Exam 1 Flashcards
Lecture 1
Be able to come up with most likely ddx, diagnostics and symptomatic treatment
Know treatments
Know control
Know prognosis
Know zoonotic potential
History - Questions to ask owner
-When was the animal last normal
-How long have the signs been going on
-Any other animals affected
-Any recent travel
-Any history of trauma
-Trouble eating/chewing
-Feed preference
-Weight loss
-Excessive salivation
-Swelling
Dentition - Aging
4 weeks of age
-All 8 incisors are present
-Premolars erupt around birth
Immature age
-20 total teeth
-2[I0/4, premolars 3/3]
Mature animal
-32 total teeth
-2[I0/4, premolars 3/3, molars 3/3]
Central incisors (1.5 yo)
-01s
-18-24 mts
Medial incisors (2.5 yo)
-02s
-24-36 mts
Lateral incisors (3.5 yo)
-03s
-3 yo
Corner incisors
-04s
-3.5-4 yo
PE - Oral cavity
-Facial symmetry
-Get accurate history
-Percussion of sinuses: symmetrical airflow?
-Nasal planum
-Oral exam
PE
-Wear gloves
-Be safe!!
-Mouth speculum
-Head: symmetry, swelling, sinuses: percussion
-Oral cavity: Lesions, salivation, tongue, lips
Oral Ulcers
DDx
Foot and Mouth Disease
Rinderpest, Vesicular Stomatitis etc. (foreign diseases)
BVDV
-Multiple systems affected: respiratory, reproductive
-Cytopathic and non-cytopathic
-GI “mucosal disease” means BVD
-Immunocompetent cattle: Mild, non-clinical signs OR Acute gastroenteritis, fever, erosions, diarrhea if stressed.
-PI cattle: severe gastroenteritis and death
Type III BVD in Alaskan Bison, 2013 Italy
BVD Mucosal disease
-Uncommon, highly fatal
-Induced when PI become infected with cytopathic form
Vesicular Stomatitis
-Incubation 3-14 days
-Unknown natural reservoir
-Periodic outbreaks
High morbidity, low mortality
Tx symptomatic
-In herds probably nothing
-Individual: supportive care, antibiotics, anti-inflammatory drugs, oral antiseptic rinses, nutrition
Malignant Catarrhal Fever
Severe keraconjuctivitis with copious mucopurulent nasal discharge and HIGH FEVER
C/S
-Productive nasal discharge
-Oral lesions
+/- Corneal edema
Etiology
-Ovine Alphagammaherpesvirus
-Sheep carriers asymptomatic
-Transmission: aerosol, can spread several kilometers
-Sporadic outbreaks
Tx
-No treatment
-Control with isolation
-No vax
Blue Tongue in Cattle
- Oribivirus
-Vector Culicoides
-Tends to be mild disease
C/S
Burns muzzle +/- oral lesions
Dx
-Serology and virus isolation
Blue Tongue in Sheep
-Can be severe
Swollen blue tongue, cyanotic
-Supportive treatment
Enzootic Hemorrhagic Disease (EHD)
-White-tailed Deer mostly
-High mortality in deer
-Not severe in cattle
Culicoides vector
-Late summer/early fall
C/S
-Febrile
Sloughing of the hoof
-Oral ulcerations
Dx
-PCR, serology
Bovine Papular Stomatitis
-Parapox virus
-Mild incidental infection usually
-Common in young stock
C/S
-Raised areas in muzzle and oral mucosa or brown spots (old lesions)
-Zoonotic? similar to viruses that cause Pseudocowpox and ORF
Caustic Substances
CaCl/ammonium Cl
-Source of calcium in oral gel treatments for milk fever
-Very irritating to damaged mucosal surfaces
-Oral administration is contraindicated in toxic or renal disease
Chemical or Poisonous plant irritation
TN
-Rhododendren
-Few differentials for true vomiting in ruminants
-Physiology based on toxins
-Ex: Grayanotoxin in Rhododendron
Tx
-IV fluids
-Charcoal + Sorbitol
+/- Rumenotomy
Rabies (differential)
Any time you examine the mouth think Rabies
Listeriosis (differential for slobbering)
Uremia (differential for slobbering)
-Salivary glands recycle ammonia
-It is not known what causes the oral lesions
-Renal disease is probably present if ammonia can be smelled orally
Sometimes referred to as “Slobbers”
Salivary Gland Disease,
Jaw Diseases,
Neoplasia,
Tooth root abscesses
Salivary gland dz
-Congenital
-Fluid filled swelling proximal to obstruction
-Usually one gland affected so treatment cosmetic
-Acquired: Laceration, trauma, ruptured duct, salivary cysts, fistula.
-Sialocele: disruption of architecture with saliva escape. Soft, fluctuant cystic lesion
-Tx: surgical extirpation, open and chemically debride Iodine, CuSO4
-Sialoadenitis: infections, penetrating wounds, plants awns.
-Tx: drain if abscessed, antimicrobials, antiinflammatories
Jaw
Abscesses
-Soft to firm swelling
-May or may not be painful
-Warm
-Dysphagic possible
Dx: Ultrasound
Tx: drain
Osteodystropha Fibrosa
-Resorption of calcium from bone
-Deficiency in calcium, phosphorous, vitamin D
-Overproduction: hyperparathyroid
Growing animal with soft, non-painful swelling
-Maxilla, mandibule, both
Neoplasia
-Lymphosarcoma is most common
-Osteosarcoma
-Other neoplasms
-Treatment usually not warranted
Tooth Root Abscesses
-Relatively uncommon
-Must differentiate from “lumpy jaw”
-Treat with tooth removal, antibiotics, lavage
-Common in Camelids
Tongue & Lumpy Jaw
Lacerations
-Debilitating
-Decreased appetite
-Dysphagia
-Excess salivation
Tx: if severe partial glossectomy
Wooden Tongue
Actinobacillus lingieresii
-Gram (-) Rod
-Normal oral flora
-Pyogranulomatous lesion
-Can occur elsewhere in the oral cavity
C/S
-Anorexia
-Facial/tongue/LN fistulous tracks
Dx
-PE sufficient
-Biopsy and culture
Tx
-Sodium Iodide (70 mg/kg slowly)
-Antibiotics
Lumpy Jaw
Actinomyces bovis
-Gram (+) pleomorphic rod
Dx
-PE and radiographs
-Hard swollen firm jaw without tracts
Tx
-Resolution of disease is dependent on how advanced it is
-Bone remodeling is often permanent
-Treatment with long term antibiotics (Penicillin, oxytetracycline, Florfenicol)
-Sodium iodide IV
-Surgical: deberidement, medical therapy, risk of mandibular fracture
Prognosis
-Depends on extent of lesion
Why do wooden tongue and lumpy jaw occur?
-Normal flora of mouth (Antinobacillus Lingieresii, Actinobacillus bovis)
-Opportunistic, needs break in oral mucosa
-Grass awns, corse roughage, trauma. Outbreaks when using overture hay
Sodium Iodide
-MOA: unknown, may improve neutrophilic function (component of neutrophil enzymes)
-Efficacy within 48 hours
Adverse effects
-Persistent cough, hyperthermia, nano-ocular discharge…
Orf (dermatology)
Laryngeal Diseases
Calf diphtheria (differential for slobbering, respiratory system)
Necrotic laryngitis “Calf Diphtheria”
-Fusobacterium necrophorum, +/- Histophilus
-Febrile, off feed
**High pitched” noise
Tx
-Long-term antibiotic
-Surgery to remove affected arytenoid cartilage
-Tracheostomy could be considered for management
Traumatic Pharyngitis
-Swelling in the throat latch area
-May be due to foreign body
-Often due to careless use of balling gun
-Boluses consider lubricating gun
Dx
-PE, C/S
C/S
-Quiet, depressed
-Occassional cough, discharge OU
-Nasal discharge
-Hypersalivation
-Halitosis
-Oral ulcerations healing
-Mass mid-neck on left ventrolateral aspect
-Painful palpation trachea
-Unwilling to swallow
Tx
-Surgical drainage, debridement of abscess and feed material
-Long term antibiotic
Prognosis
-Guarded to poor
Lymphosarcoma (BLV discussion)
Esophageal Disease - Choke
Treat as an emergency
-Relieve bloat if animal is in respiratory distress
-Rapidly fatal if complete choke
-Dysphagia or anorexia if partial
-The obstruction is nor always intramural
Common sites of choke
-Cranial part of cervical esophagus
-Thoracic inlet
-Base of the heart
Dx
-PE
-External evidence
-Radiology
-Endoscopy
-Careful stomach tube
Labwork
-Dehydration
-Metabolic acidosis
-Ruminant saliva rash in bicarbonate = loss = acidosis state
Tx
-Relieve bloat
-Rumenotomy to remove obstruction if needed
-Tube and lavage
Prognosis
-Guarded
-Stricture formation
-Mucosal damage
Ddx
-Cellulitis
-Abscess
-Perivascular injections
-Hypoderma bovis larva
-Botulism
-Tetanus
-Rabies
Foreign Bodies
General symptoms
-Difficulty eating, breathing, drinking,
-Excessive salivation
-Throwing head around
Ddx
-Rabies
Lecture 2 Rumen and Forestomachs
Pathophysiology, Diagnostic findings, Treatment and Prevention of Rumen Function, Free gas and frothy bloat, traumatic reticuloperitonitis/pericarditis, rumen foreign bodies, rumen acidosis, vagal indigestion
Diseases of the Rumen and Forestomachs
Layers
-Gas
-Coarse roughage fiber mat
-Fluid and finer particles
Two mixing cycles
Primary
-Occur ~1/minute
-Involves the reticulum
Secondary
-Does not involve the reticulum
Rumen Bacteria
-Mainly anaerobes
-Takes 1 week to respond to diet changes
-Numerous protozoan utilize starch and simple sugars. More sensitive than bacteria
Normal Rumen pH
-6.0-7.0 on roughage diet
-7+ indicates lesser quality diet
-5.5-6.5 concentrate diet
Concerned if <5.5
Other Tests
Sedimentation test
-Normal 4-8 minutes
-Frothy ingesta: nothing happen
Methylene blue reduction time
-Normal: decolorization within 3-6 minutes
-Dead bacteria: no decolorization, no reduction
Bloat - Gas or Frothy EMERGENCIES
Free Gas
-Methane and CO2 produced by fermentation and neutralization of salivary bicarbonate
Etiology
-Abnormal reticuloruminal function
-Choke
-Positional
-Vagal nerve injury
-Hypocalcemia
-Extra-esophageal enlargement: thyme lymph sarcoma, enlarge LNs, etc.
Tx
-Stomach tube, may need to do several times in chronic free gas bloat
-Trocharize if necessary to save life. Block paralumbar fossa with lidocaine. Cut through skin, pop trocar in, screw may be the only needed
-Correct underlying cause and consider: hypocalcemia, laxatives & antacids (carmilax), mineral oil, relieve choke, long term antibiotics
-Transfaunation on repeaters
-Surgery: for chronic cases
-Rumenotomy: hole in rumen takes about 2 months to heal.
-Cull
Frothy Bloat
-Diets high in soluble proteins = bubbles
Legumes, alfalfa and clover
-Winter wheat (foreign disease in East US)
-Less saliva produced due to succulent plants
-Feedlot diets (high grain) may lead to frothy bloat
-Increased mucinolytic bacteria, increased slime (insoluble) bacteria = bubbles
Tx
-Therabloat
-Home remedies: detergent, mineral oil. Reduces surface tension of the bubbles so they can dissolve and gas is released
-Solution at the cardia, quicker relief
-Walk the cow may help
-Trocar not likely to help
Prognosis - Good
-choke
-Grain overload
-Hypocalcemia
-Positional bloat
Prognosis - Guarded
-Papilloma/granuloma
-Hypoderma larvae
-Pericarditis
-Vagal indigestion
-Tumor
Bloat control
-Proloxalene
-Never let hungry cattle graze “legumes”
-Limit lush/legumes pasture access
Feedlot Bloat control
-Avoid overfeeding, too fine ground grains
Ionophores (monensin) reduces bloat potential by altering rumen microflora, bolus or in feed
Traumatic Reticuloperitonitis/pericarditis “Hardware disease”
-Foreign body penetrating through reticulum
-Lodge in reticulum
C/S
-Sudden onset
-Complete anorexia
-Low grade fever
-No rumen motility
-Precipitious drop in milk
-Mild bloat
-Increased HR
-Abducted elbow
-Grunt
-Pain
Dx
-PE: withers pinch positive, bar/Grunt test positive
-Radiology
-Metal detectors
-Ultrasound
-Centesis
Pathophysiology
-Ingested metal (fence staples, nails, etc) migrate to rumen, contractions lead to perforation, abscesses form
Clinical pathology
-Neutrophilia with left shift
-Elevated fibrinogen
+/- Mild ketosis
-Acute/diffuse Low WBC
Tx
-Depends on severity, economics, facilities, complications
Medical
-Magnet
-Antibiotics
-Anti-inflammatories
-Supportive fluids
-Decrease activity
-Elevate front
Prognosis - Guarded, vagal indigestion
Sequela
-Pericarditis
-Peritonitis
-Hepatitis
-Splenitis
-Pneumonia
-Pleuritis
-Vagal indigestion
-Sudden death
Rumen Foreign Bodies “software disease”
-Not well documented
-Fluid distended rumen without bloat
-Common objects: twine, tarps, plastic, etc.
C/S
-Often non-specific
-Intermittent appetite
-Reluctance to eat full ration
-Possible mild inflammation on the leukogram
Rumen Acidosis
Sequelae
-Obtundation
-Dehydration: increased osmolality in rumen pulls water in
-Liver abscesses
Tx
-Alkalinization of the animal
-IV fluids (Sodium bicarbonate, LRS)
-Oral fluids (Magnesium hydroxyde)
-Evacuation of rumen contents
-Tube, rumenotomy
-Replacing rumen microbiome: transfaunation
-Thiamine
-Antibiotics
Prevention
-Gradual diet change when rapidly fermentable carbs introduced
-Ionophores: favor production of propionate in the rumen
Simple Acidosis
Simple Indigestion
Minor rumen upsets
C/S
-Not specific
-Usually off feed
-Eventually diarrhea
+/- rumen motility reduced
+/- gas at ping
-Can sound just like a DA, “ping” on the right side
+/- Dehydration
Pathophysiology
-Overconsumption of non-food, operating, DAMAGED FEEDS, sudden change in diet, sporadic or herd problem
Dx
-Hx and C/S
-Wait and see
-Check rumen pH
-Rule out other things
Tx
-Restore rumen flora if necessary
-Laxative +/-
-Most recover within a few days
Prevention
-Only feed quality feed
-No moldy feeds
-Gradual changes in diet
Vagal indigestion
Key sign Abdomen distends, but fecal output is decreased and weight loss is present
-Not really a stand alone disease
-Functional disturbances
-A group of motor disturbances that hinder passage of ingesta from the reticulorumen or abomasum o both
-Omasal transport or Pylorus outflow failure
Alternate Classification
- Failure of eructation - free gas bloat
-Choke
-Mediastinal LN enlargement
-Left untreated death - Omasal transport failure
-Mechanical obstruction
-Neurogenic
-TRP
-Inflammatory conditions
-Distention high and low on left, low on right
Papple appearance
-May require rumenotomy - Abomasa transport failure - secondary to abomasal volvulus or hardware
-TPR
-Secondary to abdominal surgery
-Advanced pregnancy
-Neurogenic
Tx: treat underlying cause, +/- surgery - Vagal indigestion late gestation
-Large fetus
Key points all types
-Normal plasma and rumen Cl with distended abdomen = omasal issue
-Low plasma Cl and high rumen Cl = abomasal issue
Prognosis
-Generally poor
-Relapse some
Peritonitis
-Secondary complication
-TRP
-Ulcers
-Abscesses
-Rumenitis
-Wounds
-Bowel obstructions
-Surgery
-IP injections: DON’T
Dx
-Bloodwork: marked neutrophilia with left shift
-Neutropenia possible
-Hyperfibrinogenemia
-Ultrasound: free fluid, fibrin
-Abdominocentesis: toxic neutrophils
+/- Palpation severe cases
Tx
-Supportive care
-Long-term antibiotics = withdrawal time concerns
Carcass condemn at slaughter
Lecture 3
Abomasa Disease
Abomasal Displacements
LDA: many days before cow dies
RDA: some days “”
RTA: <1 day “”
Rarely can tell RDA from RTA
Multifactorial
-Hypomotility, atony ob the abomasum
-Concurrent disease: mastitis, metritis, ketosis, hypocalcemia
-Deficiencies in nutrition
-Ketotic cattle (3-5 days) post calving 6.1X more likely
Left side more common than right Right more complicated
Presentation
-Complete or partial anorexia
-Dehydration
-Scanty/pasty feces
-Decreased milk production
-Off-feed
-Usually ketotic
-TRP normal or elevated
Most occur shortly after calving
-Dairy more common than beef
->2yo
-Mastitis, metritis common association
“ping” in the area of suspicion
Dx
-Auscultation
-Bloodwork not always possible
-pH<4.5, from aspirated fluid but not commonly done
LDA
LDA
-Chloride sequestration in the abomasum
-Left side pings: mid thorax from point of the elbow to the hip
Hypochloremia, hypokalemia, Metabolic alkalosis
+/- Hypophosphatemia
Tx
-“Pexy”
-Return abomasum to normal anatomical position
-Right/Left abomasopexy
-Right ometopexy
-Ventral paramedian abomasopexy
-“Roll and tack/toggle”
-Laparoscopic correction
-Address metabolic disorders
Rumen
-Rumen gas cap dorsal area over last few ribs, paralumbar fossa and hips, can be tympani (bloat) or empty (void)
RDA & Volvulus/Torsion
-Can be simple or volvulus
-Less frequent than LDA
-C/S similar to LDA
-Tachycardia, decreased rumen motility, minimal to no fecal output, ping, splashes
-Emergency!
Ddx
-Abomasal volvulus
-Cecal distension, torsion
-Physometra
-Spiral colon gas
-Rectal gas after palpation
-Pneumoperitoneum
-Torsion on mesenteric root
“Pings”
-usually cranial to 8th rib
Also:
B: spiral colon
C: Cecum
D: Uterus
E: Pneumorectum
-Small intestine gas
Volvulus/Torsion
-Hypochloremia
-Hypokalemia
-Metabolic alkalosis
-Dehydration
-Hypovolemia
-Hemoconcentration
+/- Hypophosphatemia
-Metabolic acidosis can develop from reduced perfusion: poor prognosis
Paradoxic aciduria conservation of Na, Cl, K results in excretion of H+ via kidney to maintain electronegativity
Pathophysiology
-Most common between the omasum and abomasum, counterclockwise from right and rear
-Torsion near site where duodenum wraps around omasum: **functional pyloric stenosis/failure of abomasal outflow (vagal indigestion)
Tx
-Surgical correction
-Treat underlying metabolic deficiencies
+/- Antibiotics
-NSAIDs
Prognosis
-Good if simple; guarded with volvulus
Prevention of Abomasal Displacements
-Reducing fore stomach agony caused by high concentrate diets
-Increase fiber length and particle size (Penn State Sharker box)
-Maintain serum calcium levels
-Prevent ketoacidosis
Abomasal Fistula
-Most common complication from a ventral obamasopexy
-Failure to remove suture in a timely manner
-Can result from other surgeries
Abomasal Ulcers
-Caused by stress and high starch diets
-Microbiome?
Types
1. Non-perforation
2. Non-perforating and bleeding
3. Perforating with localized peritonitis
4. Perforating with diffuse peritonitis
Dx
-PE: Bruxxism
-Fecal occult blood test
-Ultrasound
-Abdominocentesis
-Bloodwork
C/S
-Inappetence
-Bruxxism: grinding the teeth habit
-Salivation
-Poor thought
-Dietary preference
Calves
-Abrasion theory
-Bacterial and fungal
-NSAIDs
-BVD or IBR
-Stress
-Nutritional deficiencies: copper, selenium VitE
Tx
-Remove starch
-Blood transfusion?
-Antibiotics?
-Mucosal protectant!!
Ex: Coating agents, Sucralfate, Alkalinizing agents, Synthetic prostaglandins, H2 antagonists, Proton pump inhibitors
-Limited options for adult ruminants
Gastroprotectants
-Bismuth Subsalicylate: GRAS
-Sucralfate
-Aloe Vera Juice
H2 antagonists
-Famotidine
-Ranitidine
-Adverse effects: electrolyte disorders (people) or drug interactions
Proton pump inhibitors
-Omeprazole
-Pantoprazole
Abomasal Impaction, Intramural/Extramural Obstruction/Lesions
-Usually beef cattle
-Surgery usually unrewarding
-Medical management: Laxatives, Detergens (DSS), fluids
Intramural obstruction/ Lesions
-Gravel, sand, etc
Extramural obstruction/lesions
-Neoplasia
-Lymphoma in cattle
-BLV status only indicates infection with the virus
Abomasal Emptying Disease
Suffolk sheep only
-Unknown cause
-Anorexia
-Wasting
-Right abdominal distention
-Tx unrewarding
Lecture 4
Non-Infectious Intestinal Diseases
Other than Diarrhea
Hemorrhagic Bowel Syndrome
C/S
-Acute onset and rapid progression
+/- painful colic (37%), abdominal enlargement, black tarry feces
-Sudden death may occur
-Mature dairy cattle primarily
-Clusters or single cases
**Clostridium perfringes Type A, potentially Aspergillus spp. **
Dx
-Hx suggestive
-Ultrasound
-Exploratory
-Necrosy
-Tests: C. perfringes, Type A, culture, toxin typing, aspregillus
Tx
-Surgical resection (poor success)
-surgical kneading: break the clotted blood down within the bowel) 60% success
-Penicillin very early or Ampicillin
-Anti-inflammatories, Lidocaine (pro kinetic effect)
Prognosis
-Guarded to grave
HBS Control
-Ration balance and feeding management
-Adequate rumen fiber
-Forage quality: avoid moldy feeds
-Vaccination: Clostridium perfringes type A, Autogenous vax, commercial vx.
-Omni-Gen AF: antifungal fed in feed, good for grain overload
Intussusception
-Pain and colic (acutely)
-Abdominal slowly distends; bilateral
-May be dehydrated (progressive)
-Feces vary: dark bloody, dry pasty scant
-Sporadic
-Adults, mass tumor may be a cause
-Usually mid to distal jejunum
-Sequelae can require intensive management
Dx
-Rectal palpation: multiple loops of SI, spongy coiled mass
-Exploratory surgery
-Ultrasound
Tx
-Supportive
-NSAIDs for pain
-Surgical correction: can be done standing, right flank approach
-General anesthesia preferred
-Prophylactic antibiotics, Lidocaine drip
-Cull
Prognosis
-Depends on duration of problem
-Ileus post-op complication
-Peritonitis poor prognosis
Spiral Colon Torsion & Cecal Dilation/Torsion
Spiral Colon Torsion
-Acute onset
-Colic
-Sporadic
Palpable per rectum
Surgery required
-Intense post-op care
Cecal dilation/torsion
-Straining, posturing, kicking at abdomen, hunched
-Scant feces
-Anorexia
-Decreased milk
-More severe C/S
-Sporadic
-Causes: high concentrate diet
Dx
-Rectal palpation: “Loaf of bread” anterior to the pelvis on the right side
-“Ping” in the upper right paralumbar fossa
Tx
-Surgery required for severe
-Anti-acids, laxatives, fluids
-Change to high fiber diet
-Cull
Prognosis
-80% dilation
-75% torsion
-10% reoccur
Aresia coli, ani, recti
-Healthy newborn with gradual abdominal distention, eventually depression and anorexia
No feces
Dx
-Rectal exam: NO FECES on glove
Tx
-Surgery: atresia ani vs. atresia recti or coli
Prognosis
-Guarded but success reported 35%
Discorage breeding
Prokinetics - Motilin receptor
Lidocaine
-Drip to stimulate gut motility
-Loading dose 1.3mg/kg per minute
-Lidocaine toxicity: syringe pump or fluid pump
Macrolides
-Erythromycin can act on the motion receptor in the gut for a pro kinetic effect
Rectal Tear & Prolapse
-Sequelae to rectal palpation
-Use lube
-Limit time palpating
Tx
-Antimicrobial
-Anti-inflammatories
-Fluid therapy
Classification
1. Conservative tx
2&3. Immediate & extensive surgery
4. Grave prognosis
Rectal Prolapse
-Common
-Tenesmus
-Rabies can cause it
-Dx based on Examination
-Abdominal pressure in late pregnancy
-Excessive coughing
-Decreased anal sphincter tone (tail docking)
-Colitis: coccidiosis, salmonella
Tx
-Replace & purse string
-Caudal epidural ~6ml lidocaine (check with tail tone)
+/- mucosal resection
-Lube lots!!
-Replace: evert completely, purse string +/- counterirritant
Review
Lecture 5 GI antimicrobials
Antimicrobial stewardship
AMDUCA
Specific drugs
Bovine Antibiotics
Ruminant GI diseases considerations
Understand the legislative acts and regulations that govern food animal antimicrobial use
AMDUCA: VCPR
Food animal considerations
-Dx and evaluation
-Establish an extended withdraw period ELDU zero tolerance
-Institute procedures to assure the animal’s identity is maintained
-Take appropriate measures to assure that assigned withdraw times are met and no illegal residues occur
Prohibited ELDU in Food animals (CCDFNN)
Group 1
-Chloramphenicol
-Clenbuterol
-Diethylstibesterol
-Fluoroquinolones-class
-Glycopeptides (Vancomycin)
-Nitroimidazole class
-Nitrofuran class
Restricted ELDU
Group 2
-Cephalosporins: 3rd generation prohibition
-Neuroaminidase inhibitors: chicken, turkey
-Gentian violet (food or feed)
-Phenylbutazone (female dairy cattle 20mts or older)
-Sulfonamide class (lactating cattle)
Grade A milk
-Non-medical grade dimethylsulfoxide DMSO prohibited
-Dipyrone
-Colloid silver
3rd Generation Cephalosporin Regulatory aspect
-ELDU prohibited
-Exception: cephapirin products that are approved
Lecture 6
Neonatal Calf diarrhea
Lecture 7
Calf diarrhea Neonate and Older
Coccidiosis
Eimeria spp.
-E. zuernii
-E. bovis
-E. alabamensis
Life cycle: 2-4 weeks
C/S
-3 weeks or older
-Common 6-12 mts of age
-Induced c/s by stressor
-Bloody mucoid diarrhea
-Tenesmus
-Rectal prolapses
-Self-limiting to death
Nervous coccidiosis
-6-12 mts old
-Tremor, ataxia, recumbency
-Unknown pathophysiology
-Tx unrewarding
80-90% mortality
Dx
-Fecal flotation
Tx
-Prevention
-Sanitation, no overcrowding, sunlight, desiccation
-Static drugs mixed with feed, thiamine co-treatment
-Sulfa drugs injectables extra label
Mycobacterium avian paratuberculosis (Johne’s)
-Endemic
-80% of all dairy herds
-10% all beef
-Few clinically affected animals
-Host ruminants
-Transmission: fecal oral, fecal exposure, in utero
Pathophysiology
-Endocytosis of pathogen in M-cells
-Reside in mesenteric lymph and submucosa
-Granulomatous immune response
-2-5 year old
-Ileum to cecum, colon, jejunum
-Malabsorption, maldigestion
-Ravenous eater with weight loss
-PLE
Dx
Reportable in some states
-ELISA
-Biopsy: acid-fast
-Culture: Gold standard, 8-12 weeks
-PCR
Stages
I: Silent, subclinical, nondetectable (<2yo)
II: Subclinical shedders (heifers, older)
III: Clinical
IV: Emanciated animals with fluid diarrhea (terminal stage)
Tx
-Recognize
-Euthanize
-Cull
-Prevent calf exposure
-Feces remova
-Colostrum management
-Pasteurization not 100% effective
-Biosecurity
Zoonosis
-Association not causation
-Pasteurized commercial milk
-Culture in meat
-Tx: human monoclonal antibodies
Lecture 8
Parasites, Liver Abscesses, BVDV control
Understand the common nematodes associated with calf parasitism and the pathophysiology behind the associated clinical disease
Gastrointestinal Nematodes
Ostertagia ostertagia: Abomasum
Cooper punctata: Small intestine
Haemonchus placed and contortus (calves).
Trcihostrongylus, etc.
-Economic losses: suboptimal milk/meat production
-Exposure dependent on: geographic region, management style (pasture vs. drylot), anthelmintic use.
O. Ostertagi
-Abomasum
-“Moroccan leather”
-Summer and autumn - North
-Winter and spring - South
-Disease of the young, older developed immunity and resistant
Type 1
-Acute, active infection
-Young naive affected
-Acute response
Type 2
-Initial host immunity evasion - hypobiosis
-Massive emergence of arrested larvae months after: activated by a number of host responses
Hypobiosis
-Remain in abomasal wall
-Activated by hormones
-Estrogen, glucocorticoids
-Caloric intake changes
-Temperature changes: overwinter
-Severe issue in small ruminants
Understand the pathophysiology associated with liver abscess development
-Fusobacterium necrophorum: predominant pathogen
-Trueperella pyogenes
-Disease of feedlot cattle
-Last 60 days of finishing
-Ration changes, longest exposure on feed, intake variation with body composition
Pathophysiology
-Ruminitis-liver abscess complex
-Ruminal acidosis, accumulation of VFAs and lactic acid
-High carbohydrate diet
-Sudden change in feeding schedule, low roughage content
-Trauma to luminal surface from sharp feed particles
-Bacteria invade the rumen wall, translocation to portal circulation, entrapment in portal capillary beds within liver.
C/S
-Uncommon unless sequela present
-Septic cardiac and pulmonary emboli
-Caudal vena cava syndrome: phlebitis and secondary thrombus, rupture, occlusion of CVC, pneumonia, infarction, endocarditis, hemoptysis epistaxis.
Tx
-Uncommon unless clinical signs
-Prevention better: vax, mitigate antibiotic use.
-Tylosin in feed (VFD required)
-Antibioitics at time of known grain overload: penicillin, ceftiofur, tetracycline, tylosin 30-42 consecutive days
Tylosin
-MOA: macrolide. R50s protein synthesis inhibition
-Oralformulation
-Bacteristatic
-Direct inhibition of Fusobacterium necrophorum
-Fermentation modulation
-VFD regulates quantity and treatments allowed “For reduction of incidence of liver abscesses associated with fusobacterium necrophorum and Arcanobacterium pyogenes”
Understand common strategies for BVD control and management
-Production loss $400-500/head
-PI calves can cause $5-10/exposed calf
-Biosecurity is crucial
-PI reservoirs
-Pregnant cows exposed to suckling calves 40-125 days gestation
-PI cows will produce PI calves
-Testing is crucial
-Vaccines MLV or kill but not a “silver bullet”
-30 day quarantine incoming animals
-If purchasing bred animals: test all progeny
Testing strategy
-Dependent on producer
-Compliance concerns
-Costs
-Herd size
-Calving window: year around?
-When in doubt call the laboratory they are helpful
Screening for PI calves
-Test all calves
-IHC or antigen capture ELISA
-Test dams of positive calves: transient infection, PI cow
-Repeat annually
Vaccines
-No vaccine protocol is perfect
-Goal is to reduce exposure to fetus
-Not aimed at preventing clinical signs of acutely infection
-BVDV 1B most common isolate in North America
-Concerns with MLV causing abortions
Lecture 9
GI Fluid Therapy
Fluid therapy overview
-Anemia
-Shock - all types
-Hypoproteinemia
-Sepsis
-Electrolyte derangements
-Dehydration
-Renal disease
-Parenteral nutrition
-Hypoglycemia
-Hypocalcemia
-Hypophosphatemia
-GI disease
-Hypovolemia
-Failure of passive transfer
-Acid/base imbalance
60% of BW if water
younger animals > water/BW than adults
Fluid Therapy overview
PE findings
-Eye recession
-Skint tent
-Suckle reflex
-Diarrhea
-Pallor
Dx
-PCV/TP
-ISTAT
-BHB
-Lactate
Understand the different types of fluids and when they can be used
Available Fluids
-Dextrose
-Isotonic
-Hypertonic
-Colloids: commercial, homemade
-Plasma
-Whole blood
Oral fluids <8% dehydration - Calf
-Clinically BAR
-Sodium 90-130mmol/L
-Glucose, citrate, acetate, proprionate, or glycine: facilitate the absorption of water
-Provide alkalinizing agent: acetate, propionate, or bicarbonate: correct acidosis
-Provide energy: do not withhold feed. Alternate milk and electrolytes; NEVER TOGETHER
Adult
-Cheap, easy, high volume deliver ability: NOT if RUMEN Distended
-Can worsen discomfort (vagal animal), obstruction, atony
-Do not add glucose: alters fermentation
-Electrolytes: YMCP/custom mix
-Alfalfa meal
Common abnormalities
Calves with diarrhea
-Acidemia
<7 DoA = base excess of -10 to -15
>7 DoA = base excess of -15 to -20
Total depletion of K
Adult Cows
-Metabolic alkalosis
-Most GI conditions
-Obstructions: hypochloremic hyponatremic alkalosis
-Metabolic acidosis
-Carbohydrate engorgement, choke (salivation), ketosis, renal failure
-Will have marked rebounding alkalosis once fixed (caution of overshoot)
Fluid Calculations
Do no harm
-Electrolyte overdose
-Cerebral edema (sodium)
-Cardiac arrest (hyperkalemia)
-Induce infection non-aseptic technique
-Replace catheter q4 days
-Monitor respiratory rate, acidotic increased RR
-Administer fluids and reassess, then repeat
Lecture 11
Food Animal Dermatology
Understand the etiology, pathophysiology, treatment, and prevention of common bovine dermatologic conditions
Bovine Skin
-Barrier to environment
-Sensory
-Vitamin D synthesis
-Body temp regulation
-Bos indicus vs. Bos taurus: hide thickness, haircoat density
Common Conditions
-Infectious: parasites, bacteria, fungi, virus
-Trauma: management conditions, frostbite, abscesses
-Neoplasia
Parasites - Flies
-Horny fly (Haematobia irritans)
-Face fly (Musca autumnalis)
Problems
-Decreased production, head shaking, bunching, twitching, tail switch, fly strike, pink eye
Peak season in TN June-July
Tx
-Topical sprays
-Dust socks
-Oral lick tubs: insect growth regulators
-Environmental traps
-Ear tags: waning efficacy ~ 2 weeks before season begins
Stephanofiliariasis
-Nematode
-Intermediate host-horn fly (Stenofilaria stilesi)
-Deposits L3 on skin
-Filarial dermatitis ventral midline
-Clinically insignificant lesions
Hypoderma
-“Warbles” “Cattle Grub”
-H. bovis “northern cattle grub”
-Eggs deposits upper body, migrate to spinal canal
-H. lineatum “common cattle grub”
-Norther and Southern USA
-Eggs deposit on legs and venture
-Migrate to esophagus
-Severe economic loss carcass/hide damage: encysts “warbles” molt to L3 “grubs” in Spring. Invade SQ fascia and migrate
Treatment
-Manual removal
-Insecticides: early autumn when eggs hatch.
-Do NOT treat Oct-March in Northern US, larvae already present, too much killed and migration = esophagitis, choke, impaired eructation, bloat. Epiduritis/CNS damage = paralysis
Lice
-Host specific
-Mallophaga: biting louse
-Anoplura: sucking louse
-Most prevalent in winter
Dx
-Visual identify, gross hair coat examination, eggs (nits) in hair, check tail head
Treatment
-Topical products for biting louse
-Topical or injectable products for sucking louse
Less common conditions
-Nutritional: mineral deficiencies vs. toxicosis
-Toxicities: photosensitization
-Anaphylaxis
-Congenital anomalies
Skin infections - Mange parasite
Some types are reportable, check with local state.
Which one burrows and causes severe pruritis?
- Psoroptic mange
-Host specific
Reportable P. bovis
-Belgium blue cattle and merino sheep susceptible
-Winter prevalence
-Survives up to 3 weeks off host
Superficial, do not burrow - Chorioptic mange
-Chorioptis bovis “leg mange”
-Host specific
Do not burrow
-Superficial infection
-Can not live off host
-Erythema, crusts, scaling, PERINEUM, hind limbs, tail/scrotum - Sarcastic mange
-SEVERE pruritis
-Head and neck or generalized
-Burrow into epidermis
-Able to live off host
Mange General Signs
-Pruritis
-Erythema, crusts, scabs
General Dx
-Skin scrapes and microscope
General treatment
-Topical and injectable ivermectin’s
-Sarcoptic mange requires sustained treatments every 2 weeks for 2-4 treatments
Other Bovine Skin infections
Screwworm
-Cochliomyia hominivorax
-Eradicated in USA
Reportable
-Found only in healthy tissue
Bacteria
Dermatophilosis
-“Rain rot/scald” “lumpy wool”
-Dermatophilus congolensis: Filamentous bacteria aerobic
-Requires skin abrasion: unable to impede skin barrier on own
Paint brush lesions
-Superficial folliculitis usually on dorsum
Dx
-Impression smear
Tx
-Topical debridement
-Topical antiseptics: lime sulfur, chlorhexidine
+/- parenteral antibiotics
-Penicillin, oxytetracycline
Superficial Pyoderma
-Semantics: Furunculosis: after follicular wall
-Impetigo: do not affect hair follicles
-S. aureus and S. pseudintermedius zoonotic potential Penicillin resistant
Dx
-Impression smear
-Biopsy
Tx
-Topical antiseptic
+/- Ceftiofur culture/sensitivity if not responsive
Udder Cleft Dermatitis
-Superficial infection
-Poor udder confirmation
-Clean and apply astringent: Granulex, Teratogen
Understand the utility of basic dermatologic testing for diagnosing of common bovine skin diseases including
- Thorough PE
- Skin cytology
- Biopsy
- Blood analyte evaluation
Lecture 12 Dermatology 2
Viral
Bovine Skin infections - Virus
- Bovine Papilloma virus
-“Warts”
-Strains 1-10 (2 most common)
-Most frequent in young animals
-Ears, teats, penis, interdigital skin, alimentary tract
-Benign lesions: can predispose to other conditions
-Spontaneously regress
-Immunocompromised may be more affected
Dx
-Visual
-Biopsy
Tx
-Crush/pinch/cryotherapy
-Leave alone
Prevention
-Clean equipment
-Tattoo equipment
-Halters
Vaccination
-Autogenous
-Commercial vax anecdotally takes 6-8 weeks
- Pseudocowpox
-Parapoxvirus
-Confined to teats
Dx: visual, papules, crusting, scabbing
-Vesiculations are rare: differentiating from herpes, vaccine, cowpox.
-Self-limiting: secondary to mastitis economic problems - Bovine Herpes Mammillitis: uncommon
-Vesiculation on teats: “leathery” texture after rupture
-Oral, udder, or generalized skin lesions
-Secondary mastitis
-Takes 3-10 weeks to heal
-Tx: supportive care - BVDV - mucosal disease
- Vesicular Stomatitis
- Foot and mouth disease
- Skin trauma
-Tail fecoliths
-Ear tags, fly tags
-Frosbite: differentiate from salmonellosis, sepsis, fescue toxicosis
-Abscesses from penetrating trauma, dirty needles, residual from a sepsis, etc.
Bovine Skin - Anaphylaxis
Urticaria
-Hypersensitivity
-Type 1: IgE
-Type 2: Cytotoxic, antibody, complement
-Type 3: immune complexes
Milk allergy
-Heritable
-Occurs during dry-off period
-Localized or generalized urticaria
-Casein allergy
Tx
-Antihistamines
-Cull
Bovine Skin - miscellaneous
Milk scald
-Fat gobbles adhere to skin
-Improper mixing
Diarrhea scald
-Can apply vaseline to reduce irritation
Telogen effluvium/defluxion
-Stressful event precedes onset: fever, sepsis
Bovine Skin - Nutritional
Copper deficiency
-Depigmentation
-Molybdenum and others can alter absorption
Congenital/Nutritional
Zinc responsive dermatosis
-Holstein-Fresians
-Autosomal recessive: lethal trait A46
-Defect in Zn absorption
-Parakeratosis
-Diet also possible cause: high calcium, bioavailability of some formulations
Skin Toxins
Hairy vetch
-Vicia villosa
-Unknwon pathophysiology
-Affect black hide
Photosensitization
-Light pigmented skin
-Photodynamic agent
-Ultraviolet light
-Types 1-3
Type 1
-Ingestion of photodynamic agent
-St. John’s Wort
-Perinneal ryegrass
-Buckwheat
-Etc
Type 2
-Congenital abnormalities in porphyrin or liver metabolism
-Heme synthesis defect
-Accumulation of photodynamic agents
-Uroporphyrin and coproporphyrin
-Holstein, Shorthorn, Jamaican breeds
-“pink tooth” and urine illuminate with Wood lamp
Bovine protoporphyria
-Limousin and Charolais cattle
Type 3
-Liver disease
-Direct liver shunt
-Accumulation of phylloerythrin/porphyrin
-Common Grousel
-Ragwort
-Tarweed
-Rattleweed
-Etc
Bovine Skin - Neoplasia
SCC
-Most common ocular tumor
-White faced cattle
-Carcass condemned
Melanoma
-Dark hided animals
-Majority are benign
Cutaneous Lymphoma
-Juvenile from BLV
-T-cell origin
-Can regress spontaneously
Congenital
-Hypotrichosis with anodontia: X-linked recessive
-Hypotrichosis with incisor anodontia: H-linked incomplete dominant
Acantholysis
-Breakdown of stratum spinosum
-Autosomal recessive
-Angus cattle
