Enterobacterales – Enterobacteriaceae & Yersiniaceae

How many genera are in Enterobacteriaceae and what is the type genus?

30 genera; type genus Escherichia (also includes Salmonella, Klebsiella, Enterobacter, Shigella, Citrobacter)

What are the general morphological and biochemical characteristics of Enterobacteriaceae?

• Gram-negative, non-spore forming rods

• Facultative anaerobes

• Catalase positive, Oxidase negative, Nitrate reductase positive

• Motile via peritrichous flagella (a few exceptions)

• Optimal growth temperature 37°C

• Genome: 38–60% GC content, ~5 Mb

What are the habitats and routes of infection for Enterobacteriaceae?

• Habitat: GI tract of humans, animals, insects; widespread in sewage, soil, water, plants, food

• Routes of infection: oral, wounds, urinary tract, respiratory tract

How many species and subspecies are in Salmonella, and how many serovars?

2 species, 7 subspecies, >2,600 serovars (based on O antigen, H antigen, K capsule)

Give examples of host-restricted vs broad host Salmonella serovars.

• Host-restricted: S. Typhi (human), S. Abortusovis (sheep)

• Broad host range: S. Typhimurium

How can Salmonella be distinguished from E. coli and Shigella in the lab?

• Non-lactose fermenter (E. coli ferments lactose; Shigella does not)

• Indole test negative (E. coli positive; Shigella variable)

• Selective media: H2S production, acid production during carbohydrate fermentation (e.g., XLD, SS media)

What is the impact of Typhoidal Salmonella (S. Typhi)?

• Causes typhoid fever (~15 million cases/year, 1% deaths)

• 1st phase: slow fever, rose spots, mild bacteraemia

• 2nd phase: gallbladder infection, ulcers, haemorrhage, death (~20%)

• Typhoid state: “muttering delirium” or “coma vigil”

How does Enteric fever caused by S. Paratyphi differ from typhoid fever?

Similar symptoms but less severe and rare.

What is the impact of Non-Typhoidal Salmonella (NTS)?

99% of human disease caused by S. enterica subspecies enterica

• Global burden: ~94 million cases/year, 155,000 deaths

• UK: 8–9,000 lab-confirmed cases/year

• Usually causes self-limiting enteritis; invasive NTS (iNTS) occurs in immunocompromised individuals

How does NTS cross the intestinal epithelium and spread?

• Via M cells, dendritic cells, or direct uptake

• Targets macrophages or re-invades epithelial cells basolaterally

• May induce macrophage apoptosis for replication

• Severe disease arises from systemic spread and bacteraemia

What are the main Salmonella virulence factors?

Type 3 Secretion Systems (T3SS) encoded on Salmonella Pathogenicity Islands (SPI)

• T3SS1 (SPI1): invasion of intestinal epithelial cells, triggers secretory/inflammatory responses

• T3SS2 (SPI2): intracellular replication, systemic infection

What are common vehicles of NTS infection in the UK?

Faecal-oral transmission, mainly poultry and poultry products, but many foods can carry Salmonella

How many species are in the genus Escherichia?

Five: E. coli, E. albertii, E. fergusonii, E. hermannii, E. vulneris

When does E. coli colonise the mammalian GI tract?

Within a few hours after birth, and maintains presence over lifetime

What is a ‘pathotype’ in E. coli?

A group of pathogenic strains causing a similar disease with similar virulence factors

What percentage of UTIs are caused by uropathogenic E. coli (UPEC)?

~75% of UTIs, affecting 50% of women in their

How does UPEC cause UTIs?

• Periurethral contamination from bowel movement or sexual activity

• P-fimbriae attach to P-antigen receptors on bladder cells

What is Neonatal Meningitis-associated E. coli (NMEC)?

• Affects 1 in 2,000–4,000 infants <1 month old

• Primary bloodstream infection with secondary CNS distribution

• 80% of NMEC strains produce K-1 capsule, key virulence factor

What are the main pathotypes of intestinal pathogenic E. coli (InPEC)?

• ETEC: mild watery diarrhoea

• EIEC: dysentery

• EHEC/STEC: severe bloody diarrhoea, HUS

• EPEC / EAEC: persistent diarrhoea

• All: vomiting, abdominal pain, fever

What virulence system do EPEC and EHEC/STEC use to attach to host cells?

Type 3 Secretion System (T3SS) → injects Tir, which acts as a receptor for intimin, causing A/E lesions

How many Shigella species exist and which is the most severe?

Four species: S. dysenteriae (most severe), S. flexneri, S. boydii, S. sonnei

How is Shigella related to E. coli genetically?

DNA-DNA hybridisation groups them as one species, but phenotypically and clinically different

What is the infectious dose of Shigella?

Very low: 10–100 organisms

Who are the main at-risk populations for shigellosis?

Children <5 years, close-contact communities (e.g., Orthodox Jewish communities, MSM)

What are the clinical symptoms of shigellosis?

Aggressive watery or mucoid/bloody diarrhoea, fever, stomach cramps; resolves in 5–7 days in immunocompetent hosts

How does Shigella invade and spread in the host?

• Crosses epithelium via M cells, taken up by macrophages

• Kills macrophages → reaches basolateral epithelium

• Escapes phagosome → disseminates intracellularly

What are the virulence factors of Shigella?

• Plasmid-borne pINV: T3SS for protein injection

• Chromosomal SHI-1: enterotoxins (SigA, Pic, Set1A/B)

• SHI-2 & SHI-3: siderophores (IucA-D, IutA)

• SHI-O: serotype conversion / O-antigen

• Stx-phage p27: Shiga toxin

How many genera and species in Yersiniaceae, and which are human pathogens?

7 genera, type genus Yersinia; 3 pathogenic species: Y. enterocolitica, Y. pseudotuberculosis, Y. pestis

What are the general characteristics of Yersinia?

• Facultative anaerobes; some lack nitrate reductase

• Motile by peritrichous flagella <30°C (Y. pestis non-motile at 37°C)

• Optimum growth 28–29°C

• GC content ~47%; genome ~4.6 Mb

How do Y. enterocolitica and Y. pseudotuberculosis affect humans?

• Self-limiting gastroenteritis

• Symptoms: fever, vomiting, abdominal pain, diarrhoea

• Mostly in children <7 years

• Rare systemic or joint complications

How is plague caused by Y. pestis transmitted and what is its impact?

• Flea-borne, occasionally aerosol

• Historical pandemics (e.g., Black Death, 1347–1352)

• Modern WHO reports 1–2,000 cases/year, 8–10% mortality

What are the clinical forms of plague?

• Bubonic: proliferates in lymph nodes (bubo), 60% mortality

• Septicemic: spreads in bloodstream, LPS-induced shock, near 100% mortality

• Pneumonic: invades lungs, highly contagious via aerosol

How does Yersinia invade the host and spread systemically?

• Entry: flea bite or inhalation

• Crosses epithelium via M cells

• Replicates in lymph nodes → bloodstream → deep tissues (liver, spleen)

 What virulence factors are key to Yersinia pathogenicity?

• Plasmid-encoded factors for flea colonisation, mammalian survival

• Type 3 Secretion System (T3SS) present in all pathogenic species

• Y. pestis lost motility and adhesion to adapt to mammalian host