FACT SHEET PS-47
Common Poultry Diseases1
G.D. Butcher, J.P. Jacob, and F.B. Mather2
before healing is complete, the surface beneath is raw
and bleeding. Unthriftiness and retarded growth are
There are many common and important diseases
typical symptoms of fowl pox. In laying hens,
which can affect the respiratory system (air passages,
infection results in a transient decline in egg
lungs, air sacs) of poultry (see Table 1). Poultry refers
to birds that people keep for their use and generallyincludes the chicken, turkey, duck, goose, quail,
In the wet form there are canker-like lesions in
pheasant, pigeon, guinea fowl, pea fowl, ostrich, emu
the mouth, pharynx, larynx, and trachea. The wet
and rhea. Due to modern systems of management,
form may cause respiratory distress by obstructing the
usually with high poultry densities, these diseases are
upper air passages. Chickens may be affected with
either or both forms of fowl pox at one time.
: Fowl pox is transmitted by direct
contact between infected and susceptible birds or by
: chicken pox (not to be confused with
mosquitos. Virus-containing scabs also can be
chicken pox in humans; the human disease does not
sloughed from affected birds and serve as a source of
affect poultry and vice versa), sore head, avian
infection. The virus can enter the blood stream
through the eye, skin wounds, or respiratory tract. Mosquitos become infected from feeding on birds with
: Most poultry -- chickens, turkeys,
fowl pox in their blood stream. There is some
pheasants, quail, ducks, psittacine, and ratites -- of all
evidence that the mosquito remains infective for life.
Mosquitos are the primary reservoir and spreaders offowl pox on poultry ranges. Several species of
: There are two forms of fowl pox. The
mosquito can transmit fowl pox. Often mosquitos
dry form is characterized by raised, wart-like lesions
winter-over in poultry houses so, outbreaks can occur
on unfeathered areas (head, legs, vent, etc.). The
lesions heal in about 2 weeks. If the scab is removed
This document is Fact Sheet PS-47, one of a series of the Dairy and Poultry Sciences, Florida Cooperative Extension Service, Institute of Food and Agricultural
Sciences, University of Florida. First published: May 1999. Please visit the EDIS Website at http://edis.ifas.ufl.edu
G.D. Butcher, extension poultry veterinarian, Faculty of Veterinary Medicine, J.P. Jacob, poultry extension coordinator, and F. B. Mather, poultry extensionspecialist, Dairy and Poultry Sciences Department, Cooperative Extension Service, Institute of Food and Agricultural Sciences, University of Florida,Gainesville, 32611.
The use of trade names in this publication is solely for the purpose of providing specific information. It is not a guarantee or warranty of the products named, anddoes not signify that they are approved to the exclusion of others of suitable composition.
The Institute of Food and Agricultural Sciences is an equal opportunity/affirmative action employer authorized to provide research,educational information and other services only to individuals and institutions that function without regard to race, color, sex, age,handicap, or national origin. For information on obtaining other extension publications, contact your county Cooperative ExtensionService office. Florida Cooperative Extension Service / Institute of Food and Agricultural Sciences / University of Florida / ChristineTaylor Waddill, Dean
: No treatment is available. However, fowl
in the egg, but Newcastle-infected embryos die before
pox is relatively slow-spreading. Thus, it is possible
hatching. In live birds, the virus is shed in body
to vaccinate to stop an outbreak. The wing-web
fluids, secretions, excreta, and breath.
vaccination method is used for chickens and the thigh-stick method for turkeys older than 8 weeks.
There is no specific treatment for
Newcastle disease. Antibiotics can be given for 3-5
Fowl pox outbreaks in poultry confined
days to prevent secondary bacterial infections
to houses can be controlled by spraying to kill
(particularly E. coli
). For chicks, increasing the
mosquitos. However, if fowl pox is endemic in the
brooding temperature 5F may help reduce losses.
area, vaccination is recommended. Do not vaccinateunless the disease becomes a problem on a farm or in
Prevention programs should include
the area. Refer to the publication PS-36 (Vaccination
vaccination (see publication PS-36, Vaccination of
of Small Poultry Flocks) for more information on fowl
Small Poultry Flocks), good sanitation, and
implementation of a comprehensive biosecurityprogram.
IB, bronchitis, cold
Newcastle disease is known as viscerotropic (attacks
Infectious bronchitis is a disease of
the internal organs) velogenic Newcastle disease,
chickens only. A similar disease occurs in bobwhite
VVND, exotic Newcastle disease, or Asiatic
quail (quail bronchitis), but it is caused by a different
Newcastle disease. VVND is not present in the United
States poultry industry at this time.
The severity of infectious bronchitis
Newcastle disease affects all birds
infection is influenced by the age and immune status
of all ages. Humans and other mammals are also
of the flock, by environmental conditions, and by the
susceptible to Newcastle. In such species, it causes a
presence of other diseases. Feed and water
consumption declines. Affected chickens will bechirping, with a watery discharge from the eyes and
There are three forms of Newcastle
nostrils, and labored breathing with some gasping in
disease -- mildly pathogenic (lentogenic), moderately
young chickens. Breathing noises are more noticeable
pathogenic (mesogenic) and highly pathogenic
at night while the birds rest. Egg production drops
(velogenic). Newcastle disease is characterized by a
dramatically. Production will recover in 5 or 6 weeks,
sudden onset of clinical signs which include hoarse
but at a lower rate. The infectious bronchitis virus
chirps (in chicks), watery discharge from nostrils,
infects many tissues of the body, including the
labored breathing (gasping), facial swelling, paralysis,
reproductive tract (see Table 1). Eggshells become
trembling, and twisting of the neck (sign of central
rough and the egg white becomes watery. (See
nervous system involvement). Mortality ranges from
publication PS-24, Egg Quality, for other causes of
10 to 80 percent depending on the pathogenicity. In
adult laying birds, symptoms can include decreasedfeed and water consumption and a dramatic drop in
Infectious bronchitis is a very
contagious poultry disease. It is spread by air, feedbags, infected dead birds, infected houses, and
The Newcastle virus can be
rodents. The virus can be egg-transmitted, however,
transmitted short distances by the airborne route or
affected embryos usually will not hatch.
introduced on contaminated shoes, caretakers, feeddeliverers, visitors, tires, dirty equipment, feed sacks,
There is no specific treatment for
crates, and wild birds. Newcastle virus can be passed
infectious bronchitis. Antibiotics for 3-5 days may aid
in combating secondary bacterial infections. Raise the
room temperature 5F for brooding-age chickens untilsymptoms subside. Baby chicks can be encouraged to
AI, flu, influenza, fowl plague
Avian influenza can occur in most,
Establish and enforce a biosecurity
program. Vaccinations are available.
Avian influenza is categorized as mild
or highly pathogenic. The mild form produces
listlessness, loss of appetite, respiratory distress,
diarrhea, transient drops in egg production, and lowmortality. The highly pathogenic form produces facial
Bobwhite quail are affected.
swelling, blue comb and wattles, and dehydration with
Japanese corturnix quail are resistant. The disease is
respiratory distress. Dark red/white spots develop in
prevalent in the southern states where bobwhite quail
the legs and combs of chickens. There can be blood-
are common. Quail bronchitis occurs seasonally as
tinged discharge from the nostrils. Mortality can range
new hatches and broods come along each year.
from low to near 100 percent. Sudden exertion addsto the total mortality. Egg production and hatchability
Respiratory distress occurs with
decreases. There can be an increase in production of
tracheal rales (rattles), sneezing, and coughing. Feed
soft-shelled and shell-less eggs (see Table 1).
and water consumption declines dramatically. Therecan also be conjunctivitis (inflammation of the eye).
The avian influenza virus can remain
Loose watery feces are seen in older and sub-acutely
viable for long periods of time at moderate
affected birds. Nasal discharges are not seen,
temperatures and can live indefinitely in frozen
differentiating quail bronchitis from similar diseases in
material. As a result, the disease can be spread
through improper disposal of infected carcasses andmanure. Avian influenza can be spread by
Once infected, quail bronchitis
contaminated shoes, clothing, crates, and other
remains on the farm for the duration of the breeding
equipment. Insects and rodents may mechanically
season, infecting each successive brood.
carry the virus from infected to susceptible poultry.
There is no specific treatment against
There is no effective treatment for avian
quail bronchitis. Quail bronchitis infections are often
influenza. With the mild form of the disease, good
complicated by concurrent mycoplasma infections.
husbandry, proper nutrition, and broad spectrum
Antibiotics can be used to combat secondary
antibiotics may reduce losses from secondary
infections. Add tylosin (500g/ton) to the feed for 10
infections. Recovered flocks continue to shed the
days, withhold the medication for 5 days, and then
virus. Vaccines may only be used with special permit.
repeat medication for 5 days. Alternate medicationregimens are tylosin (Tylan) or erythromycin
A vaccination program used in
(Gallimycin) in the drinking water for the same period
conjunction with a strict quarantine has been used to
control mild forms of the disease. With the morelethal forms, strict quarantine and rapid destruction of
There is no commercial vaccine on the
all infected flocks remains the only effective method
market. It is necessary to break the cycle by
of stopping an avian influenza outbreak. If you
depopulating and thoroughly cleaning and disinfecting
suspect you may have Avian Influenza in your flock,
pens and equipment, followed by a 30-90 day
even the mild form, you must report it to the state
veterinarian’s office. A proper diagnosis of avianinfluenza is essential. Aggressive action isrecommended even for milder infections as this virushas the ability to readily mutate to a more pathogenicform.
For more information on avian influenza, refer to
Good management and sanitation are the
publication PS-38 (Avian Influenza in Poultry
best ways to avoid infectious coryza. Most outbreaks
occur as a result of mixing flocks. All replacementbirds on “coryza-endemic” farms should bevaccinated. The vaccine (Coryza-Vac) is administered
subcutaneously (under the skin) on the back of the
roup, cold, coryza
neck. Each chicken should be vaccinated four times,starting at 5 weeks of age with at least 4 weeks
chickens, pheasants, and guinea
between injections. Vaccinate again at 10 months of
fowl. Common in game chicken flocks.
Swelling around the face, foul
smelling, thick, sticky discharge from the nostrils andeyes, labored breathing, and rales (rattles -- an
LT, ILT, trach, laryngo
abnormal breathing sound) are common clinical signs. The eyelids are irritated and may stick together. The
Chickens and pheasants are
birds may have diarrhea and growing birds may
affected by LT. Chickens 14 weeks and older are
more susceptible than young chickens. Most LToutbreaks occur in mature hens. In recent years, LT
Mortality from coryza is usually low, but
has also caused significant respiratory problems in
infections can decrease egg production and increase
broilers greater than 3 weeks of age, especially during
the incidence and/or severity of other diseases.
the cooler seasons of the year. This is believed to be
Mortality can be as high as 50 percent, but is usually
due to unwanted spread of LT vaccines between
no more than 20 percent. The clinical disease can last
from a few days to 2-3 months, depending on thevirulence of the pathogen and the existence of other
The clinical sign usually first noticed
is watery eyes. Affected birds remain quiet becausebreathing is difficult. Coughing, sneezing, and
Coryza is primarily transmitted by
shaking of the head to dislodge exudate plugs in the
direct bird-to-bird contact. This can be from infected
windpipe follow. Birds extend their head and neck to
birds brought into the flock as well as from birds
facilitate breathing (commonly referred to as “pump
which recover from the disease which remain carriers
handle respiration”). Inhalation produces a wheezing
of the organism and may shed intermittently
and gurgling sound. Blood-tinged exudates and serum
throughout their lives. Birds risk exposure at poultry
clots are expelled from the trachea of affected birds.
shows, bird swaps, and live-bird sales. Inapparent
Many birds die from asphyxiation due to a blockage of
infected adult birds added into a flock are a common
the trachea when the tracheal plug is freed (see Table
source for outbreaks. Within a flock, inhalation of
airborne respiratory droplets, and contamination offeed and/or water are common modes of spread.
LT is spread by the respiratory route.
LT is also spread from flock to flock by contaminated
Water soluble antibiotics or antibacterials
clothing, shoes, tires, etc. Birds that recover should be
can be used. Sulfadimethoxine (Albon®, Di-
considered carriers for life. LT may be harbored in
Methox™) is the preferred treatment. If it is not
speciality poultry such as exhibition birds and game
available, or not effective, sulfamethazine (Sulfa-
Max®, SulfaSure™), erythromycin (gallimycin®), ortetracycline (Aureomycin®) can be used as alternative
Incinerate dead birds, administer
treatments. Sulfa drugs are not FDA approved for
antibiotics to control secondary infection, and
pullets older than 14 weeks of age or for commercial
vaccinate the flock. Mass vaccination by spray or
layer hens. While antibiotics can be effective in
drinking water method is not recommended for large
reducing clinical disease, they do not eliminate carrier
commercial or caged flocks. Individual bird
administration by the eye-drop route is suggested.
Affected species include turkeys,
Follow manufacturers instructions. In small poultry
pigeons, ducks, psittacine (curve-beaked) birds,
flocks, use a swab to remove plug from gasping birds,
captive and aviary birds, many other bird species, and
other animals. Chickens are not commonly affected. Humans are susceptible, especially older and
Vaccinate replacement birds for outbreak
immunosuppressed individuals who are at a higher
farms. Vaccination for LT is not as successful as for
risk. Chlamydiosis in humans is an occupational
other disease, but is an excellent preventive measure
disease of turkey growers, haulers, and processing
for use in outbreaks and in epidemic areas. Refer to
workers in the live-bird areas and of workers in pet-
the publication PS-36 (Vaccination of Small Poultry
bird aviaries although the incidence is rare. For more
Flocks) for more information on LT vaccinations.
information, refer to publication PS-23 (AvianDiseases Transmissible to Humans).
Clinical signs in most birds include
TRT, rhino tracheitis
nasal-ocular discharge, conjunctivitis, sinusitis,diarrhea, weakness, loss of body weight, and a
Turkeys of all ages are susceptible,
reduction in feed consumption. In turkeys there is also
but the disease is most severe in young poults.
respiratory distress and loose yellow to greenish-
Chickens are susceptible to the virus. Experimentally,
yellow colored droppings. Chylamydiosis runs rather
guinea fowl and pheasants are susceptible, but
slowly through turkey flocks, with a maximum
waterfowl and pigeons are resistant.
incidence of around 50 percent (see Table 1).
Respiratory signs in poults include
The primary means of transmission is
snicking, rales, sneezing, nasal exudates (often frothy),
through inhalation of fecal dust and respiratory tract
foamy conjunctivitis, and sinusitis. Drops in egg
secretions. It can also be transmitted on contaminated
production can be as much as 70 percent (see Table 1).
clothing and equipment. Recovered birds remaincarriers and will continue to intermittently shed the
Spread is primarily by contact with
infective agent for long periods after clinical signs
contaminated environments, feed and water, recovered
have subsided. Environmental stress may provoke a
No drugs are available to combat the
Chlorotetracycline can be given in the
virus. Antibiotic therapy is recommended to control
feed (200-400 g/ton) for 3 weeks. Other antibiotics
are usually ineffective. Recovered birds are safe forprocessing. Permanent lesions on the heart and liver
No vaccines are currently available.
are not infectious. FDA withdrawal periods for
Prevention is dependent on a comprehensive
medications used must be strictly observed to avoid
There is no vaccine. Have a good
biosecurity program, excluding wild birds as much as
ornithosis, psittacosis, parrot fever.
The disease was called psittacosis or parrot fever
Swollen Head Syndrome
when diagnosed in psittacine (curve-beaked) birds,and called ornithosis when diagnosed in all other birds
Facial cellulitis, thick head, Dikkop, SHS
or in humans. Currently, the term chlamydiosis isused to describe infections in any animal.
Chickens and turkeys are the
known natural hosts. Experimentally, guinea fowl and
pheasants are susceptible but pigeons, ducks, and
geese are resistant to the infection. SHS does not
presently occur in the United States, but is present in
swollen, and the exudate becomes caseous and firm.
The birds have respiratory rales and showunthriftiness.
In chicks and poults, there is initial
sneezing, followed by reddening and swelling of the
With the “lower form”, infected turkeys develop
tear ducts and eye tissue. Facial swelling will extend
airsacculitis. As with chickens, birds can show no
over the head and down the jaw and wattles. Adult
outward signs if the infection is uncomplicated. Thus,
chickens have mild respiratory disease followed by a
the condition may go unnoticed until the birds are
few birds having swollen heads. Other signs include
slaughtered and the typical legions are seen. Birds
disorientation, twisting of the neck, and a significant
drop in egg production (see Table 1).
MG in chicken embryos can cause dwarfing,
The infection spreads by direct contact
with infected birds or indirectly by exposure toinfectious material.
MG can be spread to offspring
through the egg. Most commercial breeding flocks,
There is no proven medication for swollen
however, are MG-free. Introduction of infected
head syndrome. The disease is caused by a virus
replacement birds can introduce the disease to MG-
classified as a pneumovirus. A disease closely
negative flocks. MG can also be spread by using MG-
mimicking SHS is caused by a mixed infection of
respiratory viruses and specific bacteria. Antibiotictherapy may be helpful against the bacterial
: Outbreaks of MG can be controlled with
the use of antibiotics. Erythromycin, tylosin,spectinomycin, and lincomycin all exhibit anti-
A commercial vaccine is available.
mycoplasma activity and have given good results.
Swollen head syndrome is considered an exotic
Administration of most of these antibiotics can be by
disease and a live vaccine is not approved for use in
feed, water or injection. These are effective in
reducing clinical disease. However, birds remaincarriers for life.
Eradication is the best control of
MG, chronic respiratory disease (CRD),
Improvement Plan monitors all participating chickenand turkey breeder flocks.
chickens, turkeys, pigeons, ducks,
peafowl and passerine birds.
Clinical symptoms vary slightly
MS, infectious synovitis, synovitis, silent
between species. Infected adult chickens may show
no outward signs if infection is uncomplicated.
However, sticky, serous exudate from nostrils, foamy
chickens and turkeys.
exudate in eyes, and swollen sinuses can occur,
especially in broilers. The air sacs may become
Birds infected with the synovitis form
infected. Infected birds can develop respiratory rales
show lameness, followed by lethargy, reluctance to
and sneeze. Affected birds are often stunted and
move, swollen joints, stilted gait, loss of weight, and
formation of breast blisters. Birds infected with therespiratory form exhibit respiratory distress. Greenish
There are two forms of this disease in the turkey.
diarrhea is common in dying birds (see Table 1).
With the “upper form” the birds have watery eyes and
Clinically, the disease in indistinguishable from MG.
nostrils, the infraorbitals (just below the eye) become
MS is transmitted from infected
breeder to progeny via the egg. Within a flock, MS isspread by direct contact with infected birds as well as
brooder pneumonia, mycotic pneumonia,
through airborne particles over short distances.
fungal pneumonia, Aspergillus
. When the source ofthe disease is the hatchery, the disease is called
Recovery is slow for both respiratory and
brooder pneumonia. In older birds, the disease is
synovitis forms. Several antibiotics are variably
effective. The most effective are tylosin, erthromycin,spectinomycin, lincomycin, and chlorotectracycline.
All birds (domestic poultry,
These antibiotics can be given by injection while some
pigeons, canary and zoo bird species), animals,
can be administered in the feed or drinking water.
These treatments are most effective when theantibiotics are injected.
Aspergillosis occurs as an acute
disease of young birds and a chronic disease in mature
Eradication is the best and only sure
birds. Young birds have trouble breathing and gasp
control. Do not use breeder replacements from flocks
for air. Characteristically, there are no rales or
that have had MS. The National Poultry Improvement
respiratory sounds associated with aspergillosis. Feed
consumption decreases. Occasionally there isparalysis or convulsions caused by the fungal toxin.
Mortality in young birds averages 5-20 percent, butmay be as high as 50 percent. Mature birds also have
MM, N strain, H strain
respiratory distress, reduced feed consumption, andmay have a bluish and dark color of the skin
MM affects turkeys of all ages,
(cyanosis). Nervous disorders, such as twisted necks,
although poults are affected more severely than mature
may occur in a few birds (see Table 1). Mortality in
turkeys. Recently, MM has been shown to infect
mature birds is usually less than 5 percent.
Aspergillosis is caused by a fungus.
A drop-off in production and
The fungus grows well at room temperature and
hatchability can be expected in breeder flocks. There
higher. All litter and nest materials (peat moss, peanut
can be very high mortality in young poults.
hulls, sawdust, peat, bark, straw) have been known to
Unthriftiness, respiratory distress, stunting, crooked
have been contaminated with aspergillus. Feed and
neck with deformity of cervical vertebrae, and leg
water should be suspect when attempting to identify
deformation are common in young birds (see Table 1).
Egg transmission is low in the early
There is no cure for infected birds. The
breeding period, but rises as the the age of the flock
spread can be controlled by improving ventilation,
increases. Infections can be introduced into a flock by
eliminating the source of the infection, and adding a
contaminated equipment, shoes, and clothing of
fungistat (mycostatin, mold curb, sodium or calcium
propionate, or gentian violet) to the feed and/or coppersulfate or acidified copper in the drinking water for 3
Several antibiotics have been effective
days. The litter can be sprayed lightly with an oil-base
including tylosin, erythromycin, spectinomycin, and
germicide to control dust and air movement of fungal
The best preventive measure is to keep
It is important to thoroughly clean and
MM-free breeders. The MM-free status of breeders
disinfect the brooding area between broods. Use only
can be confirmed by periodic blood tests through the
clean litter, preferably soft wood shavings. Do not use
sawdust, litter high in bark content, or shavings thathave been wet.
clinical signs are not noticeable until the birds are 16
Viral Diseases (nonrespiratory)
weeks or older. Affected birds become progressivelyweaker and emaciated. There is regression of the
comb. The abdomen becomes enlarged. Greenish
acute leukosis, neural leukosis, range
diarrhea develops in terminal stages (see Table 2).
The virus is transmitted through the
Chickens between 12 to 25 weeks
egg to offspring. Within a flock, it is spread by bird-
of age are most commonly clinically affected.
to-bird contact and by contact with contaminated
Occasionally pheasants, quail, game fowl and turkeys
environments. The virus is not spread by air. Infected
Marek’s disease is a type of avian
cancer. Tumors in nerves cause lameness andparalysis. Tumors can occur in the eyes and cause
The virus is present in the yolk and egg
irregularly shaped pupils and blindness. Tumors of
white of eggs from infected hens. Most national and
the liver, kidney, spleen, gonads, pancreas,
international layer breeders have eradicated lymphoid
proventriculus, lungs, muscles, and skin can cause
leukosis from their flocks. Most commercial chicks
incoordination, unthriftiness, paleness, weak labored
are lymphoid-leukosis negative because they are
breathing, and enlarged feather follicles. In terminal
hatched from LL-free breeders. The disease is still
stages, the birds are emaciated with pale, scaly combs
and greenish diarrhea (see Table 2).
Infectious Bursal Disease
Marek’s disease is very similar to Lymphoid
Leukosis, but Marek’s usually occurs in chickens 12 to
Gumboro, IBD, infectious bursitis,
25 weeks of age and Lymphoid Leukosis usually starts
The Marek’s virus is transmitted by
air within the poultry house. It is in the feather
In affected chickens greater than 3
dander, chicken house dust, feces and saliva. Infected
weeks of age, there is usually a rapid onset of the
birds carry the virus in their blood for life and are a
disease with a sudden drop in feed and water
source of infection for susceptible birds.
consumption, watery droppings leading to soiling offeathers around the vent, and vent pecking. Feathers
appear ruffled. Chicks are listless and sit in a hunchedposition. Chickens infected when less than 3 weeks of
Chicks can be vaccinated at the hatchery.
age do not develop clinical disease, but become
While the vaccination prevents tumor formation, it
severely and permanently immunosuppressed (see
does not prevent infection by the virus.
The virus is spread by bird-to-bird
contact, as well as by contact with contaminated
visceral leukosis, leukosis, big liver, LL
people and equipment. The virus is shed in the birddroppings and can be spread by air on dust particles.
Although primarily a disease of
Dead birds are a source of the virus and should be
chickens, lymphoid leukosis can infect turkeys, guinea
fowl, pheasants, and doves, but not on a large scale.
There is no specific treatment.
The virus involved has a long
Antibiotics, sulfonamides, and nitrofurans have little
incubation period (4 months or longer). As a result,
or no effect. Vitamin-electrolyte therapy is helpful.
High levels of tetracyclines are contraindicated
50-foot strip around bird pens. This removes cover
because they tie up calcium, thereby producing rickets.
and resting areas for mosquitos. Eliminate mosquito
Surviving chicks remain unthrifty and more
breeding areas. Fog areas with malathion.
susceptible to secondary infections because ofimmunosuppression.
It is possible to immunize birds, especially
pheasants, with the vaccine prepared for horses. The
A vaccine is commercially available.
recommended dose is one-tenth of a horse dose perbird.
EE, EEE, WEE
Note: This disease should not be confused with St.
epidemic tremor, AE
Louis Encephalits (SLE). Chickens are used assentinels (test animals) in SLE suspect areas, such as
The disease is most prevalent in
southern Florida. While SLE is also carried by
chickens less than 6 weeks of age. Pheasants,
mosquitos, that is where the similarities between the
corturnix quail, and turkeys are natural hosts as well,
two encephalitis diseases end. Chickens do not get
but less susceptible than chickens. Ducklings, young
pigeons, and guinea fowl can be experimentally
Encephalitis - The Role of Chickens) for more
Signs commonly appear during the
Equine encephalitis is a contagious
first week of life and between the second and third
disease of birds (especially pheasants), mammals
weeks. Affected chicks may first show a dull
(especially horses), and people. Birds are the major
expression of the eyes, followed by progressive
incoordination, sitting on hocks, tremors of the headand neck, and finally paralysis or prostration. Affected
Two forms affect birds: eastern equine
chicks are inactive. Some may refuse to walk or will
encephalitis (EEE) and western equine encephalitis
walk on their hocks. In advanced cases, many chicks
(WEE). The clinical signs are identical and include
will lie with both feet out to one side (prostrate) and
reduced feed consumption, staggering, and paralysis.
die. All stages (dullness, tremors, prostration) can
Surviving birds may be blind, have muscle paralysis,
usually be seen in an affected flock. Feed and water
and have difficulty holding their head up. Damage to
consumption decreases and the birds lose weight. In
the bird’s nervous system varies with species. In
adult birds, a transitory drop (5-20 percent) in egg
pheasants, there is pronounced leg paralysis, twisting
production may be the only clinical sign present.
of the neck, and tremors. Mortality is high. Chukar
However, in breeding flocks, a corresponding decrease
partridges and turkeys show drowsiness, paralysis,
in hatchability is also noted as the virus is egg-
transmitted until hens develop immunity. Chickenswhich survive the clinical disease may develop
Infected mosquitoes are the primary
cataracts later in life (see Table 2).
source of the virus. The Culiseta melanuria
mosquitois the primary transmitter of the virus to poultry.
The virus can be transmitted through
Other mosquito species transmit the disease too, but
the egg from infected hen to chick, accounting for
feed mostly on other animals. Cannibalism of sick or
disease during the first week of life. The disease can
dead birds by penmates is a major source of
also be spread through a flock by direct contact of
susceptible hatchlings with infected birds, accountingfor the disease at 2-3 weeks of age. Indirect spread
can occur through fecal contamination of feed andwater. Recovered birds are immune and do not spread
Remove the source of infection by
establishing mosquito control: keep weeds mowed in a
There is no treatment for outbreaks.
The principal sign of tenosynovitis
Infected birds should be removed, killed and
with swelling of the tendon sheaths of the shank and
incinerated. Recovered chicks are unthrifty.
area extending above the hock (see Table 2). Affectedbirds are lame, sit on their hocks, and are reluctant to
A vaccine is available.
move. Rupture of the tendon can occur in olderroaster birds, resulting in permanent lameness of the
Egg Drop Syndrome
affected leg. If more than two joints are affected, theentire carcass will be condemned.
egg drop, egg drop syndrome 76, EDS-76
Infection can also play a part in broiler stunting,
The natural hosts for EDS virus are
the result of malabsorption syndrome. In chicks,
ducks and geese, but EDS has become a major cause
malabsorption due to viral enteritis is called
of reduced egg production in chickens in many parts
“helicopter disease” because feathering is affected.
of the world. No illness has been observed in ducks or
Wing feathers protrude at various angles. A reovirus is
geese. Chickens of all ages and breeds are susceptible.
believed to play only a secondary role in this
The disease is most severe in broiler-breeders and
In commercial layer flocks, increased mortality
There are no reliable signs other than
may be the first sign of the septicemia form
the effects on egg production and egg quality.
Table 2). Egg production will decrease by about two
Healthy-appearing hens start laying thin-shelled and
to three times the mortality rate. For example, a
shell-less eggs. Once established, the condition results
mortality rate of 5 percent will be accompanied by a
in a failure to achieve egg production targets.
10-15 percent drop in egg production. In the
Transient diarrhea and dullness occur prior to egg
septicemic form, joint involvement is present but less
shell changes. Fertility and hatchability are not
pronounced. Affected birds become cyanotic (blue)
and dehydrated. The tips of the comb turn purplish.
The entire comb darkens as the disease progresses (see
It is believed that the syndrome was
first introduced into chickens from contaminatedvaccine. Vertical transmission occurs from infected
The infection spreads rapidly through
breeders to chicks. Newly hatched chicks excrete the
broiler flocks, but less rapidly in caged layers. Spread
is by respiratory and digestive tract routes. The virusis shed in the feces.
There is no successful treatment. Induced
molting will restore egg production.
There is no satisfactory treatment
available. With hens, tetracycline, molasses, and
Prevention involves a good biosecurity
A vaccine is available for use in endemic
viral arthritis, tenosynovitis, teno,
Nonrespiratory Bacterial Diseases
reovirus enteritis, reovirus septicemia, malabsorptionsyndrome, helicopter disease
turkeys and chickens
avian pasteurellosis, cholera, avian
Several serotypes of the reovirus have
been identified. Some localize in the joints
Domestic fowl of all species
(tenosynovitis) while others target respiratory or
(primarily turkeys and chickens), game birds
intestinal tissues (septicemic form) (see Table 2).
(especially pheasants and ducks), cage birds, wild
Infection occurs at the time of
birds, and birds in zoological collections and aviaries
hatching or shortly thereafter, before navels are
healed. Chicks from dirty hatching eggs or eggs withpoor quality shells, or newly hatched chicks placed in
Fowl cholera usually strikes birds
dirty holding boxes, are most susceptible. Chicks
older than 6 weeks of age. In acute outbreaks, dead
removed prior to complete healing of the navel due to
birds may be the first sign. Fever, reduced feed
improper temperature and/or humidity are also more
consumption, mucoid discharge from the mouth,
susceptible. Eggs that explode in the hatching tray
ruffled feathers, diarrhea, and labored breathing may
contaminate other eggs in the tray and increase the
be seen. As the disease progresses birds lose weight,
become lame from joint infections, and developrattling noises from exudate in air passages. As fowl
There is no specific treatment for
cholera becomes chronic, chickens develop abscessed
omphalitis. Most affected birds die in the first few
wattles and swollen joints and foot pads. Caseous
days of life. Unaffected birds need no medication.
exudate may form in the sinuses around the eyes. Turkeys may have twisted necks (see Table 3).
Control is by prevention through
effective hatchery sanitation, hatchery procedures,
Multiple means of transmission have
breeder flock surveillance, and proper preincubation
been demonstrated. Flock additions, free-flying birds,
handling of eggs. Mushy chicks should be culled from
infected premises, predators, and rodents are all
the hatch and destroyed. If chick mortality exceeds 3
percent, the breeder flocks and egg handling andhatching procedures should be reviewed.
A flock can be medicated with a sulfa
drug (sulfonamides, especially sulfadimethoxine,
sulfaquinonxalene, sulfamethazine, andsulfaquinoxalene) or vaccinated, or both, to stop
bacillary white diarrhea, BWD
mortality associated with an outbreak. It must benoted, however, that sulfa drugs are not FDA
Chickens and turkeys are most
approved for use in pullets older than 14 weeks or for
susceptible, although other species of birds can
commercial laying hens. Sulfa drugs leave residues in
become infected. Pullorum has never been a problem
meat and eggs. Antibiotics can be used, but require
in commercially grown game birds such as pheasant,
higher levels and long term medication to stop the
chukar partridge and quail. Infection in mammals is
On fowl cholera endemic farms,
Death of infected chicks or poults
vaccination is advisable. Do not vaccinate for fowl
begins at 5-7 days of age and peaks in another 4-5
cholera unless you have a problem on the farm.
days. Clinical signs including huddling, droopiness,
Rodent control is essential to prevent future outbreaks.
diarrhea, weakness, pasted vent, gasping, and chalk-white feces, sometimes stained with green bile.
Affected birds are unthrifty and stunted because theydo not eat (see Table 3). Survivors become
navel ill, mushy chick disease
asymptomatic carriers with localized infection in theovary.
Pullorum is spread primarily through
Affected chicks may have external
the egg, from hen to chick. It can spread further by
navel infection, large unabsorbed yolk sacs, peritonitis
contaminated incubators, hatchers, chick boxes,
with fetid odor, exudates adhering to the navel, edema
houses, equipment, poultry by-product feedstuffs and
of the skin of ventral body area, septicemia and
Treatment is for flock salvage only.
bacitracin, neomycin, and tetracycline. However,
Several sulfonamides, antibiotics, and antibacterials
antibiotics such as penicillin, streptomycin, and
are effective in reducing mortality, but none eradicates
novobiocin are also effective. Bacitracin is the most
the disease from the flock. Pullorum eradication is
commonly used drug for control of necrotic enteritis.
required by law
. Eradication requires destroying the
As with all drugs, legality and withdrawal time
Pullorum outbreaks are handled, on an
Prevention should be directed toward
eradication basis, by state/federal regulatory agencies.
sanitation, husbandry, and management.
As part of the National Poultry Improvement Program,breeder replacement flocks are tested before onset of
production to assure pullorum-free status. Thismandatory law includes chickens, turkeys, show birds,
waterfowl, game birds, and guinea fowl. In Florida, anegative pullorum test or certification that the bird
Captive quail are extremely
originated from a pullorum-free flock is required for
susceptible and must be maintained on wire-bottom
admission for exhibit at shows and fairs. Such
pens or on preventive medications. Chickens, turkeys,
requirements have been beneficial in locating
partridges, grouse, and other species are occasionally
pullorum-infected flocks of hobby chickens.
In quail, the disease is acute with high
mortality. In chickens, signs are less dramatic. Acute
enterotoxemia, rot gut
signs are extreme depression and reduction in feedconsumption. Affected birds sit humped with eyes
Rapidly growing young birds,
closed. Other signs included emaciation, watery
especially chickens and turkeys 2-12 weeks of age, are
droppings streaked with urates, and dull ruffled
most susceptible. Necrotic enteritis is a disease
feathers (see Table 3). Accumulated mortality will
associated with domestication and is unlikely to
reach 50 percent if the flock is not treated.
threaten wild bird populations. Necrotic enteritis isprimarily a disease of broilers, roasters and turkeys.
Birds become infected by direct
Ulcerative enteritis, on the other hand, commonly
contact with carrier birds, infected droppings or
contaminated pens, feed and water. Bacteria arepassed in the droppings of sick and carrier birds.
Initially there is a reduction in feed
Infection can be spread mechanically on shoes, feed
consumption as well as dark, often blood-stained,
bags, equipment, and from contamination by rodents
feces. Infected chickens will have diarrhea.
Chronically affected birds become emaciated. Thebird, intestines, and feces emit a fetid odor (see Table
Bacitracin and neomycin can be used
singly or in combination. Other antibiotics and drugssuch as tetracyclines, penicillin, Lincomycin, and
Necrotic enteritis does not spread
Virginomycin are also effective. Consult a
directly from bird to bird. Bacteria are ingested along
veterinarian for dose, route, and duration of treatment.
with infected soil, feces, or other infected materials.
The bacteria then grow in the intestinal tract.
Ulcerative enteritis is difficult to prevent
Infection commonly occurs in crowded flocks,
in quail. When quail have access to their own
immuno-suppressed flocks, and flocks maintained in
droppings, this disease commonly occurs. To
eradicate, depopulate stock, thoroughly clean anddisinfect, and start over with young, clean stock.
The clostridia bacteria involved in
necrotic enteritis is sensitive to the antibiotics
limberneck, bulbar paralysis, western
staph infection, staph septicemia, staph
All fowl of any age, humans, and
All fowl, especially turkeys,
other animals are highly susceptible. The turkey
chickens, game birds, and waterfowl, are susceptible.
vulture is the only animal host known to be resistant tothe disease.
Staphylococcal infections appear in
three forms -- septicemia (acute), arthritic (chronic),
Botulism is a poisoning causing by
and bumblefoot. The septicemia form appears similar
eating spoiled food containing a neurotoxin produced
to fowl cholera in that the birds are listless, without
by the bacterium Clostridium botulinum
appetite, feverish, and show pain during movement.
the most common clinical sign, occurs within a few
Black rot may show up in eggs (the organism is passed
hours after poisoned food is eaten. Pheasants with
in the egg). Infected birds pass fetid watery diarrhea.
botulism remain alert, but paralyzed. Legs and wings
Many will have swollen joints (arthritis) and
become paralyzed, then the neck becomes limp. Neck
feathers become loose in the follicle and can be pulledeasily (see Table 3).
The arthritic form follows the acute form. Birds
show symptoms of lameness and breast blisters, as
If the amount eaten is lethal, prostration and death
well as painful movement (see Table 3). Birds are
follow in 12 to 24 hours. Death is a result of paralysis
reluctant to walk, preferring to sit rather than stand.
of respiratory muscles. Fowl affected by sublethaldoses become dull and sleepy.
Bumblefoot is a localized chronic staph infection
of the foot, thought to be caused by puncture injuries.
Botulism is common in wild ducks
The bird becomes lame from swollen foot pads (see
and is a frequent killer of waterfowl because the
organisms multiply in dead fish and decayingvegetation along shorelines.
Transmission: Staphylococcus aureus
and outbreaks in flocks often occur after storms when
Decaying bird carcasses on poultry ranges, wet
birds on range drink from stagnant rain pools.
litter or other organic matter, and fly maggots fromdecaying substances may harbor botulism. There is no
Novobiocin (350 g/ton) can be given in
the feed for 5-7 days. Erythromycin and penicillin canbe administered in the water for 3-5 days or in the feed
Remove spoiled feed or decaying matter.
(200 g/ton) for 5 days. Other antibiotics and drugs are
Flush the flock with Epsom salts (1 lb/1000 hens) in
water or in wet mash. It has been reported thatpotassium permanganate (1:3000) in the drinking
Remove objects that cause injury. Isolate
water is helpful. Affected birds can be treated with
chronically affected birds. Provide nutritionally
Incinerate or bury dead birds promptly.
Do not feed spoiled canned vegetables. Control flies.
Replace suspected feed.
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