Ruminant Renal Disease 1

What disease has a worldwide distribution and involves 20 species with >240 serovars?

Leptospirosis

T/F: Lepto is a very common zoonotic disease.

True!

Lepto is a —— shaped bacteria and has prolonged survival in —- environments.

Spiral

Moist

What are the THREE clinically important Lepto species?

1. Leptospira interrogans

2. Leptospira borgpetersenii

3. Leptospira kirschneri

What are the THREE major serovars of Leptospira interrogans

Hardjo type hardjoprajitno- cattle

Pomona- swine/opossums/raccoons

Icterohemorrhagiae- rats

What is the major serovar of Leptospira borgpetersenii?

Hardjo type hardjobovis- cattle

What is the major serovar of Leptospira kirschneri?

Grippotyphosa- raccons/squirrels

What are the TWO types of Leptospirosis infection?

Host adapted- maintenance hosts

Non-host adapted- incidental hosts

Host adapted Leptospirosis involves (low/high) susceptibility to infection, (sporadic/endemic) transmission, (low/high) pathogenicity, (acute/chronic) disease), (short/long) disease, and (low/high) antibody response.

High susceptibility to infection

Endemic transmission

Low pathogenicity

Chronic disease (reproductive losses)

Long disease

Low antibody response (decrease vaccine efficacy)

Non-host adapted Leptospirosis involves (low/high) susceptibility to infection, (sporadic/endemic) transmission, (low/high) pathogenicity, (acute/chronic) disease), (short/long) disease, and (low/high) antibody response.

Low susceptibility to infection

Sporadic transmission

High pathogenicity

Acute disease

Short disease

Marked antibody response (good vaccine efficacy)

What Lepto serovar is host-adapted to cattle and has a seroprevalence of 30% in US cattle with a LOW morbidity and LOW case-fatality?

Hardjo

T/F: Regionally, there is seroprevalence higher in host adapted than non-host adapted Leptospirsosis species.

False! Regionally, there is seroprevalence higher in most NON-HOST ADAPTED strains than host adapted (L. Pomona and grippotyphosa)

What animals have NO host-adapted serovars, but persistent leptospiruria has been reported?

Sheep and goats

What is the most common Lepto serovarin sheep?

Pomona

Sheep and goats have a (low/high) morbidity and case-fatality with Leptospirosis.

High

What are THREE features of Leptospirosis in sheep and goats?

1. Congenital defects/abortions

2. Fatal infections in feedlot lambs

3. Lamb losses due to agalactia

What are THREE ways Lepto can be transmitted?

1. Shedding from infected animal (pastures/water/feed)

2. Infected wildlife (deer/pigs/vermin)

3. Bacteria in urine/abortus/uterine discharge

T/F: Lepto often involves prolonged genital infections and urine contamination for 10-118 days.

True!

What is the pathogenesis of Leptospirosis?

Mucus membrane invasion -> local replication -> bacteremia -> localization in organs (kidneys, mammary gland, genital tract)

T/F: Endemic, chronic infections of Lepto, as with L. Hardjo, are often asymptomatic.

True!

What are FIVE occasional signs of endemic, chronic Lepto infection?

1. Infertility

2. Abortions weeks after infection (often only clinical sign)

3. Birth of weak calves

4. Milk drop (flabby udder; yellow to orange milk with blood clots)

5. Interstitial nephritis with prolonged shedding

Severe acute to subacute Lepto infections, as seen with L. Pomona, are most severe in what ruminants?

Young calves

What are the FIVE major signs of severe acute to subacute Lepto infections?

1. Systemic from bacteremia (fever, anorexia, lethargy)

2. Interstitial nephritis (oliguria, azotemia)

3. Hemolytic anemia with hemoglobinuria (anemia, jaundice, petechiation)

4. Reduced milk production (blood clots; limp/soft udder)

5. Abortion second half of pregnancy

What is the best way to diagnose Lepto?

Serology (MAT/ELISA)

Serology comes as a paired sera, (herd/individual) samples are better, and there is difficult interpretation with serovar —-.

What complicates the interpretation of this diagnostic?

Herd

Hardjo

Vaccine titers

T/F: For Lepto, urine samples should be the second voiding after furosemide and should be cultured to demonstrate the organism (FAT, dark field microscopy, PCR).

True!

What are TWO major treatment components involving Lepto?

1. Early antimicrobials (Oxytetracycline for chronic; Penicillin)

2. Fluid therapy (treat renal failure; prevent renal damage from pigmenturia)

What does treatment success depend on with Lepto?

Extent of renal disease

What are TWO ways to prevent Lepto?

1. Vaccination

2. Biosecurity (rodents/wildlife; carrier animals; AI with free bulls)

What are the THREE vaccines used for Lepto prevention?

1. 5-way Lepto

2. Spirovac

3. Bovi-Shield GOLD

What are THREE major categorical causes of tubular necrosis?

1. Various toxins (heavy metals, meds, plants)

2. Infectious agents (ascending UTIs, hematogenous infection)

3. Hemodynamic insults (reduced renal perfusion, thrombosis)

Name at least FIVE clinical signs of tubular necrosis.

Depression, ileus, rumen bloat, muscular weakness, dehydration, diarrhea, anuric/oliguric/polyuric

What are TWO clinical signs of renal disease in the oral cavity?

1. Breath smells like pee pee

2. Oral ulcerations from ammonia

—- is a common clinical sign with oak and heavy metal toxicity.

Melena

What are THREE signs of chronic tubular necrosis?

1. Weight loss

2. Inappetence

3. Diarrhea

There are organic and inorganic forms of arsenic, but the (organic/inorganic) form is more toxic.

Inorganic

T/F: Rodenticides, herbicides, insecticides, wood treatments, and copper chromated arsenic (CCA) are associated with organic forms of arsenic toxicity.

False! Rodenticides, herbicides, insecticides, wood treatments, and copper chromated arsenic (CCA) are associated with INORGANIC forms of arsenic toxicity.

What are the TWO major MOAs of arsenic toxicity?

1. Direct irritation (GI tract + capillaries)

2. Inhibition of TCA cycle enzyme a-ketoglutarate

What are the FOUR body systems involved in arsenic toxicity?

Liver, kidney, GI, CV

What are FIVE clinical signs of arsenic toxicity?

1. Profuse diarrhea (often bloody)

2. Abdominal pain

3. Dehydration

4. Weakness

5. Leaky vessels

How do you diagnose arsenic toxicity?

>3ppm in liver or kidney samples

Seeds treated with organic forms of fungicides is associated with what toxicity?

Mercury

What is the MOA of mercury toxicity?

Form covalent bonds with sulfhydryl groups

In mercury toxicity, binding to —- prolongs excretion.

Metallothionein

What are the first signs of mercury toxicity?

What follows it?

GI erosion + diarrhea

Nephrosis

What are the FIVE metallic nephrotoxins?

Cadmium, chromium, lead, zinc, copper

T/F: >60 species of oak may be toxic in North America.

True!

Oak toxicosis is most common in what TWO oaks?

1. Shinnery oak (Quercus havardii)

2. Gambels oak (Quercus gambelii)

In oak toxicosis, (calves/adults) are more severely affected and (young/mature) plants are more toxic.

Calves

Young

T/F: Oak buds and leaves after a snowstorm or many acorns after wind storm all contribute to oak toxicity.

True!

T/F: Oak toxicity is a sporadic disease that is enzootic under certain conditions, mainly severe weather and regionally in the southeast US.

True!

What feature of oak toxicity is irritating to mucosal surfaces, involves mucosal ulceration and GI hemorrhage, and bind to plasma and endothelial proteins to create edema?

Tannins

What does the rumen hydrolyze tannins to that then bind to tubular proteins?

Gallic acid and pyrogallol

T/F: Oak toxicosis is typically acute onset after exposure and has similar signs to other causes of acute renal failure.

True!

Many plants contain >—% oxalates and is most common in the —- plant.

>10%

Pigweed

What is the pathogenesis of oxalate toxicosis?

Intestinal absorption -> microflora not adapted -> combines with serum Ca2+ or Mg2+ -> hypocalcemia and insoluble crystals -> tubular damage

Oxalate toxicosis is most common in —-, as they graze extensively, which puts them at higher risk.

Sheep

T/F: Small quantities of oxalate consumption is enough to create noticeable clinical signs in ruminants, especially sheep.

False! LARGE quantities of oxalate must be consumed.

What are THREE risk factors of oxalate toxicosis?

1. Consumption of young plants

2. Grazing without prior rumen adaptation

3. Grazing hungry animals on at-risk pastures

What are THREE secondary conditions seen with oxalate toxicosis?

1. Hypocalcemia syndrome

2. Nephrotic syndrome

3. Ruminitis

What are the TWO treatments for oxalate toxicosis?

1. Calcium borogluconate

2. Fluids

What is the minimum lethal dose of ethylene glycol in a cow?

2-10 ml/kg

T/F: Ethylene glycol is sweet and is more common in small animals.

True!

What is ethylene glycol degraded to in the rumen?

Glycolic acid and oxalate

What medication accumulates in the proximal tubular cell and causes disruption of cellular metabolism, leading to cell death?

Aminoglycosides

What medication involves crystal formation in acidic urine, especially when overdosed or decreased water intake?

Sulfonamides

What medication involves inhibition of tubular oxidative enzymes at high doses and vascular effects by the carrier (propylene glycol)?

Oxytetracycline

What is the pathogenesis of NSAIDs becoming nephrotoxic?

Decreased PGE2 and PGI2 -> decreased renal blood flow -> medullary crest necrosis

What overdose results in increases renal Ca2+ excretion?

Vitamin D (and plant cholecalciferols)

What are the FIVE principles of therapy for tubular necrosis?

1. Remove cause as appropriate

2. Promote diuresis

3. Correct acid/base and electrolyte abnormalities

4. Plasma transfusion to correct hypoproteinemia

5. Close monitoring to access treatment success

What are FOUR ways to remove the cause as appropriate, especially with toxicity?

1. Rumenotomy

2. Activated charcoal

3. Chelation

4. Antibiotic therapy

What are THREE ways to promote diuresis?

1. IV 0.9% saline with Ca2+ or K+ as needed

2. Oral fluids

3. Diuretic in anuric or oliguric animals

What are THREE ways to closely monitor for access to treatment success for tubular necrosis?

1. Serum chemistry

2. Urinalysis

3. Quantification of produced urine