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26 Cards in this Set
- Front
- Back
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DISEASES OF OLD The plague: Yersinia pestis |
Discovered in 1900 Pneumonic plague - respiratory Bubonic plague - transmmission by rats/fleas, bacteria multiply in lymph nodes and spread to lungs Plague killed 1/3rd of europeans, outbreaks still occur in West USA, India and China |
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Anthrax |
Vetinary pathogen, vaccine developed by Louis Pasteur - toxin that destroys tissue and spreads around body - found in soil so often a farm disease - form spores than enter skin but good recovery with antiobiotics |
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Diptheria |
Common until mid 1940s Grows in throat, toxin produced which spread throughout body and inhibits protein synthesis Young people affected as do not have natural immunity |
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Streptococcus pyogenes - Scarlet fever |
Post childbirth death in late 19th/early 20th century Transmitted through air or food Secretes toxic haemolysus which lyses red blood cells Gram positive cocci, resistant to antibiotics |
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Bordetella pertussis - whooping cough |
Can cause brain damage in children 2 toxins and 2 adhesins used in vaccine Cases were recorded in 2011/2012 |
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Diseases of old still around today |
TB - biggest cause of disease today Syphillus - sexual transmission Cholera |
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Why are they considered diseases of old? |
We have vaccinations and antibiotics for them We have changed our lifestyle |
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Emerging and re-emerging bacterial disease: CHANGED LIFESTYLE |
TB - due to HIV as it targets WBCs so you become suseptible to opportunistic infection e.g TB which spreads in crowded areas. Grows slowly, not metabolically active so antibiotics are stopped so they become resistant. Legionnaire's disases - causes pneumonia, spreads in air condition and cooling water towers. Salmonella/Camplyobacter - food poisoning. Spreads quickly in barn hens |
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Emerging and re-emerging bacterial disease: RECOGNITION |
Streptococcus pyogenes - flesh eating bacterium, moves quicklly and destroys tissue Heliobacter pylori - form ulcers, found in 1970s/80s Neisseria meningitidies - decreased incidence in young adults due to vaccines |
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Emerging and re-emerging bacterial disease: NEWLY EVOLVED BACTERIA |
E.coli - pick up new genes so cause disease, 0157:H7 and O104:H4 are new toxins, aquired shiga-like toxin Cholera - lipopolysaccharide coat for protection. New strain O139 acquired O antigen which passed to another causing epidemic in Asia MRSA - antibiotic resistant strain in hospitals |
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Evolution of bacterial pathogen |
Genome acquisition - by horizontal gene transfer, acquire new phenotype to become pathogenic Genome reduction - remove genes not needed in a specific environment Mutations - produce new pathogens with enhanced survival |
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Emerging and re-emerging bacterial disease: MISUSE |
Bioterrorism using anthrax, plague and the botulinum toxin Biowarfare BOTH ARE ILLEGAL |
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Define pathogen |
Organism capable of inducing disease Commensal (non pathogenic) to parasitic (pathogenic) association with host |
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What does virulence of bacterium depend on? |
Infectivity - how many you need to establish in host Invasiveness - some remain in one area but others infect whole body Pathogenic potential - some are completely harmful |
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What is disease? |
Balance between virulence of pathogen and resistance of host If relationship moves from mutualism - commensalism - paratism then the infectious disease process begins |
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The stages of pathogenesis (Cholera as the example) RESERVOIR AND TRANSMISSION |
Vibrio cholerae is aquatic gram negative curved rod, found in contaminated water |
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MOTILITY |
To get to correct niche Transit to acid stomach, synthesise flagella and swim through mucus down chemical gradient Attach to epithelial cells and stop producing flagella to conserve energy |
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ADHERE TO AND COLONISE HOST |
Produce Pili (thin structure extending from cell surface). Terminal adhesins that bind specifically to host cell carbohydrate. Pilli interact between bacteria and multiply to produce a colony (biofilm). This may initiate invasion of host tissue |
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EVASION OF HOST IMMUNE SYSTEM |
Stays localised in gut, does not invade. Some invasive bacteria enter blood or produce capsule to avoid antibodies or other protective molecule in epithelium. Enzymes produced to destroy components of immune system or modify molecules to mimic host antigens |
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GROWTH AND MULTIPLICATION IN SELECT ENVIRONMENT (NICHE) |
Cholera responds to low pH and change in temp from 20-37 degrees. Synthesizes proteins and enzymes required for growth and multiplication. The bacteria adapt to environment and will change gene expression accordingly |
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DAMAGE |
Once well established in environment, energy is used to produce toxins (protein with active binding domain). Active domain covalently modifies adenylate cyclase so cAMP produced. Stimulates CFTR transporter so Cl- secreted blocking Na+ uptake so lots of water lost. Binding domain attaches to receptor stimulating cell to take in cholera toxin |
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DISSEMINATION |
Leave host, return to resevoir and find new host. Sneezing, coughing, diarrhhoea, decomposition, contact Move from one host to another or into the environment |
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Bacterial toxins - responsible for symptoms of disease |
Degradation enzymes - aid spread of bacterium and toxins so inter with normal physiological processes Induce inappropriate immune response |
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Examples of bacterial toxins |
Cholera - salt imbalance in intestine and fluid secretion Diptheria - inhibits protein synthesis and translation Botulinum - highly potent neurotoxin Tetanus - neurotoxin Endotoxin - overstimulation of immune response |
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Infectious disease |
Bacteria colonise GI tract, invade tissue and secret toxic which leads to symptoms of gastroenteristis E.coli O157, Salmonella, Camplyobacter |
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Intoxication |
Bacteria multiply in food, spores germinate,, so toxin produced in food which is ingested, causing symptoms Presence of living bacteria not essential Rapid onset e.g. botulinum of staphylococcal food poisoning |
