Lead Poisoning in Animals

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Presentation on Clinical signs, diagnosis and treatment of lead toxicity in animals.

Transcript of Lead Poisoning in Animals

Lead Poisoning

Lead PoisoningAmulya V.R., 2014 MVM 014Sources of LeadPaints, car batteries, fishing equipment (sinkers) and plumbing materials

Recreational shooting, ammunition, soldering, jewellery making, pottery making

Glass polishing, painting, and stained glass crafting, Ayurvedic herbal products, food products

Mechanism of ToxicityHaematopoietic ToxicityBinds to -aminolevulinic acid dehydrataseInterferes with biosynthesis of haemeInhibits pyrimidine 5 nucleotidaseBasophilic stippling (RNA aggregates)Inhibits Na+ K+ -ATP pump Increased RBC fragility and lysisincorporation of ferrous iron into the porphyrin ring of Hb

6CNS ToxicityDamage to capillary endothelium, inactivation of BBBCerebral oedema and haemorrhage, neuronal necrosisHindrance to GABA and Dopaminergic transmissionSegmental demyelination of motor neurons

Foetal ToxicityCrosses the placentaTumorigen, mutagen & developmental toxicantReproductive ToxicityGametotoxicityLow sperm count, sperm defectsInfertility, spontaneous abortion, stillbirthSkeletal SystemRedistributed to skeleton & hair via circulationBone lead release - bone resorption during pregnancy, lactationAccelerates bone mass depletion osteoporosisDisruption of structural and functional integrity of bone cells

Lead is a risk factor for osteoporosis both because it is stored in the skeleton, and because bone is a target tissue for lead toxicity. As lead, a non-bone material incorporated into bone, is released into the body during normal body processes, it accelerates the process whereby bone mass diminishes. Lead also has direct, complex toxic effects on bone cell function, and may indirectly alter how bone cells develop, and how they function. These effects appear to occur partly because lead alters critical hormone levels in the body. Lead may also alter bone cell function by disturbing the ability of bone cells to respond to hormonal stimuli; even if circulating levels of the hormones in the body are within normal range, the bone cells may not respond to them normally. Lead may also disrupt normal processes that control the activities of bone cells. It may inhibit enzymes that affect bone cell functions. In all these ways, lead in bone may threaten bone health and structural integrity9Gastrointestinal ToxicityContractions in smooth muscle lining of intestinal wallsSevere excruciating abdominal painLocal irritationRenal and hepatic toxicityYoung animals are at greater risk than mature animals because they absorb up to five times more lead following ingestion.

Toxic DoseAcuteChronicDogs: 191 to 1000 mg/kgCats: 10 - 25 mg/kgCalves: 200 400 mg/kgCattle: 600- 800 mg/kgHorses: 400 600 mg/kgPoultry: 200 600 mg/kg

Cattle: 6-7 mg/kg/day for 6 8 weeksHorses: 1-7 mg/kg/daySheep: 1-8 mg/kg/dayDogs: 0.32 mg/kg/day for 6 months Clinical SignsAnorexia, vomitingConstipation or diarrhoeaWeight lossLethargyAbdominal discomfortBehavioural changesAtaxiaTremorsSeizuresAgitationClinical Signs Contd. ..PolyuriaPolydipsiaBlindnessAggressionPicaMegaoesophagus (cats)Vestibular signsComaHyperexcitabilityDementiaVocalizationSeizuresLMN polyneuropathyDiagnosisClinical signsRadiography of GITX Ray techniques levels of lead in bones and teethBlood and urine levels of leadNormal: 10 to 15 mcg/dl (0.1 to 0.15 ppm)> 30 to 35 mcg/dl (0.3 to 0.35 ppm) - lethalAnaemia, basophilic stippling, and elevations in nucleated red blood cells

Post Mortem FindingsDegenerative changes within the white matter of the brain and the cerebrumDegenerative changes in the kidney and liverintranuclear inclusion bodies

occasionally associated with intranuclear inclusion bodies16TreatmentChelation TherapyGI decontamination must occur before chelation therapy

Renal parameters must be assessed before and during chelation

Ca-EDTABAL (Dimercaprol)PenicillamineSuccimerCa-EDTA (Calcium disodium ethylene diamine tetracetate)

Dogs: 25mg/kg4 times daily for 2-5 days 10 mg per ml of 5% dextroseSC at different sites.Max. 2 g/dog/dayCats: 27.5 mg/kg for 5 days4 times dailySC in 15 ml of 5% dextroseHorses & Cattle: 110 mg/kg2 times daily, 4-5 days1-2 % sol. In 5% DextroseIM, IP or slow IVBirds: 35-50 mg/kgIM or slow IVT.i.d for 5 daysOral zinc supplementation minimizes the GI side effects of Ca-EDTA.

each dose divided every 8 hours, diluted to a final concentration of 10 mg of Ca-EDTA per ml of 5% dextrose 19B.A.L.British Anti Lewisite or Dimercaprol2 to 5 mg/kg IM q-4-h for 2 daysT.i.d. for 1 dayB.i.d. until recovery

PenicillamineCanines: 30 to 110 mg/kg/day P.OT.i.d. for 7 days7-day hiatus before reinstitutionFelines: 125 mg per cat orallyB.i.d. for 5 daysNot for use in sheep, cattle, horseContraindicated when lead is present in GIT

Succimer10 mg/kg orally or rectally t.i.d. for 10 daysSafe for oral administration in vomiting animalsLess nephrotoxicSupportive TreatmentManage vomiting and diarrhoeaThorough bathingControl seizures with diazepam or phenobarbitalCerebral oedema: mannitol Dogs & cats: 0.5 to 1.0 g/kg IVCattle & horses: 1 2 g/kg, slow IVFurosemide :1 mg/kg IV (20 minutes after mannitol)Supportive Treatment Contd. .. Sodium or magnesium sulphate: catharticThiamine reduces deposition of leadCattle: 2-4 mg/kg, IM or SC, b.i.d for 5 daysDexamethasoneCattle & horses: 0.1 mg/kg, IV, IM or SC. Fluid therapy to counteract anorexiaRemoval of object endoscopy, exploratory laparotomy, rumenotomyTHANK YOUMeasurement of Blood Lead LevelsAtomic absorption spectrometry (AAS)Flame atomic absorption spectrometryGraphite furnace atomic absorption spectrometryAnodic stripping voltametry (ASV)Inductively coupled plasma mass spectrometry (ICP-MS)Lead LinesChronic lead intoxication in adults results in peripheral neuropathy, often accompanied by manifestations outside the NS, such as gastritis, colicky abdominal pain, anaemia, and the prominent deposition of lead in particular anatomic sites, creating lead lines in the gums and in the epiphyses of long bones in children.Acute lead exposure can lead to renal toxicityAcute organolead exposure can sensitize dopaminergic neurotransmission in the CNSChronic ToxicityTumorigen, mutagen, reproductive and developmental toxicantNeural, renal, and hematologic toxicityDisrupt learned behaviour in adult animals