lecture 4 Flashcards
Order: Vibrionales
General morphological and biochemical characteristics
family Vibrionaceae
* 4 genera including type genus Vibrio
* Gram negative straight/curved rod
* Facultative anaerobe
* Oxidase positive (most)
* Catalase positive
* Nitrate reductase positive
* Requirement for NaCl (salt) for growth
* G+C content 47%; 4-5 Mbp genome
* Two chromosomes
* Optimum growth 30-35 ˚C
* Motile (single polar flagella)
aquatic organisms, that thrive in marine and brackish water >15 ˚C
Order: Vibrionales
Genera: Vibrio
> 50 species including
V. cholerae (waterborne infections)
V. parahaemolyticus (food (shellfish) infections)
V. vulnificus (wound infections)
Similarities with members of Enterobactericeae
- Gamma proteobacteria, Gram negative rods (sometimes curved)
- Facultative anaerobes / fermentative
- Genome size 4-5Mb, G+C content ~47%, genetically tractable
Differences with members of Enterobactericeae
- 2 chromosomes
- Single polar flagella (highly motile)
- Most oxidase positive
- Most live in aquatic habitats
Vibrio cholerae
- > 200 O antigen serogroups
*O1 and O139
Pan/epidemic cholera
Cholera toxin (CT) +
Waterborne /
person-to-person
*Non-O1, non-O139
Sporadic cases
Gastroenteritis (cholera-like?)
May be cholera toxin negative
Water/shellfish
V. cholerae O1 impact
▪ acute secretory diarrhoeal disease
▪ endemic to 50 countries, and a public health
problem for the native population and for
travellers to these regions
▪ this ancient disease (5th century BC) remains a
considerable social and economic burden despite
nearly 150 years of study
▪ in midst of 7th pandemic; WHO estimates 3-5
million individuals affected by cholera per year;
current pandemic began in Indonesia in 1961 and
spread through Asia, Africa to Europe and Latin
America
Modern day cholera
Since mid-2021, the world is facing an acute upsurge of the 7th cholera pandemic characterized by the number, size and concurrence of multiple outbreaks, the spread to areas free of cholera for decades and alarming high mortality rates
Figure – Incidence of cholera cases per 100,000 population reported to WHO from 1st January to 30 November 2022
V. cholerae infection
- short incubation period (< 12 hours)
- early vomiting
- painless loss of copious amounts of watery
diarrhea (up to 1L per hour) known as
“rice-water stool” - severe and rapidly progressing
dehydration and hypovolemic shock - without treatment, severe cholera kills
about half of infected individuals
V. cholerae pathogenesis
Steps during infection:
- Ingestion and passage
through acidic stomach - Colonisation of small
intestine (distal region).;
organism remains
extracellular - Production of CT to induce
secretory diarrhoea and
mucin release - Exit from host in mucusassociated aggregates
Toxin co-regulated
pilus (TCP) – critical
colonisation factor
Cholera toxin (CT) –
responsible for
secretory diarrhoea
V. parahaemolyticus-
Enteritis (shellfish-borne infections)
- Main clinical symptoms is watery
diarrhoea, often accompanied with
abdominal pain, nausea and vomiting - Typically a self-limiting illness, with rare
severe morbidity and mortality - Sporadic cases in UK (e.g. mitten crabs in
Thames (2003-2006); pathogenic strains
in coastal waters (2012)) - Most common pathogen in Japan & other
parts of Asia where raw seafood
consumption is high
V. parahaemolyticus
- Soft tissue infections / septicaemia
- entry via wounds or skin lesions, often
linked to injury due to handling
contaminated shellfish - symptoms of skin infection (swelling,
pain, erythema, bullae (blister), necrosis
and gangrene) - symptoms of septicaemia (fever,
hypotension, bullae, pain in lower
extremities, tachycardia, shock, multiorgan dysfunction) - infections may be life-threatening
V. parahaemolyticus virulence mechanisms
- hemolysins
(e.g. thermostable direct haemolysin
(TDH) and related variant TRH); lysis of
red blood cells - Type 3 secretion system (T3SS)
Two systems in organism; T3SS1 causes
cytotoxicity (cell death) and T3SS2 is
associated with diarrhoea (enterotoxicity)
studies show that bile triggers expression
of T3SS2 genes – this provides a way for
the bacterium to know when to switch on
virulence factor production
V. vulnificus: disease and routes of
infection
Disease:
1. Wound infection / septicaemia from exposure to organism in sea water
Can be fatal; rapidly spreading systemic disease → septicaemia
- Foodborne illnesses
* Raw oysters
* USA ~ 100 cases per year
* Responsible for >95% of all seafood associated deaths in USA
* Can be fatal (septicaemia)
* Healthy individuals rarely susceptible (liver damage, high serum iron)
V. vulnificus: virulence factors
- Hemolysin
Encoded by genes vvhA and vvhB; only secreted toxin; member of the cholesteroldependent cytolysin (CDC) family of pore-forming toxins; capable of dissolving red
blood cells - Proteases
e.g. VVP – an elastase that increases vascular permeability of host cells; other
functions in promoting clotting, which prevents effective host immune response
e.g. RtxA - MARTX toxin with multiple functions including interfering with actin
cytoskeleton rearrangements and promoting necrotic cell death - Capsule
Required for infection, ‘hides’ bacterium from the host immune response (e.g.
resistance to opsonization by complement and subsequent phagocytosis by
macrophages)
One more reference & next steps…..
Baker-Austin et al. (2018) Vibrio spp. infections. Nature Disease Primers 4:1-19.
https://www.nature.com/articles/s41572-018-0005-8 .
Summary of pathogenic Vibrio spp.
detail the information for
V. cholerae
V. para
V. vulnificus regarding their
-disease
-intestinal pathology
-infectious dose
-key virulence factors
-habitat /vehicle
disease
intestinal pathology
infectious dose
key virulence factors
habitat /vehicle
