herd, bc often related to diet (and everyone eats the same thing)
3 normal urolith inhibitors?
mucopolysaccharides, ions, organic acids
WHO are the most likely to get uroliths?
CASTRATED MALE rumis, ESP if EARLY castration. (she says optimum time to castrate is at 2week- earlier is risk of urtholiths, later is inc chance of trauma and bleeding). SMALL rumis, esp Goats at higher risk. Also very common in FEEDLOT CATTLE (bc high grain diets= lot of minerals)
how common are bacterial infections playing a role in food ani uroliths?
only a minor contributor
what diet puts them at risk for urolith formation and why?
HIGH CONCENTRATE/low roughage diets--> inc urinary phosphorus excretion. OR diets high in Mg
what would Ca:P ratio be? which diet type is this skewed in?
should be (ca:p) 2:1 or 1:1....either equal or more Ca. but in high grain diets, grain high in P, P can be greater than Ca.
3 physiological contributing factors to urolith formation?
(1) NEG water balance (ESP if animals consuming a lot of grain) (2) rate of renal excretion of crystalloids (more Ca/P/electrolytes, gonna be excreting more...set them up for this) (3) ALKALINE pH (pH can determine if precipitation)
what 3 stones like to form in ALKALINE (rumi) urine? which 2 dont care what the pH is?
What are struvite stones made from? what are the likely from?
made of Mg, ammonium, phosphate (Struvite=MAP) which are constituents of a high grain diet!!! (also ammoniated feeds)
apatite stones are made of what, what most likely causes them(diet)?
Ca and P, also likely from high grain diets
calcium oxalate stones are made of what, caused by what diet?
Caused by consuming oxalate containing plants
calcium carbonate (dont confused with oxalate) caused by what diet?
diet high in legumes (LEG room in CAR)
silicate caused by what diet?
from grazing plants grown in soil with high conc of silicate
why are SMALL rumis more prone to blockage?
ANATOMY has lots more places for them to be prone to blockage. urethra with two major bends (sigmoid flexure) and a urethral process (narrow) (other possible sites for blockage include: bladder trigone, ureters, renal pelvis)
why should you always check the whole urinary tract for uroliths?
usually come in multiples
someone tells you their goat blocks a lot and they want to get a urethral process amputation- what should you tell them?
this is only a temporary fix (doesnt affect fertility)
what do you think of passing a cath to help with stones?
small rumis have a small urethral diameter and a urethral diverticulum-- not really feasable
*CSs of urolithiasis?
inappetance, lethargy (uremia makes you feel like crap), colic (abd pain), restless (prolly pain), mild bloat, straining (can be poop or urine-- make sure of think of both), posturing, vocalizing. Caution for pressure necrosis!!
major sequelae to urethral obstruction?
(1) ruptured urethra and leakage of fluid SQ: cellulitis. (2) Rupture of urinary bladder: water belly.......other complications include: urethral perforation, urethral stricture, bladder rupture, ureteral rupture, hydroureter, hydronephrosis, ruptured kidney
some ways to dx urolithiasis
(1) digital exam: pulsing urethra, urethral turgidity. not that sensitive. (2) US: easy to see if bladder intact, harder to tell about urethra. (3) rads: most uroliths visible, can use contrast (4) abdominocentesis: see if there is a rupture
how can you tell if your abdominocentesis is urine, versus sthing else?
look at odor, SG, BUN and crt levels. the urine crt:serum crt ratio should be >2:1 (Then you know its urine)
serum biochem associated with urolithiasis/rupture of urinary tract
post-renal azotemia, hyperkalemia, hyponatremia, hyperglycemia (stress), stress leukogram, hemoconcentration (might be present- are they dehydrated?), heamturia, proteinuria
How can you adjust diet to try to avoid uroliths?
PROPER Ca:P ratio (1:1 or 2:1), AVOID grain (high in P), avoid legume hay (HIGH in Ca, risk for Cacarbonates), give good quality grass hay
how can you manipulate the pH of the urine to help with uroliths? how do you do this?
ACIDIFY urine (since they have alkaline urine and they are making stones, prolly wanna do opposite), can use ammonium chloride to acidify urine. Also need to do in a PULSATILE fashion, or kidneys will catch on and adjust pH back up accordingly (careful tho, chronic tx might inc Ca loss in urine-->opsteoporosis)
tx for complete obstruction due to uroliths?
*fluid, electrolyte, acid-base adjustments (NO MORE K THO-- CAREFUL. so prolly dont want Ringers or LRS, plasma lyte, normosol)....then Sx: (1) tube cystotomy (2) amputation of urethral process (temp) (3) perineal urethrostomy, bladder marsupialization (these 2 have complications of urine scald/infections and such)
Ulcerative posthitis and vulvitis, UTI (she skipped UTI, i just made some notes)
Ulcerative posthitis and vulvitis aka?
enzootic balanoposthitis, pizzle rot, sheath rot
is this problem contagious?
yes! contagious through necrotic debris/ venereal xmission
WHO is most prone to pizzle rot? (sp, age, gender, breed..)
SMALL rumis, esp OLDER MALES>younger males>females>cattle. Most prone breeds are MERiNO AND ANGORA, because dense coat= more likely that urethral orifice is soaked with urine
what is the causative agent of pizzle rot? say a little about it
corynebacterium renale, aerobic, G+, pleomorphic. NORMAL COMMENSAL OF SKIN! survives in long wool an scabs and environment
explain pathogenesis of pizzle rot
corynebacterium renale--> produces UREASE--> breaks down urine's urea to ammonia--> ammonia causes ULCERATIONS at mucocutaneous junctions
CSs of pizzle rot
moist ulcers at mucocut. junction at prepuce, vulva, perineum. There will be little to no bleeding when picking scabs (pretty helpful sign). focal swelling of cr prepuce/enlarged vulva. Painful on palp. spreads up mucosal surface of prepuce. can get fibrinous adhesions between penis and prepuce/distortion of vulva due to scarring. Can see Dysuria, stricture of urethral process, dec breeding soundness.
deposition of insoluble protein fibrils in kidney that disrupt glom structure to cause pathology. Precursor proteins misfolded and not degraded. The misfolded proteins for BETA-PLATED sheets (these are what accumulate in tissue and disrupt tissue structure and fxn-- lesions irreversible)
what might trigger amyloidosis in cattle- how common is this?
misfolded (beta-pleated sheets) proteins can be produced in over-abundance in response to chronic infection/inflammation. This "reactive" type is the MOST COMMON TYPE IN CATTLe.
2 kinds of amyloidosis? which is more common in cattle?
(1) Reactive (2* to chronic inflammation/infection) *THIS IS MORE COMMON IN CATTLE (2) neoplasia producing overabundance of precursor proteins
what might you see on CBC/CHEM with a reactive type amyloidosis?
(1) serum amyloid A (means current ongoing inflammation) (2) hyperfibrinogenemia (indicates chronic inflammation) (3) Hypergammaglobulinemia
what can you grossly see in urine that might make you strongly consider amyloidosis? why does this happen?
FOAMY URINE. bc fluid that foams means it has a lot of protein in it. And amyloidosis is a protein losing nephropathy bc the amyloid destroys gloms
CSs of amyloidosis?
diarrhea, weight loss and poor production (PLN=weight loss), persistent, heavy proteinuria seen as very foamy urine, ventral edema (and other effusions), non-painful renomegaly, and kidneys waxy on cut surface
what is the stain/conditions under which you can see amyloidosis on histopath?
congo red stain under polarized light
DDx for amyloidosis?
johnes, chronic parasites, Cu deficiency, salmonellosis, BVDV, glom.nephritis (only other one with proteinuria, need bx to differentiate)
describe what leptospirosis is
motile, G- obligate aerobic tightly coiled spirochete. (can live in enviro for up to 6mo if wet and warm) (does NOT like dry or freezing)= seasonal incidence
what pH does lepto like?
how is lepto usually spread?
persists as a chronic infection of renal tubule of maintenance host species. In the maintenance host species, CSs are mild or they are asymptomatic. They will shed for a LIFETIME.
CSs of lepto in cattle as a maintenance host?
fever, agalactia, mastitis, soft udder, yellow to red tinged milk. ALSO can persist as a chronic infection of the GENITAL tract in maintenance host species. CS: infertility, stillbirths, abortions, birth of weak calves
infection in an incidental host for lepto can cause what probs/CSs?
ACUTE DZ IN MULT ORGAN SYSTEMS (kidney, liver, CNS, repro) can see hemolytic anemia (mediated by toxins and hemolysins), hemoglobinuria (2* pigment neuropathy), interstitial nephritis, tubular necrosis (Calves>>adults), meningitis (rare), agalactia, mastitis, abortions
how long is shedding in maintenance host? incidental host?
maintenance: lifetime. Incidental: urine shedding lasts from weeks to months
does lepto cause dz in maintenance? incidental?
causes dz in both, but in incidental much more severe
***cattle are primary maintenance hosts for what 2 kinds of lepto?
(1) L. interogans serovar hardjo. (2) L. borgperersenii serovar hardjo (so hardjos are still hardy cattle)
***cattle are the maintenance OR INCIDENTAL hosts for which 2 kinds of lepto?
(1) L. interogans serovar PAMONA (2) L. interogans serovar grippotyphosa (PAM the cow is losing her GRIP on her health)
3 most common serovars implicated in renal infection in cattle?
hardjo, pomona, grippotyphosa
how common is lepto in small rumis?
NOT common. sheep can be subclinical carriers for serovars hardjo, hardjo bovis, and pomona
if a human is infected with lepto, are they a maintenance, incidental host, or both?
ONLY INCIDENTAL (wear gloves damnit with rumi urine damnit)
where does lepto like to live in the kidney?
renal prox. tubule lumen
organs lepto really likes?
kidney, mammary gland, genital tract
explain pathophys of lepto infection
lepto enter through mucosa or macerated skin--> mult locally--> move to blood via lymphatics (leptospiremia)--> spreads to mult organs. Seroconvert by end of leptospiremic stage (soooo looking for Abs might not always be helpful)--> convalescent phase at time spirochete is localized to various organs (mammary, kidney, genital)***WHEN LOCALIZED TO ORGANS, SPIROCHETE IS PROTECTED FROM IMMUNE SYSTEM
**what determines if chronic renal lepto infection creates histological changes? what are some possible histo changes?
presence of virulence factors like LPS determine this, can be changes like: mild interstitial nephritis, diffuse severe lymphocytic interstitial nephritis, fibrosis (nephritis persists long after infection is cleared)
what is necessary for lepto to be transmitted in body fluids?
CHRONIC infection allows for this.
what is tricky about dx a carrier animal with lepto?
can be seroneg but shedding bc lepto in immune privileged sites (like mammary gland for example)
ways to dx lepto?
(1) Microscopic agglutination test (MAT) serological test. (cross reactivity with many serovars), make sure to look at CSs bc vx can confuse results (2) ELISA for Abs (common method in research) high titer during bacteremic phase. (VX CONFUSES SEROLOGY- paired serology needed) (3) urine culture, phase contrast microscopy, dark field microscopy, FAT, PCR, immunoperoxidase stained kidney sample at post mortem.