lead and copper

Question 1

lead tox, target, species

Answer 1

• Multisystemic poison:
• Target organs: CNS, blood, kidney, GIT, fetus, immune system

-all species

-90% bound to RBC, fecal excretion, transplacental transfer

Question 2

lead poisoning in cattle epidemiology

Answer 2

-one of most common**
-management disease: batteries

Characteristic:
* Turnout onto pasture or recent pasture change
* May through July: highest # of cases
* More cases in young stock
* Multiple cases per herd
-calves are more susceptible, higher GIT tract absorption

Question 3

lead tox clinical

Answer 3

-often found dead
Acute or subacute onset of neuroexcitation
* Onset: within a day or so of ingestion
* Bruxism, hypersalivation, jaw champing
* Blindness
* Aimless wandering, circling

management: remove from lead then try chelation therapy, often euthanized

Question 4

lead poisoning exam findings

Answer 4

• Blindness (PLR + Menace -)
• Polioencephalomalacia
• GI hypomotility or atony
• GI: anorexia, ruminal hypomotility or atony
• Dehydration
• Tachycardia, dyspnea
• ± hyperthermia

Question 5

lead poisoning diagnosis

Answer 5

Live animal: whole blood – purple top or green top (send-out test)
* Lead analysis
* Remember: most absorbed Pb is associated with red blood cells

dead animal: lead analysis send out: liver, kidney, brain*

necropsy: lead particles in rumen

Question 6

herd management of lead

Answer 6

Testing all animals in the herd is required**
* Many cattle will be asymptomatic and significant concentrations of lead
* BC, Alberta: reportable disease
-prevent further exposure

• The half-life of lead in blood is months to years**
• Storage in bone
• Particles stuck in reticulum

Question 7

lead to public health

Answer 7

Acute lead poisoning from animal tissues is highly unlikely
* Low-level, chronic exposure in babies and children
* Associated with cognitive deficits

Question 8

lead poisoning in companion animals

Answer 8

• Exposure to leaded paint, water

-clinical: susually subchronic,
-GI: q/d, weight loss
-CNS: dull mentation, abnormal stance, tremors if severe

clin path: BASOPHILIC STIPPLING

-management: supportive care

Question 9

metal toxicoses in pet birds

Answer 9

-zinc/ lead: from cages, toys, weights

• Clinical features:
• GI: anorexia and weight loss, regurgitation, diarrhea
• Neuro: ataxia, seizures, blindness
• Feather picking
  -green urates

Question 10

lead poisoning in predatory birds

Answer 10

High incidence of lead poisoning in eagles and other raptors
* Scavengers and opportunistic feeders
* Lead ammunition**

Question 11

copper toxicity

Answer 11

-stored in the liver

toxicity:
-excess dietary intake
-over supplementation

mechanism: oxidative damage

species: sheep»goats»cattle
-sheep have higher affinity for copper in liver. lambs> adults
-merino breed sheep are tolerant

Question 12

clinical features of Cu toxicity

Answer 12

1 acute toxicosis:
-rare, following ingestion of high copper
-* Severe gastroenteritis and mucosal erosions***
* Diarrhea ± blood, colic, recumbancy
-green/ blue feces

2 Chronic copper toxicosis
* Most common type of copper poisoning
* Hemolytic crisis triggered by a stressful event – Cu released from lysosomes in liver***
examples
* Transport
* Lactation
* Pregnancy

Question 13

pathophisiology of Cu poisoning

Answer 13

• Cu stored in lysosomes in liver bound to metallothionein
• Excessive Cu: lysosomal capacity for storage is exceeded
• Lysosomes rupture: release of free Cu ions
• Hepatic necrosis
• High free Cu in blood → oxidative damage to RBCs
• Oxidative damage hemolytic anemia
• Intravascular hemolysis: splenomegaly

Question 14

clin path of cu poisoning

Answer 14

2. Chronic copper toxicosis continued
   * Clinical pathology: hemolytic phase
   * Decreased PCV
   * Regenerative anemia: macrocytosis, polychromasia
   * Heinz bodies
   * Methemoglobinemia
   * Hyperbilirubinemia

Question 15

management of Cu poisoning

Answer 15

-identify source of excess copper, test feed, water, supplements
-supportive care
-identify other at risk animals

Clinically affected / at risk animals:
* MetHb: methylene blue
* Ammonium tetrathiomolybdate**

• Herd: individual treatment OR put on concentrate feed, zinc supplamentation

Question 16

postmortem lesions of cu poisoning

Answer 16

-jaundince
-splenomegaly-dark
-hepatomegaly-orange, friable
-dark kidneys
-urine dark red/ brown.
-histo: hepatic necrosis, kidney necrosis

Question 17

cu diagnosis live vs dead vs feed

Answer 17

Nearly pathognomonic gross lesions + elevated liver/kidney Cu = diagnosis

live animal:
-NOT BLOOD as hemolysis has started
-elevated liver enzymes, hemolysis
-LIVER BIOPSYS best antemortem test

dead animal: combination of classic PM lesions + elevated tissue copper, live and kidney

• Feed testing: ratio of Cu:M
  normal 6:1 to 10:1

Question 18

cu tox in small animals

Answer 18

• Period of no symptoms as copper accumulates
• Appear healthy for several years
• Period of chronic active hepatitis**
• Non-specific signs: weight loss, anorexia, lethargy, vomiting
• Progresses to liver failure: ascites, hepatic encephalopaty

Question 19

small animal cu tox diagnosis

Answer 19

• Diagnosis: liver biopsy
• Exploratory laparotomy, laparoscopy
• Copper concentration + histology**
• Histology grading for copper

Question 20

small animal cu tox management

Answer 20

Goals: decrease copper absorption and increase copper excretion
* Low copper diet
* Oral chelation therapy: D-penicillamine
* Zinc supplementation
* Hepatoprotectants
* Monitor liver enzymes q6 months