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3. Food Animal 3 > urinary 2 > Flashcards

urinary 2 Flashcards

1
Q

routes of infection for UTI - which are common

A
  • Ascending – most common
  • Descending (hematogenous) – less common
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2
Q

Urinary Tract Infections
* pathogenesis depends on what? what are some common possibilities?

A
  • Type of bacteria, virulence factors, quantity of “inoculated” bacteria, source of bacteria & other factors, such as trauma.
  • Trauma: difficult calving, obstetrical manipulations or catheterization
  • Bladder dysfunction may lead to reflux into the ureters, causing ascending spread of bacteria and infection. Vulvar conformation, pneumovagina and metritis are important factors.
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3
Q

Bacteria commonly implicated in bovine UTI – ascending infections

A
  • Corynebacterium renale
  • Escherichia coli
  • Other Enterobactericae
  • Other Corynebacterium spp.
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4
Q

Bacteria commonly implicated in bovine UTI – descending infections

A
  • Salmonella species
  • Trueperella pyogenes
  • Corynebacterium pseudotuberculosis (sheep & goats)
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5
Q

Corynebacterium renale
- characteristics
- survival in environment
- virulence factor important for UTI, and other factors
- transmission
- occurence
- eradication

A
  • Gram-positive, club-shaped bacterium
  • Adapted to the bovine and ovine urinary tract
  • Thought to survive for a short period in the environment
  • Pili which attach to the urinary or vaginal epithelium is a virulence factor
  • Attachment is enhanced in an alkaline environment and inhibited in an acidic environment.
  • Cattle & sheep can be carriers & cause horizontal spread
  • Venereal and iatrogenic spread also occur
  • Occurrence not as often these days due to decreased bladder catheterization by veterinarians!
  • Very difficult to eradicate once the organism becomes established on a farm
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6
Q

cystitis clinical signs

A
  • Pollakiuria, dysuria
  • Agitation - treading, twitching tail
  • Thickened bladder on rectal examination
  • Abnormal urine - red, yellow, white (although may appear normal)
  • Systemic signs of disease usually not apparent (ie. fever, inappetance)
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7
Q

pyelonephritis clinical signs

A
  • Fever, depression, inappetance, decreased milk production
  • Mild colic
  • Other signs as for cystitis
  • Rectal examination - left kidney - painful to palpation, loss of lobulation
  • Ultrasound examination - enlarged kidney, loss of lobulation, abnormal shape, enlarged calyces, presence of echogenic, flocculent material.
  • NB: chronic disease - signs are vague
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8
Q

UTI - Differential Diagnosis

A
  • Gastrointestinal disease - causing colic (normal urinalysis)
  • Urolithiasis
  • Trauma
  • Vaginitis or perivaginal abscesses
  • Enzootic hematuria (access to bracken fern, anemia, lack of pyuria, bacteriuria)
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9
Q

UTI - Dx and Treatment

A
  • Gram-stain
  • Bacterial culture & antibiotic sensitivity
  • Repeat 1 week after therapy is finished.
  • C. renale: high doses of penicillin or ampicillin for
    at least 3 weeks
  • E. coli and other coliforms - penicillin, ampicillin, ceftiofur, trimethoprim sulfonamide
  • Adequate withdrawal times
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10
Q

UTI - Prognosis

A

Depends on severity & duration of disease
* Levels of tract affected
* Unilateral or bilateral
* Antimicrobial sensitivity
* Azotemia will decrease prognosis
* Case fatality and culling: 18 - 33% of treated cases (however many variables)

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11
Q

Acute Tubular Necrosis
- causes

A

Altered perfusion
* Hypovolemia
* Disseminated intravascular coagulation
* Renal vein thrombosis

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12
Q

Acute Tubular Necrosis common causes

A
  • Antibiotics
  • Metals
  • Plants
  • Endogenous compounds
  • Other exogenous compounds
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13
Q

antibiotics implicated in acute tubular necrosis

A
  • Aminoglycosides > Neomycin, Gentamicin, Amikacin
  • Tetracyclines
  • Sulfonamides
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14
Q

metals implicated in acute tubular necrosis

A
  • Arsenic
  • Mercury
  • Lead
  • Cadmium
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15
Q

plants implicated in actute tubular necrosis

A
  • Quercus (oak)
  • Amaranthus species
  • Rumex spp.
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16
Q

endogenous compounds implicated in acute tubular necrosis

A
  • Hemoglobin
  • Myoglobin
  • Bile
17
Q

exogenous compounds implicated in acute tubular necrosis, that are not plants or antibiotics or metals….

A
  • Monensin
  • Mycotoxins
  • Oxalates
  • Ethylene glycol
  • Chlorinated hydrocarbons
18
Q

Acute Tubular Necrosis
* Clinical Signs

A
  • Poor appetite, diarrhea, epistaxis
  • Depression, nasal discharge, ileus, melena, free gas bloat (mild)
  • Fever, tachycardia, scleral injection if infectious condition is present
  • May also have muscular weakness & become recumbent
  • Rectal findings usually normal although kidney enlargement is possible
19
Q

Acute Tubular Necrosis
* Differential Diagnosis

A
  • Vague signs
  • Various causes of diarrhea (infectious & non-infectious)
  • Pregnancy toxemia
  • Other causes of recumbency (musculoskeletal, nervous, metabolic, neoplastic)
20
Q

Acute Tubular Necrosis
* Clinical Pathology

A
  • Elevated creatinine and BUN
  • Urinalysis: protein, blood, casts if early on
  • Hypochloremia due to abomasal stasis and urinary loss
  • Hyponatremia due to urinary loss
  • Hyperphosphatemia & hypocalcemia
  • Metabolic alkalosis due to abomasal atony (young ruminants may be acidotic due to diarrhea)
21
Q

Acute Tubular Necrosis
* Treatment

A
  • Correct fluid & electrolyte deficits, establish urine flow (most cases
    are oliguric or anuric)
  • Intravenous fluids are ideal; intraruminal fluids okay (via orogastric tube or rumenostomy)
  • Remove inciting agent (fluids, stop drug administration, rumenotomy)
  • Anuric/oliguric - furosemide 1 mg/kg IV or IM & repeated in 1-2 hours if needed
  • Sodium levels should be monitored
  • Mannitol (0.25 g/kg IV) or dopamine (2 - 5 mg/kg/min IV) may be needed to establish urine flow if the fluids and furosemide are not successful
  • Monitoring of acid/base and electrolyte levels is important
  • Also levels of creatinine and BUN
22
Q

Acute Tubular Necrosis
* Prognosis

A
  • Depends on cause, and duration & severity of the disease
  • Obstruction to renal blood flow - grave prognosis
  • Toxic causes are more favorable if caught early and treated aggressively
  • Monitor creatinine and BUN levels
23
Q

Ulcerative Posthitis/Vulvitis
* Description:
- cause?
- who gets it?
- precipitating factors
- effects

A
  • Ulceration of mucous membranes & skin around sheath and vulva
  • Caused by Corynebacterium renale (a normal inhabitant)
  • Small ruminants
  • Precipitating factors:
    > High urea concentration (high protein or non-protein nitrogen diet)
    > Leads to proliferation of the bacteria, resulting in disease
    > Venereal transmission occurs
  • Losses: debilitation due to pain, incapacitation of breeding animals, decreased breeding soundness, deformation of genitalia, urinary tract obstruction.
24
Q

Ulcerative Posthitis/Vulvitis
* Clinical Signs

A
  • Starts as a moist ulcer at the mucocutaneous junction
  • Progress to involve a larger area and become more severe
  • Ulcers become covered with a thin, malodorous scab; if removed, little or no bleeding occurs
  • Swelling may be noted around affected area
  • Animal is sensitive to palpation of the area
  • Can lead to scarring, adhesion formation, stricture formation, urethritis and obstruction to urinary flow.
  • Sequelae may also include weight loss and loss of breeding soundness.
25
Q

Ulcerative Posthitis/Vulvitis
* Differential Diagnosis

A
  • Viruses:
    > Unclassified poxvirus
    > Parapox virus (orf; contagious ecthyma)
  • Urethral obstruction
26
Q

Ulcerative Posthitis/Vulvitis
* Treatment

A
  • Isolate animal to prevent transmission
  • Wool or mohair should be removed – i.e. shearing
  • Topical antibiotic applied
  • Systemic antibiotics:
    > If multiple animals involved
    > Severe individual cases
    > Penicillin is preferable
    > Tetracycline is effective
27
Q

Ulcerative Posthitis/Vulvitis
* Prevention

A
  • Alter diet to decrease intake of nitrogen
  • Routine shearing may be beneficial in cases where high nitrogen levels are fed
28
Q

Ulcerative Posthitis/Vulvitis prognosis

A
  • Generally good if treated before deformities occur
  • If the diet is changed!
29
Q

Amyloidosis - what it is, where it occurs, consequences for urinary system
- signs
- clin path values

A
  • Sporadic, chronic wasting disease
  • Amyloid fibril deposition occurs in the kidney, adrenal
    gland, intestine and liver
  • Protein-losing nephropathy due to damage to glomerulus
  • Signs - chronic diarrhea, weight loss, poor production, edema, enlarged kidney
  • Clinical pathology - proteinuria, hypoalbuminemia, azotemia; amyloid protein may be detected in urine by polarized light microscopy or electron microscopy; hyperglobulinemia may occur due to chronic antigenic stimulation
30
Q

Amyloidosis
* Differential diagnosis

A
  • Johne’s disease
  • Parasitism
  • Salmonellosis
  • Copper deficiency
  • BVD
  • Glomerulonephritis
31
Q

Amyloidosis
* Pathophysiology, prognosis, tx

A

Pathophysiology
* AA protein is formed due to chronic antigenic stimulation (infection, inflammation or neoplasia) ie. secondary amyloidosis
* Source of infection may be mastitis, metritis, traumatic reticuloperitonitis or an abscess.
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* Prognosis - very poor
* Treatment - none

32
Q

Glomerulonephritis
- what is this?
- how common
- clinical signs
- prognosis, tx

A
  • Glomerular deposition of antigen:antibody complexes or antibodies directed against foreign or intrinsic glomerular antigen
  • Rare
  • Clinical signs similar to those for amyloidosis
  • Prognosis - very poor
  • Treatment - none
33
Q

Congenital Defects of the kidney
- when do we usually see them?
- what are common ones?

A
  • Usually apparent in early life but may not be evident until adulthood.
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    Renal defects
  • Renal cysts (no clinical significance unless large and multiple (polycystic kidneys)
  • Renal agenesis (less common)
  • Hydronephrosis & renal dysgenesis (least common)
  • Renal oxalosis (beefmaster calves)
34
Q

Leptospirosis – Multi-systemic Disease
- pathogen
- tissues affected
- species

A
  • Leptospira interrogans – Gram-negative spirochetes
  • Multiple serovars (hardjo (2 subtypes), pomona, canicola,
    icterohemorrhagica, grippotyphosa, szwajizak)
  • Kidneys, liver, brain, reproductive tract, udder, eyes, blood
  • Cattle are the main species affected
  • Sm. ruminants generally resistant
  • Lambs can be still born or sick at birth
  • Several serovars can cause renal disease in cattle
35
Q

Leptospira Serovar hardjo
- species adaptation
- disease
- spread, transmission
- signs

A
  • Host-adapted to cattle
  • Can cause an interstitial nephritis of varying degrees
  • Rarely causes overt renal dysfunction in cattle
  • Cattle can become shedders (urine)
  • Infected animals can be carriers for life
  • Signs:
  • Infertility
  • Stillbirth
  • Abortion
  • Birth of weak calves
  • Fever
  • Agalactia
  • Mastitis
36
Q

Leptospira Serovars pomona & grippotyphosa - diseases casued

A
  • Hemolytic disease
  • Interstitial nephritis
  • Tubular nephrosis
  • Abortion
37
Q

Leptospirosis - Detection

A
  • Microscopic agglutination test (MAT)
  • Serology (affected by vaccination)
  • Urine or urine sediment > PCR, Fluorescent antibody staining, Dark-field or phase-contrast microscope
  • Necropsy – require special stains
38
Q

Leptospirosis
* Treatment

A
  • Oxytetracycline
  • Dihydrostreptomycin
  • Penicillin
  • Ampicillin, amoxicillin
  • Tylosin
  • Tilmycosin

3. Food Animal 3 (23 decks)

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