Salmonella Organisms Produce Gastrointestinal Illnesses In Humans Contamination Biology Essay

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Salmonella organisms produce gastrointestinal illnesses in humans. Salmonella species inhabit the gastrointestinal tract of animals. Humans acquire the infection by ingesting the organisms in contaminated animal food products or insufficiently cooked poultry, milk, eggs, and dairy products. Other salmonella species are found only in humans, and infections are transmitted by human carriers.

Members of the genus salmonella produce significant infections in humans and certain animals. Salmonella organisms are gram negative , facltiveley anaerobic rod that morphologically resemble other enteric bacteria. On selective and deferential media used primarily to isolate enteric pathogens, salmonellae produce clear, colorless, non-lactose fermenting colonies; colonies with black centers are seen if the media contain indicators for hydrogen sulfide production.

The biochemical features for the genus enclude the folloing:

In almost every case they do not ferment lactose .

They are negative for endol, the voges-proskauer test, phenylalanine, and urease.

Most produce hydrogen sulfide on triple sugar iron agar.

They do not grow in potassium cyanide.


Until recently , the genus salmonella , alarge and complex group of organisms, comprised three biochemical descrete species: salmonella enteriotidis, salmonella choleraesuis, and salmonella typhi. Geneticus studies have shown, a whever, that bacterial species in the genus salmoneela are very closely related and that only one species, Salmonella enterica , must be designated . additional changes in the salmonella classification include the classification of the genus into seven subgroups with designated subspecies. Subgroup I include species that cause infections in humans. Members of subgroup I have very similar biochemical characteristics with the exception of S.typhi, S. choleraesuis, and S. paratyphi. These bacterial species are less active biochemically and are the most serious pathogens for humans, causing entric fever.

Table 16.7 shows the charectarestics feature of S.typhi, S. choleraesuis, and S. paratyphi.

Table 16.8 shows the seven salmonella subgroups.

Species in subgroup II, III, IV are usually found in cold-blooded animals, as well as in rodents and birds, which serve as their natural host. In addition to these changes, Arizona, which used to belong to its own genus, has become a member of the genus salmonella and has been reclassified into subgroup III . Arizona infection may cause symptoms identical to those of salmonella infection and may be transmitted to humans from pet turtles, snakes, and fish.

Virulence factors:

Factors responsible for the virulence of salmonella 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 that nonfimberated strains. Another factor that contribute to the invasiveness of salmonellae is their ability to traverse intestinal mucosa. Specific factors that mediate this mechanism have not been established. Last , enterotoxin produced by certain salmonellae strains that cause gastroenteritis has been implicated as a significant virulence factor.

Antigenic structures:

Salmonellae possess antigens similar to those of other enterobacteria. The somatic O antigens and falgellar H antigens are the primary antigenic structures used in serological grouping of salmonellae. A few strains may possess capsular K surface antigens, designated as Vi antigen. The serologic identification of the Vi antigen is important in identifying S.typhi. the heat â€"stable O antigen of salmonellae as the case with other entric bacteria, is the lipopolysaccharide (LPS) located in the outer membrane of the cell wall . there are many different O antigen present among the subspecies of salmonella; more than one O antigen may also be found in a particular strain. The O antigens are designated by Arabic numbers . unlike the O antigens, falgellar antegins are proteins that are heat-labile and are treatable with ethanol or acid . the H antigens of salmonellae may occur in two phases : pahse 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 1 antigens agglutinate only with homologous and antisera. Phase 2 flagellar antigens , on the other hand , occur among several strains. Shared by numerous serotypes, phase2 antigens react with heterologous antisera. The heat- labile Vi (coined from the term virulence ) antigen is a surface polysaccharide capsular antigen found in S.typhi and a few other strains of salmonella subgroup I. the capsular antigen plays a significant role in preventing phagocytosis of the organism. The Vi antigen most often blocks the O antigen during serological typing but maybe removed by heating.

Clinical infections:

In humans , salmonellosis may occur in several forms :

An acute gastroenteritis or food poisoning characterized by vomiting and diarrhea

Typhoid fever , the most sever form of entric fever , caused by S.thphi; other entric fevers are caused by other salmonella serotypes (i.e. , salmonella paratyphi, , S. choleraesuis)

Nontyphoidal bacteremia

Carrier states that follows salmonella infections.\

Humans acquire the infection by ingesting the organisms in food, water, and milk contaminated with human or human excerta. With the exception of S.typhi ans S.paratyphi, salmonellae infect various animals that serve as reservoirs, and sources of human infections. S.typhi and S.paratyphi have no known animal reservoirs, and infections seem to occur only in humans. Carriers are often the source of infection.

Salmonella gastroenteritis

One of the most common forms of "food poisoning ," gastrointestinal infection caused by salmonella results from the ingestion of the organisms through contaminated food. The salmonella strains associated with this infection are usually those found in animals; most in the United states belong to the serotypes of salmonella enteritidis. Consequently, the source of the infection has been attributed primaly 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 infection.

Cooking utensils such as knives, pans, 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, although 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 requied for shigellosis. Approximately 10^6 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 disappear usually within a few days, with little or no complication. Those who suffer from sickle cell disease and other hemolytic disorders, ulcerative colitis, and malignancy seem to be more susceptible to salmonellal infection. The infection may be more sever in the very young, the elderly, and those suffering from other underlying disease. Antimicrobial therapy is usually not indicated in in uncomplicated cases. Antimicrobial therapy is believed to prolong the carrier state. Antimicrobial agents are also restricted in cases of salmonellosis, as these agents may encourage adherence and further invasion. In case of dehydration, fluid replacement therapy may be indicated.

Dissemination may occasionally occur ; in such cases, antimicrobial therapy is required. The antimicrobial of choice include chloramphenicol, ampicillin, and trimethoprim-sulfamethoxazole. Nevertheless, susceptibility testing must be performed.


The clinical features of enteric fevers include the following:

Prolonged fever


Involvement of the reticuloendothelial system, particularly the liver, spleen , and intestines, and mesentery.

Dissemination to multiple organs

Enteric fever caused by S. 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. S.typhi doesn't have known animal reservoir; therefore humans are they only source of infection. Other enteric fevers include parathyroid fevers, which may be due to S.paratyphi serovar A, another strict human pathogen; S. paratyphi serovar B; and S. paratyphi serovar C. Other serovars that have been implicated in cases of septicemia in humans are those of S. choleraesuis. The clinical manifestations of parathyroid fevers are similar to those of typhoid fever but are less sever, and the fatality rate is lower. Therefore, the clinical features of typhoid fever are discussed here in greater details.

Typhoid fever occurs more often in tropical and subtropical countries, where foreign travelers easily acquire the infection. Improper disposal of sewage, poor sanitation, and lack of modern watery system have caused outbreaks of typhoid fever when the organisms reach a water source. This is uncommon in the United States and other developed countried, where water is purified and treated and handling of wastes is greatly improved. Pasteurization of milk has also diminished the incidence of waterborne typhoid in industrialized countries. 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 following 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 disease, the patient develops 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 poatient 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 blood stream and are further spread to the liver, spleen, and boon marrow, where they are immediately engulfed by mononuclear phagocytes. The organisms multiply intracellularly; later, they are released into the blood stream 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 16-8 shows the course of typhoid fever.

During the second and third weeks of the disease, the patient experiences sustained fever with the 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 initiate gastrointestinal symptoms as the organisms reinfect the intestinal tract. The organism now exists in large numbers and may be isolated from the stool. The gallbladder becomes the foci of the long-term carriage of the organisms, 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

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 salmonella typhmurium, S. paratyphi A and B, and S. choleraesuis.

Salmonella infection has been observed among two different groups of population: (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 disease. Cases of septic arthritis may also occur in patients who had asymptomatic salmonellosis.

Carrier state

Individuals who recover from the 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.

Serologic grouping

Once an isolate is biochemically identified as salmonella sp., serologic grouping of the isolate for the O serogroups (somatic antigen) must be performed for confirmation.

Based in the common O antigens, salmonella may be placed into major groups designated by capital; letters. Approximately 60 O antigenic groups exist; however, 98% of salmonella isolates from humans belong to serogroups A through G.

Laboratories may report isolates as salmonella group

(A-G) when specific serotyping is not available; isolates may be sent to a reference laboratory for serotyping. If an isolate is suspected of being one of these three serotypes, S.typhi, S. Choleraesuis, or S. paratyphi A, because of its medical implications, it must be biochemically identified and serologically confirmed. Their identification is very important in providing proper therapy for the patient and in limiting any possible complications that may develop. Measures may also be taken to prevent an epidemic outbreak.

It is imperative for any laboratory performing bacteriology to be able to serologically identify S.typhi, particularly, and other members of salmonella in O groups A through G. other isolates can be identified as "biochemically compatible with salmonella" and submitted to a reference laboratory for further testing.

To perform serologic grouping by slide technique, first prepare a saline emulsion from a pure culture of the organism. Serologic typing is best performed on a colony taken from a pure culture growing in nonselective media, such as blood agar plate, although TSI or macConley agar can be used for presumptive serologic identification. A slide with wells is easy to use for the agglutination test. A regular microscope slide may be used by marking separate squares with a wax pencil. The laboratory professional places one drop of antisera on the appropriately labeled slide. One drop of bacterial emulsion is added to each drop of antisera. Antisera Kits usually consist of a polyvalent A through G, Vi, and serogroups A, B, C1, C2, D, E, and G. In the event of a positive agglutination in the Vi antisera with no agglutination in the other groups, the emulsion should be heated to 100 C for 10 minutes to inactivate the capsular Vi antigen. The emulsion is then cooled and retested with antisera A to G. If the organism agglutinates with the group D antisera, it can be reported as S.typhi. larger laboratories usually maintain antisera to serotype salmonellae for all the somatic types. H antigen or flagella typing is usually performed in a reference laboratory that provides epidemiologic information of the common source in outbreaks.

Yellow book


More than any other genus , salmonella has been a favorite of those who love of subdividing and apply names to biological systems. At one time, there were over 2000 names for various members of this genus, often reflecting colorful aspect of place or circumstances of the original isolation (eg, S. Budapest, S. Seminole, S. tamale, S. oysterbeds). This has now been reduced to a single species, salmonella enterica, with with the previous species names relegated to the status of serotypes.