2. Infections of poultry with salmonellae can be grouped into two categories Nonmotile serotypes S. pullorum and S.gallinarum Which are generally host-specific for avian species

3.  Pullorum disease caused by S. pullorum  Is an acute systemic disease of chicks and poults.  Fowl typhoid, caused by S. gallinarum  Is an acute or chronic septicemic disease that most often affects mature birds.

4.  Both of these diseases have been responsible for serious economic losses to poultry producers in the past and have been addressed by the implementation of extensive testing and eradication programs.

5.  The numerous motile Salmonella serotypes referred to collectively as paratyphoid salmonellae. Found nearly in wild and domestic animals, this diverse group of serotypes is principally of concern as a cause of food-borne disease in humans.

6.  Although paratyphoid infections of poultry are very common, they seldom cause acute systemic disease except in highly susceptible young birds subjected to stressful conditions.

7.  Pullorum disease and fowl typhoid in terms of history,clinical signs, epizootiology, lesions, and control and eradication procedures have many similarities.  However,differences have been reported for these two diseases, andthey are caused by different species of bacteria (i.e, Salmonella pullorum and S. gallinarum, respectively).

8.  Pullorum disease (PD) and fowl typhoid (FT) are septicemic diseases affecting primarily chickens and turkeys, but other birds such as quail, pheasants, ducks, peacocks,and guinea fowl are also susceptible.  Both diseases can betransmitted through the egg by transovarian infection.

9.  Bacillary white diarrhea was a term used to designate PD before 1929, but the term pullorum disease has since gained universal acceptance.

10.  Pullorum disease and FT are caused by S. pullorum and S.gallinarum, respectively.

11. Pullorum disease and FT are worldwide in distribution Natural and Experimental Hosts Chickens are the natural hosts for both S. pullorum and S. gallinarum; however, naturally occurring outbreaks of PD and FT have been described in turkeys, guinea fowl, quail, pheasants, sparrows, and parrots

12.  Mortality from PD usually is confined to the first 2—3 weeks of age. Acute infections in older chickens, particularly among brown egg-producing strains, have been reported occasionally.  Similarly, mortality due to PD in semimature and mature turkeys has been observed. A certain percentage of chickens and turkeys that survive the initial infection become carriers with or without the presence of lesions.

13. Although FT is frequently referred to as a disease of adult birds, there have been reports of high mortality in young chicks. As in PD, FT losses begin at hatching time; however, in FT they also continue to laying age

14.  Like many other bacterial diseases, PD and FT can be transmitted in several ways. The infected bird (reactor and carrier) is by far the most important means of perpetuation and spread of the organism.  Birds may infect not only their own generation by horizontal transmission, but also succeeding ones through egg transmission. Egg transmission may result from contamination of the ovum following ovulation

15.  PD and FT are primarily diseases of chicks and poults.  However, FT is a more significant disease in growing and adult chickens and turkeys than PD.  The signs noted in young chicks and poults associated with both diseases are very similar as a result of the transovarian transmission of these diseases. Occasional cases of PD can be subclinical, even though the disease may originate by egg transmission

16.  If birds are hatched from S. pullorum or S. gallinarum infected eggs, moribund and dead birds may be observed in the incubator or within a short time after hatching. The birds can manifest somnolescence, weakness, depressed appetite, poor growth, and adherence of chalky white material to the vent. Death may soon follow

17.  In some cases, evidence of PD is not observed until 5—10 days after hatching, but the disease gains momentum during the following 7—10 days. Mortality usually peaks during the second or third week of life. In these situations, the birds exhibit lassitude and an inclination to huddle together under heaters, having droopy wings, and distorted body appearance.

18.  Labored breathing or gasping may be observed as a  result of extensive involvement of the lungs due to PD.  Survivors may be greatly retarded in their growth and  appear underdeveloped and poorly feathered. These birds may not mature into vigorous or well- developed laying or breeding birds.  Flocks that have passed through a serious outbreak usually have a high percentage of carriers at maturity.  In certain instances, a relatively high incidence  of infection in the joints, leads to lameness and obvious joint enlargement

19.  Infected birds may not exhibit any signs and cannot be detected by their physical appearance, especially in the case of PD.  Acute outbreaks of FT in chickens may begin by a sudden drop in feed consumption, with birds being droopy, showing ruffled feathers and pale and shrunken combs.

20.  Other signs, such as a drop in egg production, decreased fertility, and diminished hatchability, can sometimes be observed in both PD and FT, depending upon the severity of infection.  Death may occur within 4 days of exposure, but usually occurs after 5—10 days. In some cases of PD in semi-mature and mature flocks, the predominant clinical signs include anorexia, diarrhea, depression, and dehydration

21.  Chicks  In peracute cases of PD and FT, birds that die suddenly in the early stages of brooding may show no gross lesions. In acute cases, enlarged and congested liver, spleen, and kidneys may be seen.  Livers may have white foci of 2—4 mm in diameter

22.  Occasionally, those birds with respiratory signs may have white nodules in the lung, and white nodules, resembling Marek’s disease tumors, may be present in the cardiac muscle or pancreas.  Occasionally, nodules in the heart may become so large they distort the shape of the heart

23.  Lesions due to PD may be minimal in s ome birds, even though they may be active serologic reactors.  Sometimes, only a minimal lesion, such as a small nodular or regressing ovarian follicle, can be found.  However, the lesions found most frequently in chronic carrier hens with PD and FT are a few misshapen, discolored cystic ova among a few normal-appearing ovules

24.  Peritonitis and adhesions of the abdominal viscera. Fibrinous peritonitis and perihepatitis, with or without involvement of the reproductive tract, may sometimes be seen.  Ascites, pericarditis

28.  A very limited amount of information on microscopic lesions is available for PD or FT.  Most of the PD lesions described are from field cases, which might have been complicated by other bacterial and/or viral agents

29.  Diagnosis of PD or FT requires the isolation and identification of S. pullorum or S. gallinarum, respectively.  A tentative diagnosis, however, can be made based on flock history, clinical signs, mortality, and lesions.  Positive serologic findings can also be of major value in detecting infection

30.  The clinical signs and lesions produced by PD or FT are not pathognomonic.  Aspergillus or other fungi may produce similar lesions in the lungs  S. pullorum and S. gallinarum can localize in major joints and tendon sheaths of chicks.

31.  Such signs and lesions resemble those produced by organisms such as Mycoplasma synoviae, Staphylococcus aureus, Pasteurella multocida, or Erysipelothrix rhusiopathiae.  Sometimes the white nodules in the heart of young chicks may resemble Marek’s disease tumors.

32.  A definitivediagnosis of PD and FT can be made only following the isolation and identification of :  S. pullorum and S. gallinarum,respectively.

33.  It has long been established that chicken and turkey flocks can be developed and maintained free of PD and FT by adhering to well-defined procedures. Both PD and FT are good examples of diseases that have decreased in incidence over the years by the application of basic management procedures. In the simplest sense, the only requirement is to establish breeding flocks free of S. pullorum and S. gallinarum and to hatch and rear their progeny under conditions that preclude direct or indirect contact with infected chickens or turkeys.

34.  Because of egg transmission, only eggs from flocks known to be free of PD and FT should be used in hatcheries.  Under the NPIP, chicken and turkey breeding flocks and their progeny may be recognized as free of PD and FT.  Management practices should be broadly applied to prevent the introduction of PD or FT. If PD or FT are encountered, elimination of carriers must be carried out regularly until the breeder flocks are free of PD and FT.

35.  1. Chicks and poults should be obtained from sources free of PD and FT.  2. Pullorum-free and typhoid-free stock should not be mixed with other poultry or confined birds.  3. Chicks and poults should be placed in an environment that can be cleaned and sanitized to eliminate any residential salmonellae from previous flocks.  4. Chicks and poults should receive pelletized, crumbled feed to minimize the introduction of S. pullorum and S. gallinarum and other salmonellae through contaminated feed ingredients. Use of feed ingredients free of salmonellae is essential.  5. Introduction of salmonellae from outside sources must be minimized by the use of a sound biosecurity program.

36.  a. Free-flying birds are commonly found to be carriers of other salmonellae, although rarely with S. pullorum or S. gallinarum. Poultry houses should be bird proof.  b. Rats, mice, rabbits, cats, dogs, and pests may be carriers of other salmonellae, but they are infected rarely with S. pullorum or S. gallinarum. Nevertheless, poultry houses should be vermin proof.  c. Insect control is important, particularly against flies, poultry mites, and the lesser mealworm. These pests may provide a means of survival for salmonellae and other avian pathogens in the environment.

37.  d. Potable drinking water must be used, or chlorinated water should be provided. In some areas, a danger is posed by surface water collected in open ponds for use as drinking water for livestock and poultry.  e. Mechanical carriers of the organism include footwear and clothing of humans, as well as poultry equipment, processing trucks, and poultry crates. Every precaution should be made to prevent the introduction of S. pullorum or S. gallinarum by fomites.  f. Proper disposal of dead birds is essential.

38.  Elimination of Carriers.  Serologic Tests

39.  Because PD has been mostly eradicated from commercial flocks over the years and the eradication program is in place, very little incentive exists for the production of vaccines to control PD.

40.  Reasonably effective prophylactic and therapeutic drugs have been developed against PD and FT.  Various sulfonamides, nitrofurans, chloramphenicol, tetracyclines, quinolones and aminoglycosides have been found to be effective in reducing mortality from PD and FT  No drug or combination of drugs has been found capable of eliminating infection from a treated flock.

41.  Spraying eggs with neomycin sulfate prior to incubation has also been helpful in controlling PD in chicks.  Dipping contaminated eggs in antibiotic solution containing 400 ppm and 800 ppm of gentamicin In addition, resistance to chlortetracycline and nitrofurazone have been reported among isolates of S. pullorum.