KASUS NECROTIC ENTERITIS BERTAMBAH

NECROTIC enteritis yang menyerang hebat dapat dikurangi dengan menambah
temperature kandang dan mengurangi tingkat cahaya ketika ayam mulai terserang
penyakit ini.

Terjangkitnya Necrotic enteritis (NE) pada broiler telah meningkat mungkin disebabkan
bertambahnya pemberian antibiotik, kata Dr. Steven Davis, Presiden Colorado Quality
Research. Davis telah melakukan penelitian, memproduksi NE dalam satu fl ok sehingga
cara pengobatan dan pencegahan dapat ditest. Ia mengatakan bahwa konsumsi pakan
dan keadaan litter mempunyai pengaruh yang kuat pada resiko terjangkitnya NE. Konsumsi pakan yang tinggi menambah resiko terjangkitnya penyakit tetapi pemakaian cahaya yang
dibatasi sehingga mengurangi konsumsi pakan akan menurunkan resiko. Pada temperatur
dingin menambah konsumsi pakan dan menambah resiko terkena NE. Davis melaporkan
bahwa menambah temperatur kandang dan mengurangi pemakaian cahaya, keduanya
menyebabkan penurunan konsumsi pakan dapat memperbaiki kesehatan ayam untuk tidak
terjangkit NE.

NE disebabkan oleh bakteri Clostridium perfringens tetapi tidak semua ayam yang
terkena NE akan menderita NE karena tidak semua Clostridium perfringens mempunyai
kemampuan memproduksi penyakit. Type dan jumlah coccidia dan adanya Clostridium
perfringens dalam kandang adalah faktor kunci yang menyebabkan NE yang hebat.
Adalah sukar untuk menimbulkan NE atau bahkan performans yang mempengaruhi kuat
bakteri enteritis tanpa coccidiosis yang merusak usus dan memberi kesempatan bakteri
untuk menginfeksi usus. Kehebatan infeksi coccidiosis berhubungan langsung dengan
kemampuan untuk menimbulkan enteritis dan kematian fl ok, jadi kontrol terhadap bakteri dan coccidiosis dan mengurangi jumlah organisme dalam kandang dapat mengurangi resiko terjangkitnya NE.

Kondisi litter dan kemungkinan type litter dapat menambah atau mengurangi penyakit
NE. Litter yang basah dapat menambah pengaruh kedinginan pada ayam dan tantangan
adanya coccidia dan keduanya dapat menyebabkan NE. Sebaiknya litter diberi acidifi er
dalam membantu mengontrol timbulnya NE. Mengurangi bakteri dalam lingkungan broiler
terutama kandang yang pernah terjangkit NE, dapat dilakukan dengan mendesinfektan
kandang-kandang tersebut. Perhatian yang lebih terhadap efektifnya desinfektan dan
pemberian obat-obatan pada litter akan sangat membantu mengontrol NE di masa yang
akan datang. (Sumber : Large-Volume Grower, November 2006)

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Mycoplasma gallisepticum infection, M.g., Chronic Respiratory Disease - Chickens

Introduction
Infection with Mycoplasma gallisepticum is associated with slow onset, chronic respiratory disease in chickens, turkeys, game birds, pigeons and other wild birds. Ducks and geese can become infected when held with infected chickens. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). The condition occurs worldwide, though in some countries this infection is now rare in commercial poultry. In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds.

In adult birds, though infection rates are high, morbidity may be minimal and mortality varies.

The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Transmission may be transovarian, or by direct contact with birds, exudates, aerosols, airborne dust and feathers, and to a lesser extent fomites. Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. Fomites appear to a significant factor in transmission between farms. Recovered birds remain infected for life; subsequent stress may cause recurrence of disease.

The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid, and in lyophilised material. Survival seems to be improved on hair and feathers. Intercurrent infection with respiratory viruses (IB, ND, ART), virulent E. coli, Pasteurella spp. Haemophilus, and inadequate environmental conditions are predisposing factors for clinical disease.
Signs
• Coughing.
• Nasal and ocular discharge.
• Poor productivity.
• Slow growth.
• Leg problems.
• Stunting.
• Inappetance.
• Reduced hatchability and chick viability.
• Occasional encephalopathy and abnormal feathers.
Post-mortem lesions
• Airsacculitis.
• Pericarditis.
• Perihepatitis (especially with secondary E. coli infection).
• Catarrhal inflammation of nasal passages, sinuses, trachea and bronchi.
• Occasionally arthritis, tenosynovitis and salpingitis in chickens.
Diagnosis
Lesions, serology, isolation and identification of organism, demonstration of specific DNA (commercial PCR kit available). Culture requires inoculation in mycoplasma-free embryos or, more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Suspect colonies may be identified by immuno-flourescence.

Serology: serum agglutination is the standard screening test, suspect reactions are examined further by heat inactivation and/or dilution. Elisa is accepted as the primary screening test in some countries. HI may be used, generally as a confirmatory test. Suspect flocks should be re-sampled after 2-3 weeks. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks. PCR is possible if it is urgent to determine the flock status.

Differentiate from Infectious Coryza, Aspergillosis, viral respiratory diseases, vitamin A deficiency, other Mycoplasma infections such as M. synoviae and M. meleagridis (turkeys).
Treatment
Tilmicosin, tylosin, spiramycin, tetracyclines, fluoroquinolones. Effort should be made to reduce dust and secondary infections.
Prevention
Eradication of this infection has been the central objective of official poultry health programmes in most countries, therefore M.g. infection status is important for trade in birds, hatchingeggs and chicks. These programmes are based on purchase of uninfected chicks, all-in/all-out production, biosecurity, and routine serological monitoring. In some circumstances preventative medication of known infected flocks may be of benefit.

Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. Productivity in challenged and vaccinated birds is not as good as in M.g.-free stock.

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Necrotic Enteritis

Introduction
An acute or chronic enterotoxemia seen in chickens, turkeys and ducks worldwide, caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis, usually of the mid- small intestine. Mortality may be 5-50%, usually around 10%. Infection occurs by faecal-oral transmission. Spores of the causative organism are highly resistant. Predisposing factors include coccidiosis/coccidiasis, diet (high protein), in ducks possibly heavy strains, high viscosity diets (often associated with high rye and wheat inclusions in the diet), contaminated feed and/or water, other debilitating diseases.
Signs
• Depression.
• Ruffled feathers.
• Inappetance.
• Closed eyes.
• Immobility.
• Dark coloured diarrhoea.
• Sudden death in good condition (ducks).
Post-mortem lesions
• Small intestine (usually middle to distal) thickened and distended.
• Intestinal mucosa with diptheritic membrane.
• Intestinal contents may be dark brown with necrotic material.
• Reflux of bile-stained liquid in the crop if upper small intestine affected.
• Affected birds tend to be dehydrated and to undergo rapid putrefaction.
Diagnosis
A presumptive diagnosis may be made based on flock history and gross lesions Confirmation is on the observation of abundant rods in smears from affected tissues and a good response to specific medication, usually in less than 48 hours.
Treatment
Penicillins (e.g. phenoxymethyl penicillin, amoxycillin), in drinking water, or Bacitracin in feed (e.g. 100 ppm). Treatment of ducks is not very successful, neomycin and erythromycin are used in the USA. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity.
Prevention
Penicillin in feed is preventive, high levels of most growth promotors and normal levels of ionophore anticoccidials also help. Probiotics may limit multiplication of bacteria and toxin production. In many countries local regulations or market conditions prevent the routine use of many of these options.

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Colibacillosis, Colisepticemia

Introduction
Coli-septicaemia is the commonest infectious disease of farmed poultry. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys, or in young birds that are immunologically immature. It is caused by the bacterium Escherichia coli and is seen worldwide in chickens, turkeys, etc.

Morbidity varies, mortality is 5-20%. The infectious agent is moderately resistant in the environment, but is susceptible to disinfectants and to temperatures of 80°C.

Infection is by the oral or inhalation routes, and via shell membranes/yolk/navel, water, fomites, with an incubation period of 3-5 days.

Poor navel healing, mucosal damage due to viral infections and immunosuppression are predisposing factors.
Signs
• Respiratory signs, coughing, sneezing.
• Snick.
• Dejection.
• Reduced appetite.
• Poor growth.
• Omphalitis.
Post-mortem lesions
• Airsacculitis.
• Pericarditis.
• Perihepatitis.
• Swollen liver and spleen.
• Peritonitis.
• Salpingitis.
• Omphalitis.
• Synovitis.
• Arthritis.
• Enteritis.
• Granulomata in liver and spleen.
• Cellulitis over the abdomen or in the leg.
• Lesions vary from acute to chronic in the various forms of the disease.
Diagnosis
Isolation, sero-typing, pathology. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours - most strains are rapidly lactose-fermenting producing brick-red colonies on McConkey agar.

Differentiate from acute and chronic infections with Salmonella spp, other enterobacteria such as Proteus, as well as Pseudomonas, Staphylococcus spp. etc.
Treatment
Amoxycillin, tetracyclines, neomycin (intestinal activity only), gentamycin or ceftiofur (where hatchery borne), potentiated sulphonamide, flouroquinolones.
Prevention
Good hygiene in handling of hatching eggs, hatchery hygiene, good sanitation of house, feed and water. Well-nourished embryo and optimal incubation to maximise day-old viability.

Control of predisposing factors and infections (usually by vaccination). Immunity is not well documented though both autogenous and commercial vaccines have been used.

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Ascites

Introduction
Associated with inadequate supplies of oxygen, poor ventilation and physiology (oxygen demand, may be related to type of stock and strain). Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. The disease has a complex aetiology and is predisposed by reduced ventilation, high altitude, and respiratory disease. Morbidity is usually 1-5%, mortality 1-2% but can be 30% at high altitude. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition.
Signs
• Sudden deaths in rapidly developing birds.
• Poor development.
• Progressive weakness and abdominal distension.
• Recumbency.
• Dyspnoea.
• Possibly cyanosis.
Post-mortem lesions
• Thickening of right-side myocardium.
• Dilation of the ventricle.
• Thickening of atrioventricular valve.
• General venous congestion.
• Severe muscle congestion.
• Lungs and intestines congested.
• Liver enlargement.
• Spleen small.
• Ascites.
• Pericardial effusion.
• Microscopic - cartilage nodules increased in lung.
Diagnosis
Gross pathology is characteristic. A cardiac specific protein (Troponin T) may be measured in the blood. This may offer the ability to identify genetic predisposition. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis.
Treatment
Improve ventilation, Vitamin C (500 ppm) has been reported to be of benefit in South America.
Prevention
Good ventilation (including in incubation and chick transport), avoid any genetic tendency, control respiratory disease.

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