urinary 2 Flashcards
routes of infection for UTI - which are common
- Ascending – most common
- Descending (hematogenous) – less common
Urinary Tract Infections
* pathogenesis depends on what? what are some common possibilities?
- 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.
Bacteria commonly implicated in bovine UTI – ascending infections
- Corynebacterium renale
- Escherichia coli
- Other Enterobactericae
- Other Corynebacterium spp.
Bacteria commonly implicated in bovine UTI – descending infections
- Salmonella species
- Trueperella pyogenes
- Corynebacterium pseudotuberculosis (sheep & goats)
Corynebacterium renale
- characteristics
- survival in environment
- virulence factor important for UTI, and other factors
- transmission
- occurence
- eradication
- 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
cystitis clinical signs
- 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)
pyelonephritis clinical signs
- 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
UTI - Differential Diagnosis
- Gastrointestinal disease - causing colic (normal urinalysis)
- Urolithiasis
- Trauma
- Vaginitis or perivaginal abscesses
- Enzootic hematuria (access to bracken fern, anemia, lack of pyuria, bacteriuria)
UTI - Dx and Treatment
- 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
UTI - Prognosis
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)
Acute Tubular Necrosis
- causes
Altered perfusion
* Hypovolemia
* Disseminated intravascular coagulation
* Renal vein thrombosis
Acute Tubular Necrosis common causes
- Antibiotics
- Metals
- Plants
- Endogenous compounds
- Other exogenous compounds
antibiotics implicated in acute tubular necrosis
- Aminoglycosides > Neomycin, Gentamicin, Amikacin
- Tetracyclines
- Sulfonamides
metals implicated in acute tubular necrosis
- Arsenic
- Mercury
- Lead
- Cadmium
plants implicated in actute tubular necrosis
- Quercus (oak)
- Amaranthus species
- Rumex spp.
endogenous compounds implicated in acute tubular necrosis
- Hemoglobin
- Myoglobin
- Bile
exogenous compounds implicated in acute tubular necrosis, that are not plants or antibiotics or metals….
- Monensin
- Mycotoxins
- Oxalates
- Ethylene glycol
- Chlorinated hydrocarbons
Acute Tubular Necrosis
* Clinical Signs
- 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
Acute Tubular Necrosis
* Differential Diagnosis
- Vague signs
- Various causes of diarrhea (infectious & non-infectious)
- Pregnancy toxemia
- Other causes of recumbency (musculoskeletal, nervous, metabolic, neoplastic)
Acute Tubular Necrosis
* Clinical Pathology
- 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)
Acute Tubular Necrosis
* Treatment
- 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
Acute Tubular Necrosis
* Prognosis
- 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
Ulcerative Posthitis/Vulvitis
* Description:
- cause?
- who gets it?
- precipitating factors
- effects
- 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.
Ulcerative Posthitis/Vulvitis
* Clinical Signs
- 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.
Ulcerative Posthitis/Vulvitis
* Differential Diagnosis
- Viruses:
> Unclassified poxvirus
> Parapox virus (orf; contagious ecthyma) - Urethral obstruction
Ulcerative Posthitis/Vulvitis
* Treatment
- 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
Ulcerative Posthitis/Vulvitis
* Prevention
- Alter diet to decrease intake of nitrogen
- Routine shearing may be beneficial in cases where high nitrogen levels are fed
Ulcerative Posthitis/Vulvitis prognosis
- Generally good if treated before deformities occur
- If the diet is changed!
Amyloidosis - what it is, where it occurs, consequences for urinary system
- signs
- clin path values
- 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
Amyloidosis
* Differential diagnosis
- Johne’s disease
- Parasitism
- Salmonellosis
- Copper deficiency
- BVD
- Glomerulonephritis
Amyloidosis
* Pathophysiology, prognosis, tx
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
Glomerulonephritis
- what is this?
- how common
- clinical signs
- prognosis, tx
- 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
Congenital Defects of the kidney
- when do we usually see them?
- what are common ones?
- 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)
Leptospirosis – Multi-systemic Disease
- pathogen
- tissues affected
- species
- 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
Leptospira Serovar hardjo
- species adaptation
- disease
- spread, transmission
- signs
- 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
Leptospira Serovars pomona & grippotyphosa - diseases casued
- Hemolytic disease
- Interstitial nephritis
- Tubular nephrosis
- Abortion
Leptospirosis - Detection
- 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
Leptospirosis
* Treatment
- Oxytetracycline
- Dihydrostreptomycin
- Penicillin
- Ampicillin, amoxicillin
- Tylosin
- Tilmycosin
