Lead Poisoning in Waterfowl (with notes on Elephants, Bears, Lagomorphs and Great Apes)

Waterfowl photos:

Rabbit photos:

Disease Summary

Alternative Names (Synonyms)

• Plumbism
• Lead intoxication
• Lead toxicosis
• Lead toxicity

Disease Type

Infectious/Non-Infectious Agent associated with the Disease

Pathogenesis of lead toxicity

• Numerous enzymes are affected including those that are involved in haemoglobin synthesis. 
• Red blood cells become fragile and have a decreased survival time.
• Central nervous system capillaries may be damaged and this may account for the brain lesions seen. 
• Proximal tubule cells in the kidneys may be damaged.

(B609.2.w2)

Infective "Taxa"

Non-infective agents

• Lead

Physical agents

References

Disease Author

Referees

Major References / Reviews

Code and Title List

Elephants:
B455.w2

Bears:
J35.128.w1

Lagomorphs:
B600.6.w6; B600.10.w10; B601.11.w11; B602.20.w20; B603.1.w1; B603.2.w2; B603.3.w3; B603.5.w5; B606.9.w9; B606.12.w12; B609.2.w2
J4.191.w27, J13.36.w1, J14.38.w1, J213.11.w1

Great Apes:
B644.5.w5, B644.12.w12
J4.125.w2, J569.38.w1

Other References

Code and Title List

Detailed Clinical and Pathological Characteristics

General

Clinical Characteristics

• Associated with the ingestion of a large dose of lead, relatively rare form in waterfowl. No specific signs, may die in good body condition.

Chronic lead poisoning (form usually seen in waterfowl):

• Anorexia, lethargy
• Green (bile-stained) diarrhoea; tends to stain feathers around vent
• Change in voice (noted more in some species than others)
• Muscular weakness (seen progressively as weak flight, inability to fly, unsteady gait, inability to walk, coma, death)
• Progressive weight loss and atrophy of breast (flight) muscles, giving a ‘hatchet breast’ appearance
• Frequently impaction of gizzard, proventriculus and sometimes whole oesophagus.
• Neck kink (limberneck) is highly visible in swans. 'Crooked' neck position may be visible in lead-poisoned Branta canadensis - Canada geese in flight.
• Wings may be held in 'roof shaped' position or may droop
• Head tremors sometimes noted
• Swollen head (submandibular oedema) may be seen in Branta canadensis - Canada geese and Anser caerulescens - Snow geese.
• Pale mucous membranes
• Collapse and coma
• Death from starvation.
• Blood parameters: anaemia, erythrocyte abnormalities including size and shape changes (anisocytosis, poikilocytosis), hypochromia, erythrocytes without nuclei, increased reticulocytes, low MCHC. Also variable blood chemistry changes, such as low total protein, high creatinine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), high uric acid and low free fatty acid levels (J1.12.w6, J4.200.w1, J6.2.w2, J6.17.w6).
• Electrocardiogram abnormalities (associated with myocardial damage) (J5.17.w4)

Low level toxicity:

• May lead to more subtle effects on fitness, immunocompetence and possibly fecundity. Waterfowl which have ingested lead shot may be more vulnerable to hunting, have a decreased ability to migrate, be more likely to collide with objects (e.g. power lines) while flying and have a generally reduced survival rate (J1.26.w4, J46.218.w1).

(J1.29.w6, J5.11.w5, J5.36.w7, J7.S1.w2, J46.216.w1, B11.38.w6, B13.46.w1, B15, B18, B20.10.w7, B35.3.w1, B36.43.w43, B37.x.w1, P13.16.w1, P13.16.w4)

Clinical characteristics

Lead poisoning in rabbits is often a vague non-specific condition with clinical signs such as:

• Reduced appetite/inappetance
  • This seems to be linked with the slow gut motility. (B600.10.w10)
• Lethargy
• Anorexia
• Gastrointestinal hypomotility or stasis
• Gradual weight loss
• Depression
• Behavioural changes. 

(B600.10.w10; B601.11.w11; B602.20.w20; B603.3.w3; B606.9.w9; B609.2.w2, J4.191.w27, J14.38.w1, J13.36.w1, J213.11.w1)

Less common clinical signs in advanced cases include:

• Neurological defects:
  • Ataxia 
  • Head tilt / torticollis
  • Stupor 
  • Tremors 
  • Seizures 
  • Apparent blindness 
  • Weakness 
• These clinical signs result from oedema and oxygen deprivation. 
• Jaundice if there has been toxic liver damage. 
• Diarrhoea - this is rare. 

(B601.11.w11; B602.20.w20; B603.1.w1; B606.12.w12; B609.2.w2, J14.38.w1, J213.11.w1)

• Severe cases can be fatal. (J14.38.w1)
• On examination, cardiac arrhythmias may be noted due to myocarditis or intimal hypertrophy. (J213.11.w1)
• Lead poisoning may cause immunosuppression. (J213.11.w1)

Clinical pathology

• Typical changes in chronic cases are anaemia and basophilic stippling of red blood cells. (B606.9.w9)
• Anaemia may be the only abnormality found in affected rabbits that are otherwise clinically normal or have vague non-specific signs. (B602.20.w20)
• Regenerative anaemia with:
  • nucleated red blood cells
  • poikilocytosis
  • hypochromasia
  • basophilic cytoplasmic stippling
    (B600.6.w6; B601.11.w11; B602.20.w20; B603.2.w2, J14.38.w1, J213.11.w1)
• Heteropaenia and lymphocytosis have also been reported. (B601.11.w11)
• See: Clinical Pathology of Lagomorphs

• Neurological signs (e.g. apparent blindness, seizures, paresis/paralysis), anaemia, haemoglobin abnormalities, nephropathy and sudden death have been seen. (B644.5.w5, B644.12.w12)
  • Tonic-clonic seizures followed by blindness, tremor and paralysis. Often coma and death in a few hours to a few days after the onset of seizures. (J569.38.w1)
• Anorexia, inactivity and death. (J569.38.w1)
• Sometimes found dead without prior signs evident. (J569.38.w1)
• In one nine-year-old Gorilla gorilla - Gorilla, loss of full use of first one arm then both arms and favouring one leg, abnormal locomotion (bearing weight on elbows not knuckles), sweaty and slightly warm hands, reduced and hard faeces and lethargy. Clinical signs were worst on the second day then improved, with considerable improvement after one week and apparent return to normal by two weeks.(J4.125.w2)
• Clinical pathology:
  • Mild hypochromic anaemia, circulating immature erythrocytes with basophilic stippling. Sometimes elevated wbc count due to neutrophilia. Haematological changes most evident in primates with higher blood lead levels. (J569.38.w1)
  • Blood lead levels sometimes over 200 µg per 100 mL; in other individuals lower (80-200 µg per 100 mL. Normal levels 0-39 µg per 100 mL. (J569.38.w1)
  • In one nine-year-old Gorilla gorilla - Gorilla, urinary lead level 0.290 mg/L on the second day of clinical signs and 1.235 mg/L five days later. (J4.125.w2)

Incubation

• Variable. Depends on quantity of lead ingested and on rate of absorption.
• Lead may reach the gizzard in two hours to four days after ingestion and be ground down after a period of about 23-35 days (J6.2.w2).
• Average time spent in gizzard 18-21 days, maximum to full erosion six or seven weeks (for lead shot) (P13.16.w1, B15).
• Death frequently occurs about two to three weeks after the ingestion of several pieces of lead shot.

(P13.16.w1)

• "An advantage of the rabbit's rapid elimination of large particles is that flakes of lead paint will be quickly passed out in the hard faeces rather than moved into the caecum and retained in the body for longer periods before being re-ingested". (B600.10.w10)
• One week of chewing on painted floor boards was sufficient to produce clinical signs and fatal poisoning in two four-month-old dwarf rabbits. (J14.38.w1)

• In one nine-year-old Gorilla gorilla - Gorilla, nearly eight weeks from observation of eating lead paint to the onset of clinical signs (J4.125.w2)

Mortality / Morbidity

• Usually considered as a disease affecting individual birds in the UK, but simultaneous poisoning in groups of birds have been recorded, while die-offs of hundreds to thousands of birds have been reported in North America , with total mortality from lead poisoning estimated at 1.6-3.4 million waterfowl per year (2-3% of the population) in the USA before lead shot was banned for waterfowl hunting.
• Mortality is high in birds with clinical symptoms unless treated.
• Mortality may often be under-reported due to affected individuals seeking shelter and also being removed by predators and scavengers

(J36.41.w1, B35.3.w1, B36.43.w43, P13.16.w1)

• Lead toxicity is common in rabbits that are housed indoors and have ingested lead-based paint. (B601.11.w11, J213.11.w1)
• Lead toxicosis can be fatal in rabbits. (J14.38.w1)

• In the past, toxicity was affecting more than 10% of primates in some facilities each year. With the recognition of the danger from lead-containing paint, and replacement of such paint, this has been reduced. (B644.12.w12)
• Often fatal in a few days after the onset of severe nervous signs, or following non-specific signs, if untreated. J569.38.w1

Pathology

• Lead is a non-specific toxin and affects most body systems. The lead ion has a strong chemical affinity for several biochemically-reactive compounds in the body and is able to inactivate enzymes involved in major metabolic pathways.
• Lead interferes with at least two enzymes involved in haemoglobin production: delta-aminolevulinic acid and haem synthetase. The effect on haemolobin production can be measured by the accumulation of intermediary metabolites such as protoporphyrin in the blood.
• Lead also interferes with enzymes involved in cellular oxidative processes and may interfere with the release of impulses at certain nerve endings.
  (J2.28.w1, P13.16.w1, B13.37.w7, B20.10.w7, B37.x.w1).

Gross pathology

ACUTE:

• Few lesions. Normal body condition and fat deposits.
• Heart - may be pale steaks in myocardium.
• Gastro-intestinal tract - lead object(s) in gizzard.

• Emaciation, pectoral muscle atrophy (‘hatchet-breast’), loss of subcutaneous fat and internal fat deposits. Anaemic and generally pale carcass.
• Gastro-intestinal tract - Gizzard lining stained dark green (regurgitated bile). Gizzard pads often roughened, thickened, sometimes eroded and ulcerated. Lead pieces/particles may or may not be present in the gizzard. Gizzard, proventriculus and sometimes oesophagus may be impacted with food material. Proventricular and sometimes oesophageal dilatation. Intestines frequently empty and may be atrophied. Vent area stained with bright green diarrhoea.
• Hepatic - liver atrophy, gall bladder enlarged (may be five times normal size) and full of dark green bile.
• Cardiac - Heart flaccid, sometimes with myocardial infarcts (particularly in Canada geese), sometimes hydropericardium.
• Kidneys, spleen - may be atrophied.
• Other - sometimes cephalic oedema (puffy head) in Branta canadensis - Canada geese and Anser caerulescens - Snow goose.

Histopathology

• Gastro-intestinal tract - General atrophy and patchy necrosis of gizzard muscle.
• Hepatic - necrosis of hepatocytes, haemosiderosis (large quantities brown pigment in hepatic cells and Kupffer cells), variable oedema.
• Cardiac - Patchy necrosis myocardial muscles associated with fibrinoid necrosis of arterioles
• Kidneys - Nephrosis and sloughing tubular epithelium; haemosiderosis, variable formation of acid-fast intranuclear inclusion bodies in cells of the proximal convoluted tubules.
• Spleen - haemosiderin accumulation
• Respiratory - lung congestion and haemorrhage
• Nervous system - Oedema of brain and meninges (particularly Canada goose Branta canadensis), perivascular haemorrhages in the cerebellum and degenerative changes of peripheral nerves have been described.
• Bone marrow - hypoplasia, with decreased numbers of mature erythrocytes, increased numbers of early and late polychromatic erythroblasts and haemosiderin-laden macrophages in extravascular spaces.

(J1.12.w6, J1.18.w3, J1.23.w5, J5.9.w2, J5.11.w5, J5.24.w6, J5.36.w7, J6.2.w2, J7.16.w1, J46.216.w1, B15, B20.10.w7, B35.3.w1, B36.43.w43, B37.x.w1)

Gross pathology

• GIT: In the stomach, small pieces of white material mixed into the normal ingesta. (J14.38.w1)
• Hepatic: liver friable. In one rabbir diffusely pale and in the other a yellow and tan reticular pattern. (J14.38.w1)

Histopathology

• Hepatic: "massive, centrolobular to bridging, coagulation necrosis." (J14.38.w1)
  • In the rabbit which lived longer, heterophilic infiltration and foci of dystrophic mineralisation. (J14.38.w1)
• Renal: multifocal tubular degeneration and necrosis, casts of haemoglobin in the tubules. (J14.38.w1)
• Pulmonary: severe diffuse oedema. (J14.38.w1)
• Cardiac: moderate myocardial degeneration and necrosis, multifocal. (J14.38.w1)
  • In the rabbit which lived longer, heterophilic infiltration and foci of dystrophic mineralisation. (J14.38.w1)

Gross pathology

In nonhuman primates

• General: Usually normal to thin body condition. (J569.38.w1)
• Usually non-specific lesions. (J569.38.w1)
• Musculoskeletal: In two juveniles, on longitudinal section of long bones, grey-white bands ("lead lines", particularly in the distal metacarpal and metatarsal bones, radius, ulna, tibia and femoral metaphyses. Radiographically these bands were opaque. (J569.38.w1)

Histopathology

In nonhuman primates

• CNS: In nonhuman primates, neuronal degeneration, gliosis, demyelination, vascular degeneration. (B644.12.w12) µ
• Renal: In the renal proximal tubulular epithelia, multiple spherical eosinophilic intranuclear inclusions, 3 - 10 µm diameter, often with multiple inclusions in a single nucleus. More and larger inclusions were seen in individuals with higher hepatic lead concentrations. (J569.38.w1)
• Hepatic: in 40%, mainly those with hepatic lead concentrations >10 ppm, acid-fast intranuclear inclusions. (J569.38.w1)
• Musculoskeletal:
  • In "lead lines2 of long bones from juveniles, persistent cartilagenous trabeculae extending from the epiphysis well into the metaphysis, lined by a thin layer of cortical bone, with many large osteoclasts present between the trabeculae. (J569.38.w1)
  •  In about 50% of affected primates, individual or small groups of skeletal muscle cells necrotic. (J569.38.w1)
• Cardiac: In about 50% of affected primates, individual or small groups of cardiac muscle cells necrotic. (J569.38.w1)
• Reproductive: Sometimes degenerative changes of testes or ovaries: germinal cells degenerative or necrotic, spermatogenesis decreased/absent and interstitial cells apparently increased, or fewer than expected developing ovarian follicles. (J569.38.w1)

Human Health Considerations

Disease has been reported in either the wild or in captivity in:

Waterfowl:

• Trumpeter swan Cygnus buccinator, whistling swan Cygnus (Olor) columbianus in Washington state, USA (J1.18.w3).
• Whooper swan Cygnus cygnus, tundra swan Cygnus columbianus, white-fronted goose Anser albifrons in Japan (J1.29.w6).
• Blood lead levels indicating toxic exposure in American black ducks Anas rubripes and ring-necked ducks Aythya collaris in Canada (J1.29.w7).
• Snow geese Anser caerulescens in California, some with simultaneous avian cholera in California, USA (J1.29.w8).
• Spectacled eider Somateria fischeri, common eider Somateria mollissima in Alaska, USA (J1.31.w4).
• Canada goose Branta canadensis on Plum Island, Massachusetts USA associated with low water levels (J1.23.w5).
• Canada goose Branta canadensis in USA (J1.35.w2).
• Geese (and cattle) in the UK , after eating barley contaminated with lead shot (J3.114.w4).
• Greater white-fronted geese Anser albifrons, Japan (J4.200.w1).
• Whistling swan Cygnus columbianus columbianus in Wisconsin, USA (J5.9.w2).
• Canada goose Branta canadensis in Delaware, USA (J5.11.w5)
• Whooper swan Cygnus cygnus in Japan, some also with aspergillosis or gout (J5.36.w7).
• Northern pintail Anas acuta, European wigeon Anas penelope, Garganey Anas querquedula, common pochard Aythya ferina, and experimental in mallard Anas platyrhynchos and domestic ducks Anas platyrhynchos domesticus in Italy (J6.2.w2).
• Magpie goose Anseranas semipalmata, fulvous whistling-duck Dendrocygna bicolor, red-billed (black-bellied) whistling duck Dendrocygna autumnalis, Bewick's swan Cygnus columbianus bewickii, greylag goose Anser anser, Falkland Island steamer duck Tachyeres brachypterus, Salvadori's duck Anas (Salvadorina) waiguinesis, versicolor teal Anas versicolor, northern pintail Anas acuta, chestnut-breasted teal Anas castanea, mallard Anas platyrhynchos, Laysan teal Anas laysanensis, Chinese spotbill Anas poecilorhyncha zonorhyncha, New-Zealand grey duck (Pacific black duck) Anas superciliosa, Philippine duck Anas luzonica, African yellowbill Anas undulata, cinnamon teal Anas cyanoptera, New Zealand shoveler Anas rhynchotis variegata, Steller's eider Polysticta stelleri, rosybill Netta peposaca, South American pochard Netta erythrophthalmus, European pochard Aythya ferina, redhead Aythya americana, common white-eye (ferruginous duck) Aythya nyroca, Australian white-eye Aythya australis, tufted duck Aythya fuligula, lesser scaup Aythya affinis, European greater scaup Aythya marila, Brazilian teal Amazonetta brasiliensis, mandarin duck Aix galericulata, North American wood duck Aix sponsa, European goldeneye Bucephala clangula, North American ruddy duck Oxyura jamaicensis (J7.16.w1).
• Mute swan Cygnus olor, whooper swan Cygnus cygnus, and Bewick's swan Cygnus columbianus bewickii, Ouse Washes, UK (J7.26.w2).
• Mute swan Cygnus olor, whooper swan Cygnus cygnus, and Bewick's swan Cygnus columbianus bewickii, UK (J7.43.w2).
• Mute swan Cygnus olor, Scotland, UK (J7.50.w1)
• Mute swan Cygnus olor, whooper swan Cygnus cygnus, common shelduck Tadorna tadorna in Ireland (J7.S1.w2).
• Trumpeter swan Cygnus buccinator in Minnesota, USA (J7.S1.w4).
• Tundra swan Cygnus columbianus in USA (J7.S1.w5).
• Free-flying waterfowl in British Columbia, Canada (J14.19.w1).
• Mute swan Cygnus olor, mallard Anas platyrhynchos, common eider Somateria mollissima in Denmark (P13.16.w4).
• Magpie goose Anseranas semipalmata, black swan Cygnus atratus in Australia (P13.16.w5).
• Mute swan Cygnus olor in the Thames area, England, UK (J17.46.w1)
• Whooper swan Cygnus cygnus, mute swan Cygnus olor, greylag goose Anser anser in Scotland, also whooper swan Cygnus cygnus and Bewick's swan Cygnus columbianus bewicki on the Ouse Washes, England UK (J17.46.w2).
• Mute swan Cygnus olor and whooper swan Cygnus cygnus in Scotland, UK (J36.41.w1).
• Mute swan Cygnus olor and whooper swan Cygnus cygnus in Scotland, UK (J36.44.w1).
• Mute swan Cygnus olor and whooper swan Cygnus cygnus in Ireland (J46.216.w1).
• Raised blood lead levels in mute swan Cygnus olor colliding with electricity or telephone wires in Ireland (J46.218.w1).
• Whistling (tundra) swan Olor (Cygnus) columbianus, Canada goose Branta canadensis, mallard Anas platyrhynchos, American black duck Anas rubripes, lesser scaup Aythya affinis, redhead Aythya americana, canvasback Aythya valisineria, common goldeneye Bucephala clangula in Wisconsin, USA (J40.29.w1)
• Black swan Cygnus atratus in South Australia (J47.15.w1).
• Magpie goose Anseranas semipalmata in South Australia (J47.17.w1).

Elephants:

• A research study in Africa has reported lead levels in elephants. It should be assumed that these animals may be susceptible to lead poisoning. (B455.w2)

Bears:

• Clinical lead poisoning has not been reported. However, lead levels of 5.4 ppm and 7.3 ppm (wet weight) were noted in two polar bears. The source was considered probably to be paint. (J35.128.w1)

Lagomorphs:

• Lead toxicity is common in rabbits that are housed indoors and have ingested lead-based paint. (B601.11.w11, J213.11.w1)
• Lead poisoning occurred in two four-month-old dwarf rabbits which had been chewing on painted floor boards. (J14.38.w1)
• In two rabbits (separate cases), after chewing on pipes painted with lead-based paint, and plasterboard. (J4.191.w27)

Great Apes:

• Various nonhuman primates including Rhesus monkeys. (B644.5.w5)
• In 42 primates at the National Zoological Park, Washington, D.C., USA, in a wide variety of primates (Cercopithecidae, Hylobatidae, Lemuridae, Cebidae, Lorisidae, Callithricidae). (J569.38.w1)
• In a nine-year-old Gorilla gorilla - Gorilla at Lincoln Park Zoo, Chicago, USA in 1954. (J4.125.w2)

Host Species List

• Aix galericulata - Mandarin duck
• Aix sponsa - Wood duck
• Amazonetta brasiliensis - Brazilian teal
• Anas acuta - Northern pintail
• Anas castanea - Chestnut teal
• Anas cyanoptera - Cinnamon teal
• Anas laysanensis - Laysan duck
• Anas luzonica - Philippine duck
• Anas penelope - Eurasian wigeon
• Anas platyrhynchos - Mallard
• Anas platyrhynchos domesticus - Domestic duck
• Anas poecilorhyncha - Spot-billed duck
• Anas querquedula - Garganey
• Anas rhynchotis - Australian shoveler
• Anas rubripes - American black duck
• Anas superciliosa - Pacific black duck
• Anas undulata - Yellow-billed duck
• Anas versicolor - Silver teal
• Anser albifrons - Greater white-fronted goose
• Anser anser - Greylag goose
• Anser caerulescens - Snow goose
• Anseranas semipalmata - Magpie goose
• Aythya affinis - Lesser scaup
• Aythya americana - Redhead
• Aythya australis - Hardhead
• Aythya collaris - Ring-necked duck
• Aythya ferina - Common pochard
• Aythya fuligula - Tufted duck
• Aythya marila - Greater scaup
• Aythya nyroca - Ferruginous pochard
• Aythya valisineria - Canvasback
• Branta canadensis - Canada goose
• Bucephala clangula - Common goldeneye
• Cygnus atratus - Black swan
• Cygnus buccinator - Trumpeter swan
• Cygnus columbianus - Tundra swan
• Cygnus cygnus - Whooper swan
• Cygnus olor - Mute swan
• Dendrocygna autumnalis - Black-bellied whistling-duck
• Dendrocygna bicolor - Fulvous whistling-duck
• Netta erythrophthalma - Southern pochard
• Netta peposaca - Rosy-billed pochard
• Oxyura jamaicensis - Ruddy duck
• Polysticta stelleri - Steller's eider
• Salvadorina waigiuensis - Salvadori's teal
• Somateria mollissima - Common eider
• Somateria spectabilis - King eider
• Tachyeres brachypterus - Falkland steamerduck
• Tadorna tadorna - Common shelduck

Mammals:

• Bears
  • Ursus maritimus - Polar bear
• Elephants (Elephantidae - Elephants (Family))
  • Loxodonta africana - African Elephant
• Lagomorphs (Lagomorpha - Lagomorphs (Order))
  • Oryctolagus cuniculus domesticus - Domestic European rabbit
• Great apes
  • Gorilla gorilla - Gorilla

Disease has been specifically reported in Free-ranging populations of:

Waterfowl:

• Trumpeter swan Cygnus buccinator, whistling swan Cygnus (Olor) columbianus in Washington state, USA (J1.18.w3).
• Whooper swan Cygnus cygnus, tundra swan Cygnus columbianus, white-fronted goose Anser albifrons in Japan (J1.29.w6).
• Blood lead levels indicating toxic exposure in American black ducks Anas rubripes and ring-necked ducks Aythya collaris in Canada (J1.29.w7).
• Snow geese Anser caerulescens in California, some with simultaneous avian cholera in California, USA (J1.29.w8).
• Spectacled eider Somateria fischeri, common eider Somateria mollissima in Alaska, USA (J1.31.w4).
• Canada goose Branta canadensis on Plum Island, Massachusetts USA associated with low water levels (J1.23.w5).
• Canada goose Branta canadensis in USA (J1.35.w2).
• Greater white-fronted geese Anser albifrons, Japan (J4.200.w1).
• Whistling swan Cygnus columbianus columbianus in Wisconsin, USA (J5.9.w2).
• Canada goose Branta canadensis in Delaware, USA (J5.11.w5)
• Whooper swan Cygnus cygnus in Japan, some also with aspergillosis or gout (J5.36.w7).
• Northern pintail Anas acuta, European wigeon Anas penelope, Garganey Anas querquedula, common pochard Aythya ferina, in Italy (J6.2.w2).
• Mute swan Cygnus olor, whooper swan Cygnus cygnus, and Bewick's swan Cygnus columbianus bewickii, Ouse Washes, UK (J7.26.w2).
• Mute swan Cygnus olor, whooper swan Cygnus cygnus, and Bewick's swan Cygnus columbianus bewickii, UK ( J7.43.w2).
• Mute swan Cygnus olor, Scotland, UK (J7.50.w1)
• Mute swan Cygnus olor, whooper swan Cygnus cygnus, common shelduck Tadorna tadorna in Ireland (J7.S1.w2).
• Trumpeter swan Cygnus buccinator in Minnesota, USA (J7.S1.w4).
• Tundra swan Cygnus columbianus in USA (J7.S1.w5).
• Free-flying waterfowl in British Columbia, Canada (J14.19.w1).
• Mute swan Cygnus olor, mallard Anas platyrhynchos, common eider Somateria mollissima in Denmark (P13.16.w4).
• Magpie goose Anseranas semipalmata, black swan Cygnus atratus in Australia (P13.16.w5).
• Mute swan Cygnus olor in the Thames area, England, UK (J17.46.w1)
• Whooper swan Cygnus cygnus, mute swan Cygnus olor, greylag goose Anser anser in Scotland, also whooper swan Cygnus cygnus and Bewick's swan Cygnus columbianus bewickii on the Ouse Washes, England UK (J17.46.w2).
• Mute swan Cygnus olor and whooper swan Cygnus cygnus in Scotland, UK (J36.41.w1).
• Mute swan Cygnus olor and whooper swan Cygnus cygnus in Scotland, UK (J36.44.w1).
• Mute swan Cygnus olor and whooper swan Cygnus cygnus in Ireland (J46.216.w1).
• Raised blood lead levels in mute swan Cygnus olor colliding with electricity or telephone wires in Ireland (J46.218.w1).
• Whistling (tundra) swan Olor (Cygnus) columbianus, Canada goose Branta canadensis, mallard Anas platyrhynchos, American black duck Anas rubripes, lesser scaup Aythya affinis, redhead Aythya americana, canvasback Aythya valisineria, common goldeneye Bucephala clangula (J40.29.w1).
• Black swan Cygnus atratus in South Australia (J47.15.w1).
• Magpie goose Anseranas semipalmata in South Australia (J47.17.w1).

Host Species List

• Anas acuta - Northern pintail
• Anas penelope - Eurasian wigeon
• Anas platyrhynchos - Mallard
• Anas querquedula - Garganey
• Anas rubripes - American black duck
• Anser albifrons - Greater white-fronted goose
• Anser anser - Greylag goose
• Anser caerulescens - Snow goose
• Anseranas semipalmata - Magpie goose
• Aythya affinis - Lesser scaup
• Aythya americana - Redhead
• Aythya collaris - Ring-necked duck
• Aythya ferina - Common pochard
• Aythya valisineria - Canvasback
• Branta canadensis - Canada goose
• Bucephala clangula - Common goldeneye
• Cygnus atratus - Black swan
• Cygnus buccinator - Trumpeter swan
• Cygnus columbianus - Tundra swan
• Cygnus cygnus - Whooper swan
• Cygnus olor - Mute swan
• Somateria mollissima - Common eider
• Somateria spectabilis - King eider
• Tadorna tadorna - Common shelduck

General Information on Environmental Factors/Events and Seasonality

Lead poisoning can be a year-round problem, although there may be peaks of effect related to peaks in lead availability. In the USA mortality of waterfowl due to lead poisoning peaks in the spring and autumn (fall), when large numbers of waterfowl are using areas in which heavy hunting, and therefore considerable lead shot deposition, occurs.

The degree of lead ingestion problem at any one site may be affected by water depth and changes in depth, type of underlying soil/mud, and the degree of contamination of the environment with lead pellets/weights.

• In deep waters, more lead is likely to be out of reach while lying on the bottom than in shallow waters (particularly for non-diving species).
• Lowered water level (e.g. in hot summers) may make accessible lead pellets which were previously out of the reach of most species.
• Lead may sink out of reach into soft sediments, but remain accessible on the bottom if the substrate is firm (e.g. sand, gravel).
• Firm substrates are often found in areas where currents or springs keep water ice-free for longer - areas likely to be used late in autumn (fall) and early in spring, by late and early migrants respectively.
• More lead is likely to be available in areas where more lead has been deposited in the environment, for example at sites of heavy hunting.
• Lead may be more likely to be ingested where there is much lead shot and little grit.
• Dredging of lakes may expose previously-buried shot.

In general, recently deposited lead is more likely to be ingested, for example lead poisoning in Cygnus olor - Mute swans in the Thames Valley, England, was demonstrated to be closely related to lost/discarded lead fishing weights, closely follow the angling season and fishing areas (J7.S1.w1, J17.46.w1). However, lead items deposited many years earlier may also cause poisoning (J1.35.w2, J7.16.w1, J46.216.w1).

(J1.23.w5, J7.S1.w1, J17.46.w2, J40.29.w1, J46.216.w1, B11.38.w6, B20.10.w7, B35.3.w1, B36.43.w43, P13.16.w1, P13.16.w3)

In lagomorphs, lead may be found in the home environment, e.g. in paint. (B601.11.w11, J4.191.w27, J14.38.w1)

Regions / Countries where the Infectious Agent or Disease has been recorded

Regions / Countries where the Infectious Agent or Disease has been recorded in Free-ranging populations

General Information on Investigation / Diagnosis

In the field, suspect lead poisoning if small numbers of birds are becoming ill and gradually dying in an otherwise healthy flock, or if birds are staying after others have migrated from the area, and are flying weakly or not at all, and if many bright-green droppings are found.

CLINICAL SIGNS IN AN INDIVIDUAL BIRD:

• Suspect from history and clinical signs: lethargy, general weakness, weight loss (prominent keel), neck-kink in swans, greenish diarrhoea/staining feathers around vent, sometimes palpable impaction in oesophagus.
• Dorsoventral radiograph of conscious bird restrained e.g. in a swan bag or with sandbags. Centre beam in midline, about the level of the elbows, to give a view including the gizzard, proventriculus and caudal esophagus. May be radiographically visible metal in the gizzard (denser than stones). N.B. lack of visible lead on radiography does not rule out a diagnosis of lead poisoning, and metal pieces that are not lead may also be present. Lead shot embedded in the body but not in the gizzard must be distinguished from lead in the gizzard.
• Blood lead levels: Threshold indicating exposure above background generally given as 0.2-0.25 micrograms per millilitre blood (= 20-25 micrograms per decilitre, = 0.2-0.25 parts per million ); Level suggesting clinical toxicosis is generally given as 0.4-0.6 micrograms per millilitre blood (= 40-60 micrograms per decilitre, = 0.6 parts per million).
• Various references record different levels
  { -P13.16.w1: background level less than 25 micrograms per decilitre, 25-40 micrograms per decilitre indicates exposure, greater than 40 micrograms per decilitre indicates acute toxicity.
  - B20.10.w7: greater than 0.2 µg/mL (micrograms per millilitre)(0.97 µmol/L - micromoles per litre) suggests exposure; greater than 0.6 µg/ml (2.90 µmol/L) (or is compatible with clinical toxicosis; greater than 1.0 µg/mL (4.83 µmol/l) is generally found in acute lead poisoning (for birds in general).
  - B11.38.w6: 0.5 ppm to 2.0 ppm (parts per million) diagnostic of lead poisoning, with greater than 2.0 ppm considered severe toxicity.
  - B37.x.w1: greater than 2.0 micromoles per litre (µmol/L) with clinical signs, or 5 micromoles per litre in the absence of clinical signs, as a threshold for starting chelation therapy.
  - J15.15.w1: normal less than 0.4 ppm, 0.5-2.0 ppm diagnostic of lead poisoning, greater than 2.0 ppm severe toxicosis }
• Response to chelation therapy tends to confirm the diagnosis.

POST MORTEM EXAMINATION:

• History (if available), pathological findings, detection of elevated tissue lead levels. Liver and kidney are most commonly used. Liver lead level - less than 2.0 µg/g (ppm) wet weight in un-exposed birds with no effect from lead, 2-6 µg/g (ppm) wet weight indicates exposure, greater than 6-8 µg/g (ppm) wet weight indicates toxic level of lead (may frequently find levels of e.g. 20-60 ppm wet weight in lead poisoned waterfowl). N.B. variable moisture loss from liver with time, therefore determination for dry weight may be more accurate, with greater than 8ppm dry weight considered elevated (as greater than 2.0 ppm wet weight) [6-8 ppm wet weight = 20-30 ppm dry weight] (J1.15.w8, P13.16.w1, B15). Kidney lead level may be 50-100% of liver lead level.

TOXICOLOGY:

• Samples: live bird: 2-5 mL blood in lead-free tubes containing an anticoagulant such as sodium citrate or EDTA; keep chilled. Dead birds: whole carcass to laboratory or liver and kidney separately foil-wrapped and frozen.
• Alternative tests:

1. Measurement of protoporphyrin IX in red blood cells. Protoporphyrin accumulates in erythrocytes during lead poisoning, due to inhibition of haem synthetase. Levels below 40 microgrammes/dL (40 µg/100 mL) may be considered 'background' levels, with greater than or equal to 40 µg/100 mL indicating exposure to lead and levels above 200 micrograms /100 mL suggesting acute lead toxicity (J1.15.w7, P13.16.w1). Correction for haemoglobin content may be needed (since haemoglobin levels may be low in chronic lead poisoning), with levels above 3.0microgrammes/gram haemoglobin being recognized as elevated. Levels may also be high in juveniles (e.g. mute swan cygnets under four months old) due to high numbers of erythrocytes which have not completed erythropoiesis (J6.17.w6, B15). This test does not directly measure blood lead levels but requires only a few drops of blood; it is a useful screening test to identify populations/ individuals needing further tests (B36.43.w43).
2. Inhibition of serum delta-aminolevulinic acid dehydrogenase (ALAD) – very sensitive assay. ALAD activity is greatly reduced within a short time (24 hours) of lead ingestion, with inhibition persisting for about three months. Normal levels vary, but reactivation in vitro can be used to give a ration indicating the proportion of ALAD that had been deactivated. Non-activated ALAD : activated ALAD ration greater than 0.65 normal, 0.47-0.65 indicates exposure, less than 0.47 in acute exposure (P13.16.w1).

• Blood lead levels may be detected as elevated in as little as eight hours after exposure and decline to normal by one to two months following exposure.
• Bone lead levels do not indicate recent lead exposure but rather lifetime accumulation.

(J5.9.w2, J15.15.w1, B11.36.w4, B11.38.w6, B13.37.w7, B15, B18, B20.10.w7, B35.3.w1, B37.x.w1, P13.16.w1)

History

• There may be a history of the rabbit having access to lead-containing materials. (B603.3.w3, J4.191.w27) In particular, rabbits that have a tendency to lick or chew walls or metallic objects are at risk. (B602.20.w20)

Clinical pathology

• Mild anaemia with reduced MCHC, presence of poikilocytes, hypochromin erythrocytes, target cells, erythroblasts and rbc with punctate basophilic stipling, plus relative lymphocytosis with neutropaenia and eosinopaenia. (J13.36.w1)

Lead Toxicology

• "Submit whole unclotted blood; lithium heparin tube or check with diagnostic laboratory for anticoagulant preference". (B609.2.w2)
• Serum lead evaluation: Note: 1 µg/dL = 0.0483 µmol/L. (B600.6.w6)
  • >10 µg/dL is significant. (B602.20.w20, B603.1.w1, B609.2.w2, J213.11.w1)
    • Toxicosis has been defined as a level > 30 µg/dL. (J213.11.w1)
  • In two rabbits, with clinical toxicity, blood lead levels were 70 µg/dL and 22 µg/dL. (J4.191.w27)
  • or >1.1 µmol/L. (B601.11.w11)
  • <10 µg/dl needs to be interpreted in conjunction with the history and the clinical signs. (B609.2.w2)
• Blood levels may not correlate with the occurrence or the severity of the clinical signs. (B609.2.w2, J213.11.w1)
  • Blood levels fluctuate depending on the form of lead ingested and the chronicity of intoxication. (J213.11.w1)
• Two rabbits with clinical lead poisoning had blood levels of 70 µg/dl and 40 µg/dl. The normal range of blood lead levels in laboratory rabbits was given as 2 - 27 µg/dl. (B600.6.w6, J4.191.w27)
• In an experimental study, control rabbits all had blood lead levels of no more than 0.03 mg/dL. (J13.36.w1)
• A four-month-old dwarf rabbit had blood lead levels of 3.6 ppm. (J14.38.w1)
• Liver lead concentrations of two dwarf rabbits were 21.1 and 60.8 ppm (reference range 0.2 - 0.6 ppm, levels greater than 10 ppm considered toxic), and kidney concentrations 34.4 and 69.7 ppm (reference range 0.1 - 1.0 ppm, levels greater than 10 ppm considered toxic). (J14.38.w1)
• Repeat ten to fourteen days after cessation of the chelation therapy and then again two to three months later. (B609.2.w2)
• Fluorescent erythrocyte test: RBCs of rabbits with lead poisoning will fluoresce when exposed to 320 - 400 nm wavelengths. (J13.36.w1)

Radiography

• Stomach: radiopaque material may sometimes be seen. (B600.10.w10, B601.11.w11, B602.20.w20, J213.11.w1)
  • Radiopaque densities are often not present following ingestion of paint. (B609.2.w2)
• Large intestine: unevacuated hard faeces may be seen. (B600.10.w10)
• Skull: sometimes there can be metal shavings trapped in-between the teeth. This may be apparent even after the gastrointestinal lead has passed through. (B603.3.w3)

Necropsy

• In two four-month-old dwarf rabbits which had been chewing on painted floor boards, small pieces of white material were found mixed with the ingesta. (J14.38.w1)

• Whole blood lead of > 0.6 ppm or tissue lead of 1 - 10 mg/kg. (B644.12.w12)
  • Preferably fresh or frozen tissue for analysis, but formalin-preserved tissue has been used. (B644.12.w12)
• Blood lead levels in nonhuman primates: (J569.38.w1)
  • Up to 30 µg per 100 mL blood, normal. (J569.38.w1)
  • 40-80 µg per 100 mL blood, increased absorption. (J569.38.w1)
  • > 80µg per 100 mL blood, considered diagnostic of lead poisoning in humans. (J569.38.w1)
• In a Gorilla gorilla - Gorilla, clinical signs, history of eating red lead paint, and the presence of lead in urine (0.290 mg/L on the second day of clinical signs and 1.235 mg/L five days later). (J4.125.w2)

• Environmental Assessment
• History & Documentation
• Physical Examination of Mammals
• Necropsy of Mammals
• Imaging in Lagomorph Diagnosis and Treatment
• Clinical Pathology of Lagomorphs
• Chapter 2 - B36 Field Manual of Wildlife Diseases - Specimen Collection and Preservation
• Chapter 3 - B36 Field Manual of Wildlife Diseases - Specimen shipment
• Appendix A - B36 Field Manual of Wildlife Diseases - Sample specimen history form

Similar Diseases (Differential Diagnosis)

• Hunter-crippled birds (Impact Injury) (also unable to fly), botulism (Avian Botulism) (weakness, limberneck) (B14).
• Zinc (Zinc Toxicity), copper (Copper Toxicity), mercury toxicity (Mercury Toxicity)(B18).

For neurological signs: 

There are other, more common, causes of encephalopathy that should be considered during the clinical investigation. Infectious diseases are the most common, particularly bacterial and protozoal infections:

• Bacterial
  • Brain abscess
  • Meningoencephalitis
  • Extension of infection from otitis interna or media.
• Protozoal
  • Encephalitozoonosis

Rarer infectious causes of rabbit encephalopathy:

• Parasitic migration, e.g. Baylisascaris - the raccoon roundworm
• Viral 
• Fungal

Other possible causes of encephalopathy:

• Brain tumour
• Hepatic or ischaemic encephalopathy (rare)
• Heat stroke: this will be of acute onset and have a supportive history.

(B609.2.w2)

For anorexia, depression, and weight loss:

These clinical signs could be caused by almost any systemic disease process.

• Gastrointestinal disease
  • One of the most common causes particularly problems that are related to gastrointestinal hypomotility or stasis.
• Dental disease
• Pain

(B609.2.w2)

• Bacterial Meningitis and Meningoencephalitis in Great Apes
• Epilepsy

Specific Medical Treatment

Calcium disodium EDTA (ethylenediaminetetraacetate) (Sodium Calciumedetate, Veterinary Drug Company, UK; Versenate, 3M Pharmaceuticals, Northridge, California 91324, USA, CaEDTA; Versonate, Riker Labs Inc., St Paul, Minnesota, USA)

• Suggested doses vary from 10-50 mg/kg (milligrams per kilogram) twice or three times daily, usually by intravenous injection. Subcutaneous injection sometimes suggested as an alternative, or intramuscular injection, but this may be painful. If given orally, only approximately 5% of the dose is absorbed. N.B. Also chelates and removes essential metals and can be nephrotoxic. Most treatment regimens suggest periodic breaks in treatment. (J2.28.w1, B20.10.w7, B35.3.w1, B13.37.w7).
• Example suggested regimens:

• 10-40 mg/kg intravenous or intramuscular twice daily for ten days (B11.38.w6).
• 40 mg/mL diluted in lactated ringers solution (in about 30-60 mL for a swan dose) intravenously , twice daily for three to four days, then stop treatment for three to four days. Repeat for three or four series of treatments for blood levels of less than 1 ppm; six to eight treatments may be required for a bird with an initial level of greater than 2.0 ppm (J7.S1.w3). 
• 35mg/kg CaEDTA three times daily, intravenously, diluted in 10 mL/kg lactated Ringer's solution, with a break of two days after every three to four days of treatment, repeated for three to four cycles until blood lead drops below 0.5 ppm and remains at this level (P7.1.w3).
• 35 mg/kg CaEDTA three times daily, diluted with normal saline, subcutaneous injection, alternating five days treatment, five days no treatment (J3.140.w1, B37.x.w1).
• 35-50 mg/kg every twelve hours, intravenous, until blood lead levels remain low (B20.10.w7).
• 1 mL of 6% disodium CaEDTA (25.0-52.2mg/kg) every twelve hours, intravenous (J4.200.w1)

• Monitor blood lead levels every one to two weeks, continue treatment until blood levels fall below 0.4ppm and remain below that level after at least a week without treatment (J7.S1.w3).

DMSA (2,3-dimercaptosuccinic acid

• Aldrich Chemical Co., Milwaukee, Wisconsin USA) has also been used, 25-35mg/kg orally twice daily, five days a week for four to six weeks, either alone or in combination with calcium EDTA (J7.S1.w3, B13.37.w7). Treatment with DMSA at 30mg/kg/day for five days in humans reduced blood lead by 72.5% (J2.28.w1).

Oral D-penicillamine (Distamine 125mg, Dista; DiPA, Cuprimine, Merck & Co., West Point, Pennsylvania 19486, USA)

• 500mg/swan daily has also been used (J15.15.w1), but appears less effective than CalciumEDTA (J3.140.w1). N.B. possible adverse reaction (extensive pitting oedema of the head, submandibular area and neck, with cyanosis of the mucous membranes, severe respiratory distress and death) has been noted in two mute swans Cygnus olor given penicillamine at 55mg/kg twice daily (J3.140.w4). Suggestions of a possible allergic reaction (J3.140.w4) or perhaps rapid redistribution of lead from bone into the blood (J3.140.w5) have been suggested as explanations for this observed reaction.

Dimercaprol (British Anti-Lewisite, BAL)

• 2.5mg/kg every four hours for two days, followed by twice daily for up to ten days or until resolution of clinical signs occurs. N.B. low therapeutic index (B13.37.w7).

• Treatment involves facilitating the excretion of the lead from the gut by using a gastrointestinal motility agent and a chelating agent. (B600.10.w10)
• If a rabbit has suspected lead poisoning it should be started on chelation therapy whilst blood lead levels are being processed. (B603.3.w3)

Motility agents

• Cisapride (B600.10.w10)
  • 0.5 - 1.0 mg/kg orally every eight to twelve hours. (B609.2.w2)
  • [Note: this is no longer generally available, since it has been withdrawn from human use in many countries.]
• Metoclopramide (B600.10.w10; B601.11.w11)

Chelating agents

• Cheleting agents act by forming non-toxic complexes with the lead, which are then excreted in bile and urine. (J4.184.w1)
• Sodium calcium edetate (B600.10.w10; B601.11.w11) 
  • Also known as CaEDTA; calcium versenate (B602.20.w20) CaNa2EDTA, calcium disodium edetate, calcium disodium ethylenediaminetetraedetate. (J4.184.w1)
    • This must be given as the calcium disodium salt, otherwise it may lead to hypocalcaemia. (J4.184.w1)
    • Dilute to a 1% (10 mg/mL) solution with isotonic saline or 5% dextrose ( D5W) before administration, as injections of higher concentrations result in pain at the injection site. (B609.2.w2, J4.184.w1)
    • Note: Potential nephrotoxicity with prolonged continuous use, therefore wait at least five days between courses of treatment lasting 2 - 5 days. (J4.184.w1)
  • 27.5 mg/kg by subcutaneous injection every six hours for five days. (B603.3.w3; B606.9.w9, J4.184.w1)
    • Further courses may be necessary at weekly intervals. (B603.3.w3)
    • Allow a five day rest period in between treatments. (B609.2.w2, J4.184.w1)
  • 27.5 mg/kg by subcutaneous injection twice daily for five days on, five days off, five days on and then retest blood lead levels after another five days off treatment. (B601.11.w11)
  • 25 mg/kg by subcutaneous injection every six hours for five days; a second course may be required a week later. (B602.20.w20; B606.9.w9)
  • 30 mg/kg subcutaneously every 12 hours for five to seven days. Check blood lead concentrations 5 - 7 days later and repeat the course of calcium EDTA if the lead level is > 10 µg/dL. (B609.2.w2)
  • Contraindications:
    • Do not use in rabbits with renal impairment or anuria; it is necessary to establish urine flow before administration. 
    • Safety in pregnancy has not been established. (B609.2.w2)
• Alternatives to CaEDTA:
  • D-penicillamine (B600.10.w10; B609.2.w2, J4.184.w1)
    • 30 mg/kg orally every 12 hours. (B603.5.w5); 110 mg/kg body weight per day (in 3-4 divided doses) for 1-2 weeks, repeated after one week. (J4.184.w1)
    • This is the only effective oral chelating agent. (J4.184.w1)
    • It is essential to ensure, before giving this, that the rabbit no longer has access to lead-containing objects, since it will increase lead absorption from the intestines. (J4.184.w1)
  • Succimer
    • Use is not reported in rabbits. (B609.2.w2)
  • Dimercaprol (BAL) (J4.184.w1)
    • Used in humans. (J4.184.w1)

Control of seizures

• Diazepam
  • 1-5 mg/kg by intravenous or intramuscular injection. Begin with a 0.5 - 1.0 mg/kg intravenous bolus; repeat if the gross seizure activity has not stopped within five minutes. If intravenous access is not possible then diazepam can be administered rectally allowing intravenous catheter placement once the gross seizure activity has diminished or stopped. (B609.2.w2)

Expected course and prognosis

• Clinical signs should dramatically improve within twenty four to forty eight hours after starting the chelation therapy. (B609.2.w2)
• Prognosis is favourable with treatment and guarded if there are uncontrolled seizures. (B609.2.w2)

Possible complications

• Occasionally there can be permanent neurologic signs such as blindness. (B609.2.w2)

• Calcium EDTA diluted to 10% solution, 50 mg/Lb subcutaneously daily, divided between four doses, for five days. After a five day rest, a further five days of chelation. (J569.38.w1)
• Enema to remove paint chips from the colon. (J569.38.w1)

• Treatment and Care

General Nursing and Surgical Techniques

Flushing:

• Fast for 8-12 hours, Anaesthetize, (e.g. i/v ketamine, medial tarsal vein on brachial vein, or mask with isoflurane), maintain on 1-1.5% isoflurane or halothane, and oxygen, through 5-6 mm diameter endotracheal tube (for mute swan). Strap to table in sternal recumbency, incline table to 45-60°, lubricate 8-10 mm diameter soft gastric tubing, approx. 1.5 m long, advance into gizzard as far as possible, place bowl under bill, flush by pumping water into gizzard using stomach pump or large syringes and allowing water and oesophageal/proventricular/gizzard contents to flow out around the tube. (Combination of gravity and water pressure). Move tube backward and forward during the procedure to facilitate flushing. Note that volume out should match/exceed volume in … When no more particles are coming out, rotate swan laterally 90° and flush briefly. If radiograph shows lead still present, repeat after one or two days (J15.15.w1, J7.S1.w3, B11.38.w6, B13.46.w1, B37.x.w1).

Endoscopy:

• sizeable pieces of lead may be removed from a swan using a grasper under endoscopic visualization (e.g. using a human colonoscope. This may also be used in conjunction with flushing (J3.119.w1, J7.S1.w3, B13.46.w1, B37.x.w1).

Surgical:

• Anaesthetize, slowly turn onto back (dorsal recumbency), pluck minimal area (5x12cm, midline, immediately caudal to sternum), midline incision through skin and linea alba, open peritoneal membrane of left hepatic cavity: gizzard lies on left side of body cavity with ventral border attached by ventral mesentry to linea alba, gently manipulate close to incision, pack off with swabs. Incise longitudinally through tendinous area, scoop out contents of both sides using finger (N.B. lead may not be visible). Flush with saline, close (inverted Cushing, 2/0 (3 metric) Dexon, Suture abdominal incision: 2 layer, simple interrupted 2/0 chromic catgut. Follow with calcium edetate and antibiotic cover (1 wk) J3.119.w1

Supportive treatment:

Feed and water provision:

• Offer water, offer pellets or grain in a large dish or bowl, with water covering the feed; also offer e.g. pond weed or lettuce ( J15.15.w1) .
• Feeding by crop (distal oesophagus) tubing: Suggested feeds

1. 250-350 ml Reanimyl (Virbac), daily, divided into two or three meals (for a mute swan Cygnus olor - J15.15.w1);
2. waterfowl pellets in water made up to a thick gruel, 150-250 ml fed once or twice daily (for a trumpeter swan Cygnus buccinator - J7.S1.w3);
3. Complan made up in Lectade to a ‘creamy’ consistency, 60 ml may be fed by tube at one time (for a mute swan Cygnus olor - J3.119.w1).

• Fluids, 10-20 ml/kg, twice daily, lactated ringers or 5% dextrose, as a slow intravenous injection or subcutaneous, as required for treatment of dehydration; medial tarsal vein allows administration with the bird in sternal recumbency (for trumpeter swan Cygnus buccinator - J7.S1.w3).
• Offer grit freely once lead has been removed e.g. by gastric lavage (J7.S1.w3).

Iron dextran

• 2 mg intramuscular (for trumpeter swan Cygnus buccinator) if haematocrit is below 40% (J7.S1.w3).

Thiamine

• 10 mg (or 1.0 multicomplex B vitamin, small animal concentration) intramuscular, daily for at least the first week was used in Trumpeter swans - Cygnus buccinator (J7.S1.w3).

5-fluorocysteine

• 50 mg/kg orally daily for ten days as prophylaxis against development of aspergillosis, in swans and other susceptible species (J7.S1.w3).

(B20.10.w7, B35.3.w1)

• Prevent further exposure to lead. (J4.184.w1)

Fluid Therapy

• Balanced electrolyte fluids may be necessary to replace a hydration deficit. (B609.2.w2)
• Fluids may also improve movement of metal objects through the gastrointestinal tract. (J213.11.w1)
• See: Treatment and Care - Fluid Therapy

Blood Transfusion

• If the haematocrit is significantly decreased (<15%) then a blood transfusion may be necessary. (B601.11.w11)
• See: Treatment and Care - Fluid Therapy

Diet

• It is vital that the rabbit continues to eat during and after the treatment period because otherwise continued anorexia will lead to an exacerbation of gastrointestinal motility disorders leading to further derangement of microflora and overgrowth of the intestinal bacterial pathogens. 
• Offer the rabbit good quality grass hay and a decent selection of fresh greens. Note: in some rabbits, the addition of leafy greens can result in an exacerbation of the diarrhoea so for these animals only good quality hay should be offered. (B609.2.w2) See: 
  • Treatment and Care - Supportive Care and Nursing (including section on Anorexia in Rabbits)
  • Food and Feeding for Mammals - Convalescent Diets / Nutritional Support
• To encourage oral fluid intake, offer fresh water, wet leafy vegetables or flavour the water with vegetable juice.
• Syringe feeding is necessary if the rabbit is refusing to eat. 
  • See: Oral Medication and Syringe Feeding of Rabbits
• Nasogastric intubation is indicated if the rabbit refuses sufficient volumes of food. 
  • See: Nasogastric and Naso-oesophageal Tube Placement in Rabbits 
• Contraindications:
  • Avoid high carbohydrate or high fat nutritional supplements. (B609.2.w2)
  • Do not force feed if there is a suspicion of acute small intestinal obstruction or if the rabbit is in shock. (B609.2.w2)

(B609.2.w2)

Surgical considerations

• It may be necessary to remove lead objects from the gastrointestinal tract. 

(B609.2.w2)

In one Cercopithecus mona:

• Dexamethasone (2 mg initially then 0.25 mg daily, to reduce cerebral oedema. (J569.38.w1)
• Fluids and electrolytes. (J569.38.w1)
• Antibiotic cover. (J569.38.w1)
• Multivitamins. (J569.38.w1)

• Treatment and Care
• Food and Feeding for Mammals
• Oral Medication and Syringe Feeding of Rabbits
• Nasogastric and Naso-oesophageal Tube Placement in Rabbits 
• Ketamine Anaesthesia in Waterfowl
• Isoflurane Anaesthesia in Waterfowl

Preventative Measures

• Preventative Medicine for Mammals

Environmental and Population Control Measures

WATERFOWL

• Prohibiting the use of lead shot and lead fishing weights is the long-term solution. If prohibition is not possible, encourage the provision and use of non-toxic alternatives. Educate anglers and shooters regarding the problem and provide information about the validity of alternatives. Educate people in general against discarding of other sources of lead.
• In England and Wales a ban was instituted on the sale or importation of lead weights for fishing over >0.06g (number 8 split shot) and up to and including 28.36g (one ounce ledger weights) (Control of Pollution (Anglers’ Lead Weights) Regulations, 1986, made under the Control of Pollution Act 1974); the use of such weights was banned from the summer of 1987 (Fisheries Byelaw amendment to the 1978 Fisheries Bylaw (made under the Salmon and Freshwater Fisheries Act 1975). Deaths from lead poisoning in mute swans Cygnus olor on the Thames River, London, decreased considerably after the ban (J7.40.w1).
• The use of lead shot for wildfowling is banned in Denmark, The Netherlands, Norway and the USA, and regionally in Australia and Canada (J7.46.w1, P13.16.w5, B36.43.w43).
• From 1^st September 1999, under the Environmental Protection (Restriction on use of Lead Shot) Regulations use of lead shot in Britain is banned for a) shooting below the high water mark of ordinary spring tides, b) the shooting of ducks, geese, moorhen, coot, golden plover and common snipe, c) use on sites of special importance for feeding waterfowl.
• In waterfowl collections:
• Develop in sites never used previously for shooting, if possible.
• If ponds have natural earth banks know or suspected to contain lead shot, line with concrete above and below the waterline to prevent erosion which will make previously-buried shot available.
• Cover earth with large gravel and marginal shelves in shallow water (but without covering good growths of water weed).
• Make sure insoluble grit is available to the waterfowl at all times.
• Provide ample green food.
• If any pen appears to have a particular problem, consider changing the species kept, e.g. use for grazing species if dabbling below the waterline is suspected to be producing lead pellet ingestion.
• If excess earth dug from ponds is used in enclosures, ensure it has developed a good covering of grass before putting birds in the enclosures (J7.16.w1).
• In limited areas where heavy contamination with lead shot is known to be problematic, turning over of soil (tilling, deep cultivation) may be useful to bury the shot. Dredging of wetlands or excavation from shooting ranges may also be used.
• Ensuring alternative items are present for grit, particularly high-calcium grit (e.g. broken oyster shell) may reduce the severity of lead poisoning.
• Avoid supplementary feeding with whole corn (maize) and other grains in areas with lead pellet accumulation.
• Ensure plenty of green food is available
• Keep water levels high to keep pellets out of easy reach of most species, or drain to make an area unattractive to waterfowl.

(J7.46.w1, B15, B18, B20.10.w7, B35.3.w1, P13.16.w3).

• Avoid the use of lead-containing paints in enclosures. (V.w5)

• Identify the source of lead and either remove it or prevent the rabbit gaining access to it. (B602.20.w20; B603.3.w3, J213.11.w1)

• In nonhuman primates, lead poisoning is usually associated with access to paint containing lead (B644.5.w5); prevention therefore involves ensuring no lead-containing pain is used in enclosures or on items used for enrichment.

• Discourage waterfowl from using heavily-contaminated sites, e.g. by scaring (hazing).

(B15, B35.3.w1, P13.16.w3).

• Environmental and Population Management
• Preventative Medicine for Mammals
• Chapter 4 - B36 Field Manual of Wildlife Diseases - Disease Control Operations