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 ยง I-Immunosuppressives A-Feed: 1-Mycotoxins. 2-Antibiotics. 3-Pesticides. 5-Deficiency (vitamins, Protein & minerals).
4-Chemicals.
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) ยง 1-Viral agents (NDV, AIV, Avian diphtheria and Enteric viruses). ยง 2-Bacterial agents (Colibacillosis,Salmonellosis, Pasteurellosis,Spirochaetosis,TB,Clostridial infections, Camylobacteriosis and Chlamydiosis. ยง 3-Parasitic agents (Intestinal parasites). ยง 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 ( continue) Epizootiology ( 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 ยง Symptoms:
ยง 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. ยง +Specific signs of each disease. ยง Post mortem lesions:
ยง 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-transductivenecrotic changes.
3)Avian Diphtheria (Avian pox) ยง 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.
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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) orangeyellow discolouration. *Skeletal abnormalities (brittle bones).
5) Avian Colibacillosis
ยง Infectious disease of birds in which E.coli is the primary or secondary pathogen.
ยง Disease complex rather than a disease itself. ยง Blood spread infection (coli-septicemia) - Air-sac infection - Localized in any tissue of the body producing inflammation.
Avian Colibacillosis Avian Colibacillosis § Classified serologically: l l l l
Somatic “O” antigens (167). Capsular or envelope ‘K’ antigen (74). Flagellar or “H” antigens (53). 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 ยง *Bacillary white diarrhea (S.gallinarum pullorum) ยง * Paratyphoid (2300 other serotypes). Infect a very wide variety of hosts (including humans).
ยง 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 ยง Pasteurella multocida ยง gram-negative,nonmotile,non-spore-forming rods, 5 serotypes (A,B,D,E and F).
Avian Pasteurellosis ยง Transmission: ยง Cojunctiva, cutaneous wounds, upper air passages, m.m. of pharynx, carriers(chronically infected birds), carryover. ยง Dissemination within a flock is primarily by excreations from mouth,nose and conjunctiva contaminat3 feed and water.
ยง Mature chickens are more susceptible than young ones.
Avian Pasteurellosis ยง Clinical forms: ยง Peracute, acute, subacute or chronic (localized infections) forms. ยง Watery diarrhea (or whitish) later becomes whitish greenish and contains mucus. ยง Hyperemia of duodenum multiple small focal areas of coagulative necrosis in liver + septicaemic picture
8)Chlamydiosis ยง Chlamydia psittaci
ยง Latent infection ยง Stress conditions ยง Acute disease ยง (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, diarrhea containing excess bile Cyanoses greenish Cannibalism, ingestion of blood, or droppings, via and urates, inactive andwater. anorexic. contaminated feed and Use of syringes and needels sucking insects. Paresis,, blood Paralysis + anemia. Cyanoses , greenish diarrhea containing excess bile and Spleenomegaly with mottling + 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
ยง Streptococcus zooepidemicus ยง Streptococcus faecalis
ยง Gram positive spherical bacteria.(short chains)
ยง Transmission: ยง Oral, aerosol routes, skin injuries, egg transmission or fecal contamination of hatching eggs.
Streptococcosis
ยง Acute form: ยง Septicaemia - diarrhoea - decrease in egg production. ยง Spleenomegaly - hepatomegaly with white foci sanguineous pericardial or subcutaneous fluid - peritonitis omphalitis. ยง Chronic form: ยง 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 ยง Lesions along the intestinal tract; if ulcerate results in ยง severe diarrhea ยง 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 of of red red or or yellow yellow mottling mottling of of the the liver liver
Clostridial infections 13)Clostridial infections § C. perfringens colinum (Ulcerative (Necrotic Enteritis) Enteritis) § C. perfringens colinum (Ulcerative (Necrotic Enteritis) Enteritis) § Toxins § Toxins Pathological lesions lesions §§ Pathological (In some some cases, cases, the the organisms organisms are are relatively §§ (In relatively innocuous innocuous unless there there are are cofactors cofactors such such as as coccidiosis unless 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 BUlcerativeenteritis 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) ยง Lesions: ยง *Ceca: ยง ยง
(central depression filled with dark staining material) coalescing (large necrotic diphtheretic patches).
Ulcerative enteritis (UE) ยง Lesions: ยง *Liver: ยง
Yellow mottling to large irregular yellow areas along the edges.
ยง *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). ยง . *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) ยง 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 ยง * Clinicopathological picture (Tentative). ยง *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).
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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.
ยง Competitive exclusion (CE) and Probiotics ยง GIT harbors microflora (important barrier against pathogenic M.O. Colonization). ยง Depleted at hatching and following any medication with an anti- microbial product ยง 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 enterotoxins produced by pathogenic bacteria .
Maintaining beneficial microbial population in GIT
Stimulation of IgA production
(Antagonistic activity and 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.
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