Food poisoning with special reference to Salmonella -- its epidemiology, pathogenesis and control.
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Animals↗
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A study of the pathogenesis of experimental Salmonella dublin abortion in cattle.
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Abortion, Veterinary↗
Pathogenesis of Salmonella-mediated intestinal fluid secretion. Activation of adenylate cyclase and inhibition by indomethacin.
Salmonella typhimurium, an organism that invades intestinal mucosa but does not elaborate a traditional enterotoxin, evokes ileal secretion by causing alterations in active sodium and chloride transport mechanisms. To evaluate the possibility that these changes in transport might be related to the adenylate cyclase-cyclic AMP or NA+-K+-adenosine triphosphatase (ATPase) systems, mucosal adenylate cyclase, cAMP phosphodiesterase, Na+-K+ and Mg++ ATPase activities, and cAMP concentrations were measured in rabbit ileal loops infected with two strains of S. typhimurium. Strain TML invades the mucosa and evokes fluid secretion whereas strain SL 1027 invades but does not evoke secretion. Cholera toxin-stimulated loops were also studied. When compared to control loops, TML-infected mucosa demonstrated a marked increase in adenylate cyclase activity, in cAMP concentration, and no change in phosphodiesterase or ATPase activities. SL 1027-infected mucosa demonstrated no change in either adenylate cyclase or ATPase activities. Indomethacin pretreatment of cyclase activation. In contrast, indomethacin pretreatment of cholera toxin exposed animals resulted in only a partial reduction of secretion while not altering the stimulation of adenylate cyclase. These results suggest that: (1) S. typhimurium causes ileal secretion by stimulating adenylate cyclase; (2) mucosal invasion alone (SL 1027) is not sufficient to activate adenylate cyclase, and (3) Na+-K+-ATPase does not appear to be involved in salmonella-induced secretion. The mechanism of salmonella activation of adenylate cyclase is unclear but apparently differs from that of cholera toxin in that it is inhibited by indomethacin. This might be explained by the participation of prostaglandins in the salmonella activation process.
Adenosine Triphosphatases↗
Importance of the intestinal inflammatory reaction in salmonella-mediated intestinal secretion.
The ability of Salmonella typhimurium to invade the intestinal epithelium is essential to the pathogenesis of salmonella-induced intestinal secretion. This invasion is accompanied by an intense acute inflammatory reaction. The present study tests the hypothesis that the acute inflammatory reaction may have a role in the pathogenesis of salmonella-induced secretion. Two groups of rabbits infected with S. typhimurium were studied: normal animals and animals pretreated with nitrogen mustard. Nitrogen mustard depletes the polymorphonuclear leukocyte pool and thereby prevents the formation of an acute inflammatory reaction. In vivo ligated ileal loops were constructed and infected 72 h after nitrogen mustard administration when polymorphonuclear leukocytes were undetectable. Nitrogen mustard treatment markedly inhibited salmonella-induced secretion. Ileal histology in normal animals infected with S. typhimurium revealed an intense acute inflammatory reaction, while in animals pretreated with nitrogen mustard only a rare polymorphonuclear leukocyte was seen. The antisecretory effect of nitrogen mustard was not merely a nonspecific effect since nitrogen mustard treatment did not inhibit cholera toxin-induced secretion and did not alter either ileal morphology nor the activities of various intestinal enzymes in normal animals. Nitrogen mustard also did not alter the virulence of the inoculated S. typhimurium. These data suggest that the mucosal inflammatory reaction induced by salmonella invasion may be important to the pathogenesis of the salmonella secretory process. The mechanism by which the inflammatory reaction stimulates secretion is not known.
Animals↗
A Small RNA Derived From the 5' End of the IS200 tnpA Transcript Regulates Multiple Virulence Regulons in Salmonella typhimurium.
The insertion sequence IS200 is widely distributed in Eubacteria. Despite its prevalence, IS200 does not appear to be mobile and as such is considered an ancestral component of bacterial genomes. Previous work in Salmonella enterica revealed that the IS200 tnpA transcript is processed to form a small, highly structured RNA (5'tnpA) that participates in the posttranscriptional control of invF expression, encoding a key transcription factor in this enteropathogen's invasion regulon. To further examine the scope of 5'tnpA transcript integration into Salmonella gene expression networks, we performed comparative RNA-seq, revealing the differential expression of over 200 genes in a Salmonella SL1344 5'tnpA disruption strain. This includes the genes for the master regulators of both invasion and flagellar regulons (HilD and FlhDC, respectively), plus genes involved in cysteine biosynthesis and an operon (phsABC) encoding a thiosulfate reductase complex. These expression changes were accompanied by an 80-fold increase in Salmonella invasion of HeLa cells. Follow-up experimentation suggested an additional direct target of 5'tnpA to be the small RNA PinT, which has previously been shown to be a negative regulator of invasion genes through its inhibitory action on key transcription factors governing the Salmonella pathogenicity island 1 regulon. This study provides a powerful new example of bacterial transposon domestication that is based not on the production/use of a regulatory protein or regulatory DNA sequences, but on the function of a transposon-derived small RNA.
Salmonella typhimurium↗
[Pathogenesis of toxic syndrome in salmonella infections and dysentery].
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Adolescent↗
[Interaction between Salmonella and Schistosomes. Scanning electron microscopy study].
In our attempts to elucidate the pathogenesis of prolonged Salmonella bacteremia in patients with Schistosoma mansoni or Schistosoma haematobium infection, we have utilised MEB. Our results are significant. They show an association exists between Bilharziasis and Salmonellosis.
Agglutination↗
[Post-salmonella rheumatism: case report].
A twenty seven year old man had polyarthritis following diarrhoea due to Salmonella typhimurium. The role of the salmonella infection in the pathogenesis of this joint problem would appear to be confirmed by the detection of the organism on stool culture and a positive reaction for specific antigens in the blood. The arthritis was cured in six weeks under the influence of non-steroid anti-inflammatory agents.
Adult↗
Evidence of a role for permeability factors in the pathogenesis of salmonellosis.
Two clinical isolates of Salmonella typhimurium were shown to produce two skin permeability factors. One factor was heat stable and rapid in onset while the other was heat labile and elicited maximal induration by 18 to 24 hr. The rapid, erythematous permeability factor (PF) response could not be prevented by antisera to cholera toxin or Salmonella antisomatic serum, but it could be simulated by high concentrations of lipopolysaccharide from S. typhimurium. The appearance of the delayed PF reaction was indistinguishable from that of purified cholera toxin. Histological comparisons of rabbit skin injected with Salmonella-delayed PF and cholera toxin revealed that both toxins resulted in gross edema and infiltration of polymorphonuclear leukocytes after 18 hr. The Salmonella-delayed PF was shown to be resistant to a variety of enzymes, sensitive to extremes in pH, and had an isoelectric point of pH 4.8. Unlike Salmonella lipopolysaccharide skin activity, the Salmonella-delayed PF was destroyed at 100 C and was neutralized by monospecific cholera antitoxin. The Salmonella-delayed PF, which shares antigenic determinants with cholera toxin, appears to be elaborated by living S. typhimurium cells in the rabbit ligated intestine, since rabbits immunized with procholeragenoid were protected against fluid loss from live cell challenge. Finally, production of the rapid PF is a stable genetic trait, while delayed PF production is apparently an unstable characteristic among the salmonellae.
Animals↗
Studies on the pathogenesis of enteric infections caused by invasive bacteria.
Salmonellae, shigellae and some Escherichia coli must invade the intestinal epithelial cell and multiply within the mucosa to cause disease. Although the bacterial cell most likely possesses several properties essential to this invasive ability, the nature of the cell envelope complex is at present the only characteristic which has been implicated in this process. While a number of pathophysiological events result from invasion, some of our recent efforts have concerned the site and mechanism of intestinal fluid loss in salmonellosis and shigellosis. In both these disorders, bacterial invasion of the colonic mucosa, associated with an acute inflammatory reaction and mucosal damage, is regularly seen and colonic salt and water transport is abnormal. These defects may account for mild diarrhoea in salmonellosis and the dysenteric stools of shigellosis. However, in salmonella-infected animals with severe watery diarrhoea and in shigella-infected animals with diarrhoea alone or in combination with dysentery, the jejunum is in a net secretory state. This secretion occurs in the absence of bacterial invasion or morphological abnormalities. Thus, the diarrhoea caused by invasive bacteria may result from the inability of the colon to reabsorb the increased volume of fluid entering it from the small intestine. Although colonic mucosal damage is a feature of invasive-type diarrhoeas, the permeability of both the colon and small intestine to small molecules, mannitol and erythritol, is not altered. Thus intestinal fluid loss cannot be ascribed to transudation. In addition, the results of our Ussing chamber experiments, employing salmonella-infected rabbit ileum, reveal that salt and water secretion is an active process. Since secretion occurs in the jejunum in the absence of bacterial invasion, this might suggest the participation of an enterotoxin. Shigella dysenteriae I is the best-studied invasive organism in which an enterotoxin has been found, yet mutant strains which do not invade but retain the ability to elaborate enterotoxin fail to cause disease in either monkeys or man. Thus, the physiological relevance of Shiga enterotoxin and the mechanism of jejunal secretion in these disorders remain unclear. Recent data suggest that invasive enteropathogens, like the enterotoxin-producing bacteria, activate the mucosal adenylate cyclase-cyclic AMP system and that this activation may play a role in intestinal fluid secretion.
Animals↗
Identification of gene targets regulated by the IclR-like regulator SL1344_3500 in Salmonella Typhimurium.
Transcriptional regulation of metabolic operons is important for optimal carbohydrate use and for mitigating the accumulation of toxic intermediates. Here, we characterize SL1344_3500, encoding a putative IclR-like regulator in Salmonella enterica Typhimurium. We present genetic and transcriptional evidence that it regulates the expression of two neighboring operons, one designated here as xynABC, enables utilization of xylonate as a sole carbon source. Furthermore, our findings indicate that SL1344_3500 is important for luminal growth in several mouse models, exerting its effects through the suppression of the xynABC operon. Based on the observation that the ΔSL1344_3500 deletion can be stably complemented in vivo, we developed a plasmid stabilization strategy. This gene complementation approach shows promise for generating stable gene reporters for long-term colonization experiments.IMPORTANCEUnderstanding transcriptional regulation in Salmonella enterica Typhimurium is crucial for revealing how enteric pathogens optimize metabolism to compete with commensals in the gut. SL1344_3500, an IclR-like transcriptional regulator controlling genes linked to sugar acid metabolism, is essential for luminal growth in mouse models through gene suppression and represents a potential target for antimicrobial development. Based on these observations, we developed stable reporter plasmids that use gene complementation of SL1344_3500 to prevent plasmid loss during long-term in vivo studies.
Salmonella typhimurium↗
The Salmonella pathogenicity island 1-encoded small RNA InvR mediates post-transcriptional feedback control of the activator HilA in Salmonella.
UNLABELLED: Salmonella Pathogenicity Island 1 (SPI1) encodes a Type-3 secretion system (T3SS) essential for Salmonella invasion of intestinal epithelial cells. Many environmental and regulatory signals control SPI1 gene expression, but in most cases, the molecular mechanisms remain unclear. Many regulatory signals control SPI1 at a post-transcriptional level, and we have identified a number of small RNAs (sRNAs) that control the SPI1 regulatory circuit. The transcriptional regulator HilA activates the expression of the genes encoding the SPI1 T3SS structural and primary effector proteins. Transcription of hilA is controlled by the AraC-like proteins HilD, HilC, and RtsA. The hilA mRNA 5' untranslated region (UTR) is ~350 nucleotides in length and binds the RNA chaperone Hfq, suggesting it is a likely target for sRNA-mediated regulation. We used rGRIL-seq (reverse global sRNA target identification by ligation and sequencing) to identify sRNAs that bind to the hilA 5' UTR. The rGRIL-seq data, along with genetic analyses, demonstrate the SPI1-encoded sRNA invasion gene-associated RNA (InvR) base pairs at a site overlapping the hilA ribosome binding site. HilD and HilC activate both invR and hilA. InvR, in turn, negatively regulates the translation of the hilA mRNA. Thus, the SPI1-encoded sRNA InvR acts as a negative feedback regulator of SPI1 expression. Our results suggest that InvR acts to fine-tune SPI1 expression and prevents overactivation of hilA expression, highlighting the complexity of sRNA regulatory inputs controlling SPI1 and Salmonella virulence. IMPORTANCE: Salmonella Typhimurium infections pose a significant public health concern, leading to illnesses that range from mild gastroenteritis to severe systemic infection. Infection requires a complex apparatus that the bacterium uses to invade the intestinal epithelium. Understanding how Salmonella regulates this system is essential for addressing these infections effectively. Here, we show that the small RNA (sRNA) InvR imposes a negative feedback regulation on the expression of the invasion system. This work underscores the role of sRNAs in Salmonella's complex regulatory network, offering new insights into how these molecules contribute to bacterial adaptation and pathogenesis.
Genomic Islands↗
[An oral enteritis-vaccine composed of twelve heat inactivated Enterobacteriaceae. 1. Communication: Theoretical and epidemiological considerations (author's transl)].
The infectious diseases of the human intestinal tract which are caused by bacteria must be distinguished into two groups on account of their different pathogenesis: the cyclic infections (typhoid fever, parathyphoid fever) and the local infections (cholera, dysentery, Salmonella enteritis, dyspepsia coli infections). The local infections of the intestine do not cause a systemic but only a local immunity of the intestinal mucosa. It is necessary therefore to induce local immunity as active immunoprophylaxis by orally administering inactivated antigens. The twelve-fold enteritis vaccine consists of full antigens of 6 Salmonella strains, 2 Shigella strains, and 4 enteropathogenic coli strains pretreated by heat-inactivation (3 min/100 degrees C). The following should be considered as indication to effect active immunoprophylaxis against enteritis: Travelling into tropical and subtropical countries, people in emergency areas, children in developing countries, workers in food industries, secondary hospital infections, and carriers. The active mouse protection test revealed that oral immunization with enterobacteriaceae does not only deliver the well-known specific effect but also a non-specific effect which included the protection against other related enterobacteriaceae. Moreover, the specific component of the combined vaccine is enhanced by heterologous components. The resulting synergism or the adjuvantal effect, respectively, allows to employ a relatively limited number of germs which are selected on the basis of high pathogenicity, good immunogenicity, and great frequency. The first field trial with the twelve-fold vaccine was completed successfully: Following an infection with Salmonella which affected the employees of a fowl slaughtery, eight different species could be demonstrated; the above described polyvalent vaccine was orally administered and proved to be successful. The latter case clearly demonstrates the fast-acting effect of the vaccine on account of the heterologous bacterial antigens contained therein. 51 out of 60 Salmonella carriers excreted germs of a different antigen pattern not contained in the vaccine. However, the good results obtained showed that the species chosen for the vaccine were still sufficiently effective to cover the wide spectrum of other species of related enterobacteriaceae.
Administration, Oral↗
On the pathogenesis of typhoid fever.
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Bacterial Toxins↗
Experimental Salmonella typhimurium infection in calves.
The paper describes the clinical, bacteriological and pathological findings in experimental Salmonella typhimurium infection in calves. Oral doses of 10(8) and 10(9) organisms produced clinical disease and high mortality; doses ranging from 10(4)--10(7) organisms were less consistent in their action. Jersey calves appeared more susceptible to infection than Friesian calves. The clinical signs in most calves were pyrexia and a characteristic diarrhoea that lasted for up to 11 days; more severe symptoms were seen in the calves that received the higher doses. Following infection, all calves excreted S typhimurium in their faeces, the highest counts being observed in the calves that died. In the calves that survived, counts ranging from 10(2)--10(5)/g faeces occurred continuously for up to a maximum of 20 days and subsequent intermittent excretion occurred in a number of calves. In the calves that died, necrotic enteritis in the ileum and large intestine was the most striking lesion; lesions were uncommon in other organs. The findings are discussed in relation to the pathogenesis, diagnosis and control of the disease.
Animals↗
Typhoid fever. Studies of blood coagulation, bacteremia, and endotoxemia.
Patients with typhoid fever were studied to determine whether disseminated intravascular coagulation (DIC), circulating bacteria, and endotoxemia were responsible for the signs and symptoms of their illnesses. Coagulation tests in 28 patients detected thrombocytopenia in 17, hypofibrinogenemia in nine, and elevated titers of fibrinogen-related antigens in 20. Repeated testing during convalescence showed a return toward normal values. Intestinal bleeding, however, did not correlate with abnormalities of coagulation tests. Thus, DIC occurred commonly but appeared to be a subclinical event in these patients. In 25 patients with positive blood cultures for Salmonella typhi, quantitative cultures detected from less than 10 to 9 x 10(2) bacteria/ml. Limulus tests for endotoxin in plasma were negative in all 21 patients tested. These results indicated that the concentrations of circulating bacteria and endotoxin in typhoid fever are lower than in other Gram-negative bacterial infections and suggested that circulating bacteria and endotoxin do not play a major role in the pathogenesis of typhoid fever.
Antigens↗
[Studies on the bacterial causes of neonatal mortality in foals. Report on post-mortem findings (author's transl)].
The causes of neonatal mortality in foals were studied over a period of two years. The total number of foals studied was 121. Bacterial infection was found to be an important factor. Infection caused by A. equuli (1.6%) which previously was the most important one, has been superseded by E. coli infection (56%). E. coli infections particularly occur during the first weeks of life and, depending on the course of the disease, give rise to various pathological changes. Infections running an acute course are mainly marked by pathological changes of the lung and lymphoid organs. Infections running a subacute course are frequently associated with polyarthritis and polyserositis. Another important cause of infection during the first weeks of life is Klebsiella pneumonia (10%). The pathological changes occurring in this infection are markedly similar to those in subacute E. coli infection. Infections with Salmonella spp. (7%) mainly occur in the older foals (1-3 months) affected with polyarthritis. C. equi and streptococcal infections (11%) also mainly occur in the older foals (1-3 months). The pathological features are characterized by generalized purulent lesions in various organs. In spite of the fact that post-mortem findings suggested septicaemia, bacteriological examination was negative in 12% of the foals. The discussion is concerned with an assessment of the relationship between the pathomorphological findings and the pathogenesis of the various infections.
Actinobacillosis↗
Renal disease in hepatosplenic schistosomiasis: a clinicopathological study.
Thirty-nine cases of hepatosplenic schistosomiasis associated with renal disease are included. They were investigated for renal function, serum and urinary immunoglobulins, some serological tests, and bacteriological studies for evidence of associated salmonellosis. Renal biopsy was obtained from 23 subjects and studied by light microscopy. It was possible to distinguish two groups of cases "salmonella-negative" and "salmonella-positive". The former group was characterized by marked glomerular lesions, mainly membrano-proliferative, in different phases of evolution. Salmonella-positive cases were categorized into those with clinical, laboratory and histological evidence of interstitial nephropathy (six cases), that seems to result from salmonella pyelonephritis; and those with overt glomerular lesions (17 cases). The latter group differed from salmonella-negative cases in having mainly proliferative glomerular lesions with minimal or no basement membrane thickening; the lesions were diffuse and appeared in the same stage of evolution. The possible relation of schistosomiasis and associated salmonellosis to the pathogenesis of these lesions is discussed, suggesting an immunological basis for the glomerular injury and outlining the possible significance of hepatic fibrosis.
Adolescent↗