a.    Clinical signs: weakness, depression, lethargy, dementia, exercise intolerance, pallor, tachycardia, tachypnea
b.    Physical findings: pallor, icterus, abnormal urine, fever, systolic murmur (hemic murmur), blood loss (internal or external), associated hypoproteinemia

a.    Acute: rapid loss internally/externally (expistaxis, large vessel, rupture of internal organ, clotting defect, gastric ulcer
b.    Chronic: loss over time (parasitism, GI ulceration, other site of chronic hemorrhage-bladder)

a.    Anaplasmosis: worldwide, enzootic in coastal and intermountain western US
b.    Babesiosis: eradicated from North America in ruminants
c.    Eperythrozoonosis (Mycoplasma): worldwide, but considered minor dz unless in immunocompromised animal
d.    Leptospirosis: I think it’s everywhere. Zoonotic
e.    Bacillary hemoglobinuria: sporadic in western US   predominantly in irrigated areas

What is the current significance of Babesia infections in cattle in the United States ?

To third world countries?

It has been eradicated in the United States.

I imagine that it is still a big problem in third world countries, but don’t think he said
c.    Key point is that still causes hemoglobinuria (red water) b/c is intravascular hemolysis
d.    Obligate intracellular protozoan transmitted by ticks, incubation 2-3 wks, diagnose by history and area, reg. anemia, parasites in rbc, serology, treat with imidocarb, diminazene, phenamidine, and tick control

a.    Eperythrozoonosis, with some name changes to Mycoplasma and Haemoplasma
b.    Mycoplasma haemolamae is a common disease of camelids found throughout the country, anemia associated with immunosuppression. JLIDS (Juvenile llama immunodeficiency syndrome) used to be a predisposing problem to this, but don’t see JLIDS much anymore
c.    Generally a minor disease and signs usually in stressed and immunosuppressed animals, once infected are life-long carriers.
d.    Rare clinical disease in cattle: fever, stiff gait, ↓ milk yield, diarrhea, l.n. enlargement, scrotal and hind leg edema
e.    Yellow lamb disease in sheep, rare, sudden death with hemoglobinuria and icterus
f.    Treat with oxytetracyclines

a.    See hemolytic crisis in young animals and sometimes adults, hemoglobinuria and hemoglobinemia are key signs
b.    Treat with oxytetracycline and supportive care, prevent with vaccination and hygiene

a.    One of the Redwater diseases
b.    acute, fatal Clostridial diseases, see liver infarct, toxemia, and intravascular hemolysis and hemoglobinuria
c.    Caused by Clostridium hemolyticum snails and liver fluke can carry it, but not necessary part of life cycle, spores survive in alkaline soils.
d.    See sudden death usually after latent spores in the liver are activated and proliferate and produce exotoxin. If don’t die, look bad clinically and die w/in 3-4 days
e.    On necropsy the ischemic liver infarct is a key sign with rapid rigor, bloat, and autolysis, subq edema and hemorrhages, icterus, bloody fluid in cavities, abomasitis and enteritis and hemoglobinuria
f.    Diagnose based on area (western US- MT, NV, WA, ID, OR in irrigated areas), history, clinical signs and necropsy
g.    R/O postparturient hemoglobinuria, Heinz body anemia, Brassica, onions, chronic Cu toxicity, hematuria or myoglobinuria and Anthrax (sudden death)
h.    Usually dead, but can try to treat with penicillin/tetracyclines and supportive care if catch before die. Prevent with vaccination and destroy affected carcasses.

a.    Brassica: Usually get hemolytic disease within 1 week of introduction, cattle more susceptible
i.    Toxins induce oxidative damage to RBC leading to extravascular removal, can have intravascular hemolysis if concurrent with Pi, Se, or Cu deficiency
ii.    Heinz bodies formed from S-methyl cystine sulfoxide – dimethyl disulfide
b.    Allium: Toxins are N-propyl disulfide and s-methyl cystine sulfoxide → Heinz bodies and usually extravascular removal, so no red urine

a.    Usually come from rations or supplements high in copper → accumulation in liver with and acute event, liver damage may enhance storage
b.    Acute or chronic copper toxicity leads to hemoglobinuria from hemolytic anemia
c.    In pre-ruminant calves they don’t chew their cud → don’t produce as much saliva which normally will bind the Copper

a.    Iron deficiency: Associated with chronic blood loss due to parasitism or all milk diets and no dirt, ↓ Fe → ↓ hemoglobin production
i.    Dx by ↓ PCV, normal TP, ↓ iron stores in tissue biopsy, ↑ serum iron-binding capacity, ↓ serum iron, microcytic hemolytic anemia
ii.    Tx with oral iron or parenteral iron
b.    Copper deficiency: Cu needed for iron transport, so ↓ Cu → ↓ Fe transported → ↓ hemoglobin production, looks similar to iron deficiency, also may get abnormal bone and growth plates, abnormal myelin formation, ↑ risk for infectious dz b/c immune system affected, diarrhea, ill thrift and hypotrichosis
i.    Dx by ↓ PCV, ↓ Cu levels, microcytic to normal hypochromic anemia
ii.    Tx with mineral supplements, oral copper oxide needles, copper injections

a.    Four occur spontaneously (non-viral associated and T cell related)
i.    Calfhood form (either B or T cell related)
1.    Birth to 2, symmetrical lymphoid lesions, ill-thrift, anemia, leukemia, liver, kidney, spleen involvement
ii.    Thymic form (pretty common in goats)
1.    6 months to 2, beef > dairy, mass near thoracic inlet, dyspnea, dysphagia, anemia and lymphadenopathy uncommon
iii.    Cutaneous and Multicentric

1.    1 to 3 yrs, multiple skin nodules with hair loss, regress and re-appear, eventual multicentric to other lymphoid tissues and/or thymus, debilitation comes with multicentric expansion
b.    Enzootic bovine lymphosarcoma (doesn’t happen in other spp. readily)
i.    Retroviral associated, B-cell type tumors usually
ii.    Spread by blood, colostrum/milk, palpation sleeves, needles, insects, body fluids, in utero
iii.    Most common form of LSA, infection > dz, >2 yrs old
iv.    Signs: symmetrical or nonsymmetrical lymphadenopathy, weight loss, ↓ milk, exopthalmia, posterior paralysis, cardiac failure, melena, uterine involvement
v.    1° sites are in lymph nodes or lymphoid tissues
vi.    Metastasis to heart, abomasum, intestine, uterus, or spinal canal
vii.    One of common clin path signs is a persistent lymphocytosis
c.    Dx by BLV history in herd, clinical signs, biopsy, virology, serology
d.    Don’t usually treat (most infected animals are euthanized), control by identifying and isolating or removing infected animals, insect control, and colostrum management

a.    Bovine Leukocyte Adhesion Deficiency
b.    Autosomal trait of Holsteins where affected calves lack surface glycoproteins that inhibit adhesion and so the neutrophils don’t have chemotactic factors and thus more and more neutrophils are made to compensate → profound neutrophilia (>40,000/mcL)
c.    Most animals get bacterial infections and premature death
d.    Can be traced to single male ancestor and is starting to be bred out of herds
e.    Dx by recurrent infection, marked neutrophilia and DNA-PCR test

Understand the common presenting issues regarding cystitis in ruminants including:

gender issues: 
 time of occurrence:
 predisposing factors:
etiologic agents:
Signs:

gender issues: female>males
b.    time of occurrence: Not common in ruminants and camelids,
c.    predisposing factors: usually 2° to urine stasis or bladder injury
d.    etiologic agents:
i.    trauma with ascending bacteria and ↓ urine flow
ii.    E. coli most common bacteria isolated (others are Strep., Proteus, Pseudomonas, Klebsiella, Enterobacter, Corynebacterium)
iii.    Corynebacterium renale (bovis) is the cause of infectious contagious cystitis and pyelonephritis
iv.    Also associated with urolithiasis, bladder paralysis, dystocia, reproductive sepsis, catheterization, patent urachus
e.    Signs: pollakiuria, stranguria, abnormal urine (hematuria or purulent), urine scalding/dribbling, fever early on, abnormal bladder on rectal exam, abnormal cystoscopic findings (females)
f.    CBC: sepsis; Chem: BUN, Cr usually normal; UA: protein, pyuria, hematuria, other cells and debris; urine culture and sensitivity: basis of tx
g.    DfDx: urolithiasis, urinary incontinence, Pyelonephritis, neoplasia, bladder prolapsed, renal failure, urethritis, etc.
h.    Tx predisposing problems/conditions, hydration and urine flow, Abx based on C/S (7-14 days min.), urinary acidification, acute prognosis> chronic, relapses common

a.    Injury to cauda equine or 2° to obstructive urolithiasis
b.    Signs: incontinence,, dribbling/overflow, bladder full on rectal, ataxia or tail paralysis, 2° cystitis
c.    Treat cystitis and underlying causes, trauma has best prognosis

a.    Most common obstruction site is the sigmoid flexure, also in small ruminants have the urethral process, where uroliths can get stuck
b.    Urolith formation risk factors: water deprivation, high salt intake, hot arid climates high Pi from grain, high Mg intake, young animal, pelleted rations, silicates in feed, estrogenic and oxalate containing plants (alfalfa)
c.    Obstruction facilitated by an early castration, urine stasis, and nidus formation
d.    Not usually seen in renal pelvis or ureters, but will have Hardware-like signs
e.    Signs from urethral obstruction are colic like signs, frequent stretching to urinate, but can’t, dribbling urine, maybe blood tinged, pain in sigmoid area, dry prepuce or crystal on hair, rectal prolapsed could some from straining
f.    On CBC/Chem see systemic Hyponatremia, hypochloremia and normal or ↓ K
g.     
h.    Prevent by:
i.    Manage pasture or hay type
ii.    Put females on the more dangerous pasture types (will still get stones, but w/o as many complications
iii.    Put 2-3% NaCl, NH4CL, NH2SO4 in ration, Ca:P 1.2:1, salt available (helps with Mg problems), delay castration, adequate water at all times
iv.    High risk for reoccurrence
v.    Smoother the stone the better the prognosis

a.    Silicate: on dry pasture (semi-arid) in fall or on grass hay → “Jack stones”
b.    Struvite: (Mg ammonium Phosphate, triphosphate, calcium phosphates) get from high concentrate diets with high Mg → sand-like stones (lots of them)
c.    Calcium carbonate: clover pastures or legumes → smooth, pearl-like stones
d.    Calcium oxalate: oxalate containing plants → rough and irregular stones (rare in ruminants, but most common type in people)

a.    BUN > 200 mg/dl and Creatinine > 5-6 mg/dl may be seen in prerenal
b.    If azotemia with low specific gravity (<1.022) tentatively diagnose as renal
c.    Casts are frequently found with acute tubular disease
d.    Ruminants are more commonly in metabolic acidosis when in renal failure b/c of sequestration of HCl within the abomasum from GI atony
e.    ↓ K (anorexia, salivary losses), ↓ Ca (anorexia), ↑ P (b/c of lack of loss in the GI tract from anorexia, main losses of P is from the salivary glands), ↑ Mg (↓ FE of Mg in renal dz, most Mg lost through the kidneys), ↓ Na (lost in kidneys), ↓ Cl (sequestered in abomasum in anorexia and GI atony)
f.    ↑ fibrinogen not related to inflammation, but from azotemia activating the intrinsic coag pathway
g.    Bleeding disorders; be aware of these before renal biopsy

i.    Local invasion or hematogenous
ii.    Signs depend on site, duration and extent of damage
iii.    Infection est. from trauma (local invasion) or hematogenous
iv.    Infection in joint is probably in the synovial membrane, so can do synovial biopsy to diagnose
v.    Prognosis is guarded to poor

i.    Defective or abnormal bone/joint formation in both young and old
ii.    See angular limb deformities, enlargement of or pain over growth plates, lameness, DJD, pathologic fractures, systemic findings
iii.    Etiology: nutritional- Ca, Mg, and Vit. D deficiencies (Rickets), Cu def., ↑ or↓ Vit A, chronic parasitism, spondylitis in breeding bulls, chemicals, congenital or inherited, environment, unknown

i.    A group of acute diseases affecting primarily skeletal muscle caused by various species of clostridial organisms
ii.    Common clinical signs: young, prospering animals at risk, rapid course, often find dead, severe depression, high fever, tachypnea and anorexia, lameness in 1+ limbs, any muscle group, vulva, tongue, diaphragm, recent injection sites, one site/animal!!, initially skin hot and painful then cool and insensitive, possible crepitus, ~100% mortality
iii.    Blackleg: Cl. chauvoei animals <2 and taken in by mouth, sudden death
iv.    Malignant edema: Cl. septicum  deep wound associated or traumatized sites in repro tract or udder, “Braxy” is form that affects the abomasum
v.    Black neck: Cl. sordelli feedlots usually from wound or oral, black hemorrhage and muscle necrosis at base of neck and brisket
vi.    Black disease: Cl. novyi rare in cow/calf, more common in feedlot
vii.    Exposure common, disease is far less common, spores can remain quiet in tissues for long period of time
viii.    Horses have best prognosis, but grave for all spp. (treat with penicillin or tetracycline or metronidazole)
ix.    Prevent by proper disposal of carcasses and vaccinate ruminants with 2 doses initially and an annual booster while pregnant to ↑ colostral immunity

i.    Group of syndromes in animals causing inability to rise (1°ly in rear end)
ii.    Hypocalcemia is most common cause of initial recumbency in dairy cattle
iii.    Dystocia is most important cause of recumbency in beef cattle
iv.    Any condition or event that causes prolonged recumbency will cause downer animals
v.    More common in females than males
vi.    Irreversible events may occur w/in as little as 6 hours of recumbency
vii.    Stage 1: Initial event that caused animal to be recumbent (can be BAR or dull and depressed)
viii.    Stage 2: Common to all recumbent ruminants, weight leads to ischemia and pressure damage to muscles and nerves
ix.    Stage 3: Further injuries or even death from struggling (fractures, dislocations, muscle ruptures)
x.    History is very important for Dx, take blood samples before treatment to check Ca, Mg, P
xi.    Splayed legs is very bad sign and the longer recumbent the poorer the prognosis
xii.    Need to check every 2 hours and provide physical therapy or support, long, time intensive process to recovery, make sure owner is aware of this

i.    Laminitis associated
1.    White line hemorrhages
2.    Under running of the heel
3.    White line abscesses
4.    Sole hemorrhage
5.    Double sole
6.    Sole ulcer
7.    Toe ulcer
ii.    Infectious
1.    Interdigital dermatitis
2.    Heel horn erosion
3.    Digital dermatitis
4.    Toe abscess
5.    Foot rot
6.    Warts
7.    Corns