Article submitted by Mrs. G
of three to four months of age show resistance to infection. Specimens of this
parasite are found occasionally in eggs. The worm apparently wanders from the
intestine up the oviduct and is included in the egg contents as the egg in being
life history of this parasite is simple and direct. Females lay thick
heavy-shelled eggs in the intestine that pass in the feces. A small embryo
develops in the egg but does not hatch immediately. The larvae in the egg
reaches infective stage within two to three weeks. Embryonated eggs are very
hardy and under laboratory conditions may live for two years. Under ordinary
conditions, however, few probably live more than one year. Disinfectants and
other cleaning agents do not kill eggs under farm conditions. Eating eggs that
have reached the infective stage infects birds.
drugs remove only the adult parasite. The immature form probably produces the
most severe damage. The treatment of choice is piperazine. Many forms of
piperazine are produced, and all are effective if administered properly.
Piperazine is only effective for treating this parasite. It has no effect on
other internal parasites of fowl. Follow the manufacturer's instructions
parasite can be controlled by strict sanitation. If the birds are confined,
clean the house thoroughly and completely before a new group is brought in.
Segregate birds by age groups, with particular care applied to sanitation of
young birds. If birds are on range, use a clean range for each group of birds.
parasite apparently does not seriously affect the health of the bird. At least
no marked symptoms or pathology can be blamed on its presence. Its main
importance is that it has been incriminated as a vector of Histomonas
meleagridis, the agent that causes blackhead. This protozoan parasite
apparently is carried in the cecal worm egg and is transmitted from bird to bird
through this egg.
life history of this parasite is similar to that of the common roundworm. The
eggs are produced in the ceca and pass in the feces. They reach the infective
form in about two weeks. In cool weather, this may take longer. The eggs are
very resistant to environmental conditions and will remain viable for long
cecal worm can be effectively treated with fenbendazole. Since the worm itself
produces no observable damage and the eggs live for long periods, it is
advisable and necessary to keep chickens and turkeys separated to prevent spread
the lower intestinal tract there may be several different species but usually Capillaria
obsignata is the most prevalent. The life cycle of this parasite is direct.
The adult worms may be embedded in the lining of the intestine. The eggs are
laid and passed in the droppings. Following embryonation that takes six to eight
days, the eggs are infective to any other poultry that may eat them. The most
severe damage occurs within two weeks of infection. The parasites frequently
produce severe inflammation and sometimes cause hemorrhage. Erosion of the
intestinal lining may be extensive and result in death. These parasites may
become a severe problem in deep litter houses. Reduced growth, egg production
and fertility may result from heavy infections.
present in large numbers, these parasites are usually easy to find at necropsy.
Eggs may be difficult to find in droppings, due to the small size and time of
treatment for capillaria is often lacking, control is best achieved by
preventive measures. Some drugs, fed at low levels, may be of value in reducing
the level of infection on problem farms. Game birds should be raised on wire to
remove the threat of infection. As some species of capillaria have an indirect
life cycle, control measures may have to be directed toward the intermediate
host. Hygromycin and meldane may be used for control. Additional vitamin A may
be of value. Effective treatments that are not approved by the Food and Drug
Administration are fenbendazole and leviamisole.
pathology or damage tapeworms produce in poultry is controversial. In young
birds, heavy infections result in reduced efficiency and slower growth. Young
birds are more severely affected than older birds.
poultry tapeworms apparently spend part of their lives in intermediate hosts,
and birds become infected by eating the intermediate hosts. These hosts include
snails, slugs, beetles, ants, grasshoppers, earthworms, houseflies and others.
Eating the eggs of tapeworms that are passed in the bird feces infects the
several drugs are used to remove tapeworms from poultry, most are of doubtful
efficacy. In general, preventing the birds from eating the infected intermediate
host most readily controls tapeworms. Tapeworm infections can be controlled by
regular treatment of the bird with fenbendazole or leviamisole.
gapeworm is sometimes designated as the "red-worm"; or
"forked-worm" because of its red color and because the male and female
are joined in permanent copulation. They appear like the letter Y. The female is
the larger of the two and is one-fourth to one inch in length. The male gapeworm
may attain a length of one-fourth inch. Both sexes attach to the lining of the
trachea with their mouthparts. Sufficient numbers may accumulate in the trachea
to hinder air passage.
life cycle of the gapeworm is similar to that of the cecal worm; the parasite
can be transmitted when birds eat embryonated worm eggs or earthworms containing
the gapeworm larvae. The female worm lays eggs in the trachea, the eggs are
coughed up, swallowed, and pass out in the droppings. Within eight to fourteen
days the eggs embryonate and are infective when eaten by birds or earthworms.
The earthworm, snails and slugs serve as primary intermediate hosts for the
gapeworm. Gapeworms in infected earthworms remain viable for four and a half
years while those in snails and slugs remain infective for one year. After being
consumed by the bird, gapeworm larvae hatch in the intestine and migrate from
the intestine to the trachea and lungs.
infect chickens, turkeys, guinea fowl, pheasants, chukar partridge, and probably
other birds. Young birds reared on soil of infected range pens are at high risk
(pen-raised game birds). Some control or reduction in infection density
(worms/bird) is achieved by alternating the use of range pens every other year
and/or using a pen for only one brood each year. Tilling the soil in the pens at
the end of the growing season helps to reduce the residual infection. Treating
the soil to eliminate earthworms, snails and slugs is possible but the cost is
are best prevented by administering a wormer at fifteen to thirty day intervals
or including a drug at low levels continuously beginning fifteen days after
birds are placed in the infected pens. One drug that is effective for
eliminating gapeworms is fenbendazole, however, the Food and Drug Administration
do not presently approve its use for use in birds.
primary concern to the poultryman is the Northern Fowl Mite (Ornithonyssus
sylviarum) which is a frequent and serious pest of chickens. Heavy
infestations result in low condition of the birds and lower egg production, as
well as a scabby skin condition. The mite remains on the bird and does more
damage than any other species of mite. The mite does not leave the host bird, as
do may species of mites, and can be observed on birds in large numbers during
daylight hours. It prefers the feathers below the vent and around the tail, but
can be found on all parts of the body. The mite is extremely small and a
microscope or magnifying glass may be needed to see it.
female northern fowl mite lays eggs on feathers where the young mites complete
their development without leaving the host. Since they remain on the fowl most
of the time, treatment of the birds is necessary to destroy the mites.
Common Chicken Mite (Dermanyssus gallinae) is the most common mite found
on all types of poultry. It is a bloodsucker, and when present in large numbers,
loss of blood and irritation may be sufficient to cause anemia. Egg production
is seriously reduced.
mite feeds at night, and usually remains hidden in cracks and crevices during
the day. It attacks birds at night while they are on the roost. In heavy
infestations, some mites may remain on the birds during the day. About a day
after feeding, the female lays eggs in cracks and crevices of the house. The
eggs hatch and the mites develop into adults within about a week. During cold
weather, the cycle is slower. A poultry house remains infested four to five
months after birds are removed.
the mite feeds on wild birds, these birds may be responsible for spreading
infestations. However, it is more likely that spread of the mite is promoted by
using contaminated coops. Human carriers are also important. Since these mites
do not stay on the birds during the day, apply treatments to houses and
equipment as well as the birds.
Scaly-Leg Mite (Knemidocoptes mutans) lives under the scales on feet and
legs of poultry. It also may attach to the comb and wattles. It causes a
thickening of scales on the feet and legs that give the impression that the
scales are protruding directly outward, rather that laying flat on the limb. It
spends its entire life cycle on the birds and spreads mainly by direct contact.
Depluming Mite (Knemidocoptes laevis, variety gallinae) causes severe
irritation by burrowing into the skin near the bases of feathers and frequently
causes feathers to be pulled out or broken. The mite is barely visible to the
naked eye and can be found in follicles at the base of the feathers. The mites
crawl around the birds at times, spreading from bird to bird.
most effective treatment for all mite species is a regular inspection and
spraying program of both the birds and their premises. An appropriate solution
of permethrin, when sprayed on the birds, will eliminate all mites that infest
the bird. The spraying of all facilities will ensure that any mites hiding in
cracks and crevices will be destroyed. The treatment should be repeated on a one
to two month schedule or whenever populations of the mites are detected.
lice infecting poultry and birds are the chewing type. Mites may be confused
with lice, but mites suck blood. In general, each species of lice is confined to
a particular kind of poultry, although some may pass from one kind to another
when birds are closely associated. Chickens usually are infested with one or
more of seven different species; turkeys have three common species.
species of poultry lice have certain common habits. All live continuously on
feathered hosts and soon die if removed. The eggs are attached to the feathers.
Young lice resemble adults except in color and size. Lice differ in preferred
locations on the host, and these preferences have given rise to the common names
applied to various species.
general, the incubation period of lice eggs is four to seven days, and
development of the lice between hatching and the adult stage requires about
twenty-one days. Mating takes place on the fowl, and egg laying begins two to
three days after lice mature. The number of eggs probably ranges from fifty to
three hundred per female louse.
the name suggests, the Head Louse (Cuclotogaster heterographa) is found
mainly on the head, although it occurs occasionally on the neck and elsewhere.
It usually is located near the skin in the down or at the base of the feathers
on the top and back of the head and beneath the beak. In fact, the head of the
louse often is found so close to the skin that poultrymen may think it is
attached to the skin or is sucking blood. Although it does not suck blood, the
head louse is very irritating and ranks first among lice as a pest of young
chickens and turkeys. Heavily infested chicks soon become droopy and weak and
may die before they are a month old. When the chickens become fairly well
feathered, head lice decrease but may increase again when the fowls reach
louse is oblong, grayish and about 1/10-inch long. The pearly-white eggs are
attached singly to the down or at the base of the small feathers on the head.
They hatch within five days into minute, pale, translucent lice resembling
adults in shape.
Body Louse (Menacanthus stramineus) of chickens prefers to stay on the
skin rather than on the feathers. It chooses parts of the body that are not
densely feathered, such as the area below the vent. In heavy infestations, it
may be found on the breast, under the wings and on other parts of the body,
including the head.
the feathers are parted, straw-colored body lice may be seen running rapidly on
the skin in search of cover. Eggs are deposited in clusters near the base of
small feathers, particularly below the vent, or in young fowls, frequently on
the head or throat. Eggs hatch in about a week and lice reach maturity within
is the most common louse infesting grown chickens. When present in large
numbers, the skin is irritated greatly and scabs may result, especially below
Shaft Louse or small body louse (Menopon gallinae) is similar in
appearance to the body louse, but smaller. It has a habit of resting on the body
feather shafts of chickens where it may be seen running rapidly toward the body
when feathers are parted suddenly. Sometimes as many as a dozen lice may be seen
scurrying down a feather shaft.
the shaft louse apparently feeds on parts of the feathers, it is found in
limited numbers on turkeys, guinea fowl and ducks kept in close association with
chickens. It does not infest young birds until they become well feathered.
same control measures used to eliminate mite populations is effective for
treating lice. It is more important to apply the insecticides directly to the
bird's body rather than the premises.
ticks spend most of their lives in cracks and hiding places, emerging at night
to take a blood meal. Mating takes place in the hiding areas. A few days after
feeding, the female lays a batch of eggs. In warm weather the eggs hatch within
fourteen days. In cold weather they may take up to three months to hatch. Larvae
that hatch from the eggs crawl around until they find a host fowl. They remain
attached to the birds for three to ten days. After leaving the birds they find
hiding places and molt before seeking another blood meal. This is followed by
additional moltings and blood meals.
are difficult to eradicate and methods employed must be performed carefully. It
is not necessary to treat the birds, but houses and surrounding areas must be
usually attach to the wings, breasts and necks of poultry. They inject a
poisonous substance that sets up local irritation and itching. After a few days,
the larvae become engorged and drop off. Injury to grown fowl may not be
apparent or noticed until the bird is dressed; then the lesions are readily
apparent and greatly reduce the carcass value. Young chickens or turkeys may
become droopy, refuse to eat and die. Due to methods of raising poultry, turkeys
are more affected than chickens.
ages can be affected; however, the acute septicemia in young turkeys and
airsacculitis in young chickens is more common in young growing birds. High,
early mortality may occur as the result of navel infections.
symptoms of this disease is caused by the E. coli bacteria and the toxins
produced as they grow and multiply. There are many different strains or
serological types within the group of E. coli bacteria. Many are normal
inhabitants in intestinal tracts of chickens and turkeys and consequently are
common organisms in the birds' environment.
marked variation exists between different strains in their ability to cause
disease. Some are severe and by themselves can cause disease while others are
supposedly harmless. All degrees of pathogenicity exist between the two
primary routes of invasion by the organism are the respiratory system and the
gastrointestinal tract. Omphalitis and infections in young birds may result from
entry through the unhealed navel or penetration of the egg shell prior to or
symptoms vary with the different types of infections. In the acute septicemic
form, mortality may begin suddenly and progress rapidly. Morbidity may not be
apparent and birds in apparently good condition may die. However, in most cases
birds are listless with ruffled feathers and indications of fever. Additional
symptoms of labored breathing, occasional coughing and rales may be apparent.
Diarrhea may be evident. Mortality may be high in recently hatched chicks and
poults as a result of navel infection of coliforms.
acute septicemic infection may result in sudden death with very few, if any,
lesions apparent. Common lesions include dehydration, swelling and congestion of
the liver and spleen and kidneys and pinpoint hemorrhages in the viscera.
Fibrinous to caseous exudate in the air sacs, heart sac and on the surface of
the heart, liver and lungs is a characteristic lesion. The intestines may be
thickened and inflamed and may contain excess mucus and areas of hemorrhage.
Navel infections, similar to those described for omphalitis may be seen in young
by laboratory means is necessary since coliform infection in its various forms
may resemble and be easily confused with many other diseases. Isolation and
identification of the organism by culture procedures can be accomplished
relatively quickly; however, mere isolation is not sufficient to make a
diagnosis. One must take into consideration the organ from which the organisms
were isolated, the pathogenicity of the particular isolate and the presence of
other disease agents.
and sanitation practices designed to reduce the number of these types of
organisms in the birds' environment are necessary. In addition, reducing stress
factors and other disease agents can enhance the ability of birds to defend
against harmful infections. Providing adequate ventilation, good litter and
range conditions, properly cleaned and disinfected equipment and facilities and
high quality feed and water will improve the disease resisting status of the
birds. The poultryman must always avoid overcrowding, environmental stresses
like chilling or overheating and avoid vaccination or handling stress during
periods when the birds are already subjected to stressful conditions. Proper egg
handling, good hatchery management and implementing a good sanitation program is
necessary to reduce early exposure of chicks or poults to disease organisms. It
is always emphasized that problems due to one of the more pathogenic strains may
occur even under ideal conditions.
response of coliform infections to various medications is erratic and often
difficult to evaluate. Under practical conditions, treatment is often
disappointing. Drug sensitivity varies with the strain of E. coli causing
the condition. Laboratory tests to determine the sensitivity to the various
drugs are useful to select the most beneficial drugs. When practical, moving
birds to a clean environment may be of more value than medication. For example,
when outbreaks occur in growing turkeys in the brooder house, moving to range is
often the best treatment.
respiratory disease (CRD), air sac syndrome and infectious sinusitis of turkeys
have a common cause. CRD was first recognized as a chronic but mild respiratory
disease of adult chickens. It reduced egg production but caused little or no
mortality. Afterward, a condition known as "air sac disease" became a
problem in young birds. It caused high mortality in some flocks. Many birds
became stunted, feed efficiency was reduced, and many fowl were rejected as
unfit for human consumption when processed.
sinusitis in turkeys produces a sinus swelling under the eye as well as an
inflammation of respiratory organs. It is a chronic disease adversely affecting
growth and feed conversion. It may also cause significant mortality in young
peculiar bacterial-like organism known as Mycoplasma gallisepticum (MG)
is common to all three conditions. CRD and sinusitis in turkeys are caused by a
pure MG infections while the air sac syndrome is caused by an infection of MG in
combination with E. coli. These conditions are triggered by acute
respiratory infections such as Newcastle disease or infectious bronchitis.
is widespread and affects many species of birds. Eradication programs have
reduced the incidence in recent years. It is primarily spread through the egg.
Infected hens transmit organisms and the chick or poult is infected when it
hatches. Organisms may also be transmitted by direct contact with infected or
true CRD produces slight respiratory symptoms such as coughing, sneezing and a
nasal discharge. In the air sac syndrome there is an extensive involvement of
the entire respiratory system. The air sacs are often cloudy and contain large
amounts of exudate. Affected birds become droopy, feed consumption decreases and
there is a rapid loss of body weight.
sinusitis in turkeys occurs in two forms. When the "upper" form is
present, there is only a swelling of the sinus under the eye. In the
"lower" form, the lungs and air sacs are involved. The air sacs become
cloudy and may contain large amounts of exudate. Both forms of the disease are
usually present in the flock and frequently are present in the same bird.
of either condition must be based on flock history, symptoms and lesions. Blood
tests are useful in determining whether a flock is infected.
answer to the MG problem in both chickens and turkeys is eradication of the
disease organisms. This goal has been achieved in commercial breeding flocks
with voluntary programs conducted by the National Poultry Improvement Plan (NPIP)
and National Turkey Improvement Plan (NTIP). The treatment of CRD, air sac
syndrome and the lower form of infectious sinusitis is not considered
satisfactory. Many antibiotics have been used with varying success. Whether to
give treatment is a decision that must be made on each flock based on economic
factors. If treatment is attempted, give high levels of one of the broad
spectrum antibiotics (Tylosin, aureomycin, terramycin, gallimycin) either in
feed, drinking water or by injections. The "upper"; form of infectious
sinusitis can be treated with success by injecting antibiotics into the swollen
causative organism of fowl cholera is Pasteurella multocida. The organism
can survive at least one month in droppings, three months in decaying carcasses
and two to three months in soil. Pasteurella apparently enters tissues of the
mouth and upper respiratory tract. The disease is not transmitted through the
sources of infection include:
disease is seldom seen in chickens under four months of age, but is commonly
seen in turkeys under this age. In the peracute form, symptoms may be absent; in
the acute form some birds may die without showing symptoms, but many others are
visibly ill before death. Characteristic symptoms include stupor, loss of
appetite, rapid weight loss, lameness resulting from joint infection, swollen
wattles, difficult breathing, watery yellowish or green diarrhea and cyanosis or
darkening of the head and wattles.
may be lacking in birds dying during peracute outbreaks. When present, lesions
may resemble those associated with any acute septicemic bacterial infection,
often those of fowl typhoid. Typical lesions may include pinpoint hemorrhages in
the mucous and serous membranes and/or abdominal fat; inflammation of the upper
third of the small intestine; light, firm "parboiled" appearance of
the liver; enlarged and congested spleen; creamy or solid collection of material
in joints; and cheesy material in the internal ear and air spaces of the cranium
of birds having twisted necks. Turkeys may have pneumonia with solidification of
one or both lungs.
tentative diagnosis may be made on flock history, symptoms and postmortem
lesions. A definite diagnosis depends upon isolation and identification of the
administered bacterins are helpful in preventing fowl cholera, particularly in
turkeys. Their use must be combined with a rigid program of sanitation. In
general, as it applies to the use of bacterins in turkeys, complete protection
is unrealistic. Follow the manufacturer's recommendations for use of the
bacterin. Vaccination in conjunction with treatment is not recommended.
practices that aid in preventing the disease are:
is known about the spread of the disease but transmission is thought to occur by
oral contact with the droppings from infected birds. Necrotic enteritis appears
suddenly in the affected flock. Apparently healthy birds may become acutely
depressed and die within hours. Mortality is usually between two and ten
percent, but may be as high as thirty percent in severe outbreaks. Losses due to
reduced growth and feed conversion may be more costly than flock mortality.
of the disease usually involve the lower half of the small intestine, but in
some instances the entire length of the tract is involved. The intestine is
dilated, contains dark offensive fluid and a diphtheritic cauliflower-like
membrane that involves the mucosa. The lining of the intestine will have a
coarse Turkish-towel appearance and portions of the lining may slough off and
pass out with the intestinal contents. Diagnosis in based upon history, symptoms
and findings of the characteristic lesions.
or virginiamycin are effective treatments administered in the feed. Bacitracin
can also be given in the drinking water. Supportive vitamin treatment may
enhance the effectiveness of the treatments. Preventive medication may be of
value on premises where prior infections have been observed. Since coccidiosis
may be a contributing factor, attention must be given to an effective
coccidiosis control program.
cause of the disease is Clostridium colinum, a spore forming bacterial
rod. The infection spreads by the droppings from sick or carrier birds to
healthy birds. The disease organism is very resistant to disinfectants and will
persist under varying environmental conditions.
with the acute form may die suddenly while in good flesh, whereas more
chronically affected birds become listless, have ruffled feathers, whitish
watery diarrhea, and develop a humped-up posture. Such birds usually die in an
extremely emaciated condition.
dropping may be confused with those of birds with coccidiosis and the two
diseases are often seen in the same bird. Droppings of birds with only
ulcerative enteritis never contain blood.
postmortem lesions are characteristic. The entire intestinal tract often has
button-like ulcers but the lower portion is most often affected. These ulcers
often perforate, resulting in local or generalized peritonitis.
the disease is characteristic in nature, anyone suspecting the infection should
seek professional confirmation before treatment is started. Bacitracin and
penicillin are the most effective drugs in the treatment and prevention of this
disease. If bacitracin is used, it should be incorporated in the feed at levels
up to 200 grams per ton of feed. Addition of bacitracin to the water at the rate
of one teaspoon per gallon aids in controlling an outbreak of the disease.
Either method of administering bacitracin will control the disease within two
weeks, unless a bacitracin-resistant strain of the disease organism is present.
Penicillin is also used to treat the disease if bacitracin is not effective.
birds on wire is an effective preventative measure. Specific drugs (bacitracin
or penicillin) fed at low levels, are effective for controlling the disease in
operations where the use of wire flooring is impractical.
cause is a bacterium named Salmonella pullorum. This organism is
primarily egg transmitted, but transmission may occur by other means such as:
disease is highly fatal to young chicks or poults, but mature birds are more
resistant. Young birds may die soon after hatching without exhibiting any
observable signs. Most acute outbreaks occur in birds that are under three weeks
of age. Mortality in such outbreaks may approach ninety percent if untreated.
Survivors are usually stunted and unthrifty. Infection in young birds may be
indicated by droopiness, ruffled feathers, a chilled appearance with birds
huddling near a source of heat, labored breathing, and presence of a white
diarrhea with a "pasted-down" appearance around the vent. The white
diarrhea symptom instigated the term "bacillary white diarrhea" that
was commonly associated with this disease at one time. Gross lesions may be
lacking in some adult birds.
in young birds is made by isolating the causative organism in the laboratory. In
older birds, blood testing may indicate an infection but a positive diagnosis
depends upon isolation and identification of the organism by laboratory
eradication is the only sound way to prevent pullorum disease. All hatchery
supply flocks should be tested and only pullorum-free flocks used as a source of
hatching eggs. Purchase chicks or poults from hatcheries that are officially
recognized as "Pullorum Clean" by National Poultry Improvement Plan
representatives in your state.
primarily is a salvage operation and does not prevent birds from becoming
carriers. Consequently, do not keep recovered flocks for egg production. Among
the drugs used to treat pullorum disease are furazolidone, gentamycin sulfate,
and sulfa drugs (sulfadimethoxine, sulfamethazine, and sulfamerazine).
cause in the bacterium, Salmonella gallinarum. Methods of transmission
are the same as for pullorum disease, including egg transmission. However,
mechanical transmission is more prevalent with this disease than with pullorum
age bird can be infected, but the disease primarily occurs in young adults
(usually those older than twelve weeks of age). Mortality varies from less than
one to about forty percent, but higher mortality has been observed. Signs
include sudden or sporadic mortality, listlessness, green or yellow diarrhea
(accompanied with pasting of the vent feathers), loss of appetite, increased
thirst and a pale, anemic appearance of comb and wattles.
tentative diagnosis may be made from the history, signs and lesions but final
diagnosis must be based on isolation and identification of the causative
organism. Lesions observed at necropsy help verify a diagnosis of fowl typhoid.
The lesions include an enlarged and mottled spleen, enlarged liver (colored
yellow or greenish brown), small pinpoint hemorrhages in muscles and fat
surrounding internal organs, and a slimy inflammation of the front third of the
small intestine. Small, white plaque-like areas are visible through the walls of
the intestine is suggestive of fowl typhoid in turkeys. Blood tests used to
detect pullorum reactors are also used to identify fowl typhoid birds.
and control depend heavily upon basic disease prevention practices including the
hatching chicks from disease-free flocks (as determined by pullorum testing),
practicing strict sanitation on the farm, providing clean feed and water, and
proper disposal of all dead birds as approved by the state animal health agency.
The causative organism can live outside the bird body for at least six months,
thus requiring extra management precautions to break the disease cycle.
Following an outbreak, thoroughly clean and disinfect the premises. When
feasible, practice range rotation and other special precautions to prevent the
carryover of infection to the following flock.
cannot be depended upon as a means of typhoid prevention and are not recommended
for that purpose. Infected birds may be salvaged using the same drugs as used to
salvage pullorum infected birds.
is not a bacterial infection, but a condition produced by a byproduct of the
bacteria's growth. The organism is common in nature and is widely dispersed in
soils. Ingestion of the organism is not harmful. It becomes dangerous only when
conditions are favorable for its growth and subsequent toxin formation. The
organism grows best under high humidity and relatively high temperature and in
an environment containing decaying organic material (plant or animal). The
organism requires an environment in which all atmospheric oxygen is eliminated.
The organism cannot multiply in the presence of air. Stagnant pools or damp
areas with buried decaying matter are danger areas for toxin development.
Botulism results after the decaying animal or plant material containing the
toxin is consumed. Decaying carcasses are a frequent source of the toxin, as are
many insects feeding in the same tissue. The insects may contain enough toxin to
cause the disease in any bird that ingests it. Since the toxin is water soluble,
water sources may become contaminated and provide a reservoir for the disease.
toxin is one of the most potent discovered by scientists. The toxin is
relatively heat stable but may be destroyed by boiling. There are different
types of the toxin; types A and C cause the disease in birds while type B
frequently produces the disease in man.
is generally the first sign of the illness and is followed by progressive
flaccid paralysis of the legs, wings and neck. When neck muscles are affected
the head hangs limp, thus causing a condition referred to as "limberneck".
Affected birds may have a peculiar trembling, loose feathers that are pulled out
easily and dull partly closed eyes. Some birds (turkey) do not develop loose
feathers or limberneck symptoms. Because of the paralysis, birds are unable to
swallow and mucous accumulates in the mouth. Fatally affected birds may lie in a
profound coma appearing lifeless for several hours before death. Significant
lesions are not usually observed in affected birds. Examining digestive contents
may reveal insects, decomposed animal or vegetable material or other matter
suggesting that the birds have consumed the toxin.
tentative diagnosis can be made from the history, symptoms and post-mortem
findings. As an aid to diagnosis, sick birds may be given water into the crop,
kept in a cool environment and treated intravenously with antitoxin. Recovery of
a large percentage of the affected birds would substantiate diagnosis.
should be aimed at eliminating sources of toxin production and preventing access
of birds to such materials. These practices include prompt removal of all dead
animals from houses and pens, debeaking the birds, controlling fly and insect
populations and avoiding access to decaying organic material. Contaminated water
supplies are particularly dangerous.
the disease strikes, locate and remove the source of the toxin and separate all
visibly affected birds from the flock for treatment. Place sick birds in a cool
shaded area and give fresh water into the crop, twice daily. Mild laxatives may
be used for birds that have been exposed but do not show disease symptoms. Epsom
salts (one pound per 100 birds) may be mixed into feed. Adding a level
teaspoonful of Epsom salts in one ounce of water and placing in the crops of
sick birds has been beneficial in many instances. Antitoxin therapy is indicated
only in birds that have high individual value since the antitoxin is difficult
to obtain and is expensive.
disease is caused by a bacterium known as Hemophilus gallinarum.
Outbreaks usually result from the introduction of infected or carrier birds into
a flock. Transmission of the infection occurs by direct contact, airborne
infection by dust or respiratory discharge droplets and drinking water
contaminated by infective nasal exudate. Susceptible birds usually develop
symptoms within three days after exposure to the disease. Recovered individuals
may appear normal but remain carriers of the organism for long periods. Once a
flock is infected, all birds must be considered as carriers.
most characteristic symptoms of infectious coryza include edematous swelling of
the face around the eyes and wattles, nasal discharge and swollen sinuses.
Watery discharge from the eyes frequently results in the lids adhering together.
Vision may be affected because of the swelling. The disease results in a
decrease in feed and water consumption and an increase in the number of cull
birds. An adverse effect on egg production usually occurs in proportion to the
number of affected birds.
can be confirmed only by isolation and identification of the causative organism.
The organism, Hemophilus gallinarum, is extremely fastidious and often
difficult to isolate.
is the only sound approach in controlling infectious coryza. It usually can be
prevented by management programs that eliminate contact between susceptible and
infected birds. It requires only separating affected or carrier birds from the
susceptible population. In order to prevent the infection, introduce started or
adult birds only from sources known to be free of the infection. If infection
occurs, complete depopulation followed by thorough cleaning/disinfecting is the
only means for eliminating the disease.
number of drugs are effective for treating the symptoms of the disease although
the disease is never completely eliminated. Sulfadimethoxine or sulfathiazole in
the feed or water or erythromycin administered in the drinking water can reduce
the symptoms of this disease.
most problems result from mixed bacterial infections including the common
coliforms and various species belonging to the genera Staphylococcus,
Streptococcus, Proteus, and others. Omphalitis can usually be traced to faulty
incubation, poor hatchery sanitation or chilling/overheating soon after hatching
(such as in transit). The significance of isolating one of the bacterial species
mentioned above is complicated in that many of the same species can be isolated
from the yolks of supposedly normal birds immediately after hatching.
occurs during the first few days of life, so it cannot be considered
transmissible from bird to bird. It is transmitted from unsanitary equipment in
the hatchery to newly hatched birds having unhealed navels.
chicks usually appear drowsy or droopy with the down being "puffed
up". They also generally appear to be of inferior quality and show a lack
of uniformity. Many individuals stand near the heat source and are indifferent
to feed or water. Diarrhea sometimes occurs. Mortality usually begins within 24
hours and peaks by five to seven days.
lesions are poorly healed navels, subcutaneous edema, bluish color of the
abdominal muscles around the navel and unabsorbed yolk material that often has a
putrid odor. Often yolks are ruptured and peritonitis is common.
tentative diagnosis can be made on the basis of history and lesions. The
presence of mixed bacterial infections and absence of any specific
disease-producing agent is used for confirming the diagnosis.
management and sanitation procedures in the hatchery and during the first few
days following hatching are the only sure ways to prevent omphalitis. Broad
spectrum antibiotics help reduce mortality and stunting in affected groups, but
they do not replace sanitation.
in turkeys occurs most often during the fall and winter months and usually
affects birds that are four to seven months of age, although any age bird is
susceptible. Incidence has often been reported to be higher in males than in
females, possibly because fighting males receive numerous skin abrasions that
serve as portals of entry for the bacteria. In some instances the incidence is
higher in hens than toms because of artificial insemination techniques that
provide a means of transmission.
organism may survive for long periods in the soil and most outbreaks are thought
to originate from contaminated soil or premises. Sheep, swine and rodents may be
carriers of the disease organisms. Recurrence of the disease on a premise is
common. Predisposing or aggravating factors include over-crowding damp or
inclement weather and poor sanitation and range management.
first indication of the disease may be the discovery of several dead birds.
Usually several morbid birds can be found; however, most affected birds are
visibly sick for only a short period before death. Symptoms are typical of a
septicemic disease and include a general weakness, listlessness, lack of
appetite and sometimes a yellowish or greenish diarrhea. Occasionally, the snood
of toms may be turgid, swollen and purple. Some birds may be found lame with
swollen leg joints due to localization of the infection. In breeding flocks,
this disease occasionally is associated with decreased fertility and
hatchability. Daily morbidity and mortality usually are low; however, in
untreated flocks mortality may persist for some time and become excessive.
most characteristic lesions are small or diffuse hemorrhages located in almost
any tissue or organ. Such hemorrhages are commonly observed in the muscles,
heart, liver, spleen, fat and other tissues of the body cavities. Hemorrhagic
conditions of skin may result in purple blotches. The liver and spleen are
usually enlarged, congested and occasionally contain necrotic foci. Enteritis or
inflammation of the intestinal tract is commonly observed, as in most septicemic
and lesions may resemble other diseases so closely that a reliable diagnosis can
be made only through isolation and identification of the causative organism.
management practices that aid in preventing erysipelas include avoiding the use
of ranges previously occupied by swine, sheep or turkeys where erysipelas is
known to have existed. Debeaking, removal of the snoods of toms, measures that
prevent injury from fighting, avoiding overcrowding and providing well drained
ranges will aid in preventing this disease problem.
are available and are useful on premises where history indicates that outbreaks
may be a problem. The amount and duration of protection is relative to the
amount of exposure and may not be sufficient for the entire laying period.
Administer bacterins in accordance with the manufacturer's directions.
sick birds to a hospital pen for individual treatment and to prevent
cannibalism. Moving unaffected birds to a clean range may aid in preventing the
spread of the disease but may also contaminate an additional range.
antibiotics have shown efficacy in treating erysipelas; however, penicillin is
best. Penicillin injections in the leg or breast muscles of visibly sick birds
is effective in decreasing mortality. One injection is usually sufficient, but
more may be given if necessary. Water and feed medication may be of value under
and abnormal bones in adult birds is commonly present. In layers under thirty
weeks of age, the cause is usually a temporary calcium deficiency when egg
production reaches eighty percent or higher. If intake of calcium does not
satisfy the need for egg production, the hen will remove calcium stored in the
bones. Ultimately, osteoporosis develops, bones become soft and hens are subject
to bone fractures. Crippled and unable to stand, the hen suffers from the caged
hens show spontaneous recovery if removed from the cages and allowed to walk
normally on the floor. This indicates that a lack of exercise may be a partial
cause. Cage layer fatigue is more prevalent in single-hen cages than in
multiple-hen cages. When two or more hens are caged together, they get more
exercise because of competition for feed and water.
of the diet with phosphate, calcium and vitamin D3 is usually
helpful. Adding calcium to young birds by top-dressing the feed with twenty
pounds of oyster shell or limestone per one thousand hens will often help the
condition. In older hens, calcium deficiency is less likely than phosphorus or
vitamin D3 deficiencies. Recommended treatment in these birds is to
remove the hens from cages and top-dress feed with equivalent level of dicalcium
phosphate. Adding a vitamin/electrolyte supplement to drinking water is
recommended in any age bird suffering from this condition.
that do not respond to the above therapy should be submitted to a poultry
disease diagnostic laboratory to determine the cause of the problems. Several
diseases can cause symptoms similar to caged layer fatigue. Flock treatment for
the condition can be prescribed after diagnosis is completed.
within a flock that are most often affected are the high producers. This
indicates that physiological energy metabolism and production are closely
associated with this condition. Mortality varies considerably among flocks but
can become excessive in some cases. Lesions include accumulation of large amount
of abdominal fat; enlarged, easily damaged liver and presence of blood clots
that indicate that hemorrhages have occurred prior to death. Death usually is
caused by a fatal internal hemorrhage originating in a portion of the liver.
This hemorrhage is often caused as the hen is straining to lay her egg and the
enlarged, friable liver is more vulnerable to injury. When a large blood vessel
ruptures, sufficient blood is lost to cause death of the hen.
primary treatment for this condition requires an alteration of the diet or
amount of dietary energy consumed. Replacement of some of the corn in the diet
with lower energy feedstuffs like wheat bran can provide a lower energy diet. If
a complete layer ration is being fed, addition of vitamins can be of benefit. If
grains are the primary feedstuff, it is suggested that the birds be switched to
a complete layer diet. Control of body fat is the only successful remedy for
this condition and is best accomplished by regulation and reduction of total
causes are thought to initiate the problem but it is not understood why it is
uncontrollable in some cases but never becomes a problem in other situations.
Cannibalism may start as toe picking in baby chicks; feather picking in growing
birds; or head, tail and vent picking in older birds. The early symptoms of a
cannibalism problem may be difficult to detect. It is necessary that the poultry
man be on constant guard to detect any aggressive behavior and take necessary
management changes before the problem progresses into a severe case of
that can result in cannibalism include:
special method of hot debeaking has been developed for debeaking broiler chicks
at one day of age. Rather than severing or cutting the beak, a hot blade is used
to burn an area near the tip of the upper beak (egg tooth). The procedure is
designed to leave a thin base to the tip of the upper beak. This makes it easier
for the chick to eat without having a sensitive, raw beak. The tip of the upper
beak gradually drops off without apparent injury to the chick, thus leaving a
shortened upper beak and a normal lower mandible.
the mortality is a primary concern that responds well to adequate floor space.
Birds should not be crowded but instead, provide sufficient room so that weaker
birds can escape from those that are more aggressive. Reducing the amount of
floor space usually results in increased mortality and reduced growth rate. Not
only is there a monetary loss involving the cost of the chick, but the value of
the feed, labor, and other items necessary to grow a chick until the time of
death is a direct loss. There is also the lost profit that could have been
earned if the dead birds had lived until market or egg production age.
pox is caused by a virus of which there are at least three different strains or
types; fowl pox virus, pigeon pox virus and canary pox virus. Although some
workers include turkey pox virus as a distinct strain, many feel that is
identical to fowl pox virus.
virus strain is infective for a number of species of birds. Natural occurring
pox in chickens, turkeys and other domestic fowl is considered to be caused by
fowl pox virus.
pox can be transmitted by direct or indirect contact. The virus is highly
resistant in dried scabs and under certain conditions may survive for months on
contaminated premises. The disease may be transmitted by a number of species of
mosquitoes. Mosquitoes can harbor infective virus for a month or more after
feeding on affected birds. After the infection is introduced, it spreads within
the flock by mosquitoes as well as direct and indirect contact. Recovered birds
do not remain carriers.
fowl pox usually spreads slowly, a flock may be affected for several months. The
course of the disease in the individual bird takes three to five weeks. Affected
young birds are retarded in growth. Laying birds experience a drop in egg
production. Birds of all ages that have oral or respiratory system involvement
have difficulty eating and breathing. The disease manifests itself in one or two
ways, cutaneous pox (dry form) or diphtheritic pox (wet form).
pox starts as small whitish foci that develop into wart-like nodules. The
nodules eventually are sloughed and scab formation precedes final healing.
Lesions are most commonly seen on the featherless parts of the body (comb,
wattles, ear lobes, eyes, and sometimes the feet).
pox is associated with the oral cavity and the upper respiratory tract,
particularly the larynx and trachea. The lesions are diphtheritic in character
and involve the mucous membranes to such a degree that when removed, an
ulcerated or eroded area is left.
pox is readily diagnosed on the basis of flock history and presence of typical
lesions. In some cases, laboratory diagnosis by tissue or transmission studies
is no treatment for fowl pox. Disease control is accomplished best by
preventative vaccination since ordinary management and sanitation practices will
not prevent it. Several kinds of vaccines are available and are effective if
of broilers is not usually required unless the mosquito population is high or
infections have occurred previously. The chicks may be vaccinated as young as
one day of age by using the wing-web method and using a one needle applicator.
All replacement chickens are vaccinated against fowl pox when the birds are six
to ten weeks of age. One application of fowl pox vaccine results in permanent
most severe strain is called viscerotropic velogenic Newcastle disease (VVND)
and is kept from birds in the U.S. by enforcement of strict quarantines at our
national borders. It is often referred to as "Exotic Newcastle
Disease" and infection of susceptible fowl with this form usually causes
high mortality. Due to the reduced chance that poultry in this country will
become infected with this disease form, it will not be discussed.
milder form of the disease is called "mesogenic" Newcastle disease and
is the most serious strain found in the U.S. This is the form that is referred
to as Newcastle disease in this discussion.
disease is highly contagious. All birds in a flock usually become infected
within three to four days. The virus can be transmitted by contaminated
equipment, shoes, clothing and free-flying birds. During the active respiratory
stage, it can be transmitted through the air. The virus is not thought to travel
any great distance by this method. Recovered birds are not considered carriers
and the virus usually does not live longer than thirty days on the premises.
of Newcastle disease are not greatly different from those of other respiratory
diseases. The signs most frequently observed are nasal discharge, excessive
mucous in the trachea, cloudy air sacs, casts or plugs in the air passages of
the lungs and cloudiness in the cornea of the eye.
disease in young chickens begins with difficult breathing, gasping and sneezing.
This phase continues for ten to fourteen days and may be followed by nervous
symptoms. If nervous disorders develop, they may consist of paralysis of one or
both wings and legs or a twisting of the head and neck. The head often is drawn
over the back or down between the legs. Mortality may vary from none to total
loss of the flock.
adult chickens, respiratory symptoms predominate. Only rarely do nervous
disorders develop. If the flock is laying, egg production usually drops rapidly.
When this occurs, it takes four weeks or longer for the flock to return to the
former production rate. During the outbreak, small, soft-shelled, off-colored
and irregular-shaped eggs are produced. Mortality in adult birds is usually low
but may be fairly high from some virus strains.
turkeys, the symptoms are usually mild and may be unnoticed unless nervous
disorders develop. During an outbreak, turkeys will produce eggs with a chalky
white shell. Reduced production in breeder flocks is the main economic loss from
this disease in turkeys.
flock history, signs of a respiratory nervous disorder and other typical lesions
often may be sufficient to allow a tentative diagnosis. Usually, however, the
disease cannot be differentiated from infectious bronchitis and some of the
other respiratory infections, except by laboratory methods.
is practiced widely and is the recommended method for prevention. Several types
of vaccines are available but the most successful and widely used is the mild
live virus vaccine known as the B1 and La Sota types. The vaccines
may be used by drops into the nostril or eye, addition to the drinking water or
applied in spray form.
chickens are usually vaccinated when seven to ten days of age. Chickens kept for
egg production are usually vaccinated at least three times. The vaccine is given
when birds are approximately seven days, again at about four weeks and a third
time at about four months of age. Revaccination while in lay is commonly
is not widely used in turkeys. It is used to protect egg producing breeder
flocks. One dose of the mild type vaccine is given after selecting breeder
is no treatment for Newcastle disease. The disease does not always respect even
the best management programs, but good "biosecurity" practices will
help reduce the possibility of exposure to Newcastle disease virus.
bronchitis is considered the most contagious of poultry diseases. When it
occurs, all susceptible birds on the premises become infected, regardless of
sanitary or quarantine precautions. The disease can spread through the air and
can "jump" considerable distances during an active outbreak. It can
also be spread by mechanical means such as on clothing, poultry crates and
equipment. The disease is not egg transmitted and the virus will survive for
probably no more than one week in the house when poultry are not present. It is
easily destroyed by heat and ordinary disinfectants.
infection is confined to the respiratory system. Symptoms are difficult
breathing, gasping, sneezing and rales. Some birds may have a slight watery
nasal discharge. The disease never causes nervous symptoms. It prevails for ten
to fourteen days in a flock and symptoms lasting longer than this are from some
chickens under three weeks of age, mortality may be as high as thirty or forty
percent. The disease does not cause a significant mortality in birds over five
weeks of age. Feed consumption decreases sharply and growth is retarded.
infectious bronchitis occurs in a laying flock, production usually drops to near
zero with a few days. Four weeks or more may be required before the flock
returns to production. Some flocks never regain an economical rate of lay.
During an outbreak, small, soft-shelled, irregular-shaped eggs are produced.
bronchitis is difficult to differentiate from many of the other respiratory
diseases. For this reason, a definite diagnosis usually requires a laboratory
bronchitis is highly contagious and does not always respect sanitary barriers.
Vaccinate chickens being retained as layers. Whether broilers should be
vaccinated depends upon many factors and is an individual decision. Numerous
vaccines are available commercially. Most of them represent a modified or
selected strain of the infectious bronchitis virus. The vaccine used should
contain virus known to be present in the area. All vaccines contain live virus
and those that give the best protection are also capable of producing symptoms
and reducing egg production. The vaccine virus will spread to other susceptible
birds. Vaccine is usually added to the drinking water, but may be dropped into
the eye or nostril or used as a spray.
is no treatment for this disease. In young chickens it is helpful to increase
the brooder temperature and provide as nearly ideal environmental conditions as
disease is transmitted in a variety of ways. The causative viral agent is passed
out of the body of infected birds via eggs and feces. The virus may be
transmitted mechanically from infected birds to susceptibles by blood-sucking
parasites or by man in such procedures as fowl pox vaccination.
leukosis characteristically produces lymphoid tumors, particularly in the liver
and spleen. The tumors may also affect other visceral organs such as ovary and
lungs. Affected birds may die without preliminary symptoms, but the disease
usually is chronic in nature and affected birds show loss of appetite,
progressive emaciation and diarrhea. Clinically affected birds invariably die.
Losses due to the disease are most severe shortly after onset of egg production,
but losses will continue for as long as the flock is retained. Total loss may
approach twenty percent during the life of a flock.
diagnosis of lymphoid leukosis is based upon flock history and disease
manifestations. The lymphoid disease cannot be readily distinguished from the
visceral response to Marek's disease; however, there are some features that aid
in differential diagnosis.
is no treatment for lymphoid leukosis. Although the disease cannot be prevented
completely, there are certain steps that can be taken to help control the level
of infection within a flock. Some steps are:
disease is caused by a virus belonging to the Herpes virus group. Much is known
about the transmission of the virus; however, it appears that the virus is
concentrated in the feather follicles and shed in the dander (sloughed skin and
feather cells). The virus has a long survival time in dander since viable virus
can be isolated from houses that have been depopulated for many months.
usual mode of transmission is by aerosols containing infected dander and dust.
Young birds are most susceptible to infection by Marek's disease; however, since
the incubation period is short, clinical symptoms can appear much earlier than
in the case with lymphoid leukosis.
disease may produce a variety of clinical responses, all lymphoid in character.
These are acute visceral, neural, ocular, skin or combinations of the responses
that can be seen.
of the visceral type is characterized by widespread involvement with lesions
commonly seen in gonads, liver, spleen, kidney and occasionally heart, lungs and
muscles. The disease is often acute, with apparently healthy birds dying very
rapidly with massive internal tumors. The disease may appear in broiler-age
birds but the most severe losses occur in replacement pullet flocks prior to
onset of egg production.
neural type of Marek's is typified by progressive paralysis of the wings, legs
and neck. Loss of body weight, anemia, labored respiration and diarrhea are
common symptom. If lesions are present, they are confined to the nerve trunks
and plexes enervating the paralyzed extremities. Frequently no gross lesions can
(eye) leukosis or "gray-eye" is usually seen in early maturity.
Morbidity and mortality are usually low but may approach twenty-five percent in
some flocks. It is characterized by the spotty depigmentation or diffuse graying
of the iris in the eye. The pupil develops an irregular shape and fails to react
to light. Emaciation diarrhea and death follow.
leukosis produces the most severe losses in broilers. The losses result from
high condemnations at the processing plant. Enlargement of the feather follicles
due to accumulations of lymphocytes is the typical lesion. This is the most
infective virus since it is produced in the regions of the feather follicles and
is shed with the skin dander.
Marek's disease can be extremely rapid in its course, producing mortality in
apparently healthy birds. However, in some cases the lesions may regress and
clinically affected birds may make complete recoveries.
is based upon flock history and disease manifestations. Accurate diagnosis may
depend on results of laboratory procedures. As is the case with lymphoid
leukosis, there is no treatment for Marek's disease.
vaccine is available that is extremely effective (90% +) in the prevention of
Marek's disease. It is administered to day-old chickens as a subcutaneous
injection while the birds are in the hatchery. Use of the vaccine requires
strict accordance with manufacturer's recommendations in a sterile environment.
transmission or spread of the disease can occur by direct contact (bird to
bird), contaminated litter and feces, caretaker, contaminated air, equipment,
feed, servicemen and possible insects and wild birds. It is extremely
have ruffled feathers, a slight tremor at onset of the disease, strained
defecation, loss of appetite and are dehydrated. Affected birds have a tendency
to sit and when forced to move, have an unsteady gait. Vent picking is common
and a whitish diarrhea frequently develops. A sudden rise in body temperature is
followed by a drop to subnormal temperature, prostration and death. Birds
surviving the initial infection will recover rapidly within two weeks.
lesions include dehydration and changes in the bursa, skeletal muscle, liver and
kidneys. All affected birds have bursal changes characterized by swelling,
change in shape (oblong), color (pink, yellow, red, black) and the formation of
a gelatinous film around the bursa. Within a few days the bursa shrinks to half
its normal size or smaller.
of infectious bursal disease is based on flock history and postmortem lesions.
Laboratory procedures may be used to substantiate the diagnosis.
are available but must be carefully used. If given correctly, good immunity can
be developed. There is no specific treatment for infectious bursal disease and
indiscriminate medication with certain drugs may severely aggravate mortality.
Supportive measures such as increasing heat, ventilation and water consumption
is caused by microscopic animals called coccidia. There are many species of
coccidia that can infect fowl, domestic animals and humans. Each species of
coccidia is host specific and does not infect a wide variety of animals. After
an outbreak of a specific species of coccidia, the flock will develop a
resistance to the exposed coccidia species but remain resistant to other
infective species. This means that a flock may experience several outbreaks of
coccidiosis, each being caused by a different species of coccidia. Chickens are
susceptible to any of nine coccidia species, turkeys are susceptible to seven
species and quail are susceptible to at least four different species of coccidia.
is transmitted by direct or indirect contact with droppings of infected birds.
When a bird ingests coccidia, the organisms invade the lining of the intestine
and produce tissue damage as the undergo reproduction. Within a week after
infection, the coccidia shed immature descendants that are referred to as
oocysts. The oocysts shed in the droppings are not capable of infecting another
bird unless they pass through a maturation process (sporulation) in the litter.
This sporulation occurs within a one to three day period if the litter is warm
and damp but can take much longer if the conditions are cool and dry. After
sporulation the coccidia are infective if consumed by a new host bird.
number of infective coccidia consumed by the host is a primary factor as to the
severity of the resulting infection. An infection may be mild enough to go
unnoticed while a large infective dose of coccidia may produce severe lesions
that can cause death. Coccidia survive for long periods outside the bird's body.
They are easily transmitted from one house to another on contaminated boots,
clothing, free-flying birds, equipment, feed sacks, insects and rodents.
usually occurs in growing birds and young adults. It is seldom seen in birds
under three weeks or in mature birds. Signs of an outbreak include birds that
are pale, droopy, tend to huddle, consume less feed and water, have diarrhea,
and may become emaciated and dehydrated. Laying hens will experience a reduction
in rate of egg production.
coccidiosis may produce bloody droppings and anemia that is often followed by
death. Intestinal coccidiosis is not as acute and is more chronic in nature. It
produces less mortality than the cecal form.
of the infection depend on the species of coccidia causing the problem, its
severity and stage of the disease. Cecal coccidiosis may produce a ballooning of
the cecal pouches that is filled with free blood. A later stage is characterized
by cecae that are filled with a material with a cheesy consistency and being
tinged with variable amounts of blood. Lesions of intestinal coccidiosis vary
from a rather mild enteritis to a severe necrotic or hemorrhagic type.
coccidiosis may be confused with blackhead and salmonellosis due to their
similar lesions. Intestinal coccidiosis may be confused with hemorrhagic anemia
syndrome and other enteric diseases. Definite diagnosis is made from the
microscopic examination of scrapings of the digestive tract and identification
of the coccidia organisms. Since it is common for healthy birds to possess some
coccidia, consideration of flock history and lesions must be considered before
making diagnosis and treatment recommendations.
is difficult, if not impossible, to prevent coccidiosis by sanitation alone. It
is best prevented by addition of a drug (coccidiostat) to the feed that controls
the growth of coccidia in the digestive tract. Many coccidiostats are available
commercially. Coccidiostats should not be indiscriminately used and
recommendations must be followed precisely.
coccidiosis vaccine is also available commercially. The product is useful only
in certain types of poultry operations and must be used as recommended. Seek
expert advice before using the vaccine.
is caused by a protozoan parasite called Histomonas meleagridis. The
organism in passed in the fecal material of infected birds. In many instances,
the organism is shed within the eggs of the cecal worm of chickens, turkeys and
game birds. Free-living blackhead organisms do not survive long in nature, but
those in cecal worm eggs may survive for years. Therefore, most blackhead
transmission is considered due to ingesting infected cecal worm eggs.
Transmission may also occur by the earthworm.
are frequently infected without showing signs of the disease. These chickens may
shed enormous numbers of blackhead organisms, many of which are protected by
cecal worm eggs. Outbreaks in turkeys can often be traced to direct or indirect
contact with ranges, houses or equipment previously used by chickens.
Free-flying birds may also contribute to an infection.
blackhead losses occur in young birds (six to sixteen weeks). Among the symptoms
are loss of appetite, increased thirst, droopiness, drowsiness, darkening of the
facial regions and diarrhea. Morbidity and mortality are variable, but mortality
seldom exceeds fifteen percent; however, it may approach one-hundred percent in
uncontrolled turkey outbreaks. Losses are usually low in chickens.
of uncomplicated blackhead are confined to the cecae and liver, thus the reason
for the synonymous term, enterohepatitis. The cecae are ballooned and walls may
be thickened, necrotic and ulcerated. Caseous (cheesy) cores within the cecae
may be blood tinged. Peritonitis may be present if ulcers have perforated the
ceca walls. Livers are swollen and display circular depressed areas of necrosis
about one-half inch in diameter. Smaller lesions coalesce to form larger ones.
Lesions are yellowish to yellow-green and extend deeply into the underlying
liver tissue. Healing lesions may resemble those seen in visceral leukosis.
diagnosis is made readily on the basis of the lesions. Atypical forms,
particularly in chickens, must be differentiated from cecal coccidiosis and
Salmonella infections in particular. Medications may interfere with atypical
lesions. Laboratory tests may be required for positive diagnosis in such cases.
management practices can do much to control the blackhead problem. Do not
keep birds of different species on the same premises. Do not range turkeys
on ground previously used by chickens unless several years have elapsed. Rotate
ranges periodically if possible. Cecal worm control is necessary to reduce
blackhead incidence. Wire or slatted floors reduce exposure.
management is the only effective method of preventing this disease since many of
the effective drugs used in past years are no longer available commercially.
Drugs that reduce the presence of cecal worms, and thus reduce the infection
rate, are available but do not have an effect on the Histomonas organism. Refer
to the cecal worm section for recommended control practices.
is a problem in every commercial turkey-producing area. It may be a major
problem in localized areas during a particular year, followed by one or more
years in which incidence is low.
is caused by a one-celled parasite of the genus Hexamita. Hexamita
meleagridis is the cause in turkeys; in pigeons it is Hexamita columbae.
Experimentally, the Hexamita of turkeys can be transmitted to young quail,
chicks and ducklings, and that of quail and partridges can be transmitted to
poults. However, poults cannot be infected with the organism isolated from
disease is found primarily in young birds, and outbreaks seldom occur in poults
past ten or eleven weeks. Losses are most severe in birds three to five weeks
old. Apparently, resistance develops rapidly with increasing age, regardless of
primary infection source is droppings from carrier birds. About a third of
recovered birds become carriers. Most outbreaks result from a buildup of
organisms through several broods of poults, making exposure of the following
brood overwhelming. Indirect transmission may result from fecal material carried
from one location to another on shoes or equipment. Free-flying birds also may
symptoms are listlessness and foamy or watery diarrhea with rapid weight loss
due to the dehydrating effect. Birds often huddle together near the heat source
and cry or "chirp" constantly as though in pain. Convulsions due to
lowered blood sugar levels shortly precede death. Affected birds suffer losses
in weight and survivors remain stunted.
and emaciation are the principal gross lesions. Muscles are dark and dry. The
intestine usually appears to have lost muscle-tone. Intestinal contents are
usually thin and watery, or may contain mucus.
depends upon history, symptoms and microscopic examination of intestinal
contents. A definite diagnosis cannot be made unless typical flagellated
organisms can be detected in intestinal contents of the duodenum. Most
flagellate organisms in the cecae are not disease producers.
condition is caused by Aspergillus fumigatus, a mold or fungus-type
organism. Occasionally other types of molds are involved. These organisms are
present in the environment of all poultry. They grow readily on many substances
such as litter, feed, rotten wood and other similar materials.
bird comes in contact with the organisms through contaminated feed, litter or
premises. The disease is not contagious and does not spread from one bird to
another. Most healthy birds can withstand repeated exposure to these organisms.
Inhalation of large amounts of the infectious form of the mold or reduced
resistance of the bird apparently results in infection. In adult turkeys, the
disease more often affects the male.
the acute form in young birds, main symptoms are gasping, sleepiness, loss of
appetite and sometimes convulsions and death. Occasionally the organism invades
the brain, causing paralysis or other forms of nervous symptoms. The more
chronic form in older birds usually results in loss of appetite, gasping or
coughing and a rapid loss of body weight. Mortality is usually low and only a
few birds are affected at one time.
disease produces hard nodular areas in the lungs and an infection of the air
sacs. Sometimes the air sac lesions are similar to those produced by infectious
sinusitis or CRD. In some birds, colonies of mold growth can be seen on the air
is usually made from history, symptoms and lesions. It may be necessary to base
diagnosis on microscopic lesions.
disease can usually be prevented by avoiding moldy litter, feed or premises.
There is no treatment for the affected flock. Cleaning and disinfecting the
equipment is often helpful.
is caused by ingestion of toxic substances produced by molds growing on feed,
feed ingredients and possibly litter. Several types of fungi produce toxins that
may cause problems in poultry, but of primary concern are substances produced by
the Aspergillus flavus fungi and are thus called aflatoxins. Aspergillus
flavus is a common mold that grows on many substances, and grows especially
well on grain and nuts. Several other fungi also produce toxins that cause the
aflatoxins include four closely related metabolites of A. flavus known as
B1, B2, G and G2. The B1 toxin is
the most toxic and is of greatest concern to the poultry industry.
toxins cause a wide variety of signs, many difficult to recognize. The
aflatoxins under certain conditions cause death, reduced growth, reduced egg
production, reduced hatchability, signs associated with "physiological
stress" and impaired ability to develop immunity to infectious agents.
Diagnosis is difficult because characteristic lesions usually are not present,
and detection of the toxin is not conclusive.
are widespread in nature. Standing grains and other feed substances are
frequently infected with toxin-producing molds prior to harvest. The key is
proper storage to control moisture and temperature to reduce growth of the molds
while in storage. Although the mold is present, it cannot produce toxic products
unless allowed to grow freely. Aflatoxins in feeds can be detected by chemical
tests. Once the toxin is produced there is no known method for removing it from
the feed or cancelling its harmful effects. Providing a diet containing high fat
and high protein levels and augmenting the ration with vitamin supplements may
be of value.
of all ages are susceptible to the effects of this organism. Chickens, turkeys,
pigeons, pheasants, quail and grouse are species most commonly affected as well
as other domestic animals and humans. The Candida organism is widely spread
throughout the poultry producing areas of the world.
is transmitted by ingestion of the causative organism in infected feed, water or
environment. Unsanitary and unclean water troughs are an excellent reservoir of
the Candida organism. The disease does not however, spread directly from bird to
bird. The organism grows especially well on corn, so infection can be introduced
by feeding moldy feed.
malady produces no specific symptoms. Young birds become listless, pale, show
ruffled feathers and appear unthrifty. Affected caged layer hens become obese
and anemic. Some birds exhibit a vent inflammation that resembles a diarrhea
induced condition having whitish incrustations of the feathers and skin around
the area. Feed consumption may increase by ten to twenty percent.
lesions are mostly confined to the crop, proventriculus and gizzard. The crop
and proventriculus have whitish thickened areas that are often described as
having a "turkish towel" appearance. Erosion of the lining of the
proventriculus and gizzard is commonly observed, as well as an inflammation of
the intestines. Diagnosis is based on history and typical lesions in the flock.
Confirmation of the condition is by isolation and laboratory identification of
the C. albicans organism.
of the flock with an antimycotic drug will control the infection. Many broad
spectrum antibiotics will enhance this disease; therefore they should not be
used until after control of this condition is completed. Addition of Nystatin
(100 g/Ton) or copper sulfate (2-3 lb/Ton) to the feed for seven to ten days
should control moniliasis.
introduced into the flock, moniliasis is perpetuated by suboptimal management
conditions. Preventative measures include the continual use of mold inhibitors
in the feed, proper feed handling and storage, daily cleaning and sanitizing of
the watering system and periodic stirring and/or replacement of wet litter areas
to prevent caking. An inexpensive, yet effective, water treatment is the
continuous addition of household chlorine bleach to the drinking water at the
rate of five parts per million (ppm).