Shigella and Salmonella Flashcards
Presentation Cell Biology Epidemiology Transmission i. innoculum Incubation Period Pathogenesis Treatment Prevention I. Salmonella A S. Typhi B. S. cholerasuis C. S. Enteriditis/ tymphimurium II. Shigella A. most are pretty similar
shigella ___ is the most common species in the developing world
shigella dysenteriae
shigella _____ is the most common form in the US
shigella sonnei
Shigelli ____ is the most common kind in India
shigella boydii
shigella ____ also common in developing countries
shigella flexneri
shigella: cell bio
gram +
shigella: presentation
fever and diarrhea with bloody stool and tenesmus
tenesmus
the feeling of needing to constantly pass stool
shigella: bacteremia
no/ rare
shigellia: incubation
1-4 days
persists for 1-4 week after recovery
shigella: innoculum
100 bugs, acid tolerant
shigellla: vaccine?
no
shigella: treatment
fluid and electrolyte replacement
shigella: diagnosis
a. motility
b. gas production?
c. h2S
Stool Analysis 1. non motile 2 non gas producing 3. no H2S 4. PMNs= invasive disease *compare to salmonella * indole and ureas negative
indole test
ability of bacteria to convert tryptophan to pyruvate and indole, a metabolite
Kilger Iron Agar
demonstrates sugar fermentation, gas production, and H2S production
shigella: prevention
sanitation
shiga toxin
an exotoxin with two subunits A and B
shiga toxin subunit B
binds to intestinal cells
shiga toxin subunit A
binds to 60 S ribosomal RNA to prevent protein synthesis
shigella: path, T3SS
allows macrophage infiltration and escape
shigella, path, fever
IL-1 and TNF from monocytic cells
shigella, path: ulceration
Shiga toxin
S Typhi: incubation
7-14 days
S Typhi: presentation
- Fever
- bradycardia
- Rose spot (skin rash)
- leukopenia
- enlarge liver and spleen
S. Typhi: Vi antigen
may allow survival inside phagocytic vesicles
S. Typhi: SPI-1
salmonella pathogenecity island
encodes T3SS
Type III secretion systems: SPI-2
salmonella pathogenecity island
encodes endotoxin
T3SS(Type II secretion systems)
a specialized form of secretion– an injection needle allows transfer from a bacterial cytoplasm to host cytoplasm
S. Typhi: Treatment
Fluoroquinolones
Cephalosporins
Chronic Carrier: Ampicillin, Ciprofloxacin, cholecystectomy
S. Typhi: Diagnosis
Week 1; stool culture
Week 2: blood culture
Week 3: stool culture (gall bladder)
S. Typhi: Vaccines
- Typ21a (live attenuated)
2. VICPS (capsular polysaccharide)
S. Typhi: Typhoid Fever Pathogenesis
rehearse steps
- survives stomach
- adhesins attach to peithelium
- endocytosis
- ingestion by macrophages
- Vi allows survival inside vacuoles
- kill macrophages, diseeminate via thoracic duct to blood, liver, spleen, gall bladder
- reinvasion via gall bladder
- GI bleeds and diarrhea
path: endotoxic shock
the Lipid A component of endotoxin triggers cytokines
IL-1, IL-6, and TNF-α
path: T3SS
type 3 secretion system
S. Typhi: prevention
Water Sanitation
Pasteurization
2 Vaccines
S. cholerasuis: transmission
swine
S. cholerasuis: incubation
6-72 hours
S. cholerasuis: presentation
gastroenteritis followed by bacteremia and fever
S. cholerasuis: epi
rare
young age, malaria, immune dysfunciton, AIDS, ‘roids, immunsuppression, sickle cell anemia
S. Typhinmurium and Enteriditis: presentation
headache, chills, abdominal pain, vomitting, diarrhea, then fever
S. Typhinmurium and Enteriditis: duration
1-4 days
S. Typhinmurium and Enteriditis: incubation
8-48 hours after consumption
S. Typhinmurium and Enteriditis: diagnosis
- fecal culture: salmonella traits
2. PCR; O and H antigen
S. Typhinmurium and Enteriditis: treatment
self limting
fluid and electrolyte replacement
antibiotics if necessary
S. Typhinmurium and Enteriditis: path
- LPS
- T3SS
- extracellular toxins
S. Typhinmurium and Enteriditis: Sources
poultry, pork, dog food, eggs
contamination of egg shells
fruits and vegetables
reptiles
S. Typhinmurium and Enteriditis: disease
non-tyhpoidal bacteremia associated with a weakened immune system
S. Typhinmurium and Enteritidis: pathogenesis
- LPS release during epithelial cell invasion
- T3SS mediated invasion of macrophages
- extracelullar microbes produce toxins (pertussis like) that promote inflammation