The term enteric fever is frequently used to include typhoid and the paratyphoid fevers caused by salmonella typhi and salmonella paratyphi A,B or C: typhoid fever is sometime confused with typhus fever.
Typhoid and the paratyphoid fevers are clinically similar and the assumption that cases of typhoid fever are invariably more severe is not always true. Also the gross pathology of the enteric fevers is similar regardless of the casual organism and only bacteriological examination can differentiate between them.
The genus salmonella to which the enteric fever pathogens belong comprise more than 100 serotypes and unlike other salmonellae, which are primarily parasites of animals other than man, salmonella typhi and it other species, the three paratyphoid bacilli are essentially parasites of man.
When stained by Gram’s Method, members of the genus salmonella are indistinguishable from Enterobacteriaceae to which they belong. Salmonellae are motile and non-capsulate: culturally they are similar to most other enterobacteria except that on MacConkey or DCA medium they form non-lactose-fermenting colonies after incubation for 18-24 hours; on such differential media their colonies are pale-colored and similar to those of the other common pathogenic genus, Shigella.
Differentiation of salmonellae from Shigellae is a fairly straightforward matter; but to identify a member of the genus salmonella and give it serotype status is time-consuming although necessary for epidemiological purposes. The particular isolate must first have its Somatic (O) antigens and then its serotype within the particular group is determined by identifying its flagellar antigens. Strains of salmonella typhi, salmonella paratyphi A and B and salmonella typhimurium.
PATHOGENESIS OF SALMONELLA
Natural infection in the enteric fevers is most often by ingestion followed by penetration through the mucous membrane of the small intestine; possibly the bacilli sometimes enter through the pharyngeal mucosa. From the results of observations on experimental salmonella infections it appears that the bacilli attach to the epithelial cells of the intestinal villi and induce their own intake into the cells by the a process akin to phagocytosis. They pass through the cells and within 24 hour are found in the lamina propria and submucosa where they are rapidly phagocytosed by polymorphs and macrophages. The pathogenicity of the salmonellae appears to depend primarily on their ability to remain alive and to multiply the phagpcytes, which they may then kill and thus escape. From the submucosa of the small intestine the organisms pass via the lymphatics to the mesenteric lymph nodes, whence after a period of multiplication they invade the bloodstream via thoracic duct; the liver, gallbladder, spleen, kidney and bone-marrow become infected during this primary bacteriaemic phase in the first 7-10 days of the incubation period.
After multiplication in these organs, bacilli pass into the blood, causing a secondary and heavier bacteriaemia. The onset of which approximately coincides with that of the pyrexia and other signs of clinical illness. From the gallbladder a further invasion of the intestine results and lymphoid tissue – peyer’s patches and lymphoid follicles - is particularly involved in an inflammatory reaction and infiltration with mononuclear cells, followed by necroisis, sloughing and the formation of characteristic typhoid ulcers. Haemorrhage of varying degree may occur and less frequently, perforation through a necrotic Peyer’s patch may complicate the illness. Fever and illness continues for 3-4 weeks.
As well as being present in the blood, salmonellae are present in large numbers in the infected organs, in the ulcers and are found in the intestinal contents and the faeces. As a consequence of their dissemination in the bloodstream, the bacilli may localize in the kidney and appear in the urine, sometimes producing a marked bacilluria. Salmonellae may also infect other tissues and produce such occasional complications or sequelae of enteric acute suppurative periosteitis and osteitis, abscess of kidney, acute cholesystitis, bronchopneumonia, empyema and ulcerative endocarditis.
In 2-5% of convalescents from typhoid fever and in a smaller number of those who have recovered from paratyphoid fever the salmonellae persist in the body for over a year and many of these persons continue to be carriers for the remainder of their life. In such chronic carriers, the bacilli are most commonly present in the gallbladder, or rarely in the urinary tract, and are excreted in the faeces or urine. The long duration of the carrier state enables the enteric fever bacilli to survive in the community at non-epidemic times and to persist in small, relatively isolated, communities or to infect families.
The pathogenicity of salmonellae primarily depends upon the ability of the bacilli to survive and grow inside phagocytes and on the toxicity of their lipopolusaccharides endotoxin, which is associated with O antigen, the typhoid and paratyphoid C bacilli have an additional aggressive factor in the possession of a microcapsule consisting of a glycolipid called the virulence (Vi) antigen. This Vi substance appears to protect the bacillus against the lytic action of antibody and complement and to impede phagocytosis to some extent.