Bacterial Pathogens: Shigella, Salmonella, Pathogenic E. coli, and Vibrio cholerae

Vocabulary practice flashcards covering enteric pathogens: Shigella, Salmonella, pathogenic Escherichia coli, and Vibrio cholerae, including their classification, virulence mechanisms, toxins, and associated clinical diseases.

Dysentery

An inflammatory disorder of the gastrointestinal tract characterized by scant-volume stools containing blood, mucus, and pus, accompanied by fever, pain, and abdominal cramps; typically results from tissue invasion of the large intestine.

Secretory (Watery) Diarrhea

An abnormal intestinal discharge characterized by copious, watery stools lacking blood, leukocytes, or pus, resulting from disease of the small intestine where tissue invasion is absent.

Shiga Toxin

A family of $\text{AB}_5$ enterotoxins carried on STX phages and produced by Shigella dysenteriae serogroup 1 and STEC strains; the $B_5$ pentamer binds to host cell $\text{Gb}_3$ glycolipids, and the $A_1$ fragment functions as an RNA $N$-glycosidase that cleaves rRNA to shut down ribosomal protein synthesis.

Shigella Subgroups

The taxonomic divisions of Shigella based on O-antigen serotyping and D-mannitol fermentation: Subgroup A (S. dysenteriae, 15 serotypes, D-mannitol negative), Subgroup B (S. flexneri, 8 serotypes, D-mannitol positive), Subgroup C (S. boydii, 19 serotypes, D-mannitol positive), and Subgroup D (S. sonnei, 1 serotype, D-mannitol positive).

M Cells (Microfold Cells)

Specialized intestinal epithelial cells overlaying Peyer patches that sample luminal antigens and are exploited by invasive pathogens such as Shigella and Salmonella via transcytosis to access underlying macrophages and the lamina propria.

VirG (IcsA)-Mediated Actin Motility

An intracellular propulsion mechanism in Shigella where polar outer membrane protein VirG recruits host N-WASP and the Arp2/3 complex to nucleate actin polymerization at one pole, forming an actin tail that propels the bacterium through the host cytoplasm and into adjacent cells.

Zippering Model of Invasion

A bacterial entry pathway (exemplified by Listeria monocytogenes internalins InlA and InlB) characterized by direct, sequential high-affinity ligand-receptor binding that zips the host plasma membrane around a single bacterium to internalize it.

Salmonellosis

A foodborne gastroenteritis caused primarily by Salmonella enterica serovars Typhimurium and Enteritidis, presenting with fever, abdominal cramps, and inflammatory diarrhea lasting $48\text{ hours to }7\text{ days}$ after an incubation of $6\text{ hours to }2\text{ days}$.

Typhoid Fever

A severe systemic infection caused by the human-restricted Salmonella enterica serovar Typhi, characterized by prolonged high fever, headache, malaise, abdominal pain, transient diarrhea or constipation, and a salmon-colored maculopapular rash on the trunk.

Salmonella Pathogenicity Island 1 (SPI-1)

A genetic island encoding a Type III Secretion System and effector proteins (such as SopE, SopB, SipA, and SipC) that trigger localized host cell membrane ruffling and macropinocytosis to promote epithelial cell invasion.

Salmonella-Containing Vacuole (SCV)

A specialized membrane-bound intracellular compartment in which Salmonella replicates after host invasion, sustained and modulated by SPI-2 type III secretion system effectors such as SifA, SseF, and SseG.

SifA

A Salmonella SPI-2 T3SS effector protein that interacts with host SKIP and kinesin/microtubules to maintain the structural integrity of the Salmonella-containing vacuole and induce Salmonella-induced filaments (Sifs).

Signature-Tagged Mutagenesis (STM)

A negative-selection transposon mutagenesis technique developed by Hensel, Shea, and Holden using unique DNA tags to simultaneously identify bacterial virulence genes required for in vivo survival within mixed mutant pools.

Guillain-Barré Syndrome (GBS)

An autoimmune peripheral neuropathy characterized by ascending weakness and flaccid paralysis that can develop as a sequela of Campylobacter jejuni infection due to cross-reactive antibodies that recognize both bacterial lipooligosaccharide (LOS) and host gangliosides on peripheral nerves.

Escherichia coli Core Genome

The conserved genetic repertoire shared across all E. coli lineages; a comparison between non-pathogenic K-12 (MG1655), uropathogenic CFT073, and enterohemorrhagic EDL933 revealed that only $2,996$ genes ($39.2\%$ of the pan-genome) are common to all three strains.

Attaching and Effacing (A/E) Lesion

A characteristic histopathologic intestinal lesion induced by EPEC and EHEC strains via the Locus of Enterocyte Effacement (LEE) island, featuring localized destruction of host microvilli, intimate bacterial attachment, and pedestal formation from polymerized F-actin.

Translocated Intimin Receptor (Tir)

An effector protein secreted via T3SS by EPEC and EHEC into the host enterocyte plasma membrane, where it inserts and becomes phosphorylated to serve as the high-affinity receptor for the bacterial outer membrane adhesin intimin.

Enterotoxigenic Escherichia coli (ETEC)

A diarrheagenic E. coli pathotype that adheres to the small intestine via colonization factor antigens (CFAs) and produces heat-labile enterotoxin (LT, stimulating adenylate cyclase/cAMP) and heat-stable enterotoxin (ST, stimulating guanylate cyclase/cGMP), causing traveler's diarrhea.

Hemolytic Uremic Syndrome (HUS)

A severe disease triad consisting of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure, developing $5\text{ to }10\text{ days}$ after diarrheal onset from EHEC (or Shigella dysenteriae) due to circulating Shiga toxin binding glomerular endothelial cells.

Norfloxacin Prophage Induction

The process by which fluoroquinolone antibiotics induce the SOS response in enterohemorrhagic E. coli O157:H7, triggering excision of prophages carrying the stx genes and significantly elevating Shiga toxin production.

Escherichia coli O104:H4 Outbreak Strain

An enteroaggregative E. coli (EAEC) strain (harboring aggregative adherence fimbriae and antibiotic resistance plasmids) that acquired the phage-encoded Stx2 gene, causing a major outbreak of bloody diarrhea and hemolytic uremic syndrome in Germany in 2011.

Type 1 Fimbriae

Mannose-sensitive filamentous surface appendages of E. coli that bind mannosylated uroplakin receptors and undergo phase variation regulated by site-specific invertible DNA elements (fimS) that switch expression between ON and OFF states.

P Fimbriae (Pap Pili)

Uropathogenic E. coli composite pili whose PapG tip adhesin specifically binds to the $\text{Gal}(\alpha 1-4)\text{Gal}$ globobiose moiety of the P blood group antigen on human kidney and uroepithelial cells, promoting pyelonephritis and local IL-8 secretion.

K1 Polysialic Acid Capsule

An $\alpha 2,8$-linked linear homopolymer of sialic acid produced by neonatal meningitis E. coli (NMEC) that mimics host tissue carbohydrates, conferring poor immunogenicity and resisting complement-mediated alternate pathway lysis.

Cholera Toxin (CT)

An $\text{AB}_5$ protein enterotoxin encoded by the CTX$\phi$ phage; its B pentamer binds GM1 gangliosides, while the $A_1$ subunit ADP-ribosylates $G_{s\alpha}$ to constitutively activate adenylate cyclase, elevating intracellular cAMP and driving massive CFTR-mediated chloride secretion.

Toxin-Coregulated Pilus (TCP)

A type IV bundle-forming pilus encoded on the VPI-1 pathogenicity island of Vibrio cholerae that is required for microcolony formation on intestinal enterocytes and serves as the receptor for CTX$\phi$ bacteriophage entry.

ToxT

The master AraC-family transcriptional regulator in Vibrio cholerae activated by the membrane-bound regulators ToxR/ToxS and TcpP/TcpH to directly induce transcription of the virulence genes tcp and ctxAB.

HapR

The central high-cell-density quorum-sensing transcriptional regulator of Vibrio cholerae that represses biofilm formation and virulence gene expression (ToxT) while activating the HapA hemagglutinin/mucinase protease to facilitate mucosal detachment and escape.

Seventh Cholera Pandemic

The ongoing cholera pandemic that began in 1961 in Sulawesi, Indonesia, caused by Vibrio cholerae O1 biotype El Tor, which displaced the classical biotype and acquired unique genomic islands VSP-I and VSP-II.

Vibrio vulnificus

A pathogenic, halophilic marine bacterium transmitted via ingestion of raw seafood or marine wound exposure; wound infections cause severe tissue necrosis requiring surgical debridement or amputation, and can progress to secondary septicemia with fatality within $\le 48\text{ hours}$.