surface can resist microbicidal activities and potentially alter host

SALMONELLOSIS cell signaling.

Ref: Harrison’s Principles of Internal Medicine (20th edition)
Baifailah M. Mangandog (Class 2023)
 Once phagocytosed, typhoidal salmonellae disseminate
throughout the body in macrophages via the lymphatics and
 Salmonella typhi and Salmonella paratyphi is restricted to human
colonize reticuloendothelial tissues (liver, spleen, lymph nodes,
hosts, in whom these organisms cause enteric (typhoid) fever.
and bone marrow). Patients have relatively few or no signs and
 Nontyphoidal Salmonella - can colonize the gastrointestinal symptoms during this initial incubation stage. Signs and
tracts of a broad range of animals, including mammals, reptiles,
symptoms, including fever and abdominal pain, probably result
birds, and insects
from secretion of cytokines by macrophages and epithelial cells
in response to bacterial products that are recognized by innate
immune receptors when a critical number of organisms have
ETIOLOGY replicated. Over time, the development of hepatosplenomegaly
is likely to be related to the recruitment of mononuclear cells and
It is a gram-negative bacilli within the family Enterobacteriaceae the development of a specific acquired cell-mediated immune
consists of two species: response to S. typhi colonization. The recruitment of additional
 S. enterica- contains all serotypes pathogenic for humanns mononuclear cells and lymphocytes to Peyer’s patches during the
several weeks after initial colonization/infection can result in
marked enlargement and necrosis of the Peyer’s patches, which
Serotyping is based on the:
may be mediated by bacterial products that promote cell death
 somatic O antigen (lipopolysaccharide cell wall components) as well as the inflammatory response.
 Surface Vi antigen (restricted to S. typhi and S. paratyphi C)
 Flagellar H antigen
 In contrast to enteric fever, NTS gastroenteritis is characterized
by massive polymorphonuclear leukocyte infiltration into both
Salmonella the large- and small-bowel mucosa. This response appears to
-lives in intestinal tract of warm and cold blooded animals depend on the induction of interleukin 8, a strong neutrophil
-gram negative chemotactic factor, which is secreted by intestinal cells as a
-non spore forming result of Salmonella colonization and translocation of bacterial
-facultative anaerobic bacteria proteins into host cell cytoplasm. The degranulation and release
-measure 2-2 micrometer by 0.4-.06 micrometer of toxic substances by neutrophils may result in damage to the
-orally ingested salmonallae survive at low pH of stomach and evade intestinal mucosa, causing the inflammatory diarrhea observed
multiple defenses of small intestine to gain access to epithelium. with nontyphoidal gastroenteritis. An additional important factor
- produce acid on glucose fermentation, reduces nitrates and do not in the persistence of nontyphoidal salmonellae in the intestinal
produce cytochrome oxidase tract and the organisms’ capacity to compete with endogenous
-all Salmonella except Salmonella Gallinarum-Pullorum are motile by flora is the ability to utilize the sulfur-containing compound
means of peritrichous flagella and all but S. Typhi produce gas (H2S) on tetrathionate for metabolism in a microaerophilic environment.
sugar fermentation. In the presence of intestinal inflammation, tetrathionate is
-Molecular typing methods, including pulsed-field gel electrophoresis, generated from thiosulfate produced by epithelial cells through
polymerase chain reaction fingerprinting, and genomic DNA microarray inflammatory cell production of reactive oxygen species.
analysis, are used in epidemiologic investigations to differentiate
Salmonella strains of a common serotype.

PATHOGENESIS
 200 CFU to 106 CFU- the infectious dose

Increase susceptibility to Salmonella infection:

-decrease either in stomach acidity (age <1 yr, acid suppression

therapy or achlorhydric disease) or
- decrease in intestinal integrity (inflammatory bowel disease,
prior gastrointestinal surgery, or alteration of the intestinal flora
by antibiotic administration)

 Once S. typhi and S. paratyphi reach the small intestine, they

penetrate the mucus layer of the gut and traverse the intestinal
layer through phagocytic microfold (M) cells that reside within
Peyer’s patches. Salmonellae can trigger the formation of
membrane ruffles in normally nonphagocytic epithelial cells.
These ruffles reach out and enclose adherent bacteria within
large vesicles by bacterialmediated endocytosis. This process is
dependent on the direct delivery of Salmonella proteins into the
cytoplasm of epithelial cells by the specialized bacterial type III
secretion system. These bacterial proteins mediate alterations in
the actin cytoskeleton that are required for Salmonella uptake.

 After crossing the epithelial layer of the small intestine, S. typhi

and S. paratyphi, which cause enteric (typhoid) fever, are
phagocytosed by macrophages. These salmonellae survive the
antimicrobial environment of the macrophage by sensing
environmental signals that trigger alterations in regulatory
systems of the phagocytosed bacteria. For example, PhoP/PhoQ
(the best-characterized regulatory system) triggers the
expression of outer-membrane proteins and mediates
modifications in lipopolysaccharide so that the altered bacterial