Review of related literature:
The review of related literature of this study includes topics of Salmonella infection, Genus Salmonella and Pullorum disease. In addition, characteristics and features of pullorum disease was elaborated.
Salmonella infection or Salmonellosis
Infections with bacteria of the genus Salmonella are responsible for a variety of acute and chronic diseases in poultry (Gast, 1997a; Su & Chiu, 2006). Salmonella is a genus of the family Enterobacteriaceae and comprises a large and closely related population of medically important pathogens. It has long been associated with a wide spectrum of infectious diseases, including typhoid fever and non- typhoid salmonellosis, which cause public health problems worldwide (Su & Chiu, 2006).
Infected poultry flocks are among the most important reservoirs of salmonellae that can be transmitted through the food chain to humans. Poultry producers are faced with intensifying pressures from public health and regulatory authorities to protect consumers from illness transmitted by contaminated poultry meat and eggs. Poultry and poultry products are consistently among the leading animal sources of salmonellae that enter the human food supply. The increasingly international scope of the modern poultry industry has created new and more complex opportunities for the spread of Salmonella (Gast, 1997a).
Genus Salmonella
The genus Salmonella (of the family Enterobacteriaceae), named from USDA veterinary bacteriologist Daniel E. Salmon (1850–1914), consists of more than 2500 serologically distinguishable variants (or serovars) that are frequently named for the place of initial isolation (Gast, 1997a).
Infections of poultry with salmonellae can be grouped into three categories: the two nonmotile serovars, S. Pullorum and S. Gallinarum, the numerous motile and non-host-adapted Salmonella serotypes referred to collectively as paratyphoid salmonellae and the motile serotype which was for- merly designated Arizona hinshawii, the S. enterica subspecies arizonae (Gast, 1997a).
S. Pullorum and S. Gallinarum are generally host-specific for avian species. Pullorum disease, caused by S. Pullorum, is an acute systemic disease of chicks or poults. Fowl typhoid however, caused by S. Gallinarum, is an acute or chronic septicemic disease that most often affects mature birds. 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 (Gast, 1997a).
Paratyphoid Salmonellae are found nearly ubiquitously in wild and domestic animals. This diverse group of serotypes is principally of concern as a cause of foodborne disease in humans. Although paratyphoid infections of poultry are very common, they seldom cause acute systemic disease except in highly susceptible young birds subjected to stressful conditions. More often, paratyphoid Salmonella infections of chickens and turkeys are characterized by asymptomatic and sometimes persistent colonization of the intestinal tract and internal organs, potentially leading to contamination of the finished carcass (Gast, 1997a).
S. enterica subspecies arizonae, a motile serotype which was formerly designated Arizona hinshawii. This organism, although biochemically distinct, causes an acute septicemic disease that is not clinically distinguishable from other Salmonella infections. Arizonosis has reemerged as an economically significant disease of young turkeys in recent years (Gast, 1997a).
Pullorum Disease
Salmonella enterica serovar Pullorum, the causative agent for pullorum disease also known as bacillary white diarrhea is a fowl-adapted bacterial pathogen that causes severe enteritis and bacteremia in chicks during their first few days of life (Snoeyenbos, 1994; G. Liu, Rahn, L. Liu, Sanderson Johnston & S. Liu, 2002).
In its acute form, pullorum disease is almost exclusively a septicemic disease of young chickens. However, the organism may also be associated with disease in turkey poults and may be carried subclinically or lead to reduced egg production and hatchability plus a range of atypical signs in older birds. Ovarian transmission is a major route by which the organism can spread. Game birds and ‘backyard’ poultry flocks may act as reservoirs of infection, and wild birds may act as vectors for the organism and as such are important in the epidemiology of the disease (OIE, 2012).
Etiology and its characteristics
Salmonella Pullorum can be isolated by use of selective and nonselective media. Salmonella Pullorum produces rapid decarboxylation of ornithine whereas S. Gallinarum does not, an important biochemical difference between the two bacteria. Pullorum disease can be detected serologically by use of a macroscopic tube agglutination test, rapid serum test, stained antigen whole blood test or microagglutination test (Shivaprasad & Chin, 2001)
According to Shivaprasad & Barrow (2008), the organism is gram-negative, non-sporogenic, and facultatively anaerobic. It is slender rod measuring 0.3 to 1.5 mm in width and 1.0 to 2.5 mm in length. The bacilli mostly occur singly, but occasionally two or more can be found to be united. S. Pullorum is considered as nonmotile. However, motility and flagellation have been shown in S. Pullorum grown on special types of solid media. S. Pullorum grow readily on beef agar, broth, or other nutrient media. It is aerobic or facultatively anaerobic and grow best at 37°C. Colonies of S. Pullorum on meat extract or infusion agar (pH 7.0–7.2) appear as small, discrete, smooth, blue- gray or grayish white, glistening, homogenous, and entire. The growth of S. Pullorum is luxuriant and markedly translucent on liver infusion agar. Covered colonies remain small (1 mm or less), but isolated colonies may have a diameter of 3–4 mm or more.
Transmission
Like many other bacterial diseases, pullorum disease can be transmitted in several ways (Shivaprasad & Barrow, 2008; Kabir, 2010). 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, but localization of S. Pullorum in the ovules before ovulation is likely and probably constitutes the chief mode of vertical transmission. Egg transmission has been influenced by levels of antibodies in the yolk. Maternal antibodies against S. Pullorum may be critical in the prevention of embryonic mortality in infected eggs, thus allowing successful egg transmission (Shivaprasad & Barrow, 2008).
Transovarian infection resulting in infection of the egg and subsequently the hatched chicks or poults is one of the most important transmission routes for the disease (Shivaprasad & Chin, 2001 & OIE, 2012). The bacteria are passed out through the feces and lateral spread takes place through the fecal contaminated feeds, water and litter (Shivaprashad, 1997).
Epidemiology
Pullorum disease, caused by Salmonella Pullorum is widely distributed throughout the world but they have been eradicated from commercial poultry in many developed countries of Western Europe, the United States of America (USA), Canada, Australia and Japan. Salmonella Pullorum remains as a constant reservoir in wild and game birds (OIE, 2012).
Chickens are the natural hosts for the highly host adapted S. Pullorum (Shivaprasad & Barrow, 2008 & Kabir, 2010). Various routes of infection have been described. Oral route of infection represents the normal route of infection (Brito, Xu, Hinton & Pearson, 1995). Although infection in newly hatched chicks by nasal and cloacal route are also considered as the important route of transmission. Chicks may be infected early by vertical transmission either from an infected ovary, oviduct or from the infected eggs during the passage through the cloacal feces from infected or carrier hens.
Birds that survive from the clinical disease when infected during their young stage may show few signs of infection and become carriers od the disease (Berchieri, Murphy, Marston & Barrow, 2001). In adult carriers the reproductive organs are the predilection sites that often lead to the infection of ovarian follicles and as a result transovarian transmission of the disease occurs. The bacteria are passed out through the feces and lateral spread takes place through the fecal contaminated feeds, water and litter (Shivaprashad, 1995). Crowding, malnutrition, and other stressful conditions as well as unsanitary surroundings can exacerbate mortality and performance losses due to salmonellosis, especially in young birds (Waltman, Gast & Mallinson, 2008).
Pathogenesis
According to Kabir (2010), the pathogenicity of Salmonella depends on the invasive properties and the ability of the bacteria to survive and multiply within the cells, particularly macrophages (Humbert & Salvat, 1997). The main site of multiplication of these bacteria is the digestive tract, which may result in widespread contamination of the environment due to bacterial excretion through feces. Following invasion through the intestinal mucosa, cecal tonsils and Peyer’s patches, the organisms are engulfed by macrophages, and through the blood stream and/or lymphatic systems, they spread to organs rich in reticuloendothelial tissues (RES), such as liver and spleen, which are the main sites of multiplication (Barrow, Huggins & Lovell, 1994). In case of inadequate body defense mechanism, they may lead to second invasion and be localized in other organs, particularly ovary, oviduct, myocardium, pericardium, gizzard, yolk sac and/or lungs (Barrow, 1993). In the bird challenge, S. Pullorum preferentially targeted the bursa of Fabricius prior to eliciting intestinal inflammation (Henderson, Bounous & Lee, 1999). S. Pullorum disease manifests itself predominantly as an enteric disease of chickens (Shivaprashad, 1997). This biovar can cause septicemic infections, which may be acute or chronic (Christensen, 1996).
Clinical signs and lesions
Clinical signs in chicks and poults include anorexia, diarrhea, dehydration, weakness and high mortality. In mature fowl, fowl typhoid and pullorum disease are manifested by decreased egg production, fertility, hatchability and anorexia, and increased mortality. Gross and microscopic lesions due to fowl typhoid and pullorum diseases in chicks and poults include hepatitis, splenitis, typhlitis, omphalitis, myocarditis, ventriculitis, pneumonia, synovitis, peritonitis and ophthalmitis. In mature fowl, lesions include oophoritis, salpingitis, orchitis, peritonitis and perihepatitis (Shivaprasad & Chin, 2001).
Postmortem signs of pullorum disease in newly hatched chicks are those of peritonitis with generalized congestion of tissues and an inflamed unabsorbed yolk sac. Longer standing infections commonly lead to typhlitis with development of necrotic cecal casts and small necrotic foci in the liver, lungs and other viscera. Small lesions in the liver and spleen of pullorum-infected birds may show a ‘white spot’ appearance; however, this lesion is not pathognomic. Salmonella Pullorum is very poor at colonization and survival in the gastrointestinal tract and is often indicative of later stages of clinical disease. Adult birds may develop misshapen or shrunken ovaries with follicles attached by pedunculated fibrous stalks. Variant strains of S. Pullorum do not normally cause clinical disease or may result in mild, nonspecific signs but may lead to seroconversion (OIE, 2012).
According to Shivaprasad & Barrow (2008), both morbidity and mortality are highly variable in chickens and are influenced by age, strain of bird, nutrition, flock management, concurrent diseases and route and dose of exposure. Mortality from pullorum disease may vary from 0 to 100%. The greatest losses usually occur during the second week after hatching, with a rapid decline between the third and fourth week of age in pullorum disease.
Economic significance
In many developing nations, Salmonella Pullorum infections of poultry are common and pullorum disease remains among the principal disease threats to poultry producers. In most developed nations, however, the incidence of pullorum disease in commercial poultry has remained low for many years and most U.S. pullorum disease outbreaks in recent years have been reported in small or backyard poutry flocks, which may serve as potential reservoirs for disease transmission to commercial flocks (Gast, 1997b). The elimination of pullorum disease from commercial flocks in the United States in the mid-1900s was largely a result of the pullorum-typhoid control program, the National Poultry Improvement Plan (NPIP), instituted by a voluntary organization (Shivaprasad & Barrow, 2008). However, since infections with Salmonella Pullorum can result in acute systemic disease and a high incidence of mortality in young poultry (Gast, 1997b) and in mature fowls, pullorum disease are manifested by anorexia, drop in egg production , increased mortality, reduced fertility and hatchability (Kabir, 2010), this bacterial infection has the ability to devastate a poultry industry.
Vertical transmission of S. Pullorum from infected parent flocks, magnified by horizontal transmission in the hatcher, can cause economically devastating losses among chicks (Snoeyenbos, 1994).
Public health significance
Salmonella Pullorum is host adapted to avian species (Eswarappa et al., 2009; G. Liu, Rahn, L. Liu, Sanderson Johnston & S. Liu, 2002) and is considered to pose a minimal zoonotic risk (Shivaprasad, 2000), although the genome is continually evolving, which could theoretically widen the host range in future (G. Liu, Rahn, L. Liu, Sanderson Johnston & S. Liu, 2002).
According to Shivaprashad and Barrow (2008), there are only rare cases of Pullorum disease in humans that have resulted from massive exposure following the ingestion of contaminated foods or experimental challenge. The clinical signs are characterized by a rapid onset of acute enteritis, followed by prompt recovery without treatment.
Diagnosis
A definitive diagnosis of pullorum disease requires the isolation and identification of S. Pullorum. 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. However, negative results should not be considered adequate for a definite diagnosis because of the delay of 3–10 days in the appearance of agglutinating antibodies following infection (Shivaprasad & Barrow, 2008).
It is therefore necessary to confirm disease by isolation of the organisms. Serological tests can be used to establish the presence of the disease in a flock (OIE, 2012).
Treatment
According to Shivaprasad and Barrow (2008), reasonably effective prophylactic and therapeutic drugs have been developed against pullorum disease. In Canada and the United States, every effort has been made to eradicate this disease so treatment is neither feasible nor desired.
Various sulfonamides, nitrofurans, chloramphenicol, tetracyclines, and aminoglycosides have been found to be effective in reducing mortality from pullorum disease and fowl typhoid. However, no drug or combination of drugs has been found capable of eliminating infection from a treated flock. Sulfonamides, in particular, frequently suppress growth and may interfere with feed and water intake and egg production. Sulfonamides that have been used in the treatment of pullorum disease include sulfadiazine, sulfamerazine, sulfathiazole, sulfamethazine, and sulfaquinoxaline.
Most of the studies have indicated, however, that appreciable numbers of infected birds remain among medicated survivors. Spraying eggs with neomycin sulfate prior to incubation has also been helpful in controlling pullorum disease in chicks. In addition, variable resistance to chlortetracycline and nitrofurazone has been reported among isolates of S. Pullorum.
Prevention and control
Pullorum disease can be controlled and eradicated by use of serological testing and elimination of positive birds. Vaccines may be used to control the disease and antibiotics for the treatment of pullorum disease (Shivaprasad & Chin, 2001).
Management methods broadly designed to prevent the introduction of infectious agents are applicable to preventing the introduction of S. Pullorum. Only eggs from flocks known to be free of Pullorum disease should be used in hatcheries because of egg transmission. If Pullorum disease is encountered, elimination of carriers must be carried out regularly until the breeder flocks are free of Pullorum disease (Shivaprashad & Barrow, 2008). Control can best be achieved by biosecurity, hygiene, good management, monitoring and removal of infected flocks (OIE, 2012).
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