Diseases / List of Toxic Diseases / Disease description:

Avian Botulism in Waterfowl (with notes on Cranes, Hedgehogs, Elephants, Bears and Ferrets)

INFORMATION AVAILABLE

GENERAL INFORMATION

CLINICAL CHARACTERISTICS & PATHOLOGY

INVESTIGATION & DIAGNOSIS

TREATMENT & CONTROL

SUSCEPTIBILITY & TRANSMISSION

ENVIRONMENT & GEOGRAPHY

 

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General and References

Disease Summary

WATERFOWL
  • A paralytic, frequently fatal disease, caused by ingestion of toxin produced by the bacterium Clostridium botulinum. Death is usually from respiratory arrest, cardiac arrest or drowning.
  • Outbreaks affecting thousands and even millions of birds have been recorded. This is probably the most important disease of migratory birds, on a world-wide basis.

(B36.38.w38).

FERRETS
  • Botulism is a neuroparalytic disease caused by consumption of food containing toxins produced by Clostridium botulinum. (B627.14.w14)

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Alternative Names (Synonyms)

  • Limberneck
  • Western duck sickness
  • Duck disease
  • Alkali poisoning

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Disease Type

 Toxic - Bacterial Toxins

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Infectious/Non-Infectious Agent associated with the Disease

  • In Waterfowl: Clostridium botulinum producing botulinum toxin Type C, a neuroparalytic agent is the usual cause of botulism. Type E toxin may be responsible occasionally in waterfowl, and is know for causing sporadic die-offs in some other bird species such as gulls and loons (divers). Type A occasionally affects poultry but is not important for waterfowl.
  • Seven different toxin types, A-G, produced by Clostridium botulinum  have been identified. Toxin production occurs only when the bacterium is actively growing and multiplying, and is dependent on a bacteriophage (virus).
  • Botulinum type C toxin blocks the release of neurotransmitter in a three-stage process:
  1. Binds to the presynaptic cell membrane (rapid, irreversible);
  2. Penetrates membrane, enters cell;
  3. Disables mechanism for acetylcholine release (cleaves synaptobrevin, a protein found in membrane of synaptic vesicles and which is critical for acetyl choline release).

(B15, B36.38.w38, P9.1.w1).

  • In ferrets: Clostridium botulinum is a Gram-positive bacillus that produces a toxin. (B501.12.w12) The bacteria are anaerobic and spore-forming. (B627.14.w14)
  • Flaccid paralysis occurs due to acetylcholine being blocked at the neuromuscular junction. (B232.8.w8, B501.12.w12)
  • In one group of ferrets, Clostridium botulinum Type C was shown to be involved. (J3.93.w2)

Infective "Taxa"

Non-infective agents

Physical agents

-- Indirect / Secondary

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References

Disease Author

Debra Bourne, Bridget Fry BSc, RVN (V.w143)
Click image for main Reference Section

Major References / Reviews

Code and Title List

B10.26.w9, B11.38.w6, B13.46.w1, B15, B36.38.w38, B37.x.w1, B48.12.w12
P17.50.w1

Other References

Code and Title List

J1.12.w4, J1.16.w6, J1.17.w5, J1.19.w1, J1.20.w3, J1.20.w4, J1.20.w5, J1.21.w2, J1.27.w2, J1.30.w4, J1.34.w1
J3.85.w1, J3.90.w1, J3.100.w1, J3.102.w1, J3.102.w2, J3.107.w2
J4.143.w1, J4.146.w1
J7.27.w1
J10.20.w1
P1.1993.w1
P2.47.w2
P9.1.w1

In Hedgehogs:
J140.86.w1

In Elephants:
P5.21.w1

In Bears:
J4.181.w4

In ferrets:
B232
.8.w8, B501.12.w12, B627.14.w14, B628.11.w11
J3.93.w2, J4.173.w4, J34.17.w4
P20
.1992.w7

In Cranes:
B115.8.w4
J40.52.w2
P1.1993.w1
W8
.Feb07.w1
D278, D279

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Clinical Characteristics and Pathology

Detailed Clinical and Pathological Characteristics

General

WATERFOWL Flaccid paralysis, respiratory distress and death. During an outbreak it is common to see dead, sick and well birds together; dead birds may be found along the shoreline, particularly when water levels are falling. If levels are stable, affected birds may be found in vegetation, including on vegetated islands and peninsulas. Waterfowl may be found together with other types of birds. (B36.38.w38).

Clinical Characteristics

WATERFOWL Flaccid paralysis due to effect of toxin on receptor sites of peripheral (efferent autonomic and somatic) nerves, interfering with presynaptic acetylcholinesterase release at the neuro-muscular junction (J7.27.w1, B10.26.w9, B15, B36.38.w38, B48.12.w12).
  • Systemic: Depression, anorexia
  • Locomotor: Acute onset voluntary muscle paralysis (flaccid). Progression : landing/take-off problems, inability to fly, leg weakness, wing droop, inability to lift head (limberneck). Birds may use their wings to move along the surface of land or water after their legs are paralysed. The degree to which the bird is affected can be classified into three stages:
    1. Unable to fly. Able to walk, swim.
    2. Unable to fly or walk. Able to swim/flop. May be unable to keep bill out of water.
    3. Almost total paralysis of major muscle masses. Unable to keep bill out of water.
  • Respiratory: Gasping, laboured respiration.
  • Ocular: Paralysis of nictitating membrane (third eyelid), collection of fluid under membrane, clear ocular discharge which may stick eyelids shut, spasms of rapid dilation and contraction of the pupil, paralysis of the iris, loss of the eye closing reflex, conjunctivitis.
  • Gastro-Intestinal Tract: Diarrhoea. Tail feathers and vent area may be soiled with diarrhoea and urates
  • Severely affected birds may be cold to the touch: body temperature decreases from e.g. 106 F to less than 100 F.
  • Heartbeat: slow, weak, irregular.
  • Waterfowl do not appear to show the raised neck feathers described as being typical in poultry with botulism.
  • Death may be due to drowning when paralysed neck muscles are unable to keep the bill out of water, respiratory paralysis, dehydration, or exposure

(J3.85.w1, J10.20.w1, P17.50.w1, B10.26.w9, B11.38.w6, B13.46.w1, B36.38.w38, B37.x.w1, B48.12.w12)

CRANES
  • Deaths of cranes reported. (J40.52.w2, B115.8.w4B115.8.w4, W8.Feb07.w1)
  • Found dead or sick [no further details given]. (D279)
FERRETS Note: Clinical signs vary depending on the amount of toxin to which the ferret has been exposed. (B627.14.w14)

Systemic:

  • Dyspnoea. (P20.1992.w7, J4.173.w4)
  • Lethargy. (B627.14.w14)
  • Urinary incontinence. (B627.14.w14)
  • Weight loss. (B627.14.w14)
  • Death. (J3.93.w2)
    • Death occurs after one to seven days, due to paralysis of respiratory muscles. (B628.11.w11, B232.8.w8, B501.12.w12, J4.173.w4)

Locomotor: 

  • Paralysis and prostration are seen as the disease progresses. (B501.12.w12, B232.8.w8, B627.14.w14, J34.17.w4, P20.1992.w7)
  • Incoordination and stiffness usually appear 12-96 hours post infection. (B232.8.w8, B501.12.w12, B628.11.w11, J4.173.w4)
  • Hang limp when handled. (B628.11.w11, J4.173.w4)

Ocular: 

Gastrointestinal:

Incubation

WATERFOWL Several hours to days.
CRANES --
FERRETS Signs develop within twelve to seventy two hours. (B627.14.w14)

Mortality / Morbidity

WATERFOWL Mortality variable, can be high if no control measures are taken.
CRANES
  • During one outbreak in Arizona, about 150 of less than 1,000 Grus canadensis - Sandhill crane died. (J40.52.w2)
  • In 1980, 127 sandhill cranes, about 10% of the cranes present, on Willcox Plaaya, Arizona. (D279)
FERRETS
  • Botulism rarely occurs in laboratory and pet ferrets. (B628.11.w11) Ferrets are more likely to develop botulism if they are from pelt farms, rather than if they are pets or laboratory ferrets. (B501.12.w12)
  • High mortality rates have been documented in (Mustela vison - American mink) infected with Clostridium botulinum type A. (B627.14.w14)

Pathology

WATERFOWL Gross Pathology:
  • No specific gross lesions. Usually in good body condition.
  • Respiratory system: May be water in airways due to death by drowning.
  • Gastro-intestinal tract: Usually fairly empty other than grit in gizzard; occasionally maggots still present (J1.12.w4), but usually already digested (J1.20.w4). Occasional congestion of visceral vasculature (blood vessels).

Histopathology:

  • No specific lesions.

(J3.85.w1, J3.100.w1, J7.27.w1, P17.50.w1, B10.26.w9, B15, B36.38.w38, B48.12.w12)

CRANES --
FERRETS Gross Pathology:
  • Pulmonary:
    • Lungs congested. (J3.93.w2)
  • GIT:
    • Fairly empty, slightly reddened/congested mucosa. (J3.93.w2)
  • Splenic: 
    • Haemorrhage of the spleen. (B627.14.w14)
  • CNS:  
    • Haemorrhage of the cerebellum. (B627.14.w14)

Histopathology:

  • Hepatic:
    • Congestion and distension of the capillaries and veins in the liver, with haemorrhage. (B627.14.w14)
  • Splenic:
    • Congestion of the spleen. (B627.14.w14)
    • Lymphoid depletion, necrosis of the centre of the follicles, follicular hyperplasia of mononuclear cells, abnormal reticular pattern and an increase in multinucleated giant cells. (B627.14.w14)
  • Renal: 
    • Congestion of the kidneys. (B627.14.w14)
  • Lymph nodes:
    • Lymphoid depletion,, necrosis of the centre of the follicles, follicular hyperplasia of mononuclear cells, abnormal reticular pattern and an increase in multinucleated giant cells. (B627.14.w14)

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Human Health Considerations

Botulinum C is rarely problematic in humans. Botulism food poisoning usually involves toxin type A or B, and types E and F are also reported in human toxicity (P17.50.w1).

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Susceptibility / Transmission

General information on Susceptibility / Transmission

WATERFOWL Transmission:
  • Ingestion of toxin, usually in invertebrates such as maggots but also waterborne or in decaying organic matter. The toxin is produced by Clostridium botulinum growing in organic matter, including carcasses; maggots feeding on carcasses ingest toxin, ducks feeding on maggots ingest toxin in the maggots. 0.05-0.25g of maggots, or as few as 2-4 maggots can contain sufficient toxin to produce clinical botulism (J1.12.w4, J7.27.w1, B15, B36.38.w38, B48.12.w12).
  • Botulism outbreaks may also occur in the absence of maggot-infested carcasses (J1.30.w4).
  • Toxin in commercially-produced maggots has been responsible for an outbreak of botulism in birds (not waterfowl) in at least one zoological collection and for botulism in swans which had eaten fishing-bait maggots. N.B. toxin remains (in reduced amounts) even after maggots have spent several days on toxin-free food (J3.97.w2, J3.102.w2, J3.111.w1).
  • Birds may ingest toxin (e.g. in maggots), along with Clostridium botulinum spores, then fly to another site before dying, thus providing a focus for new outbreak (J1.117.w2, J7.27.w1, P17.50.w1).
  • Environmental contamination with Clostridium botulinum spores is likely to increase during an outbreak, which may increase the likelihood of future outbreaks at the same site (P17.50.w1).
  • Invasion of internal organs by Clostridium botulinum, and toxigenesis within the organs, does not appear to be of any importance for botulism in waterfowl.

Susceptibility:

  • All species of waterfowl are considered very susceptible, with dabbling and filter-feeding species most likely to ingest the toxin (as are shorebirds feeding by probing mud); other birds (waders, gulls, herons) are less susceptible to Type C toxin.
  • Raptors, gallinaceous birds including domestic poultry, songbirds, and mammals - cattle, horses, dogs, mink, cats - are affected occasionally. Vultures, however, appear to be resistant.
  • Survivors of botulism do not appear to develop any immunity: an individual may be affected several times in one summer (P17.50.w1, B48.12.w12).

(B10.26.w9, B13.46.w1,B15, B36.38.w38, B48.12.w12, P17.50.w1)

CRANES Susceptibility:
FERRETS

Susceptibility:

  • Ferrets are highly susceptible to Clostridium botulinum type C toxin (B232.8.w8, J4.173.w4, J34.17.w4), but botulism rarely occurs in laboratory and pet ferrets. (B628.11.w11)
  • Ferrets are susceptible to types A and B toxin, but even more so to type C toxin produced by Clostridium botulinum. (B501.12.w12, B232.8.w8, J4.173.w4, J34.17.w4, P20.1992.w7)
  • Ferrets are more likely to have botulism if they are from pelt farms, than if they are pets or laboratory ferrets. (B501.12.w12)
  • Females are generally more susceptible to the effects of toxin than are males. (B627.14.w14)

Transmission:

  • Ferrets developed botulism (Type C) after being fed on the carcass of a mallard (from a lake where botulism was later confirmed in waterfowl), and after being fed decomposing pigeons. (J3.93.w2)
  • Clostridium spores in the soil can cause botulism in ferrets. (B627.14.w14)
  • Uncooked food or contamination of food with soil increases the chances of botulism in ferrets. (B501.12.w12, B627.14.w14)
  • Offal that has been improperly stored in a warm environment provides the right environment for the growth of Clostridium botulinum bacteria. (B232.8.w8, J34.17.w4)

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

  • Wild mute swans Cygnus olor, Canada geese Branta canadensis, tufted duck Aythya fuligula, also grebe, moorhen and seagulls, in the UK (J3.137.w1).
  • Mallard Anas platyrhynchos, muscovy duck Cairina moschata, common pochard Aythya ferina, swans, coots and moorhens on park lake in the UK (J3.85.w1).
  • Die-off on a shallow urban lake in the UK, in which toxins blue-green algae may also have been involved: mallard Anas platyrhynchos, tufted ducks Aythya fuligula, common pochard Aythya ferina, northern pintail Anas acuta, chestnut teal Anas castanea, common teal Anas crecca, northern shoveler Anas clypeata, Eurasian wigeon Anas penelope, Carolina (wood duck) Aix sponsa, mandarin Aix galericulata, common shelduck Tadorna tadorna, pink-footed goose Anser brachyrhynchus, Canada goose Branta canadensis, mute swan Cygnus olor, (also cormorant Phalacrocorax carbo, herring gulls Larus argentatus, woodpigeons Columba palumbus, blackbirds Turdus merula, song thrush Turdus philomelos, starlings Sturnus vulgaris) (J3.90.w1)
  • Mallard Anas platyrhynchos, Canada goose Branta canadensis, Egyptian goose Alopochen aegyptiacus, gadwall Anas strepera, greylag goose Anser anser, mute swan Cygnus olor, northern pintail Anas acuta, common pochard Aythya ferina, common shelduck Tadorna tadorna, common teal Anas crecca, tufted duck Aythya fuligula, (also black-headed gull Larus ridibundus, common tern Sterna hirundo, coot Fulica atra, cormorant Phalocrocorax carbo, dunlin Calidris alpina, green sandpiper Tringa ochropus, grey heron Ardea cinerea, herring gull Larus argentatus, lapwing Vanellus vanellus, moorhen Gallinula chloropus, wood sandpiper Tringa glareola) in the Norfolk Broads, UK (J3.100.w1).
  • Pekin ducks Anas platyrhynchos domesticus in Georgia, USA (J4.146.w1).
  • Wild grey duck Anas superciliosa superciliosa, mallard Anas platyrhynchos, shoveler Anas rhynchotis variegata, black swan Cygnus atratus (also shag Phalococorax sp. and stilt Himantopus sp.) -mortality of more than 905 of the population of the lake over one month (J10.20.w1).
  • Wild wood duck Aix sponsa, northern shovelers Anas clypeata, blue-winged teal Anas discors, ring-necked duck Aythya collaris, mallard Anas platyrhynchos (also American coot Fulica americana, common gallinules Gallinula chloropus, black-necked stilt Himantopus mexicanus, snowy egret Egretta thula, semipalmated sandpiper Calidris pusillus) in Florida, USA (J1.16.w6).
  • Mallard Anas platyrhynchos, northern pintail Anas acuta, green-winged (common) teal Anas crecca, (also American coot Fulica americana) in a late autumn outbreak; lesser scaup Aythya affinis, common goldeneye Bucephala clangula, canvasback Aythya valisineria, bufflehead Bucephala albeola and Franklin gull Larus pipixcan in spring (J1.19.w1).
  • Mallard Anas platyrhynchos, American wigeon Anas (Mareca) americana, wood duck Aix sponsa, northern pintail Anas acuta, green-winged (common) teal Anas crecca carolinensis, blue-winged teal Anas discors, gadwall Anas strepera, American black duck Anas rubripes, Canada goose Branta canadensis (also shore birds, including greater yellowlegs Tringa melanoleuca) in New York State, USA (J1.20.w3).
  • Wild grey teal Anas gibberifrons, Pacific black duck Anas superciliosa, black swan Cygnus atratus, (also Australian little grebe Podiceps ruficollis, swamphen Porphyrio porphyrio) in Victoria, Australia (J1.21.w2).
  • Wild northern pintail Anas acuta, green-winged (common) teal Anas crecca, shoveler (northern shoveler) Anas (Spatula) clypeata, cinnamon teal Anas cyanoptera, mallard Anas platyrhynchos, blue-winged teal Anas discors, baldpate (American wigeon) Anas (Mareca) americana, gadwall Anas strepera, ruddy duck Oxyura jamaicensis, redhead Aythya americana, fulvous tree duck (whistling duck) Dendrocygna bicolor (also some shorebirds) with Type C botulism; oldsquaw (long-tailed duck) Clangula hyemalis, common goldeneye Bucephala clangula, bufflehead Bucephala albeola, ring-necked ducks Aythya collaris, common mergansers Mergus merganser, hooded merganser Lophodytes cucullatus, greater scaup Aythya marila, white-winged scoter Melanitta deglandi, Canada goose Branta canadensis, snow goose Anser (Chen) caerulescens were affected in small numbers in a type E outbreak affecting mainly common loons Gavia immer, and herring gulls Larus argentatus, with small numbers of other birds (grebes, other gulls etc. also recorded) (B48.12.w12).

In Cranes:

In Hedgehogs:

  • The carcass of a hedgehog found in a fodder rack following an outbreak of botulism in cattle was found to contain type C toxin (20,000 minimum lethal doses for mice per gram subcutaneous tissue). (J140.86.w1)

In Elephants:

  • Two Asian elephants in Rostock Zoo died of botulism. (P5.21.w1)

In Bears:

In Ferrets: 

  • Botulism often occurs on ferret farms, where their diet may consist of raw meat. (B627.14.w14)
  • Ferrets developed botulism (Type C) after being fed on the carcass of a mallard (from a lake where botulism was later confirmed in waterfowl), and after being fed decomposing pigeons. (J3.93.w2)

Further information on Host species has only been incorporated for species groups for which a full Wildpro "Health and Management" module has been completed (i.e. for which a comprehensive literature review has been undertaken). Host species with further information available are listed below:

Host Species List

BIRDS:

MAMMALS:

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

  • Wild mute swans Cygnus olor, Canada geese Branta canadensis, tufted duck Aythya fuligula, also grebe, moorhen and seagulls, in the UK (J3.137.w1).
  • Mallard Anas platyrhynchos, Canada goose Branta canadensis, Egyptian goose Alopochen aegyptiacus, gadwall Anas strepera, greylag goose Anser anser, mute swan Cygnus olor, northern pintail Anas acuta, common pochard Aythya ferina, common shelduck Tadorna tadorna, common teal Anas crecca, tufted duck Aythya fuligula, (also black-headed gull Larus ridibundus, common tern Sterna hirundo, coot Fulica atra, cormorant Phalocrocorax carbo, dunlin Calidris alpina, green sandpiper Tringa ochropus, grey heron Ardea cinerea, herring gull Larus argentatus, lapwing Vanellus vanellus, moorhen Gallinula chloropus, wood sandpiper Tringa glareola) in the Norfolk Broads, UK (J3.100.w1).
  • Wild grey duck (Pacific black duck) Anas superciliosa superciliosa, mallard Anas platyrhynchos, shoveler Anas rhynchotis variegata, black swan Cygnus atratus (also shag Phalococorax sp. and stilt Himantopus sp.) -mortality of more than 90% of the population of the lake over one month (J10.20.w1).
  • Wild wood duck Aix sponsa, northern shovelers Anas clypeata, blue-winged teal Anas discors, ring-necked duck Aythya collaris, mallard Anas platyrhynchos (also American coot Fulica americana, common gallinules Gallinula chloropus, black-necked stilt Himantopus mexicanus, snowy egret Egretta thula, semipalmated sandpiper Calidris pusillus) in Florida, USA (J1.6.w6).
  • Mallard Anas platyrhynchos, northern pintail Anas acuta, green-winged (common) teal Anas crecca, (also American coot Fulica americana) in a late autumn outbreak; lesser scaup Aythya affinis, common goldeneye Bucephala clangula, canvasback Aythya valisineria, bufflehead Bucephala albeola and Franklin gull Larus pipixcan in spring (J1.19.w1).
  • Mallard Anas platyrhynchos, American wigeon Anas (Mareca) americana, wood duck Aix sponsa, northern pintail Anas acuta, green-winged (common) teal Anas crecca carolinensis, blue-winged teal Anas discors, gadwall Anas strepera, American black duck Anas rubripes, Canada goose Branta canadensis (also shore birds, including greater yellowlegs Tringa melanoleuca) in New York State, USA (J1.20.w3).
  • Wild grey teal (Anas gibberifrons) gracilis, Pacific black duck Anas superciliosa, black swan Cygnus atratus, (also Australian little grebe Podiceps ruficollis, swamphen Porphyrio porphyrio) in Victoria, Australia (J1.21.w2).
  • Wild northern pintail Anas acuta, green-winged (common) teal Anas crecca, shoveler (northern shoveler) Anas (Spatula) clypeata, cinnamon teal Anas cyanoptera, mallard Anas platyrhynchos, blue-winged teal Anas discors, baldpate (American wigeon) Anas (Mareca) americana, gadwall Anas strepera, ruddy duck Oxyura jamaicensis, redhead Aythya americana, fulvous tree duck (whistling duck) Dendrocygna bicolor (also some shorebirds) with Type C botulism; oldsquaw (long-tailed duck) Clangula hyemalis, common goldeneye Bucephala clangula, bufflehead Bucephala albeola, ring-necked ducks Aythya collaris, common mergansers Mergus merganser, hooded merganser Lophodytes cucullatus, greater scaup Aythya marila, white-winged scoter Melanitta deglandi, Canada goose Branta canadensis, snow goose Anser (Chen) caerulescens were affected in small numbers in a type E outbreak affecting mainly common loons Gavia immer, and herring gulls Larus argentatus, with small numbers of other birds (grebes, other gulls etc. also recorded) (B48.12.w12).

In Cranes:

In Hedgehogs:

  • The carcass of a hedgehog found in a fodder rack following an outbreak of botulism in cattle was found to contain type C toxin (20,000 minimum lethal doses for mice per gram subcutaneous tissue). (J140.86.w1)

In Bears:

Further information on Host species has only been incorporated for species groups for which a full Wildpro "Health and Management" module has been completed (i.e. for which a comprehensive literature review has been undertaken). Host species with further information available are listed below:

WATERFOWL Host Species List

BIRDS:

MAMMALS:

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Environment/Geography

General Information on Environmental Factors/Events and Seasonality

  • Clostridium botulinum and the ‘phage responsible for type C toxin production are widely available in the environment, with some places being heavily contaminated. Spores can survive in soil for many years. Repeated outbreaks (e.g. yearly) may occur at some specific locations. (J1.30.w4, J3.100.w1).
  • Optimal bacterial growth occurs at 25-40C (particularly 30-37C). Both shallow water and the presence of decaying organic matter may increase the risk of botulism outbreaks, by increasing the temperature of water and sediments, and decreasing dissolved oxygen (B15, B36.38.w38).
  • Bacterial growth also requires a nutrient source which provides certain essential amino acids which the bacterium cannot itself synthesize; this may be provided by the carcasses of invertebrates or vertebrates, also by raw sewage and rotting vegetation. Raw sewage, in addition to directly providing nutrients for bacterial growth may also precipitate a boom-and-bust- cycle of aquatic invertebrates and oxygen depletion, with resultant deaths of aquatic plants and animals (B36.38.w38).
  • The presence of protein source, usually decaying organic matter (vegetation, decaying aquatic invertebrates, decaying vertebrates), is required for bacterial growth and toxin production. (P17.50.w1, B48.12.w12) Wetland flooding and draining can kill aquatic life, as may pesticides and other agricultural pollutants, thereby providing more substrate for toxin production. Other potential sources of energy for bacterial growth include raw sewage and rotting vegetation.
  • Aquatic and terrestrial life (vegetation, invertebrates, fish) may be killed by flooding or draining of wetlands (including fluctuating water levels), pesticides and other agricultural pollutants, also by e.g. hailstorms or power lines killing birds. Birds living in an environment rich in Clostridium botulinum spores are likely to have spores in their guts at the time of death and may then act as a focus (putrefaction, invasion of tissues by Clostridium botulinum, production of toxin) (J1.33.w7, B15, B36.38.w38). 
  • Botulism usually occurs in warmer months, in the summer and autumn (fall): July to September in North America (B36.38.w38, B48). In the UK, reports of outbreaks tend to be increased during exceptionally hot and dry summers (J3.100.w1, J3.137.w1, P17.50.w1). This may be related to the presence of maggots as well as temperatures suitable for bacterial growth and toxin production. Type E outbreaks have occurred during late autumn and spring (B36.38.w38).
  • Outbreaks of botulism in winter or early spring may be due to toxin (particularly in maggots) remaining, for example at the bottom of lakes (J1.19.w1, J3.102.w1, B15, B36.38.w38, P17.50.w1, B48.12.w12).
  • Toxin production may continue in carcasses in relatively cold weather, as carcass temperature is often higher than air temperature; this may allow outbreaks to occur earlier than expected from the temperature in spring or later than expected in autumn (J1.19.w1, J1.20.w5, J1.24.w4, B36.38.w38) .
  • Artificially increased water temperature, e.g. due to power station outputs, (thermal pollution) may assist in providing favourable conditions even in cold weather (P17.50.w1, B15)
  • Specific microenvironmental features: The likelihood of outbreaks is significantly influenced by pH, salinity, temperature, and oxidation-reduction potential in the sediments and water column. (B36.38.w38).
  • Shallow stagnant water, alkalinity, large numbers of aquatic invertebrates and oxygen depletion associated with rotting vegetation, have been thought to be contributory, also the provision of dead aquatic invertebrates or waterfowl as a 'particularly favourable growth medium and microenvironment (J3.100.w1, J7.27.w1).
  • Botulism outbreaks might be affected by variables such as number of carcasses, proportion of carcasses containing spores, rate of scavenging/carcass removal, proportion of birds ingesting sufficient toxic maggots to become poisoned and die, temperature (affecting rate of maggot infestation of carcasses etc. (J1.33.w7, B15)
  • Carcasses resulting from hailstorms (Hail storms) over botulism-prone marshes may provide suitable substrate and precipitate an outbreak of botulism (B15).

B10.26.w9, B13.46.w1

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

North America, Central America, South America, Europe, Australia, Africa. (United States, Canada, Mexico, Argentina, Brazil, Australia, Russia, New Zealand, Japan, Sweden, Denmark, England, Netherlands, Germany, Italy, Spain, Ireland, Wales, Norway, Czechoslovakia, France, South Africa, Uruguay.) (P17.50.w1).

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

United States, Canada, Mexico, Argentina, Brazil, Australia, Russia, New Zealand, Japan, Sweden, Denmark, England, Netherlands, Germany, Italy, Spain, Ireland, Wales, Norway, Czechoslovakia, France, South Africa, Uruguay.

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General Investigation / Diagnosis

General Information on Investigation / Diagnosis

WATERFOWL Presumptive Diagnosis
  • Made on the basis of history, clinical signs (ascending flaccid paralysis, good body condition), location and timing (in relation to previous outbreaks), response to treatment.
  • Post mortem examination (necropsy) can eliminate other potential diagnoses, on the basis of a lack of lesions.
  • Finding maggots in gut contents is suggestive, but rare, as maggots have usually been digested by the time of death (J1.20.w4).

Definite diagnosis: requires blood from a sick bird or heart blood from a carcass, tested using:

  • Mouse toxicity test (wasp-waist, respiratory distress, paralysis and death; protection by antitoxin). (N.B. very high botulism in serum may override antitoxin at standard dose (J3.107.w2), and low level in serum may not be mouse-lethal (J3.112.w1). Testing of blood from several birds is suggested, as the amount of toxin may vary, for example with the stage of the disease.)
  • ELISA - Sensitivity may be higher than in the mouse toxicity test, if sufficient size blood samples (at least 1ml) are available. This newly-developed test for Type C toxin is not yet commercially available (J1.34.w1). (N.B. Testing in blood from carcasses may be misleading as toxigenesis can occur after death. Ideally, blood should be collected aseptically from sick birds.)
  • Faecal examination for toxin is theoretically possible but not usually effective as these are usually free from toxin by time of capture and testing (J1.17.w5).
  • Testing gut contents for Clostridium botulinum may also be attempted, but results are of doubtful use, as the organism may be found in the gut of normal birds. Testing internal organs for Clostridium botulinum is usually of little use due to post mortem invasion by the bacterium.
  • N.B. brain acetylcholinesterase levels are not decreased in botulism (J1.27.w2).
  • (In the UK, the Central Veterinary Laboratory, Weybridge, may be contacted for detection of toxin in clotted blood (B11.38.w6)).

(J3.85.w1, J3.100.w1, P9.1.w1, P17.50.w1, B10.26.w9, B11.38.w6, B15, B36.38.w38, B37.x.w1, B48.12.w12)

FERRETS
  • Ferrets may develop botulism if they have a clinical history of ingesting spoiled or improperly handled food, with symptoms of the central nervous system and weight loss. (B232.8.w8, B627.14.w14) 
  • Diagnosis of botulism can be carried out by identifying Clostridium botulinum toxins in the blood, serum or gastrointestinal tract of ferrets or in contaminated food which the ferret has eaten. (B232.8.w8, B627.14.w14)
  • Diagnosis required neutralisation tests in mice. (J3.93.w2)
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Similar Diseases (Differential Diagnosis)

WATERFOWL
FERRETS
  • Other toxicities which produce paralysis. (B501.12.w12)

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Treatment and Control

Specific Medical Treatment

WATERFOWL Antitoxin, if available, 0.5-1 mL antitoxin per duck (B36.38.w38); 75 IU per duck intraperitoneally (B15). Recovery rates after treatment have been recorded of about 90% with moderately-affected ducks and about 55-70% with severely affected birds. (B10.26.w9, B11.38.w6, B13.46.w1, B15, B36.38.w38, B37.x.w1)
FERRETS Note: Prognosis is poor, although occasional cases will recover. (B501.12.w12)
  • Treatment of paralysis should include toxoids and oral gavage with absorbents, such as charcoal, to reduce further toxin absorption. (B232.8.w8, B628.11.w11, J34.17.w4)
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General Nursing and Surgical Techniques

WATERFOWL Remove from source of toxin.

Supportive treatment:

  • Provide clean water, food, shade and protection from predators; care with water provision for birds in Class II or II paralysis as birds may drown. (J3.137.w1)
  • For wild or feral birds, minimize disturbance once in a safe place, but remove dead birds. Allow recovered birds to fly away. Usually recovery within a few days, but several days or even weeks may be required for full recovery. Birds will begin feeding and drinking before regaining the use of the legs. (J3.85.w1, J3.137.w1).
  • Oral fluid therapy (fresh water, large volumes) given by tube into crop may be useful, particularly in birds with Class II or III paralysis (i.e. unable to drink voluntarily) and will assist to ‘flush’ toxins (J3.100.w1, B48.12.w12).
  • Intravenous fluid therapy may be of use in particularly depressed individuals - Hartmann's solution with added vitamin/amino acid supplement (Duphalyte, Duphar), through the medial tarsal (leg) vein (J3.137.w1).
  • Activated charcoal or bismuth added to fluids will absorb toxin still in the gastro-intestinal tract.
  • Injections of vitamin B12 to promote appetite (three day treatment) and antibiotic cover (five days) may be useful (J3.137.w1) (NOT penicillin, tetracyclines or aminoglycosides, as these may potentiate neuromuscular blockade).

N.B. treatment of waterfowl may allow high recovery rates of waterfowl (coot, grebes, gulls and shorebirds rarely survive even with similar treatment) (B36.38.w38).

(J3.137.w, J7.27.w1, B10.26.w9, B11.38.w6, B13.46.w1, B15, B36.38.w38, B37.x.w1, B48.12.w12)

FERRETS
  • Supportive therapy. (B627.14.w14)
  • Note: Prognosis is poor, although occasional cases will recover. (B501.12.w12)
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Preventative Measures

Vaccination WATERFOWL
  • Immunogenic toxoid may be produced by formalin treatment of toxin. Botulinum toxoid has been shown to protect waterfowl in the face of experimental exposure and in outbreaks, and to be protective for several months (J4.143.w1, J7.27.w1, B48.12.w12)
  • Commercial vaccine (produced for ranched mink) has been shown in a recent experimental trial to protect from as soon as 10 days post inoculation, and persisting to at least 90 days, which would prevent re-intoxication during an outbreak. It was not effective at 5 days post inoculation (P2.47.w2).
  • Vaccination has also appeared effective in the face of a natural outbreak. (Botumink , United Vaccines, Inc, P.O. Box 44220, Madison, Wisconsin 53744, USA) (P1.1993.w1).
  • Half the dose recommended for mink is suggested (B13.46.w1).
CRANES
FERRETS
  • Vaccinations with type C toxoid are available and recommended. (B232.8.w8, B501.12.w12, B627.14.w14, J34.12.w4)
  • Annually vaccinations are recommended for ferrets raised commercially or not on a commercially prepared diet. (B628.11.w11, P20.1992.w7)
Prophylactic Treatment

WATERFOWL

--
FERRETS
  • Prophylactic use of toxoids. (J4.173.w4)
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Environmental and Population Control Measures

General Environment Changes, Cleaning and Disinfection

WATERFOWL

Aim of all actions is to minimize toxin availability to birds:
  • Reduce the chance of initiation of outbreaks by avoiding conditions for bacterial replication - reduce organic inputs into wetlands, eliminate factors that introduce large amounts of decaying matter:
  • In avicultural conditions, increased water flow and aeration, designs to increase ease of cleaning, deepening banks, alteration of feeding practices to minimize build-up of organic and protein loads, prompt removal of carcasses
  • Avoid sudden increases of water level, e.g. flooding of dry areas, in summer (may produce drowned vegetation & invertebrates as substrate), or sudden decreases in water level (leading to death of fish, aquatic invertebrates & vegetation) or fluctuations in water level. (N.B. draw-downs are used as part of management of areas for shorebirds). Avoid discharges of wastewater or sewage into wetlands when many waterfowl or shorebirds are using the area or are likely to use an area during the following 30 days.
  • Avoid water drawdowns for e.g. fish management in the summer, and remove fish carcasses if such actions are carried out.
  • Avoid running power lines over wetlands if possible: carcasses from collisions may act as a focus - a single waterfowl carcass can allow the production of several thousand toxin-laden maggots and also seed the environment with more botulism spores as it decomposes.
  • Remove carcasses promptly and bury or burn, particularly during outbreaks and during the period when, for a particular wetland, outbreaks have occurred previously. Burning preferred, bury deep and in limed pits if necessary. N.B. carcass removal is labour-intensive and not always very efficient (J1.29.w5).
  • Flush pools with fresh water if feasible in face of outbreak.
  • Provide artificial aeration in man-made lakes and ponds during summer to keep oxygenation levels from dropping.
  • Record dates, places and environmental conditions of outbreaks; in future years increase surveillance from 10-15 days before earliest recorded outbreaks to 10-15 days after latest date, concentrating on known "hot-spots" where outbreaks are frequent, and be prepared to remove and dispose of vertebrate carcasses during this time period; perhaps deny access of the area to birds if necessary and feasible, during ‘risk’ time.
  • Where possible, monitor and modify environmental conditions to prevent the pH and salinity of wetlands from reaching or being maintained within high hazard levels.
  • If possible, construct wetlands in 'botulism-prone areas' in a way allowing complete and rapid drainage.
  • Avoid feeding maggots to birds; self-grow if they are essential.

(J1.85.w1, P9.1.w1, B11.38.w6, B13.46.w1, B15, B36.38.w38, B48.12.w12)

CRANES
  • Maintain good water quality and note the water quality. (B115.8.w4)
  • In mixed exhibits, note the health of waterfowl sharing the exhibit. (B115.8.w4)
FERRETS
  • Improve husbandry: poor husbandry practices and large groups increase the risk of botulism. (B628.11.w11)
  • Exclusion of diets contaminated with clostridial toxins, by giving a commercially prepared dry diet. (B232.8.w8, B627.14.w14, J4.173.w4, J34.17.w4)
  • Avoid feeding ferrets wild bird carcasses. (B232.8.w8)
Population Control Measures WATERFOWL
  • Remove or encourage the dispersion of birds from the site of an outbreak. Provide alternative areas for their use (e.g. make food available at a 'safe' site) and scare from the outbreak site if possible. (B36.38.w38)
CRANES
  • Harassment was used successfully to move sandhill cranes away from a botulism outbreak on Willcox Playa, Arizona. (D279)
FERRETS --
Isolation, Quarantine and Screening WATERFOWL --
FERRETS --
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