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Mikroorganisme dan Pola

Manajemen Yang Tidak Tepat

Sebagai Sumber Penyakit Pada
Unggas, dan Beberapa Tindakan
Preventif Sebagai Upaya
Sri Murtini
The Poultry Industry

Important Factors for Success in Poultry

Proper feeding
Good management
The Poultry Industry

 Advantages of Poultry Raising

 Low land requirements
 Adaptability
to small part time enterprise and large
commercial enterprise.
 The operation can be highly mechanized with high
output per hour of labour.
Disadvantages of Poultry Raising
 Serious problems with diseases and parasites.
 Need for high level of management ability, especially
for large commercial flocks.
 Need for large amount of capital for large operations.
 Limitationsof zoning on the location of flocks. Death
losses maybe high due to predators and stampeding.
 Quality of product must be carefully controlled.
 Careful marketing is required.
 High volume is needed for economical enterprise.
 Problems of waste disposal and odour.
Pola Manajemen Yang Tidak Tepat
Sebagai Sumber Penyakit Pada Unggas

 Penyakit
timbul bila fungsi normal tubuh
terganggu dan tingkat keparahan gangguan.
 Penyakit dapat terjadi akibat oleh
defisiensi nutrient penting, menelan bahan
beracun, luka atau stress fisik yang tidak
dapat diatasi, agen penyakit infeksius baik
bakteri, virus maupun parasite.
Poultry Health Programmes
Elements of health programmes in the
commercial poultry sector are
Biosecurity management (cleaning and
disinfection, clear separation between
clean and dirty),
Prophylactic vaccination against a range
of diseases (Marek, IB, ND, Gumboro, ILT,
Salmonella, etc.)
Monitoring of production data.
XIIIth European Poultry Conference, Tours
Pola Manajemen Yang Tidak Tepat
Sebagai Sumber Penyakit Pada Unggas
Pola manajemen yang salah :
 Pemberian pakan yang tidak tepat defisiensi
bias reversible maupun ireversibel.
 Distress tergantung keparahan dan lama waktu
menderita bisa menjadi penderitaan yang
 Penyakit akibat infeksi agen infeksius sangat kompleks
tergantung interaksi Antara inang dengan agen
Tanda-tanda ada masalah penyakit pada
farm unggas

Warning signs of a disease outbreak

Mortality (> 3% in 1 week or > 0.5% in 24 hours)
Production (> 5% in 1 week)
Feed or water consumption (> 20% in 1 week)
Mikroorganisme dan pola manajemen
yang tidak tepat
Penyakit oleh mikroorganisme tergantung dari :
 Jumlah
 Virulensi
 Rute masuknya
 Kondisi pertahanan tubuh inang, dipengaruhi oleh
status nutrisi, dan genetic, stress lingkungan
Health management
On-farm disease control focuses on three areas:
 decreasing susceptibility to disease
 increasing resistance
 decreasing exposure to pathogens such as bacteria,
viruses, and parasite
Health management
1. Decreasing bird susceptibility to disease is accomplished by optimal
management, including proper nutrition, good water, limited stress, prudent
antimicrobial use and proper parasite control.
2. Increasing bird resistance to disease is primarily accomplished by vaccination.
Novel to the poultry industry is increasing resistance by competitive
exclusion, the process by which beneficial bacteria are administered to newly
hatched birds to exclude pathogenic bacteria from colonizing the
gastrointestinal tract and causing disease.
3. The cheapest and most effective means of disease control is using biosecurity
to decrease disease exposure. Inadequate biosecurity can contribute to
industry-wide epidemics of highly pathogenic or exoticiseases, resulting in
quarantine and condemnation of flocks, with massive financial losses to
Survival of pathogens in a contaminated
Disease Organism Survival Time in Contaminated
Infectious Bursal Disease Months
Coccidia Months
Duck Plague Days

Fowl Cholera Weeks

Coryza Hours to Days Months to Years
Marek’s Disease
Newcastle Disease Days to Weeks

Mycoplasma Hours to Days

Salmonella Weeks
Avian Tuberculosis Years
Used of antibiotica

The target of the compound results in some

antibiotics having a narrow spectrum of microbes
that they affect while other will have a broad
spectrum of activity.
The following table shows characteristics of
antimicrobials commonly used in poultry
Mikroba bisa menjadi masalah akibat manajemen penggunaan
antibiotic yang tidak tepat ( resistensi antibiotic)

Antimicrobials approved for poultry

Growth Promotion Arsanilic acid Erythromycin Penicillin
Bactracin Neomycin Salinomycin
Bambermycin Lincomycin Sulfamethazine
Chlortetracycline Oxytetracycline Tylosin
Prophylaxis Bacitracini Neomycin Sulfaguanidine
Ceftiiofur Nitrofurazone Sulfamethazine
Chlortetracycline Oxytetracycline Tetracycline
Erythromycin Penicillin Tiamulin
Gentamycin Spectinomycin Tylosin
Lincomycin Streptomycin Virginiamycine
Therapy Ampicillin Gentamicin Spectinomycin
Apramycin Lincomycin Sulfadiazine
Chlortetracycline Neomycin Sulfamethazine
Ceftiofur Ormethoprim Tetracycline
Erythromycin Oxytetracycline Tylosin
Florfenicol Penicillin Virginiamycin
Antibiotic Activity Damages bacteria by Spectrum of Pathogen Disease
activity* Example* Example

Penicillin G Kills Cell wall synthesis Gram positive Staph. aureus Staph.
blocking arthritis
Neomycin Kills Protein synthesis Gram negative Psuedomonas Psuedomonas
blocking sp. infection

Amoxicillin Kills Cell wall synthesis Broad E. coli Colibacillosis

Apramycin Kills Protein synthesis Gram negative E. coli Yolk sac
blocking infection
Tetracycline Effects Protein synthesis Broad Pasturella Cholera
growth blocking multocida
Sulfonamides Effects Folic acid synthesis Broad E. coli Colibacillosis
growth blocking
Bacitracin Effects Cell wall synthesis Gram positive Clostridium Necrotic
growth blocking sp. enteritis
Resistensi antibiotic akibat ketidak tepatan
 The major bacterial pathogens found on poultry products
that are known for antimicrobial resistance are Salmonella
spp., Enterococcus spp.,E. coli and Campylobacter jejuni.
 The majority of human cases of campylobacteriosis and
salmonellosis are caused by contaminated food. If a
significant percentage of Salmonella or Campylobacter
become resistant to the antimicrobials used to treat these
infections in humans, there will be a significant impact on
human health.
 Antimicrobials should never be used in place of proper
animal husbandry and hygiene programs.
Strategi pengobatan dan tingkat
toksisitas obat
 The dosing strategy and length of treatment will often depend onnthe
nature of how the product works in body of the bird and the level of
product required to kill the bacteria.
 Some antimicrobials just need to reach a certain peak concentration
(concentration-dependent killers) in the blood or tissues to kill the
invading bacteria while others need to reach a steady concentration
and stay there (time-dependent killers).
 These characteristics of the antimicrobial and the bacteria causing
theinfection will determine the length and dose of treatment.
 Generally antibiotics which affect growth of bacteria require longer
Antibiotic Method Absorptio Volume of Type of killer Toxicity
of n distributio
delivery n
Penicillin G Water easily kidney, Time very low
inactivate liver, lung
Neomycin Water little oral not concentration low
absorption absorbed
Amoxicillin Water good kidney, Time very low
liver, lung
Apramycin Water first 4 kidney, concentration low
days then liver, lung
Tetracycline Feed or rapid and widely Time low
water good distributed
Sulfonamides Feed or rapid and widely Time High
water good distributed
Increase in a problem, mortalityor a decrease in production:

1. Collect a representative sample of birds with the problem, observe where in the barn the
problem is occurring.
2. Save the sample for diagnostic service
3. Based on the diagnosis and status of the flock you can make a treatment decision. In some
cases immediate treatment will be prudent and in others it may make sense to wait for a bacterial
culture and antibiotic sensitivity result.
4. Follow-up evaluation of environmental, management or other risk factors such as potential
underlying viral diseases should be done.
5. Preventative treatment may be required if the suspected risk
factors for the disease challenge cannot be identified and addressed.
Figure 4 General stages of microbial-host interactions.
Adapted from: Bailey and Scott’s Diagnostic Microbiology,

Physical encounter between host and organism

Microorganism colonization of host surface

(such as internal = gut lining or external = skin)

Microorganism entry, invasion and spread

Outcome: infection vs host defenses

Figure 5
Summary of microbial reservoirs and modes of transmission to poultry
Adapted from: Bailey and Scott’s Diagnostic Microbiology,

Microorganism Sources 1. Direct:

(reservoirs) transmitted by direct contact
between reservoir and host
Other birds
2. Indirect: Host
Food transmmitted to host via Poultry
(plant and animal intervening agent(s)
Soil Intervening agents
Bedding Vectors — animals, insects, humans
Fomites — water, food, air, equipment,
supplies, vehicles
Penyakit pada ungags terkait dengan
miss manajemen
General Signs of Disease
 Poor appetite
 Huddling
 Depression
 Runting/stunting
 poor uniformity
 Ruffled feathers
 Coughing, sneezing,
 oculo-nasal discharge,
 difficult breathing
 Bloody or wet litter
 Increased mortality
Unique Problems

 Predation
 Lack of Environmental Control
Clues To Identifying Predators
1. Several birds killed  Dogs
a. Mauled but not eaten
b. Killed by small bites-neatly
 musang /Raccoon
piled,some heads gone
c. Heads/crops eaten.
2. 1-2 birds killed  Elang
a. mauled, abdomen eaten  Owl
b. Deep marks on head and neck,
some meat eaten
3. 1 bird gone feathers left
4. Chicks killed, abdomen eaten,
lingering smell  Human
5. Several gone-no clues

From: J. Berry. Predators: Thieves in the night. OSU/CES Bull #8204

Bacterial Diseases

 Fowl Cholera Pasteurella

 Mycoplasma MG MS
 Coryza Hemophilus paragallinarum

 Botulism Botulinum toxin

 Gangrenous Dermatitis Clostridium perfringens

 Fowl Cholera  Swollen face, wattles, sinuses
 Pneumonia, Sudden death, swollen
joints, torticollis
 Mycoplasma
 MG
 MS  Coughing, swollen face and sinuses.
Bubbles in eye, sticky eye discharge
 Swollen joints and/or footpad
 Coryza

 Sticky eyelids, odor, rales, nasal

 Botulism discharge

 Dermatitis  Limberneck, flaccid paralysis





Viral Diseases

 Fowl Pox Pox virus

 Laryngotracheitis Herpes virus

 Infectious Bronchitis Corona virus
 Newcastle Paramyxovirus

 Mareks Disease Herpes virus

 Avian Influenza Orthomyxovirus (Influenza)

 Fowl Pox  Blisters, scabs,skin growths.
 Difficult breathing and swallowing, growth
in mouth, death
 Laryngotracheitis
 Cough, blood on feathers, mouth, beak,
Difficult breathing, death

 Infectious Bronchitis  Egg drop, cough, sneeze, poor egg quality

 Egg drop, soft shell eggs, chirping, cough

 Newcastle  (high mortality, diarrhea, CNS, depression,
 Avian Paramyxo
nasal discharge)

 Exotic Newcastle
 Mareks  Paralysis of legs, wings, neck, birds less
than 6 months
 Avian Influenza (AI)
 Low Path AI  High mortality, hemorrhages, similar to
 High Path AI
Exotic Newcastle




Newcastle IB/ND
Low Path AI
 Mild or no clinical signs in poultry
 Decreased egg production
 Mild respiratory signs: cough, sneeze
 Feces, ocular, oral and nasal secretions
 Bird-to-bird or contaminated equipment
 Diagnosis:
 Virus isolation
 Serology


High Path AI
Sudden death without clinical signs


High Path AI
 Decreasedactivity and decreased
feed consumption

F.A.O.- Italy


High Path AI
Decreased egg production
 Soft-shelled or misshapen eggs


High Path AI

Swelling of head, eyelids, comb, wattles

and hocks


High Path AI

Purplediscoloration (cyanosis and

hemorrhage) of wattle, comb and


High Path AI

 Nasal discharge, coughing, sneezing

 Lack of coordination
 Diarrhea

F.A.O.- Italy


Gross Lesions HPAI

 Vesicles and ulcers

on comb

 Facial edema


Gross Lesions HPAI

• Hemorrhage throughout
internal body organs and


Gross Lesions HPAI

• Hemorrhage throughout internal body

and fat


Newcastle disease
 Notifiable disease !
 Avian paramyxovirus (serotype 1, 8 genotypes)
 different pathogenity (v, m, l, a)
 chicken, pheasant, turkey, pigeon, wild birds
(water fowl)
 Sensitivity: 56 °C - 3 min
pH 3 - 3 min disinfectant
 Clinical signs:
respiratory disease
nervous signs
marked drop in egg production
 Pathology:
 haemorrhages on seromembranes,
on mucosal membranes
(proventriculi, small intestine,
ceca, -lymphoid tonsils -,
trachea, pharynx)
 enteritidis
 diphtheriod inflammation on lymphoid tonsils
on pharynx
 Isolation of virus (pathogenicity)

 Prevention / Vaccination

 Differential diagnosis
(septicaemia, CRD, IBD, ILT, IB, Fowl pox,
pneumovirus, coccidiosis, mycotoxicosis)
if NDV is observed on the farm:

In compliance with EU directive 93/119/EC,

depopulation of infected flocks may take place
using the following methods/drugs/systems:
 Electronarcosis by water dipping
 Decapitation and dislocation of the neck
 Gassing with carbon dioxide
 Vacuum tank

if NDV is observed in the slaughter-house

everything is condemned, and everything has to
be desinfected
Fowl pox
 Poxviridae, Avipox

 Sensitivity: 50°C heating 30 min

60°C 8 min
in dry scabs for months/years
pH 5-9 resistant
 cutaneous form
nodular (proliferative) lesions on the comb, wattle,
eyelids, other non feathered areas
 diphtheroid form
nodules on mucosal membranes of pharynx, trachea,
 special histopathological changes (cytoplasmic
inclusion body)
Infectious Laryngotracheitis

 Herpesvirus
 Sensitivity: mild (halogen-detergents + iodophors,
heating, but (-18° C-25° C !)
 Acute respiratory disease
 Conjunctivitis
(Histopathology: intranuclear inclusion body in
epithelial cells by 3 day PI)
Infectious bronchitis
 Coronavirus
 Sensitivity: 56°C 15 min
at room temperature 2-3 days
common detergents destroy
 Pathology:
acute catarrhal tracheitis, bronchitis
sinusitis, air sacculitis
local pneumonia
 nephritis, salpingitis (eggs !)
Infectious bursal Disease
(Gumboro Disease)

 Birnavirus
 bursa
Fabricii (B lymphoid cells)
immunsuppression !
 Sensitivity:very stabil virus!
60-70°C -30 min
0.5 % chloramines 10 min
invert soap + 0,05 sodium hydroxide
 Pathology:
in muscles (legs, breast)
on mucosal membrane of proventriculi
on lymphoid tonsils of intestine
oedema and haemorrhageous inflammation
of bursa Fabricii
 Diff. diagnosis: Newcastle disease
 Prevention: vaccination, hygiene
Marek’s Disease
 Herpesvirus (cell associated virus)
 Sensitivity: 
 Pathogenity:
„classical” form (lesions in peripheral nerves)
tumoral form
(lymphoid tumors in different organs or
in skin)
transient paralysis
 Differential diagnosis:
Newcastle disease
Internal Parasites

 Coccidia Eimeria sp.

 Blackhead Histomonas
 Tapeworms
 Gapeworms Syngamus
 Threadworms Capillaria sp.
 Roundworms Ascarids
 Coccidia  Weight loss, huddling, blood
in feces, mortality in young.

 Blackhead  Weight loss, unthrifty,

yellow diarrhea

 Gapes  Gasping, open mouth

 Tapes  Weight loss, See in feces

 Weight loss, unthrifty,

 Rounds ruffled

 Hair/Thread  Diarrhea, Unthrifty,

thickened crop.



Parasites / Protozoa
 Eimeria tenella
Eimeria necatrix
Eimeria acervulina
Eimeria truncata
 Chicken, turkey
 Anticoccidial drugs /vaccination

 immunsuppressive diseases (Marek’s disease, CAV, Gumboro

disease, Reo, mycotoxines…)
 Haemorrhagic enteritidis
(clotted blood - fibrinous inflammation)
in caecum
in small intestines
 renal coccidiosis (enlarged, yellow-greyish kidneys)
Other Health Concerns
 Mites & Lice
External Parasites

 Lice

 Mites
Feather damage, skin damage, feather picking,
 Lice 
 Numerous species

 Mites  Feather and skin damage, feathers

 Northern
look oily, anemia, feather loss.
 Northern stays on bird

 Red  Feather loss, picking, anemia,

restless at night, skin damage. Red
gets on bird at night

 Scaly Leg
 Thick dry white or yellow crusts on
leg scales.
Northern Fowl Mite Scaly leg mite Red Mite

Mites & Lice
 Lice
Size: 2-3 millimeters long

Color: Light Brown

Egg Color & Location:

White and at the base of the
Lice only live on the host, and
appear to be fast moving.
Mites & Lice

 Mites
Size: 1 millimeter in diameter

Color: Dark Reddish Black

Egg Color & Location:

White to off-white along the feather shaft

Mites live on the host and in the environment

Mites & Lice

 Decreased Food Intake

 Decreased Egg Production
 Decreased Weight Gain
 Increased Susceptibility to Other Diseases

If any of these symptoms are observed a visual

inspection around the vent for lice or mites is
Mites & Lice
 Treatment
 Sanitation and cleanliness are keys to control
 Chemical control:
 Dust bath with Sevin®
 Pyrethrin-Based spray
 Ivermectin medication
Respiratory Diseases
 Theseare some of the most common
diseases of poultry.

 They cause a wide variety of impact on the

flock, from production loss to mortality.
Respiratory Diseases
There are many causes and is
very common

 Coughing
 Sneezing
 Discharge from the
eyes and nostrils
Respiratory Diseases

 Causes:
 Viruses
 Bacteria
 Parasites (such as the gapeworm)
 High ammonia levels
Respiratory Diseases

 Vectors:
Other Chickens
Fungal infections
 Aspergillus fumigatus
Aspergillus flavus
 Respiratory disease
pneumonia (granulomes)
air sacculitis, peritonitis
 Litter, feed (toxins)
 (Antibiotics contraindicated!)
In these cases poultry meat is partial
condemned for human consumption
(the effected areas are condemned:
- parenchymal orgams
- intestines
- skin + muscles /breast, legs/ )
Pneumovirus Infections
(Turkey Rhinotracheitis/Swollen Head Syndrome)
Cause :
The disease is caused by a pneumovirus.
Transmission :
The virus may be transmitted horizontally by contaminated
water, personnel and equipment as well as from bird to bird.
Species affected
Turkeys and chickens.
Clinical signs and lesions
In young turkeys sneezing. Rales and nasal discharge, con-
junctivitis, swelling of the infraorbital and submandibularsinuses
can be seen.
In laying flocks a drop in production may occur along with respiratory distress.
Morbidity is high whereas mortality may vary being usually higher in young poults. In
chickens the pneumovirus may be involved in the so called “swollen head
syndrome” (SHS).
In such cases affected chickens may show swelling of the periorbital and infraorbital
sinuses, torticollis, cerebral disorientation and depression. Marked egg produc-
tion losses can be associated with SHS.
At necropsy the lesions seen may vary due to other microor-
ganisms that may complicate the original picture. In cases of SHS apart from
oedema in the head also purulent or caseous subcutaneous exudate can be found.
Rhinitis, tracheitis and sinusitis are frequently noted in both chicken and turkeys,
hence also the name turkey rhinotracheitis (TRT).
Poliserositis affecting the air sacs and pericardium may be
due to secondary infections (E. coli). The kidneys may be
swollen and congested as well as the lungs which may show a
fibrinous exudate in the pleural cavit
The diagnosis based only on clinical signs is difficult to
establish since other agents may be involved.
The most certain diagnosis may be obtained by the isolation
of the
organism from nasal secretions or tissue scraped from the
sinus of affected birds. Antibodies can be detected by several
serological methods such as the VN test, IFT and ELISA.
Treatment and control
Treatment with antibiotics can be given to control secondary
bacterial infections. The use of vaccines should be the best
approach to control the disease.
Inclusion Body Hepatitis

(Hydropericardium-Hepatitis Syndrome)
The disease is caused by an avian adenovirus (for example
the Tipton strain) and is usually simultaneously accompanied
by other immunosuppressive diseases such as infectious
bursal disease or infectious anaemia. There are 12 known
serotypes of avian adenoviruses that may be involved in the
development of this disease.
Egg transmission is an important factor.
Horizontal transmission from bird to bird by contact with droppings.
Once the bird becomes immune, the virus can no longer be isolated from
the droppings.
Species affected
Chickens, turkeys and pheasants and possibly other birds can
be affected by avian adenovirus.
Clinical signs
Chickens with inclusion body hepatitis are affected at usually
5 to 7 weeks of age. The birds are listless, with ruffled feat-
hers. Mortality is usually quite severe, up to 25 % in the first
10 days of the disease.
Internal lesions
Affected chickens have mottled livers, many with
pinpoint necrotic and haemorrhagic spots. Pale
bone marrow and, in some cases in presence of
infectious anemia, gangrenous dermatitis can be
seen. Kidneys are pale and swollen. The
spleen is usually quite small (atrophy
If Gumboro disease (infectious bursal disease) has been
present in the birds, even if subclinical, the bursa of Fabricius
will be very small (atrophic). Such chickens are immune-
suppressed and usually have more severe cases of inclusion
body hepatitis and/or infectious anaemia.
Mature birds do not have clinical signs of adenovirus
infection, they only start showing antibodies in their blood.
HHS was reported for the first time in 1987 in Pakistan and was referred to as “Angara
disease”. The disease has mean- while been Hydropericardium-Hepatitis Syndrome
reported from several other countries, including
India and countries in the Middle East and Latin America.
Hydropericardium-hepatitis syndrome is caused by a virus belonging to the family of
the fowl adenoviruses (FAV).
Despite of the diversity in the geographical distribution of the disease, in all areas the
infection is caused by a virus belonging to FAV serotype 4. There are three features
which underline that this condition is a new disease, different from the
known IBH. IBH and hydropericardium accompany this syndrome. Once outbreaks of
HHS occur, it remains a problem for the poultry industry. And while IBH is shown to be
caused by strains belonging to various FAV serotypes, HHS is, contrary to this, caused
by FAV serotype 4. The infected flocks show high mortality rates and beside the
lesions typical for IBH, a marked hydropericarditis is found in the affected birds
Typical mottled livers with pinpoint lesions, pale bone marrow
and kidneys, small spleen and bursa are good indications of
the disease. In the case of HHS the typical lesion (hydroperi-
cardium) is also found. Histological examination (intranuclear
inclusion bodies) of liver and/or virus isolation are helpful
means of diagnosis.
Treatment and control
No treatment exists. Antibiotics can be used to prevent
secondary bacterial infection and possible gangrenous
The best method of control is to ensure adequate immunity
against other immune suppressive diseases (e.g. infectious
bursal disease). Chickens may be vaccinated s.c. during the
first two weeks of life with an inactivated oil-emulsion
Duck Virus Hepatitis
Duck virus hepatitis is caused by a picornavirus. It is possible
that there are more serotypes.
The disease can spread rapidly to all susceptible ducklings in the flock via faeces.
The incubation period varies from around 24 hours to a few days.
Species affected
Ducklings under 6 weeks of age are susceptible.
Clinical signs
The disease has a very short course, with all affected birds
dying within a few days.
Signs, if seen at all, may include somnolence and convul-
sions, followed by quick death. Mortality up to 95 %.
Internal lesions
Principal lesions found in the liver, showing fatty degeneration, yellowish and with
many small or bigger haemorrhages
Sudden death in small ducklings is highly suggestive.
Virus isolation can confirm this diagnosis.
Treatment and control
Serum therapy is possible.
Strict isolation during the first 4-5 weeks can prevent infection. Ducklings
can be protected by maternal antibodies. To provide for this, parent stock
has to be vaccinated, preferably twice.
This will protect the progeny for two weeks, and mitigate
infection afterwards.
Ducks without maternal antibodies should be vaccinated at
day old
Duck Plague
(Duck Virus Enteritis)
Duck plague is caused by a herpes virus. Only one serotype
known. There is a difference in virulence between strains.
Duck plague virus is excreted by affected birds through
faeces and other body discharges. Via soiled drinking water,
contaminated pound water or open water other birds are
Species affected
Ducks, geese and swans, of all ages.
Clinical signs
High mortality up to 100 %, sometimes sudden death. Droppy
appearance, slow movements with hanging wings. Birds show
bloody nasal discharges and conjunctivitis, diarrhoea and they may
make a hoarse noise. The birds are very thirsty.
Birds often die in a rather characteristic position, with the neck twisted
downwards, sidewards or backwards.
In laying flocks egg production may drop 50 % or more
Internal lesions
Haemorrhagic enteritis, haemorrhagic or pseudo-membranic
pharingitis, oesophagitis and cloacitis, haemorrhagic ovaritis.
The gross lesions are rather characteristic for duck plague.
Virus isolation and neutralization confirm the diagnosis to
distinguish the disease from avian cholera (Pasteurella
multocida) or duck hepatitis.
Treatment and control
There is no treatment known. Prevention should include clean
drinking water and keeping wild, free-flying waterfowl away.
Vaccination with adapted strains can provide a reliable protec-
tion. Even in an infected flock emergency vaccination can
limit the damage, due to an interference phenomenon
between the vaccine virus and the field virus
Worms living in the intestines of chickens fall mainly into four
(Ascarids), usually 5 to 7 cm (2-3 inches) long.
(Capillaria), only measure 1-1.5 cm long.
Caecal worms
(Heterakis), usually 1.5 cm long.
Tape worms,
usually 7 to 10 cm long, consisting of many
small segments
Clinical signs
Mature roundworms are not a major cause of the disease, but
the larvae can damage the intestinal lining, causing enteritis,
anaemia, decreased egg production and at times eggs with
pale yolks.
Capillaria cause more damage to the intestinal lining and can
cause enteritis and anaemia with decreased egg production
and the appearance of pale egg yolks (“platinum yolks”).
Caecal worms
are found in the caeca and do not cause
serious damage, except that their eggs can transmit blackhead – mainly in turkeys
Examination of the intestinal contents will reveal round-
worms, caecal worms, and tape worms without difficulty.
Capillaria can usually be found when intestinal contents are
washed through a fine mesh sieve.
Treatment and control
Roundworms and caecal worm infections can be treated with
piperazine. Piperazine is not effective against tape worms and
capillaria for which other anthelmintics are required
(Histomoniasis, Enterohepatitis)
A protozoan parasite, :Histomonas meleagridis.
Direct transmission by infected water, feed, or droppings
has been proved.
Indirect transmission by infected eggs of the caecal worm
Heterakis gallinarum, is also a major factor. Raising turkey
and chickens on wire and indoors decreases the incidenc
of blackhead.
Species affected
Chickens, turkeys, and peafowl are natural hosts to blackhead
Clinical signs
Affected birds are depressed, stand or sit with ruffled feat-
hers, and have yellowish diarrhoea. Darkening of head parts,
especially in turkeys, gave the name to the disease (black-
head). Gross lesions include circular necrotic areas in livers
with a crater-like center and cheesy cores in the caeca.
Blackhead can cause high mortality, particularly in young
turkey poults, but the disease can also affect older birds. In
chickens the mortality from blackhead infection is usually
lower, young chickens being the most susceptible
Treatment and control
Treatment with protozoan chemotherapeutics is
usually effective. Such drugs can also be given
at preventive levels in turkeys starter and
grower feed. Growing turkeys on wire and
indoors can reduce the incidence of blackhead
to a large extent, but even so, strict hygiene and
elimination of caecal worms are important
control measures
(Vitamin B2)
(Curly Toe Disease)
Clinical signs
Young chicks, as early as 1-week-old, exhibit curling of the
toes, inability to walk and sometimes diarrhoea.
Treatment and control
Administering vitamin B preparations brings a rapid cure.
Only in advanced cases will birds be dehydrated and
emaciated, requiring further treatment.
It is important to ensure adequate vitamin B levels not only
in starter and grower diets, but also in the diet of parent
Vitamin E Deficiency
(Crazy Chick Disease, Encephalomalacia)
Clinical signs and gross lesions
Vitamin E deficiency in chickens affects the brain, causing degeneration, oedema
and haemorrhage, especially in the small brain (cerebellum).
Affected young chicks appear unable to walk, they fall on their sides or stand with
their heads between their legs.
The cerebellum shows gross swelling, with yellow or brown
discoloration and pinpoint haemorrhages may be observed.
Encephalomalacia can also be found in mature chickens.
Treatment and control
Adequate levels of vitamin E and selenium in the diet of
chickens and their parent breeders is of prime importance.
Treatment of affected birds with vitamin E preparations
(alpha-tocopherol) is effective if the condition is not too far
Vitamin D3 Deficiency
(Rickets, “Rubber Legs”)
Clinical signs and gross lesions
Young chickens, 2 to 5 weeks of age, with vitamin D3 defi-
ciency are unable to stand and have very soft, pliable, legs
and beaks. The rib joints are swollen like beads and
curved inward, the breastbone often twisted.
In layer chickens, vitamin D3 deficiency causes soft-
shelled eggs and a drop in production.
Treatment and control
Vitamin D3 can be given as treatment, usually in
with calcium and phosphorus