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Medical Microbiology. Salmonellosis ranges clinically from the common Salmonella gastroenteritis diarrhea, abdominal cramps, and fever to enteric fevers including typhoid fever which are life-threatening febrile systemic illness requiring prompt antibiotic therapy.
Focal infections and an asymptomatic carrier state occur. The most common form of salmonellosis is a self-limited, uncomplicated gastroenteritis. Salmonella species are Gram-negative, flagellated facultatively anaerobic bacilli characterized by O, H, and Vi antigens. There are over known serovars which current classification considers to be separate species.
Pathogenic salmonellae ingested in food survive passage through the gastric acid barrier and invade the mucosa of the small and large intestine and produce toxins.
Invasion of epithelial cells stimulates the release of proinflammatory cytokines which induce an inflammatory reaction. The acute inflammatory response causes diarrhea and may lead to ulceration and destruction of the mucosa. The bacteria can disseminate from the intestines to cause systemic disease.
Both nonspecific and specific host defenses are active. Non-specific defenses consist of gastric acidity, intestinal mucus, intestinal motility peristalsis , lactoferrin, and lysozyme.
Specific defenses consist of mucosal and systemic antibodies and genetic resistance to invasion. Various factors affect susceptibility. Non-typhoidal salmonellosis is a worldwide disease of humans and animals.
Animals are the main reservoir, and the disease is usually food borne, although it can be spread from person to person. The salmonellae that cause Typhoid fever and other enteric fevers spread mainly from person-to-person via the fecal-oral route and have no significant animal reservoirs. Salmonellosis should be considered in any acute diarrheal or febrile illness without obvious cause.
The diagnosis is confirmed by isolating the organisms from clinical specimens stool or blood. Effective vaccines exist for typhoid fever but not for non-typhoidal salmonellosis. Those diseases are controlled by hygienic slaughtering practices and thorough cooking and refrigeration of food.
Salmonellae are ubiquitous human and animal pathogens, and salmonellosis, a disease that affects an estimated 2 million Americans each year, is common throughout the world. Salmonellosis in humans usually takes the form of a self-limiting food poisoning gastroenteritis , but occasionally manifests as a serious systemic infection enteric fever which requires prompt antibiotic treatment.
In addition, salmonellosis causes substantial losses of livestock. Some infectious disease texts recognize three clinical forms of salmonellosis: 1 gastroenteritis, 2 septicemia, and 3 enteric fevers. This chapter focuses on the two extremes of the clinical spectrum—gastroenteritis and enteric fever. The septicemic form of salmonella infection can be an intermediate stage of infection in which the patient is not experiencing intestinal symptoms and the bacteria cannot be isolated from fecal specimens.
The severity of the infection and whether it remains localized in the intestine or disseminates to the bloodstream may depend on the resistance of the patient and the virulence of the Salmonella isolate. The incubation period for Salmonella gastroenteritis food poisoning depends on the dose of bacteria.
Symptoms usually begin 6 to 48 hours after ingestion of contaminated food or water and usually take the form of nausea, vomiting, diarrhea, and abdominal pain. Myalgia and headache are common; however, the cardinal manifestation is diarrhea. At least two-thirds of patients complain of abdominal cramps. The duration of fever and diarrhea varies, but is usually 2 to 7 days. Enteric fevers are severe systemic forms of salmonellosis. The best studied enteric fever is typhoid fever, the form caused by S typhi , but any species of Salmonella may cause this type of disease.
The symptoms begin after an incubation period of 10 to 14 days. Enteric fevers may be preceded by gastroenteritis, which usually resolves before the onset of systemic disease. The symptoms of enteric fevers are nonspecific and include fever, anorexia, headache, myalgias, and constipation.
Enteric fevers are severe infections and may be fatal if antibiotics are not promptly administered. Salmonellae are Gram-negative, flagellated, facultatively anaerobic bacilli possessing three major antigens: H or flagellar antigen; O or somatic antigen; and Vi antigen possessed by only a few serovars.
H antigen may occur in either or both of two forms, called phase 1 and phase 2. The organisms tend to change from one phase to the other. O antigens occur on the surface of the outer membrane and are determined by specific sugar sequences on the cell surface. Vi antigen is a superficial antigen overlying the O antigen; it is present in a few serovars, the most important being S typhi.
Antigenic analysis of salmonellae by using specific antisera offers clinical and epidemiological advantages. Determination of antigenic structure permits one to identify the organisms clinically and assign them to one of nine serogroups A-I , each containing many serovars Table 1. H antigen also provides a useful epidemiologic tool with which to determine the source of infection and its mode of spread.
As with other Gram-negative bacilli, the cell envelope of salmonellae contains a complex lipopolysaccharide LPS structure that is liberated on lysis of the cell and, to some extent, during culture. The lipopolysaccharide moiety may function as an endotoxin, and may be important in determining virulence of the organisms. This macromolecular endotoxin complex consists of three components, an outer O-polysaccharide coat, a middle portion the R core , and an inner lipid A coat.
Lipopolysaccharide structure is important for several reasons.
SALMONELLA TYPHI AND PARATYPHI -- STRUCTURE, SYMPTOMS, TREATMENT, LIFE CYCLE -- BY PHANINDRA GUPTHA
First, the nature of the repeating sugar units in the outer O-polysaccharide chains is responsible for O antigen specificity; it may also help determine the virulence of the organism. Salmonellae lacking the complete sequence of O-sugar repeat units are called rough because of the rough appearance of the colonies; they are usually avirulent or less virulent than the smooth strains which possess a full complement of O-sugar repeat units.
Second, antibodies directed against the R core common enterobacterial antigen may protect against infection by a wide variety of Gram-negative bacteria sharing a common core structure or may moderate their lethal effects.
Third, the endotoxin component of the cell wall may play an important role in the pathogenesis of many clinical manifestations of Gram-negative infections. Endotoxins evoke fever, activate the serum complement, kinin, and clotting systems, depress myocardial function, and alter lymphocyte function.
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Circulating endotoxin may be responsible in part for many of the manifestations of septic shock that can occur in systemic infections. Salmonellosis includes several syndromes gastroenteritis, enteric fevers, septicemia, focal infections, and an asymptomatic carrier state Fig.
Particular serovars show a strong propensity to produce a particular syndrome S typhi , S paratyphi-A , and S schottmuelleri produce enteric fever; S choleraesuis produces septicemia or focal infections; S typhimurium and S enteritidis produce gastroenteritis ; however, on occasion, any serotype can produce any of the syndromes.
In general, more serious infections occur in infants, in adults over the age of 50, and in subjects with debilitating illnesses. Most non-typhoidal salmonellae enter the body when contaminated food is ingested Fig. Person-to-person spread of salmonellae also occurs. To be fully pathogenic, salmonellae must possess a variety of attributes called virulence factors. These include 1 the ability to invade cells, 2 a complete lipopolysaccharide coat, 3 the ability to replicate intracellularly, and 4 possibly the elaboration of toxin s.
After ingestion, the organisms colonize the ileum and colon, invade the intestinal epithelium, and proliferate within the epithelium and lymphoid follicles.
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The mechanism by which salmonellae invade the epithelium is partially understood and involves an initial binding to specific receptors on the epithelial cell surface followed by invasion. Invasion is dependent on rearrangement of the cell cytoskeleton and probably involves increases in cellular inositol phosphate and calcium. Attachment and invasion are under distinct genetic control and involve multiple genes in both chromosomes and plasmids.
Scheme of the Pathogenesis of Salmonella enterocolitis and diarrhea. After invading the epithelium, the organisms multiply intracellularly and then spread to mesenteric lymph nodes and throughout the body via the systemic circulation; they are taken up by the reticuloendothelial cells. The reticuloendothelial system confines and controls spread of the organism.
However, depending on the serotype and the effectiveness of the host defenses against that serotype, some organisms may infect the liver, spleen, gallbladder, bones, meninges, and other organs Fig. Fortunately, most serovars are killed promptly in extraintestinal sites, and the most common human Salmonella infection, gastroenteritis, remains confined to the intestine. After invading the intestine, most salmonellae induce an acute inflammatory response, which can cause ulceration.
They may elaborate cytotoxins that inhibit protein synthesis. Whether these cytotoxins contribute to the inflammatory response or to ulceration is not known.
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These evoke an acute inflammatory response and may also be responsible for damage to the intestine. Because of the intestinal inflammatory reaction, symptoms of inflammation such as fever, chills, abdominal pain, leukocytosis, and diarrhea are common.
The stools may contain polymorphonuclear leukocytes, blood, and mucus. Much is now known about the mechanisms of Salmonella gastroenteritis and diarrhea. Figures 2 and 3 summarize the pathogenesis of Salmonella enterocolitis and diarrhea. Only strains that penetrate the intestinal mucosa are associated with the appearance of an acute inflammatory reaction and diarrhea Fig. The mechanisms of secretion are unclear, but the secretion is not merely a manifestation of tissue destruction and ulceration.
Salmonella penetrate the intestinal epithelial cells but, unlike Shigella and invasive E.
Novel Structure and Function of Typhoid Toxin
Thus, the extent of intercellular spread and ulceration of the epithelium is minimal. Salmonella escape from the basal side of epithelial cells into the lamina propria. Systemic spread of the organisms can occur, giving rise to enteric fever.
Invasion of the intestinal mucosa is followed by activation of mucosal adenylate cyclase; the resultant increase in cyclic AMP induces secretion. The mechanism by which adenylate cyclase is stimulated is not understood; it may involve local production of prostaglandins or other components of the inflammatory reaction.
In addition, Salmonella strains elaborate one or more enterotoxin-like substances which may stimulate intestinal secretion. However, the precise role of these toxins in the pathogenesis of Salmonella enterocolitis and diarrhea has not been established.
Electron photomicrograph demonstrating invasion of guinea pig ileal epithelial cells by Salmonella typhimurium. Arrows point to invading Salmonella organisms. Various host defenses are important in resisting intestinal colonization and invasion by Salmonella Table 2.
In healthy individuals, the number of ingested salmonellae is reduced in the stomach, so that fewer or no organisms enter the intestine. Normal small intestinal motility also protects the bowel by sweeping ingested salmonellae through quickly.
The normal intestinal microflora protects against salmonellae, probably through anaerobes, which liberate short-chain fatty acids that are thought to be toxic to salmonellae.