Avian Cholera and Waterfowl Biology Author(s): G. Wobeser Source: Journal of Wildlife Diseases, 28(4):674-682. Published By: Wildlife Disease Association DOI: http://dx.doi.org/10.7589/0090-3558-28.4.674 URL: http://www.bioone.org/doi/full/10.7589/0090-3558-28.4.674

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Journal

of

Wildlife

28(4), 1992, pp. 674-682 Disease Association 1992

Diseases, © Wildlife

LETTER

TO THE

Avian

Cholera

EDITOR...

and Waterfowl

Biology

In a review of the ecology of Pasteurella multocida infection in waterfowl, Botzlen (1991) indicated that many fundamental

posed individuals laboratory, birds tion of a few

questions

(Hunter and Wobesen, 1980); however, under natural conditions a larger number of organisms is likely required to result infection. The probability of infection

remain virulence

tneme

control waterfowl ca”

one

ease, and

of the management

(Bolen

Botzlen because

unanswered; yet “the of avian cholera makes

et

a!.,

highest

lack

1989).

has

development

wetlands while the

The

particularly a model

of which

of

gies. Research nomena, such

priorities for North Amen-

in

(1991) was it proposed

by

management

strate-

found of the

is increasing

managing habitat tering waterfowl

duced

phe-

to relate

and

habitat

disposing occur. In this

and

in

and winSmith et

disease

bacterium. will

If not

a bird

occur.

The

is not

to the of factors

lated lihood

is con-

on recover

but de-

is influenced

agent, that

as well influence of

enough an in-

bird being exposed, infected, and dying of avian cholera of many separate probabilities

disis the re-

to exposure and of an outbreak

resistance. occurring

long

as by the

The likeintroduces

another range of probabilities. A major unknown in the ecology of avian cholera is the source of P. multocida. I believe that avian cholera is perpetuated by fowl

carriers

of P. multocida

although

evidence

among for

water-

existence

of

carriers in wild waterfowl is inconclusive. Pasteurella multocida has been recovered from clinically healthy waterfowl (Vaught

bird

exposed,

probability

die

by its resistance the presence

dividual eased, product

between P. multocida and a susceptible bird (Fig. 1) as a starting point. Even in the most devastating outbreak not all binds

and

subsequently

ability of a sick bind to survive to recover. Thus, the likelihood

changes

interaction is not all-or-nothing. is the coming together of

cholera

of pro-

on

to avian cholera, with the intent of further stimulating interest in this disease. It is useful to consider the interaction

die, so the Exposure

Avian

consists illness

velop disease following infection is unknown, as is the proportion of diseased binds that recover. The probability that an infected bird will become diseased and

dead, disease

of carcasses letter I hope

management

infection.

Disease signs of

degree and

of

but management to control aviis reactive, consisting primarily

of collecting when outbreaks

by

and organism,

in is

sidered an acute, highly fatal infection the actual proportion of waterfowl that

interest

for migrating (Weller, 1987;

duration of the

the bird’s resistance. physical changes and

research

has centered on local as defining characteristics

There

related to the route, of exposure, virulence

valuable for the dis-

little attention. Waterfowl has, in general, focused of birds, with comparatively to reduction of non-hunting

mortality.

a!., 1989), an cholera

review

hampered

where birds were population ecology

has received management production little attention

exits

become infected. In the can be infected by injecP. multocida organisms

et a!., 1967; Konschgen

of

et al., 1978; Titche,

exposure is related to the density and distribution of bacteria and birds, the amount of time they spend together, and viability of the bacterium in the environment. The

1979) but the virulence lated from these birds

bind’s resistance has no effect on the rate of exposure. Infection involves invasion and growth of bacteria in the bird. Not all ex-

(Hughes and Pnitchett, 1930; Iliev 1964; Curtis and Ollerhead, 1981). riers have been reported in domestic

The ens

674

importance has been

of the bacteria isowas not reported.

of carrier birds in chickknown for many years et

a!., Cargeese

LETTER

and these infection

apparently for chickens

served as a source (Hellen, 1958).

of In-

TO THE EDITOR

675

BSrd

PastoiarUI

vestigators searched unsuccessfully for carriers in domestic turkeys until Carpenten et a!. (1989) demonstrated that they were

common

breaks.

among

Special

survivors

techniques,

of

as used

out-

by Car-

penter et a!. (1989), should be applied the search for carriers among waterfowl and any P. multocida isolated must characterized fully. The most likely routes of transmission

Infoot

to be

among birds are through bird-to-bind contact and via contaminated water. Different routes of transmission may explain different

disease

patterns.

Avian

among northward katchewan each but

1979)

only

a population is confined (Chen rossii),

a few

birds

occurs

are

in Saset a!.,

affected

in

of many thousands. Disease almost entirely to lesser snow

c. caerulescens) although other

lands spread white

cholera

migrating geese spring (Wobesen

and Ross’ geese (C. species share wet-

with these birds, suggesting that occurs within the population of geese through direct contact. Wind-

ingstad pattern

et a!. among

braska

and

(1988) described mallards in

Botzler

of scattered

(1991)

mortality

that

a similar western Ne-

included

reports

“never

develop

to extensive epizootics.” This form of “smouldering” avian cholera may go undetected, unless a special effort is made to search common

for dead than

example, we avian cholera since

1977

dead bers

geese of the

birds, and recognized

is probably currently.

have found in Saskatchewan

geese

but

during

have public

this

been only

more For

but

deaths

cies

migrate

in the

eider

relationship

multocida

continue

Reported

one

between

and

to occur

north.

breaks, with colonial-nesting

as some

spe-

summer

out-

exception, have species such as

(Somateria

mollissima)

been common

(Reed

(Hanson tion was which

and Mutalib, an outbreak >4,900

in

ducks,

1989). The Saskatchewan

primarily

(Aythya

americana)

moulting, 1988).

died (Wobeser common feature

breaks nificant south

period

grounds

by memexplosive

curred terfowl

A

a

and in

(Brand,

1984).

for Leighton, these out-

aggregation. Sigbirds migrating twice. One in-

birds exposed die-off on

in October of at least

in

redheads

concentrated

has been dense mortality among has been recognized involved from

excep-

The

the

to geese rebreeding second

gests

tumn outbreak. When we consider

seasonal, spring when

peaking (Friend, birds

disperse

exposure

to a common

probably outbreaks

contaminatare distinctly

in late winter 1987). Mortality from

the

epizootic

to early declines site,

oc-

1991 when >1,000 waseven species died in

Saskatchewan. Lesser snow geese sandhill cranes (Grus canadensis) from area of an earlier summer outbreak in western arctic were present during the

simultaneous

in and

outbreak, involving hundreds or thousands of birds of many species, is the more generally recognized form of avian cholera. The pattern in many such outbreaks sugsource of infection, ed water. Major

the

a bird.

Cousineau, 1967; Korschgen et a!., 1978; Jorde et a!., 1989), lesser snow and Ross’ geese (Wobeser et a!., 1979), and doublecrested cormonants (Phaicrocorax auritus)

stance turning

14-year

reported once. The

Phases

Pasteurella

dead of spring

each

1.

FIGURE

bacterium

information

from

and the the authe

entire continent it suggests that P. multocida is present in at least some waterfowl populations throughout the year. The prevalence of disease is lowest in autumn,

676

JOURNAL

increasing spring, perse.

OF WILDLIFE

to a peak

in late

VOL. 28, NO. 4, OCTOBER

winter

and then declining Outbreaks occur among

centrated

during

followed grating

by birds.

spring species,

staging while

year

DISEASES,

the

summer

mortality Outbreaks

is restricted

and

discon-

may

be

in southward on wintering

areas often mortality

involve at other

to one

or

changes

to early

as binds species

miand multiple times

a few

of

that

populations reservoirs

of

impact

of less



‘certain

white disease

large geese that

abundant

or other

local

may

have

food important

If R0 is defined

as

this

and

a

serious

ment The

of

problem

and which had resulted in loss of 53% of wetlands in the lower 48 states by the 1980’s 1990).

Stewart

et

“the rates of wintering modification have been last 25 years, and these are affecting the dance of wintering also been a change lands,

with

an

a!.

(1987)

habitat staggering changes

stated loss

and in the certainly

distribution and abunwaterfowl.” There has in the character of wet-

increase

in large

chol-

number

of

to a sininto a sus-

is intuitively

rea-

reservoirs

promote species

popuand

mixing

that

were

of once

mixing of has been the manage-

species (Anonymous, 1991). of carriers of P. multocida

waterfowl

Central lowed which

on sparse Aggregation

Recent large-scale goose populations as a problem for

of these prevalence

among

(Friend, 1981). The most obvious change has been continuation of the loss of wetlands that began at the time of settlement

(Dahl,

average

“it

and

populations

as

cause,

on avian

attributable introduced

in distribution

populations

of

diseases

as the

or dense than in a small lation” (Fine et a!., 1982).

have wild

infectious

effects

population,

changes

pop-

changes affecting as emergence

abunof

of exposure to disease in dense aggregations.

secondary infections gle infectious case

segregated. arctic-nesting recognized

habitat as well

provide

regardless

era. The probability agents is enhanced

ulations” (Anonymous, 1991). Enhanced exposure and/or reduced host resistance could facilitate transition from the enzootic form maintained by bird-to-bind transmission to a water-borne epizootic. During the past several decades there been major waterfowl,

that

but,

sonable to expect that R0 should be a function of population size on density, insofar as any individual is likely to contact more individuals pen unit time in a large

increasing

may serve may adversely

species

in agriculture

dant

ceptible

species.

Colonial-nesting species, such as lesser snow geese, may maintain the bacterium over the summer because of their dense aggregation on breeding areas. There has been speculation

1992

is unknown may

other

but

enhance

agents.

mixing

exchange

Outbreaks

of in

the

and Mississippi flyways have folmixing of populations, some of were known to have been previ-

ously exposed to avian (1984) suggested that the bacterium to new

cholera, carriers areas.

and Brand introduced Pasteurella

multocida is not the only disease agent that may be exchanged. The effect of other agents may not be dramatic but each represents a “cost” to the host (Yuill, 1987) and the aggregate cost of exchanged parasites

may

render

birds

to infection and/on to P. multocida.

more

disease

susceptible

when

exposed

(>200 ha) and a decrease in smaller wetlands (Buller, 1975; Pederson et a!., 1989; Ringelman et al., 1989). Most waterfowl

dividual may be

are gregarious, so that aggregation is normal; however, the dense concentration of binds that now occurs on staging and wintering areas (>1 million binds at some sites

cholera. For example, snow geese on traditional wintering areas along the Gulf coast were “constantly on the move from one location to another, rarely using one

(Strong et al., mal. Concentration

feeding and resting area for more than two or three weeks,” whereas many now spend the entire winter on a water area (Yancey, 1976). Pasteurella multocida persists in

loss of refuges

1991))

is probably may occur

not because

alternate habitat, development on man-made water areas,

norof of

and/or

The

long-term wetlands another

or

continual

use

throughout the change affecting

of

in-

winter avian

LETTER

water

for

days

that bacteria of the disease The

to weeks from will

probability

of

(Botzler,

1991)

carriers accumulate

or birds over

sufficient

bacteria

so

dying time. ac-

cumulating to result in water-borne tnansmission is a function of the number of binds shedding bacteria, the length of time they are present on the wetland, the number of bacteria shed, the survival time of bacteria in water and the amount of water. Bird density should be calculated measure of time, such as use of the area, to account of

accumulation.

culated

Density

in relation

although,

to include a total bird-days for this factor might

to the

if bacteria

be

volume

cal-

of water

accumulate

near

the

surface (Botzler, 1991), area may be more important than volume. Concentration of birds might reduce resistance to infection. “Crowding” is often considered a stressor in relation to disease but and

interactions infectious

predictable resistance increasing

between disease are

social pressure not consistent or

(Esch et a!., 1975). In chickens, to some agents improved with social stress, up to a point, and

then declined; resistance was inversely proportional of stress (Gross, 1984).

other agents to the amount There is little in-

formation

waterfowl.

available

on

to

study, crowded ducks retained administered dose of parasites crowded controls and parasites and caused greaten tissue crowded binds (Ould and Stress,

as a result

a direct

effect

cholera,

as well

enhancing could, in multocida.

other turn,

might effect

parasitic influence

conditions resistance

energy cranes

demands between

supplied 1989).

The

spring;

e.g.,

of mallards October and

by grain situation

many geese. Grains proteins, minerals

have

to

as an indirect

to early

one

in the 1980).

susceptibility

has been a marked to dependence

There waterfowl autumn

damage Welch,

of crowding, on

In

more of an than did lesswere larger

on

avian

through that to P.

shift by grains >90%

some from

of food

and sandhill February are

(Clark and Sugden, i probably similar for are deficient and vitamins

in specific (Baldas-

same natural

et a!., 1983; foods are

TO THE

Jorde required

balanced

diet

(Delnicki

Reinecki

and

Knapu,

et

EDITOR

677

a!., 1983) to maintain

and

and a

Reinecki,

1986;

1986;

Loesch

and

Ka-

minski, 1989). Nutritional deficiencies affect resistance to infectious disease (Watson, 1984; Chandra, 1988) and one nutrient, deficient in many grains, may be of particular consequence. Vitamin A has been called the “anti-infection vitamin” (Sommen, 1990) and effects of deficiency on resistance to disease agents are well-doeumented (Chandra and Newberne, 1977; Gross

and

Sijtsma

Newberne,

et al.,

Deficiency

1980;

1989;

Beisel,

Friedman

interferes

with

Friedman et al., 1991).

A deficiency

have

(Anas

terfowl

is unknown.

to

in black in Masmallards

overwintening

(Wobeser and of deficiency

in

Kost, among

Concentration

terfowl on wetlands riod may exacerbate through quired

reported

wintering 1950) and

platyrhynchos)

Saskatchewan but the extent

of

as barriers to production (Davis and

and Sklan, 1989; Lesions of vitamin

been

ducks (Anas rubripes) sachusetts (Hagar,

1991).

maintenance

epithelial surfaces important infection and with antibody and lymphocyte proliferation Sell, 1989; Friedman

1982;

et a!.,

1992) waof wa-

for an extended penutritional problems

depletion supplement

of

natural foods grain (Jonde et

real.,

1983).

Fungal waterfowl birds

growth might

may

in the

be infected

disease

poisoned Waterfowl

on also

grain affect

consumed disease.

by fungus,

aspergillosis;

others

by toxins produced die of mycotoxicosis

by Some

resulting may

be

by fungi. (Robinson

et al., 1982; Windingstad et a!., 1989) and sublethal exposure to mycotoxins might impair resistance to avian cholera (Smith et a!., 1990). Demand for water has increased, particularly in western North America, so that “wet” lands must compete for a share. Water

available

for

wildlife

is often

of

poor

quality and wetlands have become a method of disposing of effluent-laden water, e.g., the

Kesterson

National

Wildlife

Refuge

in

678

JOURNAL

OF WILDLIFE

California

(Zalm,

novative (Snyder

wastewater and Snyder,

DISEASES,

1986),

VOL. 28, NO. 4, OCTOBER

or a lowcost

treatment 1984). The

“in-

system” most corn-

mon contaminants are associated with agnicultural runoff. Direct toxicity, such as that associated with selenium (Zalm, 1986; Kadlec and Smith, 1989), may be the most obvious problem.

expression Effects

of

of a more sublethal

widespread exposure

to

most chemicals present in runoff water are unknown, as is the interaction between these chemicals and infectious diseases. Some contaminants increase the susceptibility of mallards to P. multocida ley and Yuil!, 1991) but methods ing such complex interactions infancy

(Porter

contaminants tle attention. herbicides duction a grain

of nutrients diet (Cain,

Fertilizers some have

et a!.,

1984).

on wetlands Turbidity, might negatively

(Whitefor studyare in their The

effect

has received insecticides affect the

increase

of litand pro-

nutrients but been implicated

production

and

occurrence

ponds

in the

Rainwater

inorganic fertilizers in the decline of sub-

of avian Basin

cholera

in

ions (Price and Brand, 1984) and protein content, increased salinelevated temperature (Bredy and 1989) enhance survival of the bac-

terium wetlands

in

to a borne

concentration transmission.

Many canadensis)

Cold, are ern

sufficient

mallards, and

winter

north

1975; Bateman

might enhance of P. multocida

Yancey, et a!., inclement

likely binds

of

of and survival in water

for

water-

Canada geese (Branta lesser snow geese now traditional

areas

1976; Jorde 1987; Pederson weather

to be common and might

and

(Buller,

et a!., et a!., food

by wells, or use natural

1984). areas

These birds often of water kept un-

turbulence deep food.

or thermal

1983; 1989).

scarcity

stressons for northreduce resistance to

pol-

reservoirs that Overwintening

provide binds

may

contribute to a decline in water qua!favorable to survival of P. multocida in water; usage of wetlands during winter, ity

as well as during spring migration, increases the potential for accumulation of the bacterium (Smith et a!., 1990). Birds ovenwintering in the north are probably more dependent

on agricultural

crops

and

lards

wintering

in

Nebraska

consumed

If asked to design a set promote frequent occurrence of avian

cholera

include:

a) a large

posed ulations

of a mixture to increase

more

than are For examthat ma!-

diet containing 37% less protein mallards wintering in Louisiana.

a

than

did

of conditions of large

on

a site,

population

I would

of birds

of species and the likelihood and to promote b) restriction

to outcom-

sub-popof in-

exchange of the birds

to a small water area for an extended time to promote accumulation of P. multocida in water, a high rate of contact among binds, a high degree of social stress and depletion

Certain increased ity and Botzler,

thermal pollution and accumulation

frozen lution, little

(Olson, small

cluding carriers of disease agents;

of Nebraska.

water. Thus, contamination with salts, organic matter

on

breaks of

merged aquatic vegetation in Chesapeake Bay (Hindman and Stotts, 1989). Contaminants might also alter survival of P. multocida in water. Windingstad et al. (1984) found a positive correlation between water salinity

infection crowd

prone to nutritional deficiencies birds that winter to the south. ple, Jorde et a!. (1983) reported

needed to supplement 1987; Reid et al., 1989).

might

1992

of

natural

ditions tocida

favorable for (e.g., increased

matter

and

thermal

dence of the in nutritional to mycotoxins; of inclement

foods;

Botzler lead

model

water

pollution);

con-

P. mu!organic d)

depen-

birds on a grain diet to result deficiencies and expose birds and e) frequent weather, food

posure to chemicals in the stnessors. These conditions similar to those experienced terfowl in North America time. The

c)

survival of salinity,

of avian

(1991)

and

to at least

three

ex-

water, and other seem perilously by many waat the present

cholera the

occurrence shortage,

above

hypotheses

proposed

by

discussion that

could

be tested. Hypothesis 1: Pasteurella tocida is maintained by carrier birds in waterfowl populations. Several

mu!withques-

TO THE EDITOR

LETTER

tions

follow

from

this

hypothesis.

Where

However, populations, to reduce

be possible wetlands and exposure of birds

679

to manipulate food resources to P. multocida

it may

is the bacterium carried in the body? What is the prevalence of carriers in different species? How long is the bacterium carried by individual birds? Does the prevalence of carriers change seasonally? What fac-

and to factors that interfere with disease resistance. Avian cholera is a complex disease but, as stated by Leopold (1933) in

tons

regard

promote

shedding

of bacteria

by

car-

riens? of

very

Hypothesis Pasteurella

major

2: Waterborne multocida

outbreaks

is

of avian

transmission involved

cholera.

in

Several

questions also follow this hypothesis. Does P. multocida accumulate in the water of wetlands overwinter? What factors influence

survival

What

of the

is the

multocida various

threshold

Questions include

the

readily raised following.

do

fect resistance prevalent is the by

dian

Wildlife

ada,

14 pp.

and contaminants on resistance to

CITED goose

(1991)

noted

of a model of avian more by a lack of

that

cholera consistency

there may ing various

be a variety combinations

ex-

available

Wildlife

H.

A.,

winter

range.

Weller

(ed).

a single of the

It is unlikely

model disease. that

to the

explain amount

all

occur-

of wetland

area available for wintering birds can increased substantially, so that dispersal birds over a greaten area solution to the problem

is not a practical of avian cholera.

be of

venture.

Venture,

A

Cana-

Alberta,

to

Can-

postbreeding

Society

water-

Bulletin

T.

JOANEN,

1 1 : 25-

History

snow geese In Waterfowl

on

1982.

pp.

their in

D.

status

Gulf

of

Coast

winter,

M.

W.

Press,

Min-

495-515.

Single

Journal

and

of Minnesota

Minnesota,

C.

AND

1987.

University

W. H.

nutrients

of Clinical

and

immunity.

Nutrition

35:

417-

468. E.

BOLEN,

involvrather

used

H. J. WHYTE, E. E. QUINLAN, 1983. Dynamics and quality

corn

American

in

avian cholera of factors are areas. Thus,

of patterns of factors

,

joint

Joint

Edmonton,

in Texas.

neapolis,

hindered in the in-

be

31.

BEISEL,

than by a paucity of data. Many that enhance exposure or reduce to infection could contribute to

the occurrence of epizootic and different combinations likely to apply in different

Goose

Service,

midcontinent

development was

Arctic

STUTZENBAKER.

avian

of at-

day

LITERATURE

BOLEN.

waste

BATEMAN,

af-

does

“this

points

some

1991. Arctic

G. A.

E. G.

fowl

hypowater-

effect

ANONYMOUS.

AND

is

the

grateful to K. F. Higgins, F. A. C. Riddell, and S. V. Tessaro for and suggestions.

G.,

G. A. BALDASSARRE, AND 1989. Playa lakes. In Habitat

GUTHERY.

cholera? Botzler

than rences

I am Leighton, comments

of

in general:

of which may measures.”

BALDASSARRE,

cholera? How of mycotox-

What

posure to mycotoxins wastewater have

deficiencies and contamavian cholera.

deficiencies

to avian consumption

waterfowl?

under

particularly wintering

nutritional

tack, one for control

prospectus.

by this hypothesis How prevalent

deficiency, A, among How

formation factors resistance

transmission

3: Nutritional to mycotoxins resistance to

nutritional vitaminosis

ins

for

of P.

diseases increases

in wetlands?

concentration

required circumstances?

Hypothesis and exposure inants reduce

fowl?

organism

to wildlife complexity

agement

for

in North

America,

and

migrating

H. M. Kaminski

and

wintering

L. M.

Smith,

(eds.).

Texas

F.

S.

man-

waterfowl

H. L. Tech

Pederson, University

Press,

Lubbock, Texas, pp. 341-365. H. G. 1991. Epizootiology of avian cholera in wildfowl. Journal of Wildlife Diseases 27:

BOTZLER,

367-395. BRAND,

C. J.

and

1984.

Mississippi

Journal

of

Avian Flyways

Wildlife

cholera during

Management

in the

Central

1979-80. 48:

The

399-406.

J. P., AND H. G. BOTZLER. 1989. The effects of six environmental variables on Pasteurella multocida populations in water. Journal of Wildlife Diseases 25: 323-339. BULLER, H. J. 1975. Redistribution of waterfowl: Influence of water, protection, and feed. International Waterfowl Symposium 1: 143-154. CAIN, B. W. 1987. Wintering waterfowl habitat in Texas: Shrinking and contaminated. In WaterBREDY,

fowl

in

winter,

of Minnesota 583-596.

M.

Press,

W.

Weller

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Avian cholera and waterfowl biology.

Avian Cholera and Waterfowl Biology Author(s): G. Wobeser Source: Journal of Wildlife Diseases, 28(4):674-682. Published By: Wildlife Disease Associat...
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