Boards Review

- Bovine – orange/ Equine – green/ Cat – red/ Dog – Blue / Sheep and Goat - yellow
Toxicology
Small Animals
- Xylitol -
o Problem in Dogs.
o Rapid release of insulin – monitor for hypoglycemia – due to rapid release of insulin
▪ Vomiting/ weakness/ ataxia/ depression/ hypokalemia seizures and coma
▪ Why hypokalemia in – storage?
o Less commonly hepatic failure ( liver issues)
o Treatment: Begin fluids -containing dextrose/ run baseline glucose/ run liver
values( coags as well)/ hepatoprotectants if necessary ( SAM – E).
- Bleach-
o Dilute stomach with milk, DO NOT induce emesis because can cause further damage,
GI protectants
- Black widow spiders = Latrodectus mactans, L. Hesperus
o Acetylcholine is the toxin binds calcium channels – leading to ascending motor paralysis
and destruction of peripheral nerves
o Recumbent, vocalizing, pain, rigidity with muscle spasms – death from respiratory/
cardiovascular failure
- Rodenticides -
o Warfarin = anticoagulant – interferes with II, VII, IX, and X
▪ Give Vitamin K1, if chronic give plasma as well
▪ Prothrombin time (PT) will be prolonged soonest after ingestion – because VII
has shortest half life and is part of extrinsic system
o Brodifacoum = D-con – inhibits epoxide reductase (loss of Vitamin K – interferes with II,
VII, IX, and X)
▪ Give Vitamin K, monitor prothrombin time (PT)
o Cholecalciferol = gets converted to active Vitamin D to cause increased resorption of
calcium and gut absorption of calcium leading to sometimes fatal hypercalcemia
- Ethylene glycol -
o High anion gap, azotemia, calcium oxalate crystalluria, metabolic acidosis, hyperglycemia,
and either polyuria or oliguria (anuria in worst case), hypocalcemia (from chelation of Ca
by EG metabolites)
o Treatment aimed at alcohol dehydrogenase – give 4- methylpyrazole (4-MP) – does not
work in CATS
▪ Ethanol competes with this enzyme when given soon after exposure
▪ 4-MP better than ethanol because doesn’t cause hyperosmolality, metabolic
acidosis, CNS depression
- Organophosphate -
o Inhibit acetylcholinesterase causing muscarinic signs such as hypersalivation,
incoordination, and bloat
o Treatment = atropine or 2-PAM (pralidoxime – anticholinesterase)
- Fleet enemas -
o High in phosphorus – leads to decrease in serum calcium due to law of mass action
▪ Hypernatremia and hyperphosphatemia – due to absorption from the colon
▪ Hypocalcemia leads to weakness, shock, tremors, and seizures
o Give calcium gluconate, phosphorus binders, with severe cases of hyperkalemia give
insulin and dextrose
- Strychnine = snail bait
o Competitively antagonizes action of glycine – loss of impulse contractility in the spinal
cord and brainstem – affects striated muscle
o Give methocarbamol (for convulsions), prevent stimulation
- Chocolate = methylxanthines (theobromine, caffeine)
o CNS excitation, tachycardia, vasoconstriction
o Highest concentration of toxin in unsweetened baking chocolate
- Pyrethrins = toxic to CATS, alters activity of sodium ion channels to increase length of
depolarization
o Depression, hypersalivaiton, ataxia, muscle tremors ! treat with methocarbamol, bathe
to remove product
- Acetominophen = toxic to CATS
o Cats lack glutathione and glucoronyl transferase – leads to methemoglobinemia (dark
brown blood – due to oxidative damage to hemoglobin), may also see Heinz bodies
o Treatment with N-acetylcysteine
- HEINZ BODY ANEMIA = methylene blue, molybdenum deficiency, rye grass, brassica family
o Zinc – from pennies minted after 1983
o Onions – can cause hemolytic anemia
▪ HEMOGLOBINURIA and hemoglobinemia – Heinz body anemia due to oxidative
damage to RBCs
o Red maple leaves = Acer rubrum – HORSES – see icterus (due to low oxygen content
of blood), colic
- RENAL FAILURE -
o Grapes and raisins –
o Lillies – ACUTE RENAL FAILURE in cats – toxic ones = Stargazer lily (Lillium family)
▪ Peace – calcium oxalate
▪ Lily of the Valley – cardiotoxin
▪ Day Lilly – Renal toxicity
▪ Easter Lilly – Renal toxicity.
▪ Cala Lilly – calcium oxalates
▪ Tiger Lilly – renal toxin
Large Animals
- Zealalenone – affects PIGS, potent estrogenic metabolite produced by Fusarium
o Hyperestrogenism and pseudopregnancy
- Salt poisoning -
o LESION = perivascular infiltration of eosinophils
o Pathogenesis = too much blood sodium causes increased osmolarity and water from
the brain diffuses into the vasculature, brain responds by forming hyperosmolar
(idiogenic osmoles) to draw water back into the brain – REHYDRATE SLOWLY or will
cause water to diffuse into the brain too rapidly
▪ See neurologic signs – head pressing, stargazing, blindness, seizures
▪ Causes hemolysis because water rushes into RBCs and they lyse
- COPPER -
o Toxicity – common in SHEEP (pigs very resistant to high copper)
▪ Cattle and horse feed contain too much copper for sheep – most common
exposure.
▪ Hemolytic anemia in sheep – liver levels build up until suddenly released causing
massive hemolysis and resulting in icterus – will see methemoglobinemia,
hemoglobinemia, hemoglobinuria
o Deficiency = see in SHEEP – enzootic ataxia, swayback
▪ Primary (low copper intake), secondary (high molybdenum, sulfur, iron, selenium,
etc.)
▪ Enzootic ataxia – see in lambs 1-2 months old
▪ Swayback – congenitally or in very young lambs, progressive ascending paralysis
- Grass tetany/staggers –
o Phalaris (canary grasses – Phalaris, Lolium, Cynodon, Paspalum) -
▪ Stiff-legged gait, hyperexcitability, nystagmus, head tremors, fall and flail wildly
▪ Remove them from the pasture and they should get better
o HYPOMAGNESEMIA -
▪ Magnesium important for nervous system function and enzyme reactions
▪ Occur in lactating animals in early spring on lush pastures that are well-fertilized
with nitrogen and potassium, high levels of these inhibit magnesium absorption
from the GI tract
▪ Restlessness, staggers, over-alert appearance, excitable, fall down with
convulsions and die
- Black walnut = LAMINITIS in horses
- GI TOXINS
o Slaframine = moldy red clover
▪ HYPERSALIVATION
▪ slobbers
o Oak leaves and acorns -
▪ Hemorrhagic diarrhea, abdominal pain, tenesmus, colic, death
▪ Cattle = renal damage, NOT in horses
o Cantharidin = aka blister beetle toxicity

▪ COLICKING in horses, cardiovascular shock, endotoxic shock, renal failure,
vesicles in mouth or tongue – watery diarrhea, neuro signs if live long enough
• Renal tubular damage (may see hematuria), cardiac arryhthmias
• Abrupt onset of colic, fever, hypersalivation, frequent urination, hematuria
o Claviceps purpura = parasitic fungus – ERGOTISM

▪ Found on rye, oats, wheat, and Kentucky bluegrass
▪ Alkaloids causes vascular constriction, thrombosis, gangrene, vomiting, colic,
diarrhea, constipation
▪ Find ergot in the grain!
- NEUROTOXINS
o Blue green algae = Anabaena, Microcystis, Aphanizomenon

▪ Toxin absorbed through mucous membranes, causes post-synaptic depolarizing
block
▪ Dead animals next to a pond – i.e. birds and cattle
▪ Miosis, ptyalism, bradycardia, diarrhea, ataxia, convulsions, death – can die
within minutes (as little as 1.5L can kill a cow)
▪ Two kinds:
• Nicotinic agonists – mimics the mechanism of acetylcholine
• Acetylcholinesterase inhibitor -
o Nightshade = atropine
▪ CNS signs – dilated pupils, progressive paralysis, depression
o Water hemlock – LEAVES very toxic
▪ Grand mal seizures, salivation, tachypnea, birth defects similar to lupine, death
o Perennial ryegrass -
▪ Ataxia and tremors as result of activating GABA receptors when infected with an
endophytic fungus
o Lead poisoning = contaminated petroleum products (i.e. used motor oil)

▪ Acute blindness, dullness, down and unable to rise, vocalizing, unaware of
presence
▪ Sample of rumen contents has oily sheen
▪ Treat with Calcium EDTA to chelate – use calcium to help prevent hypocalcemia,
do not use sodium EDTA because sodium will bind up calcium and cause
hypocalcemia
o Sorghum -
▪ Lesion = myelomalacia of lower spinal cord – pelvic limb incoordination, urine
dribbling – DEATH
o Yellow star thistle = Centaurea solstitialis

▪ Lesion = nicropallidal encephalomalacia – loss of globus pallidus and substantia
nigra
▪ Loss of prehension (dystonia of lip muscles and tongue), tremoring, dysphagia,
unable to prehend feed – GRAVE prognosis, euthanasia recommended because
die of dehydration or starvation
- REPRODUCTIVE TOXINS
o False hellbore = Veratrum californicum

▪ Teratogen called cyclopamine – cyclopia, anophthalmos, cleft palate, metacarpal
hypoplasia
• Day 14 of gestation = craniofacial deformities
• Day 30 of gestation = limb and bone shortening in metacarpal/metatarsal
joints
o Locoweeds (Astragalus, Oxytropis, Swainsona) = abortions, weak lambs, bent legs

▪ Inhibit alpha-mannosidases – widespread neurovisceral cytoplasmic vacuolation –
and abortion and neuro system abnormalities (i.e. ataxia)
▪ Grow in WEST with other forages are scarce – see in dry condition in Rocky
Mountains
o Fescue = Neotyphodium coenophialum (ergopeptine alkaloids – dopamine agonists)

▪ Prolactin suppression – inhibit lactation, thickened placenta, dystocia, agalactia,
prolonged gestation, weak or stillborn foals = REPRO FAILURE IN MARES
• Reproductive inefficiency, does not cause congenital defects
▪ Clinical signs = lameness, sloughing of rear hooves, decreased weight gain, fat
necrosis
o Lupine = “crooked calf disease”
▪ Arthrogryposis, malpositioning in the uterus, cleft palate
o Ponderosa pine needles -

▪ Abortion in LAST trimester, retained placenta
- COAGULOPATHY
o Bracken fern = bone marrow suppression (low neutrophils and lymphocytes)
▪ Toxic glycoside (ptaquiloside) and thiaminase
▪ Enzootic hematuria – hemorrhagic cystitis that progresses to neoplastic changes
in the bladder
▪ Can cause polioencephalomalacia due to thiaminase – more so in HORSES than
other animals
o CYANIDE = choke cherry (arrow grass, Sudan and Johnson grasses, Sorghum)
▪ Bright red mucous membranes – cyanide blocks cellular respiration and oxidative
transport – hemoglobin unable to release oxygen (venous blood stays
oxygenated)
▪ Bright red blood, bitter almond smell to GI tract on necropsy
▪ Treatment = sodium thiosulfate, sodium nitrate, methylene blue (NOT
supplemental oxygen)
o Carbon monoxide -
▪ Cherry red mucous membranes – differentiate from cyanide by lack of almond
smell
o Nitrates -
▪ BROWN blood
▪ Tx: Methylene blue
o Moldy sweet clover = vitamin K antagonist = dicumarol (Warfarin like)
▪ Necessary for production of factors II, VII, IX, and X – causes hemorrhage, NOT
hemolysis
▪ Prothrombin time (PT) – to diagnose because factor VII depleted first and is part
of extrinsic
o Anthrax -
▪ Common in horses and cows – sudden death, colic, fever, SQ edema – dead
horses do not show signs of rigor mortis with unclotted blood exuding from their
orifices
▪ DO NOT NECROSPY THE ANIMAL!! Could release spores into environment.
Notify the authorities!
▪ Diagnosis = obtain vitreous humor (or blood from an ear scrape)
▪ ZOONOTIC = human forms are intestinal, pulmonary, cutaneous
- CARDIAC TOXINS =
o milkweed, gossypol (in cottonseeds), oleander, rhododendron, foxglove, white
snakeroot
o All of these can cause acute death or arrhythmias
o Ionophores = i.e. monensin (also lasalocid, salmonycin) – toxic to HORSES
▪ Coccidiostat used in cattle – horses very susceptible
▪ Myocardial necrosis and dilated cardiomyopathy – heart murmur, respiratory
distress, staggering, profuse sweating, hemoglobinuria – look at fractional
shortening with ECHO to determine prognosis
▪ Empty GI tract by using mineral oil, activated charcoal, fluid therapy
▪ Tx: Atropine
- PULMONARY TOXINS
o Perilla mint = type I pneumocytes and bronchiolar epithelial cells
▪ Dyspnea, frothing at the mouth – wet, emphysematous lungs on necropsy
▪ High mortality because get permanent fibrosis of the lungs
o Moldy sweet potatoes = Fusarium solani
▪ Produces 4-ipomeanol (4-IP) – atypical interstitial pneumonia
▪ Grunting, frothing at mouth, deep cough, respiratory distress, death after 2-5
days
▪ Lungs wet, firm and fail to collapse – same lesions as seen with 3-MI
o Brassica plants = rape, kale, turnips = FOG FEVER (acute bovine pulmonary edema
and emphysema, grunts)
▪ Contain lots of tryptophan which is converted to 3-methyl-indole (3-MI) – leads to
atypical interstitial pneumonia and emphysema and cyanosis
▪ Seen in cattle on lush forage - frothy nasal discharge, SQ emphysema, loud
cough, open mouth breathing, crackles and wheezes
- HEPATIC TOXINS
o Pyrrolizidine alkaloids = fiddleneck (Amsinkia intermedia), common groundsel, ragwort,
Senecio
▪ Inhibit mitosis of hepatocytes so can’t multiple – acute liver failure, hepatic
encephalopathy, icterus
▪ Diagnostic = megalocytosis, periportal fibrosis, bile duct hyperplasia
• Presents similar to Theiler’s disease – in horses – use histopath to
differentiate
▪ May also see secondary photosensitization = sunburned white areas on skin
• Normal chlorophyll breakdown products (phylloerythrin) are usually
cleared by the liver, with liver damage this accumulates in the skin and
results in UV damage
• Primary photosensitization = St. John’s Wort, Erodium, Brassica,
Hypericum
o Contain hypericin – causes large areas of skin sloughing, mainly
unpigmented areas
• Photosensitization due to liver disease – usually chlorophyll in diet is
converted to phylloerythrin and excreted by the liver – with hepatic
disease it is deposited in skin – UV reacts with it and causes dermal
damage ! lesions on weight areas
o Aflatoxin = mycotoxin (from Aspergillus)
▪ Similar lesions to PAs - but pathologists thing megalocytes is pathogenic for PAs
• Subacute hepatic necrosis and fibrosis
▪ Primarily found in moldy grains
Clinical Pathology and Hematology
- Miscellaneous facts -
o Lactate – can measure to assess perfusion – reflection of anaerobic metabolism
(normal <2.5 mmol/L)
▪ Produced from pyruvate in anaerobic environments to keep glycolysis running
o Stress response = neutrophilia, lymphopenia, monocytosis, eosinopenia
o Polychromasia = sign of regenerative anemia (less mature RBCs being released into
circulation)
- Blood transfusions -
o Indications to perform transfusion = acute blood loss with PCV <20%
▪ To raise PCV 1% give 1ml/kg of packed RBCs
o Crossmatching
▪ Major = donor RBCs vs. recipient plasma
▪ Minor = donor plasma vs. recipient RBCs
o Transfusion reactions in cats = signs of anaphylaxis, common in cats predisposed to
having type B blood (Abyssinians, English Shorthairs, British Shorthairs, Cornish Rex,
Devon Rex)
▪ Type B have anti-A antibodies, giving B to an A cat is not as bad as vice versa,
type A is more common
o Bovine blood types = A, B, C, F, J, L, M, R, S, T, Z ! B and J appear to be most clinically
relevant
▪ Transfusion reaction = tachycardia, dyspnea, ptyalism, rough lung sounds – as
you give transfusion
▪ Treat with dexamethasone, epinephrine, antihistamine, oxygen
- Bleeding tests -
o Partial thromboplastin time (PTT) = intrinsic and common
o Prothrombin time (PT) = extrinsic and common
o Thrombin time (TT) = measure of final steps of coagulation taking fibrinogen to fibrin
o Buccal mucosal bleeding test = platelet function
o Template bleeding time = helps determine functional ability of platelets to plug a minute
wound (similar to buccal mucosal bleeding test) – helpful when hace petechial and
ecchymotic hemorrhages
o Antithrombin activity = measured when disseminated intravascular coagulation (DIC) is
a concern
- Calcium -
o With hypocalcemia check for hypoproteinemia because the calcium measured on a
chemistry is protein-bound – measure ionized calcium
▪ Causes ! renal disease, eclampsia, phosphate enema toxicity, ethylene glycol
toxicity (due to chelation by EG’s metabolites)
o Hypercalcemia ! neoplasia (lymphosarcoma, anal sac adenocarcinoma), primary
hyperparathyroidism, chronic renal failure (renal secondary hyperparathyroidism),
hypervitaminosis D, nutritional secondary hyperparathyroidism
- Joint fluid -
o Normal = small monomuclear cells without neutrophils
o Suppurative = neutrophils
o Granulomatous = mononuclear (lymphocytes, macrophages, plasma cells)
o Pyogranulomatous = mixed neutrophils and mononuclear
- Immune mediated thrombocytopenia -
o Spherocytes on blood smear
o Azathioprine for treatment
- Immune mediated hemolytic anemia (IMHA) -
o Spherocytes on bloodsmear (see with all immune-mediated disorders) – RBCs that are
smaller with lots of Hgb (so stain deep red), polychromasia
o Regenerative anemia, spherocytes, autoagglutination, positive Coombs
o Azathioprine for treatment
- Von Willebrands = deficiency of Factor VIII-related antigen
o Doberman Pinschers, platelet function abnormality due to inability to adhere to
subendothelial collagen
- Hemophilia A = inherited deficiency of Factor VIII
o Prolonged ACT and APTT – give PLASMA to treat
- Canine thrombopathia = inherited where platelets fail to aggregate and secrete their granules
o Coagulation and platelet numbers = NORMAL
o Basset Hounds
- Iron deficiency -
o RBCs will be hypochromic (less red) and smaller (microcytic) due to less volume
o Microcytic, hypochromic non-regenerative anemia
- Disseminated intravascular coagulation = severe coagulopathy where both thrombosis and
hemorrhage are occuring
o Lethargy, anorexia, bleeding from gums
o Definition = elevated PT/PTT, thrombocytopenia (low platelet count), positive D dimer
(type of fibrinogen degradation product), antithrombin III activity decreased, can look at
fibrinogen (not common in horses)
▪ 2 of these findings are enough to diagnose DIC
- Systemic inflammatory response syndrome (SIRS) -
o Fever, tachycardia, leucopenia
o Cytokine most important to SIRS = Interleukin 1 (IL-1) – major up-stream cytokine of
inflammatory response, through activation of other inflammatory cells IL-1 causes
tremendous amplification of the inflammatory response
Hypersensitivities
- Type 1 = IgE mediated, immune mediated hypersensitivity
o Causes = vaccinations
- Type 2 = antibody dependent reaction, occurs due to IgG or IgM made against normal self
antigens and some foreign antigens that resemble some molecules on the surface of host cells
- Type 3 = immune complex mediated reaction
o Soluble antigen-antibody complexes form in large amounts and overwhelm body
instead of being normally removed by macrophages in the spleen and liver
o Result in immune complex disease which can cause ! arthritis, nephritis, uveitis
o Causes = sulfa drugs in Doberman Pinschers
- Type 4 = delayed hypersensitivity – cell mediated
o T8-lymphocytes will be sensitized to an antigen and differentiate into cytotoxic T-
lymphocytes, T helper 1 type T4-lymphocytes become sensitized to an antigen and
produce cytokines
Cardiology
- ECG
o P pulmonale = tall and slender P wave = RIGHT atrial enlargement
o P mitrale = increase in duration of P wave = LEFT atrial enlargement
- Physiology
o Stroke volume x heart rate = cardiac output ! stroke volume determined by preload,
afterload, and contractility rate
o Cardiac output x oxygen content = oxygen delivery
o Response to acute bloodloss….
▪ Increased cardiac output – catecholamines induce vasoconstriction and increased
cardiac output
▪ Antidiuretic hormone release causes water and sodium resorpiton by kidney
▪ Splenic contraction occurs to inject stored RBCs into circulation
- ECF vs. ICF
o Animals tend to have 2/3 of their body weight made up of water – of TBW ! ECF:ICF
ratio = 1:2
▪ TBW = 60% of BW
▪ ECF = plasma, interstitial fluid, transcellular lymph such as CSF and synovial
fluid
- Shock
o Hypovolemic shock = critical reduction in intravascular volume (i.e. dehydration,
hemorrhage, third-spacing)
▪ Decrease in intravascular volume (preload) results in decrase in stroke volume
and subsequently cardiac output – eventually results in decrease in tissue
perfusion and oxygenation
▪ Vomiting, diarrhea, dehydration, dry mm’s, prolonged CRT, elevated HR, weak
femoral pulses
▪ Central venous pressure = direct measure of BP in cranial vena cava (estimate of
preload) - -5-5 is considered hypovolemia
o Cardiogenic shock = result of decreased myocardial contractility with subsequent
decrease in oxygen delivery
▪ ALWAYS associated with primary heart disease
o Obstructive shock
▪ Occurs with abnormal blood distribution that impairs blood return such as GDV
where obstruction of vena cava can occur or in pericardial tamponade
o Distributive or vasogenic shock
▪ Typically secondary to sepsis and anaphylactic reaction causing vasodilation
- Heart sounds
o S1 = vibration of blood during ventricular contraction and closure of the atrioventricular
valves
o S2 = heart at beginning of diastole – result of closure of pulmonic and aortic valves
o S3 = subtle, only heart occasionally in mid-diastole, caused by ventricular relaxation
o S4 = also very subtle, heard at end of diastole, associated with atrial contraction
- Murmurs
o Left = PAM – third ICS = pulmonic, fourth ICS = aortic, fifth ICS = mitral
▪ Left heart base = pulmonic stenosis, PDA, subaortic stenosis
▪ Heart apex = mitral valve dysplasia
o Right = 3-4 ICS = tricuspid
▪ Systolic at right mid thorax = tricuspid dysplasia
- Failure of closure of foramen ovale
o Small slit that allows shunting between right atrium and left atrium in fetus – when born
lungs expand (right atrial pressure decreases) and left atrium becomes higher pressure
system and should close foramen ovale – if fails to close within first 48 hours of life !
shunting of blood from left atrium to right atrium
- Ventricular septal defect
o Species
▪ Most common congenital heart defect in CATTLE!! – present at 2-3 months age
due to failure to thrive, pulmonary edema and secondary pneumonia
▪ Most common congenital defect in HORSES!! Some can perform normally, others
go into heart failure
o Pathogenesis = oxygenated blood pushed into right atrium/ventricle – right ventricular
dilatation and hypertrophy – increased flow to right side casues pulmonic stenosis
(murmur on left side at pulmonic valve)
o Murmur = loud holosystolic or constant murmur heard on BOTH sides (blood shunted
from left to right)
o Echocardiogram = small turubulent jet flowing from left to right ventricle through septum
o Treatment = small (no treatment, prognosis good), large (surgical correction)
- Tetralogy of Fallot
o *Dextropositioned aorta (overriding aorta), pulmonic valve stenosis, ventricular septal
defect, right ventricular hypertrophy
o Right sided heart failure, cyanosis, secondary bacterial endocarditis, exercise
intolerance, failure to thrive, syncope, bilateral basilar murmur, POLYCYTHEMIA
(venous blood to arterial circulation ! hypoxemia, increased EPO
▪ A RIGHT to LEFT shunt = POLYCYTHEMIA (dark red mucous membranes,
hypoxemia – see increased drive for EPO due to hypoxemia)
- Patent ductus arteriosis (PDA)
o Failure of closure after birth resulting in a shunt (usually left to right) from aorta to
pulmonary artery – shunting causes excess volume in pulmonary arteries, veins, left
atrium, left ventricle, and aortic arch
o Continuous machinery/washing machine murmur (hear on both sides of chest),
waterhammer pulses (large bounding pulse with sharp peak and rapid decline)
o Radiographs = enlarged left heart and pulmonary vasculature with aneurismal bulge of
aorta near PDA on DV
▪ Only see right ventricular enlargement with PDAs that are shunting right to left
o Rare in cats, cows, horses – MOST COMMON CONGENITAL DEFECT IN DOGS
(other species is VSD)
o Treat by surgical ligation of PDA (large cylindrical PDAs), coil embolization (funnel-
shaped PDAs)
▪ DO NOT REPAIR A right to left shunting PDA!
- Valvular endocarditis = infection of heart vales in OLDER animals
o COW = tricuspid valve is most commonly affected (right side murmur)
o SMALL ANIMALS and HORSES = aortic valve most commoly affected (also mitral)
▪ Can lead to mitral regurgitation – DDx= degenerative thickening of mitral,
ruptured chordae tendinae
▪ Aortic can cause aortic regurgitation – NO IMPACT ON PERFORMANCE – harsh
decrescendo holodiastolic murmur at left heart base – see A LOT IN HORSES
o Causes = foot abscesses, sepsis – will see signs of systemic illness (fever of unknown
origin, lethargy)
o Diagnosis = vegetative lesions on heart valves, positive blood culture
- Pericardial effusion
o Causes = hemangiosarcoma, chemodectoma, idiopathic, left atrial rupture due to chronic
mitral regurgitation, trauma, PPDH, infectious pericarditis, trauma, foreign body,
coagulopathy, heart base tumor (i.e. BLV in cattle)
o Muffled heart sounds (due to fluid), decreased milk production, lethargy, anorexia,
cough, collapse, pale mm
o Pulsus paradoxicus = exaggerations in pulse during respiration, weak as inhales, strong as
exhales
o Electrical alternans = different amplitudes of QRS due to heart shifting in fluid filled
compartment
o Radiographs = enlarged globoid heart on DV
o Necropsy = nutmeg liver (due to right heart failure which can be caused by pericardial
effusion)
o Treatment = pericardiocentesis – NOT furosemide because decreases preload on right
heart ! circulatory failure
- Atrial premature complexes
o Causes pulse deficits – usually clinically insignificant and only sometimes associated
with cardiac disease
- Atrial fibrillation
o Most common supraventricular arrhythmia in cattle – usually result of digestive
disturbance of electrolyte abnormality ! associated with vagal tone, hypokalemia,
hyperkalemia, calcium therapy
o Most common pathologic arrhythmia in horses (2nd degree AV block is most common non-
pathologic)
▪ Poor performance, exercise intolerance, may appear normal – if acute more
likely to be treatable
o PULSUS ALTERNANS ! two quick normal pulses in row followed by no pulse (pulse
deficit), irregular HR
o ECG = no P waves because SA not working, high frequency/low amplitude F waves,
QRS at irregular intervals
o Auscultation = irregularly irregular rhythm with variable heart sounds
o Treatment in horse = quinidine (class IA sodium channel blocker – prolong refractory
period of myocardium)
▪ Toxicosis = increased QRS duration of greater than 25%, colic, ataxia,
hypotension, diarrhea, edema
▪ Then try digoxin as adjunctive treatment – use if quinidine causes acceleration in
ventricular response rate, resting HR > 90 bpm, horse is exhibiting low vagal
tone, if conversion hasn’t been achieved in 24 hours
o Prognosis in horse = good for conversion if HR <60bpm, atrial fibrillation of <4m
duration, murmur < grade 3/6
o Treatment in dog = diltiazem, atenolol, digoxin, procainamide
- Ventricular fibrillation = chaotic electrical activity and mechanical activity during cardiac arrest
- Ventricular premature complexes
o Treat in dog when…HR >180 bpm, pulse deficits, clinical signs, VPCs for over 20
seconds in duration
▪ When R starts overlapping with T – definitely treat because can cause fibrillation
- Ventricular tachycardia
o Treatment = LIDOCAINE (if no response then try procainamide and quinidine)
- Ventricular asystole = no electrical or mechanical activity
- Hyperkalemia
o ECG = NO P wave, increased P-R interval, widened QRS, tall tented T waves
▪ May see atrial standstill secondary to this – ABSENT P waves!!
- Atrioventricular blocks = delay in conduction at the AV node
o First degree AV block = takes longer to get through AV node
▪ ECG = increased P-R interval and no dropped QRS
▪ This and 2nd degree block NORMAL in a horse – usually form high vagal tone –
i.e. see in healthy racetrack horses - *most common conduction disorder in horse
• No treatment necessary for this or 2nd degree because normal for
racehorses to have slower HR
o Second degree AV block
▪ Caused by a refractory AV node that is responding to a delayed atrial
depolarization
▪ Mobits type I = aka Wenkebach
• ECG = P-R interval progressively gets longer until there is dropped QRS
▪ Mobitz type II
• ECG = P-R interval is unchanged and occassionaly see P wave without a
QRS
o Third degree AV block = no impulses conducted from atria to ventricles
▪ Subservient pacemaker (i.e. in AV node or ventricle) causes ventricular
contraction
▪ Clinical signs = exercise intolerance, syncope with excitement
▪ ECG = P waves unassociated with QRS
▪ Treatment = pacemaker (for chronic cases), can also try catecholamine or
parasympatholytic (i.e. atropine) to help increast HR
• NEVER USE LIDOCAINE IN THESE PATIENTS – will abolish the
ventricular escape beat
- Heart failure
o Right heart failure
▪ In cows – can be caused by traumatic reticulopericarditis – anorexia, bottle jaw,
brisket edema, true jugular pulses, elevated HR and RR, depression
▪ Clinical signs = tachypnea/dyspnea (due to pleural effusion), exercise intolerance
(due to decrease in CO causing decrease in oxygenation), hepatomegaly (due to
venous congestion), muscle wasting (loss of protein into effusions), lethargy,
weakness, venous distention, ascites, peripheral edema
▪ Radiographs = large heart, hepatomegaly
o Left heart failure
▪ Clinical signs = cough (because of pulmonary edema), difficulty breathing
▪ Radiographs = enlarged heart, left atrial enlargement, enlarged pulmonary
arteries, hepatomegaly, alveolar pattern in perihilar region extending to right and
left caudal lung lobes
o Treatment = furosemide (decrease blood volume, to decrease edema/ascites),
nitroprusside (venodilator), sodium restricted diet, enalapril (ACEi – vasodilators to
combat vasoconstriction and increased vascular resistance)
Respiratory
- Pulse oximetry ! sigmoid shape to oxygen saturation curve, until you reach oxygen pressures
<60 mmHg there is very little change in oxygen saturation, time to intervene is early when you
see saturation percentage dropping
o An oxygen saturation of 98-100% corresponds to > 100 mm Hg oxygen in arterial blood  
▪ An anesthetized patient breathing 100% oxygen should have about 500 mmHg
oxygen in arterial blood
▪ An animal breathing oxygen should have PaO2>300 – tells you they are not
exchanging oxygen normally if not (V/Q mismatch, barrier to diffusion)
o An oxygen saturation of 95% corresponds to 80 mm Hg  
(room air is 95-100% oxygen saturated)
o An oxygen saturation of 10% corresponds to 10 mm Hg

- Acid-base status
o Metabolic acidosis
▪ Saliva loss in cattle ! rumen saliva rich in bicarb
▪ Dehydrated calf ! sunken eyes, nonresponsive – give IV fluids with bicarbonate
o Metabolic alkalosis
▪ Saliva loss in horses ! lots of chloride in saliva so causes this
▪ In sweating horse ! horse sweat is high in chloride and potassium – renal
retention of bicarb leads to this
o Respiratory acidosis
▪ Causes = hypoventilating (so there is buildup of CO2, CO2= acid), airway
obstruction, pneumothorax, flail chest, neuromuscular disease, abdominal
enlargement, pleural space disease, bicarbonate therapy
o Hypoxemia – low PO2 – ventilation/perfusion mismatch, diffusion impairment, low
inspired oxygen, hypoventilation (if severe enough), shunt
o To determine – whatever goes direction of pH is the primary problem, negative base
excess or low HCO3 means metabolic acidosis, low PaCO2 means respiratory alkalosis
or hyperventilation
- Ventilation AND oxygenation – measure with arterial blood gas
o Ventilation defined by PaCO2 ! hyperventilating = PaCO2 <30mmHg, hypoventilating
= PaCO2 > 30mmHg
▪ A normal PaCO2 (35-45) tells you animal is ventilating appropriately
▪ A high PaCO2 indicates horse is underventilating, i.e. not blowing off sufficient
CO2 – increase in CO2 leads to respiratory acidosis because CO2 is an acid
(leads to low pH)
o Oxygenation
▪ Causes of hypoxemia = hypoventilation, low FiO2 (not obtaining enough oxygen),
venous admixture (venous and arterial blood mix leading to decreased
oxygenation)
• Cyanosis indicates hyoxemia (PaO2<50mmHg) – mucous membranes are
measure of oxygenation
• Most common cause of cardiac arrest = systemic hypoxemia
o Base excess = if normal indicates there is minimal metabolic component to acidosis –
BE is amount of base that you would need to add to a solution (i.e. plasma) to achieve a
normal pH – normal HCO3 is 22-24 mEq/L and base deficit is calculated by subtracting
the patients HCO3 concentration (i.e. 10 from the normal concentration 23)
▪ How much sodium bicarb should you give to 470 kg horse that has BE of 13 to
completely correct deficit?
• Formula = 0.3 to 0.4 x BW x base deficit = 2400 mEq
• May only fix part (often half) of of total calculated bicarb and then reassess
- Stridor vs. Stertor = both audible without aid of stethescope and both indicate extrathoracic
problem
o Stertor = gurgling noise usually generated in nasal passages
o Stridor = high-pitched sound usually generated near larynx
- Pneumothorax
o NO SOUNDS DORSALLY (with audible ventral sounds) – free air moves dorsally when
lungs collapse
o Causes = trauma, damaged lung, ruptured bullae, migrating foxtail,
pneumomediastinum
▪ NEVER due to pulmonary hypertension (this causes heart failure)
▪ Always look for rib fractures, diaphragmatic hernias, pulmonary contusions, and
pleural effusion
o Respiratory distress – dyspnea, tachypnea
o Treatment = THORACOCENTESIS (on dorsal aspect) – DO NOT GIVE OXYGEN
(worsens pneumothorax)
- Aspiration pneumonia
o Fever, anorexia, lethargy, depression, harsh lung sounds and crackles cranioventral
o Cause in cows/horses = mineral oil drenches (tasteless and often aspirated),
pharyngeal paralysis (WMD), leaking nipples on bottles, gastric reflux, improper
intubation
o Causes in cats/dogs = megaesophagus (myasthenia, congenital), following anesthesia
o Radiographs = alveolar pattern in right cranial and middle lung lobes – distribution
depends on patient position at time of aspiration (usually cranioventral due to gravity in
sternal)
- Atelectasis = incomplete expansion of a lung due to loss of air from alveoli
o Common complication of prolonged recumbency and inhalation anesthesia
o Can also be due to decreased pulmonary surfactant in newborns or in ARDS or near
drownings
- Neurogenic pulmonary edema
o Causes = head trauma, seizures, electrocution, upper airway obstruction
o Rapid onset of respiratory difficulty after central nervous system insult – see
CAUDODORSAL distribution
- Lung lobe torsion = treatment is LUNG LOBECTOMY
o For procedure – use isoflurane and injectable succinylcholine (because is critical during
certain parts that dog stay completely still – including respiratory motion) – could also
use nondepolarizing neuromuscular blocking agent (i.e. pancuronium, d-tubocurarine,
atracurium)
- Smoke inhalation (from fire)
o Carbon monoxide inhalation – leads to carboxyhemoglobin formation and displacement
of oxygen
o Cabon dioxide inhalation – leads to severe acidosis
o Laryngeal edema – damage to larynx from heat causes edema and swelling
contributing to upper airway obstruction
o Smoke can inhibit pulmonary macrophage function
o Prognosis = skin burns worsen prognosis
▪ 1st degree (superficial) = epidermis only
▪ 2nd degree (partial thickness) = epidermis and may go down to the deep dermis
▪ 3rd degree = epidermis, dermis, and adnexal structures
▪ 4th degree = total destruction of skin, fat, fascia, bone, and muscle
Neurology
- UMN vs. LMN lesion localization
o UMN signs = hyperreflexia of spinal reflexes and increased muscle tone
o LMN signs = decreased or absent spinal reflexes and decreased muscle tone
▪ C1-C5 ! all 4 limbs show signs of UMN
▪ C6-T2 ! LMN signs to thoracic limbs, UMN signs to pelvic limbs
▪ T3-L3 ! UMN signs in pelvic limbs, normal thoracic limbs
▪ L4-S4 ! LMN signs in pelvic limb (and anus and bladder), normal thoracic limbs
• Dribbling urine, dropping feces
• Can tell if function is lost by checking anal reflex
o Prognosis = POOR for dog that hasn’t had deep pain for 24 hours
- Cranial nerves
o CN I – olfactory
o CN II – optic
▪ Assess with papillary light reflex
▪ Assess with dazzle reflex – examines this nerve independent of the visual cortex
(animal with cortical lesion will still have a dazzle) ! if animal does not have a
dazzle lesion is in CNII
o CN III – occulomotor
▪ Closes the eyes – levator palpebrae superioris
▪ Motor to dorsal/medial/ventral rectus muscles – movement of eye in horizontal
and vertical planes – will see strabismus of the eye
▪ Innervates palpebral levator which is responsible for raising upper eyelid
▪ Parasympathetic to this innervates iris sphincter (in mammals)
o CN IV – trochlear
▪ Innervates dorsal oblique muscle of eyeball
▪ Lesion causes medial strabismus
o CN V – trigeminal
▪ Mandibular branch ! motor to mastication muscles (pterygoid, masseter,
temporalis) – can’t close mouth
▪ Ophthalmic branch ! sensory to eyes, eyelids, cornea
▪ Maxillary branch ! sensory to face, pinnae, and nasal septum
▪ Palpebral assesses this cranial nerve (and VII)
o CN VI – abducens
▪ Motor innervation to lateral rectus - lesion would cause medial strabismus – loss
of function of this muscle will pull globe medially
▪ Motor to part of retractor bulbi muscles – not involved in pupillary light reflex, only
involved in movement of the eye
o CN VII – facial
▪ Opens the eyes – orbicularis oculi muscle
▪ Motor innervation to muscles of facial expression
▪ Taste in rostral 2/3 of tongue
▪ Inability to blink, corneal ulceration, muzzle deviation, ear droop, loss of menace
and palpebral
▪ Deficits can cause exposure keratitis – leads to lacrimation deficits (responsible
for tear production)
▪ May see deficits in animals with otitis media (runs through middle ear)
▪ Palpebral assesses this cranial nerve (and V)
o CN VIII – vestibulocochlear
▪ See vestibular signs – i.e. nystagmus
▪ Deficits can be seen with otitis media (run through middle ear)
o CN IX – glossopharyngeal
o CN X – vagus
▪ Lesion causes dysphonia, dysphagia, abnormal vocalizing, inspiratory dyspnea,
megaesophagus
o CN XI – accessory
o CN XII – hypoglossal
- Horner’s Syndrome
o 3rd eyelid protrusion, enophthalmos (retracted globe), ptosis (dropping eyelid), miosis
(constricted pupil)
▪ In cows may see regional hyperthermia, in horses see SWEATING (on ipsilateral
head and neck)
o Disruption of the sympathetic fibers to the eye (see opposite of fight/flight)
o Can be caused by idiopathic (most common), neoplasia of chest, chronic otitis,
hypothyroidism, trauma, retrobulbar disease, guttural pouch disease (horses)
- Vestibular Disease
o Central vs. peripheral
▪ With central will have vertical nystagmus and conscious proprioceptive deficits
o Clinical signs = head tilt, nystagmus, circling – TOWARD side of lesion
o PARADOXICAL vestibular disease – signs will be AWAY from lesion
▪ See peripheral signs one direction, central the other direction – lesion is on side
of central deficits
• When lesion causes vestibular signs and CP deficits – lesion is on same
side as CP deficits
- Cerebellar Disease = ataxia, usually gait appears hypermetric or exaggerated and may have a
sway
- Listeriosis vs. TEME (thromboembolic meningitis)
o Listeria monocytogenes
▪ Goats and cattle fed silage – inhabitant of spoiled silage (microaerophilic low pH
environment)
▪ Unilateral – dropped lip, lack of menace/palpebral, ptosis, drooling, fever,
dysphagia, circling
• Asymmetric cranial nerve V or XII signs – ascending infection
• Can cause abortion in cattle – fetus is autolyzed
▪ MONONUCLEAR PLEOCYTOSIS on CSF tap, microabscesses in brainstem and
cranial nerve roots
▪ Treat with procaine penicillin
▪ ZOONOTIC – foodborne illness – abortions/stillbirths in humans
o Thromboembolic Meningoencephalitis (TEME) = Histophilus somnus
▪ High fever (unlike polioencephalomalacia), may see respiratory signs before CNS
signs,
▪ NEUTROPHILIC PLEOCYTOSIS on CSF tap, xanthochromic/cloudy due to
increased neutrophils
• Xanthochromic means that there is evidence of prior hemorrhage (yellow
discoloration)
- Status epilepticus
o If in active epilepticus = diazepam RECTALLY – even in cats (some people think
causes acute hepatic necrosis)
o Idiopathic epilepsy = Beagles, Keeshonds, Dachshunds, Labs, Goldens, Shelties, Irish
Wolfhouds, Vizlas
▪ Usually 1-5 year old animal, generalized tonic-clonic seizures without interictal
abnormalities
- Head trauma
o Obtunded, most of physical exam normal
o Treatment goal = to minimize intracranial pressure need a high PaO2 – kep cerebral
blood flow relatively low without causing hypoxia
- Cushing’s reflex = BRADYCARDIA and HYPERTENSION
o Response to increased intracranial pressure (i.e. brain trauma) ! in order to perfuse
brain when there is increased ICP, the body needs ot increase systemic blood pressure
to overcome that pressure – this occurs through vasoconstriction – the increase in blood
pressure leads to decreased heart rate
o DO NOT INTERVENE TO DECREASE BLOOD PRESSURE – if you do this you might
eliminate cerebral blood flow and kill the patient
Hepatology
- Liver Bloodwork
o ALT, AST = liver specific leakage enzyme, does NOT reflect liver function
▪ AST also found in RBCs and cardiac and skeletal muscle
o ALP, GGT = hepatic enzyme induced by cholestasis
▪ ALP found in liver, intestine, kidney, bone
o SDH = liver specific in cow, sheep, horse, and goat
o LDH = found in muscle, heart, and liver
o Products of liver = bilirubin, bile acids, fibrinogen, albumin, antithrombin III, BUN (best
measure of liver function), cholesterol, glucose, coagulation factors (always do coags if
think have liver disease)
o Bilirubin in horses ! develop increased bilirubin in response to fasting (may become
icteric)
▪ Hemolysis results in increased bilirubin – damaged RBCs are removed and
hemoglobin is processed
▪ When the liver fails in the horse it is often in a hemolytic crisis as RBCs become
more fragile due to toxic metabolites in the blood – see this in TERMINAL LIVER
DISEASE
- Portosystemic shunt – in cats and dogs
o CATS = pytalism, BRIGHT ORANGE IRISES (this is pathognomonic)
o DOGS – predisposed breed = Yorkies
o BOTH = depression, lethargy, salivation, poor weight gain, aggression, failure to thrive,
hepatic encephalopathy, underweight, poor-doer
▪ Hepatic encephalopathy = head pressing, seizures, wandering, tonic-clonic
seizures after eating, circling
o Radiographs = small liver (cranial shift of gastric axis)
o Bloodwork = microcytic anemia, elevated pre and post-prandial bile acids (with shunt bile
acids can bypass liver and enter systemic circulation)
o Urinalysis = predisposed to urate stones
o ONLY veins that should enter the vena cava between the hepatic veins and renal veins
= phrenicoabdominal veins
o Treatment
▪ Lactulose – easily fermented carbohydrate that is metabolized to acid in the gut –
lowers colonic pH – keeps ammonia in ionized form (NH4+) rather than as NH3
and this form is excreted
• Cathargic and decreases GI transit time leading to decreased absorption
of ammonia
• Carbohydrate source that can be used by colonic flora as an alternative to
protein
▪ Substitute dairy and vegetable proteins instead of feeding meat proteins – feed
maximum amount of protein they will tolerate without signs of encephalopathy
▪ Oral neomycin – kills urease-producing microflora of the gut and consequently
decreases ammonia production in the gut
- Hepatoencephalopathy
o Chronic weight loss, yawning frequently, unaware of surroundings, up-to-date on
vaccinations, neuro signs
o Due to increase in ammonia, aromatic amino acids, and metacaptans to brain that
cause CNS signs
Tick Borne Disease

- Lyme Disease = Borrelia burgdorferi
o Vector = Ixodes (usually acquire it from white-footed mouse)
o Humans = erythema migrans (cutaneous rash)
o Dogs = arthritis, lymphadenopathy, fever, anorexia,
- Ehrlichia
o Canine granulocytic ehrlichiosis = E. ewingii, Anaplasma phagocytophila ! vector =
Amblyomma
o Canine monocytic ehrlichiosis = Ehrlichia canis ! vector = Rhipicephalus
o Clinical signs = fever, anorexia, edema of limbs, depression, oral vesicles, petechiation,
joint pain and swelling, aqueous flare and retinitis, hypoalbuminemia, increased ALP
- Rocky Mountain Spotted Fever = Rickettsia rickettsii
o Vector = Dermacentor
o Clinical signs = SAME AS EHRLICHIA – differentiate because RMSF’s course is over in
2 weeks
o Pathogenesis = vasculitis (why you see these clinical signs)
- Francisella tularensis = tularemia
o Cats and dogs become infected by close contact with rodents (esp. RABBITS) – vector
= TICKS
o ZOONOTIC – potential biological warfare agent (ulceroglandular, pneumonic, typhoidal)
o Dogs relatively resistant – clinical signs = depression, fever, anorexia,
lymphadenopathy, oral ulceration
- Cytauxzoon felis = CAT DISEASE
o Vector = Dermacentor
o Rapidly progressive and almost 100% fatal – dark urine, icterus, fever, prolonged CRT,
death (DIC), anemia
o Ring shaped organisms in RBCs or schizonts in spleen, liver, blood, bone marrow, or lymph
nodes
- COWS
o Anaplasma marginale
▪ TICK – but any blood feeding insect can transmit, so can needles/veterinary
instruments
▪ EXTRAVASCULAR HEMOLYSIS – NO HEMOGLOBINURIA (how you
differentiate from leptospirosis, bacillary hemoglobinuria, and anthrax)
• See in new additions to the herd – weak, depressed, staring into space,
pale, icteric, febrile
o Babesia – can see in DOGS and HORSES too – malaria-like parasite
▪ Vector = BOOPHILUS ticks
▪ Causes RBC destruction ! anemia, thrombocytopenia
▪ Greyhounds and Pitbulls predisposed
▪ Treat with imidocarb
o Heartwater disease = Ehrlichia ruminantium
▪ Vector = AMBLYOMMA – see in Africa and West Indies
▪ Fatal encephalitis in sheep, goats, cattle
o Epizootic bovine abortion (EBA) = aka foothills abortion (California foothills)
▪ Vector = Ornithodoros coriaceus (soft tick)
▪ Aborted fetus shows enlarged lymph nodes and spleen, destructive lesion to
thymus,
o Otobius megnini = soft tick with predilection for ears, cattle rub and scratch at their ears
Fungal Diseases
- Blastomycosis = Blastomyces dermatidis
o Common in Ohio, Mississippi, and Missouri River Valleys
o BELLS – bone, eyes, lymph node, lungs, skin ! skin lesions, lymphadenopathy, cough,
uveitis, boney lesions
▪ Usually doesn’t affect cats
o Broad-based budding yeast
o Treat with systemic antifungals
- Histoplasma
o Common in Ohio, Mississippi, and Missouri River Valleys
o Large bowel diarrhea
o Small intracellular yeast (small round bodies with basophilic center in mononuclear
phagocytes)
- Cryptococcosis = Cryptococcus neoformans
o Respiratory and ocular disease, facial swelling, distortion of nose (“roman nose” in cats),
lymphadenopathy
o Survives well in pigeon droppings
o Small yeast with large capsule, narrow based budding – can also diagnose by latex
agglutination
- Aspergillosis
o Branching fungal hyphae on HISTOPATH (not cytology), rhinoscopy to look for fungal
plaques
o Doliocephalics get nasal aspergillosis, German Shepherds get disseminated
o Treat with Clotrimazole (post recovery may see severe laryngeal edema)
- Coccidiomycosis = Coccidiodes immitis
o West Coast
o Similar clinical signs to Blasto – cough, lameness, draining lesions, pneumonia,
lymphadenopathy
▪ Only causes SKIN lesions in CATS
o Spherule – double-walled structure containing endospores
o Antifungals – don’t use ketoconazole in cats because causes vomiting
- Sporotrichosis
o Contagious, ZOONOTIC (esp with cat lesions!)
Parasitology
Small Animal GI Parasites
- Hookworms = Ancylostoma caninum
o = thin wall with 2-8 cells

o Dogs = anemia; humans = cutaneous larval migrans
o Treatment = NOT praziquantel – pretty much all others treat it
- Roundworm = Toxocara canis (dog), Toxocara cati (cat)
o Dog = cough in young puppy
o Transmission = transplacentally (puppies), transmammary (kittens)
o Humans = visceral and ocular larval migrans
- Tapeworm
o Echniococcus granulosus
▪ Non-pathogenic except in humans where it is fatal = hydatid cyst disease
▪ Treatment = praziquantel
o Dipylidium caninum
▪ Fleas are intermediate host, find proglottids in feces (look like white rice)
▪ Treat for fleas and tapeworms (praziquantel)
o Taenia taeniaeformis
▪
▪ Rarely causes clinical signs, get from eating infected prey
▪ Treat with praziquantel
- Whipworms = Trichuris vulpis
o Treat with fenbendazole or milbemycin oxime
- Coccidia
o Eimeria
▪ 4 sporocysts
▪ From eating rabbit feces – parasitic in birds/reptiles/herbivores, no treatment
necessary in cat/dog
o Isospora
▪
▪ Treatment = sulfadimethoxine (Albon)
o Cryptosporidium
▪ Round and slightly smaller than RBC, acid-fast or IFA stains to find these
▪ Resistant to disinfectants, humans get it from water contamination
▪ Treatment = clindamycin, azithromycin, tylosin
- Giardia
o 2 nuclei, outlined by adhesive discs, swims in “falling leaf” motion, pear

shaped, binucleate
o ZOONOTIC, treat with metronidazole or fenbedazole
o Diagnosis = trophozoites in fecal smear, IFA, giardia ELISA, cysts in fecal float
- Tritrichomonas foetus = flagellated parasite (looks like Giardia, but with one nucleus and
undulating membrane)
o Usually see in kittens with unresponsive diarrhea
o Treat with ronidazole
- Strongyloides stercoralis = threadworm
o Mucoid diarrhea and possibly anemia in kittens and puppies
o Diagnosis = Baermann fecal technique (best way to recover larvae)
- Gnathosoma = stomach worm
o 3cm long nematodes with spine-covered heads – they often vomit these up
o Need copepod (near fresh water) IH, adults live in stomach and cause gastritis
o ZOONOTIC – from ingestion of undercooked fish – gastritis, peritonitis, cutaneous or
neural migration
o Treat with albendazole
Other Small Animal Parasites
- Paragonimus kellicotti – lung worm of dogs and cats
o Crayfish and snail intermediate host
o Diagnosed by fecal sedimentation or tracheal wash – single operculum
o Treat with fenbendazole or praziquantel
- Capillaria aerophila = lung worm
o = asymmetric terminal plugs (similar to Trichuris eggs)

- Aelurostronglus abstrusus = common lungworm in cat
o Diagnose with Baermann, treat with fenbendazole
- Toxoplasma gondii = CATS are definitive host
o ZOONOTIC = infants infected in utero may have chorioretinitis and mental retardation
▪ Pregnant women should not change cat’s litter box – but if clean feces right away
should be ok because takes 1-5 days after shedding for oocysts to sporulate and
become infective
o SHEEP, kittens, pigs, dogs (NOT COWS) ! ABORTION, stillbirth, diarrhea, cough,
dyspnea, seizures, chorioretinitis, meningoencephalomyelitis, myositis
o Treatment = clindamycin
- Heartworm = Dirofilaria immitis
o Cats vs. dogs ! cats have lower adult worm burdens than dogs, in cats larvae more
likely to migrate to ectopic locations, cats are often microfilaria negative (all male
infection, occult disease), worms cannot survive as long in cat as in dog
o Wolbachia – symbiotic bacterium – treat with Doxycycline
o Prevent with ivermectin or milbemycin oxime
o Diagnosis = antigen test (detects adult female worms), Knott’s test (detects microfilaria)
o Treatment
▪ Cats = corticosteroids (NOT immiticide/adulticide because could cause
embolization and death)
▪ Dogs = melarsomine (immiticide/adulticide), and ivermectin (to kill microfilaria)
• Need STRICT ACTIVITY REST – to decrease chance of pulmonary
thromboembolism
- Dipetalonema reconditum
o Looks similar to Dirofilaria immitis – not pathogenic so must differentiate from
heartworm!
- Raccoon roundworm = Baylisascaris procyonis
o ZOONOTIC = larval migrans to the brain causing CNS disease
- Leishmania = trypanasoma
o Transmitted by sand flies
- Cuterebra = botfly
o See in cats – fistulous swelling on ventrum, erythematous and exudes small amount of
purulent material
o Eggs in environment – get on animal – heat from animal hatches eggs – larvae migrate
to SQ locations – require breathing pore in skin – eventually exit skin
o Remove in ONE PIECE – do not squeeze because rupturing larvae could cause
anaphylaxis
- Ctenocephalides felis = CAT FLEA
o Pruritis and irritation – can lead to flea allergy dermatitis – anemia, skin lesions,
tapeworm infestation
▪ DOGS can get flea allergy dermatitis too! CAUDAL HALF OF ANIMAL!
▪ Generalized military dermatitis and dark brown flecks in fur – eosinophilic plaques
• Areas of alopecia, ulceration, erythema, and pruiritis in inguinal, caudal
thigh regions
o Treat for fleas (lots of products), steroids, antihistamines, antibiotics – sometimes
hyposensitization is helpful
- Demodex canis = demodectic mange (Demodex gatoi in cats)
o Young animals = INHERITED DEFECT – do not breed – don’t treat, will clear on its own
o Adults = IMMUNE SUPPRESED – look for underlying systemic problem – treat with
Ivermectin, Amitraz, Milbemycin and antibiotics for secondary infections
▪ Amitraz (Mitaban) – only FDA approved treatment – dip that must be done in
hospital
o NON-contagious – focal areas of circumscribed alopecia and scaling – face/muzzle/
periorbital/thoracic limbs
o Diagnose by DEEP skin scrape – cigar shaped mite
- Scabies ascariasis = mite
o ZOONOTIC – though fairly host specific
o Severe pruritis around pinnae, ventral thorax, ventral abdomen, and legs – alopecia,
crusting, erythema
o Treat with ivermectin, amitraz, milbemycin, selamectin
Ruminant GI Parasites
- Haemonchus contortus
o Anemia and hypoprotenemia (NOT diarrhea) in sheep and goats – blood sucker of
abomasum
▪ Chronic weight loss, doing poorly, NO diarrhea, appear pale
o Treat with fenbendazole – may see resistant parasites if regularly give so change to
ivermectin
- Nematodirus
o Young animals with profuse watery diarrhea, anorexia, weight loss and dehydration
o Coincides with coccidiosis season in the spring
o Elliptical appearance with sharply curved poles and 2-8 blastomeres surrounded by fluid-
filled cavity
- Ostertagia ostertagii = roundworm

o Type 1
▪ Acute weight loss ( anorexia / poor growth) and diarrhea – NAÏVE cows
▪ Diarrhea in less than two year olds on pasture – a chronic disease.
▪ Occurs in winter and spring – infection with large numbers of L3 from
contaminated pastures
• EGG counts tend to be HIGH
▪ NOT associated with large numbers of larvae with few adults in the abomasum
o Type 2
▪ Chronic weight loss and diarrhea – OLDER COWS
▪ Occurs in autumn into winter
• LOW EGG COUNTS
▪ Lots of inhibited L4 that rapidly emerge – see THOUSANDS OF LARVAE IN THE
ABOMASUM
• “Moroccan leather” appearance of abomasums
o Treat with ivermectin (kills all lifestages) or fenbendazole
- Coccidiosis = EIMERIA (Isospora only affects carnivores…)

o CALF disease – can cause nervous coccidiosis in cattle less than 1 year of age( older than
21 days)
▪ Heat labile neurotoxin – usually see diarrhea followed by neuro signs
▪ Diarrhea = bloody with tenesmus.
o Treat with amprolium (Monensin, sulfa-containing drugs)
- Strongyloides spp. = intestinal threadworm

o Migrate to intestines by penetrating oral mucosa or skin, entering bloodstream, heading
for heart, traveling through lungs and trachea where they are coughed/swallowed and
enter the intestines
- Monezia = tapeworm
o Rectangular structure (or triangular)
o Usually non-pathogenic, can cause intestinal stasis
Equine GI Parasites
- Oxyuris equi = pinworm

o Anal pruritis, tail rubbing, alopecia around tail and perineal area
o Female worms crawl out of anus and cement eggs to perineal region, larvae hatch and
cause discomfort
o Scotch tape prep to look for eggs
- Parascaris equorum = roundworm (ascarid)
o Respiratory signs (because migrates through lungs and predisposes them to infection),
weight loss, diarrhea, colic (intestinal impaction) in YOUNG FOALS!
o Can cause immune mediated hypersensitivity in ADULTS
o Treat with anthelmintics – KILL THEM SLOWLY – or will cause massive die off and
impaction
▪ Likely cause if have horse that has been recently dewormed and presents
colicking
- Tapeworm = Anoplocephala magna, A. perfliata, Paranoplocephala mamillana
o GI disturbances and ulceration, unthriftiness, anemia, colic
o Treat with praziquantel, pyrantel (only effective against Anoplocephala)
- Strongyloides westeri
o Diarrhea in FOALS – transmit parasite in milk
o Treat with ivermectin or oxibendazole – give ivermectin to pregnant mare to prevent
infection in foals
- Trichostrongylus axei = small stomach worm (hairworm)
o Chronic gastritis, weight loss – penetrate mucosa causing ulceration and thickening
o Can also affect ruminants, see in horses housed near cattle
o Treat with benzimidazoles, ivermectin
- Gasterophilus intestinalis = bot fly larvae, stomach bot
o See yellowish eggs on medial aspect of forelimb cannon bones
o Usually no clinical signs – may have gastritis or stomach rupture
Ruminant and Equine Dermatology Parasites

- Hypoderma lineatum vs. Hypoderma bovis = cattle grub, heel fly, warble fly
o Female attaches eggs to hairs on feet, L1 hatch and burrow into skin….
▪ H. bovis migrates to epidural fat in spinal canal
▪ H. lineatum migrates to esophagus
▪ Then they become L2, migrate to SQ tissue of back where they become L3s and
then become …
• Nodules on dorsum with pore on top (breathing hole)
o Treat with ivermectin in early fall – emerge from back in spring, but crucial to treat in
fall!!
o Huge economic losses due to hide damage – mainly in cattle but can occur in horses
- Onchocerca cervicalis
o Dermatitis due to hypersensitivity of dying microfilaria
o Diamond shape lesions (“bull’s eye” lesion on head), ocular lesions (UVEITIS,
conjunctivitis, keratitis) due to aberrant migration of microfilaria, ventral midline
dermatitis
o Vector = Culicoides
o NONSEASONAL – non-pruritic – treat with ivermectin for microfilaria, NO treatment for
adults
- Culicoides hypersensitivity = “sweet itch”
o Saliva of gnat causes Type I hypersensitivity – very pruritic diffuse lesions
o Common in the warm months (SEASONAL), worsens with age
o Treat by decreasing exposure and steroids – antihistamines may help, topical shampoos
DO NOTHING!
o Vector for = bluetongue, Onchocerca
- Haematobia irritans = horn/face fly of cattle
o Bigger problem in cattle (reproduce in cow feces), but affects horses too – horses housed
near cattle!
o Causes ventral midline dermatitis, fairly focal lesions with wheals and crusts – crusting
on ventral midline that is NON-pruritic
- Habronema muscae = stomach worm – aka summer sores
o Larvae of worm migrate and emerge creating granulomatous lesions (eye, genitalia,
lower extremities)
▪ Inside lesions will find calicfied larvae
▪ Gastritis, eosinophilic granulomas (summer sores)
o Vector = Stomoxys calcitrans (housefly)
- Sarcoptes scabei = sarcoptic mange
o Most economically important in swine – severely pruritic, hyperkeratotic ear lesions
▪ Decreased growth, decreased milk production in cows, hide damage
▪ Around head neck and ears in horses
o ZOONOTIC and reportable – skin lesions in humans – MOST SPECIES CAN GET
THIS!
o Treat with ivermectin
- Chorioptes equi = equine mange mite
o Lesions near the foot and fetlock (esp. in draft horses) – pruritic dermatitis
- Demodex = demodetic mange
o Rare in horses (not really pruritic) – see on head, neck, and withers – diagnose with
skin scraping
▪ No treatment in horses – Amitraz in dogs but causes colic/death in horses
o Only form of mange that is NON-REPORTABLE!!
- Thelazia lacrymalis = eye worm
o Vector = Musca autumnalis (face fly of horse)
o Treat by removing manually – then add 10% levamisole drops
- Sheep keds = Melophagus ovinus
o Have six legs – they are wingless flies and the adults feed on blood
o Clinical signs = pruritis, stained wool, and potentially anemia
Ruminant and Equine Other Parasites

- LUNGWORMS
o Dictyocaulus arnfeldi = horse lungworm
▪ Definitive host = DONKEY – see in horses housed near donkeys
▪ Diagnose by Baermann (detects L1 that hatch in feces), transtracheal wash
o Dictyocaulus viviparous = horse lungworm
▪ Ingest L3 – hatch in small intestines, migrate via lymphatic’s to lungs, molt to L4,
grow to adults, cough and swallow eggs, molt in intestines, molt on ground after
being defecated
▪ Diagnose with tracheal wash, Baermann fecal analysis – not by fecal float
because too heavy to float
▪ Treatment = fenbendazole, ivermectin, levamisole, albendazole
o Dictyocaulus filarial = goat lungworm
▪ Bronchitis in goats (also Muellerius capillaris, Protostrongylus rufescens)
- Cochliomyia hominivorax = screw worms
o Eradicated from US (reportable) – eradicated by releasing lots of sterile males
o Clinical signs = myiasis – lay eggs on wounds, maggots feed on flesh creating a huge
wound
▪ May see metallic blue-green colored fly leaving the wound
▪ Sarcophaga spp (flesh flies) are another species of flies that does this to wounds
- Oestrus ovis = affects SHEEP
o Fly deposits larvae at nostrils and they migrate into nose where they develop
o Can cause sneeze, head shaking, nose rubbing, nasal discharge, stridor
▪ With heavy infestations could cause hypersensitivity response
o Cytology of nasal discharge = eosinophils and mast cells
- Hematopinus spp. = blood-sucking LICE in COWS
o Causes severe ANEMIA in calves 2-7 months old – become susceptible to pneumonia
o Diagnose by skin scraping – lice have 6 legs
- Neospora caninum
o ABORTION (4-6 months) in cattle!! – may see dog on farm that is suffering from diffuse
muscle atrophy, trouble ambulating in hind limbs (dogs have neurologic and muscular
abnormalities) – DOG = definitive host
▪ Most other abortions occur later in gestation – Brucella, Listeria, Leptospirosis
▪ Usually see autolysis of fetus with granulomas in the brain
- Sarcocystis
o S. hirsuta (CAT), S. hominis (HUMAN), S. cruzi (DOG) – all affect cattle as intermediate
host
o Lifecycle = carnivore eats cow with cyst in muscle – cysts forms sporocysts which are
shed in feces, eaten by cows – sporocysts hatch and eventually invade muscle in form
of cysts – 10 weeks!!
o In cows – fever, anorexia, salivation, weakness, muscle fasiculations, weight loss
o To prevent – prevent carnivore feces from contaminating area
- Tsetse fly = vector for Trypanosomiasis (Nagana in cattle, African Sleeping Sickness in man)
o Fever, anemia, weight loss, sleeping sickness = Trypanosoma brucei
- Reduvid beetle = vector for Chaga’s Disease = Trypanosoma cruzi
o Nervous system, digestive system, and cardiac disease
o Present in South America and some parts of U.S. – Nagana is in Africa
Porcine Parasites
- Ascaris suum = roundworm
o Migrates through liver – causing milk spots, migrates through lungs – causing thumps
(cough)
o Animal may sporadically die due to intestinal impaction, but usually not very many
clinical signs
o Necropsy = “milk spots” in liver (condemnation of meat), 20-40cm worms in intestines
o Treatment = fenbendazole (others work too)
- Trichuris suis = whipworm – MUCOHEMORRHAGIC DIARRHEA
o AFFECTS ALL AGES! – usually weaned pigs though – mucohemorrhagic diarrhea
(large bowel diarrhea)
o Double operculated egg on fecal flotation – on necropsy find eggs in cecum and colon
o To prevent give anthelmintics a week before farrowing, move to clean pasture
- Taenia solium = pork tapeworm
o ZOONOTIC – can cause cysticercosis – when eat undercooked pork!
▪ Pigs act as intermediate host by eating infected human feces – cysticerci then
form in pig’s cardiac and skeletal muscle – humans eat meat that contains cysts
and adult tapeworms develop in intestines
- Isospora suis = coccidiosis
o Diarrhea in nursing and weaning pigs – HIGH morbidity – usually affects confined 1-3
week old pigs
o Watery diarrhea, ill thrift, failure to gain weight, dehydration – other DDx for this age and
signs = E. coli
▪ To differentiate – coccidia wil not respond to antibiotics!
o Treat with amprolium – IMPROVE SANITATION!
- Strongyloides randomi = threadworm
o Transmission is transcolostrally – worms reside in small intestines of suckling piglets
o With heavy infestation see diarrhea, anemia, emaciation, death
o Treat with ivermectin, benzimidazoles
- Metastrongylus = lungworm
o EARTHWORMS are intermediate host – so to prevent keep away from soil that contains
earthworms
o Coughing, unthriftiness – may acquire secondary pneumonia and “thumps”
- Stephanarus dentatus = kidney worm
o EARTHWORMS are intermediate host – prevent access to soil that contains
earthworms
o Unthriftiness, slow growth, death – posterior ataxia/paralysis due to larvae migrating at
spinal cord
o Diagnose via urinalysis – on necropsy can find worm in kidneys, ureters, or perirenal fat
- Trichinella spiralis
o Can affect most mammals – bears, horses, rats, marine mammals, pigs
o Transmitted by ingestion of encysted larvae in muscle – infection in pigs due to eating
garbage
▪ Prevent pigs from getting it by cooking their food, preventing them from
cannibalism
o ZOONOTIC – humans get it by eating undercooked pork
Oncology
- Chemotherapeutic drugs
o Doxorubicin = adriamycin
▪ Dogs = cardiotoxic, irreversible tissue sloughing if perivascularized
▪ Cats = renal toxicity
o Cyclophosphamide
▪ Sterile hemorrhagic cystitis – encourage animal to drink lots of water, give fluids,
urinate frequently to prevent compound from sitting in bladder
o Vincristine = paralytic ileus
o L-asparaginase = anaphylaxis – because is a protein enzyme that illicits an immune
response
o Cisplatin
▪ Dogs = nephrotoxicity
▪ Cats = fatal pulmonary edema – NEVER USE IN CATS!!! “Cis-plat splats cats”
o 5-fluorouracil = neurotoxic to CATS
- Common tumor locations
o HORSE
▪ Bladder = SCC
▪ Kidney = renal carcinoma
▪ Stomach = SCC – see weight loss, colic
▪ Intestines = lymphosarcoma – VERY POOR prognosis
▪ Ocular = SCC – in ones that lack pigment in lids, older beef cattle (Herefords)
• Also get lymphoma – EUTHANIZE (meat can’t be used)
o FELINE
▪ Striated muscle = rhabdomyosarcoma
▪ Intranasal = lymphosarcoma – dyspnea due to lymph nodes compressing trachea
▪ Nasal planum = SCC
▪ Intraocular = melanoma, 2nd most common is lymphosarcoma, (ciliary body
adenomas and hemangiosarcomas are less common)
▪ Oral cavity = SCC (fibrosarcoma 2nd most common)
▪ Skin = basal cell tumor, in older cats
o CANINE
▪ Oral cavity = melanoma (1/3), SCC, fibrosarcoma, epulides
• Large cell with black melanin pigment on cytology, ONCEPT vaccine
(melanoma vaccine), usually benign
▪ Intranasal = adenocarcinoma
▪ Bone = osteosarcoma
• “Away from the elbow, towards the knee” – occur on the metaphysis (bc
cell division occurs there, metastatic at diaphysis bc blood supply there)
• Amputate + chemotherapy – because at diagnosis there are already
pulmonary mets
▪ Kidney = renal carcinoma – see polycythemia due to EPO secretion
▪ Ocular = meibomian adenoma
▪ Skin = sebaceous gland tumor (sebaceous…hyperplasia, epithelioma, adenoma,
adenocarcinoma)
▪ Spleen = hemangiosarcoma
o GOATS and SHEEP
▪ Get nasal adenocarcinoma – due to ovine/caprine nasal adenocarcinoma virus
• Expansive/destructive, not metastatic – exercise intolerance, noisy
breathing
- Types of Tumors
o CARCINOMA ! epithelial cells (i.e. skin, salivary glands, mammary glands, cells lining
most tissues)
▪ Cytology = COHESIVE CLUSTERS, see tight cellular junctions, cells often
polygonal
o SARCOMA ! mesenchymal cells (named by cell type – fibroblasts = fibrosarcoma,
osteoblasts = osteosarcoma)
▪ Cytology = isolated SPINDLE-SHAPED cells with elongated cytoplasma and
often oval nuclea
o ROUND CELL TUMORS = lymphoma, mast cell, plasma cell, histocytic, transmissible
venereal tumors
▪ Sometimes referred to as sarcomas (i.e. lymphosarcoma, histiocytic sarcoma)
▪ Cytology = large populations of cells that are not in defined clusters, round cells,
usually have unique identifiable features such as purple granules in mast cell
tumors
Renal
- Bloodwork and Diagnostics
o Elevated renal values, high specific gravity (hyperconcentrated) = pre-renal azotemia
(i.e. dehydration)
o Animals that have not been fasted or ones that have had a high-protein meal can have
an elevated BUN
o GFR = assessed by serum creatinine (rise in creatinine is proportional to fall in GFR)
o 65% = percent renal function that must be lost before a dog is unable to adequately
concentrate urine (75% in cats)
o 75% = percent of renal function that must be lost for azotemia to develop in dog
▪ HORSE = 66% of kidney must be damaged to see lab changes consistent with
renal insufficiency – isosthenuria (decreased ability to concentrate urine) –
azotemia will be seen at 75% damage to kidneys
o Urine specific gravity
▪ 1.001-1.007 (hyposthenuric) = renal function capable of diluting urine, requires
work to get here
o Indications to perform urine culture = isosthenuria (difficult to ID bacteria because too
dilute), WBCs in urine, bacteria in urine, NOT bilirubinuria
o Water deprivation test ! perform on animals that are PU/PD (after rulling out DM, renal
insufficiency, hypercalcemia, liver failure, hyperadrenocorticism, hyperthyroidism, etc.)
to determine whether the PU/PD is due to diabetes insipidus or psychogenic water
consumption
▪ Only perform in patients that have normal renal values and a low specific gravity in
the face of adequate hydration
o Azotemia
▪ Pre-renal azotemia = hypovolemia, dehydration
▪ Renal azotemia = aminoglycoside toxicity, pigment nephropathy, consumption of
oxalate containing plants
▪ Post-renal azotemia = urinary obstruction or ruptured urinary bladder
o Antidiuretic hormone (ADH)
▪ Release is stimulated by = hyperosmolality and decreased circulating blood
volume
▪ It increases renal water resorption and urine osmolality by increasing
permeability of collecting tubules
▪ Osmoreceptors in the hypothalamus detect changes in plasma osmolality and
release ADH accordingly
- Embryology
o Umbilical arteries become round ligament of bladder
o Urachus becomes middle ligament of bladder
o Umbilical vein becomes falciform
- Nervous control of bladder
o Hypogastric = sympathetic – beta receptors of detrusor muscle, alpha receptors in
internal urethral sphincter
o Pelvic = parasympathetic – detrusor muscle of bladder wall
o Pudendal = somatic – external urethral sphincter
o VOIDING = parasympathetic stimulation and sympathetic inhibition – pelvic stimulates
detrusor muscle that results in contraction of bladder and expulsion of urine
o STORAGE = sympathetic and somatic are active – hypogastric stimulates beta receptors in
detrusor muscle which causes muscles to relax, stimulates alpha receptors in internal
urethral sphincter – also external urethral sphincter contracts as result from stimulation
of pudendal nerve
- Pyelonephritis = kidney infection resulting from ascending urinary tract infection
o See bacterial or WBC casts in the urine, elevated renal values
o Fever, anorexia, depression, vomiting, pain on abdominal palpation, dysuria, pollakiuria,
hematuria, PU/PD
o Ultrasound = hydronephrosis (dilated renal pelvis), hydronephrosis of ureters, lack of
corticomedullary definition
o Need renal biopsy for definitive diagnosis
o Treat with aggressive IV fluids and antibiotic therapy – serious and life-threatening
condition
- Renal failure
o Acute vs. chronic
▪ Acute = anuria
▪ Chronic = anemia (due to decreased EPO)
▪ Both = hyperphosphatemia (excretion impaired), metabolic acidosis (low bicarb
producted by kidneys)
o Weight loss, PU/PD, anorexia
o Treatment
▪ Weekly SQ fluids and a renal diet helpful with chronic renal failure
▪ H2 receptor antagonists – decrease gastric acid secretion helping prevent
vomiting and gastric ulcers
▪ Oral phosphate binding agents (i.e. aluminum hydroxide) – prevent phosphorus
absorption in intestines
• Not a calcium based phosphorus binder because would exacerbate
hypercalcemia
▪ Often in chronic renal failure potassium starts to decrease – give RenaKare
(potassium supplement)
▪ Restrict dietary protein (and low phosphorus) – decreases formation of
nitrogenous wastes
▪ Calcium channel blocking agents (i.e. amlodipine) – palliates hypertension
o Sequelae
▪ Loss of ability to make calcitriol (the active form of Vitamin D) – calcitriol acts as
negative feedback to stop the production of PTH – thus when negative feedback
is lost the PTH becomes excessive – leads to chronic weight loss in these
patients – only supplement calcitriol if phosphorus is less than 6mg/dl
▪ Gastric ulcers – renal disease and uremia decrease mucosal blood flow and
cause gastric hypersecretion
▪ Secondary hyperparathyroidism – body’s compensation to deal with increased
phosphorus (due to decreased GFR) – body upregulates PTH which causes
decrease in phosphorus absorption in the kidneys allowing phosphorus
concentrations to return to normal early on in disease
- Urethral incontinence
o Caused by urethral hypotonicity (usually see in dogs)
o Treatment = phenylpropranolamine
- Nephrotic syndrome = occurs with protein losing nephropathies (i.e. glomerulonephritis,
amyloidosis)
o *Four components = proteinuria, hypercholesterolemia, edema/ascites, hypoproteinemia
- Renal infarct = indicative of thrombosis
o Necropsy = triangular/pyramidal shaped lesion (fanning out from medulla to cortex)
Urolithiasis
- EQUINE
o Get calcium carbonate and calcium phosphate – equine urine contains lots of calcium
▪ These form in alkaline urine
- Calcium carbonate
o Most common equine urolith
o See in sheep grazing lush pasture – clover and alfalfa contain lots of calcium and
oxalates
- Silica stones
o See in sheep that have high intake of silica in range grasses – see in dehydrated
animals
▪ Sheep and cattle grazing western rangeland
- Struvite = magnesium ammonium phosphate – made of calcium, magnesium, and phosphate
o Form in ALKALINE urine
▪ To treat give an ACIDIFYING DIET – changes in die to prevent these stones
has resulted in an increase in calcium oxalate stones
▪ Maintain USG <1.020 (dilute to prevent precipitation), low protein diet to
decrease urea
o See cocci that are urease positive bacteria and cleave urea to ammonia causing pH to
rise and make conditions even more favorable – TREAT UTI
o See in feedlot animals receiving lots of grain
- Calcium oxalate
o Common to form in ACIDIC urine
o Treat with an ALKALINIZING DIET, potassium citrate
- Cysteine
o Can’t see on radiographs
o Result of genetic defect in renal tubules, see predominantly in MALES
- Urate
o Can’t see on radiographs
o Common with PSS, DALMATIONS (defect in urate metabolism)
▪ Genetic defect in making allantoin from urates in liver, urates build up
o Treat with ALLOPURINOL (inhibits xanthine oxidase which metabolizes xanthine) –
could lead to formation of xanthine crystals
Ringworm = dermatophytosis
- Common in the winter due to crowding – healthy other than skin lesions and hair loss
- Diagnose with Wood’s lamp, fungal culture with KOH prep (definitive), DTM (dermatophyte test
media)
- Treat with topical treatments (captan/diluted bleach/lime sulfur/miconazole shampoos)
o Rarely need systemic antifungals – if use DO NOT use ketaconazole in cats because
makes them vomit
- Species
o CATTLE, GOATS ! Trichophyton verrucosum, T. mentagrophytes
o LLAMA, PIG ! Microsporum nanum
o CAT, DOG ! Microsporum canis, M. gypseum, T. mentagrophytes
▪ Hairloss and pruritis on face is common
o GOAT ! T. verrucosum
o HORSE ! T. equinum, T. mentagrophytes, M. gypseum
▪ Alopecia and pruritis on saddle/girth regions (head, neck, shoulders)
Leptospira interrogans serovar… = gram NEGATIVE

- Stains poorly so look at with dark field microscopy, microscopic agglutination test (MAT)
- ZOONOTIC – careful when handling urine
- Treat with tetracycline, vaccinate with correct serovar for the species
- Species serovars
o CATTLE = Hardjo
▪ Reproductive problems in herd
o SWINE (opossums, skunks, raccoons) = Pomona
▪ ABORTION (late term)
▪ If have infection after purchasing replacement gilts – cull replacement gilts and
vaccinate remaining pigs – because maintained by renal carriers
o DOGS = Canicola
▪ Most common serovars = Grippotyphosa, Bratislava, Pomona
▪ Acute renal failure
o RATS = Icterohemorrhagic
o SWINE, MICE, HORSES = Bratislava
o MICE (raccoons, muskrats, squirrels) = Grippotyphosa
Clostridial Diseases – gram POSITIVE

- Clostridium hemolyticum = BACILLARY HEMOGLOBINURIA, aka REDWATER
o Infection of the liver by migrating flukes (Fasciola hepatica) – results in anaerobic tracts
that allow Clostridium to bloom and cause disease
▪ Common to be near marshy areas – snail is part of liver fluke lifecycle
o Acute hemolysis, death, port wine colored urine, liver has anemic infarct, body fluids
icteric/hemorrhagic
- Clostridium chauvoei = BLACKLEG
o Ingest organism, enters bloodstream, deposits in muscle
o Acute lameness and depression, febrile, crepitant edematous swelling on muscles of
shoulder
- Clostridium septicum = MALIGNANT EDEMA
o Pitting edema that infiltrates connective tissue and subcutaneous tissue, necrosis of
damaged tissue
▪ Similar to blackleg except NO crepitus
o C. novyi type B, C. perfringens type A, C. sordelli ! all cause malignant edema
▪ Clostridium novyi type A = BIGHEAD (in rams)
• Spores enter wound through head butting – young (<9 month) old rams
develop swelling and edema of the head and neck
• Treat with wound debridement and penicillin – fatal if untreated
- Clostridium tetani = TETANUS
o Inoculation through a deep wound with a SPORE – see signs 10-14 days after injury
▪ Could be a cow that calved a week ago and had dystocia
▪ Pigs recently castrasted that are unvaccinated
▪ Lambs from unvaccinated ewes after tail docking/castration – TRISMUS
(sardonic grin)
o Erect ears, hyper-alert, stiff gait, trismus, elevated “pump-handle” tail, sawhorse stance,
lockjaw, third eyelid prolapse, extensor rigidity
▪ Causes rigid paralysis due to binding of tetanus neurotoxin to inhibitory receptors
– binds postsynaptic receptors
o Prevent by giving tetanus antitoxin (immediate protection), tetanus toxoid (protective 14
days after given)
o Treat with penicillin and muscle relaxants
- Clostridium botulinum = BOTULISM
o Toxin blocks acetylcholine release by binding presynaptic membrane
o Flaccid paralysis, rapid death (due to respiratory paralysis), tongue hanging out
o Shaker Foal Syndrome (foals 2 weeks – 6 months old) – ingest the spore, grows in their
intestines – leads to flaccid paresis/paralysis
▪ Adults only show clinical signs if they ingest the preformed toxin
- Clostridium perfringens (types A, B, and C) = CLOSTRIDIAL DIARRHEA
o Acute diarrhea in foals that results in death within 48 hours if not treated –
hemoconcentration (PCV >65%)
o Type C = PIGLETS <7 days old get hemorrhagic and necrotic enteritis – HIGH morbidity,
HIGH mortality
o Type D = SHEEP – death in lambs 4-5 months old, clostridial enterotoxemia – lambs on
rich feed
- Clostridium piliformis = TYZZER’S DISEASE – aka acute necrotizing hepatitis
o Common in FOALS (1-6 weeks old) – icterus, fever, diarrhea, jaundice, convulsions
o Hyperfibrinogenemia, hypoglycemia, increased liver enzymes, acidosis
o Randomly distributed foci of necrosis in the liver and long slender rods in hepatocytes
o Versus THEILLER’S DISEASE – serum hepatitis, serum sickness
▪ Due to administering tetanus antitoxin – to ADULT horses, causes Type III HST
• Should only give after surgery or after a wound in an unvaccinated horse
• DO NOT give to horse previously vaccinated with the toxoid!
• Give the toxoid at 3, 4, and 12 months then annually and 1-2 months prior
to foaling
o It should be repeated after wounds and surgery in a vaccinated
horse
▪ Acute diffuse necrotizing hepatitis – severe widespread hepatic necrosis
▪ Icterus, hepatoencephalopathy, malaise, weight loss – rapidly progressive and
fatal
Dentistry
- PIGS
o 44 permanent teeth
- RUMINANTS
o Dental formula = 2 (I 0/4, C 0/0, P 3/3, M 3/3) = 32 teeth
▪ NO maxillary incisors
o Aging
▪ Erupt at…in wear at…. (after eruption takes 6 months before is in wear)
• I1 = 18-24 months…1.5 years
o Fluoride toxicity
▪ If cattle are exposed to lots of fluoride at a young age it causes permanent
damage to teeth
▪ Ameloblasts prematurely reduce in size – enamel forms irregular matrix which
does not calcify
▪ Also affects bone – first palpable lesion seen on medial surface of proximal third
of metatarsals – articular surfaces are NOT affected with osteofluorosis – helps
rule in/out osteomyelitis, septic arthritis, osteoarthritis
- HORSES
o Dental formula = 2 (I 3/3, C 1/1, P 3-4/3, M 3/3) = 40-42 teeth
o Aging
▪ 5-6 months = wolf tooth (P1) erupts – is OLDEST tooth – commonly removed so
bit can fit
▪ 1 year = molar 1 erupts
▪ 2.5 year = incisor 1 erupts
▪ 4.5-5 years = canines erupt (if they ever do)
▪ 6 years = cup from I1 starts to disappear
▪ 9 years = Galvayne’s groove (longitudinal groove on I3) starts to appear
▪ 15 years = groove is halfway down tooth
▪ 20 years = groove is completely down tooth
o Float teeth on ! maxilla buccal and mandible lingual – because mandible is narrower
than maxilla
▪ Teeth continue to grow and erupt throughout horses life
o Commonly see…retained deciduous teeth, malocclusion, caudal hooks, rostral hooks
(NOT caries)
o Tooth root abscess ! common cause of maxillary sinusitis (1st molar teeth involved)
▪ See weight loss, quidding (dropping food), halitosis, unilateral purulent discharge
- CATS
o Feline odontoclastic resorptive lesions (FORL)
▪ Abnormal formation or mineralization of cementum results in cemental resorption
• Diets high in vitamin D, low in calcium/magnesium/phosphorus/potassium
▪ See evidence of endodontic necrosis on radiographs – internal and external
lesions
▪ Treat with alendronate (bisphosphonate – inhibits demineralization of bone),
extraction of affected teeth, avoid excess vitamin D
▪ Is likely other teeth will be affected in future
- DOGS
o Underbite = mandibular prognathism and maxillary brachygnathism – common in
brachycephalics
o Tertiary dentin – get from aggressive chewing, stains easily and causes teeth to look
brown, prevents exposure of pulp cavity when there is rapid wear
Reproduction
- CYCLE
o Proestrus = P4 DROPS, E2 RISES – vaginal bleeding, swollen vulva, attracts males but
doesn’t let mount
o Estrus = P4 LOWEST, E2 highest – only time female will stand to be mated, LH surge
▪ E2 causes vaginal cells to proliferate and form cornified epithelium
o Metestrus = P4 RISES
o Diestrus = P4 HIGH – when pyometra can occur
▪ P4 promotes endometrial growth, suppresses myometrial activity, inhibits
leukocyte response to infection
- PIGS
o Estrus cycle length = 21 days
▪ Reliable sign of estrus = sow stands while being mounted by boar
▪ To prevent pregnancy when using boar as estrus indicator – vasectomy or
epididymectomy
▪ To synchronize pigs = batch wean at 3-4 weeks (won’t ovulate when lactating)–
estrus in 4-6 days
• True lactational anestrus – won’t cycle until they are no longer lactating
(cats too!)
• PGF2a doesn’t work because CL is only mature and responsive for short
time in pig
• Whitten effect will not work if they are lactating
o Gestation = 113-114 days (3 months, 3 weeks, 3 days)
▪ Pregnancy dependent on OVARIAN sources of progesterone throughout
gestation
o Sows have 14 teats, dogs 10, cats 8, cows 4, sheep and goats 2
- GOAT and SHEEP
o GOAT! estrus cycle length = 21 days (duration of estrus = 1.5-3 days)
o SHEEP ! estrus cycle length = 16 days
o Gestation length = 150 days
▪ Placenta completely takes over progesterone production EARLY in pregnancy
from CL
▪ In COW – progesterone production is from the CL then augmented by the
placenta
o Breed during SHORTER DAY LENGTH – seasonally polyestrus during fall and winter
o Whitten effect = buck effect – introducing new buck causes sheep/goats to ovulate at
same time
- COWS
o Estrus cycle length = 21 days
o Estrus length = 8-18 hours (receptivity 50 hours, ovulate 24-30 hours AFTER onset of
estrus)
▪ Allows artificial insemination after estrus is over – if have post-estrual
hemorrhage means too late to breed
▪ Artificial insemination = INTRAUTERINE
o Gestation length = 9.5 months
▪ Placenta = epithelio-chorial (sow, mare, ewe, and goat)
• Retained if not passed within 12 hours – usually passed in 2 hours
▪ Placentomes = COTYLEDON (fetal), CARUNCLE (maternal)
▪ Normal fetal position = anterior presentation, dorso-sacral position, front limbs
extended
▪ Takes 40-50 days for uterus to return to normal size (25-30) with complete
histologic repair (up to 50)
o Diagnosis of pregnancy
▪ Ultrasound = 28 days (fetal gender at 58-90 days)
▪ Chorioallantoic membrane slip = 30-35 days
▪ Fetus palpable = 60 days, but may be out of reach until 4-7 months
▪ Placentomes palpable = 75-90 days
▪ Uterine artery fremitus on ipsilateral horn = 120 days
▪ Fremitus felt bilaterally = 7 months and on
o Synchronizing estrus…
▪ Give 2 injections of PGF2a 11-14 days apart – to ensure that if had immature CL
on first shot that she is synchronized on second shot – and also those that were
synchronized on first shot will have responsive CL
▪ PGF2a has no affect to synchronize if given during anestrus – need a mature CL
to work
▪ When lyse a CL with PGF2a – see estrus in 3 days
o PGF2a and Dexamethasone for abortion/induction…
▪ LESS THAN 4 MONTHS = PGF2a will lyse CL (main contributor of P4 and
induce abortion)
▪ AFTER 4 MONTHS (until 8 months) = placenta and CL contributes to P4 for few
months – use PGF2a and dexamethasone to abort in this time frame
• Never use a corticosteroid in a pregnant cow unless want to induce
abortion!!!
▪ 8 MONTHS and ON = only need PGF2a
• Placenta no longer contributes – can induce pregnancy
• Can use dexamethasone because it mimics fetal rise in cortisol – when
using dexamethasone to induce parturition it takes 48 hours for induction
of parturition
o Breeding soundness exam = sperm motility of 30%, sperm morphology of 70% normal
- HORSES
o Estrous cycle = 19-26 days – estrus = 2-10 days (on average is 6)
▪ Estrus – raising tail, frequent urination, squatting
• **Most effective way to start cycling again = provide artificial light for 16
hours per day 60 days prior to start of breeding – initiates ovarian activity
▪ Anestrus – occurs in winter, strike and avoid stallion
▪ As length of day increases at end of winter horse should return to normal cycle –
normal for horse to have inconsistent transitional period as they return to
breeding (= vernal transition)
o Gestation = 345 days (330-360) – premature if before 320 days, prolonged gestation if
greater than 365 days
▪ Most owners want them to foal in mid-January since in racing horses have
artificial birthday of January 1st
• Breed in mid-February – use artificial lighting starting in mid-December to
promote estrus in mid-February – horse is seasonally polyestrus and would
naturally start in April or May
▪ Maintenance of pregnancy = ovarian source of progesterone peaks early in
gestation and is gradually replaced by placental sources of progesterone
▪ Parturition = stage 1 is fetal repositioning into dorsosacral position, stage 2 starts
with rupture of chorioallantois and ends with birth of foal, stage 3 is passage of
the placenta
• Normal position = anterior presentation, dorsosacral position with forelimbs
extended
o Diagnosing pregnancy
▪ By ultrasound = 11-14 days
▪ Rectal palpation to detect pregnancy = day 25 – day 20-30 vesicle forms bulge –
can feel chorionic vesicle
▪ Rectal palpation to detect fetus = day 90-120
▪ Palpation of ovary location and enlarged uterine arteries = 7 months
o Uterine biopsies – performed to determine if mare can carry a foal to term – determines
amount of fibrosis present in an older mare’s uterus which indicates how able she is to
carry a foal to term
▪ Kenney categories (1-3) ! 1 = minimal change, 3 = marked changes (5%
chance of carrying pregnancy to term, but still may be abel to get pregnant)
o Spermatogenesis = takes approximately 60 days for spermatogonia to mature to sperm
– stallion with poor semen quality should be reevaluated in 2 months before making a
final judgement
▪ Oligozoospermatism = decreased numbers of sperms – old age, testicular
degeneration, testicular hypoplasia, fibrosis or testicular atrophy
▪ Acute orchitis – tends to cause morphologic or motility abnormalities in sperm
- CATS and DOGS
o DOGS
▪ Gestation = 63 days (large litters shorter gestation, small litters longer gestation)
▪ Can see fetal skeletons on radiographs = day 42
▪ Pregnancy stages
• Stage 1 = 6-12 hours (up to 36) ! pants, trembles, nesting behavior,
restless – subclinical uterine contraction and dilation of cervix
• Stage 2 = 6-12 hours (up to 36) ! abdominal straining that coincides with
uterine contraction, puppy delivery at interval of 30-60 min (up to 4 hours)
• Stage 3 = expulsion of fetal membranes and involution of the uterus –
usually passed 5-15 minutes after birth of pup before another puppy can
be delivered
▪ Thick green discharge (lochia) seen in all stages of labor, may be seen for up to
3 weeks, complete uterine involution and endometrial recovery occur in about 3
months – vaginal bleeding occurs 4-6 weeks post-whelping normally,
subinvolution can cause bleeding for 12-15 weeks
▪ Pseudopregnancy ! rise in prolactin and decline in progesterone – causes
mammary gland hyperplasia, lactation, nesting, mothering of inanimate objects
o Dystocia
▪ If hours pass since expulsion of last fetus ! give oxytocin, could also give
calcium and check viability of fetuses with ultrasound, could also perform
radiographs to look for malpositioning/malformation
▪ Brachycephalics (i.e. Boston Terriers) = predisposed due to puppies with large
heads and mothers with flattened pelvic inlets
o Mammary tumors = carcinomas – hormone-dependent
▪ 70-90% of mammary gland tumors in cats are considered malignant and majority
of them will metastasize
▪ DDx = mammary hyperplasia (usually only see in younger cats)
▪ Treatment = radical bilateral mastectomy – spay when remove mammary tumor
• Before operating do chest rads because 50% of mammary masses in
dogs and malignant
▪ Prevention = spaying a cat before 6 months of age reduces the risk of mammary
tumors by 7 fold
• Ovariohysterectomy before a heat cycle prevents hormonal effects on the
mammary glands that predispose them to developing tumors ! dogs
spayed prior to estrus are 0.05% times as likely to develop mammary
tumors as an intact dog, risk rises to 8% and 26% after one or two heats
respectively with no decrease in risk if they are spayed after the third heat
▪ Prognosis in dogs = half are benign, half are malignant – inflammatory mammary
carcinomas have a poor prognosis and cause local inflammation, dogs with
tumors greater than 3cm are considered to have a worse prognosis (2cm is cutoff
in cats)
o Ovariohysterectomy
▪ Most common complication = hemorrhage (hemorrhage of left pedicle use
mesoCOLON to retract, if right pedicle use mesoDUODENUM)
▪ Prevents = uterine neoplasia, pyometra, mammary neoplasia (if before the first
heat)
▪ Use spay hook to retrieve BROAD LIGAMENT OF THE UTERUS
o Ovarian remnant
▪ If you think your cat is spayed and then exhibits signs of being in heat…look at
vaginal cytology – if see mostly cornified epithelial cells this is confirmatory of an
ovarian remnant
• Can look at LH – if is low an ovarian remnant is likely, if high does not rule
it out
o Pyometra = occurs when dog under influence of progesterone
▪ E. coli ! most common organism – normal inhabitant of vagina, favorable
environment during diestrus (high P4, low E2) pyometra occurs
▪ Common cause in dogs older than 8 = cystic endometrial hyperplasia (CEH) –
develop from repeated exposure to progesterone, progressive thickening occurs
and glands become hypertrophied
▪ Lethargy, PU/PD, fever, tumor in caudal glands (4th and 5th)
▪ Treatment = OVARIOHYSTERECTOMY!! – can try to medically manage with
prostaglandin therapy and antibiotics (contraindicated in closed due to possible
rupture)
o Castration ! decreases ROAMING behavior, inter-male aggression, urine marking
Orthopedics
- Anatomy = from middle outwards ! diaphysis, metaphysis, epiphysis
- Salter Harris fractures = physeal fractures (commonly lead to premature closure of physis)
o Type 1 = physis
o Type 2 = physis and metaphysis
o Type 3 = physis and epiphysis
o Type 4 = metaphysis, epiphysis, physis
o Type 5 = compression/crush injury to physis
- Articular fractures
o Want…rigid fixation, anatomic realignment, early return to function (prolonged rest will
cause fibrosis and decreased range of motion of that joint)
- Hypertropic osteopathy vs. osteodystrophy
o Osteopathy – due to thoracic mass (when mass removed mass resolves)
▪ Distal extremities to proximal (metacarpal/tarsal bones affected first and may
progress to long bones) – periosteal proliferation in diaphyses
o Osteoodystrophy –
▪ Young, growing large breed dogs – may be correlated to Ca/P levels and balance
▪ VERY PAINFUL – affects metaphysis (see radiolucent lines within metaphysis –
“double physis”)
▪ Analgesia and supportive care – usually resolves on own
Ophthalmology
- Layers of the tear film
o Mucous portion – conjunctival goblet cells ! keeps tear film adhered
o Aqueous portion – lacrimal gland, gland of third eyelid ! nutrition and immunological
factors
o Lipid portion – meibomian glands ! for even spreading and prevents evaporation
- Cataracts
o Increased opacity in the LENS ! diffuse changes throughout lens
o Causes = trauma (by disrupting lens fibers or causing uveitis), most common cause in
cats = ANTERIOR UVEITIS, inherited cataracts rare in cats, aging, intraocular disease,
endocrine disease in dogs (diabetes mellitus)
o Treatment = phacoemulsification
o Incomplete vs. complete cataracts ! can see through an incomplete cataract,
incomplete cataract is not completely ossified and a tapetal reflection can be seen
through it, complete cataract is a completely opacified lens that cannot be seen through
and a tapetal reflection cannot be seen
o Incipient cataract = focal cataract, should only have minor effect on vision, does not
necessitate lens removal
o Resorbing cataract = degradation of lens proteins after development of a cataract
- Glaucoma
o Breed predispositions = purebreds, Cockers, Basset hounds, Beagles, Samoyeds
o Primary glaucoma = iridocorneal angle that becomes compromised during first few
years of life and eventually causes acute pressure spike ! decreased outflow of
aqueous leads to glaucoma because pressure increases in eye
o Secondary glaucoma = anterior uveitis (inflammatory debris plug iridocorneal angle),
intraocular neoplasia, diabetes
o Ocular pain, buphthalmos (big eye = CHRONIC), corneal edema (blue haze over
cornea), mydriasis, fundic changes (retinal vascular attenuation, tapetal
hyperreflectivity), corneal fibrosis, lens luxation, pale optic discs
o Diagnose by measuring intraocular pressures
o Treatment = increase outflow or decrease production of aqueous
▪ IV mannitol (decrease IOP through osmosis), oral or topical methazolamide/
dorzolamide (carbonic anhydrase inhibitor – decreases aqueous production),
topical latanoprost (prostaglandin analog)
o Prognosis = if have glaucoma in one eye, will develop in other eye within 6-12 months
- Anterior uveitis
o Causes = immune-mediated (lens-induced uveitis), traumatic, idiopathic, infectious,
hypertension, neoplasia
o Rubiosis iridis, aqueous flare, hyphema (blood in anterior chamber), hypopyon, keratic
precipitates, decreased IOP
o Sequelae = cataracts (CATS – inflammatory mediators break down lens proteins),
glaucoma (debris can clog angle), corneal scarring – NOT KCS (cannot extend to
lacrimal gland)
o Treatment = topical/systemic steroids (prednisone or dexamethasone, NOT
hydrocortisone), topical NSAIDs (flurbiprofen, Voltaren), systemic NSAIDs (carprofen,
flunixin), topical atropine (to relieve ciliary spasm and reduce posterior synechia
development), NOT topical antibiotics (unless infectious cause)
- Chorioretinitis
o Causes = infectious (fungi, viral, bacterial, rickettsial, toxoplasma), autoimmune disease
(uveodermatologic syndrome), systemic hypertension, lymphoma, choroidal melanoma,
coagulopathy
o Poorly defined gray spots throughout the fundus (indicated areas of cellular infiltration),
retinal hemorrhage and separation (in acute cases), hyperreflectivity (sign of previous
damage or chronic chorioretinitis)
- Anisocoria = one pupil dilated, one constricted ! can be caused by HEAD TRAUMA
- Proptosis
o Most common cause is trauma ! common in BRACHYCEPHALICS
o Treatment = replace globe, temporary tarsorrhaphy (protects eye, keeps in position
while heals – left for 3 weeks)
- Retrobulbar abscess
o Acutely painful, exophthalmos unilaterally, can be retropulsed with minimal resistance,
usually systemically ill (fever, leukocytosis, anorexia)
o Causes = penetrating wound, foreign bodies, spread from dental/sinus infection,
hematogenous spread
- Lens luxation = common in TERRIERS
o Can mechanically obstruct aqueous outflow
o Anterior luxation necessitates immediate lens removal (discomfort, uveitis, glaucoma),
posterior luxations can usually be left on floor of vitreous cavity
- Nuclear sclerosis = normal aging change to center of LENS
- Entropion = eyelid margin inverts INWARD
o Can lead to conjunctivitis and keratitis – blepharospasm, epiphora
o Fairly COMMON in foals and other young animals – usually resolves on its own as grow
o Treatment = sometimes resolves spontaneously, otherwise use local anesthetic and
evert lid and staple it (temporary fix until resolves on own), surgical correction (rarely
needed – overcorrection can cause long term problems)
- Ectropion = eyelid margin everts OUTWARD
o Can lead to exposure keratitis, very UNCOMMON in horse
- Keratoconjunctivitis sicca = abnormality of lacrimal gland and gland of 3rd eyelid
o Caused by decrease in aqueous portion of the tear film which is produced by lacrimal
gland and gland of 3rd eyelid
o Thick green ocular mucoid discharge, bilateral blepharospasm, 360 degree corneal
vascularization
o Diagnosis = Schirmer tear test (normal = 15mm/60sec)
o Treatment = cyclosporine eye drops (revereses immune mediated process, stimulates
tear production, topical steroids (reduces immune destruction of lacrimal gland)
o Causes = immune mediated adenitis (75%), trauma to lacrimal nerve, skull irradiation,
canine distemper infection
▪ Caused by these drugs = TMS, atropine, general anesthetics, EtoGesic
(etodolac)
- “Cherry eye” = prolapse of the third eyelid
o Treatment = gland replacement by Morgan pocket technique or Kaswan anchoring
technique
o Removing the gland without replacing it puts dog at increased risk of
keratoconjunctivitis sicca (KCS) becuase the third eyelid gland contributes significantly
to tear production
- Corneal ulcers
o Uncomplicated ulcer takes DAYS to heal (usually less than 5) – if it has been present for
more than a week it is considered complicated (look for source of complication)
o Treatment for complicated = conjunctival flap
o Treatment for melting corneal ucler = swab for cytology and culture (should always
assume it is infected)
- Uveal cyst vs. uveal melanoma
o Cyst = brown, round circular FREE FLOATING mass in anterior chamber – will
TRANSILLUMINATE
▪ Very spherical/ovoid and smooth
o Melanoma = brown, round circular NON-free floating mass – will NOT transilluminate
▪ Fleshier appearing
- Meibomian glands
o Adenoma = mass attached to margin of eyelid, most common ocular tumor of dogs,
usually BENIGN
o Chalazion = obstruction of meibomian gland, appears as swelling within eyelid rather
than from it
Antibiotics
- DO NOT USE IN FOOD ANIMALS (FDA rules) ! Diethyl stilbestrol, Chloramphenicol (aplastic
anemia in humans), Nitroimidazoles, Clenbuterol, Fluoroquinolones, Vancomycin, Nitrofurans,
Phenylbutazone, most sulfas, Demetridazole
o OK TO USE = penicillin (withdrawl 10 days), ionophores, sulfas (7 day withdrawl),
tetracycline (28 day withdrawl), Ceftiofur (= Naxcel, SHORTEST withdrawl of 4 days)
- Tetracyclines (i.e. doxycycline)
o Causes enamel hypoplasia and teeth staining in young animals, esophageal strictures
- Enrofloxacin
o Causes cartilage abnormalities in young animals
Food Poisoning
- *Most foodborne illness in the US is caused by viruses – 2/3 of foodborne illness in US
- Staphylococcus aureus
o Heat-stable enterotoxin – abdominal cramps/pain, vomiting, diarrhea, nausea, chills
o Usually mild illness with uneventful recovery in 1-2 days
- Campylobacter jejuni
o UNDERCOOKED CHICKEN – also in raw milk
o Diarrhea in young adults, neurologic complications are uncommon
o Guillian-Barre syndrome – acute inflammatory polyneuropathy – autoimmine disease
triggered after certain respiratory and GI infections
- E. coli O157:H7
o Enterotohemorrhagic strain of E. coli that produces Shiga-like toxins
o RAW GROUND BEEF (fecal contamination) – recent outbreaks have involved
vegetables (i.e. spinach)
o Severe acute hemorrhagic diarrhea, abdominal cramps, hemolytic uremic syndrome
(HUS)
▪ Illness usually resolves in 5-10 days
▪ Children and elderly predisposed to developing HUS – leads to renal damage/
failure
o In cattle = NO SYMPTOMS, usually get from nearby vegetable farm that is
contaminated
▪ To ID carriers – send stool to lab for O157:H7 fecal culture from random sampling
of cattle
• Grown on sorbitol-MacConkey agar (SMAC) – able to ferment sorbitol
- Clostridium botulinum
o HONEY – source of clostridial spores, do not feed infants honey = infant botulism
▪ Persistent constipation, floppy arms/legs/neck, weak cry due to muscle
weakness, weak suckling, lethargy, difficulty breathing, nervous system signs
- Listeria monocytogenes
o Grows slowly in refrigerated foods – psychrophilic (grows at low temperatures)
o Causes abortions or stillbirths in humans – also CNS signs (fevers, muscle aches)
- Yersinia enterocolitica
o Acute severe ABDOMINAL PAIN and fever (gastroenteritis) – less acute pain think
Trichenella spiralis
o Likely get it from PORK?
- Mycobacterium bovis = TUBERCULOSIS in CATTLE!
o Humans get from drinking raw unpasteurized milk! – controlled in US by pasteurization
▪ Other organisms in milk = Mycobacterium avium ssp paratuberculosis, Brucella
abortus, Salmonella dublin, Listeria monocytogenes
o Can control by testing and CULLING positive cattle from herd (report if see in cattle) –
but wildlife (deer) are also a resevoir – make eradication difficult
- Shigella
o Bacillary dysentery in humans – PRIMATE DISEASE
- Vibrio cholera
o SHELLFISH – causes GI signs in humans
Rabies = rhabdoviridae family, genus lyssavirus (bullet-shaped, enveloped)

- Maintained in wildlife reservoirs = skunks, raccoons, coyotes, foxes – transmit through saliva by
biting
- Stages
o Prodromal stage – change in behavior, voice change, attacked by wild animal
o Furious/excitable stage (1-7 days) – irritable, excitable, photophobia, hyperesthesia,
attacks imaginary objects, drooling, seizures, coma/death
o Paralytic/dumb stage – flaccid paralysis
- Clinical signs in farm animals = anorexia, depression, ataxia, aggression, single region of
pruritis and alopecia
- Diagnose by….Negri bodies in carnivores, Purkinje cells in herbivores – definitive diagnosis by
direct IFA
- Vaccination Protocols
o For dogs ! vaccinate at 3 months (no earlier because of maternal antibodies), booster
at 1 year, then every 1-3 years
o For horses ! vaccination is NOT required by law and only recommended in endemic
areas
▪ In endemic areas boosters are usually performed annually
- Protocols
o Humans
▪ Unvaccinated = inject human rabies immunoglobulin follwed by 5 injections of
approved rabies vaccine over one month
▪ Vaccinated = two injections of approved rabies vaccinem
o Cats, dogs, ferrets
▪ For pets suspected of having been bitten by wild animals
• Vaccinated = vaccinate immediately and quarantine for 45 days
• Unvaccinated = euthanize OR quarantine for 6 months then vaccinated 1
mo before release
▪ For pets that have bitten humans
• Strays = euthanize and test
• Vaccinated = confine and observe for 10 days
• Unvaccinated = euthanize and test OR quarantine for 10 days in approved
facility
Camelid Diseases
- Parelaphaostrongylus tenius = MENINGEAL WORM (aka deer worm)
o LLAMA DISEASE – definitive host is white tailed deer
o Ataxia, hindlimb paresis that progresses to forelimbs, muscle weakness, paralysis,
circling
o CSF tap = eosinophilia
o Intermediate host: snail
- Choanal atresia
o ALPACA DISEASE – opening between nasal and pharyngeal area blocked by
membranous tissue and/or bone
o See in young alpacas ! difficulty breathing and nursing, cyanosis, weakness, lack of
weight gain, aerophagia
o EUTHANIZE – usually also have polydactyly, cardiac/renal/other organ deficits
- Whipworm
o CS: weight loss, poor BCS, diarrhea. Mos common cause of diarrhea in adul camels
o Tx: panacur (fembendazole), ivermectin NOT effective
Fish Diseases
- Anatomy = 2 chambered heart, nucleated RBCs
- FDA approved anesthetic = Tricaine methanesulfonate (MS222) – 21 day withdrawl before fish
can be eaten
- FDA regulates SALMON, USDA regulates CATFISH
- Ich = Ichthyophthirius multifilis
o Fish swim erratically, white spots on skin/gills
- Aeromonas salmonicidia = furunculosis of salmonids, goldfish ulcer disease, carp erythrodermatitis,
trout ulcer disease
o Most common bacterial pathogen of fish worldwide!
- Whirling disease = Myxobolus cerebralis
o Fish swim erratically, deformed around head and spine – RAINBOW TROUT
o Histopath = diffuse necrosis of cartilage and spores in cartilage
- Hole-in-the-Head disease = HERPES – aka Channel Catfish Virus
o CATFISH – swim erratically, spin around, and eventually die
- Gill rot = Branchiomyces sanguinis and B. demigrans
o CARP and EELS – respiratory distress due gill necrosis caused by thrombosis of blood
vessels in gills
- Enteric redmouth disease = Yersinia ruckeri
o BENIGN disease, LOW mortality
- Columnaris disease = Flexibacter columnaris – aka peduncle disease, fin rot, black patch necrosis,
cotton wool disease
o Whitish plaques that may have red peripheral zone which then become erosions/ulcers,
necrosis of skin!
- Mycobacteriosis
o Common chronic disease in aquarium fish – skeletal deformities, ulcerations/erosion of
fin
- Lymphocystis disease = iridovirus
o Saltwater and freshwater fish – cauliflower growths on skin, fins, and gills
Primate Diseases
- Old World Monkeys = Colobus, Proboscis, Mandrill
o Sex skin, opposable thumbs, ischial callosities for sitting – DO NOT have prehensile tail
- New World Monkeys = lemurs, squirrel monkeys
o Have wide nasal septum
- Transmitted from primates ! humans = Herpesvirus B, Salmonella, Tuberculosis
o Herpes simiae (= Herpes B) – nonpathogenic in macaques but fatal encephalitis in man
▪ Transmit by bite/scratch, macaques are most frequent carriers
▪ Can cause mild cold sore like lesions in monkeys
- Transmitted from humans ! primates = Rubella (measles – can die!), tuberculosis (Old World
Monkeys)
o To test for tuberculosis in monkeys = intradermally in eyelid (so can read from a
distance)
Small Rodent Diseases

- Antibiotics in Rodents
o DON’T use ! streptomycin, penicillin, ampicillin, bacitracin, lincomycin, vancomycin,
erythromycin, clindamycin
▪ Can cause clostridial entertoxemia because GI tract is primarily GRAM + and
antibiotics with gram + spectrum disrupt normal balance of flora and allow for
growth of clostridial organisms
o USE ! ENROFLOXACIN, CHLORAMPHENICOL, TMS – use these because prone
to entertoxemia from others that disturb their intestinal flora
RABBIT DISEASES
- Anatomy = INDUCED OVULATOR, heat dissipation through ears (can’t sweat), 2 uterine horns,
2 cervices, require 120ml/kg/day of water (much higher than dog/cat)
- Dental formula = 2 (I 2/1, C 0/0, P 3/2, M 3/3) – diasterna between incisors and premolars
o All teeth open rooted and continuously growing – so lots of problems with malocclusion
▪ Lethargy, inappatenance, grinding teeth, absent GI sounds, painful abdomen with
no formed feces
▪ Usually fed only pellets and occasional lettuce – change diet to leafy greens and
decrease pellets/seeds
▪ Radiographs = uneven occlusal surface (improper angle of incisors), root
elongation of premolars/molars
- Bladder stones = calcium carbonate
o Rabbits absorb calcium through their GI tract at same rate of Ca in their diet regardless
if they need it or not
- Snuffles = Pasteurella multocida
o Upper respiratory signs = mucopurulent discharge, sneezing - can also cause enzootic
pneumonia, otitis media/interna, conjunctivitis, meningitis, encephalitis, reproductive
tract infections, abscesses, septicemia, rhinitis/sinusitis (NOT typhlitis)
- Vertebral fracture
o Acutely down in hindlimbs, dribbling urine, no withdrawl in hindlegs – usually dropped
by children
o Common site in caudal lumbar region = L7
- Uterine adenocarcinoma
o Common neoplasia of female rabbits – very high incidence in intact rabbits – SPAY
THEM!!!
o Hematuria, anorexia, weight loss, depression, dysuria – distinguish hematuria from
porphyrinuria
- Syphilis = Treponema paraluis cuniculi
o Sexually transmitted – skin lesions around vent, NO hematuria
- Psoroptes cuniculi = rabbit EAR mite
o ONLY species of Psorptes NOT REPORTABLE
o Scratching at ears, crusts and exorciations in ears (severe crusting and inflammation in
external canals)
o Treat with ivermectin, selamectin – NOT NOT NOT NOT Fipronil (Frontline) – VERY
toxic to rabbits
- Cheyletiella parasitovorax = rabbit FUR mite
o White flakes (resembles dandruff) – shedding, scaling, dandruff on dorsum
o Can infect dogs, cats, and humans
- Encephalitozoon cuniculi
o Neurologic and renal disease – infects LENSES and causes phacoclastic cataracts (can
break through lens capsule) and uveitis
o Remove lens with phacoemulsification (for cataracts), oral albendazole, topical steroids
(for uveitis)
- Trichobezoar = hairball stuck in stomach
o Weight loss, anorexia, scant stool production – predisposed to development if they have
decreased GI motility
o Supportive care, syringe feed high-fiber food, hope they pass without surgery
CHINCHILLA DISEASES
- Need DUST BATHS every 1-2 days to maintain coat health – too frequent of bathing can
cause conjunctivitis
- Heat intolerant – do not keep enclosure hotter than 80F
- Do not use cedar shavings – cause respiratory irritation
- DO NOT require supplemental Vitamin C, do not require dental adjustments (though dental
disease is common)
GUINEA PIG DISEASES
- Metastatic mineralization = incidental finding at necropsy
- Dental abscesses = associated with malocclusion
- Bordetella bronchiseptica
o NEVER HOUSE RABBITS and GUINEA PIGS TOGETHER! Is a normal inhabitant in
oropharynx oc rabbits but pathogenic to guinea pigs (respiratory distress, weight loss,
sudden death)
- Hypovitaminosis C = SCURVY
o Anorexia, painful/swollen stifles, loose incisors/dental malocclusion, rough haircoat,
petechiations
o Often fed only Timothy hay – leads to collagen defects with painful/swollen stifles most
common sign
o They lack enzyme to convert glucose to ascorbic acid ! have dietary requirement for
Vitamin C
o Treat with Vitamin C injections (not multivitamins, could lead to A/D toxicosis), leafy
greens
RAT DISEASES
- Lifespan = 2.5 years
- Tyzzer’s disease = Clostridium piliforme
o See in RABBITS, mice, and hamsters – usually subclinical infection unless rodent is
stressed/immune-suppressed
o Diarrhea, kyphosis, poor haircoat, death
o Histopath = focal areas of hepatic necrosis and inflammation of terminal ileum
- Cilia-associated respiratory bacillus (CAR) infection = associated with Mycoplasma pulmonis
o Severe bronchiestasis, pulmonary abscesses, atelactasis – GOOD HUSBANDRY
PREVENTS!!
- Murine respiratory mycoplasmosis (mice and rats) = Mycoplasma pulmonis
o Nasal discharge, ataxia, coughing, sneezing, dyspnea, head tilt, incoordination, circling
▪ Due to inflammation of respiratory tract and inner ear
o Treat = oxytetracycline in water
- Pseudotuberculosis (mice and rats) = Corynebacterium kutscheri
o Caseous purulent foci in lungs when stressed – dysnpea, oculonasal discharge, rough
hair coat, hunched posture
o Cytology = “Chinese character” formation of impression smears
- Ringtail = annular constriction of tail (dry gangrene, fall off) in weanling rats kept in wire-bottom
cages
o To prevent – keep temperatures 70-74F, DO NOT use wire bottom cage, provide
nesting material, increase humidity
o Factors contributing – increased temperatures, low humidity, impaired blood supply to
tail, drafts
- Sialodacryoadenitis = coronavirus
o Rat bleeding from eyes, exophthalmic, squinting, corneal drying can lead to corneal
ulcers, swollen face and neck, red discharge from eyes (porphyrin pigment – secreted
from Harderian gland in times of stress)
o Causes inflammation and necrosis of salivary and nasolacrimal gland
o Treatment = self-limiting, resolves within 2 weeks
- Mammary tumors
o BENIGN – fibroadenomas – can be anywhere based on extensive nature of mammary
tissue (females and males)
o Surgical excision is good for well-being of rat
MICE DISEASES
- Lifespan = 1.5 years
- Mammary tumors = associated with RNA retrovirus
o MALIGNANT – anaplastic and invasive – surgical exision DOES NOT have good
prognosis
o Can be found on dorsum – found at nearly any SQ part of body due to extensive nature
of mammary tissue
- Barbering of hair by cagemate = common in pigmented mice
o Black mouse presents with alopecia that started on the face and moved to trunk – other
mouse in cage normal
- Sendai virus
o Causes respiratory disease – leading to pneumonia, weight loss, dyspnea, chattering,
and mortality
▪ Usually subclinical in rats and hamsters
o VERY contagious, difficult to control
- Trichophyton mentagrophytes = ringworm (mice and rats)
o Patchy alopecia and flaking on head
o Treatment usually not necessary since is self-limiting – griseofluvin is useful antifungal
- Lymphocytic choriomeningitis (LCM) = RNA arenavirus
o EUTHANIZE colony because is zoonotic concern
- Transmissible murine colonic hyperplasia = Citrobacter freundi strain 4280
o Mice 2-4 weeks old, adults show no signs ! anorexia, dehydration, diarrhea
o Histopath = thickening and inflammation of colonic mucosa
o Highly contagious and self-limiting – treat with neomycin or tetracycline’s
-Rotavirus infection
o See in mice 1-3 weeks old ! soft yellow diarrhea that stains and dry around anus
causing obstipation and death
o Can use electron microscopy to ID the virus
o To treat – clean and remove infected feces
- Pinworms = Syphacia obvelata, Aspicularis tetraptera
o Heavy parasite load could result in rectal prolapse – inhabit the cecum, usually
subclinical infection
o Treatment = piperazine sulfate, ivermectin
HAMSTER DISEASES
- Lifespan = 2 years
- NOT an induced ovulator (unlike ferret, cat, rabbit)
- Bilaterally asymmetric intermittent swollen cheeks = FOOD STUFFED IN POUCHES
- Proliferative ileitis = Lawsonia intracellularis
o Young (3-10 week old) hamster with wet tail, lethargic, dehydrated, depressed,
dehydrated
o AGGRESSIVE treatment = SQ administation of 50ml/kg electrolyte/glucose solution,
enrofloxacin and TMS to treat bacteria – sometimes give bismuth subsalicylate for
persistant diarrhea
o GRAVE PROGNOSIS
- Amyloidosis = common renal disease in hamsters, no effective treatment
Ferret Diseases
- INDUCED OVULATOR – estrogen toxicity can occur if remain in estrus and not bred – lead to
aplastic anemia and bone marrow suppression
- Heat stroke = lethargic, inappetant, barely walking, BG = 71 mg/dl – other DDx = insulinoma
but BG is normal
- Diet = STRICT carnivores (need meat proteins and fats)
o LOW in fiber, high levels of plant proteins associated with urolithiasis, highly digestible
due to short GI
o FATAL hypoglycemia if have insulinuoma and fasted longer than 6 hours
- Cystic calculi = STRUVITE most common, but overall they are uncommon in ferrets
- Proliferative bowel disease = intracellular bacterium (formerly Campylobacter-like, related to
Lawsonia in pigs)
o Prolapsed rectum, chronic diarrhea, weight loss, green stool containing mucous
o Histopath = thickened intestines, enlarged mesenteric lymph nodes
o Treatment = antibiotics (susceptible to Chloramphenicol)
- Adrenal tumor
o Secrete ESTRADIOL – vulvar hyperplasia (females), hair loss (truncal alopecia),
pruritis, behavior changes
▪ Prostatitis/paraprostatic cysts (males) – stranguria, bilaterally symmetric alopecia,
pruritic
o Treatment = adrenalectomy, mitotane and ketoconazole are NOT successful in reducing
clinical signs
▪ Trilostane – increases 17-hydroxyprogesterone which is already elevated in
these patients
- Insulinoma
o HYPOGLYCEMIA – bouts of lethargy, dragging pelvic limbs, acute onsets of ataxia,
salivation, seizures
o To diagnose take blood glucose when they present, then insulin level
- Lymphoma
o MEDIASTINAL and MULTICENTRIC (NOT GI)
o Common ferret tumors = insulinoma, adrenal tumor, mast cell tumor, lymphoma
(melanoma is rare)
Reptile Diseases
- Anatomy = nucleated RBCs, 3 chambered heart (2 atria, single ventricle with incomplete
septum), no bladder (snakes)
o Renal portal system – blood from caudal half of body passes through kidney before
going to heart
▪ DONT GIVE GENTAMICIN IN CAUDAL HALF OF BODY!! NEPHROTOXIC
(aminoglycosides)
- Raw fish diet = neurologic signs
o Contain thiaminase – leads to vitamin B1 deficiency – weight loss with a good appetite
and neurologic signs
o Supplement with vitamins for treatment
- Metabolic bone disease = secondary nutritional hyperparathyroidism (imbalances in calcium,
Vitamin D3, phosphorus)
o Causes = low calcium, lack of UV light, vitamin D deficiency
▪ Lead to calcium being resorbed from bone in order to maintain serum levels –
weak/pliable bones
▪ Need full spectrum of UV light for conversion of inactive vitamin D to vitamin D3
in the skin – need Vitamin D3 for proper calcium absorption and metabolism
o Poor growth, osteopenia, fractures, pliable mandible/maxilla, bowing of long bones
o Treat by giving Vitamin D3 every 4 weeks (overdose can cause soft tissue
mineralization)
- Dysecdysis = inability to shed fully
o Usually due to inadequate humidity, lack of abrasive substrate to rub against, stress
(ectoparasitism), nutritional deficiencies, systemic disease
o Snakes get retained spectacles – do not use forceps to peel off eyecaps or can cause
corneal damage
o Treatment = increase humidity (humidity chamber), apply ophthalmic ointment, search
for underlying cause
- Cryptosporidium
o Regurgitation, weight loss, debilitation – NO effective treatment (euthanize due to
zoonoses)
o Thickening of GI mucosa and loss of motility – acid-fast staining
- Infectious stomatitis = Aeromonas spp., Pseudomonas
o Petechiation and caseous material build up in mouth
o Treat by debridement and antibiotics
TURTLE DISEASES
- DO NOT GIVE IVERMECTIN – crosses blood brain barrier and causes neuro signs (paresis,
paralysis, death)
- Integument
o Burned on DORSUM from heat-emitting bulbs
o Chemical exposure wounds when cage not rinsed after cleaning on VENTRUM
o Prey wounds when fed live prey
o Ectoparasites uncommon in reptiles, mite infestation causes scale loss or erythema
- Hypovitaminosis A
o Causes RESPIRATORY INFECTIONS – nasal discharge, dyspnea, open mouth
breathing, edema of eyelids, secondary infections of skin/eyes/respiratory systems (usu
Aeromonas and Pseudomonas)
▪ May also see renal disease, squamous metaplasia of epithelium, swelling of ears,
anorexia, lethargy
o Common in turtles fed imbalanced diet of fruits and insects
o Treatment = nebulization, hotter temperatures, vitamin A supplementation, antibiotics,
drain tympanic membranes
- Septicemic cutaneous ulcerative disease (SCUD) = Citrobacter freundii
o Pitted scutes that slough with underlying purulent exudate, petechia on skin and liver
necrosis
o Prevent with good husbandry, treat with chloramphenicol
- Malocclusion
o Difficulty eating, overgrown beak, history of metabolic bone disease causing distortion
of skull
o Treatment = NOT supplemental calcium (won’t help since skull fully formed), long term
corrective trimming because usually keeps recurring
SNAKE DISEASES
- Ulcerative dermatitis
o Predisposing factors = humid environment, skin lesions, exposure to feces, inadequate
UV light
o Erythema, necrosis and ulceration of the dermis, exudative discharge
o Secondary infections with Aeromonas and Pseudomonas can lead to septicemia and
death
o Treat by improving hygiene and antibiotics
- Inclusion body disease = retrovirus?
o Regurgitation, inability to right itself – transmitted by Ophionyssus natricus (maybe?)
- Meningitis = BACTERIAL
o Stargazing, mentally obtunded, twisted cervical positioning
o Supportive care, antibiotics, corticosteroids to decrease inflammation
- Entamoeba invadens
o Severe GI signs and death – weight loss, vomiting, hemorrhagic diarrhea, anorexia
o Housed with TURTLES – carriers but clinical unaffected – DO NOT HOUSE TURTLES
and SNAKES together
o Metronidazole can be used to treat (protozoa)
IGUANA DISEASES
- Normally have DARK RED TONGUE – advise owners not to be alarmed by this
- Gravid female = change in behavior (hyperactivity, irritability, stopped eating, enlarged
abdomen) – Nov-June
- Cystic calculi
o Straining to urinate, hematuria, radiographs show round calculi
o Change the diet, surgery to remove if too large to pass
- Gout = primary overproduction of uric acid or inability to excrete uric acid (renal failure)
- Renal failure
o Iguana on HIGH PROTEIN diet – signs due to hypertension due to renal failure
o Episcleral injection, swelling of pharyngeal region, pain on palpation of abdomen
- Tail trauma
o Remove tail by snapping at place of least resistance – once has lost circulation it is
more comfortable if its removed
Exotic Bird Diseases
- Anatomy and Clinical Information
o 4 chambered heart (same as mammals) – heterophils instead of neutrophils, nucleated
RBCs
o Complete tracheal rings, 9 air sacs (countercurrent airflow exchange at level of lungs,
no diaphragm)
▪ If present with swollen distended neck = ruptured cervical air sac
o Ulna bigger than radius, pneumatized bones (humerus, femur) ! IO catheter in ULNA
or TIBIOTARSUS
o Uric acid excretion = way to excrete nitrogenous waste (reptiles do this too)
o Striated muscle controlling iris
o Fused lumbosacral region = synsacrum
o Rachis = main shaft or axis of feather (what you cut when you trim wings)
o Aptera = featherless tracts, one on neck is good place to draw blood from jugular
o Rhamphotheca = horny sheath of keratin that covers boney beak
o Choana = passasge of air from nasal system to oral cavity, slit-like structure on roof of
mouth
o Esophagus lies on right side of neck – tube feed on this side
o Male ZZ, Female ZW – opposite mammals – sexual dimorphism (male eclectus green,
female red)
o Regurgitation on owner is normal courtship behavior, may regurg at themselves in a
mirror
o Can safely draw up to 1% of birds weight in blood = 100mg bird can draw 1ml from
o AVOCADOS – toxic to parrots – cause myocardial necrosis
o SQ fluids = skin fold in groin, between scapula on back (NOT lateral neck because want
to avoid air sacs)
o To stop broken blood feather from bleeding = pull the feather
o Liver specific values in birds = bile acids, AST (also in muscle cells and elevated with
CPK with muscle disorder)
o Cytology of feces from psittacine = 200 bacteria per high power field (60-80% gram +
cocci, 20-40% gram + rods, a few normal yeast) ! 2/3 gram + cocci, 1/3 gram + rods
▪ Problem when absence of bacteria, detection of WBCs, shift from gram + to gram
-, high number of budding yeast = signs of immunosuppression/infection
- Calcium deficiency
o Calcium, phosphorus, vitamin D3 imbalance ! osteoporosis, acute hypocalcemia
(weakness, tremors, seizures), egg binding, rickets, splayleg (NOT proventricular
dilatation)
▪ Excess vitamin D3 can cause mineralization in tissues, particularly the kidneys
▪ Signs = fluffed at bottom of cage, decreased appetite, red tissue from vent,
history of laying eggs
o See in birds fed ALL SEED DIETS
o Treat with fluid support and calcium supplementation
- Hypovitaminosis A
o Squamous metaplasia of mucous membranes and glands (oral mucosa, conjunctiva,
upper airways, nasolacrimal duct, GI tract) – glands can be converted to squamous
epithelium with keratin material and can look like absecesses or pustules but are
essentially keratin cysts
▪ Important in epithelial maintenance, vision, skeletal development – see in
animals fed ONLY SEEDS
o Severe dyspnea, respiratory signs, white papules in oral cavity, poor feather quality,
respiratory distress, renal disease, blunted choanal papilla ! Amazons VERY sensitive
to this condition
o DDx for white plauqes in mouth = pox, Candida, Trichomonas, capillaria, papillomatosis
- Xanthoma = accumulation of friable yellow fatty tissue, benign growth composed of lipids and
cholesterol
o COCKATIELS, BUDGES, COCKATOOS – non-aggressive, but can become locally
invasive and cause irritation and self-mutilation
o Will see yellow mass on tip of wing and/or breast, FNA reveals macrophagic
inflammation with cholesterol clefts
- Hepatic lipidosis
o Baby birds get when fed formula high in FAT (supplemented with peanut butter or oil) –
respiratory distress, heavy for their age, dyspneic
o Treat with cooling and oxygen therapy
- Cloacal papilloma = common GI tumor of birds (Amazons, Macaws) – virus?
o Cloacal prolapse with small fleshy proliferations = pink tissue blanches white with 5%
acetic acid solution
o Treat with surgical removal or chemical cautery
- Renal adenocarcinoma
o History of polydipsia, weight loss and progressive unilateral leg lameness (compression
on ischiatic nerve)
o Palpate abdominal mass, take radiographs to confirm
- Goiter = thyroid hyperplasia
o Iodine deficiency – voice change, stertor or wheezes due to pressure on syrinx,
regurgitation, engorgement of right jugular vein, palpate gross enlargement in neck that
feels like soft tissue
- Proventricular dilatation disease = avian bornavirus (ABV) – aka PDS, PDD, Macaw Wasting
Disease
o NEUROTROPIC – affects nerve cells of intestines – chronic weight loss, regurgitation,
passage of undigested seeds, nevous signs (ataxia, abnormal head movements)
o Enlarged proventriculus on radiographs, histopath of proventriculus =
lymphoplasmacytic ganglioneuritis
- RBC parasites = intraerythrocytic parasites = hemoproteus, plasmodium, leukocytozoon,
trypanosoma
o Plasmodium
▪ Transmitted by mosquitoes, on blood smear see nucleus of RBC pushed to
periphery
▪ Commonly affects passerines – often asymptomatic but may cause hemolytic
anemia
o Leukocytozoon
▪ Common in birds of prey – anemia in birds that are immunosuppressed
▪ VERY UNCOMMON in household psittacines
- Synovial gout
o When uric acid crystallizes in synovium causing lameness – shifting leg lameness,
inability to bend toes
o On aspirates may see spindle shaped crystals, on bloodwork may see elevated renal
values (due to renal disease)
o Treatment = allopurinol (to decrease uric acid formation), low-protein diet, address
underlying disease
- Hemosiderosis = aka hemachromatosis – too much IRON accumulates in liver and other
organs
o Common in TOUCANS and MYNAH BIRDS – history of poor feathering & overgrown
beak, lethargy, weight loss
o Bloodwork = elevated liver enzymes and bile acids, serum iron levels/plasma iron
binding are inconclusive
▪ Need LIVER BIOPSY to confirm diagnosis
- Egg bound = inability to expel egg from cloaca
o Contributing factors = obesity, nutrition, history of prolonged egg laying, hypocalcemia
(demand for calcium to make egg shell is VERY high, but also needed for muscle
contraction of reproductive tract)
o Abdominal straining, recent history of egg laying, obese, distended coelomic cavity (see
egg on radiographs)
o Treatment = oxytocin, place in warm/dark environment, calcium administration, gentle
manipulation with lube
▪ DO NOT jump right to surgery
- Egg yolk peritonitis
o Can be fatal – recent anorexia and dyspnea, fluffed feathers, coelomic distention
o Bloodwork = heterophilia, increased AST/CK/fibrinogen
o Treat with antibiotics, surgery, anti-inflammatories
- Capillaria = intestinal parasite that may cause diarrhea or weight loss
- Aspergillosis = Aspergillus fumigatus
o Common in raptors, penguins, and waterfowl, but NOT in psittacines – except with
stress, immunsuppression, etc.
o Inhale spores – causes long standing respiratory disease
o Histopath = white plaques on air sacs, caseous plugs in distal trachea
o Treat with amphotericin B or -azoles
- Giardiasis
o Feather pulling in cockatiels, death, emaciation in face of polyphagia, wet voluminous
feces
o Treat with metronidazole
- Pacheco’s disease = herpesvirus
o Highly acute and fatal disease of pet birds – causes ACUTE LIVER NECROSIS !
lethargy, anorexia, ruffled plumage, irregular yellow diarrhea, sudden death – NOT
emaciation (because quickly progresses to death)
o Highly contagious – often see in birds with recent change in environment (i.e. import,
quarantine, pet shop)
o Histopath = ESOINOPHILIC INTRANUCLEAR INCUSION BODIES in spleen and liver
- Psittacosis = Chlamydophila psittaci (REPORTABLE and ZOONOTIC) – aka Parrot Fever
o Respiratory and liver disease ! increased respiratory effort (due to air sacculitis),
weight loss, anorexia, lime-green urates, VERY HIGH WBC counts (2-10 times normal)
o Histopath = hepatomegaly, splenomegaly, air sac changes, fibrinous pericarditis
o Treatment = tetracyclines (i.e. doxycycline), treat for AT LEAST 45 days!
o ZOONOTIC – owner may have fever, chest tightness, sore throat
- Polyoma virus
o YOUNG (nestling) – delayed feathering, diarrhea, GI stasis, ascites, SQ hemorrhage,
melena/hematuria/green urates
o Histopath = pale mottled spleen/liver with white pinpoint foci, petechiations/ecchymoses,
intranuclear inclusions
o Prevent with vaccination
- Tuberculosis = Mycobacterium avium
o Chronic weight loss – on histopath = enlarged liver with diffuse white nodules,
granulomatous inflammation and acid-fast bacilli
o Treat with azithromycin – treatment controversial because of zoonotic potential
- Psittacine beak and feather virus
o Feather dystrophy, “powder loss”, irregular beak, nails also affected
o DDx = Cnemidocoptes (honeycomb-like beak), liver failure (always rule out with beak
abnormalities)
- Candidiasis = Candida albicans
o Thickening of crop mucosa, overgrowth of yeast in crop, secondary bacterial infections
o Predisposing factors = prolonged antibiotics, spoiled feed, vitamin A deficiency, YOUNG
birds
o Regurgitation, unthrifty, underweight, crop stasis, malabsorption syndrome
o Treatment = nystatin, itraconazole, fluconazole, vitamin A supplementaiton
- Trichomoniasis
o White caseous lesions in oral mucosa – common in falcons, raptors, and pigeons
o See motile trophozoites on saline smear, treat with metronidazole
- Heavy metal toxicosis
o Acute onset of lethargy, depression, PU/PD, hemolysis (red plasma after centrifugation),
anorexia, bright red droppings, history of chewing on windowsill
▪ Differentiate from liver disease because of red urates – with liver disease is
GREEN
o Diagnose with radiographs to look for metal in GI tract – can’t differentiate between lead
and zinc toxicosis without heavy metal panel 
Chicken Diseases
- Mites
o Knemidocoptes mutans = SCALY LEG MITE
▪ On legs and unfeathered parts – irritation can lead to feather picking and
thickened skin on legs
▪ Round, 0.5mm, short-legged mite
o Dermanyssus gallinae = COMMON RED MITE
▪ Nocturnal feeders – control through inseciticidal treatment of ENVIRONMENT
• Maintain majority of population OFF THE HOST
▪ Severe infestations can cause anemia and decrease reproductive potential
o Ornithonyssus bursae = NORTHERN FOWL MITE
▪ Affect feathered regions around vent
▪ Spend entire life ON THE HOST – apply pesticides TO BIRDS!
o Laminosioptes cysticola = SUBCUTANEOUS MITE
▪ Cause 1-3 mm nodular SQ lesions
o Trombicula alfreddusgesi = COMMON CHIGGER (of birds)
▪ Attach to wings, breast, and necks – birds that are infested may become weak,
stop eating, and die
- Fungal Infections
o Candidiasis = Candida albicans – aka thrush, sour crop, crop mycosis
▪ Develop after treatment with antibiotics
▪ White lesions in the mouth, crop, or esophagus
▪ Treat with copper sulfate in the water, nystatin in the feed
o Aspergillosis = aka brooder pneumonia, mycotic pneumonia, pneumomycosis
▪ Necropsy = cream colored plaques throughout lungs
▪ Treatment is USELESS – cull affected birds, then thoroughly disinfect all facilities
- Reproduction
o Egg drop syndrome = ADENOvirus
▪ Pretty much eradicated – only see in small operations
▪ Poor eggshell quality in healthy birds – production decreases, some have no
shells at all
o False layers
▪ Ovulate normally but yolk is dropped into abdominal cavity rather than oviduct –
usually a result of obstruction caused by E. coli or Mycoplasma gallisepticum
o Egg binding
▪ Egg lodges in shell gland or vagina – is a MEDICAL EMERGENCY (at least in
pet birds!)
- Oncology
o Reticuloendotheliosis (retrovirus) – CAUSES LYMPHOMA!
▪ Runting of birds, acute neoplasias, chronic B and T cell lymphomas
• Runting syndrome causes weight loss, abnormal feathering, occasional
paralysis, anemia
• Thymic and bursal atrophy, enlarged nerves, neoplasias of liver/heart/
spleen/intestines
▪ Similar to Marek’s and lymphoid leukosis – diagnose with virus isolation
o Avian leukosis – lymphoid leukosis (retrovirus)
▪ Causes clonal malignancy of bursal lymphoid system – transformation occurs 1-2
months after infection – tumors can take several more months to develop
▪ Vertical transmission – results in congenitally infected chicken
▪ Tumors composed of large lymphoid cells that are histologically uniform
o Renal carcinoma
▪ Unilateral paresis/paralysis
- Nutrition
o Vitamin E Deficiency = nutritional encephalomalacia and exudative diathesis and
nutritional myopathy
▪ See in chicks (15-30 days old) – ataxia, paresis, prostration, death
▪ On necropsy – ischemic necrosis, demyelinization, neuronal degeneration of
many parts of the brain
o Choline Deficiency = TURKEYS
▪ Turkeys have high choline requirement, but seen in chickens and turkeys
▪ Stunting, poor feathering, short thick bowed legs
▪ Chondrodysplasia on histopath
VIRAL DISEASES
- Infectious bursal disease = GUMBORO DISEASE – birnavirus
o Watery diarrhea, incoordination, prostration, vent pecking, poor doers in young chicks
o Neropsy = isolated from bursa of fabricius – swollen cloacal bursa that is edematous,
yellow, hemorrhagic
▪ Congestion and hemorrhage of pectoral, thigh, and leg muscles
o NO effective treatment – to prevent vaccinate breeders and progeny
- Infectious bronchitis = coronavirus
o HIGH morbidity – respiratory signs, coughing, sneezing, facial swelling
▪ DDx for these signs = Newcastle, laryngotracheitis, infectious coryza
o Virus isolation after serial passage of chick embryos (definitive diagnosis)
o Necropsy = mucoid exudate in bronchi, thickened air sacs, interstitial nephritis
- Infectious laryngotracheitis = herpesvirus
o Dyspnea with extension of neck during inspiration, coughing up mucous and blood,
decreased production, watery eyes, nasal discharge
o Diagnose with intranuclear inclusion bodies in tracheal epithelium
▪ Diphtheritic form of fowlpox produces intracytoplasmic inclusions
o Necropsy = caseous exudate and blood in trachea
o Vaccinate to prevent
- Hemorrhatic enteritis = adenovirus
o Birds 6-12 weeks old affected – depression, bloody diarrhea, sudden death
o Necropsy = intraluminal hemorrhage in small intestines, enlarged and friable spleen
o Vaccinate 4-5 week old turkeys
- Marek’s disease = adenovirus
o Neurologic signs, cutaneous signs, visceral tumors – thickened nerves, paralysis of leg/
wing/neck, gray iris or irregular pupils, raised skin around feather follicles, gray foci of
neoplastic tissue in liver/spleen/kidney/lungs/heart/muscle
o Necropsy = enlarged vagus and sciatic nerves, nodular tumors in many organs, enlarged
feather follicles
o NO treatment – to prevent give in-ovo vaccinations
- Fowl plaque = AVIAN INFLUENZA VIRUS
o If you suspect contact regulatory authorities!! – due to concern over mutation and
zoonotic potential
o History of decreased egg potential, greenish diarrhea, cyanosis, edema of head/comb/
wattle, blood tinged oral and nasal discharge
- Newcastle Disease = paramyxovirus
o Neurologic signs, coughing, death, green diarrhea, swelling of head/neck, gasping,
sneezing, dropping wings, dragging legs, circling, torticollosis, paralysis, clonic spasms
o Three strains = velogenic (highly pathogenic), mesogenic (intermediate), lentogenic (low
pathogenicity)
o Is a hemagglutinating virus
o ZOONOTIC – conjunctivitis in people
- Avian encephalomyelitis = picornavirus
o 1-2 week old birds – neurologic signs, ataxia, imbalance, head and wing tremors
o Necropsy = neuronal axon-type degeneration (ghost cells) in brainstem
o Prevent by vaccinating breeding animal to prevent vertical transmission
- West Nile Virus = flavivirus
o Chickens and turkeys don’t usually develop clinical disease – control mosquitoes
anyway as a precaution
o Affects crows, geese, exotic birds – SERIOUS DISEASE IN CROWS
BACTERIAL DISEASES
- Infectious coryza = HAEMOPHILUS PARAGALLINARUM (gram negative)
o Older chickens more susceptible – respiratory disease, nasal discharge, swelling of face
under eyes
▪ Must differentiate from fowl cholera
o Treat with antibiotics – GOOD prognosis (vs. AI, infectious bursal disease, infectious
laryngotracheitis)
- Fowl cholera = PASTEURELLA MULTOCIDA (gram negative)
o Fever, mucoid discharge from mouth, WHITISH diarrhea, petechia/ecchymoses,
increased pericardial/peritoneal fluid, acute death
o Prevent with vaccination – treat with sulfa antibiotics
o ZOONOTIC
- Salmonella enteritidis
o Causes food poisoning in people who eat eggs infected with this!
▪ Is initially only on embryo but if eggs are not refrigerated yolk membrane
weakens and Salmonella enters yolk where it multiples and can become a
significant zoonotic problem
- Clostridium perfringens (A and C) = NECROTIC ENTERITIS
o AVOID DRASTIC FOOD CHANGES – minimize levels of fishmeal/wheat/barley/rye in
diet
▪ Causes acute enterotoxemia with onset of explosive mortality due to necrosis of
small intestines
o Inappetance, ruffled feathers, dark colored diarrhea
o Necropsy = middle and distal intestine has diphtheritic membrane and contains dark
brown necrotic material
▪ DDx = Eimeria brunetti, ulcerative enteritis by C. colinum
o Most common cause of LIVER DAMAGE in broiler chickens – cholangiohepatitis
o Treat with penicillin in the drinking water
- Erysipelas = gram positive
o Sudden death after exhibiting ataxia and weakness
o Diagnose by finding gram positive slender rods in impression smears of spleen and liver
o Necropsy = darkening of skin, enlarged and friable liver and spleen
o Treat with IM sodium penicillin, give erysipelas bacterin
- Avian tuberculosis = MYCOBACTERIUM AVIUM
o Rarely seen in commercial flocks due to short life-span – see in back-yard flocks
o Acid-fast bacteria in smears from lesions
o Necropsy = granulomatous nodules in liver, spleen, bone marrow, intestines
MISCELLANEOUS DISEASES
- Coccidiosis = EIMERIA
o Numerous species specific to certain regions of the GI tract – severe diarrhea,
decreased production, death
o Demonstrate oocysts in feces to diagnose
o Treat with anticoccidial drugs – AMPROLIUM (has ZERO withdrawl time)
▪ Is a thiamine analogue that is coccidiostatic – other drugs have longer withdrawl
times
- Avian fowl pox = POX VIRUS
o Spread by contact or by mosquitoes – control mosquito populations and vaccinate to
prevent
o Two forms:
▪ Dry form: whitish wart-like lesions on unfeathered areas (head, legs, vent) –
lesions heal in about 2 weeks, mortality is low
▪ Wet form: diphtheritic membrane in mouth and pharynx, can ulcerate or erode
mucous membranes, marked respiratory involvement that can lead to mortality
o Diagnose by seeing intracytoplasmic inclusions in lesions
o NO treatment is effective
- Visceral gout
o See when there is renal damage or severe dehydration
o Urate crystals accumulate in affected organs – uric acid is produced in liver of birds as
end-product of nitrogen metabolism – this chalky substance can accumulate in liver,
myocardium, spleen, etc.
o Articular urate depsots can also occur = articular gout
- Malabsorption syndrome = runting-stunting syndrome, pale-bird syndrome
o 1-3 week chickens – poor growth and feathering, abnormal/broken feathers, pale feet
and skin, orange feces
o Necropsy = orange mucus in intestines, enlarged proventriculus, small gizzard,
atrophied pancreas
o CULL affected birds – prevent with good hygiene, good nutrition, and good egg
selection
Turkey Diseases
- Reasons not to house turkeys and chickens together…
o Mycoplasma gallisepticum
▪ MILD in chickens, SEVERE in turkeys – turkeys get nasal discharge, swelling of
paranasal sinus, decreased weight and egg production, severe sinusitis and air
sacculitis
o Histomonas meleagridis = BLACKHEAD of turkeys
▪ Affects turkeys when housed with chickens – FATAL to turkeys!
▪ GASTROENTERITIS, NOT respiratory signs – yellow droppings, dull, depressed,
ruffled feathers
▪ Heterakis gallinarum hosts the protozoan (which then causes clinical disease)
▪ Necropsy = ulcerations and thickening of cecal wall, liver has ring shaped yellow
lesions
• EXTENSIVE NECROSIS OF LIVER AND CECUM!! PATHOGNOMONIC!!
▪ Treat with Nitrasone added to feed – also use benzimidazoles (to kill Heterakis)
- Turkey coryza = BORDETELLA AVIUM
o HIGH morbidity, LOW mortality – acute respiratory disease, nasal discharge, foamy
eyes, cough
o Diagnose with MacConkey agar
o Antibiotics NOT effective, sometimes vaccine is helpful in an outbreak
- Spontaneous cardiomyopathy = round heart disease of turkeys
o Acute death in young turkeys after having labored/gasping breathing – other turkeys in
flock may have unkempt appearance and ruffled feathers
▪ Sudden death due to cardiac arrest in young turkeys (less than 3-4 weeks old)
o Necropsy = markedly enlarged heart with dilatation of the ventricles, congested lungs,
enlarged liver
o Histopath = lymphocytic infiltration and damage to myofibrils in cardiac muscle
- Ornithosis = CHLAMYDIA PSITTACI
o Nasal and ocular discharge, weight loss, inappetance, death
o Necropsy = pneumonia, necrosis of liver and spleen, severe pericarditis,
intracytoplasmic inclusions
- Deep pectoral myopathy
o Swollen edematous pectoral muscles – vigorously exercised muscle that when handled
leads to swelling, ischemia, and necrosis
▪ Thought to be due in part to selection for breast meat – not contagious, no
specific etiology
o Necropsy = degeneration, necrosis, fibrosis and green appearance of muscle
o Meat condemned at processing – economic losses – so to decrease incidence do
selective breeding
- Bluecomb = coronavirus (aka transmissible enteritis, coronaviral enteritis)
o Cyanosis and darkening of head, young turkeys die, old ones fail to gain weight,
depression, anorexia
o Diagnose via direct fluorescent antibody for viral antigens in the intestines
o Treatment is supportive care and antibiotics for secondary bacterial infections
o NO VACCINE AVAILABLE – prevent with good husbandry
Porcine Diseases
VIRAL DISEASES
- Swine influenza
o HIGH morbidity, LOW mortality – concurrent illnesses can exacerbate disease
▪ Uncomplicated infections run a short course and have low mortality
o Lethargy, respiratory illness, high fever, prostration, coughing, anorexia, conjunctivitis,
oculonasal discharge
o Important disease in pigs and aquatic fowl because by mutating could be major zoonotic
problem!!
- Porcine epidemic diarrhea and transmissible gastroenteritis (TGE) = coronavirus
o Affects ALL age groups and causes nearly 100% mortality in piglets less than 1 week of age
▪ No other disease spreads so rapidly or causes such high mortality – seldom die if
older than 1 month
o Watery diarrhea, vomiting, wet and dirty appearance of litter due to profuse diarrhea
o Treat symptomatically
- Porcine respiratory and reproductive syndrome (PRRS) = arterivirus
o Most common cause of STILLBIRTH in pigs
o 3 overlapping syndromes – affects pigs of ALL ages
▪ Reproductive impairment or failure – abortions, mummies, stillbirths, early
embryonic death
▪ Respiratory disease – weaned pigs develop cough (“thumps”), purple ear tips due
to vasculitis
• Nursery pigs get interstitial pneumonia
▪ High pre-weaning mortality – diarrhea and recurrent fevers
o Treatment = NONE – may have to depopulate herd or close herd and follow titers
o Prevention = vaccine
- Rotavirus
o Disease occurs at 5 days of age – often occurs in association with E. coli
- Blueye = tublavirus
o aka blue eye paramyxovirus
- Hog cholera = togavirus – aka classical swine fever
o USA is currently free of this REPORTABLE disease
o Closely related pestiviruses = BVD, border disease virus
o Viruse affects stem cells in bone marrow causing neutropenia and thrombocytopenia –
become immune suppressed and susceptible to enteric bacterial infections
o Oral ulceration, vomiting, diarrhea, oral petechiation, paresis/paralysis, fever, shivering,
conjunctivitis
▪ Can cross placenta and cause reproductive failure – severe systemic infection and
abortion
- African swine fever
o Fever, inappetance, hemorrhages in skin of ears, acute death – other DDx = classical
swine fever, erysipelas
o See in AFRICA (carried by warthogs, transmitted by soft ticks)
o Necropsy = petechial hemorrhages on internal organs
- Vesicular exanthema = calicivirus (aka San Miguel Sea Lion Disease in sea lions)
o Affects swine, sea lions, seals, other marine mammals
o Present in sea lions off coast of California – not present in USA in pigs
o REPORTABLE
- Pseudorabies = herpesvirus – Aujesky’s Disease
o Primary host = PIG – eradicated from pigs in US, can devastate non-immune herd
▪ Respiratory system, reproductive system, CNS (not GI) – clinical signs depend on
age group
• Young neonates (<3 weeks) – NEURO, CNS signs, tremors,
incoordination, blindness, opisthotonos, hypersalivation, ataxia,
nystagmus, paddling – DEATH (100% mortality)
o DDx for tremors = organophosphates, circovirus, hog cholera, NOT
PRRS
• Weaned pigs – NEURO and RESP – similar signs as young neonates with
respiratory signs (mortality lower in this age group)
• Grower and finisher pigs – RESP – coughing, sneezing, nasal discharge
• Older pigs at breeding age – respiratory signs, reproductive failure
(abortion, resorption, mummification)
o In RUMINANTS = first sign is paresthesia (“Mad Itch”) at site of inoculation, ataxia,
proprioceptive deficits, circling, nystagmus, strabismus – sometimes see aggression,
sometimes become depressed – death in 2 days
▪ Often have history of pigs housed nearby! Pigs are primary host of pseudorabies.
▪ NO TREATMENT – animals die, but to prevent REMOVE THE PIGS
▪ DDx for these clinical signs = rabies (Negri bodies), polioencephalomalacia, salt
poisoning, lead poisoning, hypomagnesia, meningitis
o In HORSES – VERY RARE that horses get this, if they do get it causes depression and
inability to swallow
o NO TREATMENT (older pigs recover on their own) – prevent with vaccination
- Parvovirus
o BRED SOW RETURNS TO HEAT (due to embryo resorption), unapparent infection in
sow
▪ May have mummified fetus, weak piglets, small litters, still births
▪ Abortions = RARE – endometrium is not affected so there is no PGF2a released
o VACCINATE!
o DDx for fetal loss = Parvo, Toxoplasma, Brucella, Pseudorabies, PRRS,
eperythrozoonosis, Erysipelas, Lepto
BACTERIAL DISEASES
- Lawsonia intracellularis (gram negative – curved bacteria in enterocytes) = proliferative
enteropathies
o Soft buttery (yellow) stool, sometimes acute hemorrhagic diarrhea, gradual wasting,
lethargy
o Common in weaned and older pigs – diarrhea persistent, weight loss – similar to Johne’s
in cows
o Necropsy = thickened and inflamed ileum – proliferative ileitis with edematous
mesentery
- Serpulina hyodysenteriae = SWINE DYSENTERY
o Mucohemorrhagic diarrhea – large bowel diarrhea because causes fibrinonecrotic
typhlitis and colitis
▪ Small intestines unaffected
o Bloody diarrhea and death in grower and finisher pigs
- Salmonella
o Causes RECTAL STRICTURES with chronic infections – causes “button” ulcers in large
intestine too
o See in WEANERS and GROWERS – uncommon in piglets due to passive immunity
from colostrum
- Erysipelothrix rhusiopathiae = DIAMOND SKIN DISEASE
o 3 forms ! GROWER and FINISHER pigs
▪ Peracute ! pigs found suddenly dead
▪ Acute ! pigs become lethargic, painful in their joints, anorexic, develop diamond
skin lesions
▪ Chronic ! arthritis progresses to vertebral joints and limb joints may fuse –
painful swollen joints
o Lesions = red or purple skin lesions in shape of diamonds
- Enterotoxigenic E. coli = enteric colibacillosis, EDEMA DISEASE
o Lesions = edema, pericardial and pleural effusion, ascites, hemorhages on epicardium
and endocardium
o Results from vasculitis due to heat stable enterotoxin (Shiga toxin 2e) – destroyes
endothelial cells in vessels – results in blood clots, hemorrhage, ischemic necrosis, and
edema of vital organs (including brain)
o Enteric colibacillosis
▪ Most common causes of diarrhea in NURSING piglet (less than 5 days old) – see
piglets huddled together shivering
▪ See with rotavirus – watery diarrhea, dehydration, acidosis, death
▪ To prevent ! vaccinate, NEVER MIX PIGS OF DIFFERENT AGES TOGETHER
o Edema disease
▪ FATAL disease of rapidly growing WEANED pigs – see in pigs on high-protein,
high-energy diet
▪ Fever, anorexia, SQ emphysema, dyspnea, open mouth breathing, convulsions,
diarrhea, swollen eyelids (edema of eyelids, forehead, lips), circling, acute death
- Brucellosis
o ABORTION – in any stage of gestation – placentas and aborted fetuses have NO
GROSS LESIONS
o Transmitted via venereal transmission and through aborted fetuses
o ZOONOTIC – highly pathogenic in humans!!
- Mycobacterium avium = tuberculosis in swine
- Streptococcus suis
o Affects NURSING and WEANED pigs ! polyarthritis, bronchopneumonia, sepsis,
meningitis (NOT colitis)
o Morbidity and mortality vary – improved with treatment
GASTROENTEROLOGY
- Diarrhea in different age groups…
o Unweaned (young) piglets
▪ Clostridium perfringens type C = hemorrhagic/necrotic enteritis
▪ Cryptosporidium parvum – VERY UNCOMMON IN PIGS – no drugs effective
▪ Rotavirus
▪ Isospora suis
▪ Transmissible gastroenteritis virus
▪ Enteropathogenic E. coli (enteric colibacillosis) – VERY COMMON IN NURSING
PIGLETS
o Weaned (older) pigs – growers and finishers
▪ Salmonella
▪ Lawsonia intracellularis
▪ Trichuris suis – can affect all ages but usually older pigs
▪ Serpulina hyodysenteriae – swine dysentery
- Gastric ulcers
o Caused by housing stress, type of feed, concurrent disease
o Common in GROWING swine – pale mucous membranes, dark feces,
o Necropsy = clotted blood in stomach (mainly pars esophagea portion) and duodenum
- Intussusceptions
o Occur in pigs infected with OESOPHAGOSTOMUM – vomiting with NO diarrhea
▪ Tachycardia, restlessness, signs of colic
o Treatment = surgery
DERMATOLOGIC DISEASES
- Hernias
o Inguinal ! MALES (after castration), heritable
o Umbilical ! FEMALES
- Pityriasis rosea
o 12-14 week old pigs ! unknown etiology, may be heritable
o Raised circular lesions on ventral abdomen – NO TREATMENT NECESSARY, resolves
on its own
- Staphylococcus hyicus = exudative epidermititis, aka GREASY PIG DISEASE
o Piglets less than 8 weeks of age – brown exudative spots on skin of head, axillae, groin –
brown and crusty
o Morbidity and mortality high in younger pigs, rarely affects adults
- Swine pox = poxvirus
o Transmitted by biting insects (particularly lice) – to control eliminate hog lice and insect
vectors
o 1-2cm round papules, pustules, vesicles and scabs on ventral abdomen
o Young and growing pigs most severely affected!
o Treatment usually not necessary – unless become secondarily infected by bacteria –
then antibiotics
- Aural hematomas
o Caused by bites inflicted by pen mates – or from violent head shaking (i.e. when have
mites/lice in ear)
- Dermatosis vegetans
o Semilethal hereditary defect that causes macules and papillomas around the coronary
band
RESPIRATORY DISEASES
- Atrophic rhinitis = Bordetella bronchiseptica (non-progressive), Pasteurella multocida
(progressive)
o Snorting, sneezing, snuffling, coughing, epistaxis, nasal discharge, atrophy of
turbinates, facial distortion
o Common in piglets 3-8 weeks old
o Treat with antibotics, prevent with vaccination
- Necrotic rhinitis = Fusobacterium necrophorum (gram positive)
o Necrosis of snout when enters nasal/oral mucosa
- Mycoplasma hypopneumoniae = ENZOOTIC PNEUMONIA
o Coughing in feeder pigs (persistent dry cough, fevers, inappetance, weight gains slow
(retarded growth)
▪ NOT sneezing or nasal discharge – is DRY!!
o Necropsy = purple gray areas of consolidation in cranioventral lungs with catarrhal
exudate in airways
o Prevent with vaccinations – also address air quality and ventilation
- Pleuropneumonia = ACTINOBACILLUS PLEUROPNEUMONIAE (gram negative)
o Sudden onset of respiratory distress with open mouth breathing, frothy pink oral/nasal
discharge (blood)
o Mainly affects pigs less than 6 months ! commonly have concurrent infectious
(Mycoplasma, Pasteurella PRRS, influenza) – to differentiate from influenza, influenza
affects ALL ages, doesn’t have pink discharge
o Necropsy = fibrinonecrotic and hemorrhagic lung lesions
ORTHOPEDIC DISEASES ! DDx for lameness = Strep. suis, Erysipelas, Mycoplasma hyorhinis,
Haemophilus parasuis
- Osteochondrosis dissecans
o Multiple pigs from herd present lame – usually fast growing well muscled pigs – lame at
4-8 months old
o Lesion = defects in articular cartilage – medial femoral condyle, humeral condyle,
humeral head, glenoid of the scapula, distal ulna, lumbar vertebrae
o Cull affected animals – replace with normal animals for breeding – cross-breeding DOES
NOT help
o Treatment is symptomatic and does not cure disease
- Haemophilus parasuis = GLASSER’S DISEASE
o Painful joints, pneumonia, sometimes neuro signs – swollen painful joints, shifting leg
lameness
o Affects pigs 2 weeks to 4 months old
o Necropsy = fibrinopurulent pleuritis and peritonitis (sometimes pericarditis or
meningitis)
o Treat with penicillin
- Mycoplasma hyorhinis
o Presentation similar to Glasser’s – polyarthritis, polyserosities, fever, pneumonia in 2-4
month old pigs
o LOW mortality
MISCELLANEOUS
- Eperythrozoonosis = Eperythrozoon suis
o Vectored by biting insects
o YOUNGER pigs more severely affected – anemia, fever, icterus, reproductive failure,
weakness, anorexia
o Treat with tetracycline
- Sinus arrhythmia
o VERY COMMON IN THE PIG!!!! – relatively uncommon in ruminants
o Caused by vagal tone – will see increase in heart rate on inspiration
- Vitamin A Deficiency
o Head tilt, incoordination, reduced weight gains, weak rear limbs with NORMAL VITALS
▪ Will see in MULTIPLE pigs on same farm
o Can lead to increase in middle ear infections, in sows can cause embryonic mortality or
congenital defects
- Failure of passive transfer
o Farm having increased amounts of newborn piglet diarrhea – measure IgG in piglets at
24 hours
- Management
o Piglets WEANED at 16-20 days of age in North America
o All in/all out = helps synchronize estrus and breeding in sows – have them all farrow at
the same time, wean at same time, bred at same time, vaccinated at same time – clean
house in between groups
▪ Advantages = same schedule, neonatal mortality lower, greatest return on
pounds of meat at market
▪ Disadvantages = not continuous production of piglets
Goat and Sheep Diseases
GOAT DISEASES
- Caprine arthritis and encephalomyelitis virus (CAEV) = retrovirus – affects MONOCYTES
o HARDBAG – causes fibrosis of the udder and results in agalactia
o Transmit to kids via colostrum – arthritis in adults, encephalitis in kids
▪ Leukoencephalomyelitis in kids 2-6 months old
▪ Polysynovitis-arthritis in goats 6 months or older
o Treatment is ineffective – CULL!
- Mycoplasma pneumonia = Mycoplasma mycoides ssp mycoides, M. capricolum
o M. ovipneumoniae is the species that causes pneumonia in sheep
o Transmitted by transmammary and aerosol – maintained in herd by mammary carrier
that is subclinical!
o See respiratory disease with fibrinous pneumonia on histopath
o Causes pneumonia, meningitis, mastitis, and polyarthritis
▪ *Concurrent mastitis in does and polyarthritis and pneumonia in kids (and maybe
meningitis)
• Kids 2-4 weeks old have hot swollen joints and respiratory distress
• Does have firm udders with brownish watery milk and occasional garget
▪ Diagnose by culture of milk – NON-responsive to antibiotics – so CULL all
affected (even kids)
- Brucella melitensis
o ZOONOTIC – acquired via raw goat milk – severe pathogen in humans!!
o B. abortus in cattle, B. suis in pigs, B. canis in dogs – all severe in humans!
- Squamous cell carcinoma
o Papillomas in Saanen goats tend to transform to SCC – POOR prognosis
o Warts on udder that start to develop into something more serious
- Sinusitis
o See in kids shortly after dehorning – affects frontal sinus!!
- Myotonia congenital = FAINTING GOAT SYNDROME
o Autosomal dominant mutation – abnormality in skeletal muscle chloride channel
o Marked general rigidity after visual, tactile, or auditory stimulation
- Beta mannosidosis
o Genetic in Anglo-Nubian goats (see alpha-mannosidosis in breeds of cattle)
o Storage disease that results in intraneuronal accumulation of mannose-based
oligosaccharides
o In kids – inability to stand since birth, short sternum, shortened dome head with short
curled ears, head tremors, carpal contractures, no suckle reflex
SHEEP DISEASES
- Spider lamb syndrome = SUFFOLK SHEEP (aka Ovine Hereditary Chondrodysplasia)
o Carpus valgus – hereditary, caused by semilethal autosomal recessive trait
- Bluetongue = reovirus
o Primarily affects SHEEP – cattle may have reproductive losses (hydrocephalus in
calves)
o Vector = CULICOIDES (can also be spread sexually, transplacentally)
o Causes widespread vasculitis – fever, edema of face/muzzle/lips/ears, respiratory difficulty,
mucopurlent nasal discharge, cyanotic tongue, oral lesions (differentiate from FMD and
VSVS)
▪ Teratogenic effects in both sheep and cattle
• Stillborn weak calf with “white eye calf syndrome” – congenital cataracts
• Hydrancephaly in these lambs – cerebral hemispheres like swiss cheese
▪ Lameness associated with Zenker’s degeneration of skeletal muscle – white
streaks in muscle
o Necropsy = white streaks in skeletal muscle and endothelial hemorrhage at base of
pulmonary artery, ecchymotic hemorrhages in lymph nodes and spleen – VASCULITIS
- Coxiella burnetti = Q FEVER (gram negative spore forming intracellular)
o ZOONOTIC – acquired by humans from sheep – fever, headache, fatigue, premature
delivery, abortion
o Uncommonly causes abortion in sheep!
- Ulcerative posthitis = Corynebacterium renale – PIZZLE ROT
o Bacteria contains urease which allows it to thrive in prepuce and converts urea to
ammonia which damages mucosal surfaces – leads to swelling of prepuce, stranguria,
reluctance to breed, only few animals affected
o Lesion = scabs on mucucutaneous junction of prepuce – painful ulcers under foul
smelling scabs
o See when sheep are on high protein diet – excess protein catabolized to urea
o Treat by reducing dietary protein, penicillin to control C. renale
- Mycoplasma pneumonia = Mycoplasma ovipneumoniae – ENZOOTIC PNEUMONIA,
ATYPICAL PNEUMONIA
o Transmission = AEROSOL (in contrast to goats which is spread by milk)
- Ovine progressive pneumonia (OPP) = retrovirus – aka MAEDI-VISNA
o Closely related to CAEV
o Sheep 2-4 years old – emaciation, lag behind flock, breathing difficulty, hard udders,
expiratory dysnpea, open mouth breathing, occasional NON-productive cough, fever
o Necropsy = lungs gray-blue and don’t collapse, fibrous udder (indurative mastitis) with
large lymph nodes
- Mannheimia hemolytica = ENZOOTIC PNEUMONIA< GANGRENOUS MASTITIS (blue bag)
o BLUEBAG – Staph aureus also causes bluebag, difficult to treat and many times
animals are culled
o ENZOOTIC PNUEMONIA – most common bacterial cause of pneumonia in sheep and
goats
▪ Hemorrhagic bronchopneumonia – fever, mucopurulent nasal discharge,
coughing, crackles/wheezes
▪ Necropsy = fibrinopurulent pleuropneumonia
- Entropion
o Common in newborn lambs – also common in pigs – usually lower eyelid is affected
- Cryptosporidium parvum
o ZOONOTIC - affects people handling animals or feces
o Acute diarrhea in lambs and calves
o Stains ACID-FAST
- Scrapie = PRION disease (transmissible spongiform encephalopathy)
o Afebrile neurologic disease that is chronic, progressive and degenerative – clinical signs
depend on region of brain affected – aggressiveness, failure to herd, unsteady gait, self-
mutilation (pruritis – resulting in rubbing wool off in the LUMBAR region), blindness,
seizures, inability to swallow
o CULL positives, breed for resistant flock based on pedigree – need to cull to prevent
spread of PrP gene
- Meningitis
o Associated with tail docking in sheep – causes progressive ascending paralysis and
neck pain
o Evaluation of CSF = xanthochromic, gram stain may show many bacteria
- Border Disease Virus = pestivirus – HAIRY SHAKER SYNDROME
o Antigenically related to BVD and hog cholera
o Transmitted from ewe to fetus before 80 days gestation – macerated/aborted/mummified
fetuses, ones that survive exhibit “hairy shaker” syndrome due to infection of hair
follicles and the cerebellum (domed heads, short limbs, thick trunks, tremors and fine
hairy wool)
- Campylobacter jejuni = VIBRIOSIS
o Most common cause of INFECTIOUS ABORTION in sheep in North America
o DDx for abortion = Toxoplasma, Chlamydia psittaci, Bluetongue, Brucella ovis
(epididymitis), Akbane virus (dystocia and arthrogryposis), Cache Valley virus
(brachygnathia, hydrancephaly, microencephaly, etc.)
BOTH GOATS and SHEEP
- Contagious ecthyma (CE) = ORF, SOREMOUTH – parapoxvirus
o ZOONOTIC – along with other two parapox viruses: bovine papular stomatitis,
pseudocowpox
o Virus remains in scabs that fall off lesions – virus can overwinter in scabs
o LESIONS IN MOUTH (thick brown crusts) and around nose of lambs/kids, sometimes
on TEATS of mothers
▪ Nursing problem due to sore mouths and sore teats – rarely causes mortality
o Lesion = crusting lesions of mucocutaneous junctions of mouth, in oral cavity and feet,
eyelids, and on teats
- Pregnancy toxemia
o Final stages of pregnancy (LATE gestation) with multiple fetuses
▪ Multiple fetuses become space-occupying lesion making rumen more difficult to
fill just as doe requires maximum caloric intake – tips over into negative energy
balance, utilizes fat stores and develops fatty liver, liver cannot produce enough
glucose and becomes overwhelemed with free fatty acids resulting in production
of ketones, becomes keto-acidotic and develops a pregnancy toxemia
• Body cannot produce enough OXALOACETATE for citric acid cycle –
results in mobilization of fat and production of ketones (acetoacetic acid,
B-hydroxybutyric acid, acetone)
o Anorexia, weakness, recumbency, depression, CNS signs (tremors, stargazing, circling,
teeth grinding)
o Diagnosis = multiple near term dead fetuses and pale fatty liver on necropsy, ketones in
urine, hypoglycemia, neurologic signs (circling, stargazing)
o Treatment = IV glucose/dextrose and immediate C-section – rumen transfaunation with
propylene glycol
o Prevent by increasing energy intake in late gestation – one lb/head/day of good quality
grain should be given
- Urethral obstruction = due to calculi
o Most common sites = urethral process, distal sigmoid flexure
o Vocalizing, straining to urinate, kicking at abdomen, dribbling urine, forceful abdominal
contractions, teeth grinding, restlessness, hematuria, dysuria
o Treat by amputating urethral process, if still unable to urinate do tube cystotomy
▪ Salvage procedures = bladder marsupialization, penectomy, perineal
urethrostomy
- Infectious footrot (aka contagious footrot) = Fusobacterium necrophorum and Dichelobacter
nodosus
o VERY contagious in sheep, in cattle can also be caused by (A. pyogenes, Preyotella
melaningenicus)
o Lesion = interdigital space – causes lameness and pain – malodorous exudate,
separation of horn of hoof
o Dichelobacter nodosus = microorganism essential for disease to occur, also need wet
conditions
▪ Produces proteases that cause horny wall separation – cytology = BARBELL
shaped rods
o Treatment = florfenicol SQ (esp cattle), 10% zinc sulfate bath, remove from wet
condition, regular foot trims
▪ CULL SHEEP – because is so contagious in them!
RUMINANT DISEASES
- Reportable diseases ! Brucellosis, Foot-and-mouth disease, vesicular stomatitis, Bluetongue
- Foot-and-mouth disease = picornavirus
o Only CLOVEN-HOOFED animals affected (cattle, sheep, pigs, goats – also llamas,
bears, camels, elephants)
▪ NOT horses!!!!
o Oral and foot lesions – DDx in cattle = vesicular stomatitis, bovine papular stomatitis,
pseudocowpox, bluetongue
▪ Vesicles in mouth and on coronary band and interdigital space – rupture and
result in ulceration and pain
o USA is free of FMD - REPORTABLE
- Vesicular stomatitis
o REPORTABLE – occurs about every 7-10 years in western US – reportable bc similar to
FMD
o Vector = sand flies, black flies – then spread by direct contact, high morbidity, low
mortality
o Can also affect HORSES and PIGS (NOT sheep) – way to differentiate from FMD, FMD
only affects cloven-footed
o Oral ulcerations (as result of ruptured vesicles on tongue), lesions on feet and teats,
salivation, anorexia, depression, fever, drooling and champing their mouths, ulcerated
tongue
- Malignant catarrhal fever
o 2 forms:
▪ African form – Alcephaline herpesvirus (AHV-1) – WILDEBEEST reservoir, high
mortality
▪ N. American form – Ovine herpesvirus 2 (OvHV-2) – SHEEP reservoir (goats can
be reservoir too)
• Cattle, water buffalo, deer, pigs, bison (most susceptible) are all
susceptible
o See in cattle housed near sheep – high fever, respiratory and GI lesions,
lymphadenopathy, corneal opacity, thick white nasal discharge, thick cracked skin, oral
lesions
o Affects lymphocytes and allows animal’s own killer cells to attack blood cells = acute
generalized arteritis – involves mucosa of many systems = lymphocytic vasculitis
▪ Necropsy = lymphocytic perivasculitis of the brain
- Rumen acidosis = GRAIN OVERLOAD
o History of breaking into grain meant for horses, need to SLOWLY introduce ruminants to
concentrates
o Pathogenesis = increased grain leads to replication of S. bovis and other gram positive
bacteria – lowers rumen pH below 4.5 causing increase in lactic acid – lactobacilli
multiply due to favorable condition created – crank out bunch more lactic acid – cannot
metabolize D-lactic acid made and systemic acidosis results
o Increased HR, depression, anorexia, fluid-filled rumen, scleral injection, diarrhea,
staggering
o Diagnose = rumen fluid has pH of 5.5 or less
o Treatment = oral antacids (magnesium oxide/hydroxide), IV fluids with sodium
bicarbonate, penicillin, rumenotomy if severe
o Sequelae = liver abscesses, mycotic rumenitis, death from metabolic acidosis, venal
caval thrombosis
▪ Liver absecesses – low rumen pH allows bacteria to translocate and be filtered
by hepatic circulation
▪ Venal caval thrombosis and metastatic pneumonia – bleeding from nose due to
liver abscess near posterior vena cava – thrombosis breaks off and lodges in
pulmonary arteries – pulmonary bleeding
▪ Rumen ulcers – could penetrate mucosa and cause septic abdomen
- Polioencephalomalacia = THIAMINE (Vitamin B) DEFICIENCY
o Increase in amount of grain fed, history of being fed horse feed (high in concentrates/
molasses)
▪ Strongest animals get sick first because at top of food chain
▪ Increase in grain leads to ruminal acidosis, results in thiaminase-producing
bacteria multiplying in rumen to destroy thiamine, and decreases population of
thiamine-producing bacteria
• Other causes = bracken fern, overdose of amprolium, high dietary sulfate
o Diarrhea, depression, hyperesthesia, head-pressing, stargazing, opisthotonos,
dorsomedial strabismus, odontoprisis blindness (bilateral signs) – usually progress to
recumbency
o Necropsy = soft, edematous cerebral cortex with gray-yellow discoloration and flattened
gyri
▪ Necrosis of cortical gray matter
o Treat by giving thiamine
- Dermatophilus congolensis = STRAWBERRY FOOTROT (sheep), RAIN SCALD (other
ruminants and HORSES)
o Crusty lesions at coronary band that are easy to pull off – PAINTBRUSH LESIONS –
when crusts peeled off have pink granulation tissue (“strawberry” appearance)
o Cytology – branching “RAILROAD TRACKS” of cocci bacteria
o Common in animals out in the rain/wet conditions
o Treat by removing from rain, 10% zinc sulfate baths, antibiotics
o Rain scald – crusting lesions on muzzle, ears, face, tail, dorsum – YOUNG animals
▪ Enters skin that is damaged by wetness – suppurative crusts along dorsum
- Corynebacterium pseudotuberculosis = CASEOUS LYMPHADENITIS (aka boils)
o Transmission through injury to skin (i.e. at shearing)
o Cattle affected too (large external bleeding sores on skin of cattle) – not really
systemically affected
▪ Large sore on flank with pus and blood – common on lateral thorax, neck, flank,
head
▪ Flush wound and let it heal – resolves on own in 2-4 weeks
o Most common in sheep and goats – boils and internal abscesses in sheep and goats
▪ Large submandibular and prescapular abscesses – can occur at internal lymph
nodes too
▪ Necropsy = mass has “onion ring” appearance with concentric layers of fibrous
tissue separated by inspissaed caseous exudate – greenish pus
• Culture pus = white-to-opaque colonies that can be pushed across plate like
hockey puck
o Can also affect mammary gland – cull or isolate – very difficult to treat because walled
off in absecess
▪ Life saving mastectomy can be performed if valuable
o ISOLATE AFFECTED ANIMAL (very contagious) – usually just CULL, because is a
chronic recurring disease
▪ If valuable animal – surgical drainage, abscess removal, antibiotics and isolation
o To prevent – VACCINATE, and be careful when shearing – disinfect shears well in
between sheep
- JOHNE’S DISEASE = Mycobacterium avium ssp paratuberculosis
o 2 years or older ! chronic weight loss, occasionally see diarrhea (green), submandibular
edema, emaciation, decreased production, loss of muscle mass
▪ Affected when young but don’t show signs until older and STRESSED
o Lesion = granulomatous bowel (ileocolic, ILEUM, and colitis) – lose albumin into gut,
weight loss rapid
▪ ACID-FAST rods on cytology
o CULL ALL CATTLE THAT TEST POSITIVE (no treatment!)
o ZOONOTIC? Crohn’s disease has been associated with this bacteria – debate still
ongoing
Bovine Diseases
VIRAL DISEASES
- Infectious bovine rhinotracheitis (IBR) = bovine herpesvirus type 1

o Becomes latent in trigeminal ganglia – loud hacking cough, sneezing, fever, anorexia,
open mouth breathing, mucopurulent nasal discharge, chemosis
▪ UPPER respiratory signs with WHITE PLAQUES on conjunctiva and nasal
epithelium
▪ Abortions have occurred – can kill a fetus quickly and show signs of severe
inflammation in the fetus
- Bovine papilloma virus
o See papillomas throughout herd – best treatment is to make an autogenous vaccine by
isolating some warts from the herd – commercially available vaccine not thought to be
effective
- Bovine leukosis = lentivirus (aka bovine leukemia virus (BLV), leuksosis virus)
o LYMPHOSARCOMA – lymphadenopathy, weight loss, decreased production
o Biopsy lymph node for histopathology (definitive), positive on ELISA for gp51 antigen
(herd test standard)
- Bovine respiratory syncytial virus (BRSV) = PARAMYXOVIRUS
o Rapid labored breathing, depression, salivation, nasal and ocular discharge, “honking”
cough, tachpnea, dyspnea
o Lesions = pulmonary edema and emphysema (hear crackles throughout lung fields)
o Treatment = supportive, antibiotics for secondary bacterial infections
- Bovine viral diarrhea (BVD) = flavivirus
o Maintained in herd through persistently-infected carriers that were infected as fetuses
▪ Passed to fetus when non-immune dame is viremic with a non-cytopathic BVD –
day 50-150 of gestation
• At this time fetal immune system does not recognize as foreign and
becomes persistently infected
o Congenital disorders = microphthalmia, cerebellar hypoplasia, hydrancephaly
▪ Cerebellar hypoplasia = hypermetria, hyperreflexia, nystagmus, strabismus,
opithothonus
▪ Affected less than 125 days gestation = early embryonic death, fetal death,
abortion, congenital defects, mummification or persistent infection
• Most likely to be persistently infected with nonCPE before 125 days
gestation
• Signs of persistent infection = asymptomatic, diarrhea, fever, pneumonia,
oral ulcerations, abortions, stillbirths, congenital anomalies
o Thrombocytopenia – BVD virus adheres to thrombocytes which are then removed by RE
system
▪ May see hemorrhage when platelets get low enough, hemorrhaging from scleral
vessels
▪ Diagnose via thrombocyte count (i.e. 5000) – give blood transfusion with fresh
whole blood
o Mucosal disease = chronic and severe BVD
▪ *Occurs when calf that was persistently-infected as fetus with a non-cytopathic
biotype of BVD is superinfected with a cytopathic biotype of BVD due to
rearranging of parent non-CPE viral RNA
▪ Diarrhea, acute death, oral ulcerations (on dental pad), occasionally causes
corneal opacity
▪ Lesions = severe ulcerations throughout GI tract (i.e. ileum, esophagus),
erosions on dental pad
- Pseudocowpox = parapox virus
o 3 related parapox viruses (all zoonotic) = pseudocowpox, contagious ecthyma, bovine
papular stomatitis
o Proliferative teat lesions – DDx for teat lesions = pseudocowpox, vesicular stomatitis,
bluetongue
- Bovine papular stomatitis (BPS) = parapox virus
o Fever, small raised lesions in mouth around gums and on dental pad
▪ DDx for oral ulceration = vesicular stomatitis, BVD, BPS, FMD
o Usually MILD, “calfhood” disease – if immunsuppressed may cause mortality – should
recover in 3 weeks
o Isolate calf, rule out BVD (BPS has raised lesions, lack of other oral lesions, and lack GI
signs)
-Bovine Winter Dysentery: = unknown etiology – suspect coronavirus.

o Explosive outbreak of watery diarrhea, and clotted dark blood, stabled animals in all
stages of winter.
BACTERIAL DISEASES
- Actinomyces bovis = LUMPY JAW (gram positive)
o Normal inhabitant of mouth and rumen – can infect when sustain injury to soft tissues
from scaborous feeds
o Decreased milk production, weight loss, hard non-painful swelling on mandible
(productive & destructive lesion)
▪ Radiographs show lysis and productive bone lesions with distortion of teeth in
that area
o Sodium iodide (arrests lesion), IV iodine (effective but not recommended due to food
safety), usually just CULL
- Actinobacillus lignieresii = WOODY TONGUE (gram negative)
o Normal inhabitant of rumen and mouth – when eat scaborous feeds allow access through
soft tissue lesions – causes granulomatous inflammation of tongue
o Large firm tongue (nodular, painful), decreased appetite, excessive salivation, losing
weight
o Treatment = change feed, IV sodium iodine and antibiotics (tetracycline)
- Fusobacterium necrophorum
o CALF DIPHTHERIA (3-18 months of age)
o Will die within a week if not treated – respiratory distress, moist and painful cough, loud
inspiratory stridor, head and neck extended, swelling around larynx, ozena (wasting
away of bony ridges of nose), fever, episcleral injection
▪ Can elicit cough on palpation of larynx – also can elicit pain and increased stridor
- Salmonellosis
o Salmonella typhimurium
▪ Fever, diarrhea, scleral injection, foul-smelling(septic tank odor), watery green
feces(diarrhea), death, decreased rumen contractions, septicemia, pneumonia,
meninigitis.
▪ Pseudo-diptheritic membrane of the intesintes
• Foul smell indicates serum proteins in feces, absorbed endotoxin (LPS)
cause other clinical signs
▪ Treatment = CEFTIOFUR – good activity against Salmonella (unless has been
used a lot on that dairy)
• In humans don’t treat enteric salmonellosis, in cattle is more severe and
can result in sepsis
▪ ZOONOTIC – enteric salmonellosis
o Salmonella dublin
▪ Carrier cow transmits to neonates at birth or via their milk
▪ SEPTICEMIA in dairy calves 4-8 weeks of age – death, decreaed appetite,
fever, rapid breathing
▪ Histopath = serosal and subcutaneous petechial hemorrhages, heavy wet lungs
▪ CULL carriers, vaccinate calves
- Mycoplasma bovis
o Transmission = via milk
o Respiratory signs (cough, tachypnea, nasal discharge), lameness (swollen joints,
tenosynovitis), fever
▪ Otitis media-interna – head tilt, ear droop, unilateral eye ptosis – usually recent
respiratory infection
• DDx for these signs = listeriosis, TEME
o Necropsy = lungs with multiple abscesses full of pus and casseated material
o Culture = Hayflick’s agar (microaerophilic environment)
o Treatment = tulathromycin (tetracycline, tilmicosin) – approved for respiratory disease
by M. bovis (Mycoplasma lacks cell wall so penicillin, cephalosporin are not good
choices)
- Campylobacteriosis = Campylobacter fetus ssp. Veneralis
o Obligate parasite of bovine genital tract – causes ABORTION, temporary infertility, early
embryonic death
ENDOCRINOLOGY and ELECTROLYTE ABNORMALITIES

- Milk fever = HYPOCALCEMIA in PERIPARTURIENT COWS
o Down, recently freshened, fed TMR, find barely responsive, unable to maintain sternal
recumbency, tachycardia, weak HR, no rumen motility, low body temperature, uterine
lochia red and mucoid, neck in “S” shaped curve
o Skeletal, cardiac, and smooth muscle weakness leads to signs – give IV calcium to
correct
▪ May cause heart to beat more slowly and more strongly – can lead to sinus node
arrest – be careful
o Prevention = DCAD (dietary-anion-cation difference) – makes cow more acidotic
▪ Benefits = PTH enhanced, lower incidence of milk fever, cows absorb calcium
more readily
▪ Monitor by checking urine pH (should be acidic – between 6.2 and 6.8) to make
sure cows are eating diet
▪ DCAD = (Na + K) – (Cl + S) – has more anionic salts (i.e. Cl and S) and less
cations (i.e. Na and K)
• Give this diet to cows in last 2-3 weeks prior to calving
o Treatment =
▪ As you treat the animal expect a tachycardia that slows to a bradycardia and
strong pulses.
▪ Remember Calcium Gluconate is a CARDIOTOXIN – too much too fast
- Grass tetany = HYPOMAGNESEMIA
o Occurs in cows on lush pastures that are high in potassium and nitrogen and low in
magnesium and sodium
o Several beef cows on pasture found dead, some staggering, down on side legs
paddling, elevated HR, fever, eyelids fluttering, nystagmus, champing of jaw
- Postparturient hemoglobinuria = HYPOPHOSPHATEMIA
o Decreased erythrocyte ATP which is needed for maintenance of ATP-dependent
membrane pumps – cells lyse
o Lactating cows are pale, icteric, and show hemoglobinuria – occurs in first lactational
month
o NO signs of methemoglobinemia or Heinz bodies, phosphorus levels <2 mg/dl result in
hemolysis
GASTROENTEROLOGY
- Calf diarrhea
o Big 5 = Salmonella, Coronavirus, Rotavirus, Cryptosporidia (ZOONOTIC),
enteropathogenic E. coli
o Salmonella =
o Coronavirus =
o Rotavirus =
o Cryptosporidia = 1-4 weeks old.
o E. Coli =
o White diarrhea, dehydration, hypovolemic, weak, unable ot stand, elevated HR, floppy
calf with metabolic acidosis
▪ Calf develops hypovolemia and metabolic acidosis and requires sodium containing
IV fluids which contain additional alkali such as sodium bicarbonate
▪ Hypovolemia, severe metabolic acidosis with hyperkalemia and possible sepsis
• Because of metabolic acidosis potassium leaves cells and calf becomes
hyperkalemic
• Septic as result of bacterial translocation across gut
- Abomasal ulcer = type 2 are bleeding ulcers

o Melena, anemia, collapse, weak, elevated HR and RR, heart pounds very loudly,
mucous membranes pale
o Treatment = blood transfusion (4-8 L fresh whole blood IV), omeprazole (hydrogen pump
blocker) and ranitidine can help raise abomasal pH, do NOT give NSAIDs because will
promote ulceration and decrease GI blood flow
- Abomasal volvulus/torsion = LESS common than LDA or RDA

o Recently freshened, decreased milk production, anorexia, teeth grinding, episcleral
injection, colic
o Distention of right flank, wide region of right sided monotone pinging from 9th-13th rib, no
rumen contractions
o Can SOMETIMES palpate (turgid structure to right of midline, far out of reach), fluid on
right/left on ballottment
o Bloodwork = hypochloremia hyokalemia metabolic alkalosis
▪ Sequester HCl in the abomasum (hypochloremia), become dehydrated and try to
maintain adequate BP by conserving sodium and in process retain bicarbonate
(alkalosis), because of alkalosis hydrogen will exchange for potassium and exit
cell to establish normal pH (hypokalemia)
▪ *PARADOXICAL ACIDURIA ! As result of decreased potassium and the need
to retain sodium due to hypovolemia the kidneys exchange hydrogen ions for
sodium anions (instead of K for Na) and thus hydrogen is excreted in the urine
o Surgical emergency! – correct it before cow goes into shock – IV saline (NaCl) with K
added in (no more than 0.5 meq/kg/hr of potassium) – DO NOT GIVE ORAL FLUIDS
(will add to fluid filled rumen)
- Left displaced abomasum

o Gas filled abomasum moves from its normal position near ventral midline to left of
rumen where it is trapped
o Common in first four weeks postpartum ! due to increased metabolic demands for
lactation, diet changes drastically and more gas is produced in abomasum
▪ Undergo postpartum hypocalcemia ! predisposes to decreased abomasal
motility, may contribute to displacement
o Prominent ping with VARIABLE changing pitch on left side of abdomen between 10th and
13th rib
o Recently freshened, production drops, decreased appetite, normal TPR, gaunt abdomen,
scant but normal feces
o Surgery can be done from either side
- Right displaced abomasum

o Much less common than LDA – clinical signs are more systemic/distress = episcleral
injection, elevated HR
- Intussusception
o Colic, scant dark (blackberry jam) feces (as bowel mucosa undergoes death), teeth
grinding, restlessness, kicking at abdomen, no rumen motility, dilated small bowel
proximal to lesion, distended abdomen (backed up GI tract)
▪ Fever if there is leakage – peritonitis develops
o Sausage shaped mass palpable per rectum (hard and painful mass on right – most
common in ileum)
o Hypochloremic, hypokalemic, metabolic alkalosis – chloride sequestered in abomasum
o Treat with right flank surgery – surgically remove intussussception and anastamose
intestines
- Cecal dilatation with or without cecal torsion

o Little feces passed over last 24 hours, colic, distended structure palpated just cranial to
pelvis (like loaf of bread)
o RIGHT sided ping heart from last rip to pelvis (high up)
o Treat with RIGHT flank surgery – remove gas and liquid from cecum, replace in normal
position (blind end towards pelvis), only amputate cecum if necrotic
- Gas in spiral colon

o COMMON finding in any sick cow with poor GI motility ! 8-inch circular ping high on
last rib or just behind
- Frothy bloat = consumption of LUSH LEGUMES (not due to vagal indigestion like free gas
bloat is)
o Respiratory distress due to tremendous abdominal pressure, pass stomach tube and
little or no gas esecapes, insert trocar into rumen and froth exits
o Treatment = poloxalene orally – reduces surface tension and destabilizes froth
- Vagal indigestion
o Anorexia, decreased milk production, elevated temperature and HR, no rumen motility,
scant feces, PAPPLE shape
▪ “BOINK” hollow sound over left flank – between ribs 9-13 extending to the hip
(gas-filled rumen)
▪ PAPPLE = i.e. from hardware disease – local peritonitis leads to poor motility of
forestomachs, rumen fills with fluid and develops gas cap, abomasum
accumulates fluid – pear on right, apple on left
o Type 1 = free gas bloat, FAILURE TO ERUCTATE
▪ Associated with swollen mediastinal lymph nodes – signals that detect gas
pressure and open cardia are compromised so eructation does not occur
▪ Weight loss, enlarged LEFT flank (left abdomen gas filled), rumen has poor
motility, bronchopneumonia
▪ Treat the pneumonia – create temporary rumen fistula to allow gas to escape
until eructation occurs
o Type II = FAILURE OF OMASAL TRANSPORT
▪ Results in fluid-filled rumen with some dorsal gas – lack of motility, inappetance,
depression, decreased production, dehydration, variable xiphoid pain
▪ On ballottement feel large fluid-filled rumen, monotone ping on left side from 11th
rib to hip, PAPPLE
▪ Difficult to distinguish from failure of pyloric outflow except that that has more
profound acid-base and electrolyte disturbances and the cow will appear much
sicker
o Type III = FAILURE OF PYLORIC OUTFLOW
▪ Cows have internal vomiting and accumulate chloride in rumen – hypochloremic,
hypokalemic metabolic alkalosis – appear MUCH SICKER
• Occurs as result of intestines not being able to reabsorb chloride into
bloodstream after secreted into abomasum – chloride is strong anion and
results in metabolic alkalosis when it is decreased
o Type IV = ABOMASAL IMPACTION
▪ Not common in cows – more common in Suffolk sheep
- Bristle grass irritation = Sertaria lutescens (yellow bristle grass)
o Grass contains sharp barbs that stick into mucosa of young cattle and horses and
cause oral ulcers – reluctance to eat
o Removal from diet results in healing
MASTITIS
- Lactation = reach peak lactation at 4-8 weeks postpartum, lasts around 305 days then cows
dried off for 60 days
o Oxytocin = responsible for milk letdown
o Prolactin = suckling stimulates release of this, responsible for milk production
o Somatic cell count = desirable bulk tank SCC = less than 200,000 cells/ml
o Bovine somatotropin (BST) = approved to be given to cattle to promote milk production
- To prevent mastitis….
o Fore strip each quarter, shut off vacuum befor removing claw, post dip all teats (reduce
CONTAGIOUS), pre dip all teats (reduce ENVIRONMENTAL), replace liner when
needed, only milk 5-7 minutes (when they are milked out)
- CONTAGIOUS MASTITIS = Staph. auerus, Strep. agalactiae, Mycoplasma bovis – spread by
milker’s hands/equipment
o Streptococcus agalactiae
▪ Gram positive – obligate pathogen of mammary gland – usually subclinical
mastitis, but may see high SCC
▪ CAMP reaction – plate S. aureus & S. agalactiae and see them act together to
lyse RBCs – creates clearing
▪ Treatment = ONLY ORGANISM that responds during lactation to approved
intramammary infusion
o Mycoplasma bovis
▪ See sepsis, joint infections, respiratory disease, and mastitis ! arthritis,
tenosynovitis, otitis media, reproductive disease, keratoconjunctivitis
• Spread to young calves (ear infections) via milk
• Older caws ! see pneumonia, arthritis, tenosynovitis, mastitis, abortion
▪ Fibrosis of glandular tissue – diagnose by seeing this and combination of clinical
disorders
▪ CULL – poor response to treatment and very contagious
- ENVIRONMENTAL MASTITIS = Coliform mastitis (E. coli), Prototheca, Streptococcus,
Klebsiella pneumoniae, Pseudomonas aeruginosa, Enterobacter aeruginosa, Arcanobacterium
pyogenes, Proteus
o Coliform mastitis ! absorbed endotoxin (LPS) causes many systemic signs
▪ Cow recently freshened, down and unwilling to rise, scleral injection, rumen
empty, motility poor
▪ Involuting uterus on rectal exam – discharges brownish red mucoid non-odorous
lochia through the vagina
▪ *Udder is swollen, hot and painful – serum-like secretions with clumps of fibrin in it
o Treatment = frequent milking, anti-inflammatories, antibiotics, IV fluids
RESPIRATORY
- Shipping fever = fibrinous pleuropneumonia = Mannhemia hemolytica

o Sometimes caused by Haemophilus somnus (fibrinous pneumonia), Pasteurella
hemolytica (+ viruses and stress)
o Depression, off feed, breathing hard, severe fever, increased RR and HR, injected
scleral vessels, dyspnea, cough
▪ On auscultation hear crackles and wheezes, pleural rubs (pleural effusion, septic
pleuritis), harsh inspiratory and expiratory sounds with expiratory wheezes
o Seen in OLDER (i.e. >8 months usu) animals with a recent history of being shipped/
stressed
o Necropsy = fibrinopurulent bronchopneumonia
o Treatment = DO NOT give a steroid, antibiotic (sulfadimethoxine, ceftiofur, PPG,
tetracycline)
- Enzootic pneumonia = Pasteurella multocida

o Loud cough, tachypnea, diarrhea, ill thrift for a few days – NO SIGNS of sepsis/
depression/loss of appetite
▪ Usually also have Eimeria bovis (coccidian) causing the diarrhea
▪ Crackles and wheezes, harsh bronchial tone cranioventrally (cranioventral
consolidation)
o Common in CALVES (3-8 months of age) – economically devastating – calves gain
weight slowly
o MULTIFACTORIAL – poor housing and environment, many other organisms involved
(ammonia, carbon dioxide, hydrogen sulfide, Mycoplasma, Corynebacterium, BVD,
BRSV, PI3)
- Farmer’s lung = allergies

o Episodic signs – usually animal housed indoors and exposed to allergen – keeping
animal outside will help
- Silo filller’s disease = bronchiolitis obliterans

o History of animal being housed close to silo – inhalation of toxic silo gases
- Pharyngeal trauma - .
o Causes = paste/balling gun, foreign body such as stick or wire in feed – penetrate
pharynx
o Mild bloat, inappetance, extended head, drooling, swelling and pain in throat area, fever,
coughing, reluctance to palpate throat area, breath smells necrotic (no obvious lesions
in mouth)
o Treat with antibiotics, NSAID, soft diet – prognosis good with conservative therapy
- Laryngeal papillomatosis = papovirus

o Common in feedlot cattle – stertorour respiration, cough – no systemic signs
ORTHOPEDICS
- LATERAL REAR DIGIT ! over 80% of foot disease involves this because bear most weight
here
- Coxofemoral luxation = cranial and dorsal displacement

o Usually these cows down after parturition and fail to respond to hypocalcemia therapy
o Dystocia and sciatic or obturator paralysis will increase risk of luxation
- Osteochondrosis dessicans -
o Most common site = HOCK, least common site = elbow
- Spread eagle ! ADDUCTOR muscles commonly injured (gracilis, pectineus, adductor magnus
et brevis)
- Ruptured peronesus tertius = able to extend hock and concurrently flex stifle
- Ruptured serratus ventralis = “flying scapula” if this ruptures
- Ruptured cruciate ligament = drawer movement in the stifle, difficult to perform drawer in cattle
- Flexural deformities of distal limb (in calves)

o Usually caused by contracted tendons – treat with deep digital flexor tenectomy,
superficial digital flexor tenectomy, splinting – NOT external fixator (because still
growing)
- Corns = lesion in interdigital area making cow lame
o Surgically remove mass with sedation – be careful not to invade interdigital fat pad
o Area is then bandaged and claws temporarily wired together if necessary
- Sole abscess -
o Pare out abscess and drain it
o To keep in production while resolves ! apply a wooden hoof block (if lesion is lateral –
place block medial)
- Pododermatitis circumscripta = lesion at sole/bulb junction
o Usually weight bearing claws affected first (lateral digits in hind, medial in front)
- Septic arthritis and osteomyelitis

o Causes = foreign body/puncture wound, hematogenous spread, extension of cellulitis
o See destructive lesion in both bone and joint of young animal – diagnose via culture
o Vigorously lavage or surgically open and flush – aggressive systemic antibiotics based
on culture
- Spastic paresis = Elso heel

o Hereditary disease that produces stiffness of the hocks – see signs at 3 weeks – 1 year of
age
o Combination of genetics and environment that cause overstimulation of gamma motor
neurons in spinal cord
o Calf with inability to walk, difficulty getting up, no signs of trauma, hocks will not flex due
to continuous gastrocnemius tension – signs progress over a month or two
o Treatment = tibial neurectomy or gastrocnemius tenectomy
- Spondylosis = degenerative intervertebral joint space disease in OLDER bulls

o Develop back pain due to degenerative conditions in the lumbar or thoracic vertebrae
▪ Painful osteophytes called enesiophytes develop across the intervertebral space
MUSCULAR DISORDERS
- Periodic spasticity -
o Inherited disorder of most dairy breeds (rare in beef) – first appears at 3-7 years of age
and gradually worsens
o Marked muscle spasms of hip and upper leg muscles – episodic spasms and stiffness
which can last for minutes
- Myotonia congenital-
o Inherited disorder in the skeletal muscle CHLORIDE channel – can confirm diagnosis via
electromyography
o Non-progresive general rigidity that mainly occurs after tactile, auditory, or visual
stimulation
- Myophosphorylase deficiency = glycogen storage disorder

o Myophosphorylase is a muscle enzyme – genetic disease in Charolaise cattle
NUTRITIONAL DISORDERS
- Copper deficiency
o Primary = low level of copper in feed
o Secondary = interference with absorption of copper due to presence of molybdenum and
sulfates
▪ Is usually secondary associated with low copper levels and high levels of
molybdenum (sagebrush in dry alkaline environment)
▪ *Copper levels in feed should be at least 5 times those of molybdenum
o Diarrhea, poor BCS, lameness, anemia, infertility, fever, diarrhea & respiratory disease
nonresponsive to antibiotics
▪ ACROMOTRICHIA (absence of pigment in hair) – dilusion of coat color due to
dysfunction of tyrosinase (converts L-tyrosine to melanin)
▪ Demyelination and pathologic fractures of the vertebrae
o Definitive diagnosis based on LIVER BIOPSY – before serum copper drops the liver
must be depleted of stores
o Treat with copper supplements such as copper oxide orally (in molasses or salt), or give
copper by injection
- Vitamin C deficiency = VERY RARE in ruminants, may cause crusting/alopecia/pruritis
- Vitamin D deficiency = RICKETS, bone abnormalities
- Vitamin A deficiency
o Common in FEEDLOT animals because do not have access to vitamin A rich green
plants
o Convulsions and blindness common – stargazing, diarrhea, anisocoria, strabismus
▪ Pupillary light reflex = ABSENT in both eyes – due to retinal degeneration and
constriction of CNII
▪ DDx = polioencephalomalacia, lead poisoning, salt poisoning – but papillary light
intact with these
- Selenium deficiency/Vitamin E deficiency = WHITE MUSCLE DISEASE (nutritional myopathy)
o Vitamin E deficiency = milk replacers with linseed oil, soybean oil, fish oil, corn oil !
these oils are high in polyunsaturated fatty caids so need to increase Vitamin E so it can
scavange the free radicals that will result
o Selenium = essential for glutathione peroxidase which breaks down hydrogen peroxide
and lipoperoxide to water or harmless alcohols – so involved in free radical protection
▪ WMD occurs from having excessive free radicals which cause intracellular
membrane damage – lets excess calcium into cell which causes increased
mitochondrial calcium and mitochondrial damage – causes hyperconcentration of
muscles and eventual necrosis and hyalinization
o Two forms = cardiac (acute death), skeletal (show clinical signs)
▪ Severely weak, trouble breathing, frothy nasal discharge, trouble rising, swollen
painful muscles, painful
o Necropsy = pale and dry skeletal muscle, white streaks running through muscle bundles
o To diagnose – can measure glutathione peroxidase (will be low), increased AST/LDH/CK
(NOT SDH – others released with muscle damage)
- Alpha-mannosidosis = genetic defect of the enzyme alpha mannosidase
o See in – Murray gray, Simmental, Holstein, Galloway, and Angus cattle
o Without enzyme alpha mannosidase the cleavage between N-acetyl glucosamine and
mannose will not occur and the oligosaccharide will accumulate within the lysosomes of
neurons, reticuloendothelial cells, and macrophages
o First sign at 1-15 months = mild ataxia of pelvic limbs after exercise – leads to
hypermetria, aggressiveness, intention head tremors – eventually causes diarrhea,
recumbency, and death
MISCELLANEOUS DISEASES
- Mad cow disease = Bovine Spongiform Encephalopathy (BSE) = PRION
o Dogs are only species not know to have a TSE – cats, sheep, humans, and cows all
have one
o Neurologic signs, hypermetria, ataxia, hyperexcitability, hyperesthesia
o ZOONOTIC – Creutzfeldt-Jakob disease – humans have psychiatric symptoms,
depression, schizophrenia – neurologic signs progress to difficulty walking and
involuntary movements – immobile and mute and then die
▪ Variant Creutzfeldt-Jakob disease – affects young peope and linked to exposure
of infected beef
- Maple syrup urine disease = encephalopathy
o Genetic disorder causing spongiform changes in brain – Hereford and polled Shorthorn
calves (2-3 days old)
o Deficiency in branched-chain ketoacid decarboxylase – causes accumulation of 2-keto-
methylvaleric, 2-ketoisocaproic, and 2-isovaleric acids along with their precursors
(isoleucine, leucine, valine)
▪ These are excreted in urine and result in BURNT MAPLE URINE SMELL
- Traumatic reticulopericarditis = HARDWARE DISEASE
o Decrease in milk production, fever, elevated HR, brisket edema, enlarged/dilated jugular
vein, muffled heart with occasional splashing sounds (“washing machine” murmur), poor
appetite, stiff walk, arched back
o Metallic foreign body (wire, nail) that pierced reticulum and then pericardium – leads to
lots of pericardial fluid – causes constrictive heart disease and heart failure
o Diagnose = clinical signs, scooch/xiphoid test (push down on withers – will grunt in pain)
o Treatment = magnet, antibiotics, confinement, surgery if necessary
o Prevent by giving all cows a magnet and keeping them away from wire – prognosis is
poor
- Uroabdomen = usually due to urolith
o Not eating well, normal temp/HR/RR, ventral abdominal edema, breath smells like
ammonia
o Hyponatremia, hypochloremia, hyperphosphatemia – azotemia and possibly
hyperkalemia
- Pyelonephritis = E. coli (and other coliforms), Corynebacterium renale
o Cessation of lactation, anorexia, elevated HR/RR, arched back due to pain
o Enlarged and painful kidney on rectal, cloudy and bloody urine
- Pinkeye = Infectious Bovine Keratoconjunctivitis (IBK) = MORAXELLA BOVIS
o Musca autumnalis (face fly), Moraxella bovis, and UV light!!
o Blepharospasm, chemosis, photophobia, very painful (decreases productivity)
o Central ulcer in eye ! usually resolves in a few weeks but may obseve descemetoceles
and corneal perforation
- Fatty liver syndrome = HEPATIC LIPIDOSIS
o Usually see in cows with body condition score 4.5.5 – fat cows predisposed because
when they encounter negative energy balance (i.e. postpartum when their energy needs
increase for lactation) they mobilize fat stores in such a way that the liver cannot keep
up with the triglycerides coming in
o Necropsy = enlarged liver, diffusely light yellow in color, easily friable, floats in formalin
(due to decreased density of lipid vacuoles) – DDx = lymphoma (but lymphoma liver
won’t float)
- Lipofuscinosis = storage disease that gives liver a dark appearance
o SEPSIS – in day old calves – decreased appetite, fever, elevated HR, scleral injection,
cloudy material in anterior chamber (= hypopyon)
o To diagnose = measure IgG (LOW), protein refractometry (<4.5g/dl is consistent with
failure)
o Treatment
▪ 3 day old calf ! transfuse with 1-2L plasma, antibiotics
▪ Younger calf ! colostrum (after 3 days is poor source due to poor absorption of
immunglobulins)
• IgG is immunoglobulin that predominates in bovine colostrum
- Freemartin = fusion of fetal membranes between male and female set of beef cow twins
o Freemartin results form exposure of female to Mullerian inhibiting hormone which is
being secreted by male – she is exposed as result of anastamosis between
chorioallantoic vessels
o Usually more than 90% of the cases are Freemartin when this happens
o Clnical signs = abnormally small ano-genital distance, enlarged clitoris
- Trichomoniasis = Trichomonas foetus
o Usually asymptomatic…in females causes pyometra post-coital, poor calving
percentage, early embryonic death
▪ Usually pyometra is postpartum so if post-coital strongly consider this and look
for reservoir bull
o Maintained in herd by MATURE BULL – due to increased depth of epithelial crypts of
bull’s glans penus and prepuce (increases “niche” where organism thrives) – young
bulls usually can clear it due to SHALLOW crypts
- Uterine torsion = if torsion clockwise = push forward on vagina and roll cow clockwise
- Infectious pustular vulvovaginitis = herpesvirus – white plaques on vagina
- Causes of abortion…
o Infectious causes = Akbane virus, BVD, IBR (rapid fetal death – focal necrosis of
organs), Brucella abortus (fetal inflammation, placentitis – eradicated from US so is
REPORTABLE, Rb51 is vaccine), Leptospira Pomona
o Twinning ! see twins on necropsy (at about 8m gestational age), no gross/histologic
lesions on any organs
- Endometritis = ascending infection, usually Arcanobacter pyogenes (also P. multocida,
Pseudomonas aeruginosa, E. coli)
o Normal vitals, normal appetite, normal milk production, mucous and pus running from
vulva
o Treatment = intrauterine penicillin or tetracycline, or povidone iodine and lavage with
saline if don’t want antibiotic residues in milk
Feline Diseases
VIRAL DISEASES
- Feline infectious peritonitis (FIP) = CORONAVIRUS
o Transmission = FECAL-ORAL – NOT contagious, just because one cat dies of FIP
doesn’t mean others will
▪ Feline enteric coronavirus has to mutate to FIP – see in YOUNG and
IMMUNOSUPPRESED
o Pyogranulomatous vasculitis due to Ag-Ab complexes depositing in venular endothelium
▪ Complement-mediated inflammation results in pleural and peritoneal fluids (WET
FORM)
• Dyspnea, fever, weight loss, anorexia, diarrhea, lethargy, abdominal
distention due to ascites
• Pericardial effusion = muffled heart sounds, elevated HR, weak pulses,
large globoid heart
• *Pleural effusion = high protein (5-12 g/dl), thick, cellularity low,
predominant cell type is neutrophil, clear to yellow (hazy gold), sometimes
have fibrin clots
▪ Partial cell-mediated inflammation causes slow viral replication and granuloma
formation (DRY FORM)
• Depends on organ affected – hepatopathy, splenomegaly, renal failure,
etc.
o Diagnosis = cornavirus titers (USELESS – reacts with all coronaviruses), 7B protein
ELISA (not useful because some FIP viruses do not have 7B), BIOPSY and
HISTOPATH (gold standard)
▪ Histopath = pyogranulomatous and fibrinonecrotic reaction around small veins
o Prognosis = POOR – considered FATAL disease
- Feline immunodeficiency virus (FIV)
o Transmitted by SALIVA (BITE WOUNDS) – males more aggressive so 2-3 times more
likely to be infected
▪ ***One of few viruses not passed by passive contact and sharing a litterbox***
o Affects B-cells, T helper (CD4+), macrophages, cytotoxic T-cells (CD8+)
▪ Replication occurs in lymphoid and salivary tissue – virus spreads to
mononuclear cells (viremia is suppressed by host immune response for several
years – carrier phase) – slow decline in CD4+ cells is seen resulting in failure of
immune system – cats are 10-15 years old by the time this occurs
▪ Makes animal very IMMUNOSUPPRESSED and susceptible to infections
o Diagnosis = ANTIBODY ELISA for FIV (does not produce enough antigen to measure)
▪ Kittens must be tested after 6 months (maternal antibodies), vaccination may
show positive antibody titers
- Feline leukemia virus (FeLV)
o Sheds in SALIVA – requires prolonged, close contact to transmit
o Active infections seen in cats greater than 10 years old – infected when have inadequate
immune response, persistently shed, disease occurs months-years later when stressed
or immunosuppressed
o Leads to leukemia, lymphoma, anemia, myelodysplasia
▪ Most common type of lymphoma in FeLV cats = MEDIASTINAL – see in cats
less than 3 years old – dyspnea, regurgitation, Horner’s syndrome
▪ Second most common = MULTICENTRIC
o Diagnosis = ANTIGEN ELISA for FeLV
- Panleukopenia virus (aka feline distemper, kitten “parvo”) = PARVOVIRUS
o Cats only shed virus for up to 6 weeks after they recover – most common in YOUNG
KITTENS
o Damages rapidly dividing tissues – i.e. bone marro wand GI tract = anorexia, lethargy,
vomiting, diarrhea, dehydration, fever
o If infected in utero = CERBELLAR HYPOPLASIA ! inability to regulate motor function
– ataxia, tremors, difficulty keeping balance, hypermetria, wide based stance, vestibular
signs, postural reactions, UMN signs in limbs
- Feline calicivirus
o Lethargy, anorexia, sneezing, conjunctivitis, nasal discharge, COMMONLY oral
ulcerations, chemosis, ptyalism
▪ STOMATITIS with gingivitis (with bacterial infection)
▪ Lethal feline calicivirus (highly virulent) = ulcerative and edematous lesions of skin
on head and limbs
• May be jaundiced (hepatic necrosis), thromboembolism and coagulopathy
by DIC may cause petechiations, ecchymoses, epistaxis, or hematochezia
o Treatment = clindamycin (for bacterial infection with stomatitis – NOT DOXY in cats
because of esophageal stricture), sucralfate (coat GI ulcers), analgesia, esophagotomy
tube (if won’t eat on own), L-lysine (antiviral)
- Feline herpesvirus = feline viral rhinotracheitis
o 80-100% of cats become carriers (without showing clinical signs) – flares up with
STRESS
o Conjunctivitis, coughing, fever, anorexia, dendritic ulcers in eye (LINEAR), RARELY oral
ulceration
▪ Ocular manifestations = conjunctivitis, corneal ulcers, AND eosinophilic keratitis
and corneal sequestrum (pathognomonic for herpes) – only infectious cause of
corneal ulcers in cats
o Treatment = L-lysine (antiviral), decrease stress
BACTERIAL DISEASES
- Chlamydophila felis
o Upper respiratory tract infection ! acute onset of severe chemosis, conjunctivitis,
sneezing – NO oral or cutaneous lesions (differend from herpes and calicivirus)
o Treatment = tetracyclines
- Mycoplasma haemofelis = feline infectious anemia
o Treatment = doxycycline (careful because of esophageal strictures)
- Bartonella henselae = CAT SCRATCH FEVER (humans), Bartenollosis (cats – usu
asymptomatic)
o Infects RBCs of cats and is transmitted by FLEAS – cat gets flea dirt in their claws then
scratches human
▪ ZOONOTIC – human gets fever, headache, malaise, lymphadenopathy
o Treatment = doxycycline, flea treatment – will always be carriers though, so only treat
actively bactermic cats
o Diagnosis = 5 tests (ELISA, IFA, PCR, culture, Western Blot)
- Yersinia pestis = PLAGUE
o Reservoir = RATS – transmitted by fleas or eating an infected rodent
o Lethargy, fever, mandibular lymphadenopathy with draining tract under chin, covered in
fleas, outdoor cat or stay found in area where lots of rodents (i.e. prairie dogs, rats)
▪ Also see in DOGS ! dog that ate a rat, fever, lymphadenopathy
o
Wear protection, quarantine the animal, call the state veterinarian!!!
o
Cytology = bi-polar safety-pin appearance, definitive diagnosis based on culture!
o
Treatment = lance “buboes” and flush it, usually recover on own
o
ZOONOTIC – bubonic, septicemic, pneumonic, and meningeal forms
▪ Clinical signs can occur in 1-2 days in cats, but incubation period in humans is up
to 8 days
HEPATOLOGY
- Cholangiohepatitis
o Causes = secondary to biliary obstruction (i.e. cholelith), ascending infection or immune-
mediated damage to liver
▪ See in conjunction with IBD and/or pancreatitis
o Inappetance, depression, fever, dehydration, icteric
o Bloodwork = elevated WBC, elevated ALP/ALT/GGT, elevated bilirubin
o Ultrasound = enlarged liver with normal echogenicity, hyperechoic wall of common bile
duct, distended bile duct, may see cholelith causing obstruction, enlarged gallbladder
with thickened wall
o Histopathology = infiltration of neutrophils into portal areas
o Treatment = supportive care, fluids, ampicillin, metronoidazole, ursodeoxycholic acid,
Vitamin E, milk thistle
▪ Treat for 2 MONTHS with antibiotics – one that is excreted unchanged in bile (so
not TMS because undergoes hepatic metabolism)
▪ Surgical decompression – when you see cholelith or complete biliary obstruction
– stabilize with fluids first
• Biliary-to-intestinal diversion (cholecystoduodenostomy or
cholecystojejunostomy)
o Prognosis = FAIR – half cats do poorly (dead/euthanized within 3 months), half respond
to treatment and live
- Lymphocytic portal hepatitis
o Similar to CHOLANGIOHEPATITIS in signalment, clinical signs, and lab findings – liver
BIOPSY differentiates
o Anorexia, weight loss, enlarged liver on palpation (normal gallbladder), elevated WBC,
elevated ALT/ALP
o Histopath = infiltation of lymphocytes and plasma cells (NO neutrophils) into portal areas
but not bile ducts
o Prognosis = GOOD – mean survival is greater than 2 years with treatment – disease is
slow to progress
- Hepatic lipidosis = FATTY LIVER SYNDROME
o See in OBESE – older cats (8-9 years old) – anorexia, lethargy, icterus, enlarged liver
on abdominal palpation
o Bloodwork = elevated liver enzymes (NOT GGT), elevated bilirubin, bilirubin on
urinalysis
▪ Cholangiohepatitis and neoplasia have elevated GGT
o Ultrasound = liver appears enlarged with hyperechoic hepatic parenchyma, gallbladder
is normal
o Cytology = cluster of hepatocytes with cytoplasmic lipid droplets
o Treatment = *place feeding tube for immediate and ongoing nutritional support (VERY
IMPORTANT – decreases mortality from 90% to 30%), neomycin and lactulose (to
decrease hepatic encephalopathy), Vitamin K1 (when causes coagulopathy), L-
carnitine, manage electrolyte abnormalities (i.e. hypokalemia)
GASTROENTEROLOGY
-Linear foreign body
o Acute onset of vomiting, anorexia, dehydration, painful abdomen
o Anchors in cranial GI tract (i.e. under tongue) and then causes GI tract to bunch up –
see intestines bunched/plicated in accordian-fashion on radiographs
o Treatment = exploratory surgery to remove foreign body – DO NOT PULL STRING –
could perforate intestines!
- Megacolon
o Due to chronic stretching of colon from feces impactions colon can no longer move
feces out of body
o Chronic constipation, vomiting, sraining to defecate, palpate hard feces in colon –
obstipation in cats
o Medical management = adequate hydration, remove impacted feces (enema), laxative
therapy (lactulose), promotility agents (cisapride), dietary fiber (increase transit time of
ingesta – psyllium, canned pumpkin)
o Surgical treatment (when refractory to medical therapy) = SUBTOTAL COLECTOMY
▪ Transect colon distal to cecum and desending colon proximal to pubis –
anastamose them together and preserve ileocolic junction (ileocolic artery limits
amount you can resect)
- Hairballs
o Intermittent vomiting, usually longhaired cat, chunks of hair in vomit
o Treatment = laxatone, a high quality diet, frequent brushing, metoclopramide (anti-
emetic, promotility)
DERMATOLOGY
- Psychogenic alopecia
o Systemically healthy, alopecia on ventral abdomen
o Microscopically shows short blunted hairs with normal underlying skin ! consistent with
excessive grooming
- Eosinophilic granuoma = LINEAR GRANULOMA
o Lesion = linear in shape, pink-yellow in color, no crusting/pruritis, well circumscribed
o Thought to be due to hypersensitivity and allergies to fleas, food, or inhalants
o Treatment = controlling hypersensitivity, sometimes antibiotics and corticosteroids
- Feline acne
o Deep pyoderma condition of the chin – crusting and alopecia on ventral rostral mandible
o Clean with antiseptic solution daily
RENAL
- Feline lower urinary tract disease (FLUTD) = aka feline urologic syndrome (FUS), feline
idiopathic cystitis (FIC)
o Group of clinical signs that occur with lower urinary tract obstructions (uroliths, mucous
plugs, infections, TCC)
▪ Feline idiopathic cystitis is the cause in otherwise healthy cats that have no other
problems
o Clinical signs = dysuria, pollakiuria, hematuria, crystalluria, urolithiasis, stranguria
o Treat by surgically removing stones/obstruction, is likely to recur once cat has had it
once
- Urethral obstruction
o MALE cats, difficulty urinating, lethargic, weak, vocalizing while frequently posturing to
urinate, firm bladder
o Hyperkalemia – occurs due to impaired urinary excretion of potassium – can lead to life-
threatening arrhythmias
o Treatments
▪ Immediately – give IV calcium gluconate (or calcium chloride) – to counter effects
of hyperkalemia-induced bradycardia and cardiovascular collapse
▪ Relieve urethral obstruction by placing urinary catheter
▪ 0.9% sodium chloride – because has low potassium (may also want to give
dextrose to stimulate insulin secretion and move potassium intracellularly – could
also administer insulin but give dextrose too!)
▪ Perineal urethrostomy – preserve pudendal nerves so don’t have urinary
incontinence due to loss of somatic innervation to urethral sphincter
o After go home if still straining frequently and find bladder empty on palpation but bladder
wall feels thickened…
▪ Give PHENOXYBENZAMINE – likely have hypertonicity of urethral muscle –
this drug will reduce internal urethral sphincter tone so cat can urinate easier
▪ DO NOT treat with corticosteroids to reduce inflammation because predisposes
them to developing UTIs
- Polycystic kidneys
o Common in PERSIANS – bilaterally enlarged kidneys on palpation, multiple large fluid-
filled structures in parenchyma of kidneys
RESPIRATORY
- Pleural effusions
o Rapid shallow breathing, quiet lung sounds, heart auscults normally, no crackles or
wheezes, dyspnea, open-mouth breathing, tachypnea, fever (if due to infection –
pyothorax, FIP)
o Radiographs = severe loss of detail in thorax, retraction of lung lobes, can’t visualize
heart
o Treatment = administer oxygen, chest tap to evaluate type of effusion, thoracocentesis
to drain (unless its hemothorax!), take radiographs in dorsoventral for animals in
respiratory distress
o Chylothorax = common in Siamese and Himalayans, see in dogs too
▪ Accumulation of lymphatic fluid in pleural space, clear-to-milky white fluid !
white to pink in color, opaque, variable protein level (2.6-10.3 g/dL), WBC count
can be over 7,000 cells/ul
▪ To confirm = compare pleural fluid triglycierides to serum triglyceride levels !
effusion triglycerides higher than serum triglycerides = chylothorax
▪ Cause = ruptured thoracic duct, abnormal flow or pressures in the thoracic duct
▪ Medical management = low fat diet, Rutin, intermittent thoracocentesis
• Somatostatin = useful in resolution of pleural fluid (EXPENSIVE)
▪ Surgical treatment = ligation of thoracic duct and pericardectomy – do when
medical management fails
o Pyothorax = pus in the pleural space
▪ Fluid = white with yellow tinge, foul odor, bacteria (degenerate neutrophils), fungi
(non-degenerate neutrophils)
▪ To confirm = decreased glucose in effusion compared to serum is consistent with
infectious etiology
▪ Cause = bite wound that introduces bacteria into chest, migrating foreign body,
extension of pneumonia into pleural space
▪ Teatment = chest tube with continuous suction, drainage and lavage of pleural
space (isotonic fluid), antibiotics based on C/S for 4-6 weeks, surgical exporatory
o Hemothorax
▪ Fluid = BLOOD – from trauma, coagulopathy
▪ Treatment = DO NOT REMOVE IT!!
o Other = neoplastic effusions (i.e. lymphoma), infectious effusions (i.e. FIP), effusion due
to heart failure
- Feline asthma
o Acute or chronic airway inflammation that occurs due to various stimuli – i.e.
environmental allergens
o Dyspnea, coughing, open mouth breathing, abdominal effort when breathing, increased
RR, wheezing
o Radiographs = diffuse bronchial pattern with airway thickening appearing as so called
“tracks and doughnuts”
o STABILIZE ANIMAL BEFORE DIAGNOSTICS!!! Use beta-2 agonists, oxygen, quiet
environment.
o Treatment = Beta-2 agonists (i.e. terbutaline, theophylline, albuterol), oxygen,
corticosteroids (reduce inflammation), NOT ATROPINE (thickens bronchial secretions,
encourages mucous plugging of airway)
ONCOLOGY
- *Vaccine associated fibrosarcoma
o Mass in scapular region – tumors grow slowly and metastasize but extremely
aggressive locally
o Thought to be associated with adjuvant (i.e. aluminum based adjuvants) – 3 tumors per
10,000 vaccines
o Treatment = radical excision of mass
o **VACCINE PROTOCOLS** ! rabies = distal right rear leg, FeLV = distal left rear leg,
no vaccines given in intrascapular space, give the rest in distal right front leg
▪ Do NOT give vaccines intramuscularly – will take longer to diagnose these
- Cutaneous SCC
o Common in WHITE CATS – see with solar exposure (caused by UV light)
o Usually ULCERATIVE and appear around NOSE, ears, and eyelids – common on
nasal planum
o Treat with surgery or radiation – if small enough radiation with Strontium-90, if larger
excise it
- Basal cell tumor = EPITHELIAL TUMOR
o Common in OLDER cats – most common skin tumor in cats ! firm/freely moveable, SQ
mass, hairless, may appear slightly melanotic, usually 2-4 cm, well circumscribed,
slowly growing ! HEAD, NECK, SHOULDERS
o Most (>90%) show benign behavior, even when histologically malignant with high mitotic
rate
o If diagnose prior to removal – monitor it without removal unless ulcerates and gets large
! if removed monitor the site for recurrence
- Feline traumatic sarcoma
o History of trauma to the eye, phthisis bulbi, corneal edema, scarring, no menace, no
PLR, blindness
▪ If eye has history of trauma and is now blind – suspect this!! Is VERY malignant
in cats!
o Treatment = ENUCLEATION – even if there is no pain, if you wait for signs it has
typically metastasized
MISCELLANEOUS FELINE
- Capital physeal dysplasia = young male NEUTERED cats, OBESE
o Fracture across femoral head physis
- Hyperextension injuries of carpal joint = common since cats jump from high heights and always
land on feet
o Treatment = carpal arthrodesis – conservative therapy carries guarded prognosis
▪ To do this debride articular cartilage of joints, implant cancellous autograft into
debrided joint space, fix bone plate across injured joint
- Central retinal degeneration (FCRD) = TAURINE DEFICIENCY
o Rarely see this now that commercial diets are balanced – but happens because
photoreceptors contain lots of taurine and cats cannot synthesize it
o Elliptical area of tapetal hyperreflectivity starting in area centralis dorsolateral to the optic
disk that progressies to a horizontal band and eventually can involve the entire fundus
- Blindness due to hypertension
o Causes of hypertension = hyperthyroid, renal disease, cardiac disease – treat
underlying condition
o Loss of balance, unsure of distance when jumping onto things, bumping into things
o Fundic exam = engorged retinal vessels, hazy retina and difficult to see detail of optic
nerves or vessels, markedly dilated, no menace – supect eyes have detached retina
o Blood pressure = HIGH (i.e. 260 mmHg)
o Treat with AMLODIPINE (calcium channel blocker) – slows rate at which calcium
moves into heart and into vessel walls – relaxes vessels and allows better blood flow
thus reducing blood pressure
- Diet
o Taurine deficiency ! taurine is an essential amino acid for cats because they cannot
synthesize it
▪ Develop ! dilated cardiomyopathy and central retinal degeneration
o Arachidonic acid ! also require this in their diet
o Thiamine deficiency ! rare to happen in outdoor cats because they will hunt – causes
seizures
Dog Diseases
VIRAL DISEASES
- Distemper = paramyxovirus
o Shed for several weeks after infection ! 3-6 month old puppies susceptible, esp regions
w/poor vaccine protocol
o Very contagious, spread via AEROSOL
o TRIO of signs = GI (diarrhea), neuro (seizures), respiratory (pneumonia)
▪ ENAMEL HYPOPLASIA – pathognomonic for dogs infected with distemper as a
puppy – have to be infected before eruption of permanent dentition – LOWER
CANINES
o Diagnosis = immunofluoresent assay on affected epithelium (tracheal, vaginal,
respiratory), serology for distemper IgM or increased CSF to serum virus specific IgG
- Parvovirus = canine parvovirus-2
o Sheds 7-10 days once infected, incubation is 4-14 days ! transmited via FECAL-ORAL
(survives well in feces)
o GI tract and bone marrow – selectively damages rapidly dividing tissues ! lethargy,
anorexia, vomiting, diarrhea, young puppy (6 week to 6 month old puppy), dehydrated,
fever – nonsuppurative myocarditis (if infected in utero)
- Parainfluenza virus and adenovirus 2 = canine tracheobronchitis ! can lead to pneumonia
(esp in young dogs)
BACTERIAL DISEASES
- Campylobacter = C. jejuni
o Mucus-laden diarrhea – on cytology see motile, S-shaped or “gull-shaped” rods
o Culture = streak feces on Campylobacter blood agar plate which grows in oxygen
reduced atmosphere in 3-4 days
o Kids with puppies 16 times more likely to acquire this
- Salmonella = common in dogs fed the BARF diet (raw meat and bone)
o Acute bloody watery to mucoid diarrhea, depressed, weak, slightly pale mucous
membranes, dehydrated
- Clostridium dificile = hemorrhagic gastroenteritis (HGE)
o Acute onset of hemorrhagic diarrhea with marked hemoconcentration, raspberry-jam like
diarrhea, vomiting, abdominal pain ! common in Miniature Poodles, Miniature
Schnauzers
o Diagnosis = positive fecal test for Clostridium enterotoxin, PCV 60% (HIGH), TS 6 g/dl
(NORMAL) – not as high as expected with hemoconcentration – likely due to protein
loss into intestines
o Treatment = bismuth subsalicylate (Pepto-Bismol) – causes feces to be black and lead
to misdiagnosis of melena
- Actinomyces = filamentous and branching
o Normal inhabitant of oropharynx – commonly associated with grass awn migration –
contaminated in oropharynx then migrate through body from respiratory or GI tracts
(could take years to diagnose)
o Acute onset of sneezing after running in a field, remove grass awn from nasal passage
- Nocardia = ubiquitous soil saprophyte found everywhere, usually introduced via respiratory
tract
- Bordetella bronchiseptica = canine infectious tracheobronchitis = KENNEL COUGH
o Causes primary bacterial pneumonia (Pseudomonas, Pasteurella, E. coli all require
underlying problem to cause pneumonia, i.e. aspiration, FB, viral infection, neoplasia,
etc.)
o Treatment = coupage, systemic antibiotics, oxygen therapy, nebulization
- Neorickettsia helminothoeca = SALMON POISONING DISEASE
o Severe hemorrhagic enteritis, lethargy, anorexia, history of going fishing,
lymphadenopathy, depression, vomiting
o Vector = intestinal fluke (Nanophyetus salmincola) – dogs eat salmonid fish infected with
the fluke that harbor the rickettsia – spread through lymphatic’s causing ulcerative and
hemorrhagic enterocolitis
o Treatment = oxytetracycline for the rickettsia, praziquantel for the fluke
OPHTHALMOLOGY
- Collie Eye Anomaly = congenital in Collies (see in 80% of breed)
o Choroidal hypoplasia manifested by varying degrees of visual dysfunction with signs of
bizarre choroidal vessels visible on fundic exam
o Some are completely blind and some show no visual deficits
o Other signs are optic disc coloboma, retinal hemorrhage, retinal separation
- Extraocular polymyositis = GOLDEN RETRIEVERS
o Acute onset of bilateral exophthalmos, no pain or swelling noted
o Similar to masticatory muscle myositis – occurs due to autoimmune reaction against
muscle antigens
o Treatment = prednisone +/- azithioprine
- Sudden Acquired Retinal Degneration Syndrome (SARDS) = middle-aged obese female spayed
dogs – with CUSHING’S
o PU/PD, polyphagia, increased liver enzymes and cholesterol, acute blindness
o Develop acute blindness and initially have no optic or fundic lesions – in 1-2 months
they develop vascular attenuation and tapetal hyperreflectivity
- Progressive retinal atrophy/degeneration
o Inherited disease in TOY and MINIATURE POODLES ! night blindness progressing to
complete blindness due to loss of rods prior to cones
o Fundic exam = tapetal hyperreflectivity, gray vermiform lines on fundus, retinal vascular
attenuation, pale optic disc
- Iris atrophy = normal aging change seen in almost all dogs over 10 years
o See normal fundus, iris-pupil margins are somewhat irregular (scalloped iris margin),
moth eaten stroma, PLR is slow and incomplete, menace and palpebral normal,
dyscoria, anisocoria
- Chronic superficial keratitis = PANNUS – common in GERMAN SHEPHERDS
o Corneal melanosis and vascularization along the lateral aspect of the limbus bilaterally
o Due to UV light exposure – UV light alters corneal proteins leading to immune reaction
o Diagnosis = normal Schirmer tear test, negative fluoroscein dye
o Treatment = topical steroids and cyclosporine (lifelong therapy)
RESPIRATORY
- Cricopharyngeal achalasia = pharyngoesophageal sphincter fails to relax
o Rare congenital condition usually diagnosed in dogs at weaning ! treated by
cricopharyngeal myectomy
- Cricopharyngeal dysphagia = congenital disorder characterized by in-coordination in swallowing
reflex
o Regurgitation after eating, repeatedly swallowing & bringing up food and sometimes
coughs or sneezes concurrently
- Upper airway disease
o Common in young bracycephalics ! difficulty breathing, stertor, cough
o *Tracheal hypoplasia, stenotic nares, elongated soft palate, everted laryngeal saccules,
laryngeal collapse
o Treatment = resection of soft palate for elongated soft palate, resection of everted
laryngeal saccules
- Tracheal collapse
o Common in = older toy & miniature dogs (Chihuahuas, Pomeranians, Toy Poodles, Shih
Tzus, Lhasa Apso, Yorkie)
o Weakness in tracheal rings – collapse occurs because of hypocellularity and deficient
glycoprotein’s and glycosaminoglycans in the tracheal rings (leads to decreasing
strength and loss of ability to remain firm)
o Important to take respiratory radiographs (end inspiratory thorax plus end expiratory
thorax – to demonstrate intrathoracic tracheal narrowing)
- Laryngeal paralysis
o Progressive onset of exercise intolerance, voice change, stridorous breathing on
inspiration
o Diagnosis = sedated laryngeal exam (use DOXAPRAM) – give thiopental or propofol to
sedate – can result in false diagnosis of laryngeal paralysis – therefore is recommended
to give Doxapram to help stimulate respiration
o Treatment = unilateral arytenoid lateralization
- Pulmonary thromboembolism (PTE)
o Acute respiratory distress, unremarkable radiographs, split second heart sound (due to
pulmonary hypertension)
o Diagnosis = contrast radiographs (angiography – will see sudden interruptions in
bloodflow)
DERMATOLOGY
- Acanthosis nigricans = DACHSHUNDS (inherited) – others get it secondary to other skin
diseases
o Hyperpigmentation of axillary and groin regions
o Secondary bacterial infections, yeast infections, and seborrhea commonly develop in
affected regions
- Color dilution alopecia = FAWN-COLORED DOBERMANS, YORKIES
o Hereditary alopecia that affects color diluted areas – develops animals with less melanin
in their shafts than normal
o Treatment = NONE
- Zinc-responsive dermatosis = SIBERIAN HUSKY
o Cause = zinc-deficiency (genetic defect in absorption causes an increased requirement
for zinc)
o Scaling, crusting, and alopecic dermatitis around eyes, ears, foot pads, prepuce,
scrotum, and vulva
▪ Crusting and hyperkeratosis of the mucocutaneous junctions and extremities
o Treatment = zinc supplementation
- Canine familial dermatomyositis = COLLIES, SHETLAND SHEEPDOGS
o Atrophy of muscles and erosion, crusting, and alopecia of skin which is exacerbated by
heat and sun exposure
o Treatment = UNREWARDING, high doses of corticosteroids, vitamin E, omega-3 fatty
acids
- Discoid lupus erythematosis
o Depigmentation/ulceration of nasal planum, erythema, alopecia and crusting around the
muzzle/lips/periorbitally, loss of “cobblestone” appearance of nasal planum
- Lupoid dermatosis = GERMAN SHORTHAIRED POINTERS
o Fatal disease that initially causes crusting and scaling of the dorsum and head
- Pemphigus foliaceus
o Depigmentation, erythema, ulceration of nasal planum
- Atopy = atopic dermatitis
o Pruritis and erythema of the face, ears, and feet SEASONALLY (when high pollen in
environment)
o Diagnosis = intradermal skin testing (IDST), serum ELISA (measures antigen specific
IgE in animal)
o Treatment = hyposensitization (injections of allergen into patient to increase their
tolerance) – cyclosporine, antihistamines, and corticosteroids too
- Food allergy
o Pruritis and erythema of the face, ears, and feet (also ventrum), GI signs can be seen
(less common)
o Trial diet with restricted allergens (novel protein and carbohydrate sources) – diagnosis
and treatment!
- Pyoderma = Staphylococcus pseudointermedius
o Common in dogs because the canine stratum corneum is less efficient barrier to
bacteria than in other species – dogs lack an ostial plug in their follicles, a characteristic
which allows bacteria to invade and colonize more readily
o Treatment = antibiotics
- Malassezia dermatitis = yeast
- Sebaceous gland tumor = most common skin tumor in dogs
o Older dogs – Cockers, Beagles, Poodles, Miniature Schnauzers
o Multiple small (3-6mm) skin masses that are described as wart/cauliflower like,
ulcerated – limbs, trunk, eyelids
- Otitis
o Otitis externa
▪ Causes = atopy, hypothyroidism, foreign body – these alter environment in ear
canal allowing overgrowth of bacteria or yeast ! see head shaking, ear itching
o Otitis interna
▪ Head shaking, ear itching, disorientaiton, circling, head tilt (toward side affected)
– diagnose by otoscopy
▪ Clean ears with saline and prescribe aural medications (after checking integrity of
tympanic membrane)
- Aural hematoma
o Treatment = drainage (mattress sutures parallel to blood vessels – minimizes possibility
of occluding blood vessels)
GASTROENTEROLOGY
- Familial hyperlipidemia/hypertriglyceridemia = MINIATURE SCHNAUZERS
o Predisposed to seizures, pancreatitis, acute blindness, vomiting, and corneal opacities
o Management = low-fat diets
- Megaesophagus
o Causes = myasthenia gravis, persistent right 4th aortic arch, thymomas, congenital,
endocrinopathy (hyperadrenocorticism, hypothyroidism), secondary to esophagitis,
systemic lupus, OP toxicity, dysautonomia
o Diagnosis = FNA of mediastinal masses to look for thymoma, anti-acetylcholine receptor
antibodies to test for myasthenia (edrophonium), radiographs to look for aspiration
secondary to megaesophagus
o Regurgitation, choking on saliva and bringing up white foam
o Radiographs = distended esophagus, ventral depression of trachea, tracheal stripe sign
o Treatment = small, frequent elevated feedings, high calorie diet, treat secondary
aspiration pneumonia infections
▪ Metaclopramide and cisapride – sometimes stimulate esophageal peristalsis
▪ Anti-cholinesterases = pyridostigmine – corticosteroids to decrease immune
attack on ACh receptors
- Gastric dilatation and volvulus (GDV) = LARGE DEEP CHESTED DOGS (Great Danes,
Weimeraners, Saint Bernard)
o Stomach rotates in counter-clockwise direction (looking at patient cranial-caudal) – twist
can be 180-360 degrees
o Retching, hypersalivation, abdominal distention, tachycardia, prolonged CRT, pale
mucous membranes, weak pulses, unproductive vomiting
o Radiographic view = RIGHT LATERAL RECUMBENCY – gas will fill left displaced
pylorus
o To decompress = pass tube (measure to last rib), trocarize stomach (with 14g needle)
o Preventative = GASTROPEXY (circumcostal = around rib, belt loop, incorporating =
BAD because could cut into stomach at next surgery, incisional = BEST because suture
to abdominal wall and easy)
- Mesenteric volvulus = twisting of intestines on themselves at the root of the mesentery
o ACUTE life-threatening disease – severe abdominal pain, shock, gas distention,
intestines may appear bunched
- Perforated bowel
o Lethargy, innappetance, diarrhea, vomiting, pain on abdominal palpation, dehydration,
febrile
o Evidence of ascites and gas distention in small intestines, LOW glucose
o Septic abdomen = compare blood glucose to peritoneal fluid glucose (peritoneal fluid
glucose will be >20 mg/dL less than blood glucose – provides rapid and reliable
diagnosis)
- Esophagitis
o Treatment = sucralfate (H2 blocker, proton pump inhibitors – decrease gastric acid),
broad spectrum antibiotics (with severe ulceration or aspiration pneumonia) – coats and
protects erosions in esophagus
- Perianal fistulas = GERMAN SHEPHERDS, Irish Setters, Labs
o Treatment = immunosuppressive drugs (immune mediated disease) – i.e. cyclosporine
▪ Antibiotics reduce symptoms, surgery used to be best but guarded prognosis due
to fecal incontinence
- Perianal adenoma = hepatoid tumor
o Testosterone-dependent and therefore found in intact males or in dogs that have
testosterone secreting tumors
o Treatment = castration (often shrink or resolve)
- Lymphangiectasia = protein-losing enteropathy
o Dilation and dysfunction of intestinal lymphatic’s and leakage of protein-rich lymph into
the intestinal lumen ! protein, cholesterol, and lymphocytes are all lost
o Bloodwork = PANHYPOPROTEINEMIA, calcium is also frequently low
ORTHOPEDICS
- Ruptured cranial cruciate ligament
o Progressive rear limb lameness that reaches point where it is minimally weight bearing,
localized pain to stifle
o Radiographs = joint effusion, mild degenerative changes to bones, absence of primary
bone lesion
o Cranial drawer and/or tibial thrust, may also cause medial buttress and pain on stifle
extension
o Medical management = weight reduction, strict rest for 6-8 weeks, NSAIDs,
chondroprotectives (glucosamine, chondroitin sulfate), NOT corticosteroids (lead to
weakening of ligaments)
o Surgery…
▪ Tibial plateau leveling osteotomy (TPLO) = change angle of tibial plateau to slope
cranially, converting the previous cranial thrust into caudal tibial thrust (caudal
cruciate becomes primary stabilizer)
▪ Cranial transposition of fibular head
▪ Lateral suture repair
▪ Tibial tuberosity advancement
▪ Tightrope
o Complication = MEDIAL MENISCAL INJURY – medial is most closely associated with
medial collateral ligament and causes it to slide against femoral condyle because is
stuck in place ! either bucket handle tear (caudal longitudinal tear) or “crush” of the
caudal horn of the meniscus (incomplete bucket handle tear)
- Luxated patella = small breeds (i.e. Pomeranians)
o Most commonly MEDIAL ! do a recession trochleoplasty, wedge (block) resection of
trochlear groove, lateral imbrication of retinaculum, lateral transposition of tibial
tuberosity, medial release of soft tissues
- Hip dysplasia
o Difficulty rising and laying down in pelvic limbs – do Ortolani sign to look for hip laxity
o Ortolani sign = manipulate femur – may hear/feel a “clunk” which is actually subluxation
of the coxofemoral joint
o Treatment = can try medical management with NSAIDs but may have to go to surgery…
▪ Triple pelvic ostotomy = YOUNG dog with minimal secondary degenerative
changes & deep acetabulum
▪ Femoral head ostectomy = salvage procedure for dogs where TPO or THR are not
options
▪ Total hip replacement
- Hip luxation
o Performed closed reduction and place EHMER SLING – prevent weighbearing and aid
in maintaining some degree of abduction and internal rotation of the affected limb (leave
on for 7-10 days)
- Osteochondrosis dissecans (OCD)
o Shoulder = caudal aspect of humeral head, elbow = medial aspect of humeral condyles,
tarsocrural joint = trochlear ridge of talus, stifle = femoral condyle
- Osteoarthritis
o Lameness, pain on extension and flexion of any of the joints – diagnose with
radiographs
o Treatment = medical management (NSAIDs, glucosamine, tramadol, opiods)
- Distal radial fractures
o Common in small breed dogs – as result of having decreased blood flow to distal aspect
of radius
o Best to do internal fixation with them because of decreased blood supply – results in
slower healing of fractures with higher incidence of non-union
- Elbow dysplasia = fragmented medial coronoid process, OCD, elbow incongruency
o Intermittent lameness in forelimb, pain on flexion and extension of elbow joint
o Diagnosis and treatment = arthroscopy, can do CT to evaluate boney structures better –
with FCP can perform sub-total coronoidectomy and remove diseased cartilage if OCD
is present
NEUROLOGY
- Fibrocartilagenous embolism (FCE) = embolus of disc material in spinal vasculature
o ACUTE onset of non-painful myelopathy localized to spinal segments T3L3, still has
superficial and deep pain perception and some motor function present in pelvic limbs –
hyperreflexive patellar and gastrocnemius reflexes
o Prognosis – most get better with nursing care, loss of motor neuron signs are poor
prognostic indicators
- Idiopathic polyradiculoneuritis = COONHOUND PARALYSIS
o Associated with raccoon exposure ! acutely progressive ascending paralysis in the
pelvic limbs and progressing to the forelimbs – diffusely affects all motor nerves
o Treatment is nursing and supportive care ! most dogs with this disease will recover
spontaneously in several weeks
- Canine degenerative myelopathy = GERMAN SHEPHERDS (5-9 years old)
o Often confused with hip dysplasia ! progressive degenerative spinal cord disease that
causes random axonal degeneration in all spinal cord segments but is usually most
severe in the thoracic cord
- Myasthenia gravis
o History of progressive tetraparesis, weakly ambulatory, delayed CP in all four feet
o Radiographs = megaesophagus, aspiration pneumonia, mass in cranioventral abdomen
(thymoma)
o Tensilon (edrophonium) test = edrophium (anticholinesterase) that reverses signs of
myasthenia within minutes
- Cervical spondylopathy = cervical stenosis or wedging of the vertebral canal, vertebral
malalignment, vertebral instability
o Doberman Pinschers, Great Danes, Thoroughbred horses
o Slowly progressive ataxia and paresis of all four limbs, ataxia is sporadic – ataxia and
paresis of all limbs, UMN signs to all four limbs
▪ Hyperreflexive spinal reflexes in all limbs, delayed CP in all four limbs, neck pain
on ventroflexion
- Degenerative disc disease
o Progressive lameness in hind limbs, trouble rising, drunken gait, acute hindlimb ataxia,
CP deficits, no panniculus
o Hansen’s Type I ! CHONDRODYSTROPHICS (Dachshund, Corgi, Shih Tzu) = acute,
painful, emergency
o Hansen’s Type II ! non-chondrodystrophic dogs = chronic, non-painful, NOT an
emergency
o Diagnosis = MRI (better for soft tissue), can use CT or contrast myelogram too though
o Treatment = LAMINECTOMY (to relieve disc compression)
- Discospondylitis = hematogenous spread of bacteria to spinal cord (from distant infected site)
o Look for occult infection elsewhere in dog, perform blood cultures, see vertebral
endplate lysis on radiographs
o Treatment = antibiotics, surgery if neurologic deficits are severe
- Hydrocephalus = TEACUP CHIHUAHUA
- Brachial plexus avulsion
o After trauma, thoracic limb monoplegia, Horner’s on side affected, dragging one of limbs
(no CP, motor, deep pain)
o Treatment = leg amputation (if complete nerve root avulsion)
o Prognosis = partial tear better than complete, lots of PT, lack of deep pain/motor is
negative prognostic indicator
- Trigeminal (CNV) neuropathy
o Progressive muscle loss on skull, atrophy of masseter and temporalis on affected site –
UNILATERAL!
- Masticatory muscle myositis
o Autoimmune condition that leads to atrophy of masseter and temporalis muscles –
BILATERALLY
ONCOLOGY
- Lymphoma
o Lethargy, inappetance, peripheral lymphadenopathy, HYPERCALCEMIA (produces
PTHrP)
o Population of lymphoid cells that are predominantly lymphoblasts (which are bigger than
mature lymphocytes)
o Lymphoma vs. leukemia = bone marrow affected in leukemia
o Treatment – PREDNISONE, doxorubicin, cyclophosphamide, vincristine, L-asparginase,
lomustine
- Chronic lymphocytic leukemia
o Peripheral lymphadenopathy, prominent spleen on palpation
o Bone marrow aspirate (40% small lymphocytes), FNA of lymph node (90% small
lymphocytes) – considered chronic because made up of well differentiated mature
lymphocytes
- Hemangiosarcoma = GERMAN SHEPHERDS
o Schistocytes (fragmented RBCs that are broken up due to irregular vessels and fibrin
strands as they pass through tumors), thrombocytopenia, anemia (not Heinz-body),
leukocytosis
o SPLENIC = most common malignant tumor of spleen (2/3 of malignant splenic masses,
90% chance it has metastasized by the time they are diagnosed)
o CARDIAC = right atrium ! leads to cardiac tamponade – result of excessive
accumulation of fluid in pericardium
- Mast cell tumors
o See many symptoms are related to release of histamine, heparin, and other vasoactive
amines
▪ Histamine causes GI ulcers via activation of H2’s on gastric parietal cells causing
secretion of gastric acid
▪ Heparin can cause coagulopathy
▪ May also see hypotension, vasodilation, local inflammation surrounding tumor
o Treatment = DO NOT USE MORPHINE (causes significant release of histamine)
▪ Palladia – toceranib phosphate (tyrosine kinase (RTK) inhibitor FDA approved for
mast cell tumors)
▪ H1 blockers, H2 blockers, proton pump inhibitors – diphenhydramine (H1),
famotidine (H2)
▪ Vinblastine, Prednisone – chemotherapies good for mast cell tumors
- Histocytic neoplasia (round cell tumor) = BERNESE MOUNTAIN DOGS
- Cutaneous histocytoma
o Usually BENIGN, present as small raised alopecic mass that may or may not be
ulcerated (usu on HEAD)
o Usually develop in dogs less than 3 years old ! don’t have to treat – usually ulcerate
then regress on own
- Transmissible veneeal tumor (round cell tumor)
o Can be cured in 90% or more of cases with chemotherapy (vincristine) alone
o Has different number of chromosomes than host cells – tumor has 59 chromosomes in
contrast to dogs that have 78
- Testicular tumors
o Sertoli cell tumor
▪ Common in CRYPTORCHID testes, often secrete ESTROGEN
▪ Causes male feminizing syndrome ! gynecomastia, sexual attraction of males,
bilaterally symmetric alopecia (with occasional pruritis and papular eruptions,
hyperpigmentation), aplastic anemia (bone marrow dyscrasias), urinating in
female position
o Interstitial cell tumors = usually hormonally silent, usually occur in scrotal testes
o Seminoma = can secrete androgens and estrogens and could cause feminization
- Apocrine gland anal sac adenocarcinoma (AGASAC) = SPAYED FEMALES
o Usually VERY SMALL tumors – most clinical signs are due to distant metastases or
HYPERCALCEMIA due to secretion of PTH-rP by the tumor cells
o Leads to ! renal damage, metastatic disease, pelvic canal obstructed by lymph nodes
(even from small tumors)
- Prostatic neoplasia
o Sublumbar mass and bony lysis of L6 vertebral body (more lysis than seen with IVDD,
spondylitis, or immune mediated polyarthritis)
o Castration DOES NOT decrease risk of prostatic neoplasia (only of prostatitis)
- Transitional cell carcinoma = TRIGONE of BLADDER
o Treatment = piroxicam (palliative) and platinum therapy (can extend progression-free
interval and survival with chemo – carboplatin, cisplatin, mitoxantrone)
MISCELLANEOUS
- Nutrition
o Large breed puppies = limit calcium to prevent skeletal abnormalities (OCD, retained
cartilage cores)
o Maintenance energy requirement = 30 x BW + 70 (dogs); 80 x BW (cats)
o Vitamin A deficiency = nyctalopia (night blindness) – need vitamin A for retina
o Hypoglycemia = status epilepticus from not eating, lethargy – common in young TOY
BREED dogs
▪ Neoplastic causes = insulinoma, beta cell tumor, hepatocellular carcinoma
o TPR = glucose, amino acids, lipids (carbohydrates, proteins, fats)
- Ectopic ureter
o Incontinence, unremarkable abdominal rads ! need abdominal contrast CT,
cystoscopy, abdominal ultrasound, excretory urogram vaginourethrography
- Amyloidosis = SHARPEIS
o Lethargy, PU/PD, decreased appetite, no response to supportive care, proteinuria
(suggests glomerular disease)
o Histopath = waxy kidneys, grayish in color and enlarged
o 4 signs of nephrotic syndrome = proteinuria, hypercholesterolemia, edema/ascites,
hypoproteinemia
o Treatment (same for glomerulonephritis) = ACE-inhibitors and dietary protein restriction
(both decrease proteinuria), aspirin (to decrease platelet function to alleviate
hypercoagulable state when antithrombin III is lost)
- Fanconi syndrome = BASENJIS ! proximal renal tubular disease
- Copper toxicosis = BEDLINGTON TERRIERS – accumulate copper in their livers and show
signs of liver failure
- Bile peritonitis
o To diagnose compare bilirubin concentration in fluid to serum ! concentration of
bilirubin that is twice as high as serum is considered diagnostic
Cat and Dog Diseases
ENDOCRINOLOGY
- Hyperthyroidism – CATS (8 years and older!!)
o Active form is T3, free T4 is unbound T4 that enters cells and is converted to T3 or
reverse T3 (made during illness)
o Cause = adenomatous hyperplasia – also thyroid adenomas, thyroid carcinomas
o Diagnosis = serum T4 – if this is normal and you still suspect hyperthyroidism do free T4
by equilibrium dialysis
▪ Scintigraphy can be used to determine function of gland, may see excitement
leukogram due to increased circulating catecholamines, increased catabolism of
tissues can cause increased BUN but not creatinine, GFR is increased which
may mask underlying renal disease
▪ Before treatment look at renal values (renal disease often masked by
hyperthryoidism) and liver values (treatment with methimazole is hepatotoxic)
o Palpable nodule in area of thyroid (“thyroid slip”), restlessness, polyphagia, weight loss,
low BCS, vomiting, aggression, dull haircoat, PU/PD
o Treatment
▪ Methimazole – initially – helps unmaks occult renal insufficiency that could be
hidden with hyperthyroidism – side effects = extreme facial pruritis leading to
exorciations
▪ Radioactive iodine therapy (I131 radiation) – once know renal values are stable,
use this especially if animal has bad side effects on methimazole
▪ Thyroidectomy – a lot of times thyroid tissue is left behind and disease can recur
– may also see Horner’s syndrome, hypothyroidism, hypocalcemia (due to excision
of parathyroid’s), laryngeal paralysis
o Complication = elevated blood pressure (i.e. >180-200 mmHg) – leads to ocular problems
(i.e. retinal detachment or hemorrhage resulting in blindness) – treat hypertension with
atenolol if notice animal goes acutely blind
- Hypothyroidism – DOGS (older, large breeds)
o Causes = immune mediated lymphocytic thyroiditis, idiopathic atrophy, suppression of
pituitary gland from glucocorticoids (secondary hypothyroidism)
o Weight gain (due to slow metabolism), skin changes (hyperpigmentation, alopecia,
pyoderma, seborrhea), lethargy
o Diagnosis = free T4 by equilibrium dialysis (T3 NOT beneficial to measure)
o Treatment = sodium levothyroxine (keep T4 slightly above normal and resolve clinical
signs)
- Diabetic ketoacidosis
o PU/PD, weight loss, normal to increased food intake, lethargy, vomiting
o Urinalysis = KETONES in the urine, tons of glucose in the urine
o Bloodwork = metabolic acidosis (low TCO2, due to presence of ketones which act as
acids), hyponatremia, hypochloremia, hypokalemia (these are caused by osmotic
diuresis and polyuria), hyperosmolality (due to elevated glucose and BUN), pre-renal
azotemia (due to dehydration)
o MONITOR while treating ! electrolytes, blood glucose (to make sure doesn’t become
hypoglycemic)
o Initial treatment = correct acidosis (bicarb), electrolyte abnormalities (IV fluids,
potassium and phosphorus supplementation), and hyperosmolality
▪ REGULAR insulin (Humilin-R) – potent and short acting insulin used to treat DKA
patients – give frequent doses until have glycemic control until they are stable
then can switch to longer-acting insulin
o Later treatment = regulate blood glucose, get animal to eat, control obesity and
concurrent disease
o If diagnose ketoacidosis in a controlled diabetic ! look for underlying cause of sudden
poor glycemic control (i.e. pancreatitis, cardiac disease, infection)
▪ Hyperthyroidism common in DKA cats, Cushing’s common in DKA dogs
- Diabetes mellitus
o CATS ! polyphagia, weight loss, dull hair coat, PU/PD, pelvic limb weakness,
plantigrade stance (hocks low to ground), difficulty jumping – caused by amyloid
deposition in cats, transient DM after excision of insulinoma
▪ In dogs almost always insulin-dependent, inc ats insulin-dependent 70% and non-
insulin dependent 30%
o DOGS ! bilateral cataracts - *4 classic signs = polyuria, polydipsia, polyphagia, weight
loss
▪ Glucosuria leads to polyuria – glucose in dogs spills into urine when BG = 180, in
cats at 200-280 mg/dl
o Diagnosis = elevated fasting blood glucose, glucosuria (not ketones), do a URINE
CULTURE (prone to UTIs, and if have underlying infection can lead to insulin
resistance)
▪ Glucose curve = greatly affected by stress – in cats use fructosamine because
shows average blood BG over past 2-3 weeks (so useful in stressed cat)
o Treatment = insulin injections – NPH and lente (intermediate – initially to manage
diabetics without ketoacidosis), ultralente (long-acting), glarginine (insulin of choice for
long term control once ketoacidosis has corrected)
▪ High fiber diets (delay glucose absorption and can increase insulin sensitivity),
low calorie diets and regular exercise can help treat obesity and increase insulin
sensitivity
▪ Poor glycemic control = hypoglycemia (owners give too much inulin, give when
animal not eating), infectious or hormonal disorders (i.e. hyperadrenocorticism,
pancreatitis), inappropriate storage of insulin
o Consequences of insulin deficiency ! impaired energy utilization (can’t import glucose
into cells), increased hepatic gluconeogenesis (liver upregulates in response to decreased
energy, exacerbates hyperglycemia), increased mobilization of fat (to supply body with
energy source), hepatic lipidosis and ketosis, weight loss (insulin deficient dog is essentially
starving cells of its body)
- Diabetes insipidus = lack of production or response to VASOPRESSIN
o Central = lack of release of vasopressin by the posterior pituitary
▪ Problem with function of hypothalamus (ADH production) and/or posterior
pituitary (ADH release) so patient cannot respond to changes in serum
osmolality or blood volume and pressure
▪ USG = 1.001-1.007 (kidneys have no problem responding to ADH in CDI)
▪ Treatment = DDAVP (synthetic ADH, desmopressin) – may not see response in
first 24-48 hours – takes up to 3 days to overcome medullary washout from being
PU/PD
o Nephrogenic = adequate ADH but ADH receptors of kidney do not function properly
▪ Treatment = hydrochlorothiazide, avoid excess salt, give unlimited acces to water
- Insulinoma
o Glucose = 45 mg/dl, insulin = high (normal to high insulin in face of low blood glucose –
because normal controls of insulin secretion are lost)
o Treatment = surgical removal (post-op complications = pancreatitis, recurring
hypoglycemia)
- Pheochromocytoma = tumor of adrenal medulla (secrete catecholamines) – not very common in
dogs
o Hypertension, tachyarrhythmias, seizures, collapse
o CORTEX ! zona glomerulosa = aldosterone, zona fasciculata = glucocorticoids, zona
reticularis = androgen
o MEDULLA ! chromaffin cells = catecholamines (epinephrine and norepinephrine)
- Addisons = HYPOADRENOCORTICISM – middle aged female dogs
o Destruction/atrophy of ALL layers of the adrenal cortex (deficiencies in both
glucocorticoids and mineralcorticoids)
▪ Less common form = inadequate ACTH by pituitary and results in deficiency of
glucocorticoids only
o HYPERKALEMIA, HYPONATREMIA, azotemia, hypoglycemia, acidosis, low resting
cortisol levl or low ACTH stimulation test (GOLD STANDARD – if plasma cortisol is low
after ACTH administration), absence of stress leukogram, low sodium:potassium ratio
(usually less than 23), ECG consistent with hyperkalemia (tall T’s)
o Treatment = supplemental mineralcorticoids
o Monitor = serum sodium/potassium ! will be hyponatremic and hyperkalemic if deficient
in mineralcorticoids
- Cushings = HYPERADRENOCORTICISM – most due to primary dysfunction in pituitary
(secretes increased ACTH)
o Breed predispositions = Dachshund (esp long haired)
o Calcinosis cutis (thinning and increased fragility of skin, hyperpigmentation, alopecia,
seborrhea, pyoderma), panting and lethargy (sign of muscle weakness), distended
abdomen (redistributes fat to abdomen), increased occurrence of infection (immune-
suppression), PU/PD, polyphagic
o Diagnosis
▪ ACTH stimulation ! dexamethasone prior to ACTH stim doesn’t affect it, other
steroids do
▪ Endogenous plasma ACTH assay ! after prednisone = cortisol high (due to
steroid), ACTH low (because of feedback inhibition of ACTH)
▪ LDDST and HDDST ! with Cushing’s animals have elevated cortisol at 8-hours
post-dexamethasone (normal animals will have suppressed by 8) – look at 8-
hour to see if has it, look at 4-hour to see what kind
• LDDST ! to differentiate between pituitary-dependent and adrenal-
dependent ! PDH show brief cortisol suppression at 4-hours post-
dexamethasone (maybe), with adrenal tumors do not show suppression of
cortisol at 4-hours post
• If it does not suppress you cannot tell if it’s adrenal or PDH – so do a
HDDST – with a high dose 75% of PDH patients suppress
▪ Urine cortisol:creatinine ratio ! sensitive but not specific, most dogs with
Cushings have an elevated ratio but dogs with other causes of PU/PD do as well
▪ Abdominal ultrasound
▪ Bloodwork ! elevated SAP, elevated cholesterol, elevated ALT (swelling and
death of hepatocytes), decreased BUN (secondary to diuresis that occurs with
high cortisol)
o Treatment
▪ Adrenalectomy (with adrenal dependent) – NOT NOT NOT pituitary surgery
▪ o,p’-DDD (Lysodren, Mitotane) – to treat PDH – causes selective necrosis of
zona fasiculata and reticularis
▪ Ketoconazole – inhibits production of steroids – used for functional adrenal
tumors
- Primary hyperparathyroidism = adenoma of the parathyroid glands
o Hypercalcemia, hypophosphatemia ! phosphorus decreases as calcium increases and
vice versa
o Treatment = surgical removal
▪ Monitor patient’s serum calcium for a week post-op to make sure they do not
develop hypocalcemia – then weekly for 4 weeks ! the higher the pre-op
calcium the more likely the patient will become hypocalcemic
▪ Give Vitamin D and calcium supplements as needed – maintain calcium in
normal range to stimulate production of PTH by the parathyroid cells
• Do not oversupplement Vitamin D ! can lead to high Ca, high P (causes
resorption from bone and increases absorption of Ca and P from GI tract)
• PTH causes high Ca, unchanged or normal P ! enhances renal
phosphorus secretion
CARDIOLOGY
- Hypertrophic cardiomyopathy (HCM)
o CONCENTRIC hypertrophy – thickened wall of left ventricle impairs diastolic filling, no
problem w/contractility
o CATS = Main Coons (usu less than 2 years old when diagnosed) – commonly
associated with hyperthyroidism, hypertension (i.e. due to renal disease)
▪ Aortic thromboembolism (saddle thrombus) ! dilation of left atrium with blood
stasis – thrombi form here and frequently lodge at bifurcation of aorta ! acute
paraparesis and pain in hindlimbs
▪ Test for hyperthyroidism, fundic exam to look at hypertension, blood pressure,
urinalysis (renal disease)
o Radiographs = cardiomegaly, “valentine” shaped heart
o Echocardiogram = left ventricular concentric hypertrophy, systolic anterior motion of
mitral valve (SAM)
▪ SAM = when leaflet of mitral valve obstructs left ventricular outflow tract as
chamber contracts
o Treatment = increase diastolic function by decreasing heart rate
▪ Beta blockers (i.e. atenolol) – decreases contractility and HR allowing for better
chamber filling
▪ ACE inhibitors (i.e. enalapril, benazepril) – helps decrease blood pressure by
causing vasodilation
▪ Calcium channel blockers (i.e. diltiazem)
▪ When is in failure (LEFT failure)….diuretics (i.e. furosemide), nitroglycerin,
oxygen
▪ In cats = prevent thromboembolic disease (i.e. heparin, aspirin, clopidrogel)
- Dilated cardiomyopathy (DCM)
o In CATS = taurine deficiency – rare now that commercial diets have adequate taurine
o DOGS = DOBERMAN PINSCHERS, LARGE breed dogs – taurine deficiency in Cocker
Spaniels
▪ Poor prognosis in Dobermans (die within 2 months of diagnosis)
o ECCENTRIC hypertrophy of left ventricle
o Teatment = Pimobendan (calcium sensitizer – increases cardiac contractility), diuretics,
ACE inhibitors (i.e. enalapril) +/- digoxin
- Vascular ring anomalies = rare in dogs and cats
o Diagnosed after being weaned to solid foods – constriction of esophagus does not allow
ingesta to travel causing animal to regurgitate – likely will lead to aspiration pneumonia
– usually has poor BCS with voracious appetite
o Left 5th = involutes, left 6 becomes left pulmonary artery and ligamentum arteriosum,
right 3rd becomes right internal carotid – most common to result in constriction of
esophagus = persistent right 4th aortic arch
o Breed predispositions = German Shepherds, Irish Setters
- Pulmonic stenosis = SMALL breed dogs
o English Bulldogs, Beagles, Miniature Schnauzers, Samoyeds, MASTIFFS, Fox Terriers
o Leads to dilation of pulmonary vasculature downstream of stenotic region (result of
turbulent bloodflow), increased right ventricular and atrial pressure, CONCENTRIC
hypertrophy of right ventricle – result of increase in resistance to ejection of blood
through a stenotic pulmonary outflow tract
o Systolic murmur at LEFT HEART BASE
o Treatment = balloon dilation valvuloplasty – inflate balloon to stretch stenotic region
- Aortic stenosis = LARGE breed dogs
o Boxers, Golden Retrievers, Newfoundland, German Shepherds, Rottweilers, NOT
Mastiffs or Irish Wolfhounds
o Systolic murmur at LEFT HEART BASE
o CONCENTRIC hypertrophy of left heart (due to pressure overload), post-stenotic dilation
of the aorta, ventricular arrhythmias commonly occur (may be reason for ACUTE
DEATH)
o Prognosis = guarded, sudden death may occur at anytime, dog has increased risk for
infective endocarditis
o Treatment = prophylactic antibiotics, beta blockers (i.e. atenolol – to reduce myocardial
oxygen demand and reduce frequenty of ventricular arrhythmias), balloon dilation
(results not usually good)
- Tricuspid valve dysplasia = LABS, German Shepherds, large breed males
o Signs of RIGHT heart failure (ascites, hepatomegaly), systolic murmur at RIGHT mid
thorax
o Irregular valve leaflets, chordae tendinae, or papillary muscles of valve – prognosis
depends on degree of regurge
o See severe cardiomegaly with marked right atrial and ventricular enlargement on
radiographs
- Mitral valve dysplasia ! vs. MYXOMATOUS DEGENERATION OF MITRAL VALVE
o Dysplasia = CONGENITAL defect where valves are thickened, fused, fibrosed, etc.
▪ GERMAN SHEPHERDS, GREAT DANES, other large breeds
o Degeneration = OLDER animals (most common cardiac disease in veterinary medicine)
▪ Small breeds
o Both have same physical exam and radiographic findings – regurgitant jet across mitral
valve
o Murmur at LEFT HEART APEX – can lead to pulmonary hypertension, see enlarged left
atrium on radiographs
o Treatment = none in early stages, in progressed disease = diuretics, ACE inhibitors +/-
digoxin
- Right ventricular arrhythmogenic cardiomyopathy = BOXER CARDIOMYOPATHY
o Syncope in Boxers
o Diagnosis = 24 hour Holter monitor (electrical conduction abnormality that causes VPCs
to occur)
GASTROENTEROLOGY
- Anatomy and Pharmacology
o Canine esophagus = striated muscle, feline = 2/3 striated, 1/3 smooth
o Parietal cells of stomach = produce HCl, produce in response to gastrin = G cells in
antrum
o Xylazine = induce emesis in CATS
o Cyproheptadine = stimulates appetite in small animals
- Intussusception = invagination of intestinal segment into lumen of adjacent segment –
mechanical obstruction
o More common in dogs than cats, most common site = ILEOCOLIC (second most
common is jejuno-jejunal)
o Scant bloody diarrhea, abdominal pain, palpable doughy sausage in abdomen, vomiting
o Common in young animals with history of recent enteritis (i.e. chronic diarrhea, treated
for Coccidia)
o Radiographs = obstructive pattern with dilated loops of SI with no overt mass effect,
barium study helpful
- Rectal prolapse vs. colorectal intussusception
o Tissue protruding from anus ! to distinguish pass blunt probe alongside prolapsed
tissue – if probe only goes short distance is prolapse, if goes significant distance (i.e.
5-6 cm) is an intussusception
o Rectal prolapse seen in kittens infected with GI parasites – severe diarrhea with
straining leads to prolapse
o Treatment for prolapse = manually reduce with lube, treat parasites, dextrose solution
may help decrease edema
o Treatment for intussusception = exploratory surgery
- Gastric ulcers
o Causes = corticosteroids and NSAIDs (compromise mucus-bicarbonate protection of
stomach), liver failure (decreases mucosal blood flow secondary to portal hypertension
and thrombosis)
o Treatment = omeprazole (proton pump inhibitor)
- Inflammatory bowel disease
o Chronic anorexia with intermittent vomiting and diarrhea, weight loss
o Ultrasound = multifocal-diffuse thickening of the muscularis layer of the small bowel
o Histopath = lymphoplasmacytic inflammation of the GI tract
o Treatment
▪ Novel protein diet – easily digestible with a novel protein source = hypoallergenic
diet
▪ **Corticosteroids (i.e. budesonide (concentrates on GI, less systemic effects),
prednisone) – mainstay!
▪ Metronidazole (helps with secondary bacterial infections), Fortiflora (probiotic),
vitamins
▪ Pro-motility agents (i.e. metaclopramide) – could stop vomiting but potentiate
diarrhea (bc is pro-motility)
▪ Azithioprine (only in DOGS) = immunosuppressive drug used to treat
unresponsive IBD
- Pancreatitis
o CATS = lethargy, anorexia ! feed regular commercial diet (cats don’t require low-fat diet
or period of NPO), IV fluids, H2 blocker (ranitidine)
▪ Commonly get pancreatitis with DKA
o DOGS = vomiting, painful abdomen ! fast 24 hours then feed low-fat diet, IV fluids, H2
blocker, antibiotics
▪ High fat foods can put dog at risk, surgical excision of insulinoma can predispose
to pancreatitis
o Ultrasound = hypoechoic (edema) pancreas with hyperechoic (peritonitis) surrounding
mesentery, enlarged/mottled
o Diagnosis = PLI
- Exocrine pancreatic insufficiency
o See in YOUNG animals, German Shepherds predisposed ! RAVENOUS APPETITE,
weight loss, PU/PD, voluminous pale diarrhea, polyphagic, abdominal discomfort, pica,
coprophagia
▪ Animals lose ability to digest fat and protein – leads to emaciation
o Most common cause….DOGS = pancreatic acinar atrophy, CATS = chronic pancreatitis
▪ Cats concurrently have diabetes mellitus because endocrine cells affected
▪ Dogs get small intestinal bacterial overgrowth (SIBO) – loss of antibacterial
factors in pancreatic fluid
• Cobalamin (Vitamin B12) = ILEUM, Folate = JEJUNUM ! HIGH folate,
LOW cobalamin
o Bacteria synthesize folate leading to decreased absorption of
cobalamin
o Diagnosis = trypsin-like immunoreactivity (will be low ot be diagnostic)
o Treatment = pancreatic enzyme powder, raw pancreas fed at meals, digestible diet (with
lots of protein)
- Upper GI obstruction/foreign body
o Lethargy, anorexia, vomiting
o Bloodwork (with gastric outflow) = hypochloremic metabolic alkalosis (low chloride, high
TCO2)
o Treatment = stabilize with fluids to correct electrolyte abnormalities (NaCl), enterotomy/
gastrotomy
HERNIAS
- Diaphragmatic hernia = pleuroperitoneal diaphragmatic hernia (PPDH)
o Rapid shallow breathing, quiet lung sounds, heart auscults normally, no crackles or
wheezes
o Cause = TRAUMA – may not present for months after trauma, take rads so you don’t
miss it!
o Keep animal upright and try to keep abdominal organs from invading chest cavity
o Diagnosis = barium study, thoracic radiographs
o Treatment = surgical repair
o Peritoneopericardial diaphragmatic hernia = ALWAYS CONGENITAL, never occurs from
trauma
- Perineal hernia = OLDER, INTACT MALE DOGS
o Breed predispositions = Boxers, Collies, Kelpies, Pekingnese, Boston Terriers
o Weakened pelvic diaphragm – may be hormonal component that weakens it with time
o Straining to defecate, bulge in perineal region – diagnose via rectal exam
o Correct with surgery ! could lead to fecal incontinence, infection, failure of repair (weak
muscles)
- Inguinal hernia = MALE DOGS, congenital or acquired (from TRAUMA)
o Internal inguinal ring = inguinal ligament, rectus abdominus, internal abdominal oblique
o External inguinal ring = external abdominal oblique
- Umbilical hernia = CONGENITAL (failure or delayed fusion of rectus abdominus muscle)
o Small hernias you can schedule surgery after 6 months of age if still present
o Concurrently cryptorchid – always assess for this in these patients
ONCOLOGY
- Primary lung tumor
o Treatment = lung lobectomy (excision with wide margins), chemotherapy in cases where
the tumor cannot be completely excised
o Prognosis = guarded long-term
- Osteosarcoma
o Clinical signs = persistent limb lameness that progressively worsens, can usually isolate
pain to a long bone
▪ Pathologic fractures – bone weakens from lysis from tumor – will not heal with
rest or fixation
o Radiographs = lytic lesion of bone
o Treatment = AMPUTATION
▪ Cats have MUCH better prognosis than dogs due to lower rate of metastasis – 12
months or more
▪ Dogs only usually live 3-4 months due to metastasis to the lungs
Equine Diseases
BREED PREDISPOSITIONS
- Sarcoid = Quarter Horse
- Melanoma = gray horses
- Cerebellar abiotrophy = Arabian, Oldenburg, Gotland
- Ruptured prepubic tendon = obese draft mares in late pregnancy
- Enteroliths = Arabians
- Hyperkalemic periodic paralysis = Quarter Horse, Paint, Appaloosas
- Severe combined immunodeficiency (SCID) = Arabians
- Exercise induced pulmonary hemorrhage = Thoroughbreds
- Equine recurrent uveitis/equine night blindness = Appaloosa
- Dandy-Walker syndrome = Arabians, Thoroughbreds
- Small colon impactions = Miniature horse
- Lethal white syndrome = Arabians
VIRAL DISEASES
- Equine infectious anemia = retrovirus (related to human HIV)
o Transmission = Tabanidae flies
o Clinical signs = ABORTION, anemia, history of weight loss, intermittent fevers, pale
mucous membranes
o Diagnosis = normocytic normochromic anemia (don’t see other kinds in horses!!)
▪ COOMB’S TEST ! agar immunodiffusion to detect serum antibodies against the
retrovirus
• Good for chronic infections, not enough antibody to detect in acute
infections
• False positives can occur due to acquisition of the antibody in colostrum
• *Always need to confirm an ELISA test with a Coggin’s test
▪ COGGIN’S TEST
o Can cause IMHA – if this is the cause of IMHA do not treat with corticosteroids like you
normally would because this can cause recrudescence of viremia and worsen anemia
o Treatment = isolation and supportive care
- Equine herpes virus-1 = respiratory disease in FOALS, abortion in MARES
o Transmission = AEROSOL – rapidly spreading, can also spread from aborted fetuses/
placenta
o Respiratory disease = respiratory signs in foals (copious nasal discharge), occasionally
death from pneumonia
o Abortion = most common INFECTIOUS cause of abortion
▪ Usually foals develop respiratory signs several months prior to an abortion storm –
CLASSIC
▪ Abortion in horses 7-11 months pregnant – LATE TERM ABORTION
▪ Should only be affected on one pregnancy, then normal – do not acquire
permanent immunity and can be reinfected – VACCINATE (5, 7, 9 months) to
decrease chance of abortion
o Myeloencephalitis = rarely causes neurologic disease, CNS signs
- Equine herpes virus-3 = COITAL EXANTHEMA
o BALANPOSTHITIS – papules, pustules, and ulcers to vestibular mucosa, vulvar skin,
and the penis and prepuce
o Treatment = usually not required – spontaneously recover about 2 weeks after infection
o Transmission = venereally (sexual rest to prevent transmission) – can breed once
lesions have cleared
-Equine viral arteritis (EVA) = togavirus
o Transmission = venereally – carrier stallions can infect mares, can also be aerosolized
o More mild respiratory signs than herpes, abortion during various stages of pregnancy
(won’t see lag time between foals getting sick and mare’s aborting)
▪ Vasculitis leading to edema, conjunctivitis, rhinitis, abortion – edema, oculonasal
discharge, petechia
▪ Foals = severe respiratory distress, leucopenia, thrombocytopenia, and death
after 12-24 hours
o Prevent with vaccine – immunity lasts 1-3 years – vaccinated cannot be distinguished
from infected on serology
- Equine adenovirus = UPPER RESPIRATORY TRACT
o But can cause lower respiratory tract infection in immunocompromised animals –
especially in foals with failure of passive transfer or combined immunodeficiency
▪ Most common cause of death in foals with either of these conditions – FATAL
PNEUMONIA
- Equine influenza = ORTHOMYXOVIRUS
o Transmission = AEROSOL – highly contagious
o Rapidly spreading infection with high fever and cough
o Diagnosis = nasopharyngeal swab for virus isolation – could diagnose with serology but
need paired titers are needed to yield a diagnosis
BACTERIAL DISEASES
- Endotoxemia
o Fever or hypothermia, leucopenia, tachycardia, tachypnea, obtundation, change in gut
motility
o BACTERIAL LIPOPOLYSACCHARIDE – gram negative bacteria contain LPS – signals
have evolved on monocytes/macrophages to warn the animal when a gram negative
bacterium has gained access – when the reaction to this signal is overzealous a
cascade of physiologic reactions can occur
- Brucella abortus = FISTULOUS WITHERS and POLL EVIL
o Fistulous withers = development of open draining lesion over the supraspinous bursa –
between 2-5th thoracic vertebrae – see pain, heat and swelling in this region –
eventually ruptures and drains
▪ Flush fistula and give antibiotics
o Poll evil = inflammation of bursa adjacent to nuchal ligament
- Streptococcus equi ssp. equi = STRANGLES (1-5 years old)
o Mandibular and retropharyngeal lymph node abscessation – bacterial culture confirms
diagnosis
o Treatment = ISOLATE (highly contagious), lance abscess ventrally, DO NOT GIVE
ANTIBIOTICS (prolongs course of disease – may lead to internal (bastard) strangles
where you DO use antibiotics
o Prevention = strangles vaccine – given IM has ben associated with soft tissue reaction,
now have intranasal
o Complications = puppura hemorrhagica and guttural pouch empyema
▪ Purpura hemorrhagica = type III hypersensitivity resulting in immune-complex
deposition in blood vessel walls and vasculitis that leads to urticaria, edema of
extremities, petechia and ecchymoses on mucous membranes, stiff gait
• Anemia, hyperproteinemia, hyperfibrinogenemia, hyperglobulinemia,
neutrophilia
▪ Guttural pouch empyema = purulent material in guttural pouch – chronic nasal
discharge, dysphagia, leukocytosis, swollen/tender lateral throad area, food
reflux from nose (due to pharyngeal paresis from damage to CN 9 and 12)
• Will see fluid lines in guttural pouch, need to daily catheterize and lavage
pouches (saline), if inspissated surgical drainage may be necessary
• **CN 7, 9, 10, 11, 12 cross medial pouch as well as sympathetic trunk and
internal carotid artery, external carotid crosses lateral pouch
- Streptococcus equi ssp. zooepidemicus
o Most common infectious cause of infertility in the US (NOT with abortion)
o Common inhabitant of external genitalia of mares and stallions – causes dusease when
there are predisposing factors (i.e. immunosuppression, pneumovagina, damage to the
endometrium)
o Treatment = penicillin
- Taylorella equingenitalis = CONTAGIOUS EQUINE METRITIS
o Rare in U.S. – thought to be eradicated – should NEVER BREED a horse that has had
a previous infection!!
o No clinically apparent disease – can lead to infertility
- Rhodococcus (Corynebacterium) equi = PNEUMONIA in FOALS (2-6 months old)
o *BUT Streptococcus spp are the most common etiologic agent causing pneumonia in
foals
o Cough, fever, wheezes on auscultation, abdominal tucking on inspiration, weight loss,
tachypnea – rarely diarrhea
o Diagnosis = transtracheal wash and find gram positive pleomorphic rods (CHINESE
LETTERS)
o Radiographs = abscesses within lung fields (caudodorsal)
o Treatment = *erythromycin (4 times a day) and rifampin – treat for 2 months, base on
clinical signs, radiographic signs, and bloodwork – newer antibiotics (i.e. clarithromycin)
can be used and only needs to be given 2 times a day
- Lawsonia intracellularis
o VERY common in PIGS – but in both involves WEANLING age horses
o Thickening of small intestines ! hypoproteinemia that is generally observed as ventral
edema clinically
▪ Lethargy, intermittent diarrhea, weight loss
- Corynebacterium pseudotuberculosis = PIGEON FEVER
o Ulcerative lymphangitis (of the limbs) and abscesses in pectoral region – may have
internal absceseses too
o Diagnosis = hemagglutination inhibition test (aka synergistic hemaglutination inhibition
test , ‘SHIT’)
▪ Shows for INTERNAL abscesses – leukocytosis, hyperfibrinogenemia,
hyperglobulinemia
o Treatment = hot packing and draining the abscesses
▪ Antibiotics PROLONG disease by delaying abscess formation – only useful in
horses with systemic signs
- Salmonella typhimurium
o Several different clinical presentations – subclinical, self-limiting diarrhea, acute
diarrhea with endotoxemia
o CECUM and proximal COLON – acute onset lethargy, anorexia, and explosive watery
diarrhea
o Diagnosis = serial cultures of feces for 3-5 days
DERMATOLOGY
- Pemphigus foliaceus
o Autoimmune disease where antibodies are formed against the intracellular adhesin
proteins
o Leads to vesicles, erosions, ulcerations – esp at mucocutaneous junctions – crusting
lesions on head/limbs/ventrum
o Biopsy of skin = acantholytic cells
o Treatment = immunosuppressive doses of corticosteroids ! juvenile form may have
spontaneous remission (good prognosis), adult form has worse prognosis
- Proud flesh = benign proliferation of exuberant granulation tissue (at PREVIOUS WOUND
SITE)
o Etiology is unknown but has to do with the inhibition of epithelialization
o Treatment = excision, skin grafts, irradiation
- Urticaria = HIVES
o Allergic reaction = toxins, plants, insect bites, medications, chemicals, heat, sunlight,
stress, genetic abnormalities
o Localized edema in the dermis ! acute cutaneous lesions and restlessness after
coming in from pasture
▪ Elevated, flat-topped, range in size from 2-8cm, scattered multifocally
o Treatment = dexamethasone ! can give diphenhydramine as well (NOT IV – can cause
urticaria itself if IV)
- Eosinophilic granuloma = NODULAR NECROBIOSIS OF COLLAGEN, COLLAGENOLYTIC
GRANULOMA
o Due to insect bites, trauma, multifactorial – see nodular mass lesion on lateral neck (non-
ulcerative, non-pruritic)
o Biopsy = collagen degeneration and granulomatous inflammation with eosinophils
o Treatment = sublesional steroid injections, surgical excision, systemic antibiotics
CLINICAL PATHOLOGY
- To determine if horse has regenerative or non-regenerative anemia…BONE MARROW
ASPIRATE
o Horse does not have reticulocytes in circulation – so must look at bone marrow
o If is regenerative – will see hypercellular bone marrow with low myeloid/erythroid ratio
(<0.5)
o Will ALWAYS have normocytic, normochromic anemia
- Neutrophils
o Blue aggregates in many of neutrophils = SEPSIS – Dohle bodies indicate toxic
changes – these are retained aggregates of rough endoplasmic reticulum
▪ May also see cee cytoplasmic basophilia, vacuolation, toxic granulation – often
seen these in septic foals
- Severe combined immunodeficiency (SCID) = ARABIANS
o Some Arabian foals are homozygous for the SCID gene – is now a genetic test for this
disease
o Appear normal at birth then develop fatal infections – often from unusual organisms
such as Pneumocystis carnii
o Foals born immunocompetent but lack antibodies when born, must ingest maternal
antibodies from colostrum
o Weakness, rapid breathing, fever
o Diagnosis = normal (adequate passive transfer) is >800 mg/dl
▪ ELISA (SNAP) test – good for rapid detection (takes 5 minutes)
▪ Measure of TP (refractometer) – very insensitive but can be used if no other
means available
▪ Zinc sulfate turbidity test
▪ Radioimmunodiffusion (RID) – most accurate but takes 24 hours to perform
- Neonatal isoerythrolysis = Aa and Qa are antigens involved
o Stallion positive for one of these antigens and mare negative – foal inherits either Qa or
Aa from the stallion, mare is negative for this antigen – when mare becomes exposed to
foal RBC antigens she makes antibodies against it – when she passes these antibodies
to the foal through colostrum and acute hemolytic (lysis of RBCs) event occurs
o See in 0-4 day old foals – in utero foal is protected by mare’s epitheliochorial placenta –
born to multiparous mare – weakness, depression, decreased appetite, tachycardia,
icterus, anemia, hemolysis, hyperbilirubinemia
▪ See in multiparous mares because the first time mare has a foal with the antigen
she will not produce sufficient antibodies to cause severe damage to foal – see in
multiparous mares or mares that have had a blood transfusion that exposed
themto RBC antigens
- Granulocytic ehrlichiosis = Ehrlichia equi
o Survives in NEUTROPHILS and eosinophils – look like intracytoplasmic inclusion
bodies, aggregates of purple dots (these dots are morulae)
o Depression, limb edema, petechiation, icterus, ataxia – usually MILD disease
o Diagnosis = BLOOD SMEAR
- Potomac horse fever = Ehrlichia risticii (aka Neorickettsia risticii)
o Survives in MONOCYTES (macrophages) – obligate intracellular organism, see
leucopenia and monocytosis
o Anorexia, high fever, lethargy, ileus, colic, water diarrhea, laminitis
o Diagnosis = NOT blood smear (often can’t find) – requires paired serum titers (based on
four-fold rise in paired IFA titers, or on decrease in titer between acute and convalescent
samples)
▪ PCR (of blood or feces) is more recent way to diagnose – highly sensitive and
specific
o Treatment = TETRACYCLINE (good for intracellular and rickettsial organisms) – rapid
response within 24-48 hrs
▪ Oxytetracycline = drug of choice, for 7-10 days
ONCOLOGY
- Seminoma = common TESTICULAR tumor
o Unilaterally enlarged testicle that palpates firm and fibrous – can be locally invasive and
decrease sperm production
- Granulosa-theca cell tumor = common OVARIAN tumor
o Unilateral benign tumors that secrete steroids preventing cycling by suppressing
gonadotropins
o Can cause aggression in mares because they lead to increased testosterone – DDx for
aggression = hypothyroidism
- Sarcoids = QUARTER HORSES
o One of most common skin tumors in horses – NON-MALIGNANT, NON-METASTATIC
o Locally aggressive fibroblastic tumor of the dermis and subcutis with variable proliferative
epithelial component
o Etiology = bovine papillomavirus may play a role
o Transmission = direct contact, fomites, arthropod vector
o Types
▪ Flat = slow-growing, can be confused with flat warts
▪ Verrucous = warty, look like SCC or papillomas
▪ Fibroblastic = resemble granulation tissue or proud flesh and grow rapidly
o Treatment = small lesions can do benign neglect (they do not regress), bigger lesions
do surgical excision (but usually recur even with cryosurgery and radiation therapy)
- Melanoma = GRAY HORSES (see a lot in Arabians and Percherons due to coat color)
o Common site = perineum and tail base – darkly pigmented, slowly growing, locally
invasive
o Usually benign with varying degrees of invasiveness – have potential to develop into
malignant tumors
o Treatment = surgery or cryosurgery, benign neglect, chemotherapy (systemic or
intralesional), immunotherapy - depends on location and size
o Prognosis = predisposed ot developing others in the future
- Mast cell tumor
o Often in dermis or subcutis on head or legs – may also invade underlying musculature,
often walled off by aggregates of fibrous stroma
o Excision is usually CURATIVE – good prognosis, tumors are benign
ENDOCRINOLOGY
- Cushing’s = PITUITARY TUMOR (pituitary adenoma of pars intermedia that secretes ACTH)
o See in older horses (average age about 20 years)
o Stress leukogram (neutrophilia, lymphopenia) from cortisol, hyperglycemia (counter-
insulin effects of cortisol), low USG (from PU/PD), NOT elevated ALP (horses don’t
have a corticosteroid isoenzyme of ALP)
- Equine metabolic syndrome
o Gross or severe regional obesity and clinical or subclinical chronic laminitis
o These animals are insulin resistant and often have higher than normal insulin levels in
the blood
- Hypothyroidism
o Causes = iodine deficiency (thyroid needs it), iodine excess (damages it – Wolff
Chaikoff effect) – can be from mare or foal’s diet ! NOT from pituitary adenomas (these
cause Cushing’s)
o Life threatening in foals and can cause abnormalities including physeal dysgenesis,
incoordination, limb deformities, tendon ruptures, still births, weakness, and death
OPHTHALMOLOGY
- Auriculopalpebral nerve block – blocking this branch of CN VII (facial) disrupts the motor
innervation to the orbicularis oculi, which is the muscle that closes the eye
o In the horse the orbicularis oculi is very strong and can prevent a thorough ocular exam
– lidocaine is injected SQ at the caudal aspect of the zygomatic arch where the nerve is
palpable
- Infected corneal ulcers
o Have melting appearance – indicates deepening into stroma of the cornea due to
infection
o Diagnose on cytology – usually gram negative rods because Pseudomonas – most
common bacterial keratitis
o Treatment = topical (NOT systemic) tobramycin (aminoglycoside) because effective
against most gram negatives
▪ If gram positive is likely Staphylococcus – use Cefazolin topically
- Equine recurrent uveitis = APPALOOSA = periodic ophthalmia, recurrent iridocyclitis, moon
blindness
o MOST COMMON CAUSE OF CATARACTS and BLINDNESS
o Cause = infection (Onchocerca, Leptospira, Borrelia, Toxoplasma) or immune mediated
o Recurrent bouts of ocular redness, tearing, photophobia, and cloudy cornea (“blueeye”)
for a period of years
▪ Recurrent bouts of uveitis can lead to ! cataracts, lens luxation, glaucoma,
eventually vision loss (due to damage to optic nerve – will be able to see
pigmented remnants on iris or lens capsule)
o Treatment = AGGRESSIVE – topical/systemic antiinflammatories, topical atropine (to
prevent synechia and ciliary spasm), antibiotics only necessary if horse is febrile or
infectious cause is identified
- Equine night blindness = APPALOOSA
o Congenital disease – bilateral and nonprogressive, horse has variable degree of
decreased vision in the dark
- Fungal keratitis
o Treatment = topical ocular medicine (i..e itraconazole drops) every 2 hours, if becomes
difficult to manage can place subpalpebral lavage system – allows for continuous drip of
topical meds without having to handle the horse
- Eyelid laceration
o Treatment = lavage with saline (minimal wound debridment should be done),
phenylbutazone, 2 or more layer closure (to make sure edges are opposed), tetanus
toxoid immunization
ORTHOPEDICS
- NERVE BLOCKS
o Palmar digital nerve block – blocks palmar part of foot
o Low 4 point block (palmar metacarpal nerve block) – desentizes foot, pastern, and
fetlock joint
o High 4 point block (subcarpal nerve block) – desensitizes leg distal to carpus/tarsus –
metacarpal region and below
o Abaxial sesamoid nerve block – good if there is problem at pastern joint (proximal
interphalangeal joint)
▪ Desentizes foot and proximal interphalangeal (pastern) joint
o Suspensory ligament block – desensitizes deep branch of lateral palmar nerve at level of
carpometacarpal joint
- Laminitis = P3 rotates with inflammation and degeneration of lamina
o Predisposing factors = systemic disease (i.e. endometritis, salmonellosis), high
carbohydrate diet, excessive weight bearing on single limb, corticosteroid administration
o Diagnosis = palmar digital block, change in angulation of P3 on radiographs
o Treatment = PHENOXYBENZAMINE (a-agonist that promotes vasodilation and
restoration of blood flow to the digitis) – can also use acepromazine, isoxsuprine,
hydrochloride, DMSO, heparin, nitroglycerin for this
▪ DO NOT GIVE CORTICOSTEROIDS – believed to induce this condition
- Physitis = inflammation at GROWTH PLATES – see swelling around growth plates of long
bones
o Seen in young horses – conformational defects, malnutrition, growth plate compression,
abnormal hoof growth
- Sesamoiditis = tearing of ligamentous attachments to the sesamoids (during strenuous exercise)
o Same clinical signs as sesamoid fractures – but less severe (lameness, inflammation)
o Radiographs = new bone formation or osteolytic lesions and radiolucent lines which are
prominent vascular changes
o Need to treat with long term rest and NSAIDs – prognosis is guarded to poor
- Suspensory ligament desmitis =
o Associated with apical fracture of proximal sesamoid bone, avulsion fracture of the
palmar aspect of the third metacarpal bone, or fractures of the distal third of the small
metacarpal bones
o Confirm one of these fractures with radiographs then evaluate with ultrasound
o Takes 7-9 months to heal (ligament healing rate) – only 55% of horses return to normal
use
- Splints = INTRAOSSEUS DESMITIS
o Inflammation of intraosseus ligament between 3rd metacarpal/tarsal bone with the small
metacarpal/tarsal bones
▪ Periositis occurs with new bone formation along the splint bones or small
metacarpals/tarsal’s usually due to repetitive concussion, excessive training,
poor conformation, or improper shoeing
o Need to take radiographs to distinguish from fractures of splint bones – need REST and
NSAIDs
- Carpal fractures = radial (CHIP fracture) and 3rd carpal bones (SLAB fracture)
o See immediate swelling and severe lameness – need to arthroscopically surgically
repair
- Fractures
o Tibial fractures ! usually NON-RECONSTRUCTABLE, COMMINUTED fractures – due
to lack of soft tissue coverage, highly susceptible to infection, GRAVE prognosis for
return to function
o P3 fractures ! as long as articular surface is not involved has GOOD prognosis
o P1 fractures ! repair with lag screws as long as not comminuted
o Ulnar fractures ! treat with bone plates, GOOD prognosis, about 70% return to function
- Osteochondrosis = defect in endochonrdal ossification – leads to cartilage flap
o Associated with dietary calcium and vitamin D in young horses ! diagnosis frequently
made with young horses start to train and severity of lameness can vary greatly
- Navicular syndrome
o *Palmar foot pain (due to problems with navicular bone, navicular suspensory or deep
digital flexor tendon, navicular bursa), more painful on hard surfaces than grass
o Diagnosis = hoof tester elicits pain, block of palmar digital nerves results in
improvement
▪ Radiographs = bone remodeling, enlarged vascular channels, osteophyte formation
on navicular bone
• NOT osteolysis – chronic degenerative condition
- Carpal hygroma = fluid filled swelling at carpus
o Usually see from repeated trauma leading to local bursitis – usually NOT lame but have
restricted ROM of joint
o Surgical exploration and drain placement is necessary – simply aspirating fluid or
injecting corticosteroids is not effective and swelling will usually recur – may need to
excise bursal lining if keeps recurring
- Quittor = chronic infection of CARTILAGE OF P3
o Results in draining tract from coronary band due to infection/inflammation of affected
cartilage – need SURGERY
- Subsolar abscess
o History of farrier work or penetrating foreign body, acute severe lameness, increased
heat and pain in foot that progresses to coronary band, edema over pastern and fetlock
▪ If do not treat in 2-3 weeks will see draining lesions in coronary band
o Treat with disinfectants/poultices, ensure adequate drainage, remove foreign body if
present – NO SYSTEMIC ABx
- Deep digital flexor tendon contracture = CLUB FOOT
o Distal check ligament controls stretch of long tendon of deep digital flexor – if this
becomes functionally too short flexion of the interphalangeal joint occurs resulting in
club foot – can be caused by rapid bone growth, excessive feeding, faulty nutrition, or
lack of exercise
o Treatment = distal check ligament desmotomy and corrective shoeing
▪ Distal check desmotomy = relieves DEEP digital flexor contracture
▪ Proximal check desmotomy = relieves SUPERFICIAL digital flexor contracture
- Tendonitis = BOWED TENDON
o Intermittent lameness that resolves after working the horse, palmar metacarpal bulge
and inflammation
▪ = bulge/bowing of shallowly located superficial digital flexor tendon
o Ultrasound superficial digital flexor tendon – see anechoic regions within tendon (=
hemorrhage and loss of tendon fibers – indicate an acute tendonitis)
o Tendon healing = takes 8-11 months for tendons to heal ! eventually newly formed type
III collagen is replaced by type I collagen – process is NEVER complete
o *Most commonly injured tendon in horse = superficial digital flexor tendon
- Curb = thickening of tarsal ligament due to strain
- Sweeney = supraspinatous contracture
- Stringhalt
o Myoclonic disease affecting one or both pelvic limbs (may be associated with sweet pea
poisoning) = HYPERFLEXION OF LEG ! when horse lifts hindlimb it draws foot up
sharply until it touches abdomen and then strikes it violently at ground
o Treatment = tenectomy of lateral digital extensor tendon – not all cases respond to
treatment
- Bone spavin = osteoarthritis of the HOCK
- Bog spavin = TARSAL HYDRARTHROSIS
o Chronic synovitis of tibiotarsal joint with distention of joint capsule due to increased
synovial fluid formation
o Due to poor conformation – affects both hindlimbs, horse usually not lame from this
condition
o Prognosis = distention may spontaneously appear and reappear in young horses
- Ringbone = osteoarthritis of PHALANGES
o Range of motion of joints is decreased, may palpate new bone formation in pastern
region – see on radiography
o Due to ! poor conformation, improper shoeing, trauma such as wire cuts or repetitive
concussion on hard surface
o Treatment = early on (cold packing, astringent application, radiation therapy, anti-
inflammatories), severe ringbone (surgical arthrodesis of pastern joint – curative and can
restore horse to performance status) – COMPLETE REST
- Peroneus tertius rupture ! can extend hock and flex stifle simultaneously – disrupts STAY
APPARATUS of hindlimb
- Pedal osteitis = inflammation of the structures of the feet associated with demineralization of
P3
o See in performance horses – associated with working on hard surfaces
o Treatment = prolonged rest, NSAIDs, and corrective shoeing
- PREMATURE HORSES = foal born before 320 days gestation ! ANGULAR LIMB
DEFORMITIES
o Can tell if horse is premature by….taking radiographs of carpal/tarsal bones – if
incompletely ossified indicates prematurity – as the foal ages carpal bones will ossify
but they can collapse with the weight of the foal placing pressure on soft cartilage which
may result in misshapen carpal bones and lameness ! angular limb deformities
▪ Can get carpal valgus (lateral deviation) or carpal varus (medial deviation)
▪ Result of asynchronous growth of the metaphyseal and epiphyseal growth plates
▪ Treatment = periosteal stripping of the concave side of the growth plate – promotes
growth of concave side and has little potential for overcorrection
o Also if they have….short silky haircoat, pliant floppy ears, a soft muzzle, laxity in their
flexor tendons
o
MUSCLE DISORDERS
- Creatinine phosphokinase = CPK, creatine kinase (CK)
o Stored in skeletal muscle and cardiac muscle – see elevations when you have muscle
damage (i.e. rhabdomyolysis)
- Myoglobinuria vs. hemoglobinuria
o Myoglobinuria ! brownish urine that does not clear on centrifugation along with
NORMAL colored plasma
▪ Myoglobin does not bind serum proteins and is quickly excreted before reaching
levels that would discolor plasma ! if animal has painful gait and myoglobinuria
this = MYOPATHY
o Hemoglobinuria ! reddish discoloraiton of plasma because hemoglobin is maintained
in plasma longer and is lost in the urine more slowly
- Hyperkalemic periodic paralysis (HYPP) = QUARTER HORSES, Paint, Appaloosa
o Mutation in skeletal muscle SODIUM channel – sodium channels fail to inactivate,
remain open – results in depolarization of muscle membrane (closer to threshold) and
hyperexcitability of the muscle
▪ Autosomal dominant so discourage from breeding – mutation can be tracked
back to IMPRESSIVE
▪ Causes hyperkalemia because of movement of potassium out of the muscle cell
as myocyte repolarizes
o Intermittent muscle fasiculations follwed by weakness, well-muscled, muscle stiffness,
difficulty walking, prolapsed third eyelid, recumbency – usually these signs are
intermittent
o Treatment = change diet to timothy hay (low potassium) with frequent small meals,
regular exercise
▪ Acute episodes = IV 0.9% NaCl (K+ free fluids) and 5% dextrose (drives K+ into
cell)
▪ Sometimes give diuretic (i.e. furosemide) to diurese but do not give something
like spironolactone because is a potassium sparing diuretic that would not help
decrease potassium
- Myotonia
o Mild gait abnormality at initiation of exercise which then diminishes – see in very heavily
muscled horses
o Electromyographic exam (EMG) = **crescendo-decresendo signal of high-frequency
repetitive bursts with characteristic “dive bomber” sound – produced by repetitive firing
after contraction of affected muscles
- Myositis = “TYING UP”
o Racehorse that has been overworked for past year ! presents with stiff gait, lethargy,
anorexia, oliguria
o Causes pigment nephropathy – nephrosis and subsequent renal failure is caused by
large amounts of myoglobin being filtered by the kidney – happens in animals that have
been subjected to extreme conditions that causes animal to break down a substantial
amount of muscle
NEUROLOGY
- Radial nerve paralysis
o Usually caused from laying in lateral recumbency for a long period of time – radial nerve
is susceptible to damage from pressure (advent of warm water beds for padding has
greatly decreased this incidence)
o Forelimb with dropped elbow and flexed carpus, fetlock, digits – drags limb when walks
and unable to advance leg
o Treatment = rapid and aggressive – excellent nursing care
- Fracture to basilar bones (basiphenoid/basioccipital) = see in horses that rear up and flip
backwards
o Head tilt, drooping ear, deviation of muzzle ! UNILATERAL – damage to CN VII and
VIII
o Common form of traumatic nerve injury in foals
- Equine protozoal myeloencephalitis (EPM) = SARCOCYSTIS NEURONA
o Sarcocytis neurona = migrates through spinal cord and brain (damage to white and gray
matter) - OPPOSUM
o See in horses 1-6 years old ! progressive ataxia (CP deficits), focal areas of muscle
loss noted around gluteal/quadriceps region, incoordination of all four limbs (or just one
limb may be affected)
▪ Vague ASYMMETRIC/multifocal neurologic clinical signs with MUSCLE
ATROPHY
▪ Hyporeflexia, spasticity, cerebellar signs, head tilt, facial paralysis, circling,
dysphagia, blindness, acute recumbency – see these signs if there is brainstem
involvement
o Diagnosis = serum and CSF immunoblotting
o Treatment = PONAZURIL (Marquis) – used to use TMS in COMBINATION with
pyrimethamine
- Cauda equina neuritis = inflammation of nerve roots
o Usually inflammation of the cauda equina, but sometimes CNs too – results in LMN
signs
o Paresis/paralysis, chewing the tail head, hypotonic anus, fecal retention, urinary
incontinence (urine scalding of thighs), hindlimb ataxia
o NO TREATMENT OPTIONS
- Cervical vertebral stenotic mylopathy = WOBBLER SYNDROME
o First form = cervical vertebral instability ! ventroflexion of neck causes spinal cord
compression at C3-4 or C4-5
o Second form = cervical static stenosis ! compression of spinal cord continuous
regardless of neck position
o See in horses UNDER ONE YEAR OLD
o Wide based stance, CP deficits, ataxia, paresis, spasticity which is worse in the
hindlimbs – SYMMETRICAL
o Treatment = surgery – to stabilize cervical vertebrae and decompress spinal cord
▪ Can give antiinflammatories and stall rest to decrease clinical signs short term
-Equine degenerative myeloencephalopathy (EDM)
o Seen in horses UNDER ONE YEAR OLD – usually associated with a deficiency in
vitamin E
o Ataxia, hypometria, conscious proprioception deficits, generalized weakness, normal
mentation, wide based stance, paresis, spasticity ! SYMMETRICAL ATAXIA (worse in
the hindlimbs)
o Diagnose by finding lesion in caudal brainstem nuclei and spinal cord on histopathology
- Equine herpes myeloencephalopathy (EHM)
o Vasculitis of the CNS ! hindlimb ataxia, dog sitting, intermittent dribbling of urine,
hypotonia of tail/anus
▪ Usually see MULTIPLE horses at same barn affected – signs are generally acute
- Equine encephalomyelitis = Western EE (50% mortality), Venezuelan EE (75%), Eastern EE
(90%)
o Prevention = vaccinations ! ZOONOTIC
o Eastern equine encephalomyelitis (as example, other two are similar)
▪ Transmitted by MOSQUITO – then spreads via lymphatic’s, don’t see neuro
signs until 5 days later
▪ Causes cortical and thalamic lesions – ASYMMETRICAL – progression of CNS
signs over several days – depressed, anorectic, progressing to pressing and
circling, leading to recumbency, death 2-3 days after onset of clinical signs
▪ CSF tap = protein of 80 mg/dl with primarily mononuclear pleocytosis
- Verminous myelitis = aberrant migration of parasites through CNS
o Similar to EPM – focal/multifocal/diffuse in nature – muscle atrophy, ataxia,
incoordination in all four limbs
o Parasites that undergo aberrant migration = Strongylus vulgaris, Micronema deletrix,
Draschia megastoma, Setaria
o Treatment = for strongyles – ivermectin, fenbendazole, thiabendazole
- Cerebellar abiotrophy = ARABIANS
o Common in young foals (develop around 6 months) – etiology is unknown (genetic,
toxic, infectious, etc.)
o Cerebellum is responsible for coordination and regulation of range, rate, and strength of
movement along with balance and posture ! ataxia, hypermetria, intention tremors
(head tremors), NORMAL mentation, dysmetria, hyperreflexia, spasticity, lack of
menace
o NO TREATMENT
- Dandy-Walker syndrome = ARABIANS and THOROUGHBREDS (rare in both)
o Midline defect of the cerebellum and cystic dilation of the fourth ventricle
GASTROENTEROLOGY
- Colic sedation with xylazine = causes inhibition of intestinal motility and could also transiently
decrease cardiac output in potentially hypovolemic horse with colic ! BUT is potent analgesic
that provides rapid relief to abdominal pain
- Abdominocentesis ! to RIGHT of midline (to avoid hitting many organs), normally is yellow,
nucleated cells <5000/uL, TP <2.5gm/dl
- Anaphylaxis ! horse shock organs = LUNGS and COLON
o When undergoes anaphylaxis will see respiratory and lower GI signs – dyspnea,
respiratory distress, diarrhea, anxiety, tachycardia, piloerection, sweating
o Treatment = epinephrine, corticosteroids, antihistamine
- Regurgitaiton
o If horse with colic regurges = guarded to poor prognosis – horses have extremely tight
esophageal sphincter tone and regurge will only occur when very great pressure is
exceeded (may also have gastric rupture at this pressure)
o Likely causes of regurgitaiton in foals = gastric ulcers, cleft palate, incoordination of
swallow reflex
- Small colon impaction = colic in MINIATURE HORSE
- Small intestinal obstruction
o Acute onset of colic, gastric reflux (brown to yellow fluid), CRT 3 seconds, red mucous
membranes, GI sounds absent, peritoneal fluid (cloudy yellow with protein around 3 and
WBC count around 11,000)
▪ pH >5 of gastric reflux – suggestes small intestinal contents are refluxing into
stomach
o Treatment = SURGERY – stabilize with nasogastric tube first (horses unable to vomit
due to tight sphincter so helping them reflux will relieve life-threatening pressures)
o *Causes = strangulating lipomas, mesenteric rent, intussusception, hernia, epiploic foramen
incarceration, volvulus
▪ See lipomas in OLD horses, the rest in young!!
- Duodenitis-proximal jejunitis (DJP) = ANTERIOR/PROXIMAL ENTERITIS
o May be related to Clostridium dificile
o Clinical signs closely resemble small intestinal obstruction – acute colic, increased RR
and HR, pain (but less than with an obstruction), gastric reflux, depression, decreased
gut sounds, injected mucous membranes
▪ Small intestinal obstruction is surgical, DPJ responds better to medical treatment
• Gastric reflux in DPJ = orange-brown in color, foul smelling, feel multiple
dilated fluid-filled loops of bowel, peritoneal fluid is serosanguinous with
about 3.5 gm/dl protein and 7000 WBCs
o Treatment = decompress stomach with nasogastric tube, remove excess GI fluid, IV
fluids, replace electrolyte deficiencies, analgesics, correction of acid-base abnormalities
- Nephrosplenic entrapment = LEFT DORSAL COLON DISPLACEMENT
o Left dorsal colon displacement over nephrosplenic ligament (between spleen and left
body wall) – trapped in renosplenic space
o Large horses predisposed – colic, increased HR and RR, pacing, staring at abdomen,
no gastric reflux
▪ Milder clinical signs than small intestinal obstruction – distended large colon on
palpation
o Ultrasound = unable to see left kidney but do see large colon predominantly on left side
o Treatment = surgical correction, can try to roll horse 360 degrees
- Right dorsal colon displacement
o Colic, increased HR and RR, no gastric reflux, on rectal palpation can feel colon
palpable between cecum and body wall (cecum is on RIGHT so something is going on on
right side)
- Right dorsal colitis = due to administration of NSAID (usually with chronic use)
o Innappetance, intermittent colic, hypoproteinemia
o May see concurrent RENAL MEDULLARY CREST NECROSIS with NSAID
adminstration
▪ aka RENAL PAPILLARY NECROSIS – due to limited blood flow to an area of
kidney
- Cecal volvulus = RARE in horses
o Usually see secondary to large colon volvulus – horse will ping similarly to cow and
present with acute colic
- Strongylus vulgaris (GI parasite) = thrombosis or arteritis of cranial mesenteric artery
o Migration to the cranial mesenteric artery and corresponding immune response can
result in thrombosis of cranial mesenteric ! leads to colic (by cutting off blood supply)
and infarction of bowel
o Strongylus edentatus and Strongylus equinus (GI parasites)
▪ Migrate through portal vein and into liver, through peritoneum and retroperitoneal
space, then after a few months return to gut – could be found in liver, pancreas,
or perirenal
o Treatment = ivermectin, fenbendazole, oxibendazole
- Enteroliths = ARABIANS in California and Florida
o Alfalfa hay is considered to play a role – common in California because alfalfa hay in CA
is high in magnesium
▪ Results in magnesium ammonium phosphate enteroliths
- Sand enteropathy
o Common in CA and FL becuae sandy regions – treat with Psyllium (hemicellulose
laxative that can bind sand and remove it from GI tract) – in future feed horse in stall
with hay racks to keep horse from eating off sandy ground
- Meconium impaction
o Meconium is first intestinal discharge of newborn foal – impaction usually occurs within
24 hours after birth
o Tenesmus, variable degrees of colic, straining, swishing of tail, restlessness – *most
common cause of colic in foal
o May feel numerous hard fecal balls on palpation – treat with acetylcystine enema (will
cleave disulfide bonds in mucoproteins of meconium and help break it down), warm
water and soap enema
- Gastric ulcers =
o On SQUAMOUS REGION of stomach – is nonglandular region so unable to resist injury
from acid as is the glandular region (which can secrete mucous to protect itself)
o Horses predisposed to gastric ulcers ! constantly secrete gastric fluid (others only
secrete in response to food)
o Predisposing factors = administration of two NSAIDs together
o Treatment = OMEPRAZOLE (H-K ATPase blocker), Cimetidine (ranitidine, famotidine –
H2 blocker), sucralfate (protects mucosa), Misoprostol (PGE1 analogue – increases GI
blood flow, decreases secretion of acid, increases mucous and bicarbonate secretion)
- Protein losing enteropathy = damaged bowel leaking protein into gut
o Edema, history of severe diarrhea, fever, dehydration, weak, anorexic, purple mucous
membranes, small amount of concentrated urine – NORMAL PCV with LOW TP/
albumin
o Treat with IV plasma (raise protein without raising PCV too much)
- Choke = obstruction in esophagus
o Predisposing factors = poor mastication, rapid eating, esophageal stricture, (grass
clippings, beet pulp, pellets/cubes)
o Salivation, food coming out of nose – *REMEMBER with choke you have time to resolve
it without drastic action
▪ Fist pass a stomach tube and try to gently push bolus aborally, flunixin
meglumine (NSAID), lidocaine (relieves discomfort), xylazine (to sedate), NOT
mineral oil (could lead to HARSH aspiration pneumonia)
▪ If does not resolve on first try, give horse 12-24 hours and give IV fluids then try
again – this usually does trick unless dealing with anatomical choke (i.e.
esophageal diverticulum) or very severe case
o Complications = inhalation (foreign body) pneumonia, with caustic substances may
cause rupture of esophagus
- Foal heat diarrhea = 7-14 day old foals
o Mild diarrhea in foals ! etiology unknown but may be due to consumption of grian and
hay – because may alter GI flora so that diarrhea develops
o Called foal heat diarrhea due to relationship of occurrence of post-foaling estrous in
mare
- Lethal white syndrome = offspring of PAINT mares who give birth to all white foals
o Agangliosis of intestines which leads to constipation, hypomotility, megacolon, colic, and
death
RESPIRATORY
- Recurrent airway obstruction (RAO) = chronic obstructive pulmonary disease (COPD), HEAVES
o Bronchoconstriction and accumulation of mucus/neutrophils – thought to be due to
environmental factors (i.e. in winter stabled horses housed near hay storage)
o See in horses >6 years old (MATURE horse disease) – increased RR and effort, end
expiratory wheezes (because airway diamter is reduced by inflammation/exudate/edema/
bronchoconstriction – as lung volume decreases during expiration the narrowed
bronchioles collapse trapping air distal to closure and creates wheezes heard
o Diagnosis = neutrophilic inflammation on BAL (healthy horses see macrophages on
BAL)
o Treatment
▪ Environmental changes (put horse in pasture, feed hay soaked in water, feed
pelleted diet)
▪ Beta-2 agonist – stimulate airway dilation by relaxing smooth muscle –
Clenbuterol, Terbutaline
▪ Corticosteroids – anti-inflammatory, can reduce mucous and neutrophil
accumulation
- Exercise induced pulmonary hemorrhage (EIPH) = BLEEDERS ! common in
THOROUGHBREDS
o Commonly seen in racehorses – may be due to reduced pulmonary capillary pressure
o Seen with short periods of strenuous exercise – usually speeds greater than 14 m/sec will
cause bleeding
o BILATERAL epistaxis (only 10% of time) after training – bleeding is pulmonary
(caudodorsal lung lobes)
▪ Other signs = labored breathing, loss of speed during race, poor performance,
after race swallowing excessively and sometimes coughs
o Diagnose with bronchoscopy or seeing hemorrhage on cytology of bronchoalveolar
lavage
o Treatment = FUROSEMIDE – administer before next race to decrease severity
- Pleuropenmonia
o Treatment = THORACOCENTESIS – proper site for pleural effusion removal = 7th rib
space at CC junction
▪ One of most dependent regions where fluid will accumulate, also caudal to heart
and cranial to diaphragm
- Ethmoid hematoma
o Progressive and locally destructive mass that resembles tumor but is NOT TRULY
NEOPLASTIC
▪ Mass that originates from mucosal lining of ethmoid conchae or walls of
maxillary/frontal sinus
o Unilateral intermittent epistaxis, mild increase in respiratory effort
o See smooth well-defined mass in sinus region (no osseous changes/fluid lines) –
surgically remove it!
- Laryngeal hemiplegia = recurrent laryngeal nerve is damaged
o Left side almost always affected ! caused by direct trauma, certain toxins, husbandry
o Exercise intolerance, noisy breathing, inspiratory dyspnea with audible whistling sound
on inspiration
- Pharyngeal paresis
o Can be caused by guttural pouch infections due to damage of CN 9 through 12 as they
run through pouch
o With paresis
▪ Arytenoid fails to seal glottis, epiglottis doesn’t close normal against rima glottidis
(coughing, aspiration)
▪ Soft palate no longer seals normally against roof of nasopharynx (food refluxes
through nose)
▪ Tongue fails to engage hard palate (food dropped, difficulty moving food bolus to
pharynx for swallowing)
▪ Upper esophageal sphincter remains open (no clinical sign)
- Guttural pouch tympany = pouch becomes distended with AIR
o Thought to be due to defect in Eustachian tube or pharyngeal tissues
o NONPAINFUL air-filled swelling in right parotid region, bright and alert, slightly
sterterous breathing
o Treatment = fenestrate the membrane between the normal and affected pouch
- Guttural pouch mycosis = ASPERGILLUS NIDULANS
o *CN 7, 9, 10, 11, 12 and the sympathetic trunk and internal carotid pass through the
medial pouch and the external carotid passes through the lateral pouch
o Dysphagia, Horner’s syndrome, hemorrhage if involves vasculature (epistaxis – due to
fungus eroding internal carotid artery), NOT vestibular signs (CN8 not involved)
o Treatment for persistent epistaxis = ligate internal carotid, surgical occlusion
(embolization coil, balloons) of artery
REPRODUCTION
- Persistent corpus luteum = progesterone made by CL prevents estrus
o If see anestrus during breeding season and have been non-receptive to stallions for
months but has had normal pregnancies in past – may find follicles in ovary on rectal
palpation
o Treatment = PGF2a infections – will cause lysis of CL if CL is more than 5 days old, if
you are unsure how old CL is you can repeat injection in 7 days
- Retained placenta
o Considered retained after 3 hours – usually expelled between 30 minutes and 3 hours
after birth of foal
o Treatment = oxytocin and lavage the uterus to facilitate removal – DO NOT pull on the
placenta, broad spectrum antibiotics (decrease chance of metritis)
o Mare DOES NOT eat placenta
- Uterine artery hemorrhage post-foaling
o Low PCV, tachycardia, history of foaling a few hours ago
o Treatment = aminocaproic acid – believed to facilitate clot stabilization by blocking the
activation of plasminogen to plasmin (plasmin is the active enzyme that dissolves clots
– so aminocaproic acid inhibits fibrinolysis)
- Twinning = most common noninfectious cause of abortion
o VERY RARE that both twins born alive – placental insufficiency usually leads to abortion
of both twins
o Abortions related to twinning occur at 6-9 months of gestation and may be preceded by
premature lactation
o Good to diagnose at day 13-15 with ultrasound so can manually reduce (i.e. crush) one
of twins while allowing other one to survive (90% success rate)
▪ Manual crush between 13-15 days, transcutaneous or transvaginal ultrasound-
guided twin reduction
- Gonadal dysgenesis = chromosomal abnormalitity – cannot have normal pregnancy EVER
- Pneumovagina = “WINDSUCKER”
o Usually seen in older, thin mares due to abnormal perianal conformation – in these
mares the anus is pulled forward which leads to tipping of vulva dorsally, causing
opening of the vagina
o Surgical repair = dorsal portion of labia is tipped cranially which needs to be sutured,
increasing the weight of the mare tends to realign the anatomy appropriately = Caslick
procedure
▪ Place horizontal sutures at the dorsal aspect of the labia and increase the weight of
the mare
o Predisposes to vaginitis and endometritis – aspiration of air leads to contamination,
leads to infertility
- Ruptured prepubic tendon = usually ruptures late in pregnancy
o Tendon runs along course of ventrum and provides major support for all structures in
equine abdomen
o Seen in obese DRAFT MARES – mare in last month of pregnancy develops ventral
edema from udder to xiphoid then becomes acutely painful and tachypneic
o May affect abiliaty of mare to increase intra-abdominal pressure during parturition
o Treatment = if notice ventral swelling take action immediately….restrict activity, use sling
under abdomen for support, do veterinarian assisted parturition
- Uterine torsion
o Mare in last trimester of pregnancy shows signs of colic – anroexic, frequently
attempting to urinate
o On rectal palpation = broad ligament pulled tight over the uterus from right to left
o Treatment = place mare under short-acting anesthesia and roll her (plank-to-flank),
surgery may be needed
- Uterine infection = ENDOMETRITIS
o Diagnose with uterine cytology (more reliable than cervical swab) ! will see high
percentage of neutrophils with infection especially if bacteria are seen too
▪ Culture is worthless because are so many commensal organisms – can be
helpful in choosing antibiotic
▪ If pre-ejaculate swab for culture growth has heavy growth of Pseudomonas or
Klebsiella think twice about breeding them because these organisms have a high
association of causing endometritis in mares
MISCELLANEOUS
- Chronic renal failure
o Weight loss, inappetance, PU/PD, USG = isothenuria (1.008-1.015)
o Azotemia, hypercalcemia, hypophosphatemia, hyponatremia, hypochloremia
▪ Unique to horses = HYPERCALCEMIA – see because high amounts of calcium
in diet, phosphorus levels might be low due to high calcium
- Glomerulonephritis = most common form of chronic renal failure
o Results from deposition of immune complexes in glomerular basement membrane
o Bloodwork = persistent proteinuria (may lead to serum hypoproteinemia)
- Uroperitoneum = see in FOALS
o Usually ruptures at time of parturition due to large pressures excreted on urinary
bladder at this time
o HYPERKALEMIA, hyponatremia, hypochloremia – urine is high in potassium and low
in sodium and chloride
o Diagnosis = creatinine in fluid will be TWICE as much as the serum creatinine
o Treatment = fluids – DO NOT GIVE POTASSIUM
- Ectopic ureter – YOUNG FEMALE HORSES – congenital anomaly
o Urine scalding, history of urinary incontinence ! surgically correct
Specificity and Sensitivity
- Sensitivity = the proportion of disease-positive animals that are test-positive
o A LOW sensitivity = MOST false negatives
o Because sensitivity looks at the animals that do have the disease and is the percentage
of them that will test positive
o i.e. 65% sensitivity = 65% true positives, 35% false negatives
- Specificity = the proportion of disease-negative animals that are test-negative
o Determined by percentage of true negatives versus false positives
▪ Defines the number of true negatives and false positives
- Positive predictive value = proportion of test positive animals that are disease positive (affected)
- Negative predicitive value = proportion of test-negative animals that are truly disease negative
(unaffected)

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- Bovine – orange/ Equine – green/ Cat – red/ Dog – Blue / Sheep and Goat - yellow

o Cantharidin = aka blister beetle toxicity

o Claviceps purpura = parasitic fungus – ERGOTISM

o Blue green algae = Anabaena, Microcystis, Aphanizomenon

o Lead poisoning = contaminated petroleum products (i.e. used motor oil)

o Yellow star thistle = Centaurea solstitialis

o False hellbore = Veratrum californicum

o Locoweeds (Astragalus, Oxytropis, Swainsona) = abortions, weak lambs, bent legs

o Fescue = Neotyphodium coenophialum (ergopeptine alkaloids – dopamine agonists)

o Ponderosa pine needles -

Clinical Pathology and Hematology

o An oxygen saturation of 50% corresponds to 30 mm Hg

o An oxygen saturation of 10% corresponds to 10 mm Hg

Tick Borne Disease

o = thin wall with 2-8 cells

o 2 nuclei, outlined by adhesive discs, swims in “falling leaf” motion, pear

o = asymmetric terminal plugs (similar to Trichuris eggs)

- Ostertagia ostertagii = roundworm

- Coccidiosis = EIMERIA (Isospora only affects carnivores…)

- Strongyloides spp. = intestinal threadworm

- Oxyuris equi = pinworm

Ruminant and Equine Dermatology Parasites

Ruminant and Equine Other Parasites

Leptospira interrogans serovar… = gram NEGATIVE

Clostridial Diseases – gram POSITIVE

Rabies = rhabdoviridae family, genus lyssavirus (bullet-shaped, enveloped)

Small Rodent Diseases

- Infectious bovine rhinotracheitis (IBR) = bovine herpesvirus type 1

-Bovine Winter Dysentery: = unknown etiology – suspect coronavirus.

ENDOCRINOLOGY and ELECTROLYTE ABNORMALITIES

- Abomasal ulcer = type 2 are bleeding ulcers

- Abomasal volvulus/torsion = LESS common than LDA or RDA

- Left displaced abomasum

- Right displaced abomasum

- Cecal dilatation with or without cecal torsion

- Gas in spiral colon

- Shipping fever = fibrinous pleuropneumonia = Mannhemia hemolytica

- Enzootic pneumonia = Pasteurella multocida

- Farmer’s lung = allergies

- Silo filller’s disease = bronchiolitis obliterans

- Laryngeal papillomatosis = papovirus

- Coxofemoral luxation = cranial and dorsal displacement

- Ruptured serratus ventralis = “flying scapula” if this ruptures

- Flexural deformities of distal limb (in calves)

- Septic arthritis and osteomyelitis

- Spastic paresis = Elso heel

- Spondylosis = degenerative intervertebral joint space disease in OLDER bulls

- Myophosphorylase deficiency = glycogen storage disorder

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o An oxygen saturation of 50% corresponds to 30 mm Hg  