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3. Food Animal 3 > circulatory 3 > Flashcards

circulatory 3 Flashcards

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1
Q

Copper Poisoning - what does it cause? species?

A
  • Syndrome of acute hemolysis
  • Usually, chronic copper poisoning
  • Sheep > cattle > pig > horse
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2
Q

Copper Poisoning - Etiology
-primary vs secondary, acute vs chronic - how do they arise?

A

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
<><><><><><>
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.

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3
Q

Copper Poisoning
* Pathogenesis

A
  • 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
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4
Q

Copper Poisoning
* Clinical presentation in acute cases?

A

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
<><>
If survive:
* Diarrhea
* Intravascular hemorrhage

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5
Q

Copper Poisoning
* Clinical presentation in chronic cases?

A
  • 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)
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6
Q

Copper Poisoning
Clinical pathology

A

◦ Anemia
◦ Hemoglobinemia, hemoglobinuria
◦ Elevated liver enzymes (highest just before crisis)
◦ +/- methemoglobinemia
<><><><>
◦ 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

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7
Q

Copper Poisoning
Treatment, prognosis

A

◦ If clinical signs are evident:
◦ Grave prognosis, euthanasia should be considered
◦ Symptomatic management
<><>
◦ IV fluid therapy
◦ Oxygen insufflation
◦ Blood transfusions
◦ Chelator therapy (sheep) > D-penicillamine, ammonium molybdenate, anhydrous sodium sulfate
<><><><>
◦ 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

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8
Q

Copper Poisoning
Prevention

A

◦ Keep copper in feed as low as possible (less than 15 ppm)
◦ Ensure adequate dietary intake of molybdenum
◦ Fertilize molybdenum deficient pastures

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9
Q

Leptospirosis
- characteristics of organism
> gram stain, environement, etc…

A
  • Genus: Leptospira
  • Bacterium – Spirochete
  • Gram-stain - poorly
  • Aerobic, motile, saprophytic
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10
Q

Serovars of Leptospira interrogans
* A number can cause disease in ruminants:
- most common?

A

Most common
* hardjo- considered host adapted
* Pomona- considered non-host adapted
* Widespread, zoonotic
<><><><>
A number can cause disease in ruminants
* hardjo, pomona, icterohemorrhagia, gryppotyphosa, canicola

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11
Q

Leptospirosis
Host-adapted serovars
- cause what? what sort of infections in normal vs incidental hosts?

A

◦ Special growth requirements?
◦ Often cause reproductive disorders
◦ Chronic persistent infections, endemic
◦ Acute infections in incidental hosts

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12
Q

Leptospirosis
Maintenance host characteristics

A

◦ High susceptibility to infection
◦ Renal or reproductive infections
◦ Efficient transmission between hosts

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13
Q

Leptospirosis
Non-host adapted serovars
- cause what sort of disease?

A

◦ Cause acute disease in individuals
◦ May cause acute outbreaks
◦ Cases usually sporadic

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14
Q

Leptospirosis
Accidental host characteristics
- nature of the infection and disease? transmission?

A

◦ Low susceptibility to infection
◦ Severe disease
◦ Renal infection short duration
◦ Transmission between hosts inefficient and sporadic

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15
Q

Leptospirosis
Epidemiology
- environmental survival
- how it infects
- source?
- shedding?

A

◦ 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

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16
Q

Leptospirosis
Pathogenesis

A

◦ 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

17
Q

Leptospirosis
Clinical manifestations

A
  • Acute > Hemolytic syndrome (calves and lambs)
  • Subacute
  • “Chronic” abortion/infertility
  • Occult
18
Q

Leptospirosis
Calves (Usually <1 month-of-age)
- nature of the disease, signs, serovar?

A

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

19
Q

Leptospirosis
- circulatory system effects

A

Effects on microcirculation - direct damage to vessels
* Decrease blood volume, decrease peripheral vascular resistance
* Tachycardia
<><><><>
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.

20
Q

Leptospirosis in sheep
- disease presentation, signs
- serovars

A

Sheep
◦ Outbreaks in sheep are rare
<><>
Acute/subacute
◦ Sudden death: septicemia (septic shock)
◦ Pyrexia, depression, stiffness
◦ Hemoglobinuria, pallor, jaundice
◦ Abortion
◦ All ages, lambs most susceptible
<><>
pomona, hardjo

21
Q

Leptospirosis in Adult cattle
- serovar?
- initial infection signs
- what if they are recently introduced?
- sequelae?

A
  • Primarily serovar hardjo
    <><>
    Initial infection:
  • Can see pyrexia/anorexia, agalactia, stiffness
    <><>
    When recently introduced:
  • Mastitis, agalactia in high percentage herd
  • Abortions few weeks later (<30%)
    <><>
    Sequelae:
  • Persistence in reproductive tract
  • Infertility
  • Venereal transmission
22
Q

Leptospirosis
*Adult cattle (hardjo)
- nature of abortions and mastitis

A

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
<><>
Mastitis
* No gland inflammation
* Mild yellow to orange with clots

23
Q

Leptospirosis
* Adult cattle (pomona)
- nature of the disease caused? signs?

A

Subacute disease
* Fever anorexia, stiffness, hemoglobinuria, jaundice
* Fall in milk yield +/- yellow/orange mastitis
* Abortion 3-4 weeks later

24
Q

Leptospirosis
Diagnosis, considerations, issues

A

Culture
* Requires special techniques, can take 5 weeks to months
* Only of value acute cases
<><>
Dark field microscopy
* Specialized facilities
* Acute cases
<><>
Antigen detection
* Not routine use
<><>
PCR
* Urine only, does not differentiate species
<><>
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
<><><><>
* Problems with endemic herds
* How to interpret
* Once abortions, acute phase is gone

25
Q

Leptospirosis – Antibiotic Treatment

A

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

26
Q

Leptospirosis
Vaccination, effects
- pros and cons

A

◦ 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
<><><><>
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

27
Q

Leptospirosis
Control

A
  • Difficulties with testing make it too difficult to identify carriers
    Hygiene:
  • Avoid wet areas (temporary habitats)
  • Reverse isolate unvaccinated animals
  • Isolate known affected groups
28
Q

Cold Water Hemoglobinuria
- what is this?

A
  • Ingestion of large amounts of cold water associated with intravascular
    hemolysis and hemoglobinuria
29
Q

Cold Water Hemoglobinuria
- who gets this? why? when?
- pathogenesis

A

◦ Usually seen in calves
◦ Adults - rumen acts as buffer
<><>
◦ Usually after period of water deprivation
<><>
◦ 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

30
Q

Cold Water Hemoglobinuria
Clinical signs

A
  • 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

3. Food Animal 3 (23 decks)

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