Important Poultry Diseases for all poultry keepers and those who wants to start pursuing this carrier. Only to be taken as informative.

Poultry Diseases

1. DAH 0210
LIVESTOCK DISEASES II


1: POULTRY DISEASES (16+)
2: SMALL RUMINANTS DISEASES (14+)
3: PIG DISEASES (10+)

Dr. Isaac p. Kashoma (PhD)

2. POULTRY DISEASES

3. Clinical History
Clinical signs
Necropsy/Pm lesions
Extremely useful in poultry
Requires a recently dead bird
Clear clinical picture
Laboratory diagnosis

4. 1.Respiratory signs
2.Digestive signs
3.Musculoskeletal signs
4.Neurological signs
5.Others

5. A.General clinical signs:
oIncreased mortality rates
oAnorexia/Fever/Sluggishness
oCoughing/Sneezing
oRales/Crackles (abnormal lung sounds characterized by discontinuous clicking)
oNasal/Occular discharges
oSwollen head/swollen sinuses
oInflamed eyelids

6. B.Pathological lesions:
oInflammation of
head tissues
nasal cavity
conjunctivitis
oTracheitis
oPneumonia
oAir sacculitis
oPolyserositis
Inflamed trachea
pneumonia

7. C.Examples of respiratory diseases
a)Newcastle disease
b)Infectious bronchitis
c)Infectious laryngotracheitis
d)Avian Influenza
e)Fowl Cholera (Pasteurella multocida)
f)Infectious coryza
g)Aspergillosis
h)Gape worms (Syngamus trachea)

8. A.Clinical signs:
oIncreased mortality rate
oAnorexia/Fever/tiredness
oDehydration
oDiarrhea/Loose droppings (watery/bloody)
oPasty vent/wet litter

9. B.Pathological lesions:
oInflammation of Intestinal mucosa
oChanges of intestinal content
oPresence of parasite

C.Example of Diseases
oSalmonellosis
oCoccidiosis
oIntestinal helminthes

10. A.Clinical signs:
oMortality
oParalysis
oLameness
oDown birds

11. B.Gross Lesions:
oNerve inflammation
oJoint inflammation
oFoot pad infection (Bumblefoot)
oWeak/soft bones
oBone deformities

C.Disease examples:
oMarek’s disease (nerve involvement)
oCalcium/Phosphorus deficiency
oGenetic deformities

12. A.Clinical signs:
oParalysis
oAtaxia
oTorticollis
oTremors

B.Diseases
oMarek’s Disease
oAvian Encephalomyelitis
oNewcastle Disease
oNutritional deficiency

13. a)Egg peritonitis
b)Egg drop syndrome
c)Pox virus disease
d)Vitamin deficiency
e)Tumor Viruses
-Leukosis
-Reticuloendotheliosis
Ascites Syndrome

14. 1.SALMONELLOSIS
Salmonellosis is a disease of all animals
including human being caused by a
number of different species of Salmonella.

Clinically manifested by three major
syndromes;
1.Per-acute,
2.Septicemia, and
3.Acute / chronic enteritis.

15. 1.Salmonella pullorum (poultry)
2.Salmonella gallinarum (poultry)
3.Salmonella paratyphi (man)
4.Salmonella typhi (man)
5.Salmonella typhimurium (man & animals)
6.Salmonella dublin (cattle)
7.Salmonella anatum (sheep, horses & goats)
8.Salmonella arbotus equi (horses)
9.Salmonella choleraesuis (pigs)
10.Salmonella newport (cattle and horses)
Etiology

16. This form of Salmonellosis clinically
observed in growers or adult birds,
although chicks can be affected.

Etiology: Salmonella gallinarum
a)FOWL TYPHOID
Species affected:
All types of poultry:
Chicken, Turkeys, Ducks,
Guinea fowl etc.

17. 1)Man, rats, cats and dogs may carry parts of infected
carcasses from flock to flock.

2)Movement of recovered birds frequently remain carriers
for long periods and movement of such birds spread
disease.

3)Management: attendants, feed dealers, chicken buyers
and visitors may carry infection unless precautions are
taken to disinfect foot wear, hands and clothing.

4)Inanimate: trucks, crates, and feed sacks may also be
contaminated and thus spreading the disease.

5)Wildlife: birds, animals and flies: mechanically spread,
especially if they have been feeding on carcasses of dead
birds or offal from packing plants or hatcheries.
Transmission/Spread

18. Transmission may be by transovarian or horizontal through faecal-oral
contamination
Egg transmission may result from contamination of the ovum
following ovulation or localization of the bacteria in the ova
before ovulation

Horizontal transmission may include shell penetration, feed
contamination, contact transmission either in the hatcher,
brooder, cages or floor, cannibalism of infected birds, egg eating,
and through wounds on the skin, faeces from infected birds.

Morbidity rate within the flock is high = 80 – 100%.


Mortality rate for untreated flock = 50%.


Incubation period varies with the immune status of the birds and
virulence of the strains: can be as short as 4 - 6 days in most susceptible
flocks.
Clinical signs

19. In acute outbreak, the first
sign is an increase in
mortality followed by a
drop in food consumption,
and for layers a drop in egg
production.


Affected birds: show
depression, stand still with
ruffled feathers and closed
eyes & drooping of wings.

Clinical signs: Growers and Mature birds

20. Increased respiratory
rate with rapid
breathing & gasping.







The most characteristic
clinical signs are
watery to mucoid
yellow diarrhoea, and
anemia.

21. Chronic phase (birds
that do not die within 2 or
3 days) develop chronic
stage characterized by;

progressive loss of body
condition and anemia
(shrunken, pale combs and
wattles).

Egg transmission is rare:
when occurs may lead to
increased in dead-in-shell
embryos and small, weak,
moribund or dead chick on
the hatching trays.


Gonads. The ovaries are
affected by inflammatory
and degenerative changes.

22. Chronic phase


Frequently, affected follicles are
deformed and appear like thick
pendulating masses






Sometimes, the going out of yolk
from degenerated follicles results in
fibrinous adhesive peritonitis




Sub acute outbreak of the disease
may result in a sporadic mortality
over a long period.

23. 1.Acute cases: carcasses
show septicemia and
jaundice appearance
(skeletal muscles
congested and dark in
color).


2.Swollen, friable, dark-
red liver or almost black
in color and its surface
has a distinctive coppery
bronze sheen.


3.The spleen may be
enlarged.

Post-mortem findings

24. 4.Catarrhal enteritis,
particularly involving the
small intestines.





5.Intestines contain viscous
slimy, bile stained
material.




6.The gall bladder is
engorged with viscous
slime bile.

25. Therapy with a number of
antimicrobial agents will reduce
clinical signs and mortality rate in a
flock affected with fowl typhoid.

Furazolidone (Nitrofuran)
compounds given in water for 5 – 7
days (continuously) or in feed for 10
days are generally considered to be
the best treatment routine.

Other antibacterial agents:
Sulfonamides, Norfloxacin,
streptomycin Oxytetracyclines
etc.

Resistance problems to a number of
antibiotics!

Treatment

26. Proper house hygiene: Use of strong disinfectants
to clean the poultry house, foot wash etc.

Culling of chronically affected birds.

Early diagnosis and prompt treatment of all
diseased birds.

Control of movements of birds and other animals
including man in poultry houses (Foot wash).

Proper disposal of dead birds.
Control.

27. Pullorum disease is seen predominantly in
chicks less than 3 weeks of age, and rarely
occurs in adult birds.

Species affected are chicken and turkeys.


Etiology: Salmonella pullorum

b. PULLORUM DISEASE

28. Vertical transmission occurs by the trans-ovarian (Egg transmission).

oThe infected birds carry the S. pullorum in the ovaries and being
excreted in the ova.


Horizontal transmission takes place by direct contact between clinically
affected and recovered carriers and by indirect contact with
contaminated equipment, housing, litter, and clothing of personnel.

The pathogen can remain viable in soil for up to a year.

Thus pullorum disease is passed from hen to chick by vertical
transmission and the there is rapid lateral transmission from chick to
chick in hatcheries and rearing units.
Transmission.

29. The mortality and morbidity varies considerably
and in extreme cases can be 100%.

Both morbidity & mortality are influenced by age,
strain, susceptibility, nutrition and flock
management.

The greatest losses usually occur during the 2
nd

week after hatching which rapidly decrease during
the 3
rd
& 4
th
week of age.

The first indication is usually excessive numbers of
dead-in-shell chicks and deaths shortly after
hatching (for chick hatched from infected eggs).
Clinical signs.

30. Affected chicks show variable
and non-specific signs;
depression, tendency to
huddle, respiratory
distress, lack of appetite,
and white viscous
droppings that adhere to the
feathers around the vent &
drooping of wing.

Clinical signs.

31. Sub acute form (seen in
growing birds);
lameness, swollen
hock joint and poor
growth rates.

Older birds appear
listless; have pale and
shrunken combs and
sub optimal egg
production (may be the
only signs in older
birds).
Clinical signs.

32. Chicks that die shortly
after hatching:
Peritonitis with an
inflamed, unabsorbed yolk
sac.

Congested /pneumonic
lungs

Liver is dark and swollen
with hemorrhages visible
on the surface.

Post-mortem picture.

33. In chicks that die after
showing signs for 1 - 2
days:

Caeca are enlarged and
distended with casts of hard
dry necrotic material,
discrete,

Small, white necrotic foci
found in the liver, lungs,
myocardium and gizzard
wall.

Gall bladder will be
engorged with viscous slime
bile.
Post-mortem picture.

34. In growers:
Arthritis on hock joints. The
joints are enlarged due to
the presence of excess
lemon or orange colored
gelatinous materials
around the joints.


In adult birds:
Abnormal ovary with ova
irregular cystic,
misshapen, discolored and
pendunculated with
prominent thickened
stalks.
Post-mortem picture.

35. Diagnosis:
Epidemiology – age
Clinical signs.
Pm picture.
Serological test: Agglutination test.

Treatment:
Antibacterial agents: Furazolidone , chlortetracycline, Chick
formula, Norfloxacin, Sulfonamides etc

Control:
Test and removal of the affected parent stock
Proper house hygiene.
Diagnosis / Treatment / Control.

36. 2.Escherichia coli Infection (Colibacillosis)
Synonyms: Escherichia coli infection; coligranuloma, colisepticemia
Cause: Escherichia coli.

Epidemiology:
E. coli is ubiquitous, present in intestine of birds and
mammals and is disseminated in feces (Fecal contamination
is most important).

E. coli infections often result from management failures; is
mainly a secondary infection.

Transmission:
Birds infected by direct contact with dirty litter and hatchers
or contaminated egg shells.

This is an environmental disease, not transmitted from bird to
bird.

37. 2.Escherichia coli Infection (Colibacillosis)
Synonyms: Escherichia coli infection; coligranuloma, colisepticemia
Predisposing factors
1.Contaminated water
2.Dry, dusty condition. E. coli persist for long period outside the
bird’s body in dry, dust condition
3.Overcrowding
4.Poor ventilation
5.Poor litter condition
6.Exposure to ammonia
7.Temperature extremes (too hot or too cold)
8.Stress
9.Feed/water restriction
10.Immunosuppression, for example viral infections, toxins
(mycotoxins)

38. Clinical signs: Signs are nonspecific and vary
with age, organs involved, and concurrent
disease.
ill-thrift,
ruffled feathers,
enlarged and swollen navel,
decreased appetite,
depression,
Diarrhea and pasting of feathers around vent.
Gross lesions:
A variety of lesions depending on system that is
affected:

40. a)Air-sacculitis, perihepatitis and pericarditis:
characterized by presence of white, friable material
covering air sacs, liver and pericardial sac.












Airsacculitis, perihepatitis and pericarditis

41. b)Omphalitis (navel infection). It is characterized with
reddening and tissue oedema in the umbilical region,
delayed absorption of egg sac.






Yolk infection

42. c)Salpingitis (inflammation of
the oviduct) / egg yalk
peritonitis- especially laying
hens; oviduct filled with yellow,
cheesy exudate

43. d)Cellulitis (“scabby hip”)
of broiler chickens: yellow
exudate underneath skin
of hip, leg and breast.




e)Synovitis/arthritis

44. Colibacillosis Pullorum disease
Cause: Escherichia coli Cause: Salmonella pullorum
Occurrence: chicks less than 3 weeks of
age, and rarely in growers
Occurrence: chicks less than 3 weeks of age, and
rarely occurs in adult birds
Transmission: direct contact with dirty
environment (only horizontal)
Transmission: trans-ovarian and horizontal
(contaminated environment)
Clinical signs: varieties depending on body
system affected
Clinical signs: white viscous droppings
PM:
1.Intestine is bloated and contains watery
and mucoid material tinged with blood.
2.The air-sacs and heart are thickened
and may have caseous deposits.
3.Abdominal organs are swollen and may
be covered with a layer of fibrin.
4.In adults: Inflammation of the oviduct) /
egg yalk peritonitis.

5.In grwoers: Synovitis/arthritis
PM:
1.Liver is enlarged and bile-stained, or may have
pale, dead patches.
2.The spleen and kidneys are enlarged.

3.The intestinal lining may have raised plaques,
and the caecal content is cheesy.
4.Abnormal ovary with ova irregular cystic,
misshapen, discolored and pendunculated with
prominent thickened stalks.
5.In growers: Arthritis on hock joints.
Differential diagnosis for Colibacillosis

45. Diagnosis
Histopathology and bacterial culture of affected organs is required for
tentative diagnosis.

Treatment

1)E. coli isolates from commercial poultry are often resistant to a variety of
antibiotics.

2)Enrofloxacin and other broad spectrum antimicrobial are effective
against this organism.

Prevention

a)Vigorous sanitation program in breeder house, at hatchery and at grow-
out facility; Egg fumigation; dust control in house.

b)Routinely remove dead birds from house.

c)Avoid stress and immunosuppression (IBD).

46. Infectious Coryza, as its name implies, is a disease of the
upper respiratory tract characterized by sero-mucoid nasal
discharge, conjunctivitis and facial oedema.


Etiology: Haemophilus paragallinarum (Haemophilus group of bacteria)
3.INFECTIOUS CORYZA
(Synonyms: Fowl Coryza).

47. The disease occurs principally in chicken, but has also
been reported in turkeys and other birds.

All ages are susceptible but older birds react severely.

Recovered birds from field infection has immunity lasting
for at least a year.

Main source is clinically affected and carrier birds.

Airborne spread is the major mean of transmission of the
disease.

The disease occurs worldwide.

Predisposing factors include: Intercurrent infections with
other pathogens, cold and wet conditions.
Epidemiology

48. The incubation period ranges from 3 – 10 days.

The bacteria show tropism for the mucous membranes of
nasal passages, infraorbotal sinuses, conjunctiva, and
occasionally lower trachea and lungs.

The first sign in susceptible birds: Depression, Serous
nasal discharge, Conjunctivitis, Facial edema and
swelling of wattles, Reduction in appetite and production
and Rales.

Birds may have diarrhea with foul smell when complicated
with other bacterial infection.

If uncomplicated by other infections, mortality rate is very low and
the course of illness is usually 14 – 21 days.
Clinical signs

50. Mucoid or catarrhal
inflammation of the
nasal passages,
infraorbital sinuses and
conjunctivitis

Mucoid or catarrhal
inflammation of upper
trachea and occasionally
lungs and air sacs.

Subcutaneous edema of
the face and wattles is
prominent
Gross Lesions

51. 1.Epidemiology.

2.Clinical signs.

3.Pm pictures (if any).

4.Laboratory examination: nasal exudates swabs to
culture the Heamophilus organism.

5.Serological tests: Plate and tube agglutination test,
Agar gel precipitation, and Fluorescent antibody
test
Diagnosis

52. A number of drugs reduce the worst effects of the
disease, and these include:

1.Sulphathiazole or

2.Streptomycin or

3. Tetracycline

All these are given for up to 7 days via drinking
water.
Treatment

53. The introduction of new stock should be limited to day-old
chicks or old birds, which are known to be free from the
infection.

Proper housing of all birds.

In non-endemic areas, eradication may be done by
removal of survivor flock and the thorough cleaning,
disinfection, and resting of building for at least 2 weeks
before restocking with clean birds.

Vaccination: using killed whole culture of organism
(BACTERIN) given twice at 3 weeks apart starting at 17
th

week of age.
Control

54. This is an acute disease of chicken characterized by
signs of respiratory depression, gasping and
expectoration of bloody exudates.

Etiology:

α– herpesvirus (alpha herpesvirus)
Family Herpesviridae.
4. INFECTIOUS LARYNGOTRACHEITIS (ILT)

55. The virus seems to be naturally infective only for the fowls.

All ages are susceptible, but young chicks, heavier breeds
and males are more susceptible than others.

Transmission of the disease is by aerosal route.

The virus enters the body through the upper respiratory
tract and conjunctiva.
Recovered birds act as carriers excreting the virus
intermittently for long period, perhaps for several years.

Living diseased bird excretes virus; very important source of infection.
Predisposing factors to more severe disease are:
a)Deficiency of vitamin A
b)Excess ammonia in the atmosphere
c)Concurrent infections with other pathogens e.g. NCD, Fowl pox,
Infectious bronchitis, Infectious coryza.
Epidemiology

56. The incubation period ranges from 6 – 12 days.

Three forms of disease: per-acute, acute and mild/
asymptomatic disease

i) Per-acute form:
Birds may be found dead without premonitory
signs or

Sudden acute dyspnoea with severe coughing
and expectoration of mucus and blood–stained
exudates

Death occurring between 1 – 3 days.
Clinical signs

57. ii) Acute form:
Nasal discharge
Dyspnoea; breathing with long drawn–out gaps, with a
wide-open beak and often moist rales can be heard.
Conjunctivitis with frothy exudates on eyes
Cyanosis of the faces and wattles.
Deaths usually occur in 3 – 4 days.

iii) Mild form:
Moist rales, slight coughing and head shaking, Nasal
exudates and conjunctivitis, Decrease in egg production,
and swelling of infraorbital sinuses.
Most chicken recover in 10 – 14 days.
Clinical signs

58. 1.In per-acute form: Haemorrhagic tracheitis and partial
or complete respiratory obstruction (blood stained
mucus)
2.In acute form: caseous, diphtheritic exudates, mucus
and some haemorrhages in trachea.
3.In mild form: Not severe tracheitis together with
edema and congestion of the epithelium of the
conjunctiva and infraorbital sinuses.


Differential Diagnosis
1.Infectious coryza
2.Fowlpox disease (diphtheritic form)
Post mortem lesions

60. Diagnosis:
a)Epidemiology
b)Clinical signs
c)Pm pictures

Treatment: No drug is effective in treatment of ILT

Control
1.Avoid mixing vaccinated or recovered chicken with
susceptible ones
2.Use of proper house hygiene
3.Vaccination (Eye drop, coarse spray and inclusion in water)
Diagnosis / Treatment/ Control

61. This is a disease of mammals and birds caused by
the growth of fungus Aspergillus in the tissues of the
body.

Aspergillosis in poultry usually is an infection
associated with the respiratory system and other
sites including the visceral organs, liver, eye and
brain.

Cause: Aspergillus fumigatus
5: FOWL ASPERGILLOSIS
(Synonymous: Brooder pneumonia; Mycotic Pneumonia)

62. The route of entry is by inhalation of fungal spores from
contaminated feed and water.

Fungal growth in wet litter produces large numbers of spores, and
these spread as suspended particles in air as wet litter dries.

Also can be egg borne ( A. fumigatus can grow inside the egg leading to
lowered hatchability and high embryonic mortality).

Young chicks/poults are most susceptible to the infection.

Predisposing factors to poultry include:
a)Management factors: chilling weather, deprivation of feed and/
or water, high ammonia level, and dust in the poultry house.

b)Primary bacterial or viral infections

c)Nutritional deficiencies
Epidemiology

63. Epidemiology
Outbreak of Aspergillosis is associated with:
a)high humidity and relatively warm temperature (> 25
0
C)

b)Mouldy litter materials, grain and feed

c)Dust (from both inside a poultry house and on ranges)

d)Unclean and improperly sanitized hatchery equipment

Acute outbreaks may occur in which there are high
morbidity and high mortality, particularly in young
birds.

64. Clinical signs
1.Dyspnoea, gasping and
accelerated breathing.


2.Inappetence,
emaciation, increased
thirst and pyrexia.


3.Serous nasal discharge.


4.Encephalitis; revealed
by torticollis and lack of
equilibrium
Chick with torticollis

65. 5.Eye infection -
formation of yellow
cheesy pellet beneath
mucous membrane of
conjunctiva causing lids
to bulge.

6.There may be
temporary lowered egg
production

In chicks mortality may
reach 50% especially in
confined birds

66. Post mortem findings
Post mortem findings
1.caseous nodules
(soft/cartilaginous 10 - 15
mm in diameter); are found
mainly in the respiratory
tract but occasionally in the
viscera, eyes and brain.


2.In older birds; typical
plaque – like caseous
lesions of the air sac walls
with grey-brown superficial
coloration

67. Post mortem findings
Whitish-yellow nodules (arrows) due to Aspergillosis

68. Diagnosis

Neither signs nor lesions are diagnostic of this infection.

Diagnosis depends on microscopic detection of the fungus in
tissues, followed by isolation and identification by
appropriate microbiological methodology
Treatment
At present there is no feasible treatment for Aspergillosis.

Attempts by using either Nystatin, Amphotericin B,
Trichomycin or Griseofulvin through drinking water

69. Control
Control is best accomplished by removing the cause:

1.Avoidance of mouldy litter or water leakage.


2.Daily cleaning and disinfections of feed and utensils.


3.Spraying the ground around containers with Copper
Sulphate solution e.g. 1:2000 (CuSO
4 : H
2O).


4.Careful selection of mash, grain and litter materials.

70. This is a slow – spreading viral disease
characterized by cutaneous/skin lesions and
sometimes with lesions in the mouth and upper
respiratory tract (diphtheritic form).


Etiology: Fowl poxvirus (Avipox genus and family
Poxviridae)

6: FOWL POX

71. Fowl poxvirus penetrate through a break on the skin to
enter the epithelial cells, replicate and cause disease.

Spread of the disease from one chicken to another is by
direct contact.

Also biting insects: Mosquitoes (Culex & Aedes) are
primary reservoir transmitting the disease from bird to bird
and responsible for widespread outbreak of the disease.

Fowl pox occurs in birds of all age groups, but more severe
in chicks.

Commonly in chicken, turkeys, and pigeons

The incubation period of the natural disease varies (4 – 10
days).
Epidemiology

72. Signs of typical pox infection occur in two forms or in a
combination: Cutaneous (dry form) or Diphtheritic (wet
form).


i) Cutaneous form (common): Lesions vary in appearance;

Clinical signs

First there is papules
which rapidly progress
through vesicle to
pustules (caseous
material) and finally to
crust/ scab.

73. After about 2 weeks the
scab will drop off and a
healed lesion is left
which may or may not
leave a scar.

 The lesions occur on
unfeathered skin of
the head, neck, legs
and feet.

Cutaneous lesions on
the eyelids may cause
complete closure of
one or both eyes
Clinical signs

74. ii) Diphtheritic form
White nodules in the
upper respiratory and
digestive tracts.


Then nodules coalesce to
form a raised yellow
plaques on the mucous
membrane.


Lesions are found in the
mouth, larynx, trachea,
nares, esophagus and
conjunctiva.
Clinical signs

75. ii) Diphtheritic form

Lesions in the esophagus
and larynx lead to
innapetance, in trachea give
rise to dyspnoea, and on
conjunctiva give rise to
ocular discharge and rare
cases result into blindness.



Morbidity rate is very slow
while mortality rate is
moderately high in
diphtheritic form (50%)


Clinical signs

76. Differential Diagnosis
The diphtheritic form can be confused with:
1.ILT = coughing and cyanosis of wattles
2.Avitaminosis A = No nodules, hyperkeratosis of mucous membrane of
mouth and oesophagus, corneal hyperkeratosis etc



Diagnosis
1.Epidemiology
2.Clinical signs: Cutaneous and Diphtheritic forms
3.Serological tests: ELISA



Treatment
There is no satisfactory treatment
Proper husbandry and supportive treatment.
Differential Diagnosis/Diagnosis/
Treatment

77. Vaccination (fowl pox vaccine and pigeon pox vaccine)
Three main routes are used:
a)Wing web route
For wing web method, vaccine is inoculated into the skin of the
wing web using a bifurcated needle.

b)Thigh method. Feathers are removed from the thigh and
vaccine brushed into the resulting follicles.

c)Via drinking water: Two vaccinations of high doses.

Time of vaccination
•First dose at 4 weeks old chicks
•Second dose at 1 – 2 months before egg production is expected
•For chicken held for second year of egg production, should be
revaccinated.
Control

78. Fowl pox vaccination = Wing web route

Wing web route
Fowl pox vaccine
Administering Fowl Pox Vaccine.MP4
How to do Fowl Pox Vaccine.MP4

79. Coccidiosis is contagious enteritis caused by
infection with either or both Eimeria and Isospora spp.


It occurs in all domestic animals and poultry.


A high rate of clinical infection is associated with
diarrhoea and/or dysentery and death.


In some cases there is anaemia and chronic form of
the disease which is characterized by inferior
growth rate and lowered production.
7: COCCIDIOSS

80. This is a disease of the digestive system/ tract characterized by
diarrhoea, often with blood in faeces, lack of activity, weakness,
emaciation and high mortality in chicks that looked healthy the
previous day.

Aetiology:
Seven species of Eimeria; E. tenella, E. necatrix, E. brunetti,
E. acervulina, E. maxima, E. mitis and E. Praecox.

E. necatrix and E. tenella are the most pathogenic in chickens while
other strains (E. acervulina, E. maxima, E. praecox and E. mitis) are
less pathogenic strains.

In turkeys, the most important species of Eimeria which cause
disease are E. adenoides and E. meleagrimitis.

Eimeria infections are species-specificity infection, no cross
infection and no cross immunity.
FOWL COCCIDIOSIS

81. All age groups are susceptible to the disease, although chicks of 5 – 7 days
and growing birds are highly susceptible.

a)Ingestion of the infective form of oocysts (viable sporulated oocysts) is
the only natural method of spread.

b)Oocysts can be spread mechanically by animals, insects, contaminated
equipment, wild birds and dust.

c)Spread from one farm to another is facilitated by movement of people
and equipment between farm, which may spread the oocysts
mechanically.

Oocysts may survive up to 1 year in shaded soil.

All species of Eimeria are widely distributed throughout the world.

The disease is likely to occur only under high stocking density ‘Coccidiosis
is specifically important in intensive poultry operations’
Epidemiology

82. The nature of lesion (clinical signs) varies between species of Eimeria
which are site of infection.
Two forms: 1) caecal coccidiosis, and 2) intestinal coccidiosis


The general symptoms include
1.Pale combs and wattles from blood loss in gut.
2.Ruffled feathers and depression (lack of activity).
3.Weakness, emaciation and huddling together
4.Decrease in egg production in layers at reproductive age
5.Depressed growth rate or actual weight loss may occur

NB: Early exposure to the GUMBORO agent increases severity of cecal Coccidiosis
and may decrease effectiveness of some anticoccidial drugs
Clinical signs

83. 1.Caecal coccidiosis is caused
by E. tenella, is a severe
disease characterized by
blood dropping, high
mortality, reduced weight
gain and emaciated.
oThis form has high
mortality with most of the
mortalities occurring
between 5
th
and 6
th
day
following infection
Clinical signs

84. 2.Intestinal coccidiosis
caused by E. necatrix, is
associated with severe
weight loss and mortality in
relatively older birds.
oDroppings of affected
birds usually contain
blood.
oLike E. tenella, E. necatrix
is also most harmful.
Clinical signs

85. The entire length of the external surface of the digestive tract
from the gizzard to the ceca needs to be examined.
On the serosal surface:
There may be whitish plaques or petechial or whitish streaks or
Rounded colonies of oocysts.

On opening:
Inside:- presence of mucus, blood, casts or cores (which may be
whitish, red or brown) and cheesy coagulation necrosis.
Post-Mortem picture

86. Post-Mortem picture
Lesions in Chickens vary depending on what species of Eimeria are
involved:

E. tenella: Hemorrhage in colon and cecum progressing to cores of
coagulated blood in lumen of cecum.

E. necatrix: Mid and distal small intestines (jejunum and ileum): White
spots (large schizonts) in mucosa with mucus and blood in lumen.

E. acervulina: white “tiger-striping” of upper small intestine
(duodenum).

E. maxima: Orange, mucoid material in lumen of jejunum.

E. brunetti: Mucus and blood in ileum and colon; Can occasionally see
cores of blood in cecum.

88. Caecal coccidiosis

89. Intestinal coccidiosis

91. a)Clinical signs: The presence of dysentery, diarrhoea or
soft, mucoid faeces, poor growth rate, drop in egg
production, and sudden increase in daily mortality.

b)Pm examination: A few sick birds should be sacrificed
for this purpose so that fresh material is available.
Lesions should be noted from the serosal surface and
mucosal surface.

c)Laboratory examination: examination of wet smears
diluted with isotonic saline under cover slip with
appropriate lighting will normally be sufficient to detect
schizonts, gametes and oocysts.
Diagnosis

92. Oocysts of Eimeria as observed on a mucosal scraping (40X objective).

93. Commonly anticoccidials/
Coccidiocides used are

1)Sulfa drugs: Sulphonamides;
Sulfamethazine,
Sulfaquinoxaline


2)Nitrofurans (Nitrofurazone)


3)Amprolium


4)Sodium Sulfachloropyrazine
monohydrate (Esb
3)


 All are commonly given
through drinking water.
Treatment

94. 1.Maintain good hygiene: This reduces the number of
oocysts contaminating the environment.
Prevent overflowing waterier and leaking water pipes.
Maintain birds on perforated floors.

2.Use of drugs (prophylactics/ coccidiostat, which inhibits
multiplication of parasites)
oMost of anticoccidials are formulated as feed additives

oThe most widely used drugs are: Salinomycin (Bio –
Cox
®
), Amprolium (Amprol
®
), Decoquinate (Deccox
®
),
Sulfadimethoxine + Ormetroprim (Refenaid
®
),
Nitrofurazone (Amifur
®
)
Control

95. 8: INFECTOUS BURSAL DISEASE
(GUMBORO )
Gumboro disease is an important viral disease of
poultry throughout the world.

Clinically it affects young chickens, usually up to 6
weeks of age.

The acute form is characterized by sudden onset,
short course and extensive destruction of
lymphocytes particularly in the Bursa of fabricius
(cloaca bursa) and also in other lymphoid tissues.

96. GUMBORO
Causative agent: Birnavirus (IBD virus).

The virus is highly resistant to physical conditions
and chemical agents.

It can survive temperature of 60
0
C, stable at pH 2
and resistant to most of organic solvents; it is only
susceptible to formalin and iodophors.

It can remain infective in the environment for at
least 4 months.

97. Epidemiology

Gumboro disease is of worldwide distribution.

Young birds (chicks) are susceptible, with the period of
greatest susceptibility lying between 3 – 6 weeks of age.

Viruses are transmitted only through ingestion; Neither
airborne, egg transmission nor carrier states.

The disease is highly contagious with affected chicks
excreting virus in faeces for up to 2 weeks after infection.

The disease appears suddenly and there is high morbidity
rate, usually approaching 100%.

Mortality usually begins on the 3
rd
day post infection and will
peak and recede in a period of 5 – 7 days; the mortality rate is
high 20 – 60%.

98. Clinical signs

There are no characteristic signs specific to IBD

Acute form:
oWhitish, watery diarrhoea
leading to soiling of vent
feathers.

oDepression and anorexia .

oInflamed vent and vent
picking.

oRuffled feathers, listless
and huddling together.

99. 1.Acute form:

Deaths occur within 2 days of the first signs of the disease,
reaching a peak in 2 or 3 days and rapidly decline so that
the course of the disease in a house is about 7 or 8 days.


2.Subclinical infections:
oThe severe clinical signs are absent but there may
be reduced growth and production.

Chickens infected when less than 3 weeks of age
do not develop clinical disease, but become
severely and permanently immunosuppressed.

100. Post mortem picture
1)Birds that succumb to
the infection are
dehydrated.


2)Haemorrhages are
present in the thigh
and pectoral
muscles.


3)There is increased
mucus in the
intestines.

101. Post mortem picture

4)The liver may be
swollen and show
peripheral
infarcts.





5)Occasionally
splenomegally
occurs

102. Post mortem picture
6)In acute cases the
characteristic lesion is
within the Bursa of fabricius.

oThe cloaca bursa is first
enlarged, inflamed,
oedematous with cream
coloured materials, and after
about 4 – 4 days of disease the
bursa atrophies.

oHaemorrhages may be seen
in the internal and serosal
surface of bursa and a
caseous core is formed
within the lumen from
sloughed epithelial tissues.

103. Post mortem picture
7)Occasionally,
haemorrhages are
observed in the
mucosa at the
juncture of the
proventriculus
and gizzard.

104. Differential Diagnosis

In less severe forms, or where the bursa does not
show typical lesions, Gumboro can be confused
with:
a)Coccidiosis
b)Newcastle disease
c)Haemorrhagic syndromes (for muscular haemorrhages)
d)Avitaminosis A (for caseous plugs in the bursa)

NB: Confirmation of diagnosis may be made by
serological tests

105. Diagnosis/Treatment/Control
Diagnosis
History/ epidemiology, Clinical signs and Gross lesions

Treatment
No therapeutic treatment is effective
Only supportive treatment e.g. Vitamins, & Broad spectrum
antibiotics (OTC 20%)

Control
a)Vaccination: 1
st
dose at 7
th
or 14
th
day, and 2
nd
dose at 21
st
or
28
th
day of age.

a)Sanitary precautions to prevent spread of infection by
preventing contact with infected birds and/or contact with
contaminated formats.

106. 9: NEWCASTLE DISEASE
This is a viral disease affecting chicken and is
characterized by either nervous system,
gastrointestinal or respiratory tract involvement

Causative agent
The disease is caused by a group of closely related
viruses, avian paramyxovirus type 1 (pmv-1).

Based on the disease produced in chickens under
laboratory conditions NCDVS (PMV-1) have been
classified into five pathotypes.

107. NCD pathotypes
1.Viscerotropic velogenic NDVs: causing a highly virulent form of
disease with Haemorrhagic lesions in the intestinal tract.

2.Neurotropic velogenic NDVs: causing high mortality following
respiratory and nervous signs.

3.Mesogenic NDVs: causing respiratory and sometimes nervous
signs with low mortality.

4.Lentogenic respiratory NDVs: causing mild or in apparent
respiratory infection.

5.Asymptomatic enteric NDVs: causing neither apparent enteric
infection, clinical signs nor pathology. Detected / isolated in the
guts or faeces and by presence of specific antibodies.

108. Epidemiology
Over 200 species of birds (including poultry) are
susceptible to natural or experimental infections of NDVs.

However, some species e.g. ducks and geese, tend to show
few signs of disease even when infected with the most
virulent strains of NDV.

The mode of transmission from bird to bird is clearly
dependent on the organs in which the virus multiplies:

Respiratory form - shed virus in aerosols of mucus
which may be inhaled by susceptible birds.

Intestinal form - sheds virus through feces
contaminating food or water or by inhalation of small
infections particles produced from dried faeces.

109. Epidemiology
Man seems to play the central role in the spread of
NDV, usually by the movement of live birds,
personnel and poultry product (e.g. dead birds
and faeces for fertilizers) from affected premises to
susceptible birds.


Also feral/wild birds and other wildlife
contribute to the spread of disease either by
infection or by mechanical transfer (e.g. stray
racing pigeons)

110. Clinical signs
The disease produced following infection with NDV vary
considerably with the strain of virus, species of birds,
immune status, age and conditions under which they are
reared.

1.Sudden death may be produced by infection with highly
virulent virus in fully susceptible chickens.

2.Typical signs are:

Depression
Appearance of shell-
less or soft-shelled
eggs, (due to premature
Oviposition) followed
by complete cessation
of egg laying, early sign
in adult fowl.

111. Clinical signs
Velogenic Viscerotropic
NDVs: watery greenish
Diarrhoea, sometimes
bloodstained and profuse.


Facial swelling; usually
around the eyes and throat.


Respiratory distress
(Mesogenic NDV):
increased respiration rates,
watery discharge from
nostrils, gasping and rales
especially to the disturbed
bird.

112. Nervous signs
(Mesogenic NDV):
may appear within a
day or two or later,
paralysis of legs or
wings, trembling and
twisting of the neck
(torticollis).













Mortality rate may
range from 50 –
100% and Morbidity
rate of 50 – 100%

113. Pm picture
1.Virus causing
respiratory disease may
include:
 inflammation
/hemorrhages of the
trachea.

Air sacs are inflamed
and appear cloudy
and congested.

Serous or catarrhal
exudates may be
present in nasal
passages, larynx and
trachea.

114. 2.The virulent
viscerotropic virus
usually produces:
Prominent
hemorrhagic
lesions of the
gastrointestinal
tract, particularly in
the
proventriculus .

However, the
lesions vary
considerably in
size and severity.

115. Differential diagnosis
1.Infections Laryngotracheitis (respiratory distress, nasal
discharge sometimes blood stained)

2.Infections coryza (Swelling of wattles and face, conjunctivitis, serous
nasal discharge & cyanosis of face)

3.Marek’s disease (paralysis of one leg/wing, torticolis)

4.Fowl cholera (sudden death, diarrhea with fetid, watery and greenish
feces)

5.Poisonings

116. Diagnosis/ Treatment
Diagnosis
1.History
2.Epidemiology
3.Clinical signs
4.Gross lesions; but these lesions are not
pathognomonic for any form of Newcastle disease.

Treatment
There is no specific and feasible treatment.
Antibiotics administered for 3 - 5 days to help
prevent secondary bacterial infections (especially
E. coli) in mild cases are useful.

117. Control
1.The simplest and most logical measure against
NCD is to prevent exposure of susceptible birds to
virus through:

Controlled and reduced access of personal and
equipment from outside.

Avoid introduction of new bird in the flock.

118. 2.Vaccination: Birds should be
vaccinated with low-virulence
live virus at l day old by eye
drop or coarse spray and
drinking water followed by re-
vaccination.


For layers; re-vaccination is
usually recommended at 3-4
weeks of age, then at 2 month
and lastly at 1 year old.


For broilers; great attention of
timing is required, route and
strain of virus; is
recommended to vaccinate
once when broilers are 1 – 2
weeks old.
Live vaccine

119. POULTRY VACCINATION REGIMEN
Eye drop /Drinking water
Eye drop /Drinking water

120. 10: MAREK’S DISEASE
This is a lymphomatous disease of the domestic
chicken characterized by lympho-proliferative
infiltration (mononuclear infiltration) of peripheral
nerves (leading to demyelimination of peripheral
nerves), gonads, iris, various visceral organs,
muscles and skin.

Etiology : Lyphotropic herpesvirus

Readily inactivated by common chemical disinfectants.

Remains in litter for up to 16 weeks at room temperature.

Dried feathers from infected chickens retain infectivity for up to 8
months at room temperature and for at least 3 years at 40
0
C

121. Transmission
Marek’s disease occurs in all countries throughout the world.

Natural infection to chicken occurs as early as 3
rd
week of
life and the diseases appears between the 3
nd
and 6
th
month
with losses occurring after birds reach maturity.

Direct (contact between birds) or indirect contract
(airborne) are means of spread.

Sources of infection are infected birds, carriers and
chicken in incubation period.

Incubation may be as short as 3 or 4 weeks or long as
several months.

Incidence of MD is quite variable; few birds that develop
signs and recover from the clinical disease, but in general,
mortality is nearly equal to morbidity.

122. Clinical signs
Three forms:
1.Classical Marek’s disease.

Mortality is variable 10 – 15 %.

The signs depend on the peripheral nerves affected.

Involvement of the brachial and sciatic nerves (common)
a)Sciatic nerve (leg)
involvement makes birds
to have one leg stretched
forward and the other
back as a result of
unilateral paresis/
paralysis of one legs.

123. b)Brachial nerves
involvement leads to
paralysis of a wing.
c)Vagus nerve involvement
leads to paralysis and
dilatation of the crop and/
or gasping.


d)Involvement of Vagus
and Intercostals nerves
lead to respiratory signs.

e)When cervical nerves
are involved – torticollis.

124. f)When iris is involved, blindness
occurs.

g)Non-specific signs such as weight loss,
paleness, anorexia, weak labored
breathing, enlargement of feather
follicles and greenish diarrhea

125. Post mortem picture
a)Enlargement of one or
more peripheral nerves
(brachial or sciatic
nerves) affected nerves are:
oenlarged,
olost cross-striations, gray or
yellow in colour,
oand sometimes an
edematous appearance.

 Lesions are unilateral;
compare the two nerves
in case of slight changes.

126. Diffuse lymphomatous tumor may occur in liver,
gonads, spleen, kidneys, lungs, proventriculus, heart
and muscles .

130. Diagnosis/Treatment/Control
Diagnosis
1.Clinical signs
2.Epidemiology
3.Pm picture

Treatment: None

Control
1.Management methods: isolation of growing chicken from
source of infection

2.Vaccination: at hatchery or at 18 day. The vaccine give life long
immunity

Marek’s disease is very stable in feather, and infectious virus can
remain on infected premises for very long periods of time.
Birds with clinical signs of disease will not recover and must be
culled.

131. 11. Lymphoid Leukosis
Syn: Visceral leukosis, Leukosis, Big liver
Avian leukosis is a viral disease characterized by a gradual,
persistent low mortality in the flock and diffuse or focal
neoplastic growths of lymphoblasts in viscera.

Cause: Avian leukosis viruses, family retroviruses.

Epidemiology:
The disease affects mainly chickens, occasionally turkeys,
guinea fowl, pheasants, and doves.

Transmission:
Virus transmission mainly occurs through the egg to chick.
Some bird-to-bird transmission and through contact with
contaminated environments also takes place.

132. Signs of lymphoid leukosis begin to show in birds only after
the age of 16 weeks, because it has a long incubation
period.


Clinical signs are non-specific.
oThe abdomen is distended as a result of an enlarged
liver.
oThe comb is reduced in size.
oBirds become emaciated and progressively weaker.
oIf many birds in the flock are infected, egg production
is reduced.
oGreenish diarrhea develops in terminal stages.
Clinical signs and lesions:

133. Lesions are restricted to
internal organs.

Diffuse or nodular
neoplastic growths could
be detected in many
organs, more commonly in
the liver, the spleen, the
kidneys, the heart and the
ovary.
The lesions are whitish or
grey nodules which are
cancerous lymphoid tissue
that has spread from the
bird’s bursa.
Pathological lesions:

134. Focal neoplastic lesions in kidneys
Diffuse and focal tumour lesions in the heart
Neoplastically transformed ovary in LL.
Spontaneous rupture of the neoplastically grown
spleen, leading to extensive loss of blood.

135. Lymphoid leukosis may be confused with Marek’s disease

Differential diagnosis
LYMPHOID LEUKOSIS MAREK'S DISEASE

oUsually, it is not seen in birds
younger than 14 weeks.
oObserved after the age f 4 weeks
too.
oThe lethal issues occur mostly at
the age between 24 and 40 weeks.

oThe peak mortality is seen
between the 10 - 20th week,
sometimes continues after the
20th week.
oHave distinct nodular tumors. oParalysis.
oInvolvement of eye "Grey eye".
oHave tumors in the bursa of
Fabricius.

oIn some birds, the bursa of
Fabricius is atrophied, others not
affected

136. Tentative diagnosis is easily achieved by consideration of the age of
affected birds, the lesions, and involvement of the bursa.

Confirmation is through histological examination of affected tissues /
tumors of the bursal follicles

Treatment: There is no treatment for LL.

Prevention:
Eradication is the most effective method of prevention. The virus is
present in the yolk and egg white of eggs from infected hens.
Breeder flocks should be tested and positive birds culled.

Affected flocks can be removed through slaughtering process, and
standard disease control and sanitation practices can keep chicken
flocks free of the disease.

Thus far, vaccination for tumor prevention has not been promising.
Diagnosis:

137. 12: FOWL CHOLERA
(syn: Cholera, Pasteurellosis)
Contagious disease of domestic and wild birds
characterized by acute septicemia with high
morbidity and mortality rates, and a chronic
localized disease

Aetiology: Pasteurella muttocida

138. Epidemiology
Species affected are chicken, turkeys, ducts, and many
wild birds

In poultry, semi–mature and mature birds are affected.

Turkeys are more susceptible than chicken.

Among chickens – heavy breeds are more susceptible

Distribution: Worldwide

Transmission
a)Ingestion of contaminated feed or water
b)Inhalation
c)Though conjunctival mucosa and wounds (rarely)

139. Epidemiology
Acute outbreaks associated with environmental or
management stress.

Source of infection: carrier birds, clinically
infected birds, rodents and wild birds.

Infection occurs following direct contact or
aerosol between susceptible birds and clinically
affected or recovered carriers.

Indirectly: personnel and equipment, contaminated
feed bags, livestock (cattle, cats), wild birds,
rodents, insects etc.

140. Clinical signs
Morbidity and mortality rates depend on the pathogenicity
of the strain and the susceptibility of the flock.

1. Peracute :
Death without premonitory signs (birds in good condition).

2. Acute The course of illness is short
Dead chicken may be the first sign
(laying birds dead in the nest).
Anorexia, depression, nasal
discharges,
Diarrhea: fetid water or greenish in
mucoid
Increased respiratory rates
Ruffled features

141. Clinical signs
3. Chronic
Survivors of acute diseases or affected by less virulent strain.
Signs are associated with localized infection:
a)Failure of growth and
drop in egg production

b)Swelling of joints, foot
pad, or tendons sheath
leading to lameness.

c)Torticollis and dermal
necrosis (common in
turkeys)

142. c)Wattles are
strongly distended
and filled with
fibrinous caseous
content.


d)The periorbital
sinuses are
frequently affected
by a serofibrinous
inflammation.

e)Accumulation of
cheesy exudates in
the conjunctiva,
pharynx and
infraorbital
sinuses.

143. f)In layers (commercial or breeders), acute oophorites with
regressing follicles and consequently, diffuse peritonites
are commonly observed.


Post mortem picture
1)Acute cases show
enlargement of the
spleen and liver with
hemorrhages of the
viscera: heart, intestines
and lungs.

2)Sub-acute cases may
show gray
granulomatous foci in
the liver.

144. 3)Acute oophorites with
raptured egg yolks and
consequently, diffuse
peritonitis are commonly
observed.

4)Chronic cases:
seropurulent
inflammation of the joints
and wattles.


5)In Turkeys; fowl cholera
often occurs as a
complication of air
sacculitis cased by
Mycoplasma gallisepticum

145. Diagnosis
1.Clinical signs

2.Pathological lesions

3.Identification of organism. Laboratory examination is
required to isolate and identify P. multocida from
specimens of heart blood, liver, and spleen. In acute
cases, characteristic bipolar organisms may be
observed in Giemsa-stained smears of heart blood.

4.Mice inoculation

Differential diagnosis
1.Infectious coryza
2.New castle disease
3.Avian flu
Characteristic bipolar staining Pasteurella multocida
organisms in a Giemsa-stained blood smear.

146. Treatment / Control
Treatment:
Limited value in septicemic cases
1.Sulfa drugs
2.Tetracycline
3.Erythromycin

The most efficient treatment in breeding flocks or laying hens is
individual intramuscular injections of a long-acting tetracycline,
with the same antibiotic in drinking water, simultaneously.

Control
Strictly hygiene: exclusion of livestock, wild birds & rodents.

Depopulation and disinfection of premises (removal of
reservoirs).

Vaccination.

147. 13. BUMBLE FOOT

Syn: PODODERMATITIS

Bumblefoot is an infection of the foot resulting from hard landing
off a roost, a cut that gets infected or even a Vitamin A
deficiency.
It is an injury to the lower surface of the foot and subsequent
infection with Staphylococcus bacteria
Predisposing factors:
Pododermatitis (Bumble foot) resulting from wet litter
Rough floor
Presence of sharp wire ends
Jumping repeatedly from resting/perch (heavier breeds)
Poor litter or bedding quality

148. CLINICAL SIGNS
Lameness


Swelling of the foot
pad

Hard, pus‐filled
abscess on foot pad

150. TREATMENT
Soak foot in warm water and disinfect with alcohol

If skin is open, drain pus from abscess.

Flush abscess cavity with hydrogen peroxide to cleanout
pus and debris.

Pack the cavity with antibiotic ointment.

Wrap the foot with gauze and elastic bandage.

Administer broad spectrum antibiotics through water.

Repeat daily until foot heals.

151. PREVENTION AND CONTROL
Provide good quality litter or bedding.

Keep bedding clean, dry, and deep.

Keep poultry out of rough floor to prevent foot
damage due to impact from jumping.

Remove potential sources of injury such as sharp
objects and/or surfaces.

152. 1)Vitamin Deficiency
oAvitaminosis A
oVitamin B
oVitamin D
oVitamin E,
oBiotin Deficiency

2)Mineral deficiency:
oCalcium
oPhosphorus
oManganese
oZinc

SELF READING

153. 13. Nutrient Deficiencies
Causes of Nutrient Deficiencies

a)Diets may be erroneously/mistakely formulated.

b)Biological potency of specific vitamins or availability of
minerals may be of sub-optimal quality (low quality).

c)Deficiencies may occur due to deletion of specified
ingredients or supplements from rations.

d)Destruction of nutrients in feed due to oxidation.

e)Presence of chemical antagonists in feed.

f)The nutrient quality of ingredients may be depressed by
excess moisture, mold contamination or inappropriate
processing/storage.

154. a)Low Energy Intake

oMost poultry will compensate for low energy
requirement by consuming greater quantity of feed.

oUnder conditions of feed restriction or extreme
competition, mature birds will lose weight and hens
will show a decline in both egg size and egg
numbers.

oGrowth rate of immature stock will be depressed.

oFlocks deprived of energy will show increased
susceptibility to infection.

155. b)Deficiencies of Proteins or Amino
Acids
oLow protein intake will depress growth rate, feed
conversion efficiency, immune response and
reproductive efficiency.

oDeficiency in lysine may occur in wheat and maize-
based diets and will result in depressed growth rate
and feed conversion efficiency in broilers.

oMethionine deficiency in diets containing maize
and soybean meal will result in a low growth rate.

oIn the case of mature flocks, Methionine deficiency
leads to reduced egg size and egg numbers.

156. c)Vitamin Deficiencies

oDeficiencies of vitamins may occur following
inappropriate formulation, the use of impotent/weak
commercial preparations or destruction of nutrients
in feed by oxidation.

oThe significant deficiencies encountered in commercial
poultry production include;

i.Avitaminosis A

Chicks will show poor growth and feathering and in
advanced cases, ataxia (inability to stand),
xerophthalmia (“dry eye”) and chronic purulent
conjunctivitis (accumulation of yellow caseous
material beneath the eyelids.

157. Laying hens subjected to avitaminosis A will show a
deterioration in internal egg quality and a high
prevalence of blood spots on egg shells.

Fertility and hatchability of breeders will be adversely
affected.

Flocks subjected to avitaminosis A will show a high
susceptibility to E. coli and other bacterial infections
and will be more severely affected by endoparasites
and coccidiosis.

Diagnosis of avitaminosis A: pm examination will reveal
squamous metaplasia (columnar epithelial cells
regress to multiple layers of flattened cells), kidney
degeneration, accumulation of urate in the ureters, in
advanced cases urate deposit on the viscera (visceral
gout), and accumulation of a cheesy material in
eyelids and nostrils

158. ii.Vitamin D3 (Cholecalciferol) Deficiency

oA deficiency in vitamin D3 will lead to rickets in immature
flocks.

oAffected birds aged 4 to 7 weeks show a disinclination to
walk. Swelling of the joints is noted together with depressed
growth rate and poor feathering.

oIn mature laying and breeding stock, results in osteomalacia
characterized by decreased skeletal density.

oAffected flocks show a gradual decrease in egg production
and a marked deterioration in shell quality.

oAscending mortality is associated with paresis and paralysis
in caged hens which are unable to stand to feed and drink.

oOn post-mortem examination decreased skeletal density is
evident, costochondral (rib to spine) junctions are enlarged,
and gross enlargement of the parathyroid glands.

159. v.Biotin Deficiency

oBiotin is a cofactor in carboxylation and decarboxylation
reactions involving fixation of carbon dioxide.


oThese reactions have important roles in anabolic processes
and in nitrogen metabolism.


oBiotin deficiency in chicks leads to poor hatchability, and
bony deformity in chicks


oBiotin deficiency in broiler leads to depressed growth; fatty
liver and kidney syndrome (fitty infiltrations of liver, kidney,
and heart); acute death syndrome” (or “sudden death
syndrome”) in broiler chickens

160. iii.Vitamin B1 (Thiamine) Deficiency

oAvitaminosis occurs as a result of failure to add thiamine
to vitamin premixes or occasionally as a result of
excessive addition of the anticoccidial, amprolium, to
diets.

oThe principal sign of thiamine deficiency in 10 to 20 day old
chicks comprises incoordination and an abnormal retraction
of the head (“star gazing”).


iv.Vitamin B2 (Riboflavin) Deficiency

oThis condition is characterized by rotation of the legs in
chicks aged 10 - 30 days, and is referred to as “club foot” or
“curled toe paralysis”.

oAffected flocks will demonstrate low growth rate and poor
feathering.

161. 4.MINERAL DEFICIENCY
1.Calcium and Phosphorus Deficiency

oCalcium (Ca) and phosphorus (P) are closely associated in
metabolism, particularly in bone formation.

oThe utilization of calcium and phosphorus depends on
presence of an adequate amount of vitamin D in the diet.

oDeficiencies of calcium and phosphorus in the diet of
growing broiler chicks cause rickets

oIn laying hens, calcium deficiency results in reduced egg
production and thin-shelled eggs, and weak bones which
are easily fractured.

oExcess Calcium lead to Nephrosis and visceral urate
deposition (e.g., “visceral gout”)

162. 2.Zinc Deficiency

Deficiency of zinc results in retarded
growth; poor feathering; enlarged
hocks; short, thickened long bones
(chondrodystrophy); scaling of the skin
and dermatosis, particularly on the feet;
and an awkward arthritic gait.



Excessive dietary levels of zinc induce
molt in laying hens, abrupt decline in
egg production and onset of molt
followed by rapid resumption of egg
laying after dietary zinc concentrations
are returned to normal.

163. 14. FOWL HELMINTHIASIS
a)Ascariasis
Cuases: Ascaridia galli

Clinical signs and lesions:
a)Light to medium infestations may be
tolerated without clinical signs.

b)Heavy infestations may cause
diarrhea, intestinal occlusion,
intussusceptions, emaciation,
anemia and death.

c)There is reduction in egg
production, and birds appear
unthrifty.

d)Lesions caused by this worm are
catarrhal or hemorrhagic enteritis.

164. Diagnosis is through finding worm eggs in feces or adult
worms during post mortem.
Diagnosis:

Treatment: Piperazines



Prevention:
1.Separate young birds from
old birds when kept in
enclosures.

2.Moisture levels and
ventilation should be
monitored.

165. b) Gapeworm
Cause: Syngamus trachea

Clinical signs:
dyspnoea and suffocation,
anemia, mucus production
in the airways, and
progressive emaciation.

The bird may cough and
perform gaping
movements when the
worms clog and obstruct
the airways.

Death may occur due to
asphyxiation.

166. b) Gapeworm


Diagnosis: Diagnosis is
based on clinical signs,
characteristic eggs in the
feces, and finding the
worms in the airways at
post-mortem.



Treatment: Albendazoles is
used to cure infection.

167. c) Tapeworm
Cause: Raillietina spp. (Nodular
tapeworm of poultry)

Clinical signs: Associated with
severe weight loss and anemia.

Pm lesions: Caecal wall is
congested and thickened.

Diagnosis: Diagnosis is made by
accurate identification of the
parasite during necropsy and by
identifying proglottides in feces.

Treatment: Broad spectrum
benzimidazoles are effective for
treatment of infestations of this
tapeworm.

168. 15. Ectoparasites
Mites and lice are the most common ectoparasites in poultry.

 Ectoparasites can cause decreased production and uniformity
and also provide opportunity for transmission of other
diseases.

a)Feather mites Synonyms: Acariasis
Causes: Red chicken mite (Dermanyssus gallinae).

This mite feeds on blood and is primarily
active at night (night feeder), and during
the day will leave birds to reside in nest
boxes, cracks in the poultry house.

Clinical signs: decreased egg production,

169. Mite can be observed on the feathers
of the vent and over the entire body,
particularly at night.

Treatment
In heavy infestations chemical
insecticide sprays can be used.

Commercially available acaricidal
insecticides include pyrethrins,
permethrins and rose dust (Sevin
Dust).

Prevention
Make sure the house is cleaned,
disinfected and free of mites and lice
before introducing new birds.

Maintain biosecurity to keep rodents
and wild birds out of houses.

170. b)Poultry fleas

oEchidnophaga gallinacea (stick tight flea) is the only flea
commonly affects chickens.

oIt may infest a wide variety of birds and mammals; poultry,
rodents, rabbits, canids, felids, horses, and occasionally
humans may all become infested.

oPoultry may develop clusters of the fleas around the eyes,
comb, wattles, and other bare spots.

oEchidnophaga gallinacea are difficult to remove because their
heads are embedded in the host's flesh and they cannot be
brushed off.

oOccurrence: Echidnophaga gallinacea is found in the tropics
and subtropics. Reported in Nigeria, Kenya, and Tanzania.

171. Clinical signs and pathology
oThe adult fleas attach to the skin around the face
and head, causing severe irritation, nodular
formation, and in some cases, blindness.

oThey can cause blood loss, anemia, and even
death.

oThe skin over the nodules often becomes
ulcerated, and young birds may be killed by
heavy infestations.

Diagnosis: This is based on history, clinical signs,
and identification of fleas or flea feces on birds.

Treatment: A range of insecticides can be
used; organophosphates, carbamates,
pyrethrins, and pyrethroids.

Control by treating the birds, removing them from
the infested area for three weeks, and treating the
area (removing fecal droppings and litter, and
spraying a suitable insecticide) and birds (again)
before returning them.

172. c)Scaley-leg mites
Causes: Knemidocoptes mutans.
The scaley-leg mite affects a
variety of birds including
chickens, turkeys, pheasants,
partridges, and many passerine
birds.



The mite found most often on
older birds and spends the entire
life cycle in the skin.

173. Transmission occurs through
direct contact with other
birds.

The mites burrow into non-
feathered portions of the
body, particularly the scales
of the legs, comb and
wattles, resulting in marked
proliferation of the skin with
heavy and irregular keratin
crusts.

Heavy infection on the leg
can interfere with joint
flexion and can cause
lameness, loss of toes,
decreased feed consumption
and decreased egg
production.
oAdult with scaley-let mites

oNote the enlarged and deformed feet with
excess accumulation of keratin caused by
Knemidocoptes mutans.

174. Treatment

The disease can be treated by dipping the legs in dilute insecticide (acaricidal)
solutions.

Birds that are not used for egg or meat production can be effectively treated with
a drop of ivermectin solution on the comb/wattle or Promectin® solution through
drinking water.

Treatment should be repeated after two weeks later!