Disorders Of The Renal System p903-916

Question 1

This group of animals appears to be predisposed to having a patent urachus. A) Twin calves B) Cloned calves C) AI calves D) Dystocia calves

Answer 1

B) Cloned calves

Question 2

Calves with internal urachal abscesses, adhesions or other sequelae are usually how old when they become affected? A) Neonates (under 1 mth of age) B) Yearlings C) Greater than 4 wks D) 6-8 mths

Answer 2

C) Greater than 4 wks

Question 3

What portion of the bladder communicates with the urachus, if the urachus fails to regress completely? A) Apex B) Trigone C) Along the lateral aspect of the body D) No communication with the bladder?

Answer 3

A) Apex of the bladder communicates with the pouch-like remnant, and urine can be retained here.

Question 4

What is the most common bacteria isolated from abscesses related to the urachus? A) Pseuodomonas B) Truperella C) Corynebacterium D) Fusobacterium

Answer 4

B) Truperella, along with E. coli

Question 5

What is the best treatment for urachal disorders? A) Long term abx and NSAIDs B) Euthanasia C) Surgical resection D) Benign neglect

Answer 5

C) Surgical resection, as the most problematic part is the structural abnormalities caused by adhesions and abscesses.

Question 6

What are some differentials for urinary bladder eversion or prolapse?

Answer 6

Vaginal prolapse, vaginal polyps, fat protrusion from a vaginal tear, vagina neoplasia, fetal membranes, uterine prolapse

Question 7

Describe the tx for urinary bladder prolapse vs eversion.

Answer 7

Urinary bladder eversion - must replace bladder through urethra that it came through, might need to widen urethral opening, especially if bladder is edematous; may need to perform a cystectomy if necrosis has occurred Urinary bladder prolapse - pass a catheter through urethra to reduce fill, replace into abdominal cavity and close vaginal wall tear

Question 8

What are reasons for pelvic urinary bladder entrapment?

Answer 8

Postpartum straining, perineal hernia and vaginal prolapse

Question 9

How can pelvic entrapment of the urinary bladder be treated?

Answer 9

Must reduce the urinary bladder fill and vaginally manipulate the bladder to it’s proper location. Laproscopy may also be warranted.

Question 10

Enzootic hematuria is caused by what agent? A) Clostridium hemolyticum B) Leptospirosis C) Copper toxicosis D) Pteridium aquilinum

Answer 10

D) Pteridium or aquilinum is the cause of enzootic hematuria. Also known as bracken fern, this disease causes a hematuria, not a hemoglobinuria (like C. hemolyticum or copper toxicosis does).

Question 11

Is enzootic hematuria a chronic or acute problem?

Answer 11

This is a chronic ingestion of bracken fern, of over 1-3 months. Cattle that become infected must eat a quantity approximating the animal’s body weight.

Question 12

What diagnostics can be performed to diagnosis enzootic hematuria?

Answer 12

Rectal palpation of a thickened bladder, with possible palpable masses; hematuria NOT a hemoglobinuria; US showing thickness of bladder, should be 1-2 mm; CBC may not show a regenerative anemia due to bone marrow suppression

Question 13

What are the compounds in bracken fern that are irritants, mutogenic, immunosuppressive and/or carcinogenic?

Answer 13

A) Ptaquiloside (aaquilide A), quercetin and alpha-ecdysone

Question 14

How are bracken fern and bovine papillomavirus 2 related?

Answer 14

The carcinogenic compounds in bracken fern can cause recrudescence of latent BVP-2. Local neoplasias are then induced in the bladder.

Question 15

What animals and where is enzootic hematuria seen most?

Answer 15

Adult sheep and cattle, occurring primarily in the Pacific Northwest and upper Midwest. Can see hematuria by 2-3 yo in cattle. Carcinomas seen 2-6 years after bracken feeding starts.

Question 16

UTIs in ruminants are most likely related to which bacteria?

Answer 16

C. renale or E. coli Less commonly, Salmonella, T. pyogenes, P. aeruginosa, Strep, and Staphy Corynebacterium pseudotuberculosis has been isolated from small ruminants with renal infections

Question 17

C. renale, a cause for UTIs in ruminants can be spread many ways. List common modes of transmission.

Answer 17

Direct vulvar contact; Sexual contact, spread by the bull; Splashing of urine by infected cattle; Iatrogenic transmission via contaminated OB instruments or urinary catheters

Question 18

What kind of urinary environment does C. renale thrive in?

Answer 18

pH-mediated pili are responsible for adherence of C. renale in alkaline environments. Ureolysis and ammonium production promote colonization of epithelium.

Question 19

Does infection with C. renale cause an Ab response and can this response be used to clear and protect against further infections?

Answer 19

C. renale DOES cause a serum Ab response, but this humoral response is RARELY curative, and does not provide resistance to reinfection.

Question 20

Which animals have a greater potential for developing UTIs?

Answer 20

Females, as they have a shorter urethra. Typically 90 days postpartum, is an ideal risk period.

Question 21

In regards to prognosis for animals with UTIs, what location of the infection leads to a better prognosis? What are other prognostic indicators?

Answer 21

A cystitis leads to a better prognosis in UTIs of ruminants, over a pyelonephritis, or a ureteritis. Animals with a marked azotemia (BUN > 100 mg/dL or creatinine > 1.5 mg/dL) and a pyelonephritis have a higher risk of being called. Case fatality and nonvoluntary cull rates are 18% and 47%, respectively.

Question 22

What are some clinical pathology changes seen in cattle with amyloidosis?

Answer 22

Marked proteinuria (with absence of RBCs, WBCs or bacteria) and hypoalbuminemia. Azotemia seen if renal damage is advanced.

Question 23

What is the process of development of amyloidosis?

Answer 23

Precursor proteins that are misfolded should be catabolized by proteosomes or macrophages. If this does not occur, these proteins accumulate into beta-pleated sheets that are resistant to degredation. The amyloid accumulates in renal, liver and spleenic tissues.

Question 24

How does amyloidosis occur in cattle?

Answer 24

Long-standing inflammatory diseases such as TPR or metritis causes an increase in SAA, an acute phase protein produced by the liver. If there is abnormal catabolism or a structural abnormality of the SAA, it is prone to become misfolded. This leads to its deposition in tissues.

Question 25

What are secondary consequences of amyloidosis and how does this lead to diarrhea, in cattle?

Answer 25

Amyloidosis leads to compromised glomerular filtration, leading to hypoproteinuria/hypoalbuminemia and a gradual loss of oncotic pressure. The GI, due to amyloid accumulation, can become edematous.

Question 26

Glomerulonephritis is a rare disorder of ruminants. How does glomerular injury occur from this disorder?

Answer 26

Ag to Ab complexes can become deposited in the glomerulus, or Ab can bind to intrinsic or foreign Ag localized to the glomerulus. This immune system targeting leads to glomerular injury through activation of complement and chemotaxis of leukocytes. Increased glomerular permeability allows plasma albumin to leak through and eventually leads to generalized edema.

Question 27

What are some diseases that glomerulonephritis has been associated with?

Answer 27

Cattle acutely or PI with BVDV, cattle with fascioliasis, pregnancy toxemia in ewes, mesangiocapillary GN in Finnish Landrace lambs of lineages in Scotland and Canad

Question 28

What percentage of lambs with urogenital defects were found to have one or more defects in other organ systems?

Answer 28

73%

Question 29

List some congenital defects of the urinary tract?

Answer 29

Renal cysts, renal agenesis (most common in lambs), retroperitoneal perirenal pseudocyst, renal oxalosis (metabolic dz that is suspected to have an inherited basis), ectopic ureter

Question 30

How is hemolytic uremic syndrome (HUS) characterized clinically?

Answer 30

Microangiopathies, hemolytic anemia, thrombocytopenia, and in many cases renal failure.

Question 31

Hemolytic uremic syndrome has three forms. What are they?

Answer 31

Typical - associated with consumption of food and water contaminated with Shiga toxin-producing bacteria Atypical - inherited mutations of complement-regulatory proteins and diverse causes of endothelial injury(antiphospholipid Abs, complications of pregnancy and contraceptives, vascular renal dz, chemotherapeutic and immunosuppressive drugs, radiation) Thrombotic thrombocytopenic purpura

Question 32

What is the predominant Shiga toxin-producing serotype of EHEC in human cases? Which one has been isolated in a horse diagnosed with HUS?

Answer 32

Enterohemorrhagic E. coli O157:H7 in humans E. coli O103:H2 from a mare and her foal

Question 33

What two processes drive the pathogenesis of thrombotic microangiopathy causing hemolytic uremic syndrome?

Answer 33

1) endothelial injury and activation leading to intravascular thrombosis 2) platelet aggregation

Question 34

How do E. coli toxins lead to endothelial injury in the process of hemolytic uremic syndrome?

Answer 34

EHECs (enterohemorrhagic E. coli) is not invasive, but attaches itself to the intestinal mucosa. The Shiga toxin targets the microvascular endothelium. Specific glycolipid receptors on the surface of the vascular endothelial cells are bound and the cell is injured through inhibition of protein synthesis, stimulation of prothrombotic messages or induction of apoptosis.

Question 35

List some nephrotoxins.

Answer 35

Aminoglycosides, tetracyclines, ionophores, ethylene glycol, oxalate containing plants, oak, acorn, myoglobin, hemoglobin/methemoglobin, arsenic

Question 36

What are the clinical signs of ARF in large animals? What is a specific syndrome that can result from renal failure?

Answer 36

The clinical signs of ARF in ruminants is non-specific and not indicative of overt urinary tract dysfunction. Various changes in urination patterns. Renal encephalopathy is a syndrome of brain dysfunction assoc. with renal disease. There are signs of intracranial disease (altered behavior, weakness, motor dysfunction, convulsions) that may be caused by alteration in the extracellular fluid content of acids, phosphorus, AA or certain hormones.

Question 37

What are some primary conditions in ruminants that lead to possible ARF? Describe the pathophysiology behind the diseases that lead to ARF.

Answer 37

Mastitis, metritis, enteritis, rumen acidosis, and intestinal accidents often lead to generalized loss of vascular volume, as seen with barked blood loss, septicemia, endotoxemia or severe dehydration. Thus, reduced blood flow to the kidneys causes ischemia and toxic damage to the tubular cells. ARF occurs by a sudden decrease in GFR, nitrogenous waste build up and loss of ability to manage electrolytes, protein, acid base and water build up.

Question 38

How does pigment nephrosis cause ARF?

Answer 38

Hemoglobin or myoglobin build up, resulting in renal vasoconstriction and tubular obstruction from protein coagulation.

Question 39

What is the general mechanism of toxins causing ARF?

Answer 39

Renal tubular epithelial cells have high metabolism, and are at risk of being highly susceptible to toxin that disrupt cellular enzymes. This is compounded by dehydration that concentrates the toxin in the tubular filtrate, slows toxin clearance, and can continue to severe, reduced renal perfusion.

Question 40

How do NSAIDs contribute to ARF?

Answer 40

NSAIDs block the action of prostaglandins, which are responsible for assisting in maintaining renal blood flow. In combination with dehydration, NSAIDs can contribute to ARF.

Question 41

What kind of environment does Lepto thrive in?

Answer 41

Can live up to 6 months, preferring a warm, moist environment with a pH of 7.2 to 8.0. Survival is shorter under dry conditions or at a temperature below 10*C (50*F).

Question 42

What is the prevalence of infection within a maintenance host population of Lepto?

Answer 42

30-50%

Question 43

List the ways Lepto can be spread?

Answer 43

Contact with contaminated (by urine) environment, feed or water, contact with an infected fetus or uterine discharge

Question 44

What are some maintenance hosts of Lepto?

Answer 44

Dogs, swine, opossums, skunks, raccoons, rats, pigs, mice, horses, cattle, muskrats, squirrels

Question 45

What are the important serovars typically implicated in renal infection of cattle?

Answer 45

Hardjo, pomona, grippotyphosa

Question 46

In a study of 5000 cattle in the US, what was the percentage of renal carriers?

Answer 46

2%

Question 47

A national survey showed ____% seroprevalence for L. interrogans serovars in cattle, with the highest seroprevalence found in cattle from ____. A) 2%; northwest, Atlantic coast B) 11%; Gulf Coast, southern states C) 49%; southeastern, south-central, Pacific Coast states D) 73%; Midwest, northern Canadian border states

Answer 47

C) 49%, southeastern, south-central, Pacific Coast States

Question 48

What serovar is host-adapted in cattle? What clinical signs are seen in the animals infected?

Answer 48

Serovar hardjo is host-adapted and infections are typically asymptomatic or cause non-specific repo failure or abortions. May cause chronic interstitial nephritis of variable severity. Can chronically cause infections of the genital tract of cows and bulls. Can persist in the urine for LIFE!

Question 49

How does the non host-adapted serovars affect cattle?

Answer 49

Severe systemic disease, hemolytic anemia, hepatitis, interstitial nephritis, tubular nephrosis, abortions. Urine can shed for weeks to months.

Question 50

How do renal lesions occur from infection with non host adapted serovars?

Answer 50

Direct damage to the vascular endothelium during leptospiremia, hypoxia from endothelial damage and hemolysis, tubular epithelial damage from Hg and interstitial nephritis.

Question 51

What’s the pathophysiology of Lepto, starting from infection to the convalescent phase.

Answer 51

Leptospires can penetrate external mucosal surfaces or macerated skin. Bacteria multiplies locally during an incubation period of 2-30 days. Once this is finished, the bacteria travel hematogenously. The bacteremic phase lasts 4 to 7 days. Opsonizing Abs are generated and aid in clearing infection. During the convalescent phase, leptospires can become lodged in the mammary gland, kidney, or GI tract, where they hide from the immune system.

Question 52

What are some virulence mechanisms of Lepto?

Answer 52

Toxin effect of lipopolysaccharide, adhesion to cells and extracellular matrix, bacterial motility, hemolysins and iron sequestration, motility for invasion and dissemination of the bacteria

Question 53

What is the most widely used test for diagnosis of Lepto? How are the results interpreted?

Answer 53

Microscopic agglutination test (MAT) to detect Abs to specific serovars. Need to see a fourfold increase in titers between acute and convalescent serum sample.

Question 54

Other than the MAT to diagnose Lepto, what other diagnostics are available?

Answer 54

Urine culture, phase-contrast microscopy, darkfield microscopy, FA, PCR, nucleic acid hybridization and immunoblot

Question 55

When testing a herd for endemic Lepto serovar hardjo, what is the best sample and number of samples?

Answer 55

Urine from 10 - 15 adult animals

Question 56

What treatments are considered clinically effective for Lepto?

Answer 56

Daily oxytet (100 mg/mL) 10 mg/kg IV or IM, SID, 5-7 days Long-acting oxytet 20 mg/kg IM or SC, EOD, for 2-4 tx