Disease Flashcards
‘Old’ diseases
Plague – Yersinia pestis
Anthrax – Bacillus anthracis
Botulism and tetanus – Clostridium species
Scarlet fever – Streptococcus pyogenes
Diphtheria –Corynebacterium diphtheria
Whooping cough – Bordetella pertussis
(Cholera – Vibrio cholerae)
(TB – Mycobacterium tuberculosis)
(Syphilis – Treponema pallidum)
Plague
: Yersinia pestis, Enterobacteriaceae
most feared bacterial disease, killed 1/3rd Europe middle ages, Surat -Indian outbreak 1994 (50 deaths), panic and huge economic impact
Bubonic (transmitted via flea bite - zoonosis), pneumonic (direct respiratory).
Infects lymphatic, blood, lungs
Rapid antibiotic treatment, or close to 100 % mortality
Diphtheria
: Corynebacterium diphtheriae
disease of young
characteristically shaped bacteria, grows in throat, swelling in neck
Potent toxin, spread throughout body – inhibits synthesis of proteins and kills cells. Spread by airborne route.
Toxoid, early, highly effective vaccine.
Scarlet fever
: Streptococus pyogenes
scarlet fever late 19th early 20th century – red rash, fatal, puerperal fever and death post child birth
streptococcal gangrene, necrotising fasciitis
airborne and foodborne transmission – spread rapidly within families, could loose ¾ of one family.
Strep A are generally sensitive to antibiotics.
Whooping cough
: Bordetella pertussis
Highly contagious infection of respiratory system
Dry cough, severe bouts, whoop
Complications, seizure, brain damage, pneumonia - young infants/ babies (affects all ages)
Vaccine effective, but short lived protection, last few years reappearance of disease
‘Over the next hour alone, ____people will die from an infectious disease - ______ children under five. Of the rest, most will be working-age adults
1 500 die from an infectious disease
over half of them children under five
1998 worldwide, % of children die of infectious disease; % of adults die of infectious disease
63% children
48% adults
Emerging and re-emerging bacterial diseases
Change of lifestyle
Tuberculosis – Mycobacterium tuberculosis (re-emerging) (HIV, drug resistance)
Legionnaire’s disease – Legionella pneumophila, (air conditioning and conference centre)
Food poisoning – Salmonella, Campylobacter (fast food)
Emerging and re-emerging bacterial diseases
Recognition
Flesh eating bacterium’ – Streptococcus pyogenes (apparent new disease)
Ulcers – Helicobacter pylori (association proven)
[Meningococcal meningitis – Neisseria meningitidis (more significant due to greatly decreased incidence of infectious disease in young adult)]
Emerging and re-emerging bacterial diseases
Newly evolved bacteria
Killer E. coli’ – E. coli O157:H7; E. coli O104:H4 (new toxin) – 50 deaths within a couple of months- acquired Shiga-like toxin, similar to that produced by Shigella dysenteriae
O157 is enteropathogenic causes damage to intestinal epithelial walls and produces toxin, goes into blood, kidney damage, leads to death.
O104 is enteroaggregative, produces very high levels of same toxin & antibiotic resistant strains
Cholera – Vibrio cholerae 0139 (new strain, new coat)- acquired new ‘O antigen’ – a lipopolysaccharide covering surface – hide better from immune response
Antibiotic resistant strains eg MRSA - resistance to many penicilllin based antibiotics.
Emerging and re-emerging bacterial diseases
Misuse
Bioterrorism
– Bacillus anthracis (anthrax)
- Yersinia pestis (plague)
- Clostridium botulinum (botulinum toxin)
Evolution of a bacterial pathogen
- genome reduction due to deletion events
- gene acquisition by HGT
- mutations, rearrangements
Intracellular bacteria downsize the genome, to get rid of genes where product is provided by host
Many free- living bactaria and facultative pathogens acquire new genes that help them survive in a new environment.
All bacteria undergo mutations that enhance survival.
pathogen
Organism capable of inducing damage
Commensal (non-pathogenic) -> parasitic (pathogenic) association with the host
Virulence of a bacterium depends on
(i) infectivity
(ii) invasiveness
(iii) pathogenic potential
Opportunistic pathogens
Escherichia coli (post-op/ cancer septicaemia) Staphylococcal aureus (older patients)
Disease is a balance between virulence of pathogen and resistance of host
commensalism Parasitism
Virulence of pathogen ->
Stages in pathogenesis
- Reservoir and Transmission
- Adhere to and colonise host
- Evasion of host immune system
- Growth and multiplication in select environment (niche)
- Damage
- Dissemination
Reservoir and Transmission
Microbes adapted to mode of transmission and infection.
Human respiratory system – airborne, inanimate objects, hands etc
Oral – GI tract, generally local eg most Salmonella but may become systemic eg typhoid
Water/ food- faecal/oral route
Animals (zoonoses) – insect vector often injected into blood, by passes skin
Humans; soil – direct contact; sexually transmitted; wound puncture eg rusty nail
Vibrio cholerae
infected via faecal-oral route
Vibrio cholerae is an aquatic, Gram –ve curved rod
some strains cause cholera, 60% fatal if untreated
water-borne transmission ; epidemics in disaster zones
It has pili and flagella:
Flagella required for motility, follows chemical gradient to mucosal surface / TCP pili required for attachment, bacteria also interact with each other to form a colony (biofilm) of bacteria at intestinal epithelium (required for disease)
~does not invade, localised in intestine (IgA).
~ responds to low pH and change in temperature from 20 C to 37 C
~Cholera toxin is an enzyme:ADP ribosylase acts on adenylate cyclase complex and result in Loss of Na+ and Cl- / Massive loss of water / Profuse diarrhoea, salt imbalance
Adhere to and colonise host
via pili (fimbriae) - long thin structures extending from cell surface,
- terminal adhesins, bind specifically to host cell carbohydrate
- Colonisation - establishment of a site of bacterial reproduction on or within host
- may initiate invasion of host tissue
via other surface molecules
Evasion of host immune system
Capsule - Carbohydrate, anti-phagocytic ; may mimic host molecules
Enzymes - destroy components of immune system
Modify surface molecules to mimic host antigens
Invade host cells, hide from immune system
Growth and multiplication in select environment (niche)
adapt to environment (temperature, pH, redox potential, osmolarity, nutrients, iron)
differential gene expression
Damage
responsible for symptoms of disease
degradative enzymes, aid spread of bacterium, and toxins interfering with normal physiological process eg cholera toxin
Induce inappropriate immune response, results in disease
Effects of some bacterial toxins
Cholera toxin - salt imbalance in intestine and fluid secretion (diarrhoea)
Diphtheria toxin – inhibits protein synthesis
Botulinum toxin – a highly potent neurotoxin
Tetanus toxin – a neurotoxin, lockjaw
Endotoxin, (LPS) Gram –ve bacteria, overstimulation of immune response
