Salmonella and Yersina Flashcards
1
Q
What is the bacteriology of Salmonella?
A
- gram neg rods
- motile
- seldom lactose fermenting
- oxidase negative, urease negative
- H2S producing
- > 2500 serovars exist
- usually acquired from contaminated food
2
Q
How can a salmonella infection manifest?
A
- Enterocolitis
- Enteric fevers (typhoid fever)
- Septicemia
- Risk of reactive arthritis (Reiter’s Syndrome)
3
Q
What is salmonella Enterocolitis?
A
- usually S. typhimurium, S. enteritidis, or S. heidelberg
- salmonella is a major cause in the US
- most common in children and nursing homes
- any food, many pets, some human carriers can transmit
- one outbreak in 2000 involved >182k cases
- bacteria invade epithelial and subepithelial tissue of lg and sm intestine
- inflammation and diarrhea, nausea and vomiting
- immune response restricts to gut, bacteremia is rare
- high infectious dose (100k bacteria)
- gastric acid is protective, antacids increase risk
- bacteria attach by fimbriae (pili) to cells lining the intestinal lumen
- Salmonellae selectively attach to specialized epithelial cells (M cells) of the Peyer patches
- the bacteria are then internalized by receptor-mediated endocytosis
4
Q
What are the virulence factors of Salmonella?
A
- Ipf operon enhances adhesion to M cells
- T3SS injects M cell, enhances bacterial translocation
- SipB injected by Spi1 Type 3 sys causes macrophage apoptosis
- in S. typhi, Spi2 Type 3 sys remodels phagosomes for systemic spread
- Vi antigen- S typhi capsule for immune evasion
5
Q
What is the pathogenesis of Enteric and Typhoid fevers?
A
- usually S. typhi or S. paratyphi
- human-restricted fecal oral
- high infectious dose (~100K cells)
- invades Peyer patches of distal ilieum, enters macrophages
- rides in macrophages through lymphatics, involving major organs
- once critical density is reached bacteria induce macrophage apoptosis and escape into bloodstream
6
Q
How do enteric and typhoid fevers present?
A
- onset: fever, malaise, diffuse abdominal pain, constipation (sometimes diarrhea)
- 3-4 week progression: dry cough, stupor, delerium, intestinal hemorrhage, bowel perforation, myocarditis, death (9-13%)
- necrosis of the infected Peyer patches causes hemorrhage/perforation
- most of other symptoms from toxemia
- survivors may have long term neurological sequale or chronic carriage in gallbladder (reservoir)
7
Q
Which patients get Enteric and typhoid fevers?
A
- penetration of gut is resisted by the CFTR cystic fibrosis allele; protective effect against typhoid fever, cholera, and TB may explain persistence of allele despite lethality to homozygotes
- in US, appears primarily among returning international travelers (India) and student visas
- when treated promptly, requires hospitalization but has low mortality (<1%), higher abroad (up to 30%)
- host risk factors: corticosteroids and other immunosuppressants, maliganancy, diabetes, HIV
8
Q
What is Salmonella septicemia?
A
- very rare in healthy adults
- underlying chronic disease like sickle cell anemia or predisposes
- children may be susceptible
- osteomyelitis, pneumonia, and meningitis most common sequelae
- metastatic abscesses from previously damaged tissues like aneurysms
9
Q
How do you diagnose a Salmonella infection?
A
- Enterocolitis: nonbloody diarrhea, fever, dehydration, culture from stool. Local health authority should be notified in case of a foodborne outbreak
- Typhoid fever: travel abroad, high fever, headache, tender abdomen, anorexia, sometimes rose spots (pink, blanchable, slightly raised), lethargy. Organism may be cultured from stool or blood. Bone marrow aspirate is ideal, but very painful
- Septicemia: focal symptoms related to affected organ [bone (osteomyelitis), lung (pneumonia), meninges] “nontyphoidal focal disease”
10
Q
How is Salmonella treated?
A
- Enterocolitis: normally self-limited, rehydrate, Ab-treat only very young, very old, or HIV+; culture organism and test Ab susceptibility before prescribing
- Enteric fevers and septicemia: ceftriaxone or ciprofloxacin,drain focal abscesses
11
Q
How do you prevent Salmonella?
A
- avoid uncooked food, untreated water, unpasturized milk
- wash hands after handling pets
- vaccines are available for S. typhi but not routine
12
Q
What is the bacteriology of Yersina enterocolitica and pseudotuberculosis?
A
- gram neg oval rods
- lack Y. pestis virulence factors (ie no plague)
- not lactose fermenting
- urease positive
- motile at 25C, nonmotile at 37C
- cause foodborne gastroenteritis
- enterocolitica is as common as Shigella in some countries
13
Q
What is the pathogenesis of Yersinia enterocolitica and pseudotuberculosis?
A
- Y enterocolitica causes enterocolitis, invades intestinal mucosa and destroys tissue
- virulence factors carried on both chromosome and plasmid
- high infectious dose (10^9 IUs)
- penetration of the mucosa occurs in the ileum, followed by multiplication in Peyer patches, may spread to local lymph nodes-> mesenteric lymphadenitis (aka false appendicitis)
- does not produce siderophores; virulence enhanced by iron overload
- endemic to cooler climates, but eliminated by food processing
- infection most common in young children
- bacteremia is rare but deadly (33-50% mortality)
- both species may predispose to Reactive arthritis
14
Q
What are the virulence factors of Yersinia enterocolitica and pseduotuberculosis?
A
- Pili and Inv adhesin enhance binding to M cells
- CNF- dermonecrotic toxin destroys tissue
- Yop Type 3 secretion system injects proteins into macrophages -> no phagocytosis, reduced inflammatory response
15
Q
How does Y. pseudotuberculosis infection look?
A
- similar, rarer, seen with immunocompromise or preexisting liver disease
- in children, may be associated with Izumi fever: a generalized vasculitis with symptoms of fever, rash, conjunctival injection, cervical lymphadenitis, inflammation of the lips and oral cavity, and erythema and edema of the hands and feet
