1. Necrotic Enteritis A problem in broilers.
Has become prevalent in all broiler producing areas since about 1966.
The introduction of ionophore coccidiostats has almost eliminated the disease.
Etiology
High energy feeds (broilers)
Probably a combination of events including
sub-clinical coccidiosis and Clostridium perfringens
Maybe gut stasis leading to an anaerobic environment.

2. Course of Disease
Affected birds die quickly
After treatment, usually decreases in hours.
May re-occur up to 3 times in one grow out
Mortality
If untreated maybe up to 20%.
If treated early less than 2%.
Method of Spread
Probably by humans, or may be normal soil organism that has flourished in built-up litter.
Will re-occur in infected house.

3. Clinical Signs
Ataxia, "creepers"
Water filled crop
Birds show intoxication
Usually seen first time at 3 weeks of age
Post Mortem Lesions
Extreme dehydration
Dark congested liver
Entire mid and lower small intestine have "cooked" appearance. Mucosa looks like a "dirty turkish towel".
No liver lesions as seen with ulcerative enteritis
Water in crop

4. Biological Test
Quail
Used for biological testing of this pathogen.
Homogenized suspect gut. Results in 72 hours.
Treatment
Bacitracin – gm/gal days
Pen. Strep. - high level days
Streptomycin (strep-sol) works best
Response to treatment can be used as a diagnostic tool.

5. Prevention
Low continuous levels of antibiotics:
Bacitracin g/ton in feed for chickens continuously. Lincomycin.
Ionophores such as monensin seem to have some effect against NE.
Apply salt to flooring at 60 lbs./1000 sq. ft.

6. Ulcerative Enteritis
Has been limiting disease to the commercial bobwhite quail industry.
Occurs in ground raised birds. Japanese quail (coturnix) are resistant.
Occasionally seen in white leghorn pullets and turkeys secondary to other conditions such as coccidiosis.
This disease is not seen in broilers.

7. Etiology
Quail - Clostridium colinum — Anaerobic sporeformer
Chickens - C. colinum + intestinal stress such as coccidiosis.
Quail usually on ground or reared on contaminated wire floors.
UE usually a secondary infection to Eimeria brunetti, E. tenella or E. necatrix in chickens.
These forms of coccidiosis disrupt the lamina propria and the deep lesions result in bloody feces.

8. Comment
UE seldom seen in broilers because of the good coccidiosis control program usually used in broilers (coccidiostats).
Most often seen in leghorn pullets because of weak coccidiostat program.
Incubation Period
Quail - as soon as 18 hours usually 1-3 days
Chickens - 48 hours after inoculation with UE in birds previously infected with coccidiosis for 6 days. Usually seen in chickens about 1‑2 weeks after "coccidiosis".

9. Course of Disease
Quail weeks. Acute may become chronic and have birds dying over long periods of time.
Chickens weeks. Not as severe
Mortality
Quail - Up to 100%
Chickens - Seldom over 10%
Method of Spread
Probably "carrier" birds. If one of these birds is introduced into a clean flock, it can cause disease. Bacteria build up in the soil.
Carried over in infected ground and equipment.
Spore continues to infect for years.

10. Clinical Signs
Quail
Usually seen first in 6-10 week old birds, any age may be affected.
Develop diarrhea (watery).
Sudden mortality in heavy birds.
Infected birds thirsty - birds huddle around drinkers.
Can become chronic and birds become emaciated
Usually seen in birds raised on the ground

11. Chickens
Often occurs following a coccidiosis "break" Typical "sick bird"
Birds develop diarrhea, Thirsty, Mortality
Usually in white leghorn pullets 6-14 weeks old.
Post Mortem Lesions
Quail
First seen in heavy, fat birds
Crop full of water, feed may be present indicating sudden death.
Yellow necrotic areas in liver
May be hemorrhagic infarcts in liver - this may be a good place to isolate the organism.
Discrete ulcers in small intestine and ceca.
Birds that live more than 10 days become emaciated
In peracute cases, may see liver lesion without gut lesions

12. Chickens
Same as quail, but lesions are usually where previous coccidiosis lesions were.
Intestinal lesions not as distinct as quail. Liver lesions alone frequently.
Seldom chronic.
Secondary airsacculitis may result from septicemia occurring after gut damage.
Diagnosis
Lesions are unique
May have to differentiate from necrotic enteritis in chickens
Quail - Used as a biological indicator
Liver smear - Typical organism

13. Treatment
Bacitracin gm/ton for 7-10 days Quail:
Bacitracin – gm/gal 7-10 days
Chickens: Same as quail, also can use penicillin or streptomycin

14. Staphylococcus Infections
Staphylococcus Infections
These infections are usually seen in poultry as “navel ill” (omphalitis), arthritis, and “bumblefoot.”
A differential diagnosis for this would be E. coli or Salmonella.
Not highly contagious, causes problem as chronic condition. Secondary infections occur due to poor management.
High mortality seen with omphalitis from contaminated hatchers.
Prevalent problem in replacement broiler breeders and turkeys, as arthritis.

15. Causative Agent
Staphylococcus aureus
Most pathogenic staphs are coagulase positive (+).
Very ubiquitous organism that is an opportunist.
Infection usually follows traumatic or biological injury.
Comment
Staph problems often occur following a coccidiosis outbreak and again between weeks after birds are moved to laying quarters and onto slated floors due to trauma.
Replacement broiler breeder males which are put onto slats and fed 12% protein restrictive rations.

16. Incubation Period
Three to four days in omphalitis, Two to three weeks with bumblefoot and arthritis
Course of Disease
One week to several weeks in chronic cases
Method of Spread
Primarily through injuries which allow entrance of organism.
Egg shell contamination in breeder house.
Contaminated hatchers – failure to fumigate properly.
Oral entrance possibly.
Turkeys – entrance through respiratory system.

17. Mortality
Suppurative synovitis/arthritis in replacement broiler breeder males may reach 4%.
Bumblefoot: usually low 3-6%.
Omphalitis: % mortality within 3 to 4 days after hatching.
100% of the affected birds will die.
10-15% in laying hens acutely infected with septicemic “staph.”

18. Clinical Signs
In Chicks
High mortality in 72 hours
Large scab on navel
Swollen dark greasy abdomen with very putrid odor
In Adult Chickens
“Bumblefoot” – injured footpad with severe swelling (abscess).
Arthritis and synovitis. In slatted houses.
Occasionally systemic (septicemia) but this is rare.
In Turkeys – Usually in Growing Toms
Birds reluctant to move and are crippled.
Swollen joints, synovial sheaths and bursas.

19. Postmortem Lesions
Bumblefoot” – usually there is a wound with caseous suppuration in an organized abscess (common in backyard flocks).
Omphalitis – retained yolk in emaciated baby chicks or poults. The infection has putrid odor.
Arthritis – suppuration in the joints and also, around synovial sheaths (e.g., tendon sheaths of the hocks, gastrocnemius tendon, stifle, and wing joints).
Breast blisters (synovial bursa over sternum) filled with suppurative exudate. Associated with coarse litter.

20. Septicemic “staph” lesions are similar to other bacterial diseases but usually have dark brown or greenish edges on the liver lobes. This has been related to tibial dyschondroplasia (TD) and turkey osteomyelitis complex.

21. Diagnosis
Suggestive
Swelling in joints or foot pads with suppuration present (white & creamy occasionally with flocculence).
High mortality in chicks with swollen abdomens and retained yolk sac (putrid odor), swollen foot pads and joints.
Breast blisters are filled with creamy pus.
Osteomyelitis in tibial and femoral growth plates. Discrete 1-2 mm abscesses may be found in marrow cavity. Related to TD.

22. TD will resolve with time but often associated with green livers.
In septicemia, “staph” lesions are similar to those seen in fowl cholera or any other septicemic disease. This is rare.
Positive – Isolation and identification of the causative agent.
Differential Diagnosis
The symptoms and lesions of arthritis are very similar to those found in infectious synovitis (MS) and chronic fowl cholera as well as other bacterial diseases.
Must culture to differentiate.

23. Culture Method
Staphylococcus Aureus
Visceral organs (liver, spleen, etc…) and hock exudate (swab)
Blood agar-White to yellow colonies, Hemolytic variable
Coagulase test (+) or (staphyloslide* test)
Staphtrac TM310 biochemical test strips

24. Treatment
Sensitivity tests should dictate drug being used. Penicillin is usually effective.
Drugs of choice: Novobiocin (expensive)
Others used: Chlortetracycline, Oxytetracycline, Erythromycin
Use broad spectrum antibiotics in Omphalitis at the rate of 1-2 gm per gal of water for 7-10 days.
Potassium penicillin G water soluble powder must be used for 7-10 days in replacements.
Re-treatment may be necessary before placement in laying houses (No chicken clearance).

25. Prevention
Remove sharp objects from the litter and premises. Correct rough turkey ranges.
Cleanliness and fumigation of incubators.
In turkeys, treatment of arthritis is actually a prevention method.
No vaccine available.
Anticoccidial & restrictive feeding programs in replacements can have impact on stress and resultant staph infection.

26. Avian Tuberculosis
This is a disease of older birds (5-6 years) in old contaminated chicken yards.
Due to modern methods of poultry management this disease is not considered important at present.
Spreading infected poultry litter onto cattle pastures will cause a positive tuberculin test in cattle.

27. Causative Agent
Mycobacterium avium
Can be tested for with tuberculin
Injected i/d in comb.
This is rarely done today.
The disease is characterized by granulomatous lesions.  Major lesions in liver, spleen, intestines, ceca, and bone.

28. In humans (in immunosuppressed), lymphadenitis is one of the most frequent clinical presentations of mycobacteriosis. It is assumed that human infection occurs through contact with birds.  
Swine – can be readily infected.