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Integrated Prevention of Livestock DZ > Unit 3 > Flashcards

Unit 3 Flashcards

1
Q

What is the digestive tract?

A

Muscolomembranous tube that extends from the mouth to anus

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2
Q

What is the function of mucous membranes?

A

Communicate with exterior. Direct communication with the outside of the body.

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3
Q

Where can mucous membranes be found in the body?

A

Not only line the digestive tract, but line respiratory, urogenital, etc

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4
Q

What are serous membranes?

A

Very thin, uniform, lining surrounding internal cavities

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5
Q

What is the function of serous membranes?

A

Covers surfaces closed from exterior

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6
Q

What are the functions of the digestive tract?

A
  1. Digestion
  2. Absorption
  3. Motility
  4. Excretion
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7
Q

What is a simple stomach?

A

Monogastric – vast majority of digestion and absorption is within the small intestine

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8
Q

What animal would be classified as having a simple stomach?

A

Pig

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9
Q

What animals would be classified as ruminants?

A

Sheep, cattle, goats, etc

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10
Q

What are the 4 sections of a ruminant stomach?

A
  1. Rumen
  2. Reticulum
  3. Omasum
  4. Abomasum
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11
Q

What is a ruminant stomach designed for?

A

Digestive tract is designed for fermentation (ferments feedstuff, precursor to energy

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12
Q

What is the function of the rumen?

A

Vast majority of fermentation occurs here. Can hold <40 gallons of feedstuffs + fluid

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13
Q

What is the reticulum?

A

Anterior portion. Honeycomb lining.

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14
Q

What is the function in the omasum?

A

Plays role in transporting appropriately sized feed particles

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15
Q

What is the function of the abomasum?

A

“True stomach.” Similar function to monogastric stomach.

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16
Q

What animal is known to be a hindgut fermenter?

A

Horse

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17
Q

What does a hindgut fermenter digestive tract consist of?

A

Large intestine with large diameter

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18
Q

What are the sections of a hindgut fermenter large intestine?

A

Cecum, colon, rectum

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19
Q

What is the cecum?

A

Blind sack, where most fermentation occurs

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20
Q

What are signs of disturbances of the digestive system?

A
  1. Inability to chew or swallow
  2. Depraved (bad) appetite
  3. Vomiting
  4. Excess salivation
  5. Bloating
  6. Fever
  7. Abnormal feces
  8. Pain
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21
Q

What is another name for neonatal calf diarrhea?

A

Calf scours

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22
Q

What are the infectious causes of neonatal calf diarrhea?

A
  1. Bacteria (E. coli)
  2. Viruses (Rotavirus, Coronavirus)
  3. Cryptosporidium
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23
Q

What are the non-infectious causes of neonatal calf scours?

A
  1. Stress
  2. Nutrition
  3. Oral antibiotics
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24
Q

What is the occurrence of neonatal calf scours?

A

Most important disease of neonatal calves

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25
Q

What is the economic significance of neonatal calf diarrhea?

A

Significant economic loss for producers ($95,000,000). Common cause of mortality, if the calf survives you may still have an animal that doesn’t do well

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26
Q

How is neonatal calf diarrhea transmitted?

A
  1. Oral –> contamination (environment / teat)
  2. Systemic –> umbilicus
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27
Q

What is the pathogenesis of bacterial neonatal calf diarrhea?

A

E. coli colonize intestinal epithelium. Able to attach to mucosal cells using pili (fimbriae). Then they produce an enterotoxin.

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28
Q

What is the pathogenesis of viral (rotavirus/coronavirus) neonatal calf diarrhea?

A

Damages intestinal villi. Animal will not be able to absorb nutrients (malabsorptive type diarrhea).

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29
Q

What are the three types of pathogenesis in neonatal calf diarrhea?

A
  1. Viral – damage intestinal villi
  2. Fluid passage
  3. Bacterial overgrowth
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30
Q

How does E. coli infectious neonatal calf diarrhea cause changes in fluid passage?

A

Produces enterotoxin, which increases the amount of fluid that are being secreted into lumen in comparison to what is absorbed.

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31
Q

What is the mechanism of fluid passage pathogenesis by a virus in neonatal calf diarrhea?

A

Fluid secretion is the same, but can’t absorb things anymore. Fluid stays in lumen along with what is being secreted.

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32
Q

What are the pathological changes seen associated with neonatal calf diarrhea?

A
  1. Electrolyte loss –> bicarbonate, K, Cl, Na
  2. Dehydration
  3. Blood shunting
  4. Acidosis
  5. Electrolyte imbalance
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33
Q

What percent of fluid loss in cattle will it be noticeable for producers?

A

6%

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34
Q

When do clinical signs of E. coli neonatal calf diarrhea occur?

A

1-7 days

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35
Q

When do clinical signs of Rotavirus neonatal calf diarrhea occur?

A

3-10 days

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36
Q

When do clinical signs of Coronavirus neonatal calf diarrhea occur?

A

1-6 weeks

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37
Q

When do clinical signs of Cryptosporidium neonatal calf diarrhea occur?

A

5-35 days

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38
Q

When do clinical signs of Salmonella neonatal calf diarrhea occur?

A

Usually not <14 days

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39
Q

When do clinical signs of Clostridium perfringens neonatal calf diarrhea occur?

A

Few days of age, vigorous calves

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40
Q

What is the treatment for neonatal calf diarrhea?

A
  1. TLC
    a. Warm, dry, clean environment
  2. Fluid therapy
    a. Replace what they are losing + maintenance
  3. Oral fluid therapy –>
    a. 6-8% dehydration – difference between giving oral fluid replacement vs IV fluid replacement. It is always better if we can give it orally
  4. Parental fluid therapy
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41
Q

Why is withholding milk controversial in treating neonatal calf diarrhea?

A

With fluid replacements, calves not getting a lot of energy with this. Milk sometimes is withheld but should be for >24 hours. If they are suckling, can still be giving milk even when treating for calf scours.

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42
Q

What does the amount of parental fluid therapy administered depend on when treating for neonatal calf diarrhea?

A

The amount of fluids to administer depends on clinical signs estimating the % of fluid lost.

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43
Q

How do you calculate how much parental fluid therapy should be given in treating neonatal calf diarrhea (assume 100 lb calf + 6% dehydration)?

A

100 lb. calf
6% dehydration = 6 lbs.
6 lbs. / 2 = 3 quarts (to correct dehydration)
+
10% maintenance = 10 lb.
10 lbs. / 2 = 5 quarts (milk)

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44
Q

Should antibiotics be given for treating neonatal calf diarrhea?

A

If we give antibiotics, we are messing up microflora of GI tract, which is already upset. Only reserved and administered if showing systemic signs of infection (bacterial pneumonia, swollen joints). Infection MUST be bacterial, won’t work on viral infection. If not showing systemic signs, hold off on giving antibiotics.

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45
Q

How can neonatal calf diarrhea be prevented and controlled?

A

NO specific management recommendation that can apply to every situation (differences in herd sizes, facilities, land, labor). It is unrealistic to expect total control of neonatal calf scours
a. Sanitation
b. Nutrition
c. Colostrum
d. Umbilicus

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46
Q

What are the 3 main principles to prevention and control of neonatal calf diarrhea?

A
  1. Reduce exposure to infectious agents
  2. Maximize non-specific resistance by providing good nutrition + colostrum
  3. Increase specific resistance by vaccinating dam and newborn when appropriate
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47
Q

What can the aftereffects of recovering from neonatal calf diarrhea?

A

a. Pneumonia
b. Unthrifty
c. Arthritis
d. Abomasa ulcers

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48
Q

What is vesicular stomatitis?

A

This is a viral disease of livestock. We see it sporadically in the United States. Primarily effects horses and cattle.

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49
Q

What is the cause of vesicular stomatitis?

A

Caused by family Rhabdoviridae genus Vesiculovirus

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50
Q

What animals is vesicular stomatitis seen in?

A

Cattle and horses most commonly. Also, swine, sheep, llama, goats

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51
Q

How is vesicular stomatitis transmitted?

A
  1. Arthropods –> insect vectors
  2. Direct contact
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52
Q

What are the clinical signs of vesicular stomatitis?

A
  1. Oral vesicles
  2. Excessive salivation
  3. Anorexia
  4. Teat lesions
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53
Q

How is vesicular stomatitis diagnosed?

A

Reportable and quarantinable disease until officially diagnose because lesions look identical to foot and mouth disease.
1. History
2. Clinical signs
3. Lab tests

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54
Q

How can vesicular stomatitis be controlled?

A
  1. Regulatory agency
  2. Management
  3. Control arthropods
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55
Q

What is another name for Actinobacillosis?

A

Wooden tongue

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56
Q

What is the cause of Actinobacillosis?

A

Caused by bacterium Actinobacillus lignieresii

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57
Q

What is the occurrence of wooden tongue?

A

Widespread

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58
Q

How is wooden tongue transmitted?

A

Infected discharges

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59
Q

What is the pathogenesis of Actinobacillus lignieresii causing wooden tongue?

A

Part of the normal flora of the oral cavity / pharynx region. Gains access to SQ tissue by trauma (eating course material, puncturing mucosa with nail or wire). This allows bacteria to get into area that it normally doesn’t have access to, and it spreads.

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60
Q

What are the clinical signs of wooden tongue?

A
  1. Swelling*
  2. Excessive salivation
  3. Inability to chew
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61
Q

How is wooden tongue diagnosed?

A

Clinical signs. Definitive diagnosis is lab exam (biopsy + culture organism).

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62
Q

How is wooden tongue treated?

A

Sodium iodine. Given IV. Give one dose and 7-10 later, repeat as needed.

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63
Q

What needs to be considered with using sodium iodine to treat wooden tongue?

A

Can be toxic to the animal, need to monitor for signs of iodine toxicity. Decrease dose or increase time in between doses

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64
Q

What is another name for Actinomycosis?

A

Lumpy jaw

65
Q

What is the cause of Actinomycosis?

A

Caused by bacterium Actinomyces bovis

66
Q

What type of tissue does lumpy jaw affect?

A

Soft tissue AND bone

67
Q

What is the occurrence of lumpy jaw?

A

World-wide

68
Q

How is lumpy jaw transmitted?

A

Oral wounds

69
Q

What are the clinical signs of lumpy jaw?

A

Bony swelling. Also, can see erosion of bone, honey-comb type pockets. Can lose teeth, jaw can fracture.

70
Q

How is lumpy jaw treated?

A

Same treatment as wooden tongue. Usually give antibiotics as well, can be difficult to penetrate bone. May have to go in surgically and scrape material out in conjunction with sodium iodine + antibiotics.
1. Antimicrobials
2. Sodium iodide
3. Surgical debridement

71
Q

How can lumpy jaw be prevented?

A
  1. Isolate infected animals –> When draining fistulas are seen
  2. Management –> Make sure feed is good; avoid course, stemmy type feed. If there has been any demolition in pasture, pick up metal / nails.
72
Q

What is the cause of choke?

A

Obstruction of the esophagus

73
Q

What are the predisposing factors of chose in cattle, calves, and horses?

A
  1. Cattle –> rapid ingestion
  2. Calves –> boluses
  3. Horses –> dry grain
74
Q

What are the clinical signs of choke?

A
  1. Bloat
  2. Extension of head
75
Q

How is choke diagnosed?

A

Clinical signs are obvious
1. Palpate
2. Stomach tube

76
Q

How is bloat secondary to choke treated in cattle and calves?

A

Relieve bloat (free gas bloat). Pass trocar through lumbar fossa and relieve gas pressure. Often if gas pressure is released, it will pass into rumen. If it doesn’t, need to get more aggressive, could require surgery.

77
Q

How is choke treated in horses?

A

Withhold feed and water, sedation + muscle relaxant properties will resolve usually. If not, pass NG tube, sedate, slowly gently flush. Endoscopy, possibly surgery.

78
Q

What are other names for lactic acidosis?

A
  • Rumen overload
  • Toxemia
  • Rumenitis
  • Grain overload
  • Founder
  • Laminitis
79
Q

What is the cause of lactic acidosis?

A

Feed: high energy rations with grains, rumen microflora not adapted.

80
Q

What is the pathogenesis of lactic acidosis?

A
  1. Ingestion of highly fermentable carbohydrates
  2. Impaired rumen activity
  3. Rise in osmotic pressure
  4. Dehydration
81
Q

What are the clinical signs of lactic acidosis?

A
  1. Anorexia
  2. Lameness*
  3. Atonic rumen
  4. Feces
  5. Incoordination
82
Q

How is lactic acidosis treated?

A
  1. Rumenotomy –> Severe cases – open rumen and physically remove grain + add healthy rumen material from donor cow. Flushing out rumen will not be enough.
  2. Adjust rations (roughage) –> Give good quality hay (NO GRAIN). Add grain back SLOWLY so that microbial flora has time to accommodate
83
Q

How is lactic acidosis prevented?

A

Avoid sudden changes in ration

84
Q

What is rumenitis – liver abscess complex?

A

One step further beyond lactic acidosis. See when put on high energy diet ration. Lactic acid erodes rumen wall. Bacteria escapes to portal vein and go to liver where abscesses occur.

85
Q

What is the cause and occurrence of rumenitis – liver abscess complex?

A
  1. Cattle on finishing rations
  2. Concentrate : roughage ratio
86
Q

What is the pathogenesis of rumenitis – liver abscess complex?

A
  1. Lactic acid
  2. Bacteria (Fusobacterium necrophorum and Trueperella pyogenes)
  3. Abscess
87
Q

What are the clinical signs of rumenitis – liver abscess complex?

A
  1. Depression and intoxication
  2. Fluid diarrhea
88
Q

How can rumenitis – liver abscess complex be prevented?

A
  1. Adjust ration
  2. Adaptation
89
Q

What is ruminal tympany?

A

Bloat

90
Q

What is another name for primary ruminal tympany?

A

Frothy bloat

91
Q

What is the mechanism of pathogenesis of frothy bloat?

A

Instead of having a lot of gas, have tiny bubbles of gas in foamy mixture and the bubbles can’t get rid of them. Young plant material pastures. Can see in feedlot but is thought to be more a result of high grain / high energy rations and change to microflora creates biofilm which mixed with gas and causes frothy bloat.

92
Q

What is frothy bloat caused by?

A

a. Gas entrapment*
b. Legume pastures

93
Q

What is another name for secondary ruminal tympany?

A

Free gas bloat

94
Q

What causes free gas bloat?

A

Obstruction of esophagus

95
Q

What are the clinical signs of bloat in ruminants?

A
  1. Sudden death
  2. Rapid onset
  3. Dyspnea –> Difficulty breathing (head extended, trying to breathe)
96
Q

How can free gas bloat be diagnosed in a postmortem exam?

A

Bloat line on esophagus; pressure in thorax from bloat. Not being able to be profuse with blood, causes constriction of esophagus. Hemorrhagic type response on outside.

97
Q

How can free gas bloat be treated?

A
  1. Rumenotomy
  2. Stomach tube / Trocar
  3. Resolve choke
98
Q

How can frothy bloat be treated? Gas can’t be released with trocar

A
  1. Introduce antifoaming agent into trocar in rumen (surfactant + oil – changes surface tension)
  2. Stomach tube
99
Q

How can bloat be controlled?

A
  1. Ration
    a. Add good quality hay (1/3 diet)
    b. Wait until legume is more mature
  2. Antifoaming agents
    a. Introduce ionophores into diet which help to prevent bloat
100
Q

What are other names for traumatic gastritis?

A

Traumatic reticuloperitonitis, hardware disease

101
Q

What is the cause of traumatic gastritis?

A

Perforation of the reticulum wall.

102
Q

What are the predisposing factors of traumatic gastritis?

A
  1. Cow eating habits
  2. Late gestation –> Uterus is taking up space of abdomen, more likely to push material through membranes during contractions.
  3. Grazing conditions
103
Q

What is the pathogenesis of traumatic gastritis?

A
  1. Metallic object swallowed
  2. Penetration
  3. Perforation of reticulum
  4. Peritonitis
104
Q

What is peritonitis secondary to traumatic gastritis?

A

Infection / fibrous material around heart + abdomen, adhesions.

105
Q

What are the clinical signs of traumatic gastritis?

A

Easier to diagnose earlier than later. Initially will see decrease in rumen / reticulum activity (contraction). Rectal temperature and HR may be slightly increased. Careful about gait if they move just right it will poke.
1. Decreased milk production
2. Resistant to movement

106
Q

How is traumatic gastritis diagnosed?

A
  1. History
  2. Clinical signs –> Clinical signs more prominent early with initial penetration + peritonitis
107
Q

How is traumatic gastritis treated?

A
  1. Surgery
    a. Get rid of metal material (surgery –> rumenotomy)
    b. Drain abscess
  2. Antibiotics
108
Q

How is traumatic gastritis prevented?

A
  1. Magnets –> Pass magnet over feed. Bar magnets administered orally at about 1 year of age)
  2. Management
109
Q

What are abomasal disorders caused by?

A

Abnormal anatomy / movement of the abomasum.

110
Q

What is abnormal anatomy that results in abomasal disorders caused by?

A

Multifactorial causes such as abomasal atony or gas production. Usually, a result of hypomotility.

111
Q

What are the clinical signs of abomasal disorders?

A

Anorexia, decreased milk production

112
Q

How are abomasal disorders diagnosed?

A

Evaluate for displacement, use stethoscope to listen for ping sound. Also, can diagnose based on history.

113
Q

What is the treatment for abomasal disorders?

A
  1. Surgery –> Incision on paralumbar fossa, take tube attach to needle and let air be released. Pull abomasum back to where it belongs +/- tack in place
  2. Cast –> Put animal down on side, hold on back. Should go back to normal ventral side of animal
114
Q

How can abomasal disorders be prevented?

A

Adjust rations (good dry matter rations, maintain 3.5 BCS during calving, good quality and quantity of forage)

115
Q

What Is the cause and pathogenesis of abomasal ulcers?

A

Poorly understood (ulcers can be result of going off feed after giving birth, changes pH, etc)

116
Q

What is the occurrence of abomasal ulcers?

A
  1. High producing cow
  2. Hand fed calves
  3. Suckling calves
117
Q

What are the clinical signs of abomasal ulcers?

A
  1. Anorexia
  2. Blood in feces
  3. Abdominal pain
  4. Death
118
Q

How are abomasal ulcers diagnosed?

A

Feces with blood (caused by peritonitis)

119
Q

How are abomasal ulcers treated?

A

Ration management (Want them to eat again. Food acts as good buffer in abomasum, helps stabilize pH).

120
Q

How can abomasal ulcers be prevented?

A

Management and ration adjustments (withholding / decreasing concentrates, adequate roughage, increase concentrate particle size)

121
Q

What is another name for paratuberculosis?

A

Johne’s disease

122
Q

What is the cause of paratuberculosis / Johne’s disease?

A

Mycobacterium paratuberculosis

123
Q

What is the occurrence of paratuberculosis / Johne’s disease?

A

Worldwide

124
Q

How is paratuberculosis / Johne’s disease transmitted?

A
  1. Oral fecal route
  2. Carriers –> usually introduced into carrier animal b/c it has long incubation period
  3. Milk
125
Q

What is the incubation period of paratuberculosis / Johne’s disease?

A

Up to 2 years

126
Q

What are the clinical signs of paratuberculosis / Johne’s disease?

A
  1. Cattle over 2 years
  2. Diarrhea
  3. Decreased milk production
  4. Emaciation
127
Q

What will postmortem examination look like for animals that have paratuberculosis / Johne’s disease?

A

Look at distal small intestine region. SI will be thick, rough. Not necessarily ulcers. Minimal clinical signs and intestinal tract can look horrible. Other sever dz can have S.I. that isn’t that bad. No direct correlation btwn clinical signs and severity of infection.

128
Q

How is paratuberculosis / Johne’s disease prevented and controlled?

A
  1. Management –> To control / limit – as soon as animals are born, move away from mom, feed pasteurized colostrum / milk, -rear in isolated area
  2. Eradication –> can be eradicated but takes a lot of testing & won’t happen overnight. Pay attention to replacements that come in – quarantine + test appropriately
129
Q

What is BVDV?

A

Bovine Viral Diarrhea Virus

130
Q

What is Bovine Viral Diarrhea Virus caused by?

A

Genus Pestivirus, Family Flaviviridae

131
Q

What are the biotypes of BVDV?

A
  1. Cytopathic –> When cells get infected, virus kills cells
  2. Noncytopathic –> Cells get infected with virus, live in harmony. Infecting fetuses that are persistently infected
132
Q

How many species / genotypes of BVDV are there? Are they similar?

A

Type one and type two. Antigenically diverse.

133
Q

What is the occurrence of BVDV?

A

Worldwide

134
Q

How is BVDV transmitted?

A

Contact (direct or across placenta)

135
Q

What is the morbidity and mortality of BVDV?

A

Highly variable. Some strains are severe and will kill adult cow, some are very mild.

136
Q

What is the pathogenesis of BVDV and mucosal disease (MD)?

A
  1. Predilection of virus for lymphoid organs
  2. Persistent infections
  3. Immunotolerance
  4. Immunosuppression
137
Q

How does BVDV / MD cause immunotolerance?

A

Does not mount immune response to BVDC in persistently infected calves

138
Q

How does BVDV / MD cause immunosuppression?

A

Does not mount immune response to other pathogens (animal has increase susceptibility to other bacteria / virus)

139
Q

What systems are affected by BVDV?

A

All systems within body can be affected (digestive, respiratory, immune, reproductive)

140
Q

What are the clinical signs of BVDV / MD?

A
  1. Diarrhea
  2. Respiratory tract signs
  3. Unthrifty
  4. Reproductive failure
  5. Fetal anomalies
  6. Persistent carriers
141
Q

What is the pathogenesis of fetal infection of BVDV?

A
  1. Oronasal passages
    Initial replication – tonsils, epithelium
  2. Phagocytic cells
    Lymphoid tissues
  3. Viremia
    Fetus
142
Q

What age of animals are persistent carriers of BVDV?

A

Fetal infections

143
Q

What biotype of BVDV do persistent carriers have?

A

Noncytopathic BVDV

144
Q

When do fetuses become susceptible to being persistent carriers of BVDV?

A

First 1/3 of gestation, before they are immunocompetent / have developed immune response.

145
Q

How long are persistent carriers of BVDV?

A

Carrier status = lifetime

146
Q

What will necropsy of BVDV animals show?

A

Postmortem examinations will show lesions that are erosions of the GI tract and lymphoid organs

147
Q

What is mucosal disease (MD) and how is it related to BVDV?

A

Sequel to persistently infected animals. When they have both biotypes – sets them up for MD and severe erosions + ulcerations

148
Q

How is BVDV / MD diagnosed?

A
  1. History –> tentative diagnosis from history, clinical signs, gross / microscopic lesions
  2. Necropsy findings
  3. Lab tests –> viral antigens, ear notch as minimally invasive technique
149
Q

What are the differential diagnoses of BVDV / MD?

A
  • Vesicular stomatitis, bluetongue –> ulcerations
  • Johne’s disease, winter dysentery –> diarrhea, GI upset
150
Q

How can BVDV / MD be controlled?

A

Management (biosecurity, avoid PI carriers)

151
Q

What management practices can be done to avoid PI carriers of BVDV?

A

Test animals, focus on calves, quarantine / test replacement animals

152
Q

How can BVDV / MD be prevented?

A

Vaccination

153
Q

What is winter dysentery caused by?

A

Bacteria and/or virus

154
Q

What bacteria causes winter dysentery?

A

Campylobacter jejuni

155
Q

What virus causes winter dysentery?

A

Bovine coronavirus

156
Q

What animals does winter dysentery occur in?

A

Adult dairy cattle

157
Q

How is winter dysentery transmitted?

A

Fecal-oral route

158
Q

What are the clinical signs of winter dysentery?

A

Diarrhea. The cows may go off feed, may be depressed, significant drop in milk production.

159
Q

What is the mortality of winter dysentery?

A

Mortality tends to be low (usually recover)

Integrated Prevention of Livestock DZ (2 decks)

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