49. Salmonella and Shigella Flashcards
1
Q
what is the real species of S.typhinurium?
A
Salmonella enterica, subspecies enterica, serovar Typhinurium
2
Q
typhoid vs NTS disease?
A
- Typhoid: systemic syndrome, enteric fever (life threatening
- NTS: diarrhea (inflammatory)
3
Q
Typhoid vs NTS - which can you treat w/Abx? which has vaccines?
A
Typhoid for both
4
Q
NTS epidemiology?
A
- infections assoc w/poultry eggs, and dairy
- raw meat, fruits, veggies
- contaminated prep area
- animal hosts
- infectious dose is low
- self-limiting infections
- carried asymptomatically by lots of vertebrate species
- some NTS in kids
5
Q
NTS disease?
A
- gastroenteritis (“inflammatory enteritis”)
- watery diarrhea: blood, pus, and mucous
- abd pain, fever
- immunocompromised hosts: bacteremia and systemic suppurative foci (bone, lung, meninges, etc)
6
Q
NTS tx?
A
- antidiarrheals
- NO ABX
7
Q
Typhoid Salmonella Epi?
A
- adapted to cause disease in humans only
- world health problem
- ingestion of contaminated food/water
- asymptomatic excretion from gallbladder colonization chronic carriers (gallstones and bile induced biofilm formation may be impt)
8
Q
Typhoid salmonella disease?
A
- “typhoid fever” = enteric fever
- generalized systemic infection of the reticuloendothelial system
- No diarrhea
- 5-21 days inc period
- malaise, headache, cough, sore throat, constipation, muscle aches, CNS abnormalities
- febrile and ill-appearing
- rose spots, hepatosplenomegaly, abdominal tenderness
- 10-30% mortality untreated (1% treated)
- can lead to pna, meningitis, or intestinal perforation (intestinal hemorrhage is the most common cause of death)
9
Q
typhoid salmonella tx and vaccine?
A
- remember to think of typhoid fever in febrile pts who have traveled to developing areas as problem when undiagnosed early
- FQ (ciprofloxacin)
- S.enterica MDR to many first line Abx (ie ampicillin, chloramphenicol, TMP-SMX)
- live attenuated oral vaccine (Ty21a)
- Vi capsular polysaccharide (parenteral)
- no vaccine for pts
10
Q
salmonella pathogenesis?
A
- all salmonella are invasive (mucosal invasion)
- bacterium adheres to small bowel mucosa
- via T3SS, internalized into M cells and enterocytes (cell membrane disrupted transiently to engulf organism, has effects on actin dynamics causing cytoskel alterations)
- 2nd T3SS to prevent lysosomal fusion – multiplies w/in vacuole
- bacteria escape and infect others
- cause inflammation: Typhoidal involves minimal inflammation and neutrophil transmigration w/restrained immune response while NTS causes significant inflammation and neutrophil recruitment which may contain the infection
- inflammation re: T3SS-1 creating inflammasome, LPS binding TLR4, and Flagella binding TLR5
- *Inflammation induced by salmonella confers competitive advantage in the intestine:
- host releases antimicrobial peptide lipocalin-2
- lipocalin binds enterobactin (siderophore produced by enteric bacteria)
- salmonella produces salmchelin that is not bound by lipocalin
- thus salmonella has an advantage over other gut microbes (gets the iron it wants)
- also use of tetrathionate for respiration
11
Q
salmonella virulence?
A
- T3SS encoded on PAIs (pathogenicity islands)
- regulators
- adherence fimbriae
- salmochelin expression - tetrathionate utilization (NTS only)
S.typhi only:
- Vi antigen: capsule that reduces inflammatory response by evading TLR4
- altered flagellin gene regulation evades TLR5
- genome degradation
12
Q
Shigella microbiology?
A
- GNR
- non-motile
- closely related to EIEC
- enterobacteriaceae
13
Q
most common shigella in US?
A
S.sonnei - traveler’s diarrhea
14
Q
most common shigella in the world?
A
S. flexneri - traveler’s diarrhea
15
Q
most severe shigella?
A
S. dysenteriae
- Most severe – more virulent and infectious
- explosive outbreaks and epidemics
- all age groups
- high attack rates
