lead and copper Flashcards
lead tox, target, species
- Multisystemic poison:
- Target organs: CNS, blood, kidney, GIT, fetus, immune system
-all species
-90% bound to RBC, fecal excretion, transplacental transfer
lead poisoning in cattle epidemiology
-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
lead tox clinical
-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
lead poisoning exam findings
- Blindness (PLR + Menace -)
- Polioencephalomalacia
- GI hypomotility or atony
- GI: anorexia, ruminal hypomotility or atony
- Dehydration
- Tachycardia, dyspnea
- ± hyperthermia
lead poisoning diagnosis
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
herd management of lead
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
lead to public health
Acute lead poisoning from animal tissues is highly unlikely
* Low-level, chronic exposure in babies and children
* Associated with cognitive deficits
lead poisoning in companion animals
- 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
metal toxicoses in pet birds
-zinc/ lead: from cages, toys, weights
- Clinical features:
- GI: anorexia and weight loss, regurgitation, diarrhea
- Neuro: ataxia, seizures, blindness
- Feather picking
-green urates
lead poisoning in predatory birds
High incidence of lead poisoning in eagles and other raptors
* Scavengers and opportunistic feeders
* Lead ammunition**
copper toxicity
-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
clinical features of Cu toxicity
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
pathophisiology of Cu poisoning
- 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
clin path of cu poisoning
- Chronic copper toxicosis continued
* Clinical pathology: hemolytic phase
* Decreased PCV
* Regenerative anemia: macrocytosis, polychromasia
* Heinz bodies
* Methemoglobinemia
* Hyperbilirubinemia
management of Cu poisoning
-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
postmortem lesions of cu poisoning
-jaundince
-splenomegaly-dark
-hepatomegaly-orange, friable
-dark kidneys
-urine dark red/ brown.
-histo: hepatic necrosis, kidney necrosis
cu diagnosis live vs dead vs feed
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
cu tox in small animals
- 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
small animal cu tox diagnosis
- Diagnosis: liver biopsy
- Exploratory laparotomy, laparoscopy
- Copper concentration + histology**
- Histology grading for copper
small animal cu tox management
Goals: decrease copper absorption and increase copper excretion
* Low copper diet
* Oral chelation therapy: D-penicillamine
* Zinc supplementation
* Hepatoprotectants
* Monitor liver enzymes q6 months
