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914 Cards in this Set
- Front
- Back
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What are the cardinal signs of pregnancy?
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1. Amniotic Vesicle
2. Fetal Slip 3. Fetus 4. Placentomes |
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Whan can you feel Amniotic Vesicle, Fetal Slip, Fetus?
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35 days
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Whan can you feel Placentomes?
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90 days
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Name ways to manage dystocia in bovine.
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1. Epidural
2. Stand up 3. C-section 4. Pull 5. Drug Induction |
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Why do you give an epidural?
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To stop straining.
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Why do you make the cow stand up?
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Get rumen off uterus
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What are the 3 P's you should consider before pulling a calf?
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Presentation, posture, position
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What are the orientations of Presentation?
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cranial, caudal, dorsal, ventral, lateral.
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What are the orientations of Position?
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All cranial presentation-decide what part is dorsal:
Dorso-sacral, pubic, ileal(R or L) |
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What are the orientations of posture?
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Limbs: extended, retained, flexed
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What do you do if pulling is not successful?
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Fetotomy
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Where do you place chains on a calf?
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Hitch above and below pastern.
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Types of fetotomy?
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Percutaneous, subcutaneous, decapitation.
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What are the approaches for a C-section in a cow?
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1. Ventral Midline
2. Left Flank- R. lateral recumbancy 3. Left standing flank |
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Pros vs cons of Ventral Midline?
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Pro- Good exposure
Con- Chance to dehis. |
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Pro Vs cons on left flank c-section?
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Pro- Good restraint
Con- Right lateral- breathing - Have to elevate uterus |
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Pro Vs cons on Left standing flank c-section?
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Pro- Easiest restraint
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DOC for induction of parturition?
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Prostaglandin F2- alpha and Dex
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What is the first thing you think of when a cow presents with a Fever and fibrinous pneumonia?
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Bovine Respiratory Disease Complex (BRDC)
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What makes animal susscepitble to Bovine Respiratory Disease Complex?
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Shipping
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What is the viral etiology of Bovine Respiratory Disease Complex?
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1. Bovine resp syncytial virus
2. IBR (bovine herpes 1) 3. BVD 4. Parainfuenza 3 |
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What is the bacterial etiology of Bovine Respiratory Disease Complex?
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1. Manheima hemolytica
2. Past Mult 3. Heamophilus somnus 4. Mycoplasma 5. Arcanobacter pyogenes |
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What are your necropsy findings with Bovine Respiratory Disease Complex?
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Fibrinous pneumonia
Coagulative necrosis |
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AB treatment for Bovine Respiratory Disease Complex?
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LA200, PPG, TMS, Mictil,Forfenicol
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Prevention of Bovine Respiratory Disease Complex?
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1. LA200 upon arival
2. Seperate ages 3. Wean calves before shipping 4. Vax with Pasteurella and viral |
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A placenta is considered retained if it is longer than?
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24 hours after parturition
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What can a retained placenta induce?
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post partem metritis
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what can retained placenta be confused with?
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Ketosis, LDA, RDA, milk fever, peritonitis
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Do not give what with retained placenta?
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Ecbolic drugs
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What are ecbolic drugs?
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Prostaglandins, ergots, oxytocin, B2 antagonists
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What nutritional status may retained placenta be caused by?
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Low selenium and Vitamin E
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Treatment of retained placenta?
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1. Will expel in 4-6 days on its own
2. Manual 3. LA 200 4. Intra uterine infusion |
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What are the 3 categories of infertility?
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1. Decreased conception rate
2. Fertilization failure 3. Early embryonic death |
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What factors would cause a decrease in conception rate?
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1. Timing
2. Inadequate energy 3. Maternal gene abnormalities 4. Neoplasia 5. Infectious disease |
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What neoplasia will result in decreased conception rate?
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Granulosa Cell tumor
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What infectious disease will cause pyometra?
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Trichomonas fetus
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What infectious disease will cause endometritis and salpingitis?
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Campylobacter fetus
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What infectious disease will cause Mastitis?
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Leptospirosis
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What lepto affects bovine?
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Lepto interrogans hardjo
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What infectious disease will cause papules on vestibule and vulva?
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IBR-herpes I
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What infectious disease will cause early embryonic death?
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BVD, trichomonas, campylobacter.
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What disease is only an AI disease and why?
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Brucella abortus- cannot penetrate cervix
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What infectious disease will cause nodular lesions?
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Mycoplasma
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What do you culture trichomonas with and how many times?
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Diamons media-3x's
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What do you collect on Clark's media?
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Campylobacter
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What disease is the bull an asymptomatic carrier and is often called peter pan?
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Trichomonas
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How do you manage campylobacter?
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Treat bull with dihydrostreptomyacin.
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What disease is the cow the carrier?
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campylobacter
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What are the AI diseases?
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Ureaplasma, Hemophilus, Chlamydia, Brucella
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How do you prevent AI diseases?
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Double Sheath or Double rod pipette.
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What are some causes of fertilization failure?
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a. Bull semen
b. AI technique c. Segmental aplasia d. Intralumenal adhesion e. Paraovarian cysts f. Double cervical g. Persistent hymen |
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What are some causes of early embryonic death?
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a. Trichomo/Campy
b. Heat stress c. High cortisol d. Aged gametes e. Lethal genes f. Growth implants |
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What happens if a cow has paraovarian cysts?
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Prevents follicle from dropping.
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What is the disease of shipping fever?
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Pasteurellosis.
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What is the etiology of shipping fever?
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1. Past Multocida
2. Mannheima hemolytics |
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Which of the etiologies of shipping fever is the septicemic form of pasteurellosis?
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Pasturella Multocida
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Which of the etiologies of shipping fever is the Pneumonic form of pasteurellosis?
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Mannheima hemolytics
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Pasturella Multocida causes
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acute fibrinous pneumonia
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M. Hemolytica causes
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coagulation necrosis
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What are Growth implants –
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endometrial glands don’t develop properly and creates a toxic environment for embryo
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What is the first sign of Pasteurellosis?
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Fever
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What is the diagnostic test for Pasteurellosis?
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ELISA-blood or nasal swab
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What is the pathogenesis for Pasteurellosis?
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part of normal flora that becomes virulent when the animal is stressed and obtaines a virus in the respiratory complex
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What are the Four virulence factors of Pasteurellosis?
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a.Fimbriae
b.Polysaccaride capsule c.LPS (endotoxin) d.Leukotoxin |
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Action of fimbriae in Pasteurellosis?
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Of organism:enhances colonization in the upper resp tract
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MOA of Polysaccaride capsule
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– inhibits complement and phagocytosis and inc seg infilatration into the lung
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MOA of LPS (endotoxin)?
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– directly toxic to bovine endothelium
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MOA of Leukotoxin
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exotoxin that directly destroys cow’s cells
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What part of intestines absorbs?
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Villi
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What part of intestines secretes?
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Crypts
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Ages of onset of D+ in calves- in days
< 3 E coli 5-15 Rotavirus 5-21 Coronavirus 5-35 Cryptosprodiosis 5-42 Salmonella 5-15 Clostridium C > 30 Coccidia |
Ages of onset of D+ in pigs- in days
<3 E coli 1-7 Clostridium C 5-25 Coccidiosis TGE 1-5 w Rotavirus |
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What is the mechanism of diarrhea in Rotavirus
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-Villus tips
-Maldigestion -Malabsorption |
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What is the mechanism of diarrhea in Corona virus
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-Entire villus destroyed
–More severe D+ |
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What is the mechanism of diarrhea in Cryptosporidiosis?
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-villus blunting
–malabsorption, -maldigestion |
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Stain for Cryptosporidiosis?
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-Acid fast
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What causes bloody diarrhea
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salmonella T.
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What breed is carrier of salmonella?
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Dublin
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What diarrhea causes "flat calves" and why is it called this?
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Cryptosporidiosis-hypoglycemia
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What type of coccidia is seen in cows?
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Eimeria
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Major cause of diarrhea in calves less than 3 days old?
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E.coli
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Mechanism of pathogenicity for e.coli?
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1. enterotoxigenic-K99 fimbriae- attach to mucosal recptors.
2. Stable enterotoxin (ST)- inhibits absorption of villous 3. Inhibits NaCl absorption- loss of Na, CL, Bicarb, K, H20 |
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Type of diarrhea seen with e.coli?
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profuse/watery
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Chemical profile seen with E.coli?
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1. Metabolic acidosis- underperfused kidney
2. Hyperkalemia(cells hypo) |
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Diagnosis of e.coli
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1. CS
2. Fecal bacteriology |
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What is a Brodie's abcess?
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chronic fibrous osteomyelitits and chronic bone abscess
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Describe a Brodie's abcess.
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form of osteomyelitis that is circumscribed lined w/ granular membrane surrounded by sclerotic bone
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Etiology of Brodie's abcess?
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•Fusobacterium necrophorum and Actinomyces pyogenes
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Iatrogenic SQ injections
mostly caused by? |
Actinomyces pyogenes
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Where are you supposed to inject cattle?
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Middle third of the neck, about 1/3 of the way down instead of the gluteal region.
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In abcesses of the jaw: If the abscess is hard all over how do you treat?
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Delay treatment until it is softened and pittling of one area is noticeable (called Pointing of the abscess)
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What if an abscess is opened and drained prematurely?
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Have a tendency to recur
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Retropharyngeal abscess
may be caused by? |
1. Actinobaccillosis (wooden tongue)
2. Infection entering pharyngeal wound |
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Liver abscessess caused by?
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Actinomyces pyogenes or Fusobacterium necrophorum
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Liver abscessess may be due to?
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Rumen acidosis
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Liver abscessess may cause
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1.peritonitis, rupture of a major vessel causing hemorrhage and sudden death, or vena cava thrombosis
-->Vena cava thrombosis may produce pulmonary thromboembolism leading to pulmonary abscess (painful cough, dyspnea w/ rupture of abscesses into blood vessels producing severe and recurrent epistasix and blood out of the mouth) |
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Explain the clinical features of myocardial abscessess.
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Produces a similar clinical picture to chronic vegetative endocarditis, but with a slower temperature rise and slower course
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Abscess in the preputial epithelium are caused by?
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Actinomyces pyogenes and Staphylococcus aureus
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M/c breeds to have abscesses in the preputial epithelium?
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1.Angus
2.Hereford 3.Bos indicus breeds and crosses |
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What is pediculosis?
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Lice
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What are the biting lice?
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Anoplura-bovicola(damalina)
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Where are the biting lice usually found?
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neck, withers, tail head
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What are the sucking lice?
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- Mallophaga-Hematophiunus eurysternus
- Linognathus - Solenopotes |
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Where are the sucking lice usually found?
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generalized
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Is the life cycle indirect or direct?
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entirely on host
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What is the cardinal sign for lice infestation?
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itching
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What is the treatment of lice?
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-organophosphurus, pyrethroid, Coumaphos, Diazinon and permethrin
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Can you use ivermectin for lice?
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Ivermectin injectable gets sucking lice but not biting spp
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What is the most common metabolic disorder affecting cattle?
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Postparturient paresis
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Predispositions to milk fever:
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a. Dairy cattle
b. Inc w/age& milk yield c. High prepartum ca+ d. Low mg+=restricts ability to absorb calcium e. Estrogens-can inhibit Ca immobilization f. Low feed intake at part g. Fatty liver |
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Postparturient paresis AKA?
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Milk fever, hypocalcemia, Eclampsia
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Pathophysiology of milk fever?
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a.hypocalcemia stimulates PTH which inc kidneys ability to synthesize 1,25, OH2D3 from Vit D3.
b.1,25 OH2D3 stimulates inc gut absorption of Ca and Ca from bone |
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Clinical signs of milk fever
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a. Recumbancy
b. S bend to her neck c. Incordination, ataxia d. Dystocia e. Low Ca, Low Ph and high Mg (even though milk fever is due to low Mg intake |
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DDx for a recumbant cow are:
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a. Acute toxic mastitis paralysis
c. Pelvic fxs d. Grass tetany e. Downer cow syndrome f. Inanition g. Pregnancy toxemia h. Acidosis i. Hypothermia j. BSE |
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In acute toxic mastitis you must make sure you do what?
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Examen milk in all 4 teats
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Calving paralysis due to what?
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-Obturator paralysis at L4-L6
-Abduction of hindlimb or straddled |
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Pelvic fractures may be due to what?
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Osteoperosis in dairy cattle-rare
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Grass tetany aka?
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hypomagnesia
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What is inanition
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-starvation-lack of food and water.
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Pregnancy toxemia is primarily a disease of what?
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sheep
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What do you see with pregnancy toxemia in cattle when yoe do see it?
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1. Starvation
2. Acetonemia- b/c of lack of energy |
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Treatment of pregnancy toxemia?
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1. Slow IV Ca+ borogluconate warmed to body temperature.
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Prevention of pregnancy toxemia?
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Feed Mg or high anionic diets to prepartum cows.
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Metritis-Pyometra complex induced by?
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dystocia, retained placenta and milk fever
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Why do the listed resasons for Metritis-Pyometra complex cause this?
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They cause delayed return to cyclicity
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Why is Metritis-Pyometra related?
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Metritis will delay involution after calving, and develop into pyometra.
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Pathophys of Metritis-Pyometra complex?
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If the uterus is still infected after calving and ovulation and CL still develop, the progesterone created by the uterus reduces normal uterine defense mechanisms
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Do not use what in Metritis-Pyometra complex?
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progesterone
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Why do you not want to use prog in Metritis-Pyometra complex?
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Defense mechanisms inhibited by progesterone:
a.Decreases protection against purulent infection b.causes cervix to close tightly c.reduces myometrial contractions |
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Etiology of pink eye?
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-Moraxella bovis is most common known cause.
-May also be induced by IBR (infectious bovine rhinotracheitis) and Mycoplasma bovirhinits and M. laidlawii |
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Factors contributing to IBK – Infectious Bovine keratoconjunctivits (IBKC)
isolation, Abs topically, subconjunctival and parenterally · Pedersen’s suggests sulphadimidine IV injection · Sx – Third eyelid flap (membrana nictitans) to protect ulcerated cornea |
UV light, flies and dust
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Tx of (IBKC)?
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1. isolation
2.Abs topically, subconjunctival and parenterally 3.sulphadimidine IV injection 4.Sx – Third eyelid flap (membrana nictitans) to protect ulcerated cornea |
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Coccidiosis type in cattle?
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Eimeria zuernii and bovis
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Coccidiosis occur in what age?
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Affects groups of cattle less than one year old
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Usual time on onset of coccidiosis
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Occurs three or four weeks after groups of purchased calves are mixed or sudden stress of extreme temperature reductions
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In Coccidiosis what is the infective stage?
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Trophozite
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Gi signs of coccidia seen mostly as?
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GI hemorrage of cecum
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Treatment of coccidia?
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a.Sulpha drugs (Albon)
b.Amprolium |
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Metritis-Pyometra complex induced by?
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dystocia, retained placenta and milk fever
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Why do the listed resasons for Metritis-Pyometra complex cause this?
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They cause delayed return to cyclicity
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Why is Metritis-Pyometra related?
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Metritis will delay involution after calving, and develop into pyometra.
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Pathophys of Metritis-Pyometra complex?
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If the uterus is still infected after calving and ovulation and CL still develop, the progesterone created by the uterus reduces normal uterine defense mechanisms
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Do not use what in Metritis-Pyometra complex?
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progesterone
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Why do you not want to use prog in Metritis-Pyometra complex?
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Defense mechanisms inhibited by progesterone:
a.Decreases protection against purulent infection b.causes cervix to close tightly c.reduces myometrial contractions |
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Etiology of pink eye?
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-Moraxella bovis is most common known cause.
-May also be induced by IBR (infectious bovine rhinotracheitis) and Mycoplasma bovirhinits and M. laidlawii |
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Factors contributing to IBK – Infectious Bovine keratoconjunctivits (IBKC)
isolation, Abs topically, subconjunctival and parenterally · Pedersen’s suggests sulphadimidine IV injection · Sx – Third eyelid flap (membrana nictitans) to protect ulcerated cornea |
UV light, flies and dust
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Tx of (IBKC)?
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1. isolation
2.Abs topically, subconjunctival and parenterally 3.sulphadimidine IV injection 4.Sx – Third eyelid flap (membrana nictitans) to protect ulcerated cornea |
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Coccidiosis type in cattle?
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Eimeria zuernii and bovis
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Coccidiosis occur in what age?
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Affects groups of cattle less than one year old
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Usual time on onset of coccidiosis
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Occurs three or four weeks after groups of purchased calves are mixed or sudden stress of extreme temperature reductions
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In Coccidiosis what is the infective stage?
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Trophozite
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Gi signs of coccidia seen mostly as?
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GI hemorrage of cecum
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Treatment of coccidia?
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a.Sulpha drugs (Albon)
b.Amprolium |
|
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Metritis-Pyometra complex induced by?
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dystocia, retained placenta and milk fever
|
|
|
Why do the listed resasons for Metritis-Pyometra complex cause this?
|
They cause delayed return to cyclicity
|
|
|
Why is Metritis-Pyometra related?
|
Metritis will delay involution after calving, and develop into pyometra.
|
|
|
Pathophys of Metritis-Pyometra complex?
|
If the uterus is still infected after calving and ovulation and CL still develop, the progesterone created by the uterus reduces normal uterine defense mechanisms
|
|
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Do not use what in Metritis-Pyometra complex?
|
progesterone
|
|
|
Why do you not want to use prog in Metritis-Pyometra complex?
|
Defense mechanisms inhibited by progesterone:
a.Decreases protection against purulent infection b.causes cervix to close tightly c.reduces myometrial contractions |
|
|
Etiology of pink eye?
|
-Moraxella bovis is most common known cause.
-May also be induced by IBR (infectious bovine rhinotracheitis) and Mycoplasma bovirhinits and M. laidlawii |
|
|
Factors contributing to IBK – Infectious Bovine keratoconjunctivits (IBKC)
isolation, Abs topically, subconjunctival and parenterally · Pedersen’s suggests sulphadimidine IV injection · Sx – Third eyelid flap (membrana nictitans) to protect ulcerated cornea |
UV light, flies and dust
|
|
|
Tx of (IBKC)?
|
1. isolation
2.Abs topically, subconjunctival and parenterally 3.sulphadimidine IV injection 4.Sx – Third eyelid flap (membrana nictitans) to protect ulcerated cornea |
|
|
Coccidiosis type in cattle?
|
Eimeria zuernii and bovis
|
|
|
Coccidiosis occur in what age?
|
Affects groups of cattle less than one year old
|
|
|
Usual time on onset of coccidiosis
|
Occurs three or four weeks after groups of purchased calves are mixed or sudden stress of extreme temperature reductions
|
|
|
In Coccidiosis what is the infective stage?
|
Trophozite
|
|
|
Gi signs of coccidia seen mostly as?
|
GI hemorrage of cecum
|
|
|
Treatment of coccidia?
|
a.Sulpha drugs (Albon)
b.Amprolium |
|
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What is physiologic anestrus?
|
Normal anestrus
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What does the causes of physiologic anestrus include?
|
1. Pregnancy
2. Postpartum anestrus 3. Prepubertal |
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Postpartum anestrus is caused by? 60 days, dairy will cycle back in 18 days
3. Prepubertal – not reached puberty yet; should be cycling by the time 65% of body weight |
Suckling of the calf
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How long does it take for beef cattle to cycle back after parturition?
|
45-60 days
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How long does it take for dairy cattle to cycle back after parturition?
|
18 days
|
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When do cows begin their first cycle?
|
-Should be cycling by the time 65% of body weight
|
|
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Causes of abnormal anestrus?
|
1. Nutrition
2. Cystic ovaries 3. Free martin 4. Ovarian hypoplasia 5. Retained fetal membr 6. Dystocia 7. Milk fever 8. Excess feeding 9. Metritis and pyomet |
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What happens with cystic ovaries?
|
-not enough GnRH from hypothalmus
-not enough LH receptors on ovary - not producing or releasing LH; |
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Treatment for cystic ovaries?
|
1.GnRH or hCG to create luteal tissue-->give PGF2 alpha 10 days later to destroy luteal tissue
-If continues put on progesterone to suppress the hypothalmus and create a hyperactive state when progesterone is removed |
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Why do you see pyometra-metritis complex in anestral cows?
|
-due to prolonged progesterone production and decrease in uterus defense mechanisms
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What are the two types of bloat?
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Free gas and frothy
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Clinical signs of bloat?
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a. Severe distention of Left paralumbar fossa
b. Respriatory distress c. Circulatory compromise d. Death |
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What is Secondary Rumen tympany?
|
Free Gas Bloat
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What are some reasons Free Gas Bloat occurs?
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Esophageal obstruction or interference with eructation
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How do you usually distinguish free gas bloat from frothy bloat?
|
Usually only one animal is affected with free gas bloat.
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Free gas bloat is usually caused secondary to?
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a. Vagal dysfunction
b. Impaction/ choke c. Abscess d. Tumor or enlarged LN e. Choke f. Milk fever g. Tetanus h. Rumen acidosis i. Rumenitis |
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Vagal dysfunction can be caused by?
|
1.omasal or pyloric transport failure
2. salmonella |
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Treatment of free gas bloat?
|
1. Pass a stomach tube
2. Only when a tube won’t go down put in a rumen fistula or trocar to relieve tension |
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Is frothy Bloat (Primary Rumen tympany)more common or gas bloat?
|
Primary is more common
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Frothy Bloat is associated with?
|
- pasture feeding – legumes such as alfalfa, clover or green chop
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Is frothy bloat relieved by passing a stomach tube?
|
No-(a trochar and cannula will become blocked if used)
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Treatment of frothy bloat?
|
1. Tx is given when froth is seen on stomach tube of surfactants (Therabloat), mineral oil
2. May perform an emergency rumenotomy in the middle of the sublumbar fossa. |
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Name the many causes of Downer Cow Syndrome.
|
1. Mastitis, milk fever or metritis
2.Injury to spine or legs 3. LSA infiltration to spinal canal 4.Toxic infectious 5.Compartmental syndrome 6.Crush syndrome 7.Pressure syndrome 8.Calving paralysis |
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What is the chemistry picture in a cow with Mastitis, milk fever or metritis?
|
– due to Decreased Ca, P, Mg & K
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Whatshould you observe in cows with Mastitis, milk fever or metritis?
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LOOK AT THE VAGINA AND TEATS
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Injury to spine or legs should you be worried about in downer cows?
|
sacroiliac or coxofemoral luxation, or pelvic fx
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What do you do to diagnose injuries in downer cows?
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NEED RECTAL PALPATION
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In Compartmental syndrome and a downer cow what happens?
|
increased pressure develops in an osteofascial compartment
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In downer cows what happens in Crush syndrome?
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– release of myoglobin from muscle damage
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What is Pressure syndrome ?
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-ischemic necrosis if cow is sitting in same position for 6 hours or more
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What is damaged in Calving paralysis?
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– obturator or sciatic nerve damage
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What are the treatment measures for downer cows?
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1.Good nursing care – soft bedding, physical therapy, hoist, Aqua Cow (best for muscles)
2. Prognosis decreases dramatically each day she is down 3.Avoid IM injections b/c of muscle damage |
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What are many causes of abortion in cows?
|
1. Salmonella dublin
2. Listeriosis 3. Brucelosis abortus 4. Campylobacteriosis 5. Leptospirosis hardjo and pomona – mainly pomona in US 6. Candidia 7. BVD 8. IBR 9. Tritrichomonas 10. PGF2 before day 150 11. Toxic plants 12. Braddica 13. Trauma/stress 14. Fusarium spp 15. Nutrition 16. Twin pregnancy 17. Genetics |
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What Toxic plants cause abortion?
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Ponderosa Pine, Broomweed, Montery cypress, Sumpweed
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What is the MOA of Braddica?
|
Inhibits iodine into thyroxine inducing a hypothyroidism
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Samples submited of aborted feti should include?
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Entire aborted calf w/ associated fetal membranes
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The ticks that infest cattle are:
|
1.Babesia bigemina and Babesia bovis
2. Anaplasma marginale -Boophilus – Texas Cattle fever tick -Argas – fowl tick -Dermacentor variablis – American dog tick -Ixodes scapularis – Black legged tick -Rhipicecephalus sanguineus – Brown dog tick 3.Epizootic bovine abortion – Spirochete; Ornithodorus coriaceus 4.Theileria – foreign countries |
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What transmits Texas Cattle fever?
|
Boophilus
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What transmits RMSF?
|
Dermacentor variablis – American dog tick
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What is a host for babesia canis?
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Rhipicecephalus sanguineus – Brown dog tick
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What transmits Epizootic bovine abortion ?
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Ornithodorus coriaceus
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Ticks in general serve as intermediate hosts for?
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Babesia, Thelieria and Cytauxzoon
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Ticks in general serve as vectors for?
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RMSF and lyme
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What is the general term for flies?
|
Myiasis
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Simuliidae flies are aka?
|
blackflies or buffalo flies
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Where are Simuliidae flies mostly found?
|
around swiftly flowing streams
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Simuliidae flies intermediate hosts for?
|
Leukocytozoon, Onchocerca
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Simuliidae flies vectors for?
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EEE and vesicular stomatitis
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What are Phlebotomus?
|
Old world sand flies
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What are Phlebotomus intermediate hosts for?
|
Leishmania
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Vector for bluetongue?
|
Cullicoides – biting midges
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What are Tabanus?
|
horseflies
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Tabanus are carriers of what?
|
– anthrax, anaplasmosis, trypanosomiasis, EIA, tularemia, ricketsial
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Name the species of Deerflies?
|
– Chrysops, hematopota, Pangonia
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What transmitts pinkeye? (Moraxella bovis)
|
Face fly – Musca autumalis
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What transmits Thelazia eradesii?
|
Face fly – Musca autumalis
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What is Thelazia ?
|
Eyeworm
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What is the species of stable flies?
|
Stomoxys calcitrans; Habronema musca
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What is a Glossina?
|
Tsetse fly
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What does a Tsetse fly transmit?
|
Trypanosoma
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What is a species of horn flies?
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Haematobia irritans, Siphoma irritans
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What do Heel flies cause?
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gadding; cattle gallop madly to water; Warbles
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What is the species name of a heel fly?
|
Hypoderma bovis and lineatium;
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Hypodermatosis aka? • Look like bumble bees
• Life cycle ae. Produce large domed nodules under the skin on either side of the spine and produce a ventral breathing pore f. In the spirng the larva emerge from the cyst and fall to the ground and pupate • Cattle should NOT be treated between December and March b/c the larva are migrating through the esophagus or spinal cord and can cause bloat or paralysis if killed then. |
Warbles or Grubs
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Etiology of Hypodermatosis?
|
Hypoderma bovis and lineatum from heel flies.
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Heel flies that transmit hypoderma look like what?
|
Look like bumble bees
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What is the lifecycle of heel flies?
|
1.In the spring and lay eggs on lower legs of cow in a row of six or more on a hair
2. Cattle becomes irritated by the flies and will “Gadding” or gallop madly to water 3. Eggs hatch in 4 days and crawl to skin surface and penetrate to C.T. and migrate to esophagus (lineatum) or spinal canal and epidural fat (bovis) 4. Remain here for autumn and winter |
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Which species of hypoderma will migrate to esophagus/spinal canal?
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-esophagus (lineatum)
-spinal canal and epidural fat (bovis) |
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In treatment of hypoderma when would you not want to treat?
|
•Cattle should NOT be treated between December and March b/c the larva are migrating through the esophagus or spinal cord and can cause bloat or paralysis if killed then.
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What are the four biggest criteria in BSE of bulls?
|
1.PE
2.Minumum scrotal circumference based on age 3.Minimum progressive motility of sperm of 30% 4.Minimum morphology of 70% normal cells |
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Do a BSE when ?
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60 days prior to breeding season
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What on the sheath will you look for in BSE?
|
hematomas, lacerations, abscesses, adhesions
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What on the penis will you look for in BSE?
|
papillomas, hair rings, persistent frenulum
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What do you check in a bull BSE per rectum?
|
• Rectal exam:
a.Urethralis muscle – covering the urethra, massage to feel pulsations b.Prostate – firm like a wedding band c.Vesicular glands – most problems here d.Ampullae – enlarged end of the vas deferens near the urethra e.Internal inguinal rings – not larger than 3 finger sizes f.Bladder, kidneys, LN, peritoneum, omentum |
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Most problems in bulls occur where?
|
Vesicular glands
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Internal inguinal rings on BSE must be?
|
not larger than 3 finger sizes
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What are the size of testicles supposed to be based on age?
|
-1 year old-at least 30 cm
-2 years old-at least 34 cm |
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What anatomy should you be able to locate in the Epididymis for a BSE?
|
1. head is readily palpable at proximal pole of testicle on anteriolateral surface
(sperm granulomas found here) 2. tail on distal pole |
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Where are sperm granulomas normally found?
|
head of epididymis
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What anatomy should you be able to locate in the Ductus deferens for a BSE?
|
– 2-3 mm cord ascending on medial surface of testicle
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What criteria must be met as far as sperm evaluation on a BSE?
|
•Electroejaculation
a.Evaluate libido b.Minimum progressively motile sperm is 30% c.Should have only 1-2 spheroids (immature sperm that are large, grainy & non-segmented nucleus) d.Classify as normal, Primary, or secondary |
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Primary classification of sperm means?
|
-head or midpiece or tail rolled; bigger problem b/c can compete with normal sperm
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Seconday classification of sperm means?
|
- tail or loose, normal head
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Abaxial attachment of sperm confirmation is problem in?
|
-ruminants only
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What is the abomasal diseases?
|
LDA. RDA. ulcers
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Normal anatomy On left side of bovine include?
|
-mostly rumen with some abomassum and most of reticulum
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Normal anatomy On right side of bovine include?
|
1.Liver: covers the omassum, with the abomassum and reticulum below
2. The descending duodenum immediately in the right paralumbar fossa |
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|
Describe local anesthesia in the bovine.
|
a.Line block – Inverted L; T13, L1 & L2
b.Regional – Over and under L1, L2 and L4 |
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List causes of a ping on the left side:
|
1.LDA – variable pitch ping
2.Gas cap on rumen 3.Pneumoperitonitis 4.Rumen void |
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|
LDA type of ping?
|
– variable pitch ping b/c of peristalsis
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Is an LDA torsion?
|
NO
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M/C breed with LDA?
|
Dairy
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Cause of LDA?
|
Could be...
-Can have concurrent disease (milk fever, metritis, mastitis, hardware, ketosis, fatty liver, abomasal ulcers) |
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Clinical findings of LDA?
|
a.Off feed/ dec milk
b.Variable pitch ping on left side c.Ballotment |
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Where is ping located in LDA?
|
Left-sided ping between ribs 9-13
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Which is more common: LDA or RDA?
|
LDA
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Treatment of LDA?
|
a.Rolling – put on right side, and tie Grymer Sterner toggle suture loosely while cow is in dorsal recumbancy
b.Left flank laparotomy -Preplace abomaspexy suture in Ford continuous pattern w/ Braunamid cranial from pylorus -Decompress gas in abomassum -Blindly put sutures between xyphoid and milk well and tie the sutures -Explore abdomen last -Contraindicated in occult LDA (has gone away); will have a low ping line c.Right flank laparotomy -will see duodenum first -Explore the abdomen first -Decompress abomassum completely -Pull abdomassum around |
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Is RDA displacement?
|
No- dilation and torsion
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Which one comes first? Dilitation or Torsion.
|
Dilitation
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Clinical signs of RDA?
|
a. Dec rumination and contractions and fecal quantity
b. Distension of right flank c. Inc HR d. Signs become peracute once torsion occurs e.Cold extremities and extreme dullness (shock) f.Ping on right side g.Metabolic alkalosis b/c of loss of Cl ions |
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LDA and RDA are most common in?
|
Dairy cattle
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|
When are dairy cattle more prone to LDA and RDA and Why?
|
-Within one month of parturition or prepartum. Due to hypocalcemia resulting in abomosal atony.
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What kind of chemistry picture do you see with LDA and RDA and why?
|
-metabolic alkalosis
-hypochloremia -hypokalemia -due to sequestration of acid, chlorine and potassium in abomasum. |
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What is a poor prognostic sign when dealing with LDA and RDA?
|
Diarrhea
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Differentials for left pings?
|
1. LDA
2. pneumoperitoneum 3. atonic rumen. |
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|
Differentials for right pings?
|
1.Spiral colon
2. rectum/colon 3. RDA, RAV (palpable). |
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|
Who is predisposed to abomasal impaction?
|
Pregnant beef cattle in winter with poor quality feed.
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Abomasal ulcers are most common in?
|
high-producing dairy cows in first 6 weeks of production.
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|
Why do abomasal ulcers happen?
|
1.Stress decreases protective prostaglandins
2. Hypocuprosis (low copper) 3. LSA in older cattle |
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|
Ulceration occur where in abomasum?
|
-Ulceration at the ventral portion of the fundic region of the greater curvature.
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|
|
Clinical signs of abomasal ulcers?
|
See melena, anorexia, occult blood, abdominal pain.
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|
How do you tell between bleeding ulcers and perforating ulcers?
|
-Bleeding ulcers don’t perforate and perforating ulcers don’t bleed.
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|
Perforating ulcers seen in?/bleeding ulcers seen in?
|
Perforating-calves
Bleeding- adults |
|
|
How do you treat RDA?
|
a.Correcting dilatation without torsion is much easier
b.Reports of metochlopramide to tx dilatation w/o torsion c.IV fluids w/ Ringers or isotonic (lactated ringers Nabicarb should not be used) b/c of loss of Cl- ions d.Right standing laparotomy technique: -decompress w/ 12 g needle, the direction of the torsion should be identified and an attempt made to correct the torsion w/out removing the fluid -Perform abomasopexy as LDA |
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|
Teat/udder injury is usually colonized by?
|
Staph and Strept aggalacita
|
|
|
You can repair a teat laceration surgically if?
|
within 12 hours
|
|
|
IBR – Infectious Bovine Rhinotracheitis etiology?
|
Bovine herpes virus –1
|
|
|
Source of infection of IBR?
|
nasal, eye, vaginal or preputial discharge, semen and fetal tissue
|
|
|
IBR Spread via?
|
aerosol or venereally
|
|
|
IBR is what type of infection?
|
1. Latent infection – shed during times of stress
2. Respiratory dz 3. Reproductive dz 4. Alimentary DZ |
|
|
Respiratory symptoms of IBR?
|
a.Most common manifestation
b.Mild, subacute, acute to peracute c.Discharge out of nose d.Mild rise in temp e.Short, expressive cough f.Rapid and shallow breathing |
|
|
Reproductive symptoms of IBR?
|
a.Infectious pustular vulvovagintits – discharge of pus from vulva
b.Infectious bovine penoposthitis – purulent discharge form prepuce c.Endometritis d.Abortion |
|
|
Alimentary symptoms of IBR?
|
– newborn calves due to FPT
- CNS – calves less thant six months old; rare - Inclusion bodies may be seen |
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|
Acetonimia (Ketosis) is seen most commonly in?
|
High yielding lactating cows
|
|
|
Ketosis caused by what in general?
|
1. Negative energy balance
2. LOW proprionic acid or 3. HIGH butyric acid |
|
|
CS of ketosis?
|
1. Dec milk yield
2. Wt loss 3. Inappetance 4. Nervous signs |
|
|
Pathophys of ketosis?
|
a.Negative energy balance causes the mobilization of fat reserves to meet the energy deficit
b.Fatty acids are broken down to acetyl-CoA, which enter the citric acid cycle c.Medium and short chain Fatty acids enter the mitochondria (long chain Fas are bound to Carnitine from lysine and methionine) d. Beta oxidation removes two carbons from the FA to produce a lot of energy e.If there is a decrease in acetyl CoA entering the citric acid cycle b/c of dec supply of glucose metabolites, OR if there is an accumulation of acetyl CoA, then more acetate is formed in the liver. The ability of the tissues to oxidize the ketones is soon exceeded and they accumulate in the blood |
|
|
What are the Ketone bodies and their function?
|
-Acetate - ketogenic
-Butyrate – ketogenic -Proprionate – glucogenic |
|
|
Physical diagnosis of ketosis in bovine?
|
-Sweet smell (pear drops) of acetone on breath and in milk
|
|
|
Treatment of ketosis?
|
a.500 mL of 50% dextrose
b.Propylene glycol c.One dose of steroids to increase appetitie and increase glucose d.Monensin – 300-500 mg SID PO; selects for proprionic acid |
|
|
Prevention of ketosis?
|
a.Prevent excess fat at calving
b.Good transition c.Niacin d.Dec Cereal grain silaages containing high butyric acid |
|
|
Calf coronavirus affects what age?
• More watery and more severe than rotavirus • Loss of Na, K, Cl and bicarb • Yellow, watery feces • Effects entire villus – malabsorption |
1-3 weeks old
|
|
|
Differentiate Calf coronavirus from rota.
|
More watery and more severe than rotavirus
|
|
|
Chemistry picture of coronavirus.
|
Loss of Na, K, Cl and bicarb
|
|
|
What type of diarrhea is seen with coronavirus?
|
1.Effects entire villus – malabsorption
2.Yellow, watery feces |
|
|
Traumatic reticulopericarditis aka?
|
Hardware disease
|
|
|
What is most likely cause of penetration in hardware dz?
|
Ruminal and reticular contraction the wire penetrates until it reaches the peritoneum
|
|
|
Sequela of penetration in hardware dz?
|
A.A localized peritonitis occurs causing a local abscess and adhesion
2.The diaphragm and pericardium may be punctured |
|
|
Clinical signs of hardware dz?
|
a. Anorexia
b. Dec milk production c.Arched back and tucked abdomen d.Grunt positive, scootch negative e.Fever f.Shallow resp (may even look like pneumonia) g.Jugular pulse h.Muffled heart sounds – splashing and tinkling sounds over the heart i.Secondary ketosis |
|
|
Treament of hardware dz?
|
Tx and prognosis depends on whether or not pericarditis is present
a.Magnet or sx if pericarditis is NOT present b.If it is present, then immediate slaughter must be recommended |
|
|
Cystic follicular degeneration can be caused by?
• Will not have a crown or papillair • Uteruse is flacid when has a cyst, but may have a CL on other ovary or may even be pregnancy • More common in dairy cows during high lactation (rare in heifers or beef cattle) • Biggest sign is anestrus • Tx: a. Give GnRH or hCG to create luteal tissue, give PGF2 10 days later to destroy luteal tissue b. If cyst is still there, put on progesterone to suppress the hypothalamus, then remove progesterone and hypothalamus becomes hyperactive and proeduces GnRH on own |
a.Not enough GnRH from hypothalamus
b.Not enough LH receptors on ovary c.Not producing or releasing LH from pituitary |
|
|
Types of Cystic follicular degeneration?
|
1. Can be luteal (thick walled)
2. Or thin walled (follcular cyst) |
|
|
Gross description of follicular cysts?
|
1. Will not have a crown or papillair
2.Uterus is flacid when has a cyst, but may have a CL on other ovary or may even be pregnant |
|
|
Follicular cysts most common in?
|
- Dairy cows during high lactation (rare in heifers or beef cattle)
|
|
|
Biggest sign of Follicular cysts?
|
anestrus
|
|
|
Treatment of follicular cysts?
|
a.Give GnRH or hCG to create luteal tissue, give PGF2-alpha 10 days later to destroy luteal tissue
b.If cyst is still there, put on progesterone to suppress the hypothalamus, then remove progesterone and hypothalamus becomes hyperactive and proeduces GnRH on own |
|
|
Causes of early embryonic death?
|
a.heat stress
b.high cortisol (stress) c.Endometritis - A pyogenes, Campylobacter fetus, Ureaplasma, H somnus, Tritrichomonas fetus, IBR d.Aged gametes e.Trauma from hand of palpator f.Lethal genes g.Growth implants – endometrial glands don’t devleop properly when embryo embeds in uterus, has toxic envirnonment ito embryo |
|
|
Most common bovine neoplasm?
|
Squamous Cell Carcinoma (cancer eye)
|
|
|
Contributing factors to Squamous Cell Carcinoma?
|
a.Long term exposure to intensive sunlight
b.Herford most common breed (lack of pigment or melanin around eye) c.IBR d.Dust e.Flies f.High level of nutrition |
|
|
MC breed of cattle w/ SCC?
|
hereford
|
|
|
Treatment of SCC?
|
a. Sx excise, enuc
b. Cryosurgery c. Hyperthermia d. Radiation therapy e. Immunotherapy |
|
|
Bovine rotavirus m/c in what age?
|
Calves at about 10 days old
|
|
|
Describe feces in rotavirus?
|
Yogurt-like feces
|
|
|
What type of villous damage does rota cause?
|
Fuses and stunts tips of villi causing columnar epithelium to become cuboidal or squamous oreven completely flat
|
|
|
Prevention of rota?
|
- dam vaccination
|
|
|
DX rota
|
-virus antigen in feces
– examine for affected calves and for normal calves and compare b/c healthy calves can excrete the virus |
|
|
Laminitis caused by?
|
1. Poor perfusion to the claw
2. Rumen acidosis is mc cause 3. Fatty liver can detoxify endotoxins |
|
|
CS of laminitis?
|
a. Arched back
b. Front legs are crossed and hind legs wide apart. c. Shifts weight, painful walking d. Inc HR and RR e. Warm hooves |
|
|
Laminitis mc in what feet?
|
Lateral hind claws
|
|
|
What disease can healthy calves transmit?
|
Rota
|
|
|
What is tha pathophys of laminitis?
|
Locally released mediators in inflammation and perfusuion in capillary circulation causing degeneration of the stratum germinatinum
|
|
|
Treatment of laminitis?
|
a.Alter initial process – mastitis, endometritis, lactic acidosis
b.Abs c.Bute and banamine d.Soft bedding e.Warm water bats f.Steroids g.Corrective shoeing h.Sulphur-containing aas i.Claw blocks |
|
|
What is the Hamophilus comnus complex?
|
Part of respiratory complex
|
|
|
Hamophilus comnus complex most commonly affects?
|
feedlot cattle
|
|
|
Hamophilus comnus complex characterized by?
|
1. pleuritis
2. myocarditis 3. pneumonia |
|
|
Hamophilus comnus complex cs?
|
• Clinical signs:
a. Fever b. Ataxia c. Joint swelling d. Fundic lesions e. Weakness f. Recumbency g. Death h. meningoencephalitis i. pleuropneumonia j. myocarditis septicemia) |
|
|
Bovine respiratory syncytial virus causes what?
• Causes necrosisi of type I pneumocytes and type II pneumocytes show hypertrophy, hyperplasia and syncytial formation |
-viral pneumonia in dairy and beef calves under 6 months old
|
|
|
Diagnosis of Bovine respiratory syncytial virus?
|
1. virus isolation
2. TTW in early stages |
|
|
Bovine respiratory syncytial virus damages what in the lung?
|
1. necrosis of type I pneumocytes
2. type II pneumocytes show hypertrophy, hyperplasia and syncytial formation |
|
|
*****Cornybacterium spp******
|
*****Cornybacterium spp******
|
|
|
Which cornybac causes mastitis?
|
Corynebacterium bovis
|
|
|
Contagious Bovine Pyelonephritis Causes?
|
pyelonephritis or balanoposthitis
|
|
|
What causes Contagious Bovine Pyelonephritis Causes?
|
Corynebacterium renale
|
|
|
Corynebacterium renale found where on bovine?
|
Found on vagina or prepuce of carrier animals
|
|
|
Corynebacterium renale spread by?
|
trauma (breeding or catheterization)
|
|
|
Corynebacterium renale most pathogenic type?
|
Type I and III
|
|
|
Corynebacterium renale Clinical findings ?
|
-hematuria, pyuria, colic, straining to urinate, fever
- inc Crea and urea - pH urine alkaline (> 8.5) |
|
|
What make Corynebacterium renale cross with when testing for disease in?
|
Johne’s
|
|
|
Diagnosis of Corny renale?
|
Culture urine
|
|
|
Tx for corny renale?
|
PPG for 3 wks
|
|
|
Corny renale can also cause what?
|
Enzootic Posthitis; Pizzle Rot; Balanoposthitis
|
|
|
More common species for Enzootic Posthitis?
|
sheep
|
|
|
CS of Enzootic Posthitis?
|
Pustules and scabs at preputial orfice
|
|
|
Vectors of Enzootic Posthitis?
|
Flies are mechanical vectors
|
|
|
Ulcerative Lymphangitis of horses and cattle caused by?
|
Corynebacterium pseudotuberculosis
|
|
|
Clinical picture of horse or cow with Ulcerative Lymphangitis?
|
-Lymphangitis of lower limbs
-Usually in work horses - Cattle have lymph node enlargement |
|
|
**Staphylococcal species**
|
**Staphylococcal species**
|
|
|
Staph that causes mastitis?
|
Staph aureus
|
|
|
Defining property of staph aureus?
|
coagulase positive
|
|
|
Primary cs seen in infection with s. aureus?
|
abnormal milk
|
|
|
How many tests do you run to be 100% positive cow is s. aureus free?
|
3
|
|
|
Common cause of infection with S. aureus?
|
Heiffers fed milk and turned into herd
|
|
|
Treatment of S.aureus?
|
1. will go into remission if left untreated
2. Dry cow therapy most effective |
|
|
What is a coagulase (-) staph?
|
all others
|
|
|
Source of coag (-) staph?
|
-environment
-normal inhabitant of skin |
|
|
What causes a causes a chemical rumenitis ?
|
Lactic acidosis
|
|
|
Chemical rumenitis can induce what?
|
This can induce a mycotic rumenitis w/ (Mucor, Rhizopus and Absidia) 4-6 days later
|
|
|
MOA of mycotic rumenitis
|
-invade the ruminal vessels and cause a thrombosis and infarction
-Hepatic abscesses can result b/c F. necrophorum and A. pyogenes |
|
|
Umbillical hernias
Most common in? |
Holstein or Fresian (dominant, or recessive)
|
|
|
Uncomplicated Hernia?
|
omentum, intestine or abomassum, completely reducible w/ ring; no systemic signs
|
|
|
Fibrous core Hernia?
|
-abscess
– one part will be reducible, the other will not |
|
|
Omphalophelbitis
|
umbillical vein, connects to liver
|
|
|
Omphaloarteritis
|
umbillical artery
|
|
|
Urachal abscess?
|
– most common, abscess in urachus
|
|
|
Umbillical abscess?
|
– feels warm, painful, non-reducible, firm; no hernia ring palpated; systemic signs seen; lance, drain and flush
|
|
|
Enlarged umbillical stalk?
|
-usually only cosmetic issue; usually secondary to omphalitis, persistent patent urachus, or post tx w/ chemical retraint
|
|
|
What is your diagnosis... A firm coarse cauliflower like lesion on the head, neck, and udder of a cow?
|
Papillomatosis
|
|
|
What strains of papilloma are seen in bovine?
|
1-5
|
|
|
What types of papilloma virus will spontaneosly regress?
|
I and II
|
|
|
Treatment of papilloma virus?
|
-Cryosurgery or cold steel surgery
-Lithium antimony thiomalate 6% solution 15 mL by deep IM injection every other day 4-6 times |
|
|
Primary condition you must differentiate from papillomatosis?
|
Interdigital fibroma
|
|
|
Interdigital fibroma is mc in?
|
sheep
|
|
|
Treatment of Interdigital fibroma?
|
If detected early, sx removal (cryosurgery and electrocautery) is successful
|
|
|
Hairy foot warts Aka?
|
Bovine digital dermatitis, Papillomatosis digital dermaitis, Mortellaro’s dz, Foot warts, heel warts
|
|
|
MC area Hairy foot warts are found?
|
Between the heel bulbs of the plantar surface at the junction of skin and periople
|
|
|
Appearance of Hairy foot warts?
|
Red, granular appearance
|
|
|
Hairy foot warts most common in?
|
dairy cattle
|
|
|
Etilogy of Hairy foot warts ?
|
Spirochetes (Treponema denticola)
|
|
|
CS of hairy foot warts?
|
Causes lameness, wt loss, dec milk production
|
|
|
Treatment of hairy foot warts?
|
Tx is topical....
-oxytetracycline and bandaging -Footbaths w/ tetracycline, lincomycin, spectinomycin, or 5% Cu sulfate can be used for control, but must be watched for contamnation |
|
|
What are the 3 types of Ostertagia ostertagi?
|
Type I, Type II, Hypobiosis
|
|
|
Type I Ostertagia ostertagi cs?
|
-profuse watery D+ of calves on grass
|
|
|
Type I Ostertagia caused by?
|
-Caused by immature adults leaving the gastric glands
|
|
|
Type I Ostertagia ostertagi found where and when?
|
-Fall in the north; winter in south
|
|
|
Type II Ostertagia disease predilection?
|
-Yearlings following their first season of grazing
|
|
|
Type II Ostertagia ostertagi caused by?
|
-Caused by arrested L4 resuming development after hypobiosis
|
|
|
Type II Ostertagia ostertagi found where and when?
|
-Spring in north; fall in the south
|
|
|
What is hypobiosis with Ostertagia ostertagi?
|
-L4 accumulate in gastric glands b/c of harsh weather conditions
|
|
|
Hypobiosis seen what time of year?
|
-Winter in the north, Summer in the south
|
|
|
Pathophys of infection in hypobiosis?
|
-Animal ingests L3 and encysted larvae invade the gastric gland of the abomassum causing a ‘morrocan leather’ appearance. The gastric glands (parietal- HCL and chief – pepsinogen) are affected and the tight junctions that maintain the integrity of the epithelial sheet in diminished.
•The alkaline pH in the abomassum causes bacterial overgrowth and hypoproteinemia b/c of lack of pepsinogen. |
|
|
Ostertagia ostertagi tx?
|
Tx: ivermectin, doramectin and moxidectin
|
|
|
***Lactic Acidosis***
|
***Lactic Acidosis***
|
|
|
Lactic acidosis aka?
|
-Acute CHO engorgement, rumen overload
|
|
|
Lactic acidosis caused by?
|
- Ingestion of large amounts of highly fermentable CHO (cereal gains, corn, grapes, apples)
|
|
|
Pathophys of LA?
|
-The increase in CHO causes a marked change in microes, specifically Streptococcus bovis which utilize the CHO to produce large quantities of lactic acid, causing the rumen pH to be < 5. This causes destruction of bacteria and protozoa in the rumen. Both D and L forms of lactic acid are produced. This increases ruminal osmolality and water is drawn in from the circulation, causing hemoconcentration and dehydration. L lactic acid is utilized much more rapidly than D, so it accumulates and causes a severe D-lactic acidosis.
|
|
|
Clinical signs of Lactic acidosis?
|
a. Profuse D+ w/ sweet/sour odor of feces – may have undigested kernels
b. Anorexia c. Depression d. Dehydration e. Rumen stasis f. Ataxia leading to recumbency g. Fluid splashing sounds on ballotment\ |
|
|
Complications of Lactic acidosis? (3 Ls)
|
a.Liver abscess – Fusobacterium necrophorum and Arcanobacter pyogenes from rumenitis break down of vessels
b.Laminitis – unknown pathogenesis c.Lactic acidosis d.Fungal hepatitis – Mucor, Rhizopus, Absidia |
|
|
Clin path of Lactic acidosis?
|
a.Ruminal fluid pH < 5
b.Rumen microbes abscent c.Dehydration d.Hypocalcemia – temproary malabsorption e.Hypochloride – loss of serum Cl due to sequestration in the rumen f.Hyperphosphatemia – renal failure g. inc blood lactate |
|
|
Tx of Lactic acidosis if animal is found engorging herself (before clinical signs)?
|
a.Off water for 12-24 hours
b.Offer good quality hay at ½ day ration c.Exercise every hour for 12-24 hours to encrouage movement of ingesta through GI tract |
|
|
Tx of Lactic acidosis if animal is showing clinical signs?
|
a.Rumenotomy – severe cases; empty rumen w/ a siphon and replace with cud transfer and few handfuls of hay
b.Sodium bicarb – systemic acidosis c.Rumen lavage – rubber tube and warm water pumped in until obvious distension of L paralumbar fossa, then empty via gravity d.Alkalinizing agents – Mg hydroxide or Mg oxide pumped into rumen, then kneading to promote mixing e.Antihistamines form lamintits f.NSAIDs – shock therapy g.Thiamin or brewer’s yeast to promote metabolism of lactic acid h.Parasympathomimetics – Ach-like effect, cholinergic drugs; stimulates smooth muscle contraction - Choline - Ach - Methacholine - Carbachol - Bethanechol - Pilocarpine i. Ca borogluconage – tx hypocalcemia |
|
|
In LA you have hypocalcemia due to what?
|
- temporary malabsorption
|
|
|
In LA you have hypochloride due to what?
|
loss of serum CL sue to sequesterization in rumen.
|
|
|
In LA you have hyperphosphatemia due to what?
|
renal failure
|
|
|
What are some alkalinizing drugs you can use in LA?
|
MG hydroxide and MG oxide
|
|
|
Antihistamines must be used with precaution because they can cause what?
|
laminitis
|
|
|
What can be used as shock therapy in cattle?
|
NSAIDS
|
|
|
What can be used to promote metabolism of lactic acid?
|
Thiamin or brewers yeast
|
|
|
What do you use to treat hypoglycemia?
|
Ca borogluconate.
|
|
|
BVD etiology?
|
RNA pestivirus
|
|
|
BVD related to?
|
Hog Cholera and Border dz
|
|
|
2 genotypes of BVD.
|
Type I (Ia & Ib) and Type II
|
|
|
Most BVD are type ?
|
Type I
|
|
|
2 biotypes of BVD?
|
Cytopathic – cell death in culture
b.Noncytopathic – does not cause death in culture |
|
|
Naïve animals exposed to BVD will show?
|
a. D+
b. Fevere c. inc RR d. dec milk production e. Abortions, EED; fetal wastage |
|
|
Fetus with BVD will show?
|
a. Micro-phthalmia
b. Juvenile cataracts c. Cerebellar hypoplasia d. Arthroporosis e. Curly hair coat – like border dz in sheep |
|
|
BVD is a primary virus to set up secondary infection of what?
|
-Mannheimia and Pasteurella along w/ stress and shipping
|
|
|
Persistently infected animals are those that are what?
|
– calf exposed in utero
|
|
|
Persistently infected animals are caused by and what happens?
|
a.Noncytopathic biotype exposure to cow at < 150 days of gestation
b.Could abort, develop congenital lesions, develop persistent infection, or nothing could occur |
|
|
PI infected animals are what clinically- how do they present?
|
-Smaller, chronic poor-dooers or could be normal
|
|
|
Mucosal Disease is what?
|
-When persistently infected aniamsl are expposed to a cytopathic virus you get ‘mucosal dz’
|
|
|
Mucosal dz Looks similar to?
|
Looks similar to Foot and Mouth
|
|
|
Mucosal dz must be similar strain of ?
|
NCP and CP
|
|
|
Mucosal dz pathophys?
|
1. Can be induced by modified live vaccine, mutation inside the calf changes from NCP to CP, or animal gets an acute infection of CP
|
|
|
Dx of BVD?
|
a. Virus isolation on whole blood
b. Test poor doers c. Test again in 3 weeks d. Ear notching – punch biopsy IMHC (immunohistochemistry) e. If BVD +, then test every animal via virus isolation or ear notch. Cull all +; retest when born. f. Retest w/in a year and cull the positive g. Herd screening - >5 months old calves b/c after maternal antibodies but has not been vaccinated yet; “Canary in the mineshaft” |
|
|
Prevention of BVD?
|
a.Vaccinate w/ killed or MLV
b.Close the herd – test incoming pregnant heifers via ear notch and test fetus when born; isolate her until she gives birth and then quarantine for 3 weeks |
|
|
Clostridial enterotoxemia etiology?
|
Clostridium perfringens types B,C & E (Beta toxin)
|
|
|
Enterotoxemia causes what?
|
-Enterotoxemia in calves, lambs, foals and piglets
|
|
|
Enterotoxemia occurs in calves how old?
|
5-15 days old
|
|
|
The beta toxin is readily inactivated by what? and so what happens?
|
-trypsin, but b/c the young animal has absence of mature flora, C. perfringens colonizes
|
|
|
Carefule because of what with enterotoxemia?
|
bacteria can for spores
|
|
|
CS of enterotoxemia?
• |
D+, abdominal pain, nervous signs (tetany, opisthotonos); Violent bellowing and aimless running
|
|
|
Localized lesions seen with what type of enterotoxemia?
|
Type B
|
|
|
More extensive lesions seen with what type of enterotoxemia?
|
Type C
|
|
|
Treatment enterotoxemia?
|
Tx is hyperimmune serum
|
|
|
Prevention enterotoxemia?
|
All pregnant animals should be vaccinated to provide colostral immunity to babies.
-Antiserum will protect susceptible animals and is give immediately after birth |
|
|
Omphalitis AKA?
|
Navel ill
|
|
|
Is inflammation on th external aspects of the umilicus or internal aspects?
|
External
|
|
|
Age mc for navel ill?
|
w/in 2-5 days of birth and often persists for several weeks
|
|
|
Tx naval ill
|
surgical excision
|
|
|
Winter dysentery etiology?
|
Bovine corona virus
|
|
|
Predisposing factors to Winter dysentery?
|
-Northern climates
-Adult lactating dairy cows during winter months |
|
|
CS of Winter dysentery?
|
-Explosive D+ affecting almost entire herd w/in several days
-May have mild respiratory signs |
|
|
DX Winter dysentery?
|
-Detection of virus in feces (ELISA)
|
|
|
TX/Prevention winter dysentery?
|
No tx or control available
|
|
|
Calves bellowing aggressively and aimlessly wandering, what is your dx?
|
enterotoxemia
|
|
|
Explosive diarrhea affecting entire herd, what is your dx?
|
Winter dysentery
|
|
|
Fat Cow syndrome aka?
|
Fatty liver
|
|
|
Overall MOA Fat Cow syndrome?
|
-Mobilization of excessive body fat to liver during periods of negative energy balance at time of parturition or in early lactation in dairy and beef cows
|
|
|
Predisposition to Fat Cow syndrome?
|
a. High producing dairy cows
b.Over-conditioned beef cows just before or after calving (when energy intake suddenly decreases) c.Twins d.Lead or challenge feeding during dry period e.Milk fever, detosisi and LDA can complicate fatty liver f.Starvation diet of dry cows right before calving b/c farmer thinks is too fat which may increase dystocia (untrue) |
|
|
Is this disease(Fat Cow syndrome) fatal?
|
Highly
|
|
|
Pathogenesis of Fat Cow syndrome?
|
-After calving there is a large increase in fat accumulation in the liver; b/c of the metabolic demands of lat pregnancy and early lactation, there is a gradual increase in NEFAs (nonesterfied FA) and glucose during final days of gestation and a decrease in BHBA (betahydroxyburtyrate).
-Immediately after parturition, there is an increase in energy demands. This causes a mobilization of fat from body reserves (SQ fat) to the blood which transports fat to the body tissues (particularly the liver) but also muscle and kidney a. inc NEFAs and glucose and dec BHBA pre-parturition b.inc energy demands immediately after parurtion c.Mobilization of fat from SQ fat to blood to liver, muscle and kidney d.If there is a decreases in energy intake (she can’t eat enough or there is not enough food) then there is an excess mobilization of FFAs to the liver e.Hepatic lipogeneissi – enlarged hepatocytes, dec liver glycogen, inadequate lipoprotein transport f.Most lipids in the liver are triacylglycerols b/c inc NEFAs and inc deacylglycerol acyltransferase (enzyme activated by FA) g.May be exacerbated if the liver has dec ability to export VLDL (very low density lipoprotein) |
|
|
Clinical signs of Fat Cow syndrome?
|
a. High BCS
b. Anorexia c. Recumbancy d. Scant feces e. Unresponsive ketosis f. Nervous signs – especially beef cows g. Increase in liver enzymes, increase in blood ketones |
|
|
Tx of Fat Cow syndrome?
|
a. IV glucose and electrolyes
b. Transfaunation c. Dexamethasone d. BSE e. Propylene glycol – promotes gluconeogenesis and inculin f. Offer good quality hand and water g. Steroids |
|
|
Control of Fat Cow syndrome?
|
a. Prevent pregnant cattle from becoming fat during last trimester (especially during dry period)
b. BCS often to monitor nutrtional starus of herd |
|
|
What is cryptosporidium?
|
Coccidia
|
|
|
What age does it affect adult or babies?
|
Calves 1-2 wks
|
|
|
Infective stage of crypto?
|
oocysts
|
|
|
Is crypto of bovine able to spread to other species?
|
oh yes
|
|
|
What anticoccidial drugs can you use for crypto?
|
Unaffectd by existing anticocccidial drugs
|
|
|
Clinical signs of cryptosporidiosis?
|
-Profuse watery green D+ w/ occasional mucus and blood
Dehydration -Destroys mature enterocytes in small and large intestine causing a malabsorption and secretory dz |
|
|
Diagnosis of cryptosporidiosis?
|
-Giemasa, Acid fast and Auramine to stain oocysts in fecal smear from flotation technique
|
|
|
Treatment of cryptosporidiosis?
|
No specific tx, but sulfaquinooxaline w/ Vit B & K may decrease mortality
|
|
|
Grass However, CSF and vitreous humor will be depressed even after death
• Tx: a. Be quiet and gentle – can die from any stress or sudden stimulus b. IV 6% Mg salt (Mg sulfphate) slowly– can cause resp or cardia failure c. Ca borogluconate – hypocalcemia d. Sodium pentobaritone (euthaniasia) solubiont IV to reduce convulsions e. Relapses are common – SQ Mg sulfphate solution f. Orally give 4 Mg bullets |
Hypomagnesemia
|
|
|
Hypomagnesemia seen most commonly in what?
|
-Lactating cows (beef or dairy) when grazing grass in spring or autumn
|
|
|
CS of Hypomagnesemia?
|
1. Hyperastesia
2. Incorrdination 3. Tetany and convulsions 4. Reluctance to enter the parlor (subclinical) 5. Sudden death |
|
|
Hypomagnesemia is most commonly seen when?
|
-Peak lactation b/c of increased secretion of Mg in milk
|
|
|
Pathophysiology of Hypomagnesemia?
|
-There are no Mg stores in the body, so if there is a reduction in the amount of Mg in the diet w/ an increase in milk production, grass tetany can occur
|
|
|
What is high in Mg?
|
Clover
|
|
|
What is low in Mg?
|
ryegrass
|
|
|
What will reduce absorption of Mg in soil?
|
K+ fertilizers in late winter/early spring
|
|
|
What interferes w/ body uptake of Mg?
|
Ca, K and ammonium (Nitrogen) ions
|
|
|
What forms in calves if they are deficient in Mg? How does this occur?
|
Milk Tetany: calves 2-4 months old fed whole milk diets w/o Mg supplement
|
|
|
Mg below this number is classified as hypoMg
|
0.85
|
|
|
Common blood chemistry picture seen with Grass tetany?
|
Hypocalcemia and Hyperkalemia
|
|
|
What are the only 2 things you can use for diagnosis of Grass Tetany and why?
|
CSF and vitreous humor-Mg stays same after death
•After death, blood or tissue levels are meaningless b/c Mg rises |
|
|
TX of grass tetany?
|
a.Be quiet and gentle – can die from any stress or sudden stimulus
b.IV 6% Mg salt (Mg sulfphate) slowly– can cause resp or cardia failure c.Ca borogluconate – hypocalcemia d.Sodium pentobaritone (euthaniasia) solubiont IV to reduce convulsions e.Relapses are common – SQ Mg sulfphate solution f.Orally give 4 Mg bullets |
|
|
Be extra careful with Mg sulfphate give slowly because of what?
|
– can cause resp or cardia failure
|
|
|
Bovine Leukemia Virus AKA?
|
Bovine lymphosarcoma (LSA) or Enzootic bovine leukosis
|
|
|
Bovine Leukemia Virus Most common in?
|
-Hereford
-3-8 years old |
|
|
Description Bovine Leukemia Virus?
|
A.Exogenous C-type RNA oncovirus in retroviridae family
b.Present in circulating B lymphocytes c.P24 internal protein antigen and gp51 glycoprotein antigen is important for dx |
|
|
Bovine Leukemia Virus affects what structures?
|
LNs, right side of heart, abomasum, uterus, kidney, eye, spinal cord
|
|
|
Bovine Leukemia Virus can be transmitted by?
|
1. Iatrogenic transmissionneedles; multidose syringes can spread, same rectal gloves, dehorning and ear tattooing
2. Contact transmission- via saliva, vaginal disharges, tracheal fluids |
|
|
Clinical signs of Bovine Leukemia virus?
|
a. 60% are asymptomatic
b. May show persistent lymphocytosis c. Enlarged LNs d. Depression, indigestion, chronic bloat, LDA, lamness or paralysis |
|
|
Bovine Leukemia virus found where in blood?
|
Circulating lymphocytes
|
|
|
Dx Bovine Leukemia virus?
|
a. Persistent lymphocytosis
b.AGID Ab to viral antigens p15, p24, and gp51 c.ELISA to detect BLV Abs |
|
|
Control Bovine Leukemia virus?
|
a.isolate and separate BLV positive cows
b.Test all incoming cows c.Separate and raise calves on BLV-free milk |
|
|
How old do calves have to be tested and if serologically negative for Bovine Leukemia virus then can join negative herd?
|
at 7 months
|
|
|
What id Sporadic bovine leukosis?
|
-LSA (Bovine lymphosarcoma) in young animals in absence of BLV
|
|
|
Three forms of sporadic bovine leukosis?
|
a. Juvenile
b. Thymic c. Cutaneous |
|
|
Age and characteristics of sporadic bovine leukosis?
|
- < 6 months old LNs, liver , spleen and bone marrow; death
|
|
|
Age and characteristics of Thymic bovine leukosis?
|
– 6-30 months old; massive tumor in thymus and nods of neck and thorax; death
|
|
|
Age and characteristics of Cutaneous bovine leukosis?
|
– 18 months-3 years; nodular lymphocytic neoplasia in seen in the skin; if animal survives, will recover in several weeks but will have remission and die
|
|
|
White muscle disease aka?
|
Subacute enzootic muscular dystrophy
|
|
|
What is the cause of White muscle disease?
|
-Selenium and Vit E deficiency causes a myopathy
|
|
|
White muscle disease results in and from?
|
-Myodegeneration in calves and lambs of dams that received selenium-deficient feed during or before gestation
|
|
|
What is low in selenium naturally?
|
Legumes are low in selenium
|
|
|
Clinical signs of White muscle disease
|
a. sternal recumbency but will attempt to stand
b. The hocks will rotate c. Muscle tremor d. Dyspnea e. ‘Flying scapula’ – scapula protrudes above the vertebral column and is widely separated from the thorax; bilateral rupture of the serratus ventralis muscles f. Paralytic myoglobinura – stiffness, recumbancy, myoglobinuria, hyperpnea, and dyspnea |
|
|
Natural role of selenium in the body?
|
-Selenium is component of GSH-PX enzyme needed to protect RBC membranes and a component of thyroid gland hormones to convert T4 T3
-Selenium contouracts toxicty of heavy metals |
|
|
Natural role of Vit Ein the body?
|
-Vit E is an antioxidant that prevent oxidant damageby decreasing hydroperoxid formation
|
|
|
Treatment of White muscle disease?
|
Tx is a mixture of selenium and alpha-tocopherol (Vit E)
|
|
|
Etiology of Wooden tongue?
|
Actinobacillus lignieresii
|
|
|
Infection enters through what in Wooden tongue?
|
-Abrasion of the tongue (ulcer, teeth, spiny awns, prickly forage) ;
|
|
|
Actinobacillus is a normal inhabitant of?
|
-The oral cavity and rumen
|
|
|
Clinical signs Wooden tongue?
|
a.salivation and gentle chewing
b.Tongue is swollen and hard particularly at the base c.Manipulation of the tongue causes resentment d.Lymphadenitis e.Loud, snoring respiration •Can also occur in sheep but involves the lower jaw, face and nose (not the tongue) |
|
|
Tx Wooden tongue?
|
Iodides (Potassium iodide, Sodium iodide) until iodism develops
|
|
|
What is the disease : A cow with a flying scapula?
|
White muscle disease
|
|
|
Signs of iodism?
|
• Lacrimation
• Anorexia • Coughing • Appearance of dandruff |
|
|
What is iodism?
|
Poisoning by iodine
|
|
|
What is the etiology of Lumpy jaw?
|
Actinomyces bovis
|
|
|
Lumpy jaw caused by?
|
-wounds to the buccal mucosa through wounds or dental alveoli
|
|
|
Clinical signs Lumpy jaw?
|
-Iniatially painless, hard, immovable bony swelling on mandible or maxilla at the level of the central molars
- Eventually discharge small amounds of pus through one or more openings in skin |
|
|
Clin path Lumpy jaw?
|
show ‘club’ colonies of Gram-positive filaments
|
|
|
Lumpy jaw can spread to ?
|
esophageal groove and even reticulum
|
|
|
**Streptococcal diseases**
|
**Streptococcal diseases**
|
|
|
What causes Contagious udder?
|
Streptococcus agalacia
|
|
|
Streptococcus agalacia properties?
|
CAMP positive, esculin negative
|
|
|
Is there a 100% eradication of Streptococcus agalacia?
|
Yes-dry cow therapy
|
|
|
Name the environmental Strepts:
|
S. uberis, dyslactia
|
|
|
Environmental Strepts properties?
|
Non-ag, CAMP test and esculin fermentation
|
|
|
Is there a 100% eradication of Environmental Strepts ?
|
-No, it is ubiquittous
-Dry cow theraoy is highly effective |
|
|
What are the Neonatal Streptococcus?
|
Streptococcus genitalium
|
|
|
Streptococcus genitalium causes what?
|
•Causes acute painful swelling of joints, lameness, and fever
•May show signs of meniingitis, omphalophlebitis, and ophthalmitis |
|
|
Source of Streptococcus genitalium?
|
-Source is contaminated uterine discharged from infected dams through umbilicus
|
|
|
Tx Streptococcus genitalium?
|
Tx w/ PPG
|
|
|
Paratuberculosis aka?
|
Johne’s disease
|
|
|
Etiology of Johne’s disease?
|
Mycobacterium avium paratuberculosis (MAP)
|
|
|
Johne’s disease related to?
|
Crohne’s dz
|
|
|
What is your dx: A calf with acute swelling and pain in joints ans later meningitis?
|
Streptococcus genitalium
|
|
|
Clinical signs of Johnes Disease?
• |
a.D+ - often contains bubbles
b.Progressive wasting dz over several weeks or months c.Bottle jaw d.Normal to increased appetite (parasites will have a decreased appetite) e.3-5 years old |
|
|
Johnes Disease
Transmitted via? |
feca/oral, colostrum or transplacental
|
|
|
Dx Johnes Disease?
|
.Clumps of acid fast bacteria in smears of feces stained w/ Ziehl-Nielsen stain of rectal mucosa
b.Culture – 16 weeks; positive is useful (high specificity) |
|
|
Tx Johnes Disease?
|
*Tx is not recommended; Control via:
a.Test everybody w/ ELISA b.Those that are positive, culture to confirm positive c.Cull fecal culture cows d.Cull offspring of culture positive cows e.Multiple/yearly testing – cull accordingly |
|
|
Polioencephalomalacia affects what part of brain?
|
-Gray matter of brain
|
|
|
Polioencephalomalacia Caused by ?
|
1. Thiamin inadequacy or ingestion of thiaminase plants in cattle and sheep
2. sulfate toxicity |
|
|
What is your DX.... A calf with bubbly diarrhea?
|
Johne's
|
|
|
Clinical signs of Polioencephalomalacia?
|
a. Sudden blindness
b. muscle tremors c. opisthotonus d. nystagmus e. convulsions f. staggers • Plants containing thiaminase (will also cause bone marrow suppression) |
|
|
What plants contain thiaminase?
|
a. Bracken fern
b. Horstail. |
|
|
Treatment of Polioencephalomalacia?
|
-Thiamin hydrochloride (there is no tx for sulfate toxicity)
|
|
|
What is your dx... a Cow with sudden blindness?
|
Polioencephalomalacia
|
|
|
Bottle Jaw in calves with diarrhea seen with?
|
Johnes
|
|
|
What is Lumpy wool?
|
Dermatophilosis/cutaneous streptotrichosis
|
|
|
Etiology of Lumpy wool?
|
Dermatophilus congolensis
|
|
|
Description of disease of Lumpy wool?
|
Infection of the epidermis characterized by exudative dermatitis w/ scab formation
|
|
|
Lumpy wool seen mostly in?
|
cattle, sheep and goats most commonly (occasionally horses)
|
|
|
Is Lumpy wool contagious to humans?
|
Has been documented ocassionally
|
|
|
What is Strawberry fot rot?
|
Dermatophilosis
|
|
|
Cause of Lumpy wool/factors predisposing an animal to this?
|
-Prolonged wetting by rain, high humidity, high temp and flies and ticks can increase it
|
|
|
What will attract the zoospore of lumpy wool?
|
Carbon dioxide released from breaks in the skin.
|
|
|
Lumpy wool Scabs look like what?
|
raised and circular
|
|
|
Lumpy wool lesions look like?
|
– pyramid-shaped masses of scabs on wool
|
|
|
Strawberry foot rot looks like ?
|
– skin from coronet to carpus or hock
|
|
|
Treatment of Dermatophilus?
|
-Most recover w/in 3 weeks of initial infection or during dry weather
-PPG or streptomycin injections |
|
|
Urolithiasis Seen mostly in what?
|
1.housed calves fed milk substitute
2. weaned animals fed high concentrates |
|
|
Urolithiasis Occur most commonly at what place in urogenital system?
|
-sigmoid flexure of the penis
|
|
|
Housed animals get these uroliths?
|
1. Ca or Mg ammonium phosphate
2. Struvite 3. Oxalate |
|
|
Pastured animals get these uroliths?
|
Ca carbonate, Mg carbonate and Ph carbonates
|
|
|
Factors predisposing to Urolithiasis?
|
a.High concentration of grain
b.Vit A deficiency has been suggested a factor c.Estrogesn from plants or growth promoters d.Pelleted ration e.Castrated males |
|
|
Clinical signs Urolithiasis?
|
a. Palpate preputial hairs, will feel gritty
b. Straining to urinate c. Colic – kicking at belly, paddling movement, tail swishing d. If there seems to be a sudden relief, probably a urethral or bladder rupture (will see abdominal distension) |
|
|
Tx Urolithiasis is?
|
sx
|
|
|
**Salmonella**
|
**Salmonella**
|
|
|
What type of bacteria is Salmonella?
|
Enterobacteria- anaerobic gram (-) rod
|
|
|
How is it usually zoonotic to humans?
|
Food contaminated with animal material.
|
|
|
2 types of Salmonella that affect cattle?
|
S. Dublin, S. Typhimurium
|
|
|
Age salmonella occurs in calves?
|
< 5 days, or 2-6 wks old, or adult
|
|
|
CS of salmonella in adults?
|
Severe Diarrhea?
|
|
|
CS of Salmonella in calves?
|
Putty, smelly diarrhea
|
|
|
3 Syndromes of Salmonella?
|
a. Peracute systemic infection
b. Acute enteritis c. Chronic enteritis |
|
|
What salmonella serotypes are pathogenic to man?
|
All
|
|
|
What salmonella is host adapted and cause dz only in man?
|
-S typhi, partype A and sendai
|
|
|
What salmonella is Sheep specific?
|
S abortusovis
|
|
|
What salmonella is Poultry specific?
|
S pullorum
|
|
|
What salmonella Causes dz in pigs, but are opportunist pathogens for other spp?
|
S cholerasuis
|
|
|
What salmonella Causes dz in cattle but is opportunist pathogen for other spp?
|
S dublin
|
|
|
What salmonella is Ubiquitous and causes dz in many animals including cattle and humans?
|
S typhimurium
|
|
|
Dx of salmonellosis?
|
Fecal sample before AB's for culture.
|
|
|
Control of salmonellosis?
|
a.Uncontaminated food and water
b.Control of rodents and birds c.Biologic control d.Vaccination |
|
|
Name some common stifle injuries in cattle?
|
1. Patellar luxation
2. Cranial cruciate ligament rupture 3. Collateral ligament torn 4. Patellar fx 5. Proximal tibial epiphyseal separation – young cattle |
|
|
Name 3 types of patellar luxation?
|
Dorsal, medial, lateral
|
|
|
Type of luxation seen in adult cattle?
|
dorsal, lateral
|
|
|
Congenital luxation occurs in what direction?
|
medial
|
|
|
CS of cattle with dorsal patellar luxation
|
-hindlimb remains extended caudally longer than usual, then pulled forward and upward (looks like stringhalt)
|
|
|
TX of dorsal patellar luxation?
|
Tx is medial patellar desmotomy if signs persist form more than one week
|
|
|
Lateral patellar luxation secondary to what?
|
Quadriceps atrophy from femoral paralysis.
|
|
|
CS of Lateral patellar luxation ?
|
-Lateral and medial fixation show characteristic posture of a markedly flexed stifle and the limb collapses on weight bearing (exactly as in femoral paralysis)
-Bilaterally affected calves may be recumbant |
|
|
Tx of Lateral patellar luxation ?
|
-Both medial and lateral fixation are tx w/ a joint capsule overlap procedure
|
|
|
Cranial cruciate ligament rupture occurs due to what?
|
Heavy weight, sudden twists and falls (mounting, being mounted by cows in estrus)
|
|
|
Problems associated with Cranial cruciate ligament rupture?
|
-Subluxation of femarotibial joint, CrCL rupture, damage to tibial menisci, secondary osteoarthritic changes
-Soft tissue swelling and creptus |
|
|
Diagnosis of Cranial cruciate ligament rupture?
|
Can get tibial drawer sign
|
|
|
Blackleg is caused by what?
|
Clostridium Chauveoi
|
|
|
Clostridium Chauveoi mannifests itself where?
|
spleen, liver and muscles
|
|
|
Clinical signs of Blackleg?
|
a.Initial – hot and painful lameness on a limb
b.Cold and emphysematous limb c.Respiratory distress if involves the tongue d.Stiffness and reluctance to move when sublumbar muscles are involved e.Depression, anorexia, inc HR and inc temp f.Death occurs in 12-24 hours |
|
|
Signs of Blackleg postmortem?
|
•After death, carcass becomes bloated and putrefaction occurs rapidly
•Bloodstained froth exudes form all body orfices •Muscle is black, dry and crepitant w/ spongy and rancid odor |
|
|
Dx of Blackleg ?
|
a. Anthrax must be ddx
b. FA stain |
|
|
Tx of blackleg?
|
-Ab of PPG only if early
|
|
|
Prevention of blackleg?
|
-via vaccines of all animals > 6 months old
|
|
|
Malignant edema aka?
|
Clostridial myositis –
|
|
|
Malignant edema caused by?
|
-Acute wound infection caused by Clostridial organsism C. novyi, C perfringens, C septicum,
or C sordelli -Caused by deep puncture wounds, sx operations, injections, parturition |
|
|
Malignant edema affects whole herd of individuals?
|
-individual or small number of animals
|
|
|
CS of disease with Malignant edema?
|
-Swelling, tense and emphysematous
•Lameness, stiffness, and muscle tremors may be evident – can die w/in 48 hrs |
|
|
Necropsy findings with Malignant edema?
|
-all body cavities contain blood stained fluid
-The side of infection is surrounded by an extensive edema of SQ tissue and IM fascia |
|
|
DX of malignant edema?
|
FA tests or culture
|
|
|
Pregnancy toxemia is considered primarily a dz of what species?
|
sheep
|
|
|
Pregnancy toxemia is similar to what?
|
-ketosis only during 7-9 months of gestation
|
|
|
Pregnancy toxemia predisposing factors?
|
beef cattle in late pregnancy
• Starvation, energy deficient diet in fat cows induces causing massive mobilization of fat reserves |
|
|
Clinical signs of Pregnancy toxemia?
|
Same clinical signs as ketosis
|
|
|
Clin path of Pregnancy Toxemia?
|
-hypoglycemia, hyperketonemia and ketonuria
|
|
|
Dx Pregnancy Toxemia?
|
-clinical signs, nutritional status and stage of pregnancy
|
|
|
Tx Pregnancy Toxemia?
|
-same as ketosis
|
|
|
Pregnancy Toxemia overall is a result of?
|
-Even though it is more common in fat cows, it is essentially the result of starvation; therefore, supply good quality forage throughout gestation
|
|
|
Leptospirosis that causes synovitis and dermatitis?
|
-L interrogans
- serovar icterohemorrhagica - serovar canicola |
|
|
Carrier of Leptospirosis (serotypes icterohem and canicola)?
|
Rodent
|
|
|
Spread of Leptospirosis (serotypes icterohe and canicola)via?
|
feed or water
|
|
|
CS of Leptospirosis (serotypes icterohem and canicola)?
|
-Fever, dullness & anorexia
-Jaundice and hemoglobinuria -Synovitis and dermatitis |
|
|
TX of Leptospirosis (serotypes icterohem and canicola)?
|
Dihydrostreptomycin, tetracycline, blood transfusion
|
|
|
Leptosprirosis (serotypes hardjo) causes what?
|
-abortion
|
|
|
Leptosprirosis (serotypes hardjo) Transmitted to humans by contact via?
|
-urine by milking
|
|
|
Leptosprirosis (serotypes hardjo) Spread cow to cow via?
|
-urine, fetus and uterine discharge and semen
|
|
|
Two main syndromes of Leptosprirosis (serotypes hardjo)?
|
1. Udder – sudden drop in milk in all quarters, udder secretion is thickened and clotted; Flabby bag
2.Abortion – second half pregnancy |
|
|
DX/TX/Prevention of Leptosprirosis (serotypes hardjo)?
|
DX- urine
Tx: dihydrostreptomycine Prev: Vaccination w/ killed, but should use Ab in all cattle before vaccination program b/c infected cows may still excrete bacteria |
|
|
Coxofemoral luxation – hip joint occur mc in what?
|
2-5 year cattle w/ parturition and early postpartum
|
|
|
Coxofemoral luxation occur due to?
|
Obturator or other nerve injury during dystocia
|
|
|
Coxofemoral luxation displacement most common in what direction?
|
Craniodorsal
|
|
|
Coxofemoral luxation only consistent sign is?
|
Sudden onset of lameness
|
|
|
Other cs of Coxofemoral luxation?
|
-Leg may be rotated outward, hock medial and stifle more lateral
-Leg may appear shortened and asymmetrical femoral trochanters |
|
|
Dx of coxofemoral luxation?
|
Rectal palpation may locate crepitance
|
|
|
Tx coxofemoral luxation?
|
a.Manipulative reduction – position cow so that the body is fixed while the affected upper leg can be extended in various direction (deep sedation is advisable)
|
|
|
Retropharyngeal abscess treatment?
|
Same as abscesses of the jaw, wait until there is a softening to lance open
|
|
|
Causes of retropharyngeal abscess?
|
May be induced by balling gun, actinobacillosis or foreign object
|
|
|
MC causes of Choke?
|
Apples and potatoes most common
|
|
|
Predisposing factors to choke?
|
Fed in groups where cows will hoard food
|
|
|
Signs of choke include?
|
a. Profuse salivation followed by bloat (prevents swallowing and eructation)
b. Head extended c. Frequent attempts to swallow |
|
|
Diagnosis of choKe?
|
-pass a stomach tube to see if there is an obstruction (or will dislodge it!)
|
|
|
Differentials for choke?
|
-rabies (excess salivation is either choke or rabies!)
|
|
|
Tx for choke?
|
a.cannula for rumen tympany
b.spasmolytics (hyoscine butylbormide and dipyrone) c. Prevent by cutting food into small pieces |
|
|
Mycoplasmosis aka?
|
mastitis
|
|
|
Most common cause for mastitis?
|
Mycoplasma bovis
|
|
|
Type of bacteria Mycoplasmosis?
|
Not a bacteria, lack a cell wall
|
|
|
AB treatment for Mycoplasmosis?
|
•Refractory to Ab tx – cull postitive cows
|
|
|
Contagious bovine pleuropneumonia etiology?
|
Mycoplasmosis – respiratory-
Mycoplasma mycoidies |
|
|
Occurence of Mycoplasmosis and cs?
|
-Eradicated
-Sudden pyrexia and respiratory distress and pain |
|
|
Contagious bovine pyelonephritis etiology?
|
Corynebacterium renale
|
|
|
Effects of Corynebacterium renale?
|
Urinary tract of cattle causing inflammation of kidneys, ureters and bladder
|
|
|
Corynebacterium renale
contracted how? |
by ascending infection, females are far more susceptible than males
|
|
|
Age Contagious bovine pyelonephritis mc in?
|
> 3 years old
|
|
|
CS of Contagious bovine pyelonephritis?
|
-Hematuria, colic, painful urination w/ progression to anemia and uremia
|
|
|
TX Contagious bovine pyelonephritis?
|
-Tx w/ PPG
-Acidification of urine w/ Na phosphate |
|
|
In a bacterial infection you you want to acidify urine or alkalanize it?
|
Acidify
|
|
|
Hemoglobinuria causes intravascular hemolysis or extravascular?
|
intravascular hemolysis
|
|
|
Name some DDx for Hburia?
|
1. Red maple – wilted leaves (BUT ONLY IN HORSES)
2. Scented thorn 3. Murcury 4. Cereal rye 5. Babesiosis (bigemina and bovis) – severe jaundice 6. Tropical theileriosis – Hyalomma ticks, LN enlargment 7. Postparturient Hburia – no jaundice, 2-4 weeks postcalving in cows 3-6th lactation 8. Bacillary Hburia 9.Leptosporosis (interrogans pomona) – mostly in young calves, jaundice, petechia, pallow, adults have orange milk 10. Chronic copper poisoning – copper supplement in swine diet by mistake |
|
|
Orange milk in adult cows?
|
Leptosporosis
|
|
|
Is red maple leaves toxic effect cause hemoglobinuria in all species?
|
No-only horses
|
|
|
Cows would get accidental copper poisoning if ?
|
get into copper supplement in swine diet by mistake
|
|
|
Bacillary hemoglobinuria etiology?
|
Clostridium hemolyticum
|
|
|
Area affected by Clostridium hemolyticum?
|
-Liver
|
|
|
Time of year Clostridium hemolyticum prevalent?
|
-Summer and autumn in endemic areas (irrigated or poortly drained pastrue)
|
|
|
Clostridium hemolyticum
causes what? |
-Causes toxemia, Hburia, and jaundice, brisket edema, sudden death, urine is dark red
|
|
|
Tx of Clostridium hemolyticum?
|
1. Immediate PPLG or tetracyclines
2. Antitoxic serum if available 3. Vaccination available |
|
|
Type of diarrhea caused by Campylobacter jejuni in calves?•
|
NOT A CAUSE OF INTESTINAL DZ IN CALVES
|
|
|
Name campy's causing abortion in cattle?
|
Abortion
•Campylobacter fetus spp venerealis – venereal infection •Campylobacter fetus spp fetus – ingestion |
|
|
Herd problem abortions in cattle include?
|
IBR, BVD, brucellosis, leptospirosis, campylobacteriosis, trichomoniasis, anaplasmosis, ureaplasmas, mycoplasmas.
|
|
|
Sporadic abortions in cattle include?
|
Mycotic(Aspergillus, Mucor spp)., Listeria, Haemophilus, Corynebacterium pyogenes, Staphylococcus, bluetonque. Nitrates, lupine, locoweed, mycotoxins
|
|
|
***Abortion***
|
***Abortion***
|
|
|
Asymptomatic in bull
|
Tricho fetus
|
|
|
Causes postcoital (not post partum) pyometra?
|
Trich fetus
|
|
|
Not zoonotic in cattle (zoonotic in sheep)?
|
Campy vibriosis (Vibriosis)
|
|
|
Affects developing embryo at the time of maternal recognition of pregnancy (DOES NOT affect conception)?
|
Vibriosis
|
|
|
Herd hx of gradual ‘infertility’?
|
Trich fetus
|
|
|
Endometritis and Salpinitis
|
Vibriosis
|
|
|
CARRIERS from one breeding season to the next
|
Vibriosis
|
|
|
DOES NOT prevent conception, but EED (early embryonic death)
|
Trich fetus
|
|
|
Dx of Vibriosis?
|
CLARK’s medium
|
|
|
Dx of Trich fetus?
|
Diamond’s media so will multiply, & culture for 24-48 hrs. THREE TIMES
into prepuce fold |
|
|
Conceive, but then return to estrus 40-45 days later/Get a ‘scattered calf crop’.
|
Trich fetus
|
|
|
What do you use flagyl to treat in bovine?
|
Flagyl is illegal in food animals
|
|
|
Protozoan w/ 3 anterior and 1 posterior falgella and an undulating membrane.
|
Trichomonas
|
|
|
Tx of vibriosis?
|
Tx bull w/ Dihydrostriptomycin
|
|
|
Venereal dz of cattle
Transmitted by coitus |
Trich fetus
|
|
|
Transmitted by raw foods such as eggs, meat, milk, water etc?
|
Campylobacteriosis
|
|
|
Anaplasmosis etiology?
|
Anaplasma marginale
|
|
|
Anaplasmosis Transmitted by ?
|
1. Ticks (Boophilus microplus, Dermacentor), tabanids
2. Iatrogenically 3. Transplacentally |
|
|
CS anaplasmosis?
|
Anemia, jaundice, severe debility, death
|
|
|
Anaplasmosis found in blood stream in what cell?
|
RBC
|
|
|
Major pathogen of college students in US
|
Campylobacteriosis
|
|
|
Treatment of Anaplasmosis?
|
1. Tetracycline or imidocarb, blood transfusion
2. Weekly dipping in acaricides is vacciantion inendemic arease |
|
|
May be confused w/ appenticitis?
|
Campylobacteriosis
|
|
|
AMOUNT OF ALTERNATING CURRENT THAT CAN AFFECT BEHAVIOR in cattle?
|
0.5 TO 1.0 VOLT
|
|
|
Stray voltage amount that can kill a cow?
|
110-220 volts
|
|
|
Survives refrigeration and freezing well and has low infective dose
|
Campylobacteriosis
|
|
|
Cow will respond to this amount of voltage?
|
2 volts
|
|
|
Name the campylobactors transmitted through food?
|
1. C jejuni – cattle, swine, fowl
2. C fetus, hyointestinalis – swine 3. C coli – fowl |
|
|
Anaplasmosis subclinical in what species?
|
Sheep/goat
|
|
|
Can cause abortions in all species of animals by eating affected foods?
|
Campylobacteriosis
|
|
|
Listeria monocytogenenes is dangerous to humans and man why?
|
-Ubiquitous in farm enviroment
-Resistant because psychrophillic and thermoduric |
|
|
Listeria monocytogenenes assocaiated w/ what causing it?
|
-feeding silage w/ high listerial growth (found at bottom abd top of silo)and management induced stress
|
|
|
Lesion with listeria seen where?
|
brainstem and CN
|
|
|
Abortion with Listeria occur during?
|
last trimester
|
|
|
Other disease manifestations with Listeria?
|
-septicemia in pregant and neonatal sheep and goats, enteritis in weanlings, spinal myelitis, ophthalmitis and occasionally masitis
|
|
|
CSF analysis of listeria?
|
CSF – pleocytosis of mononuclear cells and lymphocytes & inc protein
|
|
|
Pathopneuminic lesion with listeria?
|
Microabscesses in brainstem, spinal cord, intestin or viscera
|
|
|
Tx of listeria?
|
Tx is chlortetracycline or PPG EARLYin clinical dz
•Zoonotic implications |
|
|
Fescue toxicosis
|
Neotyphoidium coenophialum – ergovaline from ergot alkaloids
|
|
|
Aflatoxin
|
Aspergillus flavus
|
|
|
Zearalenone
|
Fusarium roseum
|
|
|
Trichothecenes
|
moldy corn toxiciosis; Fusarium sprorotrichoides and roseum
|
|
|
Ochratoxin
|
Aspergillus ochraceus and Pnicillin vindicatum; Ochratoxin A
|
|
|
Slaramine
|
Rhizoctonia legumincoola
|
|
|
Fumoninsins
|
– moldy corn toxicosis; Fumonsins
|
|
|
Name common trematodes affecting bovine?
|
•Schistosomes
•Fasciola hepatica Flukes •Paramphistomum and Coylophron |
|
|
Blood trematode?
|
•Schistosomes
|
|
|
What auses hyperplastic cholangitis and what is that?
|
Fasciola hepatica Flukes– where the biliary mucosa becomes permeable to albumin
|
|
|
Rumen flukes?
|
•Paramphistomum and Coylophron -non pathogenic
|
|
|
Predisposes cattle to Clostridium hemolyticus (red water dz)
|
Fasciola hepatica
|
|
|
Most susceptible species to tetanus?
|
Horse
|
|
|
Most pathogenic fluke in cattle
|
Fasciola hepatica – major cause of liver condemnation
|
|
|
Most resistant species to tetanus?
|
birds
|
|
|
Causes aboriton via placentits and is found in moldy hay or straw?
|
Aspergilosis, Candiasis, Zygomycosis (Mucor, Rhizo)
|
|
|
What mycosis causes pneumonia, hepatic insufficiency, placentitis?
|
Histomonas-MIssissippi river
|
|
|
Chronic dz of nasal mucosa in cattle and horses.
|
Rhinosproidiosis
•Rhinosprodidium seeberi |
|
|
Generalized dz or granulomatous, abortion, can be a cause of bovine mastitis?
|
cryptococcosis
|
|
|
Mycosis common in dogs but rare in other species?
|
Blasto
|
|
|
What happens with Intussusception?
|
• Small intestine telescopes into the small intestine or the ileo-cecal valve into the cecum
|
|
|
Tx in Bovine with Intussusception?
|
-Sx remove and anastomosis performed – DO NoT UNRAVEL
|
|
|
What is your dx? Basophillic stippling of RBC?
|
Lead poisoning
|
|
|
Lead toxicosis most common source is?
|
electric storage batteries
|
|
|
Tx of lead toxicisis in bovine?
|
Tx Mg sulphate, Ca EDTA, thiamine
|
|
|
What is the condition of lead poisoning called?
|
plumbism
|
|
|
Species that tend to be resistant to lead?
|
Swine and poultry
|
|
|
Use Calcium EDTA as a chelating agent in all species except?
|
Birds-use Dimercaptosuccinic acid 25-35 mg/kg BID for 5 days.
|
|
|
Pathway of lead through body?
|
Residue problem b/c stored in bone, kidney and slowly excreted in the bile
|
|
|
Common Sources of lead?
|
1. Lead arsenate in pesticide
2. Older buildings – putty, shingles, paints, plaster 3. Lead shots 4. Fishing wts 5. Solder 6. Bell clangers 7. Lead acid batteries – cattle |
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A farmer tells you he added an ingredient to improve digestibility and nitrogen content in his hay cows are now presenting with Hyperesthesia, rapid blinking, ear flicking, frequent urination and defecation, dyspnea, circling and convulsions
•Blood ammonia levels are normal, what is your dx? |
Anhydrous ammonia was added to hay-Ammoniated feed toxicosis
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Treatment in the above situation?
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Tx – sedation and dilute toxic forage w/ normal feed is NOT recommended b/c can get an accumulatory effect
•Maximum rate of ammoniation to avoid toxicity is 3% for poor quality forage and 1% for high moisture forage |
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Ergot toxicosis Includes?
|
a.Neothypohdium (Acremonium) - ergovaline (fescue toxicosis), lolitrem (ryegrass staggers via tremorgens)
b.Clavicepts paspali – paspalum staggers; dallis grass, bahiagrass, CNS c.Claviceps purpurea – ergotism; ergotomine; cereal rye grasses, ingestion of large quantities |
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What is your diagnosis?a.Gangrene of extremities
b.Hyperthermia syndrome c.Reproductive syndrome -lack of udder development and agalacia |
•Claviceps purpura
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Rabies etiology?
|
Rhabdovirus
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% mortality wih rabies?
|
100%
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Who does rabies affect?
|
Affects all warm blooded animals
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Transmission of rabies introduced into?
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striated muscle
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Rabies path of infection?
|
Replicates until reaches nerve ending
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Why does rabies reach nerve endings?
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tropism for Ach
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Amt/ day that rabies migrates?
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50-100mL/day in nervous system toward brain
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T or F- The longer the bite is from the brain, the longer it takes to be fatal!
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True
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Rabies replicates in?Moves to?
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limbic system of lower brain-moves to cortex
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Phase of rabies is called what after moves to cortex?
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‘Dumb rabies’
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Destination of rabies virus?
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The moves to salivary gland & is excreted via a bite in extremely high concentrations
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DDX of Rabies
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distemper in racoons; pseudorabies in swine
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3 stages of rabies?
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Prodromal
Furius Dumb |
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Clinical signs of Prodomal stage?
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-humans, vague changes in temperament 1-3 days before clinical signs
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Clinical signs of Furious stage?
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-Dogs, cats, horses, CNS ; loses emotional control – bizarre behavior; will move after anything that moves, will break teeth
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Clinical signs of dumb stage?
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– cattle, pharyngeal paralysis, ‘choke’
Wild animals – aberrant behavior, animals come out in middle of day Drool b/c swallowing is painful |
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Dx of rabies?
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- IFA test of head to state lab
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Protocol for rabies suspect?
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Confine dog/pet for 10 days after bite
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Rabies animal will shed virus for how long?
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6 days before showing signs (4 extra days are precautions)=10 days confinement
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If vaccinated pet bitten by rabid animal what do you do?
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revaccinate immediately, release to O, and observe for 45 days
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If unvaccinated pet bitten by rabid animal what do you do?
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isolate for 6 months and vaccinate 1 month before release
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Susceptibility of rabies in different animals from greatest to least?
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Coyotes, Foxes, Skunks > racoons > Dogs > Pigs > Human > Opossums
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Most common sign in cattle with rabies?
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bellowing
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Bangs disease aka?
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Brucellosis- Contagious abortion
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Describe Brucellosis?
|
Zoonotic, AI dz
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Does Brucellosis occur during coitus?
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No- because natural service cannot penetrate cervix
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How long are animals infertile following infection with Brucella?
|
4-12 months
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Brucella Bacteria may be found in what in pregnant cows?
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Uterus
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Dx of Brucella in cow via?
|
stomach and lungs of aborted fetus
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Test cow for Brucella via ?
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serum agglutination test from milk, whey and plasma or ELISA Abs in milk and serum and vaginal mucus
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Treatment for Brucella?
|
none
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Prevention of Brucella?
|
- vaccinate w/ B abortus strain 19
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Nocardiosis is a disease causing what?
|
Chronic infection from soil borne organisms
|
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Clinical manifestation of Nocardia?
|
generalized, purulent granulomatous nodular lesions
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MC in what species (Nocardia)
|
Cattle
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Most common sign of nocardia in cattle?
|
Mastitis
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Nocardia has the ability to cause other problems in the body via?
|
Metastasis to lungs and supramammary LNs
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Nocardia is known to cause what other disease?
|
bovine farcy – puruelent lymphadentitis and lymphangitis
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DX of nocardia
|
Easily cultured on blood ro brain-heart agar for more than 3 days
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Tx of nocardia
|
-successfully w/ udder infusion; Erythromycin and miconazole are most effective
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**** Chlamydiosis****
|
**** Chlamydiosis****
|
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•Causes seminal vesiculiis syndrome – semen contain chlamydia
•Causes an endometritis and infertility and abortion •Severe placentitis |
•Chlamydia psittaci
|
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•Fever w/ good appetite
•ADR, incoordination and staggering •Vascular damage in many organs – peritonitis, pleuritis, pericarditis |
Sporadic bovine encephalomyelitis
•Chlamydia psittaci |
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Will chalmydia cause intestinal disease in cattle?
|
yes
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Chlamydia psittaci will cause eye infections in these species?
|
cats, lambs, goats and guinea pigs
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Enzootic pneumonia in calves
|
Chlamydia psittaci
|
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Polyarthritis-serositis Infectious dz of sheep, calves, goats and pigs
|
Chlamydia psittaci- from GI
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Arthritis in calves with no naval involvement?
|
Chalmydia psittaci
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Ionophore/Monensin/Lasalocid toxicity due to uses for coccidiostat and growth promotion in cattle will cause what cs?
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Cause myopathy,Myocardial necrosis and pulmonary congestion
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Monensin is also used to tx?
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ketosis, lactic acidosis and bloat
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Monensin is potentiated by?
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Abs and sulfonamides
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Highest toxicity to monensin seen in what animal?
|
horse
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D+ and black erosions of abomasal and duodenal mucosa? is DX?
|
Na chlorate- a Herbicide
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•Inhibites aconitase – Myocardial depression w/ ventricular fibrillation and CNS causing convulsions-what is your dx?
|
Na fluoroacetate- Compound 1080 as a rodenticide
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V+/D+, dehydration, opisthotonus, nystagmus, blindness, convulsions, death
,Polioencephalomalacia what is your dx? |
Na chloride poisoning- water deprivation
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What is your dx? eosinophilic perivasculitis, meningitis, laminar cortical necrosis w/ gitter cells and edema?
|
Salt poisining- NACL
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Mad Itch aka?• Rare, but Suid Herpesvirus 1 can be spread from the pig to cattle via nasal discharge in contact w/ abraded skin or nasal mucosa
• • Most cause death • MAD ITCH |
Pseudorabies
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|
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Etiology of Pseudorabies?
|
Herpesvirus 1
|
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How do cattle get pseudorabies?
|
spread from the pig to cattle via nasal discharge in contact w/ abraded skin or nasal mucosa
|
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MC clinical sign of Pseudorabies?
|
-Intense, local pruritis w/ violent licking, chewing and rubbing of the part
-May cause intesne excitiment including bellowing and convulsionsm manic behavior, circling and spasm and opsthotonus |
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Vesicular stomatits affects who?
|
Disease of cattle, horses and pigs
|
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Are all vesicular diseases reportable?
|
yes
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|
Vesicular lesions in vesicular stomatitis seen where?
|
on oral mucosa, teats and prepuce
|
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|
DX of vesicular stomatitis ?
|
Virus isolation or PCR, serology w/ rising titers
|
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|
Most vesicular stomatitis outbreaks occur when?
|
Late summer and early autumn
|
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|
Human manifestation of vesicular stomatitis ?
|
flu-like symptoms
|
|
|
Mechanical transmission of vesicular stomatitis ?
|
Windborne, black fly, Culicoides fly, eye gnats may transmit
|
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|
Is vesicles a definitive diagnosis in vesicular stomatitis ?
|
No-Vesicles only occur in 30% of cases – hard to detect
|
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Definitive diagnosis in vesicular stomatitis ?
|
FA Ab used to dx
|
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|
Tuberculosis etiology?
|
Mycobacterium bovis
|
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|
Main source of infection of Mycobacterium bovis
to pigs and all other spp (all ages and all spp!) |
Infected cattle
|
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|
Reservoir of Mycobacterium bovis which prevents eradication in some countries?
|
Wildlife
|
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|
Transmission of Mycobacterium bovis?
|
Transmitted by inhalation or ingestion – drinking water and feed troughs, infected milk, intrauterine infection, feeding TB cattle carcasses, stockmen urinating in cattle environment
|
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|
More resistant breed of cattle to Mycobacterium bovis?
|
Zebu (Bos indicus)
|
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|
Important zoonosis of Mycobacterium bovis?
|
infected milk
|
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|
Mycobacterium bovis Spread by two stages?
|
a. Primary complex – lesion at point of entry and in local LN; calcification of lesion 2 weeks later; and spreads to lung or liver
b. Post primary dissemination – discrete nocular lesions in various organs or chronic organ tuberculosis |
|
|
Pathognomonic for Mycobacterium bovis
|
monocytes and plasma cells surrounded by granulation tissue “tubercle’
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|
Clinical signs Mycobacterium bovis?
|
a. Progressive emaciation
b. Capricious appetite and fluctuating temperature c. Chronic soft cough d. Dyspnea – bronchopneumonia in sheep & goats e. Crackles over caudal lobes f. May have infertility or abortion – uncommon g. Mastitis – important b/c cause of public health; palpate supramammary LNs h. Painful osteomyelitis in cervical vertebrae in horses |
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|
M/C Dx of Mycobacterium bovis?
|
Tuberculin test
a. Single intradermal (SID) test – intradermal injection of 0.1 mL of tuberculin into a caudal tail skin fold made of bovine tuberculin purified protein derivative (PPD) b. Reaction is read 48-72 hours later for sensitivity and 96 hours for specificity c. NVLs – no visible lesion reactors and lack of specificity (M bovis, M avium, tuberculosis, paratuberculosis, Nocardia d. May not be sensitive to to old cows or cows which ahbe rectnly calved e. Cannot retest for 60 days |
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|
Other Dx of Mycobacterium bovis?
|
a. Short thermal test – intradermal TB (4 mL) injected SQ in the neck which have NO temperature. If temp at 4,6 and 8 hours later goes above 104, the animals is a positive reactor
b. Stormont test – same as above, w/ further injection at same site 7 days later, an increase in skin thickness of 5 mm or more 24 hours after 2nd injection is a positive; cannot retest for 6 months c. Comparative test – Avian and bovine TB are injected simultaneously into two separate sites on same side of neck and read 72 hours later. Good to differentiate between vaccination against Johne’s and TB d. Serological tests – Interferone gamma assay • Other spp: a. Pigs – SID in base of the ear b. Horses – SID – false positives occur; smaller doses required, may provoke an anaphylacitic rxn c. Sheep and goats – Stormont test |
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|
Treatment for Mycobacterium bovis?
|
test and eradicate
|
|
|
Atypical mycobacterium seen in bovine?
|
Mycobacterium avium-intracelluar
|
|
|
Mycobacterium avium-intracelluar source?
|
Domestic or wild birds
|
|
|
Mycobacterium avium-intracelluar cs?
|
Draining LNs of GI tacts; most are subclinical but can cause carcass condemnation
|
|
|
Human origin TB?
|
Mycobacterium tuberculosis
|
|
|
CS of Mycobacterium tuberculosis in cattle?
|
Usually causes LNs of GI and respiratory system to enlarge
|
|
|
Confused w/ bovine farcy – Mycobacterium farcinogens
|
Skin tuberculosis
|
|
|
What is Skin tuberculosis
? |
Chronic tuberculoid granuloma lesions of the skin on lower limbs
• Acid fast organsism • Not pathogenic • |
|
|
Malignant Catarrhal Fever
Etiology? |
Caused by two agents:
1. Alcelaphine herpes virus-1 (AHV-1) from wildabeast 2.Ovine herpes virus-2 from sheep |
|
|
AHV occurs where in world?
|
occurs in Africa in cattle comingled w/ wildabeast
|
|
|
OHV occurs where in world?
|
a. occurs in USA in low incidence in cattle that comingle with sheep
b.Unknown how it is spread |
|
|
Outcome of AHV and OHV?
|
1. fatal
2. Some recovered cattle show a persistent viremia |
|
|
Considered one of the most important dzs of what?
|
farmed deer
|
|
|
Gossypol toxicosis ocurs from ingestion of what?
|
cotton seed seeds and hulls
|
|
|
Gossypol toxicosis Causes what?
|
damage to myocardium and liver
|
|
|
Most susceptible species to Gossypol toxicity?
|
Preruminant lambs
|
|
|
Seen in farmed deer?
|
MCF
|
|
|
Outbreaks of gossypol seen mostly in?
|
Pigs
|
|
|
CS of Gossypol toxicity?
|
-Thin, exercise intolerance, dyspnea, jugular vein distension, reduced fertility in bulls, generalized edema
|
|
|
In a herd of cattle youare finding opacity of the cornea is always present, and persistant bilateral ocular leukomata,necrotizing vasculitis,what is your diagnosis?
|
MCF
|
|
|
Whatcan you add to an animals diet to prevent gossypol poisoning?
|
a.iron to pig diet
b.cations c.Ca carbonate – prevents repro effects in cattle d.Cookiing in Ca hydroxide or Ferrous sulfate |
|
|
Botulism is what type of toxin?
|
Clostridium botulinum neurotoxin
|
|
|
Does clostridium botulinum cause spores?
|
yes
|
|
|
Spore forming anaerobe of botulism can suvive in environment for ?
|
30 years
|
|
|
Type of Clostridium botulinum causing diseae in animals?
|
Animal dz from subtypes B, C & D
|
|
|
Where are the different types of botulism found?
|
Type B – not found in south, horse
•Type C – acid soils in Gulf coast, cattle and sheep •Type D – alkaline soils in the west, cattle and sheep |
|
|
Other source of botulism
|
1. Forage botulism
2. Carrion Associated botulism 3. Wound botulism |
|
|
Source of forage botulism?
|
a.ingestion of preformed toxin in spoiled stored forages or decaying vegetable material
b.Usually cereal or big bale silage |
|
|
Type of botulism in forage?
|
Type B
|
|
|
Most susceptible to forage botulism?
|
horse
|
|
|
Source of Carrion associated botulism?
|
a. Animals on pasture
b. Includes dead animals and birds |
|
|
Type of botulism in Carrion associated botulism?
|
Most type C & D
|
|
|
Type of botulism that persists in carcass/how long can it remain infective?
|
Carrion assoc- 1 yr
|
|
|
Phosphorus deficient diet (cattle) or Protein deficient diet (sheep) can predispose to thi botulism?
|
Carrion associated botulism-type C & D
|
|
|
Drinking from lakes w/ avian botulism has been a source of this type of botulism?
|
Carrion associated-type C & D
|
|
|
Found in poultry manure?
|
Carrion associated-type C & D
|
|
|
Wound botulism foundin what species?
|
a.rare but recoded in horses following castration or injection abscess
|
|
|
Causes shaker foal syndrome in horses?
|
Type B botulism
|
|
|
MC species affected with botulism?
|
birds
|
|
|
Type of paralysis with botulism?
|
Flaccid-compete with ACh
|
|
|
Pathogneumonic for Botulism infection?
|
•Animal dies of respiratory paralysis
•Progressive symmetric muscular paralysis |
|
|
Botulism aka____ in sheep
|
limber neck
|
|
|
Botulism aka____ in foals
|
muscle tremor
|
|
|
DX of botulism?
|
a. detection of toxin using mouse bioassay
b. spores in the feed or feces of affected animals c. Ab via ELISA |
|
|
Tx of botulism
|
b. Polyvalent antiserum – early
c. Mineral oid – consitpation d. Bladder catheterization e. Avoid drugs that deplete neuromuscular junction (Ach) |
|
|
Bovine Spongiform Encephalopathy (BSE) first occurence?
|
Occurred in United Kingdom when meat and bone rendering processing changed from organic solvent to steam
|
|
|
Bovine Spongiform Encephalopathy (BSE) is a derivative of ?
|
Scrapie changed spp
|
|
|
Is BSE zoonotic?
|
possibly
|
|
|
Incubation of BSE?
|
2-8 years
|
|
|
Spongiform encephalopathies have also been identified in?
|
-ungulates and domestic cats and zoo felids (Feline spongiform encephalopathy) and ther is a Transmissible mink encephalopathy in the US in subclinical form
|
|
|
Clinical signs BSE?
|
nervousness, aggression, abnormal posture, incoordination, difficulty rising, decmilk prod
|
|
|
Cases of fatality of BSE is?
|
100%
|
|
|
Pathognomonic signs of BSE?
|
-Brain will have bilaterally symmetric intracytoplasmic vacules in neurons and degeneration of gray matter
|
|
|
DX BSE
|
-Dx via demonstration of prion protein PrPSc
|
|
|
Human form similar to FSE and BSE
|
Variant Creutzfeld-Jakob disease
|
|
|
Is anthrax reportable?
|
Duh
|
|
|
Anthrax etiology?
|
Bacillus anthracis
|
|
|
Anthrax spores can be picked up where?
|
-from infected soil, directly from the soil, fodder contaminated bone meal or protein, or from infected excreta
|
|
|
Transmission of Anthrax?
|
a.Inhalation – minor importance
b.Ingestion – causes most death c.Through the skin |
|
|
Anthrax Outbreaks occur mc when ?
|
after a major climate change
|
|
|
Anthrax organism is resistant to?
|
-phagocytosisi b/c poly-D-glutamic acid capsule
|
|
|
Anthrax forms a lethal toxin which causes?
|
edema and tissue damage and death
|
|
|
Anthrax death from?
|
shock and acute renal failure and termnal anoxia
|
|
|
After death by Anthrax what will you find?
|
a. discharges of blood form orfices of the body
b.absence of rigor mortis c.Gaseous decomposition d.CARCASS SHOULD NOT BE OPENED IF ANTHRAX IS SUSPECTED e.Blood will not clot f.Spleen is soft, large and looks like blackberry jam |
|
|
Prevention of anthrax?
|
1.Vacicnation w/ modified live ‘Sern avirulent spore vaccine does not present a hazard to humans
2.Disposal of infected animals is the biggest single factor in the prevention of spread of dz – should be buried at least 2 meters deep or burned |
|
|
Redwater dz aka?
|
Babesiosis, Texas Cattle tick fever
|
|
|
Etiology of babesiosis?
|
Babesia bigmina and bovis
|
|
|
In horse babesiosis is called what?
|
In the horse, is equine piroplasmosis
|
|
|
Natural vector of babesia?
|
Ticks (Boophilus) is natural vector
|
|
|
Iatrogenic factors of babesia transmission,
|
Affected adults are carriers for life -Iatrogenic infections via contaminated needles and sx instrument
|
|
|
Resistant breed of cattle to Babesiosis?
|
Zebu are relatively resistant b/c they have a resistance to ticks
|
|
|
Do you get immunity after exposure?
|
Strong immunity occurs after natural infection
|
|
|
CS of babesia?
|
a. Intravascular hemolysis
b. High fever c. ADR d. Jaundice e. Dark-red to brown urine f. Abortion g. May show CNS signs w/ Bigemina w/ cerebral babesiosis |
|
|
DX of babesia?
|
-Giemsa stain on blood smear in RBCs
-Complement fixation test most common serologic test |
|
|
TX of babesia?
|
-babesidcide - Diminazen aceturate, Imidocarb, Amicarbalide and phenamide
|
|
|
Prevention of babesia?
|
-giving the vaccination at the same time as a babesidide
|
|
|
Rinderpest aka?
|
Cattle plague
|
|
|
Etiology of Rinderpest?
|
Rinderpest virus (morbillivirus)
|
|
|
Need to control disease caused what?
|
establishment of the first veterinary school in 1762 in Lyon, France
|
|
|
Susceptible species to rinderpest?
|
All ruminants and cattle
|
|
|
Rinderpest virus is excreted by infected animals in?
|
-urine, feces and nasal discharges and perspiration
-Transmission occurs through contaminated feed or by inhalation |
|
|
Good thing about control of Rinderpest?
|
Cannot persist outside the body
|
|
|
Clinical signs Rinderpest virus?
|
a. high fever
b. Oculonasal discharge c. Slaivation d. Ulcerative stomatitis e. D+ f. Dehydration and death • Causes necrotic stomatitis and esophagitis, ulcerative and hemorrhagic enterocolitis and massive necrosis of lymphocytes in Peyer’s patches, LN and spleen |
|
|
Diagnosis Rinderpest virus?
|
-Dx via virus isolation, s-erology and immunohistochemistry
|
|
|
Control Rinderpest virus via?
|
-Effectively controled by slaughter and rigic quarantine measures
•Annual vaccination and surveillance |
|
|
Footrot etiology?
|
Fusobacterium necrophorum
|
|
|
Where on the foot does it affect?
|
-dermatitis in interdigital space w/ characteristic odor
|
|
|
Foot rot caused by what?
|
-Caused by wet, unhyginic or abrasive conditions
|
|
|
Footrot M/C in what?
|
-dairy cattle in first month of lactation and beef cattle on irrigation
|
|
|
cs of foot rot?
|
-Severe foot lameness, fever and swelling of coronet and claw
-Typical lesion in skin at top of interdigital cleft -Long continued irritation may cause interdigital fibroma (see below) |
|
|
Tx of foot rot?
|
-Tx Abs and local tx of foot lesion
-Cu sulfate may be used -Bandage to keep clean and dry |
|
|
How do cattle get interdigigtal fibromas?
|
inherited defect of foot confirmation in heavy animals
|
|
|
Area of foot most interdigital fibrimas are found?
|
Anterior part of cleft
|
