Efficacy of Salmonella enteritidis-immune lymphokines on horizontal transmission of S. arizonae in turkeys and S. gallinarum in chickens

Lowry, Virginia K.

doi:10.1016/s0168-1605(99)00036-7

Cited by 16 publications

(14 citation statements)

References 38 publications

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“…Taken together, it was perceived that the pathogenesis of fowl typhoid by serovar Gallinarum would be different from that of murine typhoid by serovar Typhimurium, as suggested previously (59,60). It was previously shown that serovar Gallinarum preferentially invaded the cecal tonsil and Peyer's patch in chicken lacking peripheral or mesenteric lymph (5,41). It is therefore possible that the uptake of serovar Gallinarum may not require SPI-1 genes even though these were clearly expressed (Fig.…”

Section: Discussionmentioning

confidence: 53%

Salmonella enterica Serovar Gallinarum Requires ppGpp for Internalization and Survival in Animal Cells

et al. 2008

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To elucidate the pathogenic mechanism of Salmonella enterica serovar Gallinarum, we examined the expression of the genes encoded primarily in Salmonella pathogenicity island 1 (SPI-1) and SPI-2. These genes were found to be induced as cultures entered stationary phase under high-and low-oxygen growth conditions, as also observed for Salmonella serovar Typhimurium. In contrast, Salmonella serovar Gallinarum in the exponential growth phase most efficiently internalized cultured animal cells. Analysis of mutants defective in SPI-1 genes, SPI-2 genes, and others implicated in early stages of infection revealed that SPI-1 genes were not involved in the internalization of animal cells by Salmonella serovar Gallinarum. Following entry, however, Salmonella serovar Gallinarum was found to reside in LAMP1-positive vacuoles in both phagocytic and nonphagocytic cells, although internalization was independent of SPI-1. A mutation that conferred defects in ppGpp synthesis was the only one found to affect animal cell internalization by Salmonella serovar Gallinarum. It was concluded that Salmonella serovar Gallinarum internalizes animal cells by a mechanism independent of SPI-1 genes but dependent on ppGpp. Intracellular growth also required ppGpp for the transcription of genes encoded in SPI-2.

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Section: Discussionmentioning

confidence: 53%

Salmonella enterica Serovar Gallinarum Requires ppGpp for Internalization and Survival in Animal Cells

et al. 2008

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“…This is in agreement with some of the observations of Murray and Lee (25) for the role of SPI-1 in serovar Typhimurium in murine typhoid-like disease. We have previously shown that serovar Gallinarum appears to preferentially invade the cecal tonsil and Peyer's patch during the early stages of fowl typhoid (6,23). This apparent tropism for lymphoid tissue is also displayed by serovar Typhimurium in infection of mice (24).…”

Section: Discussionmentioning

confidence: 89%

Salmonella enterica Serovar Gallinarum Requires the Salmonella Pathogenicity Island 2 Type III Secretion System but Not the Salmonella Pathogenicity Island 1 Type III Secretion System for Virulence in Chickens

et al. 2001

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Salmonella enterica serovar Gallinarum is a host-specific serotype that causes the severe systemic disease fowl typhoid in domestic poultry and a narrow range of other avian species but rarely causes disease in mammalian hosts. Specificity of the disease is primarily at the level of the reticuloendothelial system, but few virulence factors have been described other than the requirement for an 85-kb virulence plasmid. In this work, by making functional mutations in the type III secretion systems (TTSS) encoded by Salmonella pathogenicity island 1 (SPI-1) and SPI-2, we investigated the role of these pathogenicity islands in interactions between Salmonella serovar Gallinarum and avian cells in vitro and the role of these pathogenicity islands in virulence in chickens. The SPI-1 mutant showed decreased invasiveness into avian cells in vitro but was unaffected in its ability to persist within chicken macrophages. In contrast the SPI-2 mutant was fully invasive in nonphagocytic cells but failed to persist in macrophages. In chicken infections the SPI-2 mutant was attenuated while the SPI-1 mutant showed full virulence. In oral infections the SPI-2 mutant was not observed in the spleen or liver, and following intravenous inoculation it was cleared rapidly from these sites. SPI-2 function is required by Salmonella serovar Gallinarum for virulence, primarily through promoting survival within macrophages allowing multiplication within the reticuloendothelial system, but this does not preclude the involvement of SPI-2 in uptake from the gut to the spleen and liver. SPI-1 appears to have little effect on virulence and survival of Salmonella serovar Gallinarum in the host.

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“…Infected birds, contaminated eggs, water, feed, and other materials play an important role in spreading the bacteria (Lowry et al, 1999;Berchieri et al, 2001;Kokosharov, 2001;Oliveira et al, 2005). In the present study, the continuous contamination of feed and the hatching eggs with faeces and other environmental material, the absence of an effective hatchery sanitation programme and the mixing of the outside adult budgerigars in all of the flocks probably played a major role in the occurrence and spread of S. Gallinarum in the young and adult budgerigars.…”

Section: Discussionmentioning

confidence: 99%

“…The disease usually follows the ingestion of food or water contaminated by the excreta of clinically infected birds or carriers but can also be transmitted by attendants through contaminated hands, feet and clothes (Lowry et al, 1999;Berchieri et al, 2001). In the subacute and chronic stages of the disease, the liver and spleen are mostly affected, with multiple white foci, severe swelling and discolouration being observed (Hossain et al, 2006;Shivaprasad & Barrow, 2008).…”

Section: Introductionmentioning

confidence: 99%

Pathomorphological, immunohistochemical and bacteriological findings in budgerigars (Melopsittacus undulatus) naturally infected withS.Gallinarum

et al. 2012

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The present study describes the pathological and bacteriological findings and diagnosis by immunoperoxidase and immunofluorescence methods in budgerigars (Melopsittacus undulatus) naturally infected with Salmonella gallinarum obtained from three commercial budgerigar rearing farms. The course of the disease in young budgerigars was peracute or acute, whereas in adult budgerigars the disease was acute or chronic. Clinically, yellowÁwhite diarrhoea was observed in the young budgerigars with the acute form. In the adult budgerigars with the acute and chronic forms, a decrease in feed and water consumption with loss in body condition together with greenish-yellow diarrhoea was generally noted. Peritonitis and pericarditis were the most common findings in young budgerigars at necropsy, while in adult budgerigars scattered greyÁwhite necrotic foci were found in the livers. Histopathologically, the lesions in young budgerigars were characterized with fibrinonecrotic peritonitis and/or pericarditis and necrotic hepatitis. In adult budgerigars with acute infection, hepatic necrosis with focal heterophil infiltration was present; whilst lesions in the chronic cases were granulomatous in nature with the infiltration of macrophages, lymphocytes and histiocytes. For the detection of S. Gallinarum in formalin-fixed, paraffin-embedded tissues, the avidinÁbiotin peroxidase complex and immunofluorescence methods were used. Both methods showed bacteria to be localized in the liver, kidney, peritoneum, heart, spleen and intestines of both young and adult budgerigars. The results of the present study indicate that the avidinÁbiotin peroxidase complex method was more sensitive than the immunofluorescence method in the detection of the bacteria.

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Efficacy of Salmonella enteritidis-immune lymphokines on horizontal transmission of S. arizonae in turkeys and S. gallinarum in chickens

Cited by 16 publications

References 38 publications

Salmonella enterica Serovar Gallinarum Requires ppGpp for Internalization and Survival in Animal Cells

Salmonella enterica Serovar Gallinarum Requires ppGpp for Internalization and Survival in Animal Cells

Salmonella enterica Serovar Gallinarum Requires the Salmonella Pathogenicity Island 2 Type III Secretion System but Not the Salmonella Pathogenicity Island 1 Type III Secretion System for Virulence in Chickens

Pathomorphological, immunohistochemical and bacteriological findings in budgerigars (Melopsittacus undulatus) naturally infected withS.Gallinarum

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