Bovine Flashcards
1
Q
What is the causative agent of Anthrax?
A
Bacillus anthracis
2
Q
Why is Bacillus anthracis considered a resilient pathogen?
A
Its spores are resistant to heat
3
Q
What animals are most commonly affected by Anthrax?
A
Herbivores such as cattle
4
Q
How does Bacillus anthracis cause disease?
A
Spores germinate in the host
5
Q
What are key clinical signs of Anthrax in animals?
A
Sudden death
6
Q
What are hallmark findings of Anthrax on postmortem examination?
A
Bloody discharge from orifices
7
Q
Why should necropsy NOT be performed on suspected Anthrax cases?
A
Opening the carcass exposes vegetative bacteria to oxygen
8
Q
How is Anthrax diagnosed?
A
Blood or tissue sample submission following diagnostic lab protocols (do not open the carcass).
9
Q
Why is Anthrax considered a zoonotic and reportable disease?
A
It can infect humans and requires mandatory reporting for disease control.
10
Q
What are the key prevention strategies for Anthrax?
A
Rapid detection
11
Q
What is the recommended disposal method for animals suspected of Anthrax?
A
Burial or burning of the carcass without opening it to prevent spore formation.
12
Q
What post-exposure prophylaxis is recommended in herd outbreaks?
A
Prophylactic antibiotic treatment of asymptomatic animals.
13
Q
What are the three primary forms of Anthrax in humans?
A
Cutaneous
14
Q
What is the most common form of Anthrax in humans?
A
Cutaneous Anthrax (~95% of cases).
15
Q
How does Cutaneous Anthrax occur?
A
Entry of spores through breaks in the skin.
16
Q
What are clinical signs of Cutaneous Anthrax?
A
Papule formation
17
Q
Can Cutaneous Anthrax become systemic?
A
Rarely
18
Q
How is GI Anthrax acquired?
A
Consumption of contaminated meat.
19
Q
What are the clinical signs of GI Anthrax?
A
Severe sore throat
20
Q
What is the prognosis for GI Anthrax?
A
May become systemic and fatal if untreated.
21
Q
How is Inhalational Anthrax acquired?
A
Inhalation of Bacillus anthracis spores.
22
Q
What are clinical signs of Inhalational Anthrax?
A
Flu-like symptoms progressing to massive bacteremia
23
Q
Why is Inhalational Anthrax highly fatal?
A
Antibiotics kill the bacteria but do not neutralize the bacillus exotoxins
24
Q
What is the treatment for Anthrax?
A
Early antibiotic therapy with ciprofloxacin
25
Why is extended treatment needed for Anthrax?
A 60-day course is required to fully eliminate the organism and prevent relapse.
26
What are the two major transmissible spongiform encephalopathies (TSEs)?
Bovine Spongiform Encephalopathy (BSE) in cattle and Scrapie in sheep.
27
What is the theorized causative agent of TSEs?
A prion (abnormal protein)
28
How is Bovine Spongiform Encephalopathy (BSE) primarily transmitted?
Through contaminated commercial feed containing ingredients from infected cattle (e.g.
29
Why are young animals more susceptible to BSE?
Their immune system and gut barrier may be less effective at preventing prion absorption.
30
Is BSE contagious through casual contact between cattle?
No
31
What is the key public health concern related to BSE?
Variant Creutzfeldt-Jakob Disease (vCJD) in humans
32
What is the primary neurological sign of BSE in cattle?
Hyperesthesia (exaggerated reflexes)
33
What are other clinical signs of BSE?
Nervousness
34
What systemic signs are associated with BSE?
Weight loss and decreased milk production.
35
Over what time period does BSE develop?
Over several months
36
How is BSE definitively diagnosed?
Histology of the brain showing bilaterally symmetric intracytoplasmic vacuolation of neurons.
37
What confirmatory test can be used for BSE?
Immunohistochemistry for prion protein fibrils.
38
What is the treatment for BSE?
There is no effective treatment; affected animals must be culled.
39
Why is BSE a reportable disease?
Due to its zoonotic potential and severe public health risk.
40
What regulations have been implemented to control BSE?
Banning non-ambulatory cattle from the food chain
41
What is variant Creutzfeldt-Jakob Disease (vCJD)?
A fatal neurodegenerative disease in humans linked to BSE exposure.
42
When was vCJD first identified?
In 1996 in the UK.
43
What changes were made in the food industry to prevent vCJD?
Banning non-ambulatory cattle from human food
44
What type of virus causes Bovine Viral Diarrhea (BVD)?
A Pestivirus in the Flaviviridae family.
45
What are the two genotypes of BVDV?
Type 1 and Type 2.
46
What are the two biotypes of BVDV?
Cytopathic (CP) and non-cytopathic (NCP).
47
Does biotype indicate virulence in BVDV?
No
48
What is the most common clinical presentation of BVD?
Subclinical infection.
49
What are the clinical signs of acute BVD?
Fever
50
What is the age group most commonly affected by acute BVD?
Cattle 6 to 24 months old.
51
What additional complications can occur with acute BVD?
Immunosuppression and secondary bacterial pneumonia.
52
What is hemorrhagic syndrome in BVD?
A form of BVD that induces thrombocytopenia
53
How does BVD affect reproduction?
It causes infertility
54
What congenital defects occur with BVD infection at 100-150 days of gestation?
Hydrocephalus
55
When does persistent fetal infection with BVD occur?
If the fetus is exposed to a NCP biotype between 40-125 days of gestation.
56
What is the significance of persistently infected (PI) animals?
They are immunotolerant and shed BVDV continuously
57
What causes mucosal disease in BVD?
A PI animal is superinfected with a CP biotype or the NCP biotype mutates to CP.
58
What is the prognosis for mucosal disease?
Peracute and often fatal.
59
What is the prognosis for chronic BVD?
Eventually fatal.
60
What methods are used to detect BVD antigen?
Fluorescent antibody
61
What sample is commonly used for immunohistochemistry in BVD diagnosis?
Ear notches.
62
What additional diagnostic methods can be used for BVD?
PCR and serology.
63
What diseases should be considered as differentials for BVD?
Malignant catarrhal fever (MCF)
64
What is the primary treatment for acute BVD?
Supportive care
65
What are the key strategies for BVD control?
Biosecurity
66
What is the vaccination strategy for young cattle?
Vaccination as maternal immunity wanes.
67
What is the vaccination strategy for breeding cows?
Vaccination prior to breeding season with modified live virus vaccine containing Type 1 and Type 2 strains.
68
What type of vaccine is safer for pregnant cows?
Killed vaccine; however
69
How many doses are required for killed BVD vaccines?
Two doses.
70
How many doses are required for modified live BVD vaccines?
One dose.
71
What type of bacteria are Clostridia?
Gram-positive
72
How do Clostridial bacteria cause disease?
They produce toxins when in favorable conditions in the host.
73
Are Clostridial diseases contagious between animals?
No
74
What species are most affected by Blackleg?
Cattle (6 months - 2 years)
75
How do animals acquire Blackleg?
Ingestion of spores that enter the bloodstream and settle in tissues.
76
What are clinical signs of Blackleg?
Lameness
77
How is Blackleg diagnosed?
Presumptive based on gaseous swelling; necrotic muscle with gas bubbles on necropsy.
78
What is the treatment for Blackleg?
Early penicillin
79
How is Blackleg prevented?
7-way Clostridial vaccine (two doses).
80
What is Malignant Edema?
A Clostridial infection causing severe swelling and tissue death.
81
How is Malignant Edema acquired?
Bacteria enter through wounds (castration
82
What are clinical signs of Malignant Edema?
Swelling
83
How is Malignant Edema treated?
Early administration of penicillin; often fatal.
84
How is Malignant Edema prevented?
7-way Clostridial vaccine
85
What is another name for Redwater Disease?
Bacillary Hemoglobinuria.
86
What is the pathogenesis of Redwater Disease?
Spores lodge in the liver and proliferate when liver flukes cause damage.
87
What are key clinical signs of Redwater Disease?
Hemoglobinuria (red urine)
88
What is the primary lesion found in Redwater Disease?
Large necrotic liver areas with pale carcass and thin
89
How is Redwater Disease treated and prevented?
Penicillin/tetracycline early
90
What species are most affected by Black Disease?
Sheep (most common)
91
What is the pathogenesis of Black Disease?
Spores lodge in the liver
92
What are the clinical signs of Black Disease?
Sudden death; in cattle
93
What are the necropsy findings for Black Disease?
Large gray-black necrotic liver areas with foul odor.
94
How is Black Disease prevented?
7-way Clostridial vaccine
95
How is Tetanus acquired?
Spores enter through wounds and produce neurotoxins.
96
What are the clinical signs of Tetanus?
Sawhorse stance
97
How is Tetanus diagnosed?
Clinical signs; no specific necropsy findings.
98
What is the treatment for Tetanus?
Penicillin
99
How is Tetanus prevented?
Tetanus toxoid vaccine
100
How does Botulism cause disease?
Toxin blocks acetylcholine release
101
How is Botulism acquired?
Ingestion of contaminated feed
102
What are key clinical signs of Botulism?
Flaccid paralysis
103
How is Botulism diagnosed?
Toxin detection in serum
104
What is the treatment for Botulism?
Botulinum antitoxin
105
How is Botulism prevented?
Type B vaccine (3-dose series with booster before foaling).
106
What species are most affected by Enterotoxemia?
Calves
107
What are the clinical signs of Enterotoxemia?
Weakness
108
What are the necropsy findings in Enterotoxemia?
Purple gut appearance with fluid-filled small intestines.
109
What is the treatment for Enterotoxemia?
Supportive therapy
110
How is Enterotoxemia prevented?
Herd vaccination
111
What is another name for Overeating Disease?
Pulpy kidney disease (in sheep).
112
What is the cause of Overeating Disease?
Rapid fermentation of excess carbohydrates in the gut leads to toxin production.
113
What are the clinical signs of Overeating Disease?
Weakness
114
What is the key laboratory finding in Overeating Disease?
Glucosuria (high glucose in urine).
115
How is Overeating Disease prevented?
7-way Clostridial vaccine (two doses).
116
What diseases are caused by Clostridium perfringens Type A?
Jejunal hemorrhage syndrome (JHS) in dairy cattle
117
What are the clinical signs of Jejunal Hemorrhage Syndrome (JHS)?
Sudden death
118
What are the clinical signs of Yellow Lamb Disease?
Hemolysis
119
How is Clostridium perfringens Type A diagnosed?
Abdominal ultrasound (dilated intestines)
120
What is the prevention strategy for JHS?
Increased dietary fiber; no vaccine available in the U.S.
121
What is the causative agent of Infectious Bovine Keratoconjunctivitis (IBK)?
Moraxella bovis.
122
Why is IBK economically important in cattle?
It causes decreased weight gain
123
What are other organisms that can contribute to pinkeye in cattle?
Chlamydia
124
How does ultraviolet (UV) light contribute to IBK?
UV damage sensitizes the eye to infection
125
Why are Hereford cattle selectively bred for pigmented periocular skin?
To reduce susceptibility to pinkeye and squamous cell carcinoma.
126
What environmental factors contribute to IBK?
UV light exposure
127
Which flies are vectors for IBK?
Musca domestica (house fly)
128
How do flies transmit IBK?
They irritate the eye while feeding on secretions and remain infected for up to 3 days.
129
How is IBK transmitted?
Direct contact
130
During which seasons is IBK more common?
Summer and fall due to increased fly activity
131
What age group is most commonly affected by IBK?
Younger cattle.
132
What are the clinical signs of IBK?
Conjunctivitis
133
What is a distinguishing feature of IBK corneal ulcers?
They start as a small opaque region in the center of the cornea and progress to a deep ulcer.
134
How is IBK diagnosed?
Clinical signs and culture from conjunctival swab or lacrimal secretions.
135
What is the first-line antibiotic treatment for IBK?
Oxytetracycline (LA-200) administered systemically.
136
What are other antibiotic options for IBK treatment?
Ceftiofur (Naxcel) SQ
137
When is surgical intervention used for IBK?
In severe cases
138
What environmental modifications help prevent IBK?
Eye patches for UV protection
139
What vaccinations can help reduce IBK severity?
IBK vaccine (mixed results)
140
Why is IBK vaccination not widely used?
Inconsistent efficacy; protection depends on humoral IgG and secretory IgA responses.
141
What virus causes Infectious Bovine Rhinotracheitis (IBR)?
Bovine Herpesvirus-1 (BHV-1).
142
What are the three subtypes of BHV-1?
BHV-1.1 (respiratory)
143
What are the six main forms of IBR?
Respiratory
144
How is IBR transmitted?
Airborne
145
What is a key feature of BHV-1 infections?
Latency in ganglia with reactivation under stress.
146
What are the key clinical signs of the respiratory form of IBR?
Fever (104-107°F)
147
Why is IBR considered an important feedlot disease?
It plays a role in bovine respiratory disease complex and affects the entire herd.
148
What is a potential complication of IBR respiratory infection?
Secondary bacterial pneumonia
149
What are the clinical signs of the ocular form of IBR?
Severe conjunctivitis
150
What are the clinical signs of infectious pustular vulvovaginitis?
Vulvar discharge
151
What genital lesions can occur in bulls with IBR?
Pustular balanoposthitis with exudate and penile inflammation.
152
At what stage of pregnancy do most IBR-induced abortions occur?
5-6 months of gestation.
153
What is a characteristic finding in IBR-related abortion cases?
Fetal death with a partially decomposed fetus.
154
How can vaccines cause abortion in IBR?
Modified live virus (MLV) vaccines can induce abortion if given to pregnant animals or those in contact with pregnant animals.
155
What organs are affected in the generalized neonatal infection form of IBR?
Respiratory tract
156
What is the prognosis for neonatal generalized infection due to IBR?
Usually fatal.
157
What is the treatment for IBR?
No specific antiviral treatment; supportive care with antimicrobials to prevent secondary infections.
158
What supportive care measures are recommended for IBR?
NSAIDs (flunixin)
159
What are key control strategies for IBR?
Isolating new additions for 30 days
160
What are important considerations for IBR vaccination?
Use intranasal or IM live vaccines for feedlot and adult cattle; do not use live vaccines in neonatal calves.
161
Why should vaccine selection be done carefully in pregnant cattle?
Modified live vaccines can cause abortion; killed vaccines are safer for pregnant cows.
162
What is the primary cause of ketosis in ruminants?
Negative energy balance and inadequate feed intake.
163
Why does ketosis occur in lactating cows?
The energy (glucose) needed for heavy milk production exceeds caloric intake.
164
What are the three main ketone bodies elevated in ketosis?
Acetoacetic acid
165
What is pregnancy toxemia in ewes and does?
Ketosis occurring in late gestation due to increased energy demands from fetuses.
166
What are common primary diseases that can lead to secondary ketosis?
Displaced abomasum
167
How does the liver contribute to ketosis?
When overwhelmed
168
What metabolic pathway is disrupted in ketosis?
The citric acid cycle slows down due to reduced oxaloacetate
169
What are common clinical signs of ketosis in cattle?
Depression
170
What are clinical signs of pregnancy toxemia in small ruminants?
Anorexia
171
How is ketosis diagnosed?
History of recent parturition and heavy lactation
172
What is the most common diagnostic test for ketosis in ruminants?
Urine ketone detection.
173
What is the primary treatment for ketosis?
IV glucose administration.
174
What oral treatment is commonly used for ketosis?
Propylene glycol
175
How do corticosteroids help in ketosis treatment?
They promote gluconeogenesis and stimulate appetite.
176
What adjunct therapy can be used with IV glucose for ketosis?
Insulin.
177
What is the treatment approach for pregnancy toxemia?
Induced parturition or cesarean section
178
How can ketosis be prevented?
Proper feeding strategies during late lactation and the dry period to maintain good body condition at calving.
179
What is the equivalent of ketosis in ponies and miniature horses?
Hyperlipemia or hyperlipidemia.
180
How does hyperlipemia differ from ketosis?
Equids accumulate fat in plasma and liver rather than forming significant ketones.
181
What is the primary cause of hyperlipemia in ponies?
Negative energy balance caused by a primary disease leading to anorexia.
182
What is mastitis?
Inflammation of the mammary gland
183
What are the two main categories of mastitis?
Subclinical mastitis and clinical mastitis.
184
What is subclinical mastitis?
A form of mastitis where infection and inflammation occur without visible abnormalities in the milk.
185
How is subclinical mastitis detected?
Somatic cell count (SCC)
186
What SCC level suggests inflammation in milk?
>100
187
How does the California Mastitis Test (CMT) work?
It lyses cells in the milk and causes gelling
188
How does electrical conductivity help detect mastitis?
Mastitis increases sodium and chloride while decreasing potassium
189
What are the different severities of clinical mastitis?
Mild
190
What are the signs of mild clinical mastitis?
Abnormal milk (flakes
191
What are the signs of moderate clinical mastitis?
Abnormal milk
192
What are the signs of severe clinical mastitis?
Systemic illness
193
How can clinical mastitis be detected during milking?
Stripping milk onto a black surface or strip plate to identify abnormalities.
194
What are the major contagious mastitis pathogens?
Streptococcus agalactiae and Staphylococcus aureus.
195
What is a minor contagious mastitis pathogen?
Corynebacterium bovis.
196
Why is Mycoplasma a significant cause of mastitis?
It spreads from other body sites and becomes highly contagious when it reaches the mammary gland.
197
How is contagious mastitis diagnosed?
Milk culture for bacterial identification.
198
What is a key control method for contagious mastitis?
Post-milking teat dipping with an iodine-based germicidal solution.
199
What is the role of dry cow therapy in mastitis control?
Intramammary antimicrobial treatment eliminates infections
200
Why are Staphylococcus aureus and Mycoplasma difficult to eradicate?
They are intracellular
201
What milking protocols help prevent mastitis spread?
Milking infected cows last
202
What are the main environmental mastitis pathogens?
Coliform bacteria and environmental streptococci (e.g.
203
What are the sources of environmental mastitis infections?
Bedding
204
Which bacterial species can act as both contagious and environmental pathogens?
Coagulase-negative Staphylococcus species (e.g.
205
What other uncommon bacteria can cause mastitis?
Arcanobacterium pyogenes
206
What bedding materials help reduce mastitis risk?
Sand is preferred; wood products increase the risk of Klebsiella infections.
207
What hygiene practices help control environmental mastitis?
Frequent manure removal
208
Why is dry cow management important in mastitis control?
Dry cows are often infected
209
Which plants contain cyanide or cyanogen compounds?
Chokecherry (Prunus sp)
210
What is the toxic principle of cyanogenic plants?
Hydrogen cyanide inhibits mitochondrial cytochrome oxidase
211
What are the clinical signs of cyanide poisoning?
Acute death
212
What is the treatment for cyanide poisoning?
Sodium nitrite (induces methemoglobin to bind cyanide) and sodium thiosulfate (enhances cyanide excretion).
213
Which plants accumulate nitrates?
Pigweed (Amaranthus)
214
What is the toxic principle of nitrate plants?
Nitrate is reduced to nitrite in ruminants
215
What are the clinical signs of nitrate toxicity?
Muddy (chocolate-colored) mucous membranes
216
What is the treatment for nitrate poisoning?
1% methylene blue to reduce methemoglobin back to hemoglobin.
217
Which plants are cardiotoxic?
Oleander
218
What is the toxic principle of cardiotoxic plants?
Cardiac glycosides or alkaloids that inhibit depolarization or increase contractility.
219
What are the clinical signs of cardiotoxic plant poisoning?
Salivation
220
How is cardiotoxic plant poisoning treated?
Emesis (if recent ingestion)
221
Which plants cause primary photosensitization?
St. John's Wort (Hypericum perforatum).
222
Which plants cause secondary photosensitization?
Rape (Brassica)
223
What is the mechanism of photosensitization?
Photosensitive compounds cause UV light-induced membrane and free radical damage.
224
What are the clinical signs of photosensitization?
Erythema
225
Which plants are neurotoxic?
Lupine
226
What are the clinical signs of lupine poisoning?
Salivation
227
What is a teratogenic effect of lupine in cattle?
Crooked calf syndrome (torticollis
228
What are the clinical signs of poison hemlock poisoning?
Salivation
229
How does Larkspur toxicity present in cattle?
Bloat
230
What toxin is found in Bracken Fern?
Thiaminase (leads to polioencephalomalacia in monogastrics) and ptaquiloside (bone marrow suppression
231
Which plant causes acute laminitis in horses?
Black Walnut (Juglans nigra).
232
Which plant causes severe gastroenteritis and multi-organ failure?
Castor Bean (Ricinus communis).
233
Which plant causes severe respiratory distress and pulmonary edema?
Perilla Mint (Perilla frutescens).
234
Which plant causes 'Chewing Disease' in horses?
Yellow Star Thistle (Centaurea solstitialis).
235
What are the clinical signs of Yellow Star Thistle toxicity?
Dystonia of lips/tongue
236
Which plant causes abortions in cattle?
Ponderosa Pine (Pinus ponderosa).
237
Which plant causes myocardial necrosis in horses?
White Snakeroot (Eupatorium rugosum).
238
Which plant causes red blood cell lysis in horses?
Red Maple (Acer rubrum).
