Lect 18: Salmonella

salmonella

gram negative rods, motile, do not ferment lactose, produce H2S, facultative anaerobe

Salmonella enterica

Salmonella subspecies infects warm blooded hosts while the other five infect cold blooded hosts

Typhimurium

Salmonella enterica serovar has a broad host range, also known as non typhoidal salmonella (NTS), causes gastroenteritis

Salmonella enterica

bacteria (genus and species) has around 1454 serotypes, host surface has been modified, Abs only protect against one serotype

false, human adapted

(true/false) salmonella enterica serovar typhi main reservoir is cold blooded reptiles

accumulation of pseudogenes

likely reason Salmonella enterica serovar typhi is human adapted (genes disabled due to mutation)

cd4

Salmonella enterica will cause infection in immunocompromised patients lacking this immune cell type

true

(true/false) salmonella enterica serovar typhi is relatively acid labile, resistant to desiccation, not readily killed by freezing, and is a facultative intracellular pathogen

M cells

Salmonella enterica serovar typhi uses T3SS to inject bacterial effectors into these cells allowing invasion of GI mucosa and spread to peyers patches

pyroptosis

caused by Salmonella enterica pathogenicity island 1 (SPI-I) in which T3SS inject effects infecting M cells, spreading to peyers patches, and inflammation resulting in diarrhea and macrophage attraction

salmonella pathogenicity island 1 (SPI-I) genes

Salmonella enterica causes membrane ruffling due to GI cell pyroptosis

SPI-2

salmonella pathogenicity island, essential component of pathogenesis allowing survival in macrophages

phagolysosome modification, block ROS accumulation, prevent phagolysosome maturation

mechanism in which Salmonella enterica SPI-2 allow survival in macrophages

true

(true/false) Salmonella enterica strains without SPI-2 are avirulent

Salmonella enterica

(bacteria genus, species) survives in target organs inside macrophages

flagella

Salmonella enterica allows a rapid colonization of peyers patches, helps with environmental fitness via chemotaxis, not required for virulence

TLR5 in GI mucosa, NLRC4 mediated pyroptosis

mechanisms of innate immune system recognize Salmonella enterica

pyroptosis

key host defense mechanism for Salmonella enterica promotes inflammatory state

IL-1b endogenous pyrogen

production and release promotes inflammatory state, key host defense mechanism for Salmonella enterica serovar typhi releasing intracellular Salmonella and allowing uptake by PMNs

polysaccharide Vi antigen

capsule expressed by Salmonella enterica, increases infectivity and virulence by limiting immune recognition and increasing intracellular survival

non typhoidal salmonella (NTS)

Salmonella causes gastroenteritis, recovery usually occurs spontaneously, taking AB can prolong infection

diarrhea (can be bloody), nausea, vomiting

non typhoidal salmonella (NTS) symptoms

undercooked poultry, eggs, dairy, reptile exposure

transmission of non typhoidal salmonella (NTS)/where you can contract it

Pierre Louis

introduced “typhoid fever” after identifying infected abdominal lymph nodes in autopsies in patients with gastric fever

Karl Ebert

pathologist who in 1880 identified what we now know as Salmonella enterica

Salmonella enterica serovar typhi

(bacteria genus, species, serovar) infectious dose is 10³-6, abdominal pain always present as disease progresses, can have pea soup diarrhea, systemic spread can lead to severe cases

typhoid fever

disease characteristic includes rose spots on chest and neck

cholecystitis

caused by S. typhi, swelling and redness of gallbladder resulting chronic carrier state

small intestine→lymph nodes→ transient bacteremia → multiplication in macrophages → gallbladder

Salmonella typhi infection cycle leading to cholecystitis and carrier state

septicemia

systemic inflammatory response, occurs when Salmonella typhi multiplies in macrophages and spread to liver, spleen, and bone marrow

true

(true/false) chronic carriers of Salmonella typhi typically have high anti-Vi Abs and do not exhibit clinical illness

stool culture, blood, bone marrow

S. typhii becomes easier to diagnose the more invasive the disease, list the order from least to most easy to diagnose from culture

typhoid vaccination

vaccine is live attenuated, oral, causes symptoms, effective but short lived and requires boosters every five years

rehydration

treatment for NTS localized gastroenteritis

antibiotics

treatment for NTS in immunocompromised individual with septicemia

blood cultures

specimen obtained to diagnose cases and evaluate systematic spread of NTS

fluoroquinolones

treatment for typhoid

4 weeks of antibiotics

treatment for chronic carriers of S. typhii, more common in elderly and those with gallbladder disease