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Avian Digestive

problems
The enteric tract has many functions:

1- Providing a means by which the body


derives nutrition.

2- Furnishes protective mechanisms to


safeguard the host.

3- Serves as an environment for other living


organisms.
Economic losses
§ 1-High mortality e.g. coccidiosis.
§ 2-Down grading of carcasses e.g.
§ Enteroviruses infection (ISS).
§ 3-Lowering fertility and hatchability e.g.
§ Salmonellosis.
§ 4-Loss of weight and poor feed conversion
§ e.g. Colibacillosis.
§ 5-Severe drop in egg production e.g. TB.
Predisposing factors
§ I-Immunosuppressives
A-Feed:
1-Mycotoxins. 2-Antibiotics. 3-Pesticides. 4-Chemicals.
5-Deficiency (vitamins, Protein & minerals).

B-Environment:
1-Bad ventilation (ammonia and dust-cilliary apparatus).
2-Temp. Extremes: Air drafts chilling, over heating.
3-Relative Humidity.

C-Organisms:
1-Viral:
*Vertically transmitted (CAV, ALV,REV & Reo).
*Horizontally transmitted (IBDV, MDV, NDV & AIV).
2-Bacterial:E.coli, MG & MS.
3-Coccidiosis (7 Eimeria species).
Predisposing factors (Continue)
II-Management factors
1-System of management (Multiage).
2-Distance to the nearest farm.
3-Distance between houses.
4-Stocking density (over crowding leads to social stress)
5-Chick quality.
6-Feeders and waterers (the amount and quality of feed and
water).
7-Poor biosecurity (Rodents,Insects, Animals, personnel).
8- Litter (dry or wet).
9-Duration between successive cycles.
10-Vaccination and medication.
Classification of Enteric Diseases according to
etiological agent(s)
§ 1-Viral agents (NDV, AIV, Avian diphtheria and
Enteric viruses).

§ 2-Bacterial agents (Colibacillosis,Salmonellosis,


Pasteurellosis,Spirochaetosis,TB,Clostridial infections,
Camylobacteriosis and Chlamydiosis.

§ 3-Parasitic agents (Intestinal parasites).

§ 4-Non-infectious causes (Avitaminosis A, toxicity


and Mycotoxicosis).
Epizootiology
I-Susceptibility:
a-Species:
*Species specific(Coccidiosis).
*Many species (AI, ND, Salmonellosis).
b-Age:
*First few weeks (E.coli, Salm.).
*Semimature and Adults (FC).
*All ages (ND).
Epizootiology( continue)

II-Mode of infection and transmission:


*Ingestion (All).

*Conjunctival infection (FC).

*Vertical transmission (Salmonellosis, E.coli)


Epizootiology
Epizootiology ( continue)
( continue)

III-Incubation period:
*Very short (1-3 days e.g. AI).

*Moderate (4-6 days e.g. ND).

*Long (Over 6 days e.g., TB).


Clinicopathological
picture
§ Symptoms:
§ Diarrhea is the main clinical sign of enteric diseases. +
General clinical signs of ruffling of feathers, loss of
appetite, huddling together, constant peeping young
birds, and depression.
§ +Specific signs of each disease.
§ Post mortem lesions:
§ Enteritis and /or typhlitis (catarrhal to hemorrhagic
or even necrotic) + Specific lesions of each disease.
Specific
clinicopathological
picture of certain Enteric
diseases
1)Newcastle disease
§ Septicaemic contagious- respiratory and/or nervous, facial edema,
greenish diarrhea, Lowering egg production (quantity and
quality).
§ Variation of clinicopathology depends upon
§ 1- Virus agent (Virulence, degree of exposure).
§ 2-Host (Age, general health condition, immune status).
§ Different forms:
§ I- Acute lethal VVND (Doyle’s form).
§ II- Acute often lethal respiratory + nervous NVND
§ (Beach’s form).
§ III- Less pathogenic NVND-mesogenic (Beaudett’s
§ form).
§ IV- Mild respiratory-lentogenic (Hitchener’s form).
§ V- Non obvious disease (Asymptomatic-enteric form)
2) Avian influenza
Variety of disease syndromes ranging
from subclinical to acute generalized fatal
disease (Fowl plague).

Fowl plague
Rapidly fulminating - increasing
mortality - periorbital edema - edema
of the head - swollen sinuses - cyanotic
hemorrhagic wattles, comb and legs.

Post mortem lesions consist of a variety


of congestive-hemorrhagic-transductive-
necrotic changes.
3)Avian Diphtheria
(Avian pox)
§ Contagious disease - Skin eruptions of
unfeathered parts and / or diphtheritic
lesions on mucus membranes of upper
respiratory and digestive tracts
(pseudomembrane).
4) Enteric viruses

Reoviruses, Parvoviruses,
Adenoviruses, Caliciviruses, Rotavirus,
Togavirus Coronaviruslike particles,
Togaviruslike agent, Coronaviruslike
particles.
particles
Infect villous epithelial
cells in the mid-small intestine

Decreased Wt. gains

Dysfunction of the intestine impaired digestion and


absorption of lipids and fat-soluble vitamins A, D and E
and carotenoids. – Stunts (Uneven growth)

Runts
(Very small birds about 120-150 g)
*Poor FCR (Malabsorption or
maldigestion syndrome).
*Increased mortality.
*Irrigular feathers(helicopter appearance)
or (umbrella bird).
*Encrustation at the commissars of the
mouth, and Granulation in the eye lids.
*Catarrhal enteritis (white color, dilated
and may contain undigested feed with
degeneration of intestinal villi) orange-
yellow discolouration.
*Skeletal abnormalities (brittle bones).
5) Avian Colibacillosis

§ Infectious disease of birds in which E.coli is the primary or


secondary pathogen.
§ Disease complex rather than a disease itself.

§ Blood spread infection (coli-septicemia) - Air-sac


infection - Localized in any tissue of the body
producing inflammation.
Avian Colibacillosis
Avian Colibacillosis
§ Classified serologically:
l Somatic “O” antigens (167).
l Capsular or envelope ‘K’ antigen (74).
l Flagellar or “H” antigens (53).
l Fimbriae or Pili ‘F ’ antigens (17).

§ E.coli is common inhabitant of the intestinal tract of


man and animals.
§ Transmission: Vertical, horizontal, Sequestered E.coli in
intestine, nasal passages, air sacs or reproductive tract
may be a latent source of infection.
6) Salmonellosis

§ *Bacillary white diarrhea (S.gallinarum pullorum)

§ * Paratyphoid (2300 other serotypes). Infect a very wide variety of


hosts (including humans).
§ Paratyphoid is common in all types of birds. They are
mainly chronic and subclinic infections, yet occasionally
produce high morbidity and mortality during the first few
weeks of life.
Salmonellosis
§ Transmission: Vertical, horizontal, carryover.
§ Recently; all Salmonellae are considered to be one species called S.
enterica which is divided into 6 groups:
§ *Salmonella subgroup 1 : Subspecies enterica - Majority of
pathogenic Salmonellae. So, e.g. Salmonella typhimurium is called
now Salmonella enterica subspecies enterica serovar typhimurium
and for simplification is called S.serovar typhimurium.
§ *Salmonella subgroup 2 : Subspecies salamae.
§ *Salmonella subgroup 3 : Subspecies arizonae.
§ *Salmonella subgroup 4 : Subspecies diarizonae.
§ *Salmonella subgroup 5 : Subspecies houtenae.
§ *Salmonella subgroup 6 : Subspecies indica.
7) Avian Pasteurellosis
§ Pasteurella multocida
§ gram-negative,nonmotile,non-spore-forming rods, 5
serotypes (A,B,D,E and F).
Avian Pasteurellosis
§ Transmission:
§ Cojunctiva, cutaneous wounds, upper air passages,
m.m. of pharynx, carriers(chronically infected birds),
carryover.
§ Dissemination within a flock is primarily by
excreations from mouth,nose and conjunctiva
contaminat3 feed and water.
§ Mature chickens are more susceptible than
young ones.
Avian Pasteurellosis

§ Clinical forms:
§ Peracute, acute, subacute or chronic (localized
infections) forms.
§ Watery diarrhea (or whitish)
whitish later becomes
greenish and contains mucus.
§ Hyperemia of duodenum multiple small focal areas
of coagulative necrosis in liver + septicaemic picture
8)Chlamydiosis
§ Chlamydia psittaci
§ Latent infection

§ Stress conditions

§ Acute disease
§ (Respiratory signs, diarrhea, trembling, locomotor
disturbances, leg paralysis, spleenomegaly and
hepatomegaly, serofibrinous exudates in abdominal
cavity, peritonitis, airsacculitis, pericarditis, and
perihepatitis).
9)Spirochetosis
Spirochetosis
B. anserina (Spirochaeta gallinarum).
Transmission:
Cyanoses,
Cyanoses greenish
Cannibalism, diarrhea
ingestion containing
of blood, excess bile
or droppings, via
and urates, inactive
contaminated andwater.
feed and anorexic.
Use of syringes and
needels
Paresis,, blood sucking
Paralysis insects.
+ anemia.
Cyanoses , greenish diarrhea
Spleenomegaly containing
with mottling excess bile and
+ Hepatomegally
urates, inactive and anorexic.
with hemorrhage and marginal liver infarcts.
Paresis, Paralysis + anemia.
Spleenomegaly with mottling + Hepatomegally with
hemorrhage and marginal liver infarcts.
Spirochetosis
Avian intestinal Spirochetosis
Spirochaeta gallinarum and others
Etiology:
Spirochaeta gallinarum and others
Transmission:
Fecal-oral-route.
Diarrhea, pasty vent, retarded growth rates.
Infected chickens have slimy to frothy, yellowish to
brown, fluid-filled ceci
Avian
Avian intestinal
intestinal Spirochetosis
Spirochetosis
Etiology:
Spirochaeta gallinarum and others

Diarrhea, pasty vent, retarded growth rates.


Infected chickens have slimy to frothy, yellowish to
brown, fluid-filled ceci
10)Streptococcosis
§ Streptococcus zooepidemicus
§ Streptococcus faecalis

§ Gram positive spherical bacteria.(short chains)


§ Transmission:
§ Oral, aerosol routes, skin injuries, egg transmission or
fecal contamination of hatching eggs.
Streptococcosis
§ Acute form:
§ Septicaemia - diarrhoea - decrease in egg production.
§ Spleenomegaly - hepatomegaly with white foci -
sanguineous pericardial or subcutaneous fluid - peritonitis -
omphalitis.
§ Chronic form:
§ Loss of weight and lamness - head tremors - Blood stained
tissue around head - Yellow droppings - pale combs and
wattles. Fibrinous arthritis - osteomyelitis - salpingitis,
fibrinous pericarditis - perihepatitis - necrotic myocarditis -
vulvular endocarditis.
Streptococcosis
11)Tuberculosis

Mycobacterium avium
§ Lesions along the intestinal tract; if ulcerate results in

§ severe diarrhea

§ Extreme weakness (sitting position)


Campylobacteriosis
12) Campylobacteriosis
§§ *Depression
*Depression and
and diarrhea.
diarrhea.
§§ *Mortality
*Mortality up
up to
to 32
32 %% ..
§§ *Distention
*Distention of
of the
the intestinal
intestinal tract
tract extending
extending
§§ from
from the
the distal
distal duodenal
duodenal loop
loop to
to the
the
§§ bifurcation
bifurcation of
of the
the ceca
ceca..
§§ *Accumulation
*Accumulation of of mucus
mucus and
and watery
watery fluid
fluid
§§ occurs
occurs with
with presence
presence ofof red
red or
or yellow
yellow
§§ mottling
mottling of
of the
the liver
liver
Clostridial
13)Clostridial infections
infections
§ C. perfringens
colinum (Ulcerative
(Necrotic Enteritis)
Enteritis)
§ C. perfringens
colinum (Ulcerative
(Necrotic Enteritis)
Enteritis)
§ Toxins
§ Toxins
§§ Pathological
Pathological lesions
lesions
§§ (In
(In some
some cases,
cases, the
the organisms
organisms are
are relatively
relatively innocuous
innocuous
unless there
unless there are
are cofactors
cofactors such
such as
as coccidiosis
coccidiosis or
or
immunosuppressive
immunosuppressive infections
infections).
).
ANecrotic
-Necroticenteritis
enteritis(NE)
(NE)
§ Predisposing factors:
§ *High level of fish meal or wheat.
§ *Damage of intestine.
§§ .Lesions:
§ Friable intestine, distended with gas and Necrosis of the intestinal
mucosa
§
§ Fibrino-necrotic Enteritis
§ (Diphtheretic membrane)
§ i.e. adherent yellow or green pseudomembrane on mucosa.
Necrotic enteritis (NE)
§ Friable intestine, distended with gas and Necrosis of the intestinal
mucosa
§

§ Fibrino-necrotic Enteritis
§ (Diphtheretic membrane)
§ i.e. adherent yellow or green
§ pseudomembrane on mucosa.
Ulcerative
B- Ulcerativeenteritis
enteritis(UE)
(UE)
§ Predisposing factors:
§ Coccidiosis, Aplastic Anemia, IBD, or Stress
Conditions.
§ Lesions:
§ *Intestine: Hemorrhage,
§ Necrosis and Ulceration
§ (Small yellow foci with
§ Hemorrhagic borders)
Ulcerative enteritis (UE)
§ Lesions:
§ *Ceca: (central depression filled with dark staining
§ material) coalescing (large necrotic
§ diphtheretic patches).
Ulcerative enteritis (UE)
§ Lesions:
§ *Liver: Yellow mottling to large irregular yellow areas along
§ the edges.

§ *Spleen: Congested, Enlarged, and Hemorrhagic.


14) Helminthiasis
(Ascariasis, Heterakiasis, Cestodiasis, Capillariasis)
§ *Diarrhea, loss of weight, general clinical signs.

§ *lesions of enteritis, typhlitis (mucoid or hemorhagic).

§ *Presence of the worms

§ *Intestinal obstruction with the worms

§ *Intestinal nodules e.g. Ralliatena echinobothridia


§ infestation.
Protozoal Diseases
A- Coccidiosis
*Signs vary with various species; (less pathogenic
species produce few or no signs, while more
pathogenic species often cause diarrhea which
may be
§ . mucoid or bloody).

*Drop in egg production and depigmentation of the


skin may occur in layers.
*Mortality may reach up to 30 %.
*Specific coccidial lesions in intestinal tract (host
and tissue specific.
Protozoal Diseases
B- Histomoniasis
(Enterohepatitis- Blackhead disease).

§ *Enlarged ulcerated ceci containing large


§ cores of necrotic material.
§ *Sulfur colored diarrhea
§ *Liver lesions (cream colored circular necrotic
§ area surrounding haemorrhagic depressed
§ central areas).
Protozoa Diseases
C- Trichomoniasis:

§ *Affects upper and lower digestive tract.


§ *The lower tract form show yellowish
§ diarrhea and death within 2-3 days with
§ lesions of caseous cecal cores and necrosis
§ with raised granular yellowish-creamy
§ liver lesions.
Avitaminosis A (Nutritional Roup)

§ Poor growth - Inflamed eyes - Nasal


catarrh - Swelling of sinuses -
Keratoconjunctivitis -Excessive
lacrimation -Drop in egg production.
Mycotoxicosis
Ochratoxins:
§ *Poor growth, reduced feed efficiency,
§ increased water consumption, and
§ increased manure moisture due to
§ diarrhea.
§ *Nephritis, nephrosis Gout
§ *Reduced breaking strength bones
§ *Increased intestinal fragility
Mycotoxicosis
Trichothecenes (TCT)
• Necrosis and hemorrhage throughout the digestive
tract
• Circumscribed proliferative yellow caseous plaques
occurring at the margin of the beak, mucosa of the
hard palate, angle of the mouth, and tongue.
• Growth retardation, neural disturbances, abnormal
feathering.
• Decreased egg production and eggshell quality
(thinner eggshells).
• Hemorrhages of the large intestine.
Diagnosis
§ * Clinicopathological picture (Tentative).
§ *Laboratory methods of diagnosis (Definite diagnosis):
l Early stages (Isolation and identification of pathogenic

agent-Direct methods). Diagnosis of parasitic diseases


could be confirmed by demonstration of the parasite or
their eggs either macroscopically or microscopically
from intestinal contents
l Convalescent stages (Detection of rising Ab titers in

sera).
l N.B.: Lab. Diag. is necessary to rule out the possibilities

of a mixed infection.
Prevention
and Control
1-Veterinary biosecurity + hatchery hygiene.

2- Destruction of large numbers of


invaders using:
*Disinfectants
*Feed decontamination
*Physical destruction of microorganisms ( irradiation,
pelleting, pasteurization).
*Chemical mechanisms (Dietary acid additives).
.

3-Strengthen resistance of the host.


Strengthen resistance of the host
A- Breeding for resistance.
B- Improved nutrition.
C-Vaccination (Viral, Bacterial or parasitic
vaccines).
D- Chemotherapy (Prophylactic and
Therapeutic).
E-Competitive exclusion (CE) and Probiotics.
§ Competitive exclusion (CE) and
Probiotics
§ GIT harbors microflora (important barrier against
pathogenic M.O. Colonization).

§ Depleted at hatching and following any medication


with an anti- microbial product

§ Competitive exclusion (CE) describes the protective


effect of natural flora of GIT for limiting
colonization pathogenic bacteria.
bacteria First CE products
were simply fecal contents.
Probiotics
*Pure cultures of one or more living M.O.
*Proliferate in the host-bird’s GIT.

Adequate gut microflora

Counter pathogenic bacteria in GIT by:


Increase feed intake and digestion:
Intestinal bacterial flora takes part in the metabolism of nutrients
and synthesis of vitamins.

Neutralizes Maintaining
beneficial
enterotoxins Stimulation of
microbial
produced by IgA production
population in GIT
pathogenic (Antagonistic activity and
bacteria . competition for attachment sites)

Altering metabolism by:


* Increase digestive enzyme activity(amylase, protease and lipase).
* Decrease bacterial enzyme activity ( Reduction in
b-glucuronidase ).
* Reduce ammonia in the excreta and litter of broilers.
Thank you

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