Zootecnica International - World Poultry Journal

Dr. Bernie Beckman
Hy-Line International
Dallas Center, IA, U.S.A.

By courtesy of Hy-Line

Peritonitis is not a new disease. As poultry production has intensified, however, its occurrence has also increased, as has the need for identification, prevention, control methods, and treatment. Dealing with peritonitis can be confusing and frustrating when it appears to be increasing at a farm or complex. On the other hand many producers have never seen peritonitis as a cause for elevated mortality. In the majority of field cases, peritonitis is the end result of the bird being challenged by a primary agent of infectious, physical, toxic or nutritional origin.

Definition of Peritonitis

The peritoneal cavity contains the internal organs of the bird. Peritonitis is an inflammation or infection within the peritoneal cavity that causes sudden increased mortality levels in a flock. The condition is marked by exudations in the peritoneum of serum, fibrin and inflammatory cells (pus). Fibrin is the white to yellow material that is a product of the inflammatory response of the chicken and can be found covering the oviduct, ovary, intestine, air sac, heart, lungs and liver.

Terminology

Peritonitis is a lesion and several other lesions are used to describe this condition:

• Omphalitis (navel/yolk sac)
• Fibrinous Polyscrositis:
• Pericarditis (heart)
• Perihepatitis (liver)
• Pneumonia/Pleuritis (lungs)
• Airsacculitis
• Salpingitis (oviduct)
• Pulmonary Edema and Congestion (lungs)

Terms or phrases used to mean the same as peritonitis:

• Egg yolk peritonitis
• CRD – Chronic Respiratory Disease
• Colibacillosis – a general term for any primary or secondary infection caused by E. coli
• Colisepticemia – a more specific term that refers to the widely disseminated presence of virulent strains of E. coli in the bloodstream. This is the most accurate definition of what we all refer to as peritonitis.
• E. coli – a bacteria Escherichia coli that is most commonly recovered from birds with peritonitis.

Causative agent

1. A bacterium known as E. coli. E. coli is not just one organism but instead there are hundreds, if not thousands, of different serotypes with 10-15% of the serotypes being considered pathogenic for birds. Other bacteria can also cause the lesion peritonitis, such as salmonella, Mannheimia haemolytica, Proteus sp., streptococcus sp., Klebsiella sp., and pasteurella.
2. From the 10-15% of pathogenic serotypes, some serotypes are considered primary pathogens while the remaining serotypes are considered opportunists that invade following other diseases or stresses. We spend a lot of time on peritonitis trying to determine what those stresses or diseases are and what impact they have on any given case of bacterial peritonitis.
3. E. coli is a common inhabitant of the intestine of birds and mammals at approximately 104-6 organisms per gram of feces and is disseminated widely in the feces. Birds are then continuously exposed to E. coli through the dust, which can be carrying as many as 106 CFU of bacteria per gram. This disease can affect laying chickens, broilers, or turkeys and other birds any time during the birds' life.
4. E. coli can be the cause of omphalitis or yolk sac infection in baby chicks but it is the condition of E. coli peritonitis in sexually mature birds that I will concentrate on.
5. As fecal E. coli contamination goes up, the likelihood of exposure to other infectious agents and reduction of environmental quality goes up as well.

Possible Causes:

1. Selective evolution of more pathogenic infective or virulent strains of E. coli
2. Microbial genetics resistant to common antibiotics used for treatment
3. Regulatory loss of antibiotics used for treatment
4. Environment of the birds – cage space, water availability, air quantity and quality, feed that is sub-optimal, etc.
5. Intensified poultry production (complex) vs. single standing houses
6. Attention to details is lost when profit margins are tight
7. Other diseases and stressors
8. Combination of all of the above. As these factors are mixed and matched, the causes of peritonitis becomes pure speculation because in a number of situations we have not been able to identify a primary pathogen other than E. coli.

Routes of transmission

Bacteria can gain entrance into the body to cause peritonitis by a variety of routes:

1. Gastrointestinal Tract – Coccidiosis, enteritis, mycotoxins, antibiotics, abrupt feed changes causing indigestion can disturb the normal flora of the intestine. These good bacteria normally cover the lining of the intestine keeping bad bacteria from invading the intestine. When this natural barrier is disturbed, the door is opened for invasion by pathogenic E. coli. A resulting enteritis can also then increase fecal E. coli contamination. Water contaminated with coliform bacteria E. coli is a risk factor for intestinal and respiratory infections. Contaminated feed ingredients or post manufacturing contamination of finished feed with rodent or wild bird droppings, or the practice of feeding byproducts of processing (i.e. eggshell). Although this is believed to be a sporadic event, it may be more common than we think.
2. Skin – The skin protects vulnerable tissues beneath from infection. Breaks in the skin from scratches (overcrowding), old cages, rough handling by crews, or ectoparasites opens the door for pathogenic bacteria.
3. Reproductive Tract – Ascending infections up the oviduct is a direct route to the body cavity of the hen. Pecking of the vent by other birds and prolapse, caused by excessive egg size, can cause infections, which result in peritonitis. Yolks (ova) laid outside the oviduct can be the result of oviduct infection, respiratory infections, or handling birds after egg production has begun (late transfer). This can cause egg yolk peritonitis to develop. Another factor is birds coming into production have high estrogen levels. High estrogen levels make birds more susceptible to infection. This may be an important factor of why we don't see peritonitis in pullets.
4. Immune System – Possible increased susceptibility of the flock from immunosuppression caused by early IBD, REO, CAV, Marek's or adenovirus type challenges.
5. Respiratory Tract – The most likely source of infection is inhalation of contaminated dust containing E. coli (fecal-oral route). Primary respiratory pathogens like Newcastle, bronchitis, ILT, MG, MS, ORT, dust, and ammonia can cause respiratory tract damage, which opens the door for an E. coli infection. Adverse vaccine reactions to NC, IB, ILT vaccinations can also be a primary cause for respiratory tract damage. The breakdown of mucosal lining of the trachea allows the bacteria to enter the blood stream and cause a septicemia. The dust in a poultry house is important, maybe the most important factor, because under dry conditions bacteria can persist for long periods of time and spread readily on the farm.

In modern layer complexes, the ventilation systems may not effectively remove the dust from houses. This is particularly true during the winter season when overzealous use of house temperature is used to control feed intake. A balance is established between the rate of resuspension of settled dust by the turbulent ventilating air and the rate of dust removal. When the balance is tipped in favor of the accumulation of dust, the mechanism within the trachea for the removal of dust is overwhelmed. Accompanying poor ventilation are ammonia levels of 20-100 ppm, which paralyzes the small hair like structures lining the trachea (cilia) reducing its ability to clear dust and bacteria.

Only dilution with clean incoming air has a significant effect in reducing the dust (bacterial load of air), but this is often negated by the proximity of other houses and the resulting house-to-house recycling of dust and contaminates. Blowing dust with leaf blowers can stir up the dust levels to high levels causing outbreaks of peritonitis. Cleaning out manure with birds in the house can release large amounts of ammonia causing an outbreak of peritonitis. In-house dead bird disposal/grind is a risk factor.

Prevention and control

E. coli can be viewed as a numbers game. Below a certain level of exposure, disease will not occur even though the birds are infected. At higher levels of exposure, the bacteria overcome the natural defense of the birds and clinical disease results. The number of any bacteria able to cause disease, even a pathogenic one, is in a constant state of flux depending on the health of the bird's immune system.

The goal of prevention and control is not to prevent infection from occurring but to prevent disease by minimizing the level of exposure. Principles for accomplishing this task are:

• Biosecurity: Prevent the introduction of other infectious agents.
• Sanitation: Down time between flocks, cleaning and disinfection lowers the numbers of E. coli until the birds can build up immunity to E. coli.
• Nutrition: Higher levels of Vitamin E or C may be beneficial in building a stronger immune system.
• Immune System: Protection of immune function by preventing immunosuppressive disease like Gumboro. Having vaccination program matching vaccines to field strains for MD, IBD, ND, IB, LT, pox and cholera.
• Environment: Leaf blowers and power mowers to be used at a minimum. Do not compost dead birds in the pit. Do our procedures and insecticides used to control flies contribute stress to the bird? Temperature Extremes/Air Quality vs. Economics.

NOTE: Preventative steps can and should be taken regardless of stage of disease.

Treatment

The results obtained from antibiotic treatment of infected flocks have been variable. Several factors can contribute to this variability:

1. Level of infection/exposure
2. Types of organisms involved – symptoms and lesions provide a tentative diagnosis, but confirmation requires isolation and identification of the organism
3. Improper identification of disease
4. Duration of antibiotic
5. Level of antibiotic
6. Lack of early detection
7. Antibiotic resistance/overuse of antibiotics

At this time, these are the currently approved drugs and levels for treatment of peritonitis in the feed:

drug dose duration
Chlortetracycline 400-500 g/T 7-14 days (longer may be required)
Erythromycin 100 g/T 7-14 days (longer may be required)
Neomycin/Oxytetracycline 35-140 g/T/100-200 g/T 7-14 days (longer may be required)
Tylan 4-50 g/T as long as required

In addition to antibiotic treatment, several other factors are needed for a successful outcome:

1. Lower dust exposure/clean cool air – spraying a disinfectant (Virkon-S) in the house
2. Adequate nutrition
3. Clean water/chlorination if needed – to obtain 3 ppm at the drinker, use 2 oz of 5% bleach per gallon of stock solution
4. Early detection of peritonitis by posting/early treatment
5. Once E. coli is diagnosed, one should seek to identify the primary disease or management factors predisposing the flock to E. coli

Treatments-Prevention as current-future alternatives

1. Competitive Exclusion – Probiotics
2. Multivalent E. coli bacterins
3. Subunit vaccines
4. New antibiotics (quinolones)
5. Controlling the effects of endotoxemia with the use of anti-inflammatory therapy (i.e. aspirin)
6. Treatment of feed with products that lower bacterial levels

- Pelleting
- Formaldehyde
- Organic acids, etc.

From Proceedings of the "Midwest Poultry Federation Convention", St. Paul, Minnesota, U.S.A.