circulatory 3 Flashcards
Copper Poisoning - what does it cause? species?
- Syndrome of acute hemolysis
- Usually, chronic copper poisoning
- Sheep > cattle > pig > horse
Copper Poisoning - Etiology
-primary vs secondary, acute vs chronic - how do they arise?
Primary copper poisoning:
* Acute poisoning
> Acute ingestion of large quantities
*Chronic poisoning
> Ingestion of small quantities of excess copper over time (most common form)
> > 10-15 ppm dry matter
> Concomitant low dietary molybdenum levels
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Secondary copper poisoning
◦ Syndromes in which intake of non-toxic/ normal quantities of copper in association with certain plants result in toxicity and an acute hemolytic crisis
- Trifolium subterranium, Helitropium euranium, Senecio spp.
Copper Poisoning
* Pathogenesis
- Hemolysis caused by copper induced auto-Ab?
- Hemoglobin oxidation by copper promotes RBC fragility
- Oxidation → methemoglobin → Heinz bodies → mechanical hemolysis
- Episodes precipitated by stress
- PCV can drop rapidly - from normal 40% to 10% in <48 hrs
- All animals in a group are at risk
- Same animal at repeated risk
Copper Poisoning
* Clinical presentation in acute cases?
Acute
* Chemical damage GI mucosa (protein coagulation), fluid loss, circulatory collapse, shock - most die
* Gastroenteritis
* Diarrhea, abdominal pain, shock
* Dysentery & jaundice if survive >12-24 hrs
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If survive:
* Diarrhea
* Intravascular hemorrhage
Copper Poisoning
* Clinical presentation in chronic cases?
- Poorly understood
- Initially no clinical signs as liver copper levels rise > Liver stores copper, excreted in bile but reabsorbed
- Acute hemolytic crisis preceded by hepatic necrosis
- Release of copper into bloodstream
- Severe hemolytic crisis and further liver damage
<><> - Anorexia, depression, tachycardia, tachypnea
- Pallor, jaundice, hemoglobinuria, if survive >24 hrs,
may show neuro signs - Anemia (+ methemoglobinemia) may show
hypoxemia, dyspnea (anemic hypoxia)
Copper Poisoning
Clinical pathology
◦ Anemia
◦ Hemoglobinemia, hemoglobinuria
◦ Elevated liver enzymes (highest just before crisis)
◦ +/- methemoglobinemia
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◦ Blood copper levels elevated during crisis
◦ Blood copper levels 5- 20 ppm (normal <1 ppm)
◦ Liver copper levels >1000 ppm (normal <350 ppm)
◦ Kidney copper levels >50 ppm
Copper Poisoning
Treatment, prognosis
◦ If clinical signs are evident:
◦ Grave prognosis, euthanasia should be considered
◦ Symptomatic management
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◦ IV fluid therapy
◦ Oxygen insufflation
◦ Blood transfusions
◦ Chelator therapy (sheep) > D-penicillamine, ammonium molybdenate, anhydrous sodium sulfate
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◦ All exposed animals
◦ Minimize stress
◦ Dietary ammonium molybdenate > May reduce blood copper levels
◦ Ammonium tetra-thiomolybdate 50-100 mg/sheep, twice weekly,
orally
◦ Cattle (used in outbreaks) > Sodium molybdate 3g and sodium thiosulfate 5g daily PO
Copper Poisoning
Prevention
◦ Keep copper in feed as low as possible (less than 15 ppm)
◦ Ensure adequate dietary intake of molybdenum
◦ Fertilize molybdenum deficient pastures
Leptospirosis
- characteristics of organism
> gram stain, environement, etc…
- Genus: Leptospira
- Bacterium – Spirochete
- Gram-stain - poorly
- Aerobic, motile, saprophytic
Serovars of Leptospira interrogans
* A number can cause disease in ruminants:
- most common?
Most common
* hardjo- considered host adapted
* Pomona- considered non-host adapted
* Widespread, zoonotic
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A number can cause disease in ruminants
* hardjo, pomona, icterohemorrhagia, gryppotyphosa, canicola
Leptospirosis
Host-adapted serovars
- cause what? what sort of infections in normal vs incidental hosts?
◦ Special growth requirements?
◦ Often cause reproductive disorders
◦ Chronic persistent infections, endemic
◦ Acute infections in incidental hosts
Leptospirosis
Maintenance host characteristics
◦ High susceptibility to infection
◦ Renal or reproductive infections
◦ Efficient transmission between hosts
Leptospirosis
Non-host adapted serovars
- cause what sort of disease?
◦ Cause acute disease in individuals
◦ May cause acute outbreaks
◦ Cases usually sporadic
Leptospirosis
Accidental host characteristics
- nature of the infection and disease? transmission?
◦ Low susceptibility to infection
◦ Severe disease
◦ Renal infection short duration
◦ Transmission between hosts inefficient and sporadic
Leptospirosis
Epidemiology
- environmental survival
- how it infects
- source?
- shedding?
◦ Environmental survival appears dependent on warm, wet climatic conditions
◦ Skin abrasions, mucous membranes
◦ Source: urine, fetus, uterine fluids, venereal
◦ Recovered cases still shed > Intermittent. Cows shown up to 500 days
Leptospirosis
Pathogenesis
◦ Multiplication in bloodstream
◦ Invasion spleen, liver, brain
◦ Direct damage to blood vessels and liver
◦ Invasion of kidney favoring proximal tubules
◦ Placental invasion- fetal infection
◦ If recovery: antibodies eliminate, except: renal, eye, uterus
◦ Some serogroups: hemolysin -> hemoglobinuria
Leptospirosis
Clinical manifestations
- Acute > Hemolytic syndrome (calves and lambs)
- Subacute
- “Chronic” abortion/infertility
- Occult
Leptospirosis
Calves (Usually <1 month-of-age)
- nature of the disease, signs, serovar?
Acute disease
◦ High mortality, slow recovery
◦ First sign may be sudden death
◦ Severe pyrexia, anorexia, depression
◦ Petechiation
◦ Acute hemolytic anemia, hemoglobinuria, pallor
◦ Dyspnea, tachycardia, tachypnea (shock)
◦ Usually pomona
Leptospirosis
- circulatory system effects
Effects on microcirculation - direct damage to vessels
* Decrease blood volume, decrease peripheral vascular resistance
* Tachycardia
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Hemolysis- severe
* Loss of oxygen carrying capacity
* Tachycardia, tachypnea
* Peripheral constriction to attempt to maintain blood volume - but vessels are
damaged.
* Vascular damage results in edema.
* Hypoxia also causes vasodilation and causes cell death which potentiates
edema.
* In the lungs, this worsens the tachypnea and causes dyspnea.
Leptospirosis in sheep
- disease presentation, signs
- serovars
Sheep
◦ Outbreaks in sheep are rare
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Acute/subacute
◦ Sudden death: septicemia (septic shock)
◦ Pyrexia, depression, stiffness
◦ Hemoglobinuria, pallor, jaundice
◦ Abortion
◦ All ages, lambs most susceptible
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pomona, hardjo
Leptospirosis in Adult cattle
- serovar?
- initial infection signs
- what if they are recently introduced?
- sequelae?
- Primarily serovar hardjo
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Initial infection: - Can see pyrexia/anorexia, agalactia, stiffness
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When recently introduced: - Mastitis, agalactia in high percentage herd
- Abortions few weeks later (<30%)
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Sequelae: - Persistence in reproductive tract
- Infertility
- Venereal transmission
Leptospirosis
*Adult cattle (hardjo)
- nature of abortions and mastitis
Abortions
* Systemic infections lead to fetal death
* Placentitis may not be present
* Abortion may occur at any stage (endemic)
* Last trimester fetus may mount immune response and recover
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Mastitis
* No gland inflammation
* Mild yellow to orange with clots
Leptospirosis
* Adult cattle (pomona)
- nature of the disease caused? signs?
Subacute disease
* Fever anorexia, stiffness, hemoglobinuria, jaundice
* Fall in milk yield +/- yellow/orange mastitis
* Abortion 3-4 weeks later
Leptospirosis
Diagnosis, considerations, issues
Culture
* Requires special techniques, can take 5 weeks to months
* Only of value acute cases
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Dark field microscopy
* Specialized facilities
* Acute cases
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Antigen detection
* Not routine use
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PCR
* Urine only, does not differentiate species
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Serology (e.g. microagglutination test – MAT)
* Antibodies inconsistently detected and significance difficult to interpret
* Rising titres (4-fold) suggests recent infection
* Have to take acute and convalescent
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* Problems with endemic herds
* How to interpret
* Once abortions, acute phase is gone
Leptospirosis – Antibiotic Treatment
Acute onset:
◦ Tetracycline, oxytetracycline, penicillin, ceftiofur, tilmicosin, tulathromycin
◦ Erythromycin, tiamulin, tylosin– may not eliminate the renal carrier state
◦ Long-acting oxytetracycline & sustained-release ceftiofur will eliminate the renal carrier state
Leptospirosis
Vaccination, effects
- pros and cons
◦ Serovar specific
◦ Animal infected with same serovar will show anamnestic response to vaccine
◦ Vaccine reduces urinary shedding
◦ Can vaccinate as young as 4 weeks
◦ Vaccinating calves reduces their risk of becoming urinary shedders
later in life
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But
◦ Need to repeat vaccination (6 months- 1 year)
◦ Does not prevent abortion/renal carriage shedding of hardjo in endemic
herds
◦ Despite vaccination hardjo can become established in clean herds
◦ By reducing natural immunity may make herd more susceptible to outbreak
Leptospirosis
Control
- Difficulties with testing make it too difficult to identify carriers
Hygiene: - Avoid wet areas (temporary habitats)
- Reverse isolate unvaccinated animals
- Isolate known affected groups
Cold Water Hemoglobinuria
- what is this?
- Ingestion of large amounts of cold water associated with intravascular
hemolysis and hemoglobinuria
Cold Water Hemoglobinuria
- who gets this? why? when?
- pathogenesis
◦ Usually seen in calves
◦ Adults - rumen acts as buffer
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◦ Usually after period of water deprivation
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◦ Intravascular hemolysis in the intestinal wall
> Absorption of water lowers blood electrolytes
> Decreased osmotic pressure
> Osmotic fragility of red cells highest at 4-5 months
> Cold water (12-14°C) at an amount of 12% of their body weight
◦ Hemolysis - ~1 hour after ingestion
Cold Water Hemoglobinuria
Clinical signs
- Tachycardia due to anemic anoxia
- If carrying capacity sufficiently low then “perfusion” fails even if volume
sufficient- oxygen not supplied - Cell death
- Vasodilation, vascular integrity fails
- Edema, cell death
- Convulsions, coma, pulmonary edema, brain edema, death are all
possible
