POULTRY PARASITES AND DISEASES

A disease can spread rapidly among chickens because they are usually kept together in a cage or chicken house.
They also share the same food and water bowls, which can spread disease and infections from sick to healthy
chickens.

In an intensive system we place a great deal of pressure on the chickens to grow fast and to lay many eggs. This
situation can cause disease to spread resulting in a lot of damage because of the stress the chickens experience

FACTORS CONTRIBUTING TO DISEASE

Factors that can contribute to disease include management, environment and the chickens themselves

Management

 Poor-quality food and water

 Poor hygiene and inadequate cleaning programme
 Leaking water bowls
 Rat and fly problems
 Overcrowding of chicks
 Chickens of mixed ages reared together
 No security measures to prevent people and animals from entering the chicken house

Environment

 Too hot or too cold conditions

 Wet litter
 Dusty bedding
 High build-up of chicken droppings
 No air circulation
 Sharp wires in the cages

ACTIONS AT FIRST SIGNS OF DISEASE

You must act quickly at the first signs of disease. The chickens must be treated, and
management that may have led to the problem must be corrected to prevent the disease from
occurring again

 Consult your animal health technician or veterinarian to help you find a correct
solution to your problem as soon as possible
 Call your animal health technician or veterinarian. They will kill some of the sick
chickens and cut them open. They will also cut open dead chickens and take samples.
They may take blood or egg samples, depending on the disease. The samples taken will be sent to a
laboratory.
 You and your animal health technician or veterinarian should then go through the
entire system to identify possible problems in the management and environment that
can be corrected
GENERAL TREATMENT
 There are not many forms of treatment or in certain cases no treatment for some diseases, which is why
prevention is so important
 The treatment will depend on the cause of the disease
 If it is at all possible, try to separate all sick chickens from the healthy ones daily. The sick chickens should
be handled and treated last to prevent the spread of the disease
 Correct management problems

GENERAL PREVENTION
Diseases can be prevented through management, environmental and chicken factors

Management

 Apply correct methods for raising young chicks (temperature, food, water, bedding)
 Disinfect and clean the housing of the different groups of chicks
 Maintain the correct stocking density (avoid over-crowding)
 Use the best-quality food that is available and provide clean water daily
 Use bedding that is not dusty
 Prevent the buildup of gases by cleaning and ventilation
 Control rats and flies
 Ensure that no people from outside your farm visit the chicken house
 Have bird-proof houses to keep out wild birds that eat the food and bring diseases to your chickens

Environment

 Ensure that the building or house you are going to use is large enough for the chickens
 Fix leaky watertroughs
 Feed and waterbowls should be cleaned daily and fresh food and water should be supplied
 Houses should be warm in winter and cool in summer and well ventilate
 Dust causes irritation of the respiratory tract and the environment must therefore not be dusty
 Use cages for laying hens that do not have sharp edges that can injure the hens. Make sure that there is
sufficient space per hen

Chickens

 Get only first-grade chicks from a good, reliable supplier

 Vaccinate chicks against important diseases
 Keep chickens of the same age together in one house

DIARRHOEA
Signs in sick chickens

 Diarrhoea (also known as scours or dirty vent). The stool or droppings of the chickens
are not firm but very loose, watery, not of the normal colour and may contain blood.
 This may cause the feathers of the vent to be soiled and caked together
 Depression
 Reluctance to eat, drink and move about
 Poor growth
  Death

Signs in dead chickens

 Poor condition
 The intestines may be red and swollen and the contents watery
 There may also be a yellow butter-like substance around the heart, liver and intestines

Causes

There are many different types of organisms that can cause diarrhoea, which include:

 Bacteria (Salmonella, E. coli, Pasteurella)

 Viruses (Newcastle disease, gumboro disease)
 Parasites (coccidiosis, worms)
 Fungi (Candida, Aspergillus)

Treatment

 Use an antibiotic or coccidiostatic drug in the water that was recommended by the animal health technician
or veterinarian in the water for 3 to 5 days.
 Stress preparations that contain electrolytes, vitamins and minerals can be added to the water.

UPPER RESPIRATORY DISEASES

Signs in sick chickens

 The sinuses of the chicken (the area between the eye and the beak) are swollen. These may be swollen in
such a way that the eyes are closed.
 Tears and wetness often occur around the eyes and nostrils. The discharge from the nostrils may look like
clear water in the early stages but can become cloudy and yellow when secondary bacterial infections cause
complications.
 Sneezing
 Coughing
 Difficulty in breathing. They breathe with an open beak and you can hear a snoring or clicking sound
 Loss of appetite
 Weakness
 Weight loss

Signs in dead chickens

 A very red windpipe and throat

 Fluid in the windpipe

Causes

There are many different types of organisms that can cause disease in the upper respiratory tract. These include:

 Mycoplasma
 Bacteria (E. coli, Pasteurella, Haemophilus)
 Viruses (Newcastle disease, influenza, infectious bronchitis, infectious laryngotracheitis)
  Parasites (mites and worms)
 Fungi (Aspergillus)

Treatment

 Use an antibiotic drug that was recommended by your animal health technician or veterinarian in the water
for 3 to 5 days
 Stress preparations that contain electrolytes, vitamins and minerals can be added to the water

NERVOUS SIGNS AND LAMENESS

Signs in sick chickens

 Signs may vary, but usually chickens lie down because they cannot stand up
 They also walk with a limp or are reluctant to move
 Nervous signs may include staring into the sky, not knowing where they are, pulling the head and neck
over their backs, paralysis
 Sores on the breast muscles from lying down

Causes

There are many different types of organisms that can cause nervous signs and lameness. These include:

 Bacteria (Salmonella, Botulism)

 Viruses (Newcastle disease, Mareks disease, avian encephalo- myelitis)
 Fungi (Aspergillus)

Treatment

 A complete hygiene and disinfection programme should be planned together with the animal health
technician or veteri- narian
 Antibiotics will only be effective against bacteria and can be used as recommended. If it is a viral disease,
such as Newcastle disease, urgent steps have to be taken to prevent possible spread because it causes
serious production losses

DROP IN EGG PRODUCTION OR QUALITY

 You will notice that the hens are not producing as many eggs as they should for their age
 You may see unusually-shaped eggs, eggs with no shell, soft eggs, eggs that break easily, or that have
abnormal contents when you break them
 Often the people buying the eggs will complain of poor quality
 The only way these changes will be noticed is if you keep good records

Causes

There are many different types of organisms that can cause a drop in egg production or quality. These include:

 Bacteria (E. coli, Salmonella)

 Mycoplasma
  Viruses (Newcastle disease, influenza, infectious bronchitis, infectious laryngotracheitis, avian
encephalomyeli- tis, egg drop syndrome)
 Parasites

Treatment

 Your animal health technician or veterinarian may recom- mend a short course of antibiotics but usually it
may only help for bacterial infections
 Adding vitamins and minerals to the water or feed may help

NEWCASTLE DISEASE
 Newcastle disease is probably the most important disease for poultry farmers around the world. This is a
production disease that causes a large number of deaths in chickens and huge losses to farmers and the
industry
 Because there is no treatment and the disease spreads so quickly, sick chickens should be slaughtered
immediately
 This disease is caused by a virus

Signs in sick chickens

 A large number of chickens will die suddenly without any of the following apparent causes:
o Depression
o Nervous signs
o Sneezing, swollen eyes, difficulty in breathing
o Diarrhoea
o Death

Treatment

 There is NO treatment for the disease and all the chickens may die within a few days.
Very few chickens survive
 It is best to prevent the diseases by good management and a vaccination programme
 Your animal health technician or veterinarian will give you the best advice in a
Newcastle disease outbreak, especially as this is a controlled disease

Prevention

 You should vaccinate all the chickens against this disease by using a good vaccination programme before
any signs appear
 It is a very contagious disease, which means it spreads easily to other farms. You should not visit your
neighbours without washing and putting on new clothes and shoes. You should also recommend that your
neighbours vaccinate their chickens as soon as possible
 You should clean the chicken house thoroughly with soap and water. All equipment must be washed.
Everything should then be disinfected. You should also wash and disinfect your clothes and shoes. All
chicken litter or dead chickens should be burned to prevent the spread of the disease

For many poultry diseases there is still no treatment.

Prevention is therefore the only option!
There are four main types of disease affecting poultry: metabolic and
nutritional diseases; infectious diseases; parasitic diseases; and behavioural
diseases.
Metabolic and nutritional diseases
These are conditions caused by a disturbance of normal metabolic functions
either through a genetic defect, inadequate or inappropriate nutrition or
impaired nutrient utilisation. These include Fatty Liver Syndrome, Perosis
(or slipped tendon), Rickets and Cage Layer Fatigue.
Infectious diseases
An infectious disease is any disease caused by invasion of a host by a
pathogen which subsequently grows and multiplies in the body. Infectious
diseases are often contagious, which means they can be spread directly or
indirectly from one living thing to another. These include Avian
Encephalomyelitis, Avian Influenza, Avian Tuberculosis, Chicken Anaemia
Virus Infection (or CAV), Chlamydiosis, Egg Drop Syndrome (or EDS), Fowl
Cholera (or Pasteurellosis), Fowl Pox, Infectious Bronchitis, Infectious
Bursal Disease (or Gumboro), Infectious Coryza, Infectious
Laryngotracheitis, Lymphoid Leukosis, Marek’s
Disease, Mycoplasmosis, Necrotic Enteritis, Newcastle Disease and
Salmonellosis.
Parasitic diseases
Parasitic diseases are infections or infestations with parasitic organisms.
They are often contracted through contact with an intermediate vector, but
may occur as the result of direct exposure. A parasite is an organism that
lives in or on, and takes its nourishment from, another organism. A parasite
cannot live independently. These include
Coccidiosis, Cryptosporidiosis, Histomoniasis, Lice and Mites, Parasitic
Worms (or Helminths), Toxoplasmosis and Trichomoniasis.
Behavioural diseases
Abnormal behavioural patterns can lead to injury or ill health of the
abnormally behaving bird and/or its companions. These
include Cannibalism (or aggressive pecking).
 LIST OF POULTRY DISEASES

Ascites is considered a metabolic disorder and is common in commercially

grown chicken and ducks. It is thought that in fast growing breeds, organs are
unable to supply the body’s cells with oxygen. The high oxygen requirement is
a result of accelerated metabolic rates.

Avian encephalomyelitis (AE) is a viral infection of the central

nervous system of poultry, primarily chickens, turkeys, Japanese (coturnix)
quail, and pheasants. It is found worldwide and is characterised by ataxia
(loss of muscle coordination) and tremors, especially of the head and neck,
and a drop in egg production and hatchability in hens. Ducklings, pigeons,
and guinea fowl can be infected experimentally. The mortality rate from this
disease can be high.
The disease is most common in chickens 1-6 weeks of age. Symptoms
usually appear at 7-10 days of age, although they may be present at
hatching or delayed for several weeks. Affected chicks may first show a dull
expression of the eyes, followed by unsteadiness, sitting on hocks, tremors
of the head and neck, paresis (weakness or partial paralysis), and finally
total paralysis. Feed and water consumption decreases and birds will lose
weight. All stages of the disease can usually be seen in affected flocks.
Muscle tremors are best seen after exercising the bird and head tremors are
best seen by holding the bird inverted. In adult birds a slight transient drop
in egg production may be the only symptom. The disease in turkeys is often
milder than in chickens.
What causes avian encephalomyelitis?
AE is caused by a picornavirus. Vertical transmission is the most common
way the disease is spread but it is also spread by direct contact between
susceptible hatchlings and infected birds. Most commercial poultry are
exposed in the hatchery when 1 day of age, although further spread occurs
later within the flock. The virus present in droppings may survive for more
than 4 weeks. Recovered birds are immune and do not spread the virus.
Prevention and treatment of avian encephalomyelitis
There is no treatment for AE. Control of the disease is through prevention.
To prevent flocks becoming infected, hatcheries should only accept hatching
eggs from immune breeder flocks. Lifetime immunity is acquired
through vaccination or recovery from the disease. Breeder pullets should be
vaccinated between 9-16 weeks of age. It is also recommended for
replacement egg layer pullets to be vaccinated at this age to prevent a
temporary drop in egg production.
To minimise the impact of the disease in an infected flock, remove all
affected birds and provide good nursing, including fresh food and water, to
the remaining birds. Affected birds should be killed and incinerated.

Avian influenza (AI) is a highly contagious viral infection which may

cause up to 100% mortality in domestic chickens or turkeys. The disease is
caused by a virus that belongs to the family Orthomyxoviridae. Influenza
viruses have two surface proteins, haemagglutinin and neuraminidase, that
determine their subtype and the animal species they infect; there are 16
haemagglutinin and nine neuraminidase types. When AI viruses of two
haemagglutinin types, H5 and H7, infect domestic poultry (chickens or
turkeys) they often mutate and virulent disease arises in these birds which
is called highly pathogenic avian influenza (HPAI). The initial infection that
does not cause or causes minimal disease is called low pathogenic avian
influenza (LPAI). Wild water birds act as reservoir hosts of influenza viruses,
however these viruses generally do not cause disease in these birds
Birds susceptible to AI
All commercial, domestic and wild bird species are susceptible to infection
with AI viruses but disease outbreaks occur more frequently in chickens
and turkeys. LPAI viruses are traditionally spread by migratory wild birds.
Many species of waterfowl, especially geese, ducks and swans, carry the
virus but generally show no signs of disease. The recent HPAI outbreak in
eastern Asia has seen the H5N1 virus cause disease and high mortality in
ducks, geese, swans and other wild birds.
Avian influenza in Australia

Avian influenza causing depression Source: CSIRO

While LPAI viruses are probably ubiquitous throughout the world in wild
water birds, outbreaks of HPAI have occurred as sporadic events that were
controlled and eradicated until the recent eastern Asia outbreak. The H7
subtype HPAI virus has caused outbreaks of clinical disease in commercial
poultry in Australia in Victoria (1976, 1985 and 1992), Queensland (1994)
and NSW (1997). All outbreaks were quickly eradicated. Avian influenza as it
occurs in Asia as H5N1 subtype virus has not been recorded in Australian
poultry flocks.

AUSVETPLAN
The Australian strategy is to eradicate the virulent disease by immediate
culling and disposal of infected and in-contact birds to remove the major
source of the virus. Additionally, there will be strict quarantine and
movement controls to prevent the spread of infection, decontamination to
remove and destroy the virus, tracing and surveillance to locate the source
of infection, locate other infected premises and determine the extent of the
infection and zoning to define infected and disease-free areas. Vaccination
may be an option in some circumstances and provisions have been made for
emergency vaccine supplies to be available for use in Australia. The current
Emergency Animal Disease Response Agreement applies to both HPAI and
LPAI outbreaks (see AUSVETPLAN – Avian Influenza). Government and the
poultry industries share the costs of eradication under the Emergency
Animal Disease Response Agreement, which is administered by Animal
Health Australia.
H5N1 virus
The spreading Asia outbreak is unprecedented in recent history. The H5N1
virus was first detected in China in 1996 and the infection spread to other
eastern Asian countries in 2003 and evolved to produce severe disease and
deaths in domestic and wild water birds, which is an unusual feature for AI
viruses. Altogether more than 150 million domestic birds have died or been
killed in the attempt to control AI infection in eastern Asia. In mid-2005, the
infection spread eastwards to countries bordering the Black Sea with
infection occurring in both wild birds and poultry. In early 2006, H5N1
infection spread to Nigeria, India and Egypt in poultry and to many
countries in Europe with deaths in wild birds, particularly swans.
Significance of AI outbreaks
Since 1997 when H5N1 virus was shown to infect humans in Hong Kong,
there has been increasing concern about HPAI poultry outbreaks. With more
than 170 confirmed human infections and over 90 deaths in Asia, the World
Health Organisation (WHO) is concerned about a pandemic of human
influenza arising from mutation(s) of the poultry virus or its recombination
with a human influenza virus that will enable the virus to infect and spread
between people easily.
Recently the World Organisation for Animal Health (OIE) has redefined avian
influenza infection as both HPAI and LPAI viruses of the H5 and H7
subtypes and in so doing indicated there is a need to control both LPAI and
HPAI infections in domestic poultry and other domestic birds. It is not
practical to control AI infections in wild bird populations and it is
recommended that action not be taken to control infection in these species
when outbreaks occur.
Avian influenza in poultry and impact on the poultry industries
The clinical signs of infection with HPAI virus are variable and can be
affected by the existence of other diseases, the age of the birds, the
environment and the severity of the virus itself. In very severe forms the
disease appears suddenly and birds die quickly. Some may appear
depressed, egg production falls and softshelled eggs are produced. There
may be profuse watery diarrhoea, combs and wattles may become blue and
respiration may be laboured. With less virulent forms of HPAI, the clinical
signs may include decreased egg production, depression, respiratory signs
suggestive of a cold, swelling of the face, possibly some nervous signs and
diarrhoea. With LPAI, there may be no clinical signs seen following infection
or mild signs relating to the respiratory, alimentary or reproductive systems
may be seen.
Spread of infection

Avian influenza causing swollen head Source: CSIRO

Direct or indirect contact (likely through drinking water) with migratory
waterfowl is the most likely source of infection for domestic poultry. Once
established in domestic poultry, infection can also spread through contact
with contaminated equipment or humans. Transmission through the egg is
uncommon, although contamination of the shell does occur. Avian influenza
virus is highly concentrated in the manure and in nasal and eye discharges.
Persistence of AI virus
Environmental conditions have a marked effect on virus survival outside the
bird. Avian influenza virus can survive for at least 35 days at 4°C in manure
and can be isolated from lake water where waterfowl are present. The virus
can survive for up to 23 days if refrigerated and for several days in carcases
at ambient temperature. The virus can persist in poultry meat products but
is eliminated by cooking.
Prevention of infection
Australia has developed industry plans (called biosecurity plans) to prevent
avian influenza viruses gaining entry to commercial poultry flocks. The
plans are aimed at limiting possible contact between wild birds and
domestic poultry through contaminated water and food supplies and
transfer of infection by the mechanical movement of infection on fomites
such as on the clothing and footwear of persons and on equipment,
containers, vehicles etc. Treatment of surface water by chlorination to
inactivate the virus is essential if it is to be supplied to poultry and aviary
birds.
Suspicion of AI
If you are in contact with commercial poultry which present with any
unusual disease signs, abnormal behaviour or unexplained deaths, or with
pet birds with depression, rapid breathing and a sudden rise in mortality,
report this to your veterinarian or Department of Primary
Industries/Agriculture Officer or alternatively call the Emergency Animal
Disease Watch Hotline on 1800 675 888 at once.
Control of AI outbreaks
Australia has very strict quarantine procedures that seek to prevent the
entry of live birds and poultry products from countries that have
experienced AI outbreaks and increased surveillance is undertaken at
airports, seaports and international mail exchanges when AI outbreaks
occur overseas. There is nothing that can be done to control the infection in
wild birds but the likelihood of migratory birds introducing H5N1 infection
to Australian poultry is regarded as highly unlikely given wild birds become
rapidly ill or die after becoming infected and the main reservoir hosts
(ducks, geese and swans) do not migrate into Asia. The use of AI vaccination
will likely be considered in future in the event of an outbreak that is not
readily controlled by eradication techniques.
Control of AI outbreaks Avian influenza viruses and human infection
Generally, outbreaks of AI infections in poultry or wild birds have not been
associated with cases of human influenza. However cases of human
influenza due to H5 and H7 subtype HPAI viruses have been recorded in a
few humans associated with recent poultry outbreaks in Europe (2003),
eastern Asia (1997–2006) and western Asia (2006).
Human pandemic influenza
Human pandemic influenza occurs irregularly, having occurred in 1919,
1957 and 1968 when strains of influenza virus with a novel haemagglutinin
type adapted to humans and spread rapidly around the world. It is feared
that another human pandemic will arise from the current AI outbreak in
eastern Asia. Illness and death have been associated with outbreaks of HPAI
viruses of both H5 and H7 subtype, particularly the H5N1 virus in eastern
Asia. The pandemic of human influenza will not occur until there have been
mutations in the poultry H5N1 virus or its recombination with a human
influenza virus that will allow the resulting virus to easily infect and
transmit between humans. To this time, contact with live infected birds or
their manure has been necessary for infection to establish in humans and
few human cases have infected other humans in contact with them. A
pandemic cannot commence without an AI virus acquiring the ability to
easily infect and spread between humans. Avian influenza in birds and
human pandemic influenza can be expected to be caused by genetically
different viruses.
Dangers for humans consuming poultry products
The recognised source of AI infection for humans is direct contact with
infected live birds or their manure, so poultry products are relatively safe.
Handling raw poultry meat products or eggs and eating cooked poultry
products have not been recorded as causing infection. Cooking poultry
products in the normal way destroys AI viruses.

Avian Intestinal Spirochaetosis (AIS) is a disease that affects

commercial laying and meat breeding hens and results from the colonisation
of the caeca and rectum by one or more species of anaerobic spirochaetal
bacteria. AIS was first described in the 1990s in commercial chickens from
the United Kingdom, The Netherlands and the United States. Seven species
of the bacterium are capable of colonising poultry hosts, but only three are
considered to be pathogenic. Of these, Brachyspira intermedia is considered
the most common and significant species.
AIS is characterised by chronic diarrhoea in diseased birds, and
subsequently results in faecal staining of eggs and wet litter. The resultant
wet litter is an industrial problem and necessitates the mechanical cleaning
of cages. A delay and (or) reduction of egg laying capacity is also observed,
and hatched broiler chicks from eggs of infected parents show reduced
performance compared to those of healthy parents. The significance of AIS is
often unappreciated due to the variable clinical signs of the disease. In
addition, the isolation of the bacterium can only be achieved using
specialised media and techniques.
Treatment
Currently there are no antimicrobial compounds that are registered for
treatment of, or vaccines for prevention of , AIS. Compounds that are used
to treat or prevent spirochaetosis in pigs have also been used in laying
chickens with limited success, and importantly have not provided any long
term control with recurrence of infection and reduction in performance
occurring within 3 weeks to 3 months.
Research is currently in progress to develop a diagnostic immunological test
method and a recombinant vaccine to detect antibodies and provide
sufficient protection against AIS in chickens.

Avian tuberculosis is chronic bacterial infection that spreads slowly

through a flock. All bird species appear to be susceptible, however
pheasants seem highly susceptible whereas turkeys rarely succumb to the
disease. The disease is more common in captive than wild birds, however it
is uncommon in poultry flocks due to the poultry husbandry practices and
their short life span. Tuberculosis has been found in emus and other ratites
and has also shown to cross-infect other animal species, such as pigs,
sheep, rabbits, rodents and calves. The bacterium can be carried
asymptomatically by adult cattle and has been isolated from people with
acquired immunodeficiency syndrome.
Symptoms do not usually develop until late in the infection and affected
hens are usually more than one year old. The disease in birds is
characterised by gradual weight loss, sluggishness and sometimes
lameness. Combs and wattles shrink and become pale. The disease causes
multiple granulomas (a small mass of firm tissue formed as a result of
inflammation) to form in a number of organs, predominantly in the liver,
spleen, intestine and bone marrow.
What causes avian tuberculosis?
Avian tuberculosis is caused by the bacterium Mycobacterium avium. This
bacterium is closely related to the human and bovine TB bacteria. It can
survive for as long as four years in the soil or when protected by organic
matter. It is also resistant to acid and alkali. Infected birds with advanced
granulomas excrete the bacteria in their faeces. Infected dead birds and offal
may infect penmates, rodents and predators if eaten. The bacterium can
spread from bird to bird, animal to bird and bird to animal. The incubation
period is several weeks to months.
Prevention and treatment of avian tuberculosis
There is not treatment for avian tuberculosis. Control is achieved through
depopulation and good biosecurity practices including rodent control,
screening against wild birds, isolation from other birds and animals and
good sanitation. Dirt-floored houses should have several inches of the floor
removed and replaced with dirt from a place where poultry have not been
maintained.

CANNIBALISM
Pecking is the natural means by which poultry investigate their
surroundings and establish a stable social order, however this behaviour
can escalate to the stage where birds will literally peck each other to death
(cannibalism). All forms of commercial poultry can experience cannibalism
as it a behavioural problem that can develop into a habit that will persist
and spread within a flock as a learned behaviour, even after the initial
causes of the behaviour have been corrected.
What causes cannibalism?
Cannibalism often starts as feather pulling or picking while the birds are
only a few weeks old, or as investigative pecking at any age. These
behaviours can escalate to aggressive pecking, particularly if injury occurs.
Scientific study has shown that any stressor (or combination of stressors)
can trigger this behaviour and can lead to serious aggressive pecking and
cannibalism.
These stressors include crowding, bright light intensity, high room
temperature, poor ventilation, high humidity, low salt, trace nutrient
deficiency, insufficient feeding or drinking space, nervous and excitable
birds (hereditary), external parasites, access to sick or injured birds, stress
from moving, boredom and idleness, housing birds of different appearance
together and birds prolapsing during egg-laying.
Prevention and treatment of cannibalism
As cannibalism can become a learned behaviour it can be difficult to treat
once it has started in a flock. Therefore prevention should be the main aim
and as such, good husbandry practices should aim to minimise the
stressors listed above as potential causes for cannibalism. Some strains of
birds have been shown to have a higher tendency towards developing
aggressive pecking behaviour and therefore strains that are more placid
should be preferred.
The broad range of factors that can trigger cannibalism can make it very
difficult for management to control all of these factors for the entire life of
the flock. Bright light is a known factor that leads to cannibalism but
control of lighting levels in some poultry housing systems can be very
difficult, if not impossible (such as in free range systems). Where outbreaks
of cannibalism have occurred in a flock, or where there is a reasonable
concern that management strategies can not be guaranteed to prevent an
outbreak, then beak trimming of the birds may be used as a control
measure. Trimming of the sharp tip of the upper, and sometimes also lower,
beak reduces the damage that is caused by aggressive pecking. Further
information on the practice of beak trimming can be found in the section
on Beak Trimming.
The spread of the behaviour may be able to be controlled if the injured and
aggressive birds can be rapidly identified and removed from the flock.
Provision of escape areas may also help in floor-housed flocks. Other control
methods that have been tested include the use of spectacles to prevent
forward vision, bits that prevent complete closure of the beak and coloured
contact lenses to prevent the identification of blood on another bird.
There is evidence that cannibalism may be alleviated through the use of
high fibre diets. It is believed that high fibre diets enhance gut development
and gizzard function, which in turn help reduce aggressive behaviour in
hens.

Chicken anaemia virus infection (known generally in the

industry as CAV) is an acute viral infection of chickens that is found
worldwide. The disease is not known to affect any other bird species,
although antibodies have been found in Japanese (coturnix) quail. Prior to
confirmation that the disease was in fact caused by a virus it was known as
Chicken Anaemia Agent or CAA.
CAV can infect chickens of all ages but disease is only seen in young
chickens and is characterised by depression, anaemia, inappetence,
haemorrhage and a sudden rise in mortality. CAV depresses the immune
system and therefore leaves affected birds more susceptible to other
infections and mortality can often be a result of secondary infections.
What causes chicken anaemia virus infection?
CAV is a small DNA virus. In healthy chicks, susceptibility to disease
declines rapidly with age and chicks are resistant to the clinical signs of the
disease at 2 weeks of age. The virus can be spread both vertically (from
parents to offspring) and horizontally (between birds within a flock), via the
faecal-oral route.
Infected birds are viremic (shed virus) for up to 35 days. Infected roosters
will shed the virus in their semen and hens will shed the virus into eggs
during this viremic period. Chicks infected through their parents can spread
virus to other susceptible chicks with which they have contact, either
directly or indirectly.
Recovered or immunised birds have neutralising antibodies that protect
them from further infection. Chicks from immune breeder hens will be
protected by maternal antibody until their own age resistance develops.
Protection by maternal antibodies can however be overcome if the chick is
affected by another severe immunosuppressive disease, such as infectious
bursal disease, Marek’s disease or reticuloendotheliosis.
Prevention and treatment of chicken anaemia virus infection
There is no specific treatment. Secondary bacterial infections may be treated
with antibiotics and minimised through good biosecurity practices,
including hygiene and management. Vaccination of antibody-negative
breeder flocks prior to the start of egg production is recommended. The
control of other diseases that suppress the immune system is also
important. At present, there is no vaccine available to prevent subclinical
losses in broilers.

Chlamydophilosis is a bacterial infection that can range from

subclinical through to acute or chronic disease states. It is characterised by
respiratory, digestive or systemic infection. Chlamydophilosis can affect a
wide variety of bird species, including turkeys, pigeons, ducks, psittacines
(such as parrots), although chickens are not commonly affected.
Chlamydophilosis can affect other animal species and is a zoonotic disease
(can be transmitted to humans). Symptoms in birds include fever,
discharges from the nostrils and eyes, green to yellow-green droppings,
conjunctivitis, sinusitis, inactivity, ruffled feathers, weakness, loss of
appetite and weight loss. The disease in humans is usually respiratory and
characterised by rapid onset of flu-like symptoms. Pneumonia, organ
failure, and death can result if the disease is severe or left untreated.
What causes Chlamydophilosis?
Chlamydophilosis is caused by the bacterium Chlamydophila psittaci. This
bacterium can only multiply within host cells and spread is primarily
through inhalation of faecal dust. Recovered birds remain carriers and
continue to shed the organism for up to 42 days after clinical signs subside.
The same strain of the bacterium may cause mild disease or asymptomatic
infection in one species, but severe or fatal disease in another species. The
disease is not egg transmitted.
Prevention and treatment of Chlamydophilosis
There is no effective vaccine available for use in birds. Treatment with
tetracycline antibiotics will prevent mortality and shedding but cannot be
relied upon to eliminate latent infection and therefore shedding may recur.
Treatment of infected flocks with tetracyclines a minimum of two weeks
prior to slaughter can effectively eliminate the transmission risk to
processing workers. Effective biosecurity procedures are an important factor
in preventing infections from occurring. The bacterium can survive in dried
faeces for many months but is susceptible to heat and most disinfectants,
however it is resistant to acid and alkali.
Coccidiosis is one of the most common and economically important
diseases of chickens worldwide. It is caused by a parasitic organism that
damages the host’s intestinal system, causing loss of production, morbidity
and death. This disease has a major economic impact on the global poultry
industry.
Coccidia life-cycle
Coccidial parasites are protozoa belonging to the phylum Apicomplexa.
Chicken coccidiosis is caused by seven species, all from the
genus Eimeria: E. acervulina, E. brunetti, E, maxima, E. mitis, E. necatrix, E.
praecox and/or E. tenella. The life-cycles of these species are direct.
Chickens ingest sporulated oocysts (the parasite ‘egg’) from contaminated
litter, and these pass into the intestinal tract, where the parasites invade the
cells of the intestinal wall. Several cycles of replication occur which lead to
the formation of new oocysts which are shed in the faeces. Depending on
environmental conditions (including temperature and humidity), the oocysts
sporulate and become infective. The entire cycle takes 4 to 6 days. This
short, direct, life-cycle combined with the potential for massive replication
during the intracellular phase, makes this group of parasites a serious
problem under intensive farming conditions.
Intestinal damage
The following photos show intestinal damage caused by various species
of Eimeria in chickens. Source: The Merck Veterinary Manual

E. brunetti E. necatrix E. tenella

E. acervulina
It is the replicative phases of the parasite which lead to damage in
the intestinal tissues. Individual birds may show no clinical signs, or may
suffer a mild loss of appetite, weight loss or decreased weight gain,
diarrhoea (which can be bloody), dehydration and death. Resistance
develops rapidly and infections can be self-limiting, but naïve birds which
consume large numbers of oocysts can be severely affected and
die. Immunity is strictly species-specific which means that birds exposed to
one Eimeria remain susceptible to infection from all other species. The
degree of injury caused by the seven species varies, with some developing
deep in the intestinal mucosa, causing wide-spread damage and distinct
gross lesions (e.g., E. tenella). Other species are less destructive but may
still have a significant impact on production. All species are potentially of
importance economically.
The following diagrams show the intestinal sites parasitised by various
species of Eimeria in chickens. Source: The Merck Veterinary Manual

E. acervulina E. maxima E. mitis

E. brunetti

E. praecox E. tenella
E. necatrix
Methods of Control
Eimeria are present world-wide, and are ubiquitous under intensive farming
methods. Up to six species have been shown to occur simultaneously on one
farm. The omni-present nature of Eimeria precludes eradication as a
practical option for control. Since species-specific immunity develops
rapidly, the management of coccidiosis aims to achieve a balance between
allowing natural immunity to build up and preventing high oocyst exposure
to naïve birds. Hygiene, anticoccidial drugs and vaccines all play major
roles.

Oocysts of E. maxima Source: The Merck Veterinary Manual

Hygiene
As species of Eimeria have direct life-cycles, mechanical transmission is the
primary means of spread between farms and between sheds on a farm.
Oocysts are resistant in the environment, both to climatic extremes and
disinfectants, and can survive for weeks in soil. However, they only last for
days in litter due to heat caused by fermentation and the presence of
ammonia. Good hygiene, such as cleaning boots and exchanging clothes
between sheds, and the eradication of rodents, assists in minimizing the
transmission of oocysts. Effective farm management, such as well
maintained, drip-free water lines, minimize the level of infective oocysts in
the litter, as desiccation significantly reduces sporulation.
Anticoccidial Drugs

Release of merozoites Source: The Merck Veterinary Manual

Chemotherapy has been the main approach for controlling coccidiosis in
chickens. Anti-coccidial drugs are usually used preventatively and if a
farmer were to wait for overt signs of disease before treating the flock,
morbidity and mortality would be high and the economic damage already
done. Almost all commercial, intensively farmed flocks are administered
anti-coccidial drugs prophylactically. When given at the correct low
preventative doses, Eimeriaspecies are able to complete their life-cycles
without large numbers of infective oocysts building up in the environment.
Such subclinical infections result in the development of strong, specific
natural immunity without overt disease.
Vaccination
Live, virulent vaccines have been utilized since the 1960s and live
attenuated vaccines have become available since the 1980s. The attenuated
strains have been selected for rapid passage through the host.
Consequently, they have low reproductive potential and have lost their
virulence, but still have strong immunogenicity. Importantly, they cause no
post-vaccinal decrease in weight gain, and are therefore suitable for use in
broiler flocks.
Colibacillosis is an infectious disease caused by the bacterium Escherichia
coli (also known simply as E. coli), and is seen in poultry flocks worldwide. E.
coli can cause an infection under the skin, known as cellulitis, and is
commonly associated with respiratory disease in birds, which in severe
cases leads to septicaemia and death. Avian colibacillosis primarily affects
broiler chickens between the ages of 4 and 6 weeks and is responsible for a
significant proportion of the mortality found in poultry flocks. This
mortality, treatment of the disease and decreased feed conversion efficiency
result in significant costs to the poultry
industry.

Symptoms
Signs of colibacillosis are respiratory distress, reduced appetite and poor
growth. Lesions seen at post mortem are airsacculitis, pericarditis,
perihepatitis and peritonitis. Figures 1, 2 and 3 illustrate the clear airsac of
an uninfected bird, the foamy exudate seen early in infection, and the
caseous exudate later in infection.

Figure 1. Clear airsac ofFigure 2. Foamy exudateFigure 3. Caseous

an uninfected bird seen early in infection exudate later in infection
E. coli are gram negative facultatively anaerobic (can be both aerobic an
anaerobic depending on environmental conditions) bacilli that are part of
the normal intestinal microflora of poultry. Although most E. coli are non-
pathogenic, some strains are able to establish themselves outside of the
intestines and cause disease. These strains are known as Avian
Pathogenic E. coli (APEC). High numbers of E. coli are maintained in the
poultry house environment through faecal contamination and the common
route of infection is inhalation of the faecally contaminated dust that
contains large numbers of pathogenic E. coli.
Predisposing Factors for Colibacillosis
Respiratory disease attributed to infection with E. coli is most commonly
seen after respiratory stress caused by infections with Mycoplasma
gallisepticum or viral agents such as infectious bronchitis virus (IBV) and
Newcastle disease virus (NDV). Environmental influences, such as
temperature, humidity, and high concentrations of ammonia and dust in
poultry houses, also contribute to the respiratory stress of birds.
Virulence Factors Encoded on a Plasmid
Strains of Avian Pathogenic E. coli are known to possess specific virulence
factors that are commonly carried on a large virulence plasmid. Many
factors have been associated with the virulence of these E. coli strains,
including the production of colicin V, resistance to serum, temperature
sensitive haemagglutination and adhesins. Adherence to epithelial cells is a
fundamental requirement for colonisation of the respiratory tract by E. coli.
Iron scavenging mechanisms are thought to be one of the more important
factors, as iron is essential for bacterial growth and therefore the
establishment of infection. Numerous systems exist for iron acquisition,
most of which are plasmid encoded. It is believed that a combination of
these factors increases the pathogenicity of E. coli.
Diagnosis of Colibacillosis
Colibacillosis causes typical pathology, which can be seen during post
mortems of affected birds. Isolation of a pure culture of E. coli from the
heart, liver or other lesions confirms the diagnosis.
Control and Treatment of Colibacillosis
Control measures taken to prevent E. coli infection in chickens primarily
involve elimination of predisposing factors, which includes vaccinating birds
against mycoplasmas, IBV and NDV. E. coli is susceptible to disinfectants
and temperatures greater than 80oC, so thorough cleaning of poultry
houses, thereby reducing exposure to pathogenic strains of E. coli, can help.
Ensuring proper ventilation and chlorination of drinking water also reduces
the levels of environmental contamination. Treatment of colibacillosis relies
on antimicrobial therapy, but with isolates of E. coli becoming increasingly
resistant to frequently used antibiotics, this treatment may fail.

Cryptosporidiosis is a parasitic disease that affects quail, pheasants,

peafowl, waterfowl, chickens, turkeys, finches and psittacines (such as
parrots). Cryptosporidia are poorly host-specific and can affect other animal
species including humans, other mammals, reptiles, amphibians and fish.
However, species that infect birds are rarely infectious to humans. The
disease is not egg transmitted.
Some infections are asymptomatic (infected hosts show no symptoms),
however often the disease in birds is characterised by acute and/or chronic
disease of the respiratory and digestive tracts. The disease is usually fatal in
quail and more serious in turkeys than chickens. Symptoms of the
respiratory forms of the disease include discharge from the nostrils and
eyes, swollen sinuses, coughing, sneezing, breathing difficulties and rales
(clicking, bubbling or rattling sounds in the lungs). The intestinal form is
characterised by diarrhoea, weight loss and ruffled feathers.
What causes cryptosporidiosis?
Cryptosporidiosis is caused by protozoan parasites of the genus
Cryptosporidium and are related to coccidia, but have much smaller oocysts
(the spore-like infective stage of the lifecycle that is passed from the infected
host to the new host). Cryptosporidium baileyi can cause respiratory disease
in chickens and turkeys and can also cause infections of the hindgut and
cloacal bursa in chickens, turkeys, and ducks. C. meleagridis also infects
chicken and turkey species. The organism is transmitted by susceptible
birds inhaling or ingesting oocysts passed in the droppings of infected birds.
The oocysts are very resistant in the environment. Oocysts can also be
carried between flocks by people on shoes and clothing and equipment.
Prevention and treatment of cryptosporidiosis
There are no satisfactory control measures except isolation and good
sanitation. All known anticoccidial drugs are ineffective against
Cryptosporidium spp and they are extremely resistant to chemical
disinfection. Supportive therapy may reduce mortalities. Steam cleaning is
effective in reducing infection as oocysts are inactivated above about 65°C.
Treatment and prevention are both based on good hygiene, sanitation
and biosecurity practices. All dead infected birds should be incinerated.

Egg drop syndrome (EDS) is caused by a viral infection in laying

hens. It is characterised by production of soft-shelled and shell-less eggs in
apparently healthy birds, and leads to a sudden drop (10-40%) in recorded
egg production or a failure to achieve a normal peak in production. It can be
difficult to identify the early stages of the disease as hens will eat the shell-
less eggs, and the only evidence that may remain is the membranes, which
is a sign that is easy to miss. In flocks where some birds have acquired
immunity due to the spread of the virus, a failure to reach expected
production targets is observed. Clinical signs include diarrhoea and brief
loss of shell colour and egg yolk pigment prior to the production of soft-
shelled eggs and mortality is usually negligible. Ducks and geese are the
natural hosts for the EDS virus and are asymptomatic carriers. Chickens of
all ages and breeds are susceptible but the disease is most severe in broiler
breeders and brown-egg layer strains. EDS was first introduced into
chickens through contaminated vaccine and spread through breeder flocks.
EDS is a notifiable disease in some states of Australia.
EDS can be distinguished from Newcastle disease and influenza virus
infections by the absence of illness, and from infectious bronchitis by the
eggshell changes that occur at or just before the drop in egg production.
What causes egg drop syndrome?
EDS is caused by infection with the EDS virus which is an adenovirus. The
incubation period is three to five days and the course of the disease is four
to 10 weeks. The virus is transmitted through any of the conventional
means of viral disease spread and is also transmitted on and in the egg
(horizontal and vertical transmission). The main method of horizontal
spread is through contaminated egg trays, however, droppings are also
infective. Contact with wild ducks or geese, or water or ranges frequented by
these birds, may be a source of infection. Humans and contaminated
fomites (such as crates or trucks) can spread virus, which can also be
transmitted by needles when vaccinating and drawing blood. Insect
transmission has not been proven but is considered possible. Chicks
hatched from infected eggs may develop antibodies and excrete virus
however it is more common that the virus will remain latent (alive but
inactive) and subsequently the bird will not produce antibodies. The virus
reactivates and grows in the oviduct when the hens go into lay, at which
point the viral cycle begins again. Birds which are immune to the virus
(already have antibodies) reduce the rate of spread of the virus. EDS has no
effect on fertility or hatchability of eggs that are suitable for setting.
Treatment and prevention of EDS
There is no successful treatment of EDS. The classical form has been
eradicated from primary breeders and the maintenance of EDS-free breeding
stock is the main control measure. In layers, induced moulting will restore
egg production after an episode of EDS infection. The prevention of
horizontal spread relies on good biosecurity and washing and disinfecting
plastic egg trays before use can control the endemic form. The sporadic form
can be prevented by ensuring that chicken flocks do not come into contact
with other birds, especially waterfowl. As such, potentially contaminated
water should be chlorinated before use and general sanitary precautions
should always be followed. There are vaccines available to prevent infection,
and if appropriately produced and administered, these inactivated vaccines
can prevent clinical disease but will not prevent virus shedding.

Fatty liver syndrome is a condition that affects only hens, primarily

caged layers. It is a metabolic or nutritional disease and is characterised by
general obesity with an enlarged, fatty liver that becomes soft and easily
damaged. Mortality rates vary and death is often caused by internal
haemorrhage due to rupture of the liver.
What causes fatty liver syndrome?
The principal cause is thought to be excessive calorie intake, but it may also
be related to exposure to the mycotoxin aflatoxin, calcium deficiency and/or
stress. An incorrect protein:energy balance may also be to blame. Some
strains of laying hen appear to be more susceptible. The higher producing
hens appear the be the birds within a flock that are most affected. Fatty
liver syndrome has been seen in conjunction with cage layer fatigue.
Prevention and treatment of fatty liver syndrome
The principal causes of fatty liver syndrome are related to feed
ingredient quality or inappropriate feed formulation. Unless caused by
aflatoxin or calcium deficiency, the main treatment for this condition is to
reduce the amount of dietary energy consumed. If aflatoxin is involved, the
contaminated feed must be replaced. If a calcium deficiency is suspected,
adding large particle calcium to the diet is recommended, as this allows the
hen to select an increased calcium intake without over-consuming the
energy component of the diet. Some farmers add choline chloride to feed as
a treatment, however effects are variable. If a complete layer ration is being
fed, addition of vitamins can be of benefit. However, control of body fat is the
only successful remedy for this condition and is best accomplished by
regulation and reduction of total energy intake.

Fowl cholera is a contagious bacterial infection. The disease can range

from acute septicaemia (blood poisoning) to chronic and localised infections.
Domestic fowl, game birds and small feral birds are susceptible. Turkeys are
more susceptible than chickens, older chickens are more susceptible than
younger ones, and some breeds of chickens are more susceptible than
others. The disease is rare in broiler-aged chickens.
Clinical findings vary greatly depending on the course of the disease. In
acute cases, increased mortality is usually the first indication. Affected birds
have swelling of the face or wattles, discharge from the nostrils, mouth and
eyes which may become “cheesy”, laboured breathing and, in some cases,
lack of coordination. The face, combs and wattles may become cyanotic
(turn a bluish colour). Other symptoms include depression, loss of appetite,
lameness, diarrhoea and ruffled feathers.
What causes fowl cholera?
Fowl cholera is caused by the bacterium Pasteurella multocida. Chronically
infected birds are considered to be a major source of infection and recovered
birds remain carriers. Transmission is from bird to bird or from infected
premises.
Prevention and treatment of fowl cholera
Fowl cholera can be treated with sulfonamides and antibiotics. Vaccines are
available but give variable results. A live attenuated vaccine has been
developed in Australia by Poultry CRC partners Bioproperties Pty Ltd, under
the trade name Vaxsafe ® PM. A live vaccine will give more widespread
protection than the individual inactivated types.
The disease is best controlled by eradication. Prevention relies on
good biosecurity practices, with good sanitation and rodent control and
separation of birds by age with thorough cleanout between flocks. This
bacterium is susceptible to ordinary disinfectants, sunlight, drying, and
heat.

Fowl pox is a relatively slow-spreading viral infection that affects most

bird species, including all commercial forms of poultry. It occurs in both a
wet and dry form. The wet form is characterised by plaques in the mouth
and upper respiratory tract. The dry form is characterised by wart-like skin
lesions that progress to thick scabs. The disease may occur in any age of
bird, at any time. Mortality is usually not significant unless the respiratory
involvement is severe. Fowl pox can cause depression, reduced appetite and
poor growth or egg production. The course of the disease in the individual
bird takes three to five weeks.
What causes fowl pox?
Fowl pox is caused by an avian DNA pox virus. There are five or six closely
related viruses that primarily affect different species of birds but there is
some cross-infection. Infection occurs through skin abrasions or bites,
through the respiratory route and possibly through ingestion of infective
scabs. It can be transmitted by birds, mosquitoes or fomites (inanimate
objects such as equipment). The virus is highly resistant in dried scabs and
under certain conditions may survive for months. Mosquitoes can harbour
infective virus for a month or more after feeding on affected birds and can
subsequently infect other birds. Recovered birds do not remain carriers. A
flock may be affected for several months as fowl pox spreads slowly.
Prevention and treatment of fowl pox
There is no treatment for fowl pox and prevention is through vaccination of
replacement birds. Where preventative vaccination is used, all replacement
chickens are vaccinated when the birds are six to ten weeks of age and one
application of fowl pox vaccine results in permanent immunity. Vaccination
of broilers is not usually required unless the mosquito population is high or
infections have occurred previously. Chicks may be vaccinated as young as
one day of age. During outbreaks, unaffected flocks and individuals may be
vaccinated to help limit the spread. If there is evidence of secondary
bacterial infection, broad-spectrum antibiotics may help reduce morbidity
and mortalities. As mosquitoes are known reservoirs, mosquito control
procedures may be of some benefit in limiting spread in poultry confined in
houses.

Histomoniasis is a parasitic protozoan infection of turkeys, chickens,

peafowl and several game bird species. Most infections are fatal in turkeys,
but mortality is less common in other birds. Although chickens are relatively
resistant to the condition, significant disease has been observed in breeding
chickens and free-range layers. Clinical signs include depression,
inappetence, poor growth, increased thirst, mustard-yellow diarrhoea,
listlessness and dry, ruffled feathers. The common name for this disease is
‘blackhead’, which stems from the clinical sign where the bird’s head may
become cyanotic (blue-black in colour). Chronically sick birds will become
dehydrated and emaciated before dying and young poults may die within a
few days of signs appearing.
What causes histomoniasis?
Histomoniasis is caused by the protozoan Histomonas
meleagridis which acts with existing intestinal bacteria, such as Escherichia
coli, to cause the condition. After the protozoan is ingested it first infects
the caeca then migrates through the blood stream to the liver. It is then
passed out in the droppings and also within the eggs of the caecal
worm Heterakis gallinae, if that is also present in the bird. Most infections
are caused by birds ingesting infected caecal worm eggs and sometimes
directly by contact with infected birds. Outbreaks spread quickly through
flocks by direct contact. Earthworms also feed on caecal worm eggs and
birds can be infected by ingesting infected earthworms. The protozoa is very
resistant when inside worm eggs, larvae or earthworms and can be
perpetuated from flock to flock in this way. It has recently been
demonstrated that infection occurs readily via the cloaca when turkeys are
on contaminated litter.
Prevention and treatment of histomoniasis
Drugs have been produced that will control the disease but there may be
restrictions on their use in commercial flocks, and currently no treatments
have been approved for use in Australia. As control primarily relies on
management and control of H. gallinae, frequent worming of flocks with
benzimidazole anthelminthics helps reduce exposure to the caecal worms
that carry the infection. Good management, biosecurity, and sanitation and
housing birds on wire or concrete floors, or intensive re-littering for floor-
housed birds, can reduce the level of infection.

Infectious bronchitis is a highly contagious viral

respiratory infection of chickens, however the virus will also infect the
urogenital and gastrointestinal tracts. The clinical signs of infectious
bronchitis are non-specific and so laboratory tests are required to confirm
diagnosis. Clinical signs are strongly dependent on the tropism (preferred
tissue to infect) of the strain, but commonly include include coughing,
sneezing and gasping in young birds, loss of appetite and wet litter. Feed
intake decreases sharply and growth is retarded. Mortality in young birds
can be high (up to 30%), however minimal mortality is experienced in older
birds (> 5 weeks old). Less common strains can cause a sharp drop in egg
production in layers, and production usually drops to near zero within a few
days. Recovery occurs within 3 – 4 weeks, however some flocks never regain
an economical rate of lay. During an outbreak, small, soft-shelled, irregular-
shaped eggs are produced.
What causes infectious bronchitis?
Infectious bronchitis is caused by a coronavirus. The virus is highly variable
and new serotypes and genotypes continue to appear. The virus dies quickly
outside of the host but can spread through the air and can travel
considerable distances during an active outbreak. It can also be spread via
fomites such as clothing, poultry crates and equipment. The disease is not
egg transmitted and the virus does not survive much more than one week in
the house when poultry are not present. Classical Australian strains are
nephropathogenic (cause kidney damage) and treatment using electrolytes
may be beneficial in an outbreak. Insufficient work has been done on
antigenic variants in Australia and there is a limited range of vaccines
available (all local strains). Variants are continually being detected, the most
recent to cause problems was detected in NSW broiler flocks.
Prevention and treatment of infectious bronchitis
The highly contagious nature of this disease generally results in all
susceptible birds on the premises becoming infected, often in spite
of biosecurity measures such as sanitary or quarantine precautions, which
should always be maintained. There is no treatment for this disease.
Secondary infections with bacterial diseases are common and antibiotics
may reduce losses from these infections. The virus is easily destroyed by
heat and ordinary disinfectants. In young chickens it is helpful to increase
the brooder temperature and to optimise environmental conditions.
Chickens that are kept as layers should be vaccinated. Whether broilers are
vaccinated depends upon many operation-specific factors as numerous
vaccines are commercially available. These vaccines represent a modified or
selected strain of the infectious bronchitis virus and therefore the vaccine
used should contain specific virus known to be present in the area. All
vaccines contain live virus and those that give the best protection
unfortunately can also produce clinical signs of disease and 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.

Egg shell defects caused by infectious bronchitis Source: Merck Veterinary

Manual

Infectious bursal disease (IBD), also known as Gumboro, is a

highly contagious viral infection that is found in chicken flocks in most
countries. The severity of the disease will depend on the age and breed of
chicken (White Leghorns are more susceptible than broilers and brown-egg
layers) and the virulence of the virus. Signs of the disease can include a
rapid drop in feed and water consumption, mucoid (slimy) diarrhoea with
soiled vent feathers, ruffled feathers, listless chicks with unsteady gait or
sitting in hunched position, picking at own vent and sleeping with beak
touching the floor.
Infections before 3 weeks of age are usually subclinical (no detectable
symptoms). Chickens are most susceptible to clinical disease at 3-6 weeks
and severe infections have occurred in Leghorn chickens up to 18 weeks old.
Early subclinical infections are the most economically important as the
disease can cause severe, long-lasting suppression of the immune system.
Chickens that are immunosuppressed by early IBD infections do not
respond well to vaccination and are more susceptible to other diseases,
including those that don’t normally affect healthy chickens.
In clinical infections, onset of the disease is sudden after an incubation of 3-
4 days. Mortality is usually low but has been reported to be as high as 20%.
Recovery from the disease usually occurs in less than a week, however
broiler weight gain is delayed by 3-5 days. The presence of maternal
antibody (antibody passed to the chick from the mother) will modify the way
the disease progresses. The virulence of field strains varies considerably.
Very virulent (vv) strains of the virus that cause high mortality and
morbidity were first detected in Europe, and have not yet been detected in
Australia.
What causes infectious bursal disease?
Infectious bursal disease is caused by a birnavirus (IBDV) that is most
readily isolated from the bursa of Fabricius which is an organ of
the immune system. The virus can also be isolated from other organs. It is
shed in the faeces and spreads between birds or by contact with a
contaminated environment and is possibly also carried in dust. The virus
can be transferred from house to house on fomites (any inanimate object or
substance that is capable of carrying infectious organisms from one
individual to another) and rodents. The virus is very stable and difficult to
eradicate. There is no vertical transmission (from parents directly to
offspring) and mealworms and litter mites may harbour the virus for 8
weeks. Infected birds shed large amounts of virus for up to 2 weeks after
infection.
Prevention and treatment of infectious bursal disease
There is no treatment for IBD but support therapies such as vitamin and
electrolyte supplements and antibiotics to treat any secondary bacterial
infections, may reduce the impact of the disease.
Depopulation and rigorous disinfection of contaminated farms have
achieved some limited success in preventing disease spread. Prevention is
through good biosecurity and vaccination, including passive protection via
breeders and vaccination of progeny depending on virulence and age of
challenge. In most countries, breeders are immunised with a live vaccine at
6-8 weeks of age and then re-vaccinated with an oil-based inactivated
vaccine at 18 weeks. Birds that have recovered from a natural infection have
a strong immunity. If maternal antibody was still high at the time of
vaccination, immunity in chicks that receive live vaccine can be poor.
Due to the high degree of variation between naturally occurring IBD viruses
there are a number of vaccines available. Vaccines need to be selected based
on the types of viruses present in the area. The disease is believed not be
present in New Zealand. The Australian field strains of IBD are relatively
mild and live vaccination of broilers is not regarded as necessary. The main
method of control relies on vaccination of parent chickens and transmission
of maternal antibody to the chicks.

Infectious coryza is a contagious bacterial respiratory infection of

chickens. While there are reports of a similar disease in other birds such as
pheasants and guinea fowl, there is considerable doubt if these non-chicken
cases are associated with the same aetiological agent. The disease occurs
most often in adult birds. Infection can spread slowly, with chronic disease
affecting only a small number of birds, or rapidly, with a higher percentage
of birds being affected. Clinical signs include swelling around the face and
wattles, watery or pus-like discharge from the eyes and nostrils, difficulty
breathing, sneezing, loss of appetite, weight loss and a drop in egg
production.
What causes infectious coryza?
Infectious coryza is caused by the bacterium Avibacterium paragallinarum.
Earlier names for this organism, including Haemophilus
paragallinarum and Haemophilus gallinarum should no longer be used. The
bacterium is spread through contact with infected birds or exudates.
Recovered birds remain carriers of the bacteria for long periods and as such,
once a flock is infected all birds must be considered as carriers. Birds can
be more susceptible if already infected with other respiratory viral or
bacterial infections.
Prevention and treatment
Infectious coryza can be treated with a number of antibiotics
and vaccines are used to prevent infection in high incidence areas. However,
control of the disease requires good husbandry practices. Prevention is best
achieved using biosecurity principles based on an all-in/all-out replacement
policy and ensuring replacement birds are not infected. If infection occurs,
complete depopulation followed by thorough cleaning/disinfecting is the
only means for eliminating the disease. The bacterium survives 2-3 days
outside the bird but is easily killed by heat, drying and disinfectants.
Swollen sinuses from infectious coryza Source: The Merck Veterinary Manua

Infectious laryngotracheitis (ILT) is a highly contagious viral

respiratory infection of chickens and pheasants and the disease is notifiable
in most Australian states. A number of other bird species such as turkeys,
ducks, geese and quail can be carriers of the virus and recovered birds are
long-term carriers. Mortality and morbidity rates vary but mortality in young
birds can be as high as 80% and the disease can cause a severe drop in egg
production in laying flocks. Clinical signs include watery eyes, wheezy and
gasping breathing, watery discharge from nostrils, sneezing and coughing of
mucous and blood.
What causes infectious laryngotracheitis?
ILT is caused by a herpesvirus. The virus is spread by direct contact with
infected birds or through contact with contaminated dead birds, bird tissue,
equipment, housing, humans or other animals. Although the virus is easily
killed by disinfectants, fumigants and direct sunlight it can survive in
infected litter for up to 2 months and dead carcasses for up to 12 months.
Outbreaks tend to occur in areas of high broiler farm density and
vaccination may be the only avenue of control.
Prevention and treatment of infectious laryngotracheitis
There are no specific treatments for the disease but antibiotics to control
secondary bacterial infections may reduce losses. Vaccination is available
using attenuated live vaccines but this approach perpetuates the disease.
Good biosecurity principles such as effective sanitation and quarantine
procedures are important control measures. The A20 vaccine strain was
developed in Australia and is mild enough to be used in young broilers
(when it’s available).
Leg and skeletal problems are a very important area especially
from welfare points of view and are common in some breeds of broilers.
Issues include rickets, TD, spondylolisthesis, slipped tendons, tibial rotation
and femoral head necrosis.
Slipped tendon
Slipped tendon or Perosis is a metabolic disease that causes deforming leg
weakness in chickens, ducks and turkeys. It is usually seen in poultry less
than six weeks of age, and results in flattened and enlarged hocks. This
causes slippage of the Achilles tendon at the hock which causes the foot and
shank to extend laterally from the body, and only appears in one leg. It is
called ‘spraddle legs’ if both legs are affected, and is most often caused by
injuries received when other chicks pile upon it or when the chick is placed
on slick flooring soon after hatching.
What causes perosis?
Perosis is caused by a deficiency of a number of trace nutrients, primarily
manganese and choline, but zinc, pyridoxine, biotin, folic acid and niacin
may also be involved. In turkeys it may be an inherited galactosamine
deficiency.
Prevention and treatment of perosis
It is important to provide starter and grower diets that are formulated to
contain adequate amounts of all trace minerals and vitamins, especially
manganese and choline. Water that contains vitamin supplements will
ensure that perosis does not develop in young chicks. Most perosis-affected
flocks will respond to supplementation with manganese.

Lice and mites are common external parasites of poultry. Lice are
insects, while mites belong to the same family as spiders. There are a large
number of lice and mite species that can infest poultry under the
appropriate conditions. They are either blood-suckers or live on dry skin
scales, feathers or scabs on the skin. Adults can survive for 4-5 days away
from the host. Therefore, infestation can be spread by direct contact
between birds but also through contact with infested litter etc. They are
more common and difficult to control in floor-based housing systems than
in cage systems. Symptoms of infestation can include scratching, poor
feather condition, unthriftiness, nervous behaviour and anaemia can occur
with severe blood-sucking infestations.

The chicken mite (Dermanyssus gallinae) Source: The Merck Veterinary

Manual
Prevention and treatment of lice and mites

Skin lesions caused by chicken mite Source: The Merck Veterinary Manual

Skin lesions caused by scaly leg mite (Knemidocoptes mutans) Source: The
Merck Veterinary Manual
Flocks should be kept away from backyard or wild birds and individual
birds examined regularly for adult parasites and eggs. Infestations can be
treated with appropriate chemical pesticides, either as dry powders or liquid
sprays. Effective biosecurity procedures such as an all-in/all-out clean out
between flocks will help manage these pests.

Lymphoid Leukosis is a neoplastic (tumour causing)

viral infection of chickens that is found in flocks worldwide. The virus has
been eradicated from some SPF (specific pathogen free) flocks. Globally, the
frequency of infection has been reduced substantially in the primary
breeding stocks of several commercial poultry breeding companies. This
control program has led to infection becoming infrequent or absent in
commercial flocks. The frequency of avian Leukosis tumours, even in heavily
infected flocks, is typically low (<4%), and disease is not often apparent in
infected flocks. However, mortality up to 1.5% excess mortality per week has
been reported in commercial broiler-breeder flocks naturally infected with
an avian Leukosis virus.
Affected birds show non-specific clinical signs including reduced feed intake,
weakness, diarrhoea, dehydration, weight loss, depression and reduced egg
production. Palpation often reveals an enlarged bursa of Fabricius and
sometimes an enlarged liver. The disease can be immunosuppressant which
increases susceptibility to other diseases.
A subclinical disease syndrome characterised by depressed egg production
in the absence of tumour formation is economically more important than
mortality from Lymphoid Leukosis.
The incubation period for Lymphoid Leukosis is 4-6 months and as a
consequence the disease is usually seen in broiler flocks.
What causes Lymphoid Leukosis?
Lymphoid Leukosis is caused by certain members of the Leukosis/sarcoma
group of avian retroviruses. These viruses are commonly called avian
Leukosis viruses and belong to subgroups A, B, C, D, E, and J. Subgroups A
and B have been most prevalent in western countries, until the emergence
of subgroup J.
The virus can be vertically transmitted (passed directly from parent to
offspring). Hens with subclinical disease usually shed virus or viral antigen
into the albumen of eggs. Chickens infected at hatching shed virus their
entire lives. Horizontal transmission (spread from bird to bird) can occur by
the faecal-oral route but is of secondary importance to vertical transmission.
Prevention and treatment of Lymphoid Leukosis
There is no treatment for Lymphoid Leukosis. Lymphoid Leukosis appears
to be controlled best by reduction and eventual eradication of the causative
virus, which are rapidly inactivated at ambient temperature and on
exposure to most disinfectants. Prevention is also helped by obtaining
chicks from breeder flocks that are free of the virus and rearing birds in
isolation with adequate ventilation. Follow good biosecurity and
management procedures to prevent stress and control other diseases, and
dispose of dead birds by composting, incineration or deep burial.
Some chickens have specific genetic resistance to infection with certain
subgroups of avian Leukosis virus, although genetic resistance is unlikely to
replace the need for reduction or eradication of the virus. Thus
far, vaccination for tumour prevention has not been promising. However,
recombinant vaccines have been developed that can induce antibodies in
breeders to ensure protective maternal antibodies in chicks and these may
be useful to assist with eradication programs.
Reticuloendotheliosis or Lymphoid Tumour Disease is
a retrovirus infection that is common in chickens, turkeys, ducks, geese and
quail with morbidity rates up to 25%. A gradual increase in mortality and
reduced weight gain in broilers may be the first clinical signs of the disease.
Clinical signs also include diarrhoea and leg weakness.
What causes Reticuloendotheliosis?
Transmission is lateral and possibly transovarian (from ovary to egg; type of
vertical transmission), and the infection can be spread by mosquitoes or in
contaminated Marek’s disease vaccines. There is an incubation period of 5-
15 days.
Prevention and treatment of Reticuloendotheliosis
Formal control programmes have not been documented as the condition is
sporadic and relatively self-limiting. Avoidance of live vaccine contamination
is the main control measure practised.

Marek’s Disease Virus (MDV) is a highly contagious

viral infection that predominantly affects chickens but can also affect
pheasants, quail, gamefowl and turkeys. It is one of the most common
diseases that affects poultry flocks worldwide. Clinical disease is not always
apparent in infected flocks, however subclinical disease is often more
economically important as it reduces weight gain and egg production.
Mortality rates can be very high in susceptible birds. Marek’s Disease (MD)
results in enlarged nerves and in tumour formation in nerve, organ, muscle
and epithelial (cells that line the internal and external surfaces of the body)
tissue. Clinical signs include paralysis of the legs, wings and neck, weight
loss, grey iris or irregular pupil, vision impairment and the skin around
feather follicles can be raised and roughened. Affected birds are
immunosuppressed and as a consequence are more susceptible to other
infectious diseases.
The clinical signs associated with MD can look similar to those caused by
Lymphoid Leukosis and Reticuloendotheliosis, however the rareness of
bursal tumours with MD helps distinguish this disease from Lymphoid
Leukosis. Also, MD can develop in chickens as young as 3 weeks old,
whereas Lymphoid Leukosis is typically seen in chickens older than 14
weeks old. Reticuloendotheliosis, although rare, can easily be confused with
MD because both diseases feature enlarged nerves and T-cell lymphomas (a
type of tumour that involves white blood cells called T-cells, which are part
of the active acquired immunity system) in visceral (soft internal) organs.
What causes Marek’s Disease?

Leg paresis (partial paralysis) from

Marek’s disease Source: The Merck
Veterinary Manual
Grey iris and irregular pupil from Marek’s disease
MD is caused by a highly cell-associated (virus particles that remain
attached to or within the host cell after replication) but readily transmitted
herpesvirus. The route of infection is usually respiratory. The serotypes that
exist are ‘virulent’ (disease causing) chicken isolates (serotype 1) and
‘avirulent’ (non-disease causing) chicken isolates (serotype 2). The avirulent
virus that is commonly found in turkeys is designated serotype 3.
Serotypes are identified by reaction with serotype-specific monoclonal
(clones from a single cell) antibodies or by biological characteristics such as
host range, pathogenicity (severity of disease), growth rate, and plaque
morphology (the physical appearance of laboratory grown viral cultures).
Currently, virulent serotype 1 strains are further divided into pathotypes
(classification based on the severity of disease caused by that particular
strain of virus), which are often referred to as mild (m), virulent (v), very
virulent (vv), and very virulent plus (vv+) MD virus strains.
The virus matures into a fully infective, enveloped virus in the cells that line
the feather follicle and is released into the environment in dander (small
scales from feathers which flake off and can become airborne). The virus
may also be present in faeces and saliva. When cell-associated, the virus
may survive for months in poultry house litter or dust and is resistant to
some disinfectants. Infected birds become carriers of the virus for life and
are a source of infection to susceptible birds. A Poultry CRC epidemiological
study has revealed that MDV is less prevalent in the environment than
previously thought, however, it is long lasting and remains infective in dust
despite wide variations in atmospheric temperature.
Prevention and treatment of Marek’s Disease

Skin lesions from Marek’s disease Source: The Merck Veterinary Manual
There is no treatment for MD. Vaccination is the central strategy for the
prevention and control of MD. While vaccination will prevent clinical disease
and reduce shedding of infective virus it will not prevent infection. Cell-
associated vaccines are generally more effective than cell-free vaccines
because they are neutralised less by maternal antibodies. Over time,
increasingly virulent strains of MD virus have emerged, which has resulted
in an ongoing need to develop new vaccines and vaccination programs to
combat the disease. It was found that better protection from MD was
obtained when certain combinations of serotypes were used together in a
vaccine rather than one serotype alone (protective synergism). This
phenomena, which is unique to MD and is strongly serotype specific, has led
to the development of polyvalent vaccines (vaccines containing more than
one vaccine strain). The efficacy of vaccines can be improved by strict
sanitation to reduce or delay exposure and by breeding poultry for genetic
resistance to MD. Vertical transmission (from parents to offspring) is not
considered to be important. Vaccines administered at hatching require 1-2
weeks to produce an effective immunity, therefore exposure of chickens
vaccinated at hatching to virus should be minimised during the first few
days after hatching. Vaccines are also effective when administered to
embryos at the 18th day of incubation. In ovo vaccination (vaccination of the
embryo prior to hatching) is now performed by automated technology and is
widely used for vaccination of commercial broiler chickens, mainly because
of reduced labour costs and greater precision of vaccine administration.
The history of Marek’s Disease control in Australia
In the early 1970’s, the success of vaccination against MD became apparent
in other countries but Australian quarantine restrictions prevented the
importation of any international vaccines. This necessitated the
development of a local vaccine. In 1974, field trials began using an
Australian isolate of herpesvirus of turkeys (HVT). This serotype 3 vaccine
was shown to be safe and gave an overall protection of 85.2%, which
compared favourably with results reported in other countries. Vaccination
with this strain was very effective and controlled MD in Australia until about
1980. HVT is generally produced as a cell-associated form of vaccine. A cell-
free form also exists but is less protective than its cell-associated
counterpart.
Despite the availability of serotype 1 and 2 vaccines in other countries, HVT
was the most commonly used vaccine throughout the world until the late
1970’s when MD outbreaks of increasing severity were reported in
vaccinated chickens. Viruses isolated at this time were classified as very
virulent Marek’s Disease viruses (vvMDV). The discovery of protective
synergism (better protection when combinations of serotypes were used
together in a vaccine rather than each serotype alone) between Marek’s
Disease vaccines prompted the use of bivalent vaccines (a mixture of two
vaccine strains) containing serotypes 2 and 3.
The importation of breeding stock coincided with increased problems from
Marek’s disease in the Australian poultry industry Source: Australian Egg
Corporation Limited
MD continued to be widespread in Australia, with disease outbreaks despite
vaccination programs during the 1980’s. Consequently, an Australian cell-
associated serotype 2 vaccine “Maravac”, which was licensed for sale in
1977, was used alternatively with HVT or in combination.
In the early 1990’s, despite the use of Maravac, polyvalent vaccines and
increased doses of HVT, an increase in the prevalence of MD was once again
observed. During this time, imported breeds of chickens became available in
Australia. The influx of imported pullets into Australia coincided with
increases in MD mortality to over 50%, which had never been seen
previously in Australia. Field and breed comparison trials demonstrated that
imported breeds were responding poorly to Australian-derived MD vaccines.
The incidence of MD in imported breeds appeared to be higher than in
existing Australian strains of birds.
In view of this situation, and the emergence of strains of increased
virulence, changes in vaccination strategies included the vaccination of
broiler chickens, previously not routine practice in Australia.
Due to concern from the Australian poultry industry over the apparent
failure of Australian vaccines, a meeting was convened by the vaccine
manufacturer, Websters, and the Australian Veterinary Poultry Association
(AVPA) in 1993, where the industry reported to the government and vaccine
manufacturers the full extent of MD in Australia. Websters proposed that a
serotype 1 vaccine be imported from overseas. This option was unpopular
with the majority of the poultry industry and instead, the industry decided
to increase its funding of MD research, particularly aimed at providing
evidence that a serotype 1 vaccine would give better protection than existing
Australian vaccines and to develop an Australian serotype 1 vaccine. An
Australian serotype 1 vaccine was developed by RMIT with industry funding,
however prior to the commercialisation of the vaccine approval was given for
the importation of the Rispen’s serotype 1 vaccine. The Rispen’s vaccine is
derived from a mildly virulent serotype 1 MDV isolate which was further
attenuated (weakened) by 20 cell culture passages. Rispen’s vaccine has
been used extensively for protection against MDV strains of very high
virulence. It has been shown to be mildly virulent for highly susceptible
lines of chickens and maintains its ability to spread by
contact. Bioproperties now has an important role in importing Rispens
vaccine.
Future control of Marek’s Disease in Australia
The introduction of the Rispen’s vaccine to the Australian chicken industry
has lessened the need for an Australian serotype 1 MD vaccine.
Nevertheless, the RMIT vaccine seed has been stored as it may be useful if
further change occurs in the evolution of MDVs. Since the RMIT vaccine
virus is derived from an Australian isolate, it may share more antigens with
recent strains. The Rispen’s vaccine was derived from a mildly virulent
serotype 1 MDV isolated in the 1970s in The Netherlands and, as such, may
not possess antigens common to recent Australian strains.
Trivalent combinations of all three serotypes were introduced in 1990. As at
2004, trivalent vaccines were available in the USA, recommended only for
high risk flocks, but were not available in Australia. Using fowlpox virus and
herpesvirus of turkeys as vectors (an organism that does not cause disease
itself but which spreads infection by conveying pathogens from one host to
another), experimental recombinant (genetically engineered to contain DNA
from different organisms) vaccines have been shown to be effective against
challenge with virulent Marek’s disease virus. As at 2004, recombinant
vaccines were not commercially available.
For an existing farm, other than providing clothing for visitors (disposable
overalls) and using hard fibre based litter materials (wood shavings), risk
can be reduced by being aware that there is a higher seasonal incidence of
MD in Summer/Autumn, which peaks in March. This being so, it is
important to vaccinate broiler flocks that will mature at the end of Autumn,
not just those grown for the Christmas market. In terms of biosecurity, it is
more economically feasible to provide disposable overalls for visitors than to
clean vehicles between farms as cleaning vehicles does not reduce the
spread of MDV.
Future research
The Rural Industries Research and Development Corporation (a core partner
in the Australian Poultry CRC) is investing in a new project to develop a
DNA based test to quickly differentiate between wild-type MDV and MDV
from the Rispens vaccine, commonly used to vaccinate broiler-breeders and
layers. Armed with this test, it will be possible to ascertain if MDV on farms
is caused by spread of the vaccine amongst the progeny of broiler-breeders
or if it is a potentially dangerous wild-type. Meanwhile the Poultry CRC will
also look into the possibility of arranging a comparison between the
international reference strains of MDV with the known Australian strains to
establish, once and for all, just how virulent the Australian strains are. This
knowledge will help in the development of new vaccines against MDV. Given
that this work involves moving highly pathogenic virus between countries, it
will be carried out at either an Australian or overseas laboratory with the
highest possible levels of biosecurity.

Mycoplasmosis is a collective term for infectious diseases caused by

the micro-organisms called mycoplasmas. There are a number of
mycoplasmas that can infect poultry, with Mycoplasma gallisepticum (MG)
(which affects a number of bird species including chickens, turkeys,
gamebirds and pigeons), M. synoviae (MS) (which affects chickens and
turkeys), and M. meleagridis (MM) (which only affects turkeys) being the
main species.
MG can cause chronic respiratory disease and decreased growth or egg
production and affected carcasses sent to slaughter may be downgraded.
Some chickens may not show symptoms. Observable clinical signs may
include rales, coughing, sneezing, nasal discharge, frothiness and swelling
around the eyes or difficulty breathing. Signs are often more severe in
turkeys. MS can cause respiratory disease similar to MG but if it becomes
systemic it can cause lameness, swollen joints, loss of weight and breast
blisters. Greenish diarrhoea can also be present in dying birds. MM is a
venereal disease that can result in high mortality of young poults through
starvation. Signs in young poults include unthriftiness, difficulty breathing,
poor growth and neck and leg deformations. Breeder flocks may experience
a drop in egg production and hatchability.
What causes Mycoplasmosis?
All of these mycoplasmas can be transmitted vertically and so can be
introduced into the flock through infected eggs, including venereal
transmission by males for MM. Vertical transmission has been greatly
reduced through the establishment and maintenance of MG, MS and MM-
free breeder flocks. They can spread through bird-to-bird contact and
contact with exhaled respiratory droplets either as aerosols or on
equipment, people and surroundings. Birds recovered from MG and MM
remain carriers of the organisms and continue shedding for life.
Treatment and prevention of Mycoplasmosis
All of these mycoplasmas are sensitive to several antibiotics,
however vaccines for some mycoplasmas are also available.
Good biosecurity procedures are critical for prevention. Mycoplasmas are
destroyed by disinfectants and sunlight.
Necrotic Enteritis (NE) is the most common and financially
devastating bacterial disease in modern broiler flocks. Early signs of an NE
outbreak are often wet litter and diarrhoea, and an increase in mortality,
that may not be significant. However, the depression of growth rate and feed
efficiency of birds become noticeable by day 35 due to intestinal damage and
the subsequent reduction in digestion and absorption of food. Subclinical
infections are more economically damaging due to these factors.
Furthermore, increased condemnations at processing due to liver lesions
associated with subclinical NE can occur. The severity of clinical signs
varies with the age of the birds.
NE is a complex, multifactorial disease with many unknown factors that
influence its occurrence and the severity of outbreaks. In particular,
sporadic outbreaks of NE can occur frequently in farms where antibiotics
are not used as growth promoters, coccidial infections are not controlled,
the husbandry practice is not strict, and diets based on viscous grains with
animal protein sources.
Predisposing factors for the rapid proliferation of C. perfringens and the
onset of NE include other dietary and husbandry factors such as damage to
the intestinal mucosa through coccidial infection or a change in the normal
intestinal microflora as a result of a change in diet formulation, such as
inclusion of a high level of viscous cereal grains and/or animal by-
products like fish and meat meal.
What causes Necrotic Enteritis?
It is an infectious disease caused by Clostridium perfringens, which is a
gram-positive, anaerobic bacterium that can be found in soil, litter, dust
and at low levels in the intestine of healthy birds. Clostridium
perfringens only causes NE when it transforms from non-toxin producing
type to toxin producing type. There are five types of C. perfringens (A, B, C,
D and E) which produce a number of toxins (alpha, beta, epsilon, iota and
CPE). The α-toxin, an enzyme (phospholipase C), is believed to be a key to
the occurrence of NE. However, a recent study has shown that an isolate
that does not produce α-toxin can still cause disease and additionally, a new
toxin called NetB has been recently been identified in disease causing C.
perfringens isolates.
Prevention and treatment of Necrotic Enteritis

Necrotic enteritis (Score 1-mild; 4-severe )

Poultry CRC Deputy CEO, Vivien Kite; Monash University PhD student,
Anthony Keyburn; and Poultry CRC Chairman, Jeff Fairbrother at the
Cooperative Research Centres Association (CRCA) Conference in Perth (May
2007)

Outbreaks of NE can be effectively prevented by including antibiotics such

as bacitracin and avilamycin in the feed. In addition, an effective control of
coccidial infections can greatly reduce the risk of NE outbreaks.
Furthermore, if antibiotics are not used in the feed, strict on-farm hygiene
management practice, good climate control of the buildings and careful
selection of feed ingredients for diet formulation are all important in
maintaining production efficiency. In the Nordic countries, where antibiotics
have been removed from the feed, ionophorous anticoccidials have been
used to manage NE.
Following the ground-breaking discovery that alpha-toxin is not the main
causative factor for NE, by a Monash University PhD student funded by
the Poultry CRC, Anthony Keyburn, CSIRO Livestock Industries researchers
have patented NetB, the toxin they believe is the causative agent. The
research team has identified the novel toxin and is now working on how it
might be used to create the first truly effective vaccines against NE.

Newcastle Disease is a highly contagious viral infection that affects

many species of domestic and wild birds to varying degrees. Domestic fowl,
turkeys, pigeons and parrots are most susceptible while a mild form of the
disease affects ducks, geese, pheasants, quail and guinea fowl. The disease
can result in digestive, respiratory and/or nervous clinical signs, which
range from a mild, almost inapparent respiratory disease to very severe
depression, drop in egg production, increased respiration, profuse diarrhoea
followed by collapse, or long-term nervous signs (such as twisted necks), if
the birds survive. Severe forms of the disease are highly fatal.
What causes Newcastle Disease?
Newcastle Disease is caused by a paramyxovirus that can vary in
pathogenicity from mild to highly pathogenic. Spread is usually by direct
physical contact with infected or diseased birds. The virus is present in
manure and is breathed out into the air. Other sources of infection are
contaminated equipment, carcasses, water, food and clothing. People can
easily carry the virus from one shed or farm to another. Newcastle Disease
virus does not affect humans in the same way that it does birds but it can
cause conjunctivitis in humans.
Prevention and treatment of Newcastle Disease
There is no treatment for Newcastle Disease, although treatment with
antibiotics to control secondary infections may assist. The virus can remain
alive in manure for up to 2 months and in dead carcasses for up to 12
months, however it is easily killed by disinfectants, fumigants and direct
sunlight. Prevention relies on good quarantine and biosecurity procedures
and vaccination. Newcastle Disease vaccination of commercial meat and egg
layer chickens has been made compulsory in many Australian States. For
information on compulsory Newcastle Disease vaccination in your State
contact your State department of primary industries or agriculture. Further
information on the national situation in regard to Newcastle Disease can be
found at The Animal Health Australia website.

Signs of ND – conjunctivitis, depression and neurological signs Source: CSIRO

PARASITIC WORMS
All birds are naturally subject to infection by parasitic worms,
or Helminths. The majority of Helminths infect the digestive tract but some
are also found in other organs, such as the brain, trachea and eye. Not all
Helminth infections cause obvious clinical disease. The roundworms (or
nematodes) and the flatworms (including cestodes and trematodes) are
the two major classes of Helminth.

Roundworms in small intestine Source: The Merck Veterinary Manual

Parasitic worm lifecycles

Ascaridia galli eggs Source: The Merck Veterinary Manual

Capillaria eggs in an earthworm as intermediate host Source: The Merck

Veterinary Manual

Parasitic worms have either a direct or indirect lifecycle. Worms that have a
direct lifecycle only need to infect a single host species in order to complete
their entire lifecycle, although some development may take place outside of
the host. Worms that have an indirect lifecycle require two different hosts to
complete their lifecycle – a main host and an intermediate host. Worms with
an indirect lifecycle spend some of their immature phase in an intermediate
host but must then infect the main host in order to be able to reach
maturity and reproduce. Some worms may require very specific intermediate
and/or main host species.
Roundworms (nematodes)
Syngamus trachea (gapeworm) Source: The Merck Veterinary
Manual

Roundworms are the most common intestinal worm of

commercial poultry and cause the most economic
impact. They are called roundworms because they are
spindle-shaped and non-segmented with a smooth cuticle or skin. Some
may have transverse grooves. With few exceptions, roundworms have
separate males and females. Roundworms can have either a direct or an
indirect lifecycle. Roundworms that have a direct lifecycle pass through four
developmental stages before becoming adults. Mature roundworms living in
the infected bird produce eggs (1) that pass in the droppings, where they
embryonate (2) in the environment, and when ingested, they hatch (3) in the
proventriculus of the host and undergo larval growth (4) to maturity.
Flatworms

Tapeworms Source: Kansas State University

Flatworms that infect poultry include tapeworms (cestodes) and flukes

(trematodes).
Tapeworms are white or yellowish ribbon-like segmented flatworms.
Tapeworms grow by forming new segments (called proglottids) just behind
their head (scolex). Each segment contains both male and female sexual
organs. The tapeworm attaches itself to the wall of the intestine with the
scolex. As it grows, segments on the tail end mature and break off, passing
out of the intestine with the droppings. The excreted segments are filled with
“eggs”, which are actually first stage larvae. Tapeworms have an indirect
lifecycle. Insects and other arthropods eat the excreted segments and
become intermediate hosts for the parasite. Many tapeworms require a
specific intermediate host. Poultry become infected by eating infected
intermediate hosts.
Flukes are flattened, unsegmented, leaf-like parasites. Flukes are
hermaphroditic (each individual has both male and female sex organs) and
all trematodes that infect poultry have an indirect lifecycle. Their lifecycles
vary in complexity and can involve up to four hosts. More than 500 species
have been found in birds but only a few are known to cause disease.
Prevention and treatment of parasitic worms

Effects of tapeworm infestation (top) on growth Source:

Kansas State University
Control of either class requires accurate species identification and
knowledge of the parasite’s lifecycle. Control of worms with indirect
lifecycles may require both control in the main and intermediate hosts. As
with most diseases, prevention is better than cure and while many parasitic
worms can be killed using appropriate medications it is desirable to
minimise exposure through good biosecurity management practices. Worms
that are transmitted through the oral-faecal route can be greatly reduced by
housing the birds on clean wire away from their droppings. In floor-based
housing systems stocking rates, shed cleanout and litter and range
management are important factors. However, in some cases, such as with
the common roundworm (Ascaridia galli), insects such as flies can carry
worm eggs and so may also need to be controlled to prevent infection.

Rickets and cage layer fatigue are nutritional diseases of

chickens, turkeys and ducks that results in soft bones. Often the leg bones
become bowed and hamper the bird’s ability to stand and walk. The term
‘rickets’ is generally used to describe the condition in young poultry, while
‘osteomalacia’ is often the term used for the disease in adult birds. Caged
layer fatigue is a related condition observed in caged laying hens, usually
around peak egg production, that may also be associated with osteoporosis,
a condition causing brittle bones as a result of reduced bone density.
What causes rickets and cage layer fatigue?
Rickets is caused by a deficiency or imbalance of circulating calcium,
vitamin D3 and/or phosphorous. It can be caused by an imbalanced or
deficient diet, some medications and also some mould toxins. Caged layer
fatigue is thought to be caused primarily by depletion of body stores of
calcium as a result of delay in feeding high calcium feeds during high egg
production or a metabolic malfunction that impairs calcium absorption or
bone calcification during this production stage.
Prevention and treatment of rickets and cage layer fatigue
For normal bone calcification, calcium and phosphorous need to be supplied
in adequate amounts as well as in a ratio of 2:1. Excess of either calcium or
phosphorous can cause rickets. Vitamin D3 plays a critical role in
regulating the absorption and metabolism of calcium. Therefore, in addition
to ensuring that poultry diets have an appropriate level and balance of
calcium and phosphorous, they must be adequate in vitamin D3. Bone
mineralisation is a constant process and therefore correction of dietary
deficiencies or imbalances can ease the condition if identified early enough.
Mould or fungal toxins, called mycotoxins, can have a range of effects on
poultry including interference with the absorption of nutrients. Rickets
caused through the presence of dietary mycotoxins can be treated by
replacing the toxin-contaminated feed and by supplementing vitamin D3 to
three or fourfold of the usual levels. There is a higher incidence of bone
calcification problems in high producing layer hens housed in cages rather
than floor-based housing systems, hence the term cage layer fatigue. This
indicates the role of exercise in preventing or treating this condition.

Toxoplasmosis is a zoonotic (can be transmitted from animals to

humans) parasitic protozoan disease and is rare in poultry. It is more
common in aviaries and backyard poultry than commercial producers. It is
characterised by disorders of the central nervous system but can also
affect reproductive, musculoskeletal (muscles and bones) and visceral
organs (internal organs of the chest and abdomen). Clinical signs in poultry
include weight loss, inappetence, shrunken comb, drop in egg production,
whitish diarrhoea, incoordination, trembling, opisthotonos (severe spasm in
which the back arches), torticollis (twisting of the neck) and blindness. All
chickens infected before eight weeks of age develop clinical signs. In older
birds, infection can be asymptomatic (infected hosts show no symptoms) or
latent (symptoms only develop under certain conditions).
What causes toxoplasmosis?
Toxoplasmosis is caused by the parasitic protozoa Toxoplasma gondii. Cats
are the only definitive hosts (a host in which the parasite can sexually
reproduce) and so both wild and domestic cats serve as the main reservoir of
infection. There are three infectious stages in the lifecycle of this protozoa.
Stage one is within the tissue of the host, stage two is when the protozoan is
excreted by the host in the faeces and stage three is when the protozoan
transferred across the placenta in mammals to their offspring. Transmission
can therefore occur by eating infected tissue, contact with infective faeces or
transfer from an infected mother to a developing foetus (in mammals only).
Prevention and treatment of toxoplasmosis
Drugs are available that suppress multiplication of the parasite within the
host but they will not usually eradicate the infection. Good biosecurity and
management procedures are the principle forms of control in commercial
poultry flocks. Pet animals should be kept away from poultry and poultry
feed. Establish good rodent control and use separate staff for infected and
uninfected flocks. Infected flocks should be depopulated as soon as possible
after diagnosis is confirmed. Oocysts (the spore-like infective stage of the
lifecycle that is passed in the faeces of the infected host) are resistant to
detergents, acids and alkalis. Effective methods of disinfection include
steam cleaning, ammonia, drying and heating (to 55oC for 24 hours).
Concrete floors assist disinfection. Buildings should remain empty for four
weeks after cleaning and disinfection.
Trichomoniasis is a parasitic protozoan disease that affects domestic
fowl, pigeons, doves, and hawks. It occurs in the digestive as either the ‘lower’
form, which is characterised by depression, weight loss and watery yellow
diarrhoea or the ‘upper’ form, which is characterised by depression, drooling
and repeated swallowing movements, sunken and empty crop, open-mouth
breathing and bad odour. The upper form is rare in turkeys and chickens. Most
caged, domestic and game birds (except waterfowl) are susceptible but the
disease is more serious in young birds. Recovered birds remain carriers for life.

Exudate from Trichomoniasis in pigeon oral cavity Source:

The Merck Veterinary Manual

What causes trichomoniasis?

Trichomoniasis is caused by infection with the parasitic
protozoa Trichomonas gallinae. This protozoa has variable pathogenicity
(ability to cause disease). Transmission of the protozoa is by bird to bird
contact or by contact with infected litter, feed or water. The protozoa is shed
in the faeces of infected birds and can be regurgitated in crop milk.
Treatment and prevention of Trichomoniasis
Treatments are available that will control the disease but there may be
restrictions on their use in commercial flocks. Prevention requires
good biosecurity and management practices to eliminate the sources of
infection. Drain water pools on ranges, screen out wild birds, separate
young birds from adults as well as susceptible birds from recovered (carrier)
birds.

Viral Arthritis also known as Tenosynovitis is caused by

reoviruses, and the clinical signs and manifestation of disease varies
markedly depending on the pathogenicity and tropism (preferred tissue to
infect) of the virus. Some can cause other disease syndromes such as early
chick mortality and malabsorption syndrome, while others have shown
severe systemic disease including pericarditis in chickens. Clinical signs
include reduced growth and mobility, lameness, hock inflammation, swelling
of the tendon sheaths and unthriftiness.
What causes Viral Arthritis?
Viral arthritis is a classic manifestation of reovirus infection of chickens,
and there are at least five serotypes of the virus. Morbidity is high but
mortality is usually low. Transmission is by faecal contamination and birds
can remain carriers for over 250 days. Diagnosis may be based on the
history, lesions, IFA and rising antibody titre. Isolation may be readily
achieved in in vitro cultures and serology may be by DID, FAT or Elisa.
Subclinical infections (not associated with clinical disease signs) are
common. Diagnosis is primarily to exclude Mycoplasmosis, Salmonellosis,
Marek’s Disease, Pasteurella and Erysipelas as potential causative agents of
the observed clinical signs.
Prevention and treatment of Viral Arthritis
Vaccination is ideally carried out by administration of a live vaccine in rear
followed by an inactivated vaccine prior to lay. Most vaccines are based on
strain 11/33. The virus is resistant to heat, ether, chloroform, pH and
environmental factors, therefore, good biosecurity and hygiene practices and
an all-in/all-out production system are the best preventative measures.