Members of the genus Salmonella produce significant infections in humans and in certain animals. Salmonella organisms are gram-negative, facultatively anaerobic rods that morphologically resemble other enteric bacteria. On selective and differential media used primarily to isolate enteric pathogens, salmonellae produce clear, colorless, nonlactose-fermenting colonies;
colonies with black centers are seen if the media contain indicators for hydrogen sulfide production.cyanide.
Previously the genus Salmonella comprised three biochemically discrete species: S. enteritidis, S.
choleraesuis, and S. typhi. Genetic studies have shown, however, that bacterial species in the genus Salmonella are very closely related and that only two species, S. enterica (the type species of the genus) and S. bongori should be designated. A recently published Taxonomic Note by Tindall et at. and an opinion issued from the Judicial Commission of the International Committee on the Systematics of the Prokaryotes in 2005 both clearly support this two-species designation and have placed nearly all former species as serotypes below the level of S. enterica subsp. enterica (e.g., S. enterica subsp.
enterica serotype Typhi). This is often more simply written as Salmonella Typhi. Table 20-8 shows the characteristic features of Salmonella serotype Typhi, Salmonella serotype Choleraesuis, and Salmonella serotype Paratyphi.
Many Salmonella serotypes are usually found in cold-blooded animals as well as in rodents and birds,
which serve as their natural hosts. Members of the former genus Arizona, now a subspecies of S. enterica, are found in infections with symptoms identical to those of Salmonella infections and may be transmitted to humans from pet turtles, snakes, and fish
Factors responsible for the virulence of salmonellae have been the subject of speculation and still remain uncertain. The role of fimbriae in adherence in initiating intestinal infection has been cited. It is apparent that fimbriated strains appear more virulent than nonfimbriated strains. Another factor that contributes to the virulence of salmonellae is their ability to traverse intestinal mucosa. Specific factors that mediate this mechanism have not been established. Lastly, enterotoxin produced by certain Salmonella strains that cause gastroenteritis has been implicated as a significant virulence factor.
Salmonellae possess antigens similar to those of other enterobacteria. The somatic 0 antigens and flagellar H
antigens are the primary antigenic structures used in serologic grouping of salmonellae. A few strains may possess capsular K surface antigens, designated Vi antigen. The serologic identification of the Vi antigen is important in identifying Salmonella serotype TyphL Figure 20-8 shows the antigenic structures used in
serologic grouping and their locations.
The heat-stable 0 antigen of salmonellae, as is the case with other enteric bacteria, is the lipopolysaccharide
(LPS) located in the outer membrane of the cell wall. Many different 0 antigens are present among the subspecies of Salmonella; more than one 0 antigen may also be found in a particular strain. The 0 antigens are designated by Arabic numbers.
Unlike the 0 antigens, flagellar antigen proteins are heat labile. The H antigens of salmonellae occur in one of two phases: phase 1, the specific phase; and phase 2, the nonspecific phase. Phase 1 flagellar antigens occur
only in a small number of serotypes and determine the immunologic identity of the particular serotype. Phase
۱ antigens agglutinate only with homologous antisera.
Phase 2 flagellar antigens, on the other hand, occur among several strains. Shared by numerous serotypes,
phase 2 antigens react with heterologous antisera.
The heat-labile Vi (coined from the term virulence) antigen is a surface polysaccharide capsular antigen found in Salmonella serotype Typhi and a few strains of Salmonella serotype Choleraesuis. The capsular antigen plays a significant role in preventing phagocytosis of the organism. The Vi antigen often blocks the 0 antigen during serologic typing but may be removed by heating.
One of the most common forms of “food poisoning,” GI infection caused by salmonellae results from the ingestion of the organisms through contaminated food. The Salmonella strains associated with this infection are usually those found in animals; most such strains in the United States belong to the former designation S. enteritidis, now considered a heterotypic synonym for S. enterica subsp. enterica. Consequently the source of
the infection has been attributed primarily to poultry, milk, eggs, and egg products as well as to handling pets.
Insufficiently cooked eggs and domestic fowl, such as chicken, turkey, and duck, are common sources of
Cooking utensils such as knives, pans, and cutting boards used in preparing the contaminated meat can spread the contamination to other food. Direct transmission from person to person has been reported in
institutions. Salmonella gastroenteritis, also referred to as food poisoning, occurs when a sufficient number of organisms contaminate food that is maintained under inadequate refrigeration, thus allowing growth
and multiplication of the organisms. The infective dose necessary to initiate the disease is higher than that required for shigellosis. Approximately 106 bacteria may initiate infection, but infections resulting
from lower infective doses have been reported.
The symptoms of intestinal salmonellosis, which may appear 8 to 36 hours after ingestion of contaminated food, include nausea, vomiting, fever, and chills, accompanied by watery diarrhea and abdominal pain.
The role of enterotoxins in the pathogenesis of Salmonella infection remains unclear. Most cases of Salmonella gastroenteritis are self-limiting. Symptoms usually disappear within a few days, with few or no complications.
Those who suffer from sickle cell disease and other hemolytic disorders, ulcerative colitis, and malignancy seem to be more susceptible to salmonellae infection. The infection may be more severe in very young patients, elderly patients, and those suffering from other underlying disease. Dissemination may occasionally occur; in such cases, antimicrobial therapy is required.
The antimicrobials of choice include chloramphenicol, ampicillin, and trimethoprim sulfamethoxazole. Nevertheless, susceptibility testing must be performed.
However, antimicrobial therapy is usually not indicated in uncomplicated cases. Antimicrobial therapy is believed to prolong the carrier state. Antidiarrheal agents are also restricted in cases of salmonellosis because these agents may encourage adherence and further invasion. In cases of dehydration, fluid replacement therapy may be indicated .
The clinical features of enteric fevers include the following:
· Involvement of the reticuloendothelial system, particularly the liver, spleen, intestines, and
·Dissemination to multiple organs
Enteric fever caused by Salmonella serotype Typhi has been known as typhoid fever, a febrile disease that results from the ingestion of food contaminated with the organisms originating from infected individuals or carriers. Salmonella serotype Typhi does not have a known animal reservoir; humans are the only source of infection. Other enteric fevers include paratyphoid fevers, which may be due to Salmonella serotype Paratyphi and Salmonella serotype Choleraesuis. The clinical manifestations of paratyphoid fevers are similar to those of typhoid fever but are less severe, and the fatality rate is lower.
Typhoid fever occurs more often in tropical and subtropical countries, where foreign travelers are
more likely to acquire the infection. Improper disposal of sewage, poor sanitation, and lack of a modern water system have caused outbreaks of typhoid fever when the organisms reach a water source. This is uncommon in the United States and other developed countries, where water is purified and treated and handling of wastes is greatly improved. Carriers, particularly food handlers, are important sources of infection anywhere in the world. Direct transmission through fomites is also possible. Laboratory workers in the microbiology laboratory have contacted typhoid fever while working with the organisms.
Typhoid fever develops approximately 9 to 14 days after ingestion of the organisms. The onset of symptoms depends on the number of organisms ingested;
the larger the inoculum, the shorter the incubation period. Characteristically, during the first week of the disease, the patient develops a fever, accompanied by malaise, anorexia, lethargy, myalgia, and a continuous dull frontal headache.
When the organisms are ingested, they seem to be resistant to gastric acids and, on reaching the proximal end of the small intestine, subsequently invade and penetrate the intestinal mucosa. At this time, the patient experiences constipation rather than diarrhea.
The organisms gain entrance into the lymphatic system and are sustained in the mesenteric lymph nodes.
They eventually reach the bloodstream and are further spread to the liver, spleen, and bone marrow, where they are immediately engulfed by mononuclear phagocytes.
The organisms multiply intracellularly; later they are released into the bloodstream for the second time.
The febrile episode becomes more evident during this release of the organisms into the circulatory system. At this time, the organisms may easily be isolated from the blood. Figure 20-9shows the course of typhoid fever.
During the second and third weeks of the disease, the patient experiences sustained fever with prolonged bacteremia. The organisms invade the gallbladder and Peyer’s patches of the bowel. They also reach the intestinal tract via the biliary tract. “Rose spots” (blanching, rose-colored papules around the periumbilical region) appear during the second week of fever.
Involvement of biliary system sites initiates GI symptoms as the organisms reinfect the intestinal tract.
The organism now exists in large numbers in the bowel and may be isolated from the stool. The gallbladder
becomes the foci of long-term carriage of the organism, occasionally reseeding the intestinal tract and shedding
the organisms in the feces. Necrosis in the gallbladder leading to necrotizing cholecystitis and necrosis of the
Peyer’s patches leading to hemorrhage and perforation of the bowel may occur as serious complications.
Pneumonia and thrombophlebitis are other complications that occur in typhoid fever as well as meningitis,
osteomyelitis, endocarditis, and abscesses.
Salmonella bacteremia, with and without extraintestinal foci of infection caused by nontyphoidal Salmonella, is
characterized primarily by prolonged fever and intermittent bacteremia. The most commonly associated
serotypes of Salmonella are Typhimurium, Paratyphi, and Choleraesuis. Salmonella infection has been observed
among two different groups: (1) young children, who experience fever and gastroenteritis with brief episodes of bacteremia and (2) adults, who experience transient bacteremia during episodes of gastroenteritis or develop symptoms of septicemia without gastroenteritis.
The latter manifestations were observed among patients who had underlying illnesses, such as malignancies and liver disease. The risk of metastatic complications could be more severe than the bacteremia itself, even in individuals who do not have underlying diseases. Cases of septic arthritis may also occur in patients who had asymptomatic salmonellosis.
Individuals who recover from infection may harbor the organisms in the gallbladder, which becomes the site of chronic carriage. Such individuals excrete the organisms in their feces either continuously or intermittently;
nevertheless, they become an important source of infection for susceptible persons. The carrier state may be terminated by antimicrobial therapy if gallbladder infection is not evident. Otherwise, cholecystectomy has been the only solution to the chronic state of enteric carriers