LECTURE - Salmonella Flashcards
Characteristics of Salmonella
- facultatively anaerobic
- gram neg rods; catalase pos and oxidase neg
- subdivided into serovars based on LPS O antigen, flagellar H (2 types), capsular Vi (Kaufmann-White system)
- formerly, each serotype was given a distinctive ‘species’ name
- NOW, each serotype is termed a variant of one species (ex: Salmonella enterica serovar Typhimurium or simply S. Typhimurium)
T or F. Salmonella is motile
T! peritrichous flagella
characteristic core sugars of LPS
heptose and KDO (2-keto-3-deoxy-D-manno-octanoate)
Depending on this, Salmonella can infect multiple vertebrate hosts
serovar
- some serovars cause different diseases in different hosts (S. Typhimurium causes gastroenteritis in humans and a typhoid-like disease in mice)
The exception in Salmonella; this serovar grows exclusively in humans
S. Typhi
These cause disseminated disease in humans
S. Typhi and S. Paratyphi
sopE gene in Salmonella
- affects the severity of disease symptoms
- carried on a bacteriophage that is not present in all strains
- NOT ALL Salmonella strains contain the sample complement of T3SS effectors or plasmids
Two main groupings of Salmonella based on disease
- NTS (Non-typhoidal Salmonella): S. Typhimurium = common cause of self-limiting gastroenteritis; in immunocompromised, ma cause bacteremia; severity depends on strain, complement of virulence factors and HEALTH of individual
- Typhoidal strains: able to spread throughout the body to cause typhoid fever regardless of health of an individual; early treatment with antibiotics is effective and saves lives
Genetic sources of Salmonella virulence factors
- virulence plasmids = occurs in all Slamonela whether typhoidal or not; ex: pSLT Typhimurium, pSLV in Enteritidis; encode fimbriae (attachment to enterocyte microvilli); spv = including SpvB (ADP-ribosylating toxin)
- SPIs (Salmonella Pathogenecity Islands) in bacterial chromosome; T3SS apparatus and effector proteins
T or F. Shigella is much less common than Salmonella or Campylobacter
T!
Comparison between the two Salmonella serovars helped to define the molecular basis for …
systemic disease vs. gastroenteritis and to begin to identify host specificity determinants
S. Typhi PIs
- more PIs than other serovars
- SPI-7 carries the viaB locus for Vi exopolysaccharide (capsule) synthesis which is missing from most other Salmonella species. This island also contains genes for type IV pili.
Salmonella Typhimurium Pathogenicity Islands
S. Typhimurium: SPI-1 encodes a T3SS that mediates invasion of enterocytes..
S. Typhimurium: SPI-2 encodes a second T3SS essential for intracellular replication, escape from phagosomes (e.g., in Mϕ) and for systemic spread of bacteria.
SPI-1
SPI-1 mutants are attenuated for virulence because they cannot invade host cells.
Invasion is an active process, not simply receptor-mediated endocytosis
Attachment induces cytoskeletal rearrangements, seen as membrane ruffling in host epithelial cells.
Entry results in formation of the Salmonella-containing vacuole (SCV). Surrounded by a membrane that is derived from the host cell membrane.
SPI-2
- Maintenance of the SCV and formation of Salmonella-induced filaments (SIFs) are phenotypes that correlate with virulence (although the function of SIFs is still a mystery!)
- SCV and SIFs are dependent upon the translocated effector SifA.
- SPI-2 effectors such as SopD2 and SpiC mediate the altered trafficking of the SCV.
- SPI-2 effectors are essential for bacterial replication inside the SCV.
SPI-1 vs SPI-2 regulation
regulated differently:
- SPI-1 is expressed during invasion, and then down-regulated during the intracellular phase.
- SPI-2 is specifically induced during the intracellular phase in response to pH and nutrient conditions within the SCV.
Co-regulation occurs with each T3SS and the effectors that it translocates.e
Vi antign
Salmonella Typhi
This capsular polysaccharide is not present in other Salmonella serovars and not present in all S. Typhi strains that cause typhoid fever, thus its role in virulence is still unclear.
- When present it renders the bacteria resistant to complement-mediated killing and phagocytosis but induces an antibody response.
- Plays a role in modulating the host innate immune response.
s. Typhi may use CFT to enter intestinal epithelial cells
S. Typhi Treatment
Antibiotic treatment essential.
Resistance to chloramphenicol and ampicillin had developed by the 1990s. Current treatment uses fluoroquinolones and third-generation cephalosporins.
S. Typhimirium treatment
Only systemic infections require antibiotics.
Emergence of antibiotic-resistant strains, e.g., S. Typhimurium DT104 have been related to antibiotic use in animals.
T or F. No vaccine for humans for S. Typhimurium
T! focus on detection and public education
Salmonella as a vector to make vaccines against other targets
S. Typhi Ty21a
•Shigella virulence plasmid products
•Cloned O-antigen gene from Vibrio cholerae
•S. Typhi tetanus vaccine gives protection in mice
S. Typhimirium aroA mutatant
•Live bacterial vaccines
•Oral delivery of DNA vaccines
