of the lumbar vertebrae)

150
Q

Why should the caudal abdomen be explored first in an abdominal exploratory in cattle?

A

(The chances of there being something infected in the cranial portion of the abdomen is higher (traumatic reticulopericarditis) than something in the caudal portion, do not want to track cranial bacteria everywhere else you go)

151
Q

Sort the following surgeries into if you would perform a left or right paralumbar celiotomy for them.

  • Abomasal surgery
  • Intestinal surgery
  • C-section
  • Cecal surgery
  • Rumenotomy
A
  • Abomasal surgery (Either)
  • Intestinal surgery (right)
  • C-section (left)
  • Cecal surgery (right)
  • Rumenotomy (left)
152
Q

How far should your paralumbar celiotomy incision be caudal to the last rib and ventral to the transverse processes of the spine?

A

(4-6 cm caudal to the last rib and 6-8 cm ventral to the transverse processes)

153
Q

What layers are you going through in a right or left paralumbar celiotomy?

A

(Skin, EAO, IAO, transversus abdominis, and peritoneum)

154
Q

What layers are you going through in a right paramedian celiotomy?

A

(Skin, external sheath of rectus abdominis, rectus abdominis, internal sheath of rectus abdominis, and peritoneum)

155
Q

What cases are ventrolateral celiotomies used for?

A

(C-section or removal of emphysematous feti)

156
Q

What surgical approach is good for c-sections or removal of emphysematous fetus(es) in pigs and horses?

A

(Ventral midline celiotomy)

157
Q

What cases are left oblique celiotomies used for?

A

(C-section or removal of emphysematous feti)

158
Q

What cases are right paracostal approaches reserved for?

A

(Needing abdominal access in calves → better exposure)

159
Q

Pair the following clinical signs with the stage of PEM:

Recumbency with opisthotonus, coma or seizures

A - Early signs
B - Later signs
C - Latest signs

A

(C - Latest signs)

160
Q

Pair the following clinical signs with the stage of PEM:

Ataxia, head pressing, dorso-medial strabismus

A - Early signs
B - Later signs
C - Latest signs

A

(B - Later signs)

161
Q

Pair the following clinical signs with the stage of PEM:

Dullness, inappetence, blindness, hyperesthesia and muscle tremors

A - Early signs
B - Later signs
C - Latest signs

A

(A - Early signs)

162
Q

What are the five components of milk?

A

(Water, solids, protein, fat, and ash)

163
Q

What is significant about the differences in ewe versus cow/doe milk?

A

(Bc of the differences in solids/protein/fat/ash, cow/doe milk cannot be used as milk replacer in lambs)

164
Q

Cow and sheep milk are apocrine/merocrine (choose).

A

(Merocrine)

165
Q

Goat milk is apocrine/merocrine (choose) and that can explain the low/high (choose) somatic cell count when compared to other species.

A

(Apocrine, high)

166
Q

What are the two DNA specific counting methods used for measuring SCC?

A

(Fossomatic electronic cell counter and direct microscopic counts using DNA specific stains)

167
Q

Why do goats tend to have a better response to infectious agents in their mammary glands?

A

(Bc they already have a high number of circulatory neutrophils at that site)

168
Q

The first lactation SCCs are the lowest/highest (choose) in cattle.

A

(Lowest)

169
Q

An increased lactation number in goats is associated with an increase/decrease (choose) in SCC.

A

(Increase)

170
Q

(T/F) Lactation number has very little influence on the SCC of sheep milk.

A

(T)

171
Q

What are the normal SCCs for early, mid, and late lactation goats?

A

(Early → 600-700k, mid → 800k, late → 1.8-3.4mil)

172
Q

Why do SCCs increase during estrus?

A

(Estrogen increases alveolar sloughing and regeneration)

173
Q

Which of the following is FALSE:

A - Goats have a higher SCC in the evening
B - Sheep have a higher SCC in the morning
C - Cows have a higher SCC in the evening
D - Cows have a higher SCC in the morning

A

(D)

174
Q

(T/F) In goats infected with caprine arthritis encephalitis, her SCCs will be increased compared to other goats as soon as her first lactation.

A

(F, 2nd and greater lactation)

175
Q

(T/F) We know that CAE is a factor for increased SCCs, but OPP and BLV have not been shown to be a factor in increased SCC is sheep and cattle respectively.

A

(F, OPP is a factor for increased SCCs, BLV is not)

176
Q

Hand milking is associated with a lower/higher SCC.

A

(Lower)

177
Q

Do vaccines increase or decrease SCC for up to 7 days post vaccination?

A

(Increase)

178
Q

What bacteria is the most common cause of clinical mastitis in goats and which causes blue bag?

A

(Staph aureus)

179
Q

Coagulase negative Staph species are most commonly associated with subclinical mastitis/clinical mastitis/toxic mastitis (choose).

A

(Subclinical mastitis)

180
Q

Why is coliform mastitis rare in goats?

A

(Bc udder is better protected)

181
Q

What three clinical signs do you look for to indicate whether you should treat a goat with acute mastitis?

A

(Fever over 104, severe depression, and/or no rumen motility)

182
Q

The withdrawal time for goat milk is suggested to be equal/doubled/tripled (choose) when compared to cattle milk.

A

(Doubled)

183
Q

Pair the following location with the bacteria that are likely to affect that area:

Milk and epithelial lining

A - Strep agalactia/dysgalactia, coagulase negative staph
B - Staph aureus, Strep uberis, Trueperella pyogenes
C - Coliforms

A

(A)

184
Q

Pair the following location with the bacteria that are likely to affect that area:

Deep tissue

A - Strep agalactia/dysgalactia, coagulase negative staph
B - Staph aureus, Strep uberis, Trueperella pyogenes
C - Coliforms

A

(B)

185
Q

Pair the following location with the bacteria that are likely to affect that area:

Milk and systemic

A - Strep agalactia/dysgalactia, coagulase negative staph
B - Staph aureus, Strep uberis, Trueperella pyogenes
C - Coliforms

A

(C)

186
Q

What is the causative agent of summer mastitis and how is it spread?

A

(Trueperella pyogenes and flies)

187
Q

Pair the following colony formation on a blood agar plate with the appropriate bacterial isolate:

Moderately sized round colonies with hemolysis

A - Staph aureus
B - Coagulase negative staph
C - Strep spp.

A

(A)

188
Q

Pair the following colony formation on a blood agar plate with the appropriate bacterial isolate:

Moderately sized round colonies with no hemolysis

A - Staph aureus
B - Coagulase negative staph
C - Strep spp.

A

(B)

189
Q

Pair the following colony formation on a blood agar plate with the appropriate bacterial isolate:

Pinpoint sized colonies with hemolysis

A - Staph aureus
B - Coagulase negative staph
C - Strep spp.

A

(C)

190
Q

What group of bacteria are indicated if your mastitis sample grew colonies on a MacConkey plate?

A

(Coliforms)

191
Q

Of the following products, which can be used to treat CoNS, Strep dysgalactia, and E. coli mastitis?

A - Pirsue
B - Today
C - Spectramast
D - Amoxi-Mast

A

(C)

Pirsue (Staph aureus, Strep ag/dysgalactia/uberis)
Today (Staph aureus, Strep ag, and CoNS)
Spectramast (CoNS, Strep dysgalactia, E. coli)
Amoxi-Mast (Staph aureus, Strep ag, CoNS)

192
Q

What SCC and higher is considered high for a newly freshened cow?

A

(200k → bc just off dry period and should have received a dry cow tx, i.e. teats should be the healthiest they possibly could be)

193
Q

What are some causes for high somatic cell counts in heifers? 5 answers.

A

(Drinking waste milk when young, poor management (particularly pertaining to flies), dirty environment, dirty calving area, milking (not as used to it as cows, may kick at machine or move around))

194
Q

What practices can be implemented by a farm that has a history of increased SCCs in heifers? 5 answers.

A

(Pasteurize waste milk, fly management fix environment, proper milking, and tx 10-14 days prior to freshening with mastitis tube)

195
Q

What organisms are orbeseal especially good for because it blocks the teat canal?

A

(Environmental streps and coliforms)

196
Q

What molecule is pulled from adipose tissue when a cow is in a negative energy balance state?

A

(NEFAs → non-esterified fatty acids)

197
Q

What are NEFAs converted to in the liver that are useful for the body?

A

(Ketones → provides fuel to muscles and eventually the brain if the NEB is bad enough)

198
Q

What is the purpose of the liver forming ketones from NEFAs when a cow is in a negative energy balance state?

A

(To spare limited glucose for cells that only utilize glucose → fetus, mammary glands, inflammatory cells and follicles questionable, and tumors)

199
Q

What is the net result of the altered adipose and insulin sensitivity that has been bred into today’s cows?

A

(An excessive release of NEFAs when faced with an NEB state)

200
Q

What are the three ketone bodies, which provide 10%+ of daily energy in a normal cow?

A

(Acetoacetate, beta-hydroxybutyrate, and acetone)

201
Q

What is ketosis?

A

(Metabolic disorder that occurs in cattle when ketone production exceeds ketone utilization by the cow)

202
Q

What are the clinical signs of ketosis in cows?

A

(Dullness, lack of appetite, hard feces, dull hair coat, decrease in milk production, and signs of nervous ketosis (other question))

203
Q

What are the clinical signs of nervous ketosis in cows?

A

(Ataxic, hyperaesthetic, aggressive, wandering, heading pressing)

204
Q

Spontaneous or primary ketosis is associated with a high producing cow and what range of DIM?

A

(3-6 weeks so 21-42 DIM)

205
Q

What are some causes for secondary ketosis in the first month of lactation? 5 answers.

A

(Retained placenta, metritis, mastitis, hypocalcemia, DA)

206
Q

(T/F) All cows have elevated ketones during the periparturient period.

A

(T, its when concentrations exceed a limit (there is disagreement on that limit) that she becomes ketotic)

207
Q

(T/F) The blood ketone concentration will be higher if you sample the mammary vein versus the jugular.

A

(T)

208
Q

Ketones are highest/lowest (choose) right before a cow’s next meal.

A

(Highest)

209
Q

Ketone concentration will be higher/lower (choose) in urine compared to blood/milk.

A

(Higher in urine)

210
Q

What is the most recommended treatment and treatment protocol for ketosis in cows based on current literature?

A

(Propylene glycol, 300mls once daily for 3-5 days, do not repeat because it may decrease appetite)

211
Q

In what cases would you add 500mls of 50% glucose to your treatment place for a ketotic cow in addition to propylene glycol?

A

(Nervous ketosis cases)

212
Q

What causes the immune suppression associated with parturition in cows and which causes metritis, mastitis, and pneumonia to be more severe in fresh cows when compared to mid-lactation cows? 3 answers.

A

(Cortisol surge at calving (inhibits pro-inflammatory cytokines), ketone bodies (generally considered immunosuppressive), and colostrum (transferring dam IgG into colostrum, can’t defend the dam))

213
Q

You are presented with a 4 day old calf with diarrhea, what infectious causes will be on your rule out list?

A

(E. coli (1-4 day old calves), rotavirus (4-14 day old calves), clostridium (0-28 day old calves), and salmonella (any age))

214
Q

You are presented with a 7 day old calf with diarrhea, what infectious causes will be on your rule out list?

A

(Rotavirus (4-14 day old calves), coronavirus (7-30 day old calves), crypto (7-21 day old calves), salmonella (10 days-3 month old calves more commonly affected but can happen at any age), and clostridium (0-28 day old calves))

215
Q

You are presented with a 17 day old calf with diarrhea, what infectious causes will be on your rule out list?

A

(Coronavirus (7-30 day old calves, crypto (7-21 day old calves), salmonella (any age), clostridium (0-28 day old calves))

216
Q

You are presented with a 25 day old calf with diarrhea, what infectious causes will be on your rule out list?

A

(Coronavirus (7-30 day old calves), coccidiosis (21+ day old calves), salmonella (any age), and clostridium (0-28 day old calves))

217
Q

How are rotavirus and coronavirus diagnosed besides the commercially available SNAP test (which also tests for E. coli)?

A

(Either fluorescent antibody testing at necropsy or electron microscopy on a fecal sample)

218
Q

Why can you accurately assume that a calf under 21 days of age likely doesn’t have coccidia?

A

(Bc the incubation period for coccidia is 21 days, doesn’t mean it’s not impossible just highly unlikely)

219
Q

ETEC E. coli is most commonly seen in calves, lambs, kids, and piglets during what age?

A

(1-4 days of age)

220
Q

What are the goals for fluid therapy? 5 answers.

A

(Correct dehydration, correct electrolyte deficits, correct acid-base imbalances, supplement energy, and provide maintenance fluids)

221
Q

How many mEq/L of potassium can be administered to correct hypokalemia and what needs to be added to the fluids in addition to the potassium?

A

(20 mEq/L, glucose and bicarb need to be added as well)

222
Q

How many mEq of bicarb are in 1 ml of 8.4% bicarb solution?

A

(1 mEq)

223
Q

What is the typical dose of bicarb given to animals with acidosis either over 10 minutes or added to their first bag of fluids?

A

(5-10 ml/kg body weight)

224
Q

What is the daily maintenance fluid requirement for large animals?

A

(50-100 ml/kg)

225
Q

What should the fluid rate be set at for intravenous replacement of fluid deficits in large animals that are not equids?

A

(50-80 ml/kg/hr for the first 2-4 (what he said in lecture)/4-8 (what his doc says) hours then drop to maintenance fluids)

226
Q

Calves should be administered no more than how many liters of oral fluids at a time?

A

(2 L)

227
Q

What bloodwork change in cows with BLV infections indicates that those cows are likely to be more infectious (and you could possibly use this information to select cows for culling to decrease spread of BLV)?

A

(Persistent lymphocytosis, WBC count of 10,000 or greater)

228
Q

(T/F) Sporadic bovine leukosis is not associated with a virus.

A

(T)

229
Q

Which form of sporadic bovine leukosis is described → cows with recurrent bloat, muffled heart sounds, +/- heart failure with distended jugulars, caudal ventral lung sounds difficult to hear, febrile?

A

(Thymic form)

230
Q

Which form of sporadic bovine leukosis is described → rare, usually cattle less than 30 months of age are affected, numerous lesions that enlarge over time, enlarged lymph nodes, and BCS/health deterioration over 6-12 months?

A

(Skin form)

231
Q

(T/F) The diarrhea of a cow with Johne’s disease is highly infectious.

A

(T)

232
Q

Why can you not confirm that cattle less than 18 months of age have Johne’s via serology?

A

(Bc Johne’s takes a long time to stimulate the immune system → antibody levels are not usually detected before 18 months of age)

233
Q

What diagnostic tests can be used to confirm a case of anaplasmosis?

A

(PCR or blood smear (look for morulae))

234
Q

What diagnostic test can be used to confirm a case of Theileria?

A

(PCR)

235
Q

What is the treatment of choice for anaplasmosis and does that same tx work for Theileria?

A

(Oxytet, no)

236
Q

What is the purpose of recommending tick and fly control to farmers who have anaplasma or theileria cases?

A

(Bc both are vector borne, specifically Haemaphysalis longicornis for Theileria and dermacentor/biting flies for anaplasma)

Food Animal Med Surg (32 decks)

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