Necrotic enteritis

Causes: Necrotic enteritis is caused by Clostridium perfringens types A or C. The organism is transmitted by soil, dust, litter and faeces. Can be induced by choice of raw materials in feed and/or coccidiosis. Clostridium perfringens can become especially prevalent in the small intestine when no antibacterial growth promoters are used.

Effects: Ataxia, intoxication, diarrhoea, depression, ruffled feathers, reluctance to move. It may also cause dysbacteriosis, leading to vitamin or mineral deficiency.

Detailed causes:

All types of chickens from two weeks onwards are susceptible to this acute to chronic disease. The agent involved in the aetiology of the disease is Clostridium perfringens which produces types A and C alpha toxin and type C beta toxin. It is also called creepers because chickens are sometimes ataxic (can’t move).

Mode of transmission

Soil, dust, litter and faeces spread the organism.

Special note

It may cause malabsorption syndrome leading to vitamin or mineral deficiency.

Clinical signs:

Ataxia, intoxication, diarrhoea, depression, ruffled feathers and reluctance to move may be seen.

In acute cases death can occur within hours of the disease onset.

Postmortem lesions

Dehydration (darkened skin), emaciation (no breast muscle), congested liver, cooked (ruffled up) intestinal mucosa – primarily of the jejunum and ileum can be seen. Intestines are often distended and filled with gas. There is water in the crop.

In acute cases enteritis occurs with just a grey layer of necrotic material on the mucosa.

Diagnosis:

Diagnosis is based on the gross lesions (ruffled intestinal mucosa), clinical signs and bacterial isolation on blood agar plate. Colonies are surrounded by an inner zone of complete haemolysis and an outer zone of discolouration and incomplete haemolysis.

It simulates coccidiosis and ulcerative enteritis.

Treatment and control:

Prevention

Bacitracin 50 g/ton given continuously in the feed, improved sanitation, lincomycin in feed or water. Rearing birds on wire will prevent the disease.

Treatment

Bacitracin (200 g/T) in the feed and vitamins and minerals in the water to reduce the disease.

Lincomycin, ozytetracycline, amoxicillin and tylosin can also be used to treat the disease.

Note

Bacitracin is now banned in most countries.

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Haemorrhagic enteritis (HE)

Causes: HE virus is a double stranded DNA Adenovirus.

Effects: Incubation period is less than 24 hours. Depression, bloody droppings, dark red to brownish blood on the skin and feathers around the vent can be seen. Mortality is 10-80%.

Detailed causes:

Turkeys of 4 weeks or older may develop this acute viral disease. HE virus is an unenveloped, icosahedral, double-stranded DNA virus. It replicates in the nucleus forming basophilic inclusion bodies (viral factories seen under light microscope).

Mode of transmission

Spreads orally from infectious faeces or litter.

Clinical signs:

(Incubation period is less than 24 hours).

Depression, bloody droppings, mortality (10-80%), dark red to brownish blood on skin, feathers and around vents can be seen.

Postmortem lesions

The skin and flesh are pale, anaemic and dark in colour.

The jejunal mucosa is read and highly congested, spleens are enlarged, friable and mottled, lungs are congested and vascular organs are pale, and the livers are enlarged with haemorrhage.

Diagnosis:

Clinical signs, and gross and microscopic pathology are useful.

Intranuclear inclusion bodies in the reticuloendotheial (RE) system and intestine are diagnostic.

Spleens show RE hyperplasia and inclusion bodies. ELISA or AGP tests can be used to detect antibody.

Treatment and control:

Prevention

Use of a live vaccine in drinking water at 4 and 6 weeks of age can prevent the diseases.

Treatment

None.

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Cannibalism

Occurrence: Worldwide.

Species affected: All.

Age affected: All.

Causes: Predisposing factors include insufficient feed or feeder space, high density rearing, excessive light, too much heat, nutritional deficiencies or irritation from external parasites.

Effects: Injuries to the vent, head or feet, missing feathers. Injuries can be severe.

Detailed causes:

Predisposing factors include insufficient feed or feeder space, high density rearing, excessive light, too much heat, nutritional deficiencies or irritation from external parasites.

Clinical signs:

The following are common forms of cannibalism seem in commercial poultry operations:

Vent-picking

Picking of the vent or region of the abdomen several inches below the vent is the most severe form of cannibalism. This is generally more common in high-production or overweight pullet flocks. Predisposing factors are prolapse or tearing of the tissues by passage of an abnormally large egg. Vent picking can result in anaemia.

Feather-pulling

Frequently seen in flocks kept in close confinement resulting in lack of sufficient exercise. Nutritional deficiencies may contribute to the problem.

Toe-picking

Most commonly seen in young birds. Inadequate feeder space or inability of the chick to find the feed will lead to toe-picking.

Head picking

Follows injuries to the comb or wattles.

Diagnosis:

Injuries seen around the head, vent and feet, or observation of cannibalistic activity are indicative.

Treatment and control:

Prevention

Provide adequate feed and feeding space, reduce bird density, reduce light, beak trimming, toe and comb trimming in breeders and wattle trimming in cage birds. Coloured light can help to reduce the problem. Give "toys" for the birds to play with like straw, branches etc.

(beak trimming, toe and comb trimming and wattle trimming will soon be forbidden in Western Europe).

Chick feeder lids or paper should be filled with feed and be in place prior to the reception of the chicks.

Automatic feeders (pan-shaped or troughs) should be available no later than 7 days of age. Feed lids and automatic feeders should overlap by 3 days to ensure smooth transition between the two feeding systems.

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Colibacillosis

Occurrence: Worldwide.

Species affected: All.

Age affected: All.

Causes: Gram negative bacteria- Escherichia coli. It is the most common bacterial pathogen of poultry, and the second most common of all poultry pathogens.

Effects: Low performance in older birds, or high mortality in younger birds. High embryonic mortality, respiratory distress and enteritis can be evident.

Detailed causes:

This disease has a number of names because it causes granulomas in adults and yolk sac infection in chicks.

Coli Granuloma is chronic in mature birds of all species, and may be acute in chicks occurring as omphalitis.

Escherichia coli are gram-negative, non-acid-fast, non-spore-forming bacilli, and many strains have flagella.

Mode of transmission

E. coli may be a primary or secondary invader. It is the most common bacterial pathogen in poultry and second most common of all pathogens of poultry.

Faecal contamination of eggs, transovarian contamination, contaminated water and feed with bacteria can occur commonly.

Aerosol spread may occur.

Special note

E. coli is a normal contaminant in the intestines and may complicate mycoplasma, IBV, LT, and/or NDV in the air sacs, heart, liver and lungs causing air sacculities and/or chronic respiratory disease (CRD). Several serotypes make vaccination difficultur. E. coli is a very important cause of economic losses in poultry due to mortality, drops in weight gain, hatchability and an import cause of Septicemia-toxemia (sept-tox), air sacculities, and IP condemnations in processing plant. Sept-tox is the leading infectious cause of condemnation in the broiler processing plant in the US, air sacculities is the second, and IP the third.

Clinical signs:

Low performance in older birds or high mortality in younger birds, high embryonic mortality, respiratory distress and enteritis (diarrhoea) can be evident.

Postmortem lesions

Cauliflower-like nodules on viscera (granuloma), omphalitis in chicks, discoloured and misshapen yolk (mushy chick) are seen. These lesions are characteristic. Air sacculitis, salpingitis (inflammation of the oviduct), enteritis, synovitis, arthritis, pericarditis, peritonitis, panophthalmitis, or swollen head syndrome are common. Cellulitis, an inflammation of the cellular or connective tissue, can be caused by E. coli. The soft tissue is heavily necrotic and may be gangrenous. It can result in extensive processing plant condemnation. It is sometimes called infectious process or IP.

Diagnosis:

Laboratory isolation of E. coli for lesions, yolk, blood on MacConkey’s or methylene blue agar (EMB). Colonies are pink on MacConkey’s and dark with metallic sheen. It simulates Salmonella, Staphylococcus, Tuberculosis, Fowl cholera, Marek’s disease and Aspergillosis.

Treatment and control:

Prevention

• Use mycoplasma-free stock to prevent interaction with E. coli.
• Pellet feed to kill bacteria.
• Bacterin for breeders or turkeys (serotype 02, 078) egg and hatchery sanitation to reduce organisms.
• Chlorinate water (3 to 5 ppm) and use nipple drinkers to reduce transmission in water.
• An inactivated vaccine is available for breeders and layers.

Treatment

Chlortetracycline (CTC) (400 g/ton), Oxytetracycline (OTC), Quinolones (Flumequine), Sulfadimethoxine and Ormetroprim or Trimethoprim, can be used.

Gentamicin can be given by subcutaneous injection at 1 day-of-age.

Chlorox® in water at 2 to 4 oz/gal for 1-3 weeks or Quinolone in water for 3-5 days to treat clinical signs.

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Aspergillosis

Causes: Fungal infection caused by Aspergillus fumigatus, A. flavus and A. niger.

Effects: High mortality, respiratory distress, central nervous dysfunction, sleepiness, inappetance and emaciation. Conjunctivitis and cloudy eyes can be seen.

Detailed causes:

Aspergillosis is mainly seen in young birds as an acute disease. Chronic disease occurs in adults. The fungi Aspergillus fumigatus, A. flavus and A. niger are responsible. It spreads by the aerosol spread of spores, which are common in the hatchery, and less commonly by contaminated dust and litter in the house.

Clinical signs:

Signs include high mortality, respiratory distress (dyspnoea and gasping), central nervous dysfunction (tremors, ataxia, and torticollis) somnolence (sleepy), inappetance, and emaciation (very thin), conjunctivitis and cloudy eyes can be seen.

Postmortem lesions

Yellowish-green or whitish, caseous (cheesy) nodules and/or green, fur-like down in mouth, palate, lungs, trachea, syrinx, viscera, air sacs, brain and eyes may be seen.

Diagnosis:

Fungus can be identified microscopically (20% KOH stain) from culture or special stain of tissues (hyphae, mycelia, conidophores). Isolation of culture in 48 hours on Sabouraud dextrose agar is diagnostic. Stain colony with lactophenol cotton blue to see conidophores. It is similar to colibacillosis, MD, and lymphoid leukosis. Nodules in the lungs and fungal fur-like down in the air sacs are diagnostic.

Treatment and control:

Prevention

Hatchery sanitation includes regular fumigation of eggs, machines and air ducts and regular (monthly) plating of hatchery with media to examine for the presence of fungi. Use clean dry litter and dry cups of nipples to reduce water spills. Quality of the feed is important. An aerosol of thiabenidazole or Clinafarm® pellets can be placed in the hatchery to kill fungus. Formalin fumigation is an effective method to kill Aspergillus in the environment (not in the chicken). This is not allowed in most of the USA.

Treatment
Quaternary ammonium, chlorine, and/or copper sulphate can be added to the water to help reduce the spread of the organism and reduce clinical signs. However, taking preventative measures is more effective.

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