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
Fat necrosis
-Overconditioned animals
-Channel Island breeds
C/S - Dx
-Bloody stool
-Colic
-Treading, eventually intestinal obstruction
-Hard masses via rectal palpation
-Rectal strictures
Tx
-Slaughter
-Isoprothiolane (anti fungal)
Prognosis: poor
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 concepts of antimicrobial stewardship, and the classes of antibiotics used in veterinary medicine that are highest importance for human health
-Safe food supply
-Animal welfare
Violations
-Residue in edible tissues
-Litigation: malpractice coverage does not apply for an “illegal” act
Highest priority antimicrobials
1. Cephalosporins 3,4,5 generation
2. Fluoroquinolones
Highly important antimicrobials
1. Cephalosporins 1,2 generation
2. Tetracyclines
Stewardship
-Preventing common diseases through multimodal strategies
-Evidence based approaches
-Judicious and sparingly use
For drug regimen needs
-Appropriate diagnostics
-Disease severity and prevalence
-Likelihood of antimicrobial response
-PE consistent with infection
-Lab work: CBC, Culture and sensitivity, diagnostics
-Consider non-antimicrobial options prior/instead/in conjunction
-Select drugs and optimize regimen following regulations AMDUCA, FDA
What is a food animal?
Major species: cattle, pigs, chickens, turkey
Minor species: sheep, goat, pheasants, quail, farmed cervids, camelid, etc.
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
Review the common parenterally administered food animal antibiotics in an organized (SPACED) approach
Bactericidal with low volume of distribution but broad-spectrumish?
- Procaine Penicillin G
Spectrum: Gram (+ & -), anaerobes, Gram (+) aerobes.
Pk/PD: Cidal, time above MIC; low volume of distribution.
Adverse reactions: Anaphylaxis
Compliance: PPG IM/SQ
Environment: concentrate in kidney and bladder, decreased with beta lactamases
Diagnostics: validated breakpoint only with novobiocin for bovine mastitis
- Oxytetracycline
Spectrum: Gram (+ & -) aerobes & anaerobes.
-Rickettsia, leptospira, protozoa, mycoplasma
Pk/PD: Static; time above MIC, Vol Dis 0.8-1.0 L/kg
Adverse effects: Nephrotoxic, collapse, injection site reactions
Compliance: Approved and legal ELDU
Environment: resistance, binds to cations
Diagnostics: human-derived breakpoints
- Enrofloxacin
Spectrum: Gram (-) aerobes
Pk/PD: cidal, AUC above MIC, high vol dis.
Adverse effects: cartilage foals/young damage, seizures, retina, AI, other drug interaction.
Compliance: no permissible ELDU
Environment: not anaerobes, increased in kidneys and bladder
Diagnostics: for cattle BRD
- Tulathromycin
Spectrum: Effective for Mycoplasma
Pk/PD: static, time above MIC; vol dis >1L/kg
Adverse effects: rectal edema in pigs, reactions if given IM
Compliance: Injection site
Environment: poor in acidic environments
Diagnostics: cattle and swine resp dz
- Sulfadimethoxidine
Spectrum: Gram (+ & -) plus coccidia
Pk/PD: static
Adverse effects: everything
Compliance: Injection site reactions, loading dose
Environment: poor in purulent materials/debris
Diagnostics: human derived breakpoints
- Florfenicol
Spectrum: Gram (+ & -) anaerobes, Gram (+) aerobes (enterobacter)
Pk/PD: static? time above MIC, Vol dis > 1l/kg
Adverse effects: anorexia in cattle, milk residues, bone marrow suppression
Compliance: risks with ELDU in dairy animals
Environment: Good tissue penetration
Diagnostics: cattle & swine resp dz
- Ampicillin
Spectrum: Everything except enterobacter
Pk/PD: Cidal, time above MIC; low vol dis.
Adverse effects: anaphylaxis
Compliance: SQ
Environment: concentrates in kidney and bladder, decreased with beta lactamases
Diagnostics: UTI data
- Ceftiofur
Spectrum: Gram (+) aerobes, Strep (+), Staph (-).
Pk/PD: Cidal time above MIC
Adverse effects: IV injection can be fatal (Excede, Excenel)
Compliance: 3rd gen cephalosporin order of prohibition
Environment: increased in kidney and bladder, decreased with beta lactamases
Diagnostics: Resp dz
Critically consider the application of antimicrobials in specific bovine disease cases
Lactating Dairy Cattle
-Grade A milk: DSMO non medical prohibited, dipyrone, colloidal silver
-Short milk withdrawal times: Ceftiofur, Ampicillin
-Fluoroquinolones: no ELDU
-Cephalosporins 3rd gen: no disease prevention, unless surgical prophylaxis
-Respiratory disease prophylaxis: strict label adherence
-Surgical prophylaxis: Ampicillin, Penicillin, Tulathromycin
Rumen inactivation of Meds
-Trimethoprim and Trimethoprim-sulfa
-Most Clostridium infections respond to Penicillin or Beta-lactams. Be prepared for diarrhea, transfaunation required typically
Aminoglycosides
-Gentamicin, Amikacin, etc
-Not prohibited
-“Voluntary” bans AABP, AASRP
-Prolonged residues in kidney, withdrawal times 18-24 mts
Coccidiosis and HBS
Sulfonamide effective
-Water-based
-Oral boluses
-IV formulation
Labelled formulations for food animals
-IV, water-based, boluses
-Not permissible to use sulfonamides in extra label in lactating cattle
HBS
-Beta lactase effective
-Increased dosing frequencies
-IV penecillin potassium
-IM Ampicillin
E. Coli and Salmonella
-Treatment may lead to the development of resistance
-Salmonella and fluoroquinolones resistance
-Oral ampicillin or amoxicillin best
Lumpy jaw and Wooden tongue
-Need the drug to penetrate into tissue
-Vol of dis: ability to concentrate in tissues of the body other than blood.
-Oxytetracycline med-high Vol dis
Lecture 6
Neonatal Calf diarrhea
Understand the different mechanisms behind diarrhea
- Malabsorption
-Cell destruction: blunted, less surface area
-Lack of cell production - Osmotic
-“Solution to pollution is dilution”
-Solutes pull water into lumen: sugar, undigested ingesta, microbial fermentation byproducts
-Intentional: miralax, lactulose - Increased hydrostatic pressure
-24% blood flow
-Uncommon in calves
-Secondary to heart failure, renal or liver disease - Secretory
-cAMP, cGAMP stimulation
-Secretion of Cl, Na, K.
-Movement of water into lumen - Motility abnormalities
-Decreased transit time = less ability to absorb
-Maldigestion leading to osmotic changes
-Malabsorption increases luminal fluid volume - Inflammatory
-Pro-inflammatory mediators “protect” GIT-secretion
-PGE2
-Appropriate in moderation
-NSAIDs induced ulcers
Neonatal calf diarrhea syndrome
Cause
-Colostrum deficiency
-Poor management of colostrum, milk replacer, calf, organic debris.
-Infectious: very small contributor
Colostrum
->5.7 g/dl needed
-QC checkpoint 1 day <7 days old
Understand the etiology, common susceptibility periods, diagnosis, treatment and infection/non-infectious causes
There are few to no pathopneumonic appearances
Virus (Rota/Corona)
-Osmotic diarrhea, maldigestion, malabsorptive, fecal-oral, PCR dx.
-5 days to 14 days (Rota): Proximal jejunum, self limiting, enterotoxin released.
-5 days to 1 mt (Corona): Distal SI and colon, mucohemorrhagic, crypt cell invasion.
-Vax at birth (oral) or dams late gestation
Enterotoxigenic E. coli (ETEC)
-0-7 days old
-F5 (K99) fimbria
-Attachment ability decreases with age
-Distal jejunum
-Secretory diarrhea
-Net loss of Na, K, Cl, HCO3, water
-Minimal lesions in intestines
-PCR/culture
-Tx: antiendotoxic drugs, flunixin meglumine (caution ulceration if chronic use)
-Rehydration
Cryptosporidium
-1-4 weeks old
-Ileum, abomasum.
-Malabsorptive: enterocyte invasion, lysis, blunting.
-Osmotic from maldigestion
-“Flat calf syndrome”
Zoonotic
-Calf hypoglycemic, comatose, emancipate, minimally dehydrated, energy deprived.
-Tx: Ammonia or peroxide disinfecting products
-Dx: acid fast staining, fecal flotation
Salmonella spp
-5-14 days, anytime
Clostridium
-Varies
-Abomasitis, and or enteritis
-Type A and C most common in USA
-Young calves <10 days old
C. perfringes: hemorrhagic enterocolitis. Beta toxin. 10-21 days old. Distal jejunum and ileum affected.
-IV fluids, Abomasal decompression
-Oxytetracycline, Penicillin
-Antitoxin: oral or parenteral
-Vax Dam late gestation
Giardia
-2wk-2mts old
-ISTAT: Acidemia
-Loss of HCO3 in feces
-Decreased renal excretion of H+
-Organic acids: D-lactate, VFAs
Hyperkalemia
-Hypoglycemia
Bovine Enteric Panel: Corona/Rota-virus, Salmonella spp, E. coli K99, Crypto
Know the major metabolic abnormalities of calves with neonatal diarrhea syndrome
- Self-limiting, mucohemorrhagic, 5 days old, vax orally or late gestation. Osmotic and malabsorptive
- 0-5 days old, K99, loss of electrolytes = secretory, flunixin meglumine.
- Malabsorptive, 10-30 days old, hypoglycemia, hypothermic, comatose, zoonotic
- Hemorrhagic enterocolitis, penicillin, tetracyclines, late gestation vax
- Acidemia, hyperkalemia, hypoglycemia, malabsorptive,
Diagnostics
-Fecal flotation
-Direct fecal smear
-Total protein
-Pseudo-hyperproteinemia >7.5g/dl with PCV>45%
Understand the zoonotic potential of etiologic agents associated with Calf diarrhea
Giardia, Salmonella, Crypto
Lecture 7
Calf diarrhea Neonate and Older
Understand the etiology, common susceptibility periods, diagnosis and treatment of common infectious associated with diarrhea in calves and older cattle
Salmonellosis
Etiology
-Salmonella enterica spp.
serovar/subtypes DUBLIN
-Primary bovine adapted stain
-Typhimurium, Newport, Montevideo
-Fecal-oral: feces asymptomatic carrier
-Cattle of all ages affected
Salmonella Dublin Zoonotic
Pathogenesis
-Enterocyte attachment and destruction
-Local inflammation, macrophages/neutrophils
-Bacteremia
-Predilection for lymphoid tissues: Peyer’s patches through M-cells
C/S
-Fever, depression, anorexia, recumbency
-Bloody, fetid diarrhea, fibrin casts
-Malabsorptive, maldigestion.
-Pneumonia
-Abortions
Dx
-Fecal culture
-PCR
-Necropsy: GIT, mesenteric lymph node, Gall bladder, lung
Tx
-Aggressive IV fluids
-Antiendotoxin therapy: flunixin meglumine
-Antimicrobials: tetracycline, streptomycin, ampicillin, ceftiofur, ahminoglycosides, fluoroquinolone, trimethoprim sulfa.
Enterohemorrhagic E. coli
Etiology
-EHEC, STEC
-Secretory diarrhea
-Attaching and effacing
-Shinga toxin producing
-Mucosal damage
-GI hemorrhage
-PCR
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
Winter dysentery Coronavirus
Hemorrhagic diarrhea
-During winter and housed animals
-Self limiting
-Reduced milk production
-Decreased feed intake
-Seldom pyrexia
-Histologic lesions confined to colon
-Tx: supportive care
Understand the process for control and eradication of Johne’s in endemic herds
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
Understand the zoonotic potential of Salmonella spp found in cattle
Etiology
-Salmonella enterica spp.
serovar/subtypes DUBLIN
-Primary bovine adapted stain
-Typhimurium, Newport, Montevideo
-Fecal-oral: feces asymptomatic carrier
-Cattle of all ages affected
Salmonella Dublin Zoonotic
Pathogenesis
-Enterocyte attachment and destruction
-Local inflammation, macrophages/neutrophils
-Bacteremia
-Predilection for lymphoid tissues: Peyer’s patches through M-cells
C/S
-Fever, depression, anorexia, recumbency
-Bloody, fetid diarrhea, fibrin casts
-Malabsorptive, maldigestion.
-Pneumonia
-Abortions
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
C. punctata
-Parasite of young cattle <12 mts old
-SI damage
-High fecundity: shed lots of eggs
-Resistant nematode species to macrocyclic lactones (Ivermectins)
Dx
-McMasters fecal flotation
-Modified Wisconsin: single or double centrifugation
-FLOATC protocol: more sensitive with lower egg counts. Calves/adults
Tx
-Methodical deworming
-80% of the problem in 20% of the herd
-No extended release product in young animals <700-900 lbs
-No cookie cutter method
-Benzimidazole: Cooperia spp. susceptible
-Macrocyclic lactones
-Injectable, pour on, product limitations
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
Understand different routes of fluid administration and when they are appropriate
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
IV Fluids
-Neonatal calf diarrhea
-Hurry to improve severe acidemia
-Jugular or ear vein
-Sodium bicarbonate - ISOTONIC (1.3%) first choice in most instances
-Commercial product is 8.4% (1mEq/ml HCO3)
-Baking soda NaHCO3: 13 g/L is isotonic since 1g = 12mEq HCO3. 1ml = 1g so use syringes
-Add 10-15 mEq KCl to fluids (1g = 14mEq K+)
-Commercial products available or lite salt from grocery store.
-Potassium will be driven into cells as pH rises
-No more than 0.5mEq/kg/hr
-Add glucose usually 1-5%, phlebitis if over 7% given in peripheral vein
Adult
Oral
-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
IV Fluids
-Volume delivery issues based on weight
-Max flow rate 14 gauge catheter limiting step
-Roughly 230 ml/min with pressure bag
-Multiple catheters if necessary
-Hypertonic solution (7.2% NaCl)
-4ml/kg
-Rapid volume expansion.
-Lasts ~ 30min
-Must give with oral fluids: strongly recommend giving oral BEFORE IV hypertonic: needs to be rapidly available
-Commercial/homemade solution via carboys
-Lacatated ringers comes in 5L bags convenience rather than ideal solution
Intraperitoneal Fluids
Small ruminants neonates
-Dextrose administration NO SQ = abscesses
-CMPK
-Subcutaneous: cervical region recommended
-Rectal fluids: case dependent for efficacy
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)
Be able to calculate fluid rates in various scenarios based on physical exam findings and basic diagnostic results
Replacement of current deficit
Fluid volume
Electrolyte concentration
Replacement of ongoing loss
Daily requirements
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
Calf Fluid Calculations
Replacement IV
-50-80 ml/kg/hr
-Isotonic 300-450 mosmols/L
-Sodium and chloride concentrations at physiologic concentration
-Potassium 10-20 mEq/L: 1g KCl = 14 mEq K/L
-Dextrose 10-20 g/L (1-2%)
-Bicarbonate or suitable precursor
<7 DoA = Base excess of -10 to -15
>7 DoA = Base excess of -15 to -20
Lecture 10 - Cases
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
Bovine Skin infections - Fungi
Dermatophytosis
-Ringworm
-Trichophyton spp. T. verrucosum, T. mentagrophytes
-Microsporum spp.
-INvade only fully keratinized “nonliving tissue”
-Younger cattle most susceptible
-Transmission by direct contact or fomites
Dx
-Circular alopeic regions “classic”
-Superficial or deep lesions
-Variable pruritic
-Trichogram
-Fungal culture: peripheral samples found up to 4 inches around edge
Tx
-Self limiting
-Topical: Lime sulfur, water/bleach,
-azoles/chlorhexidine solutions
-Sytemic: Nal, antifungal (extra label and expensive)
Infectious even if it looks dead
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
