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39 Cards in this Set
- Front
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How do we identify the causative pathogen (Koch's postulates, 1870s) |
1. Organism must be present in all cases (absent in healthy person) 2. Organism must be isolated from host and grown as pure culture 3. Disease must be reproduced by inoculation of experimental host with pure culture (put back into host) 4. Microorganism isolated from experimentally infected, diseased host |
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When was the golden era of Bacteriology? |
1877-1900 - identification of many causative agents of disease e.g. anthrax, cholera, typhoid, diptheria and TB |
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Limitations of Koch's postulates |
Inability to grow in pure culture - carriers will not show symptom so unaware of disease Experimental animal - cannot put back in humans so need a similar animal, but this animal may not be able to get disease Opportunistic infection of healthy individual Intoxication - disease without microorganism |
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Relevance of Koch's postulates - gastric ulcers |
1. 95% of patients with gastric ulcers and 100% with chronic gastritis had Helicobacter pylori in biopsies 2. Organism isolated with appropriate media, increased CO2 and reduced O2 3. Reproduced by inoculation of experimental host with pure culture using animal model 4. Treatment with antibiotics clears H.pylori and prevents recurrence. |
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Infectious disease epidemiology - 6 points |
What causes disease (monitor new disease Factor contributing to disease Monitor public health/disease Detection - source of disease Preventative control PHE, CDC, WHO |
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Define epidemiological factors |
Influence frequency and distribution of diseasee.g. temperature, animals, humidity, vegetation, is there a natural commondistribution or a sudden peak? |
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Define sporadic and outbreak |
Occurs occasionally and at irregular intervals - no key pattern Sudden unexpected occurrence of disease above normal numbers e.g. MRSA |
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Define endemic and epidemic |
Steady, low level and occurs at moderately regular intervals e.g. malaria in certain countries Epidemic - outbreak that affects many people at once within a community e.g. cholera after Haiti |
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Define pandemic and index case |
Pandemic - increase in disease involving at least 2 countries, generally worldwide due to people travelling Index case - first case in an epidemic e.g. Ebola. See where it starts so you can track down sources |
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The cholera epidemic in Haiti |
Killed 8,231 in 2 years More than 6% of population have had disease Endemic since 2010 Transmitted by faecal oral route |
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John Snow - father of epidemiology |
1849 - cholera transmitted via water 1854 - major outbreak in Soho He studies water supply and when he removed broad street pump, epidemic ende |
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Water transmission of disease |
Dirty drinking water and poor sanitation leads to diarrhoeal disease Enterotoxigenic E.coli, Salmonella typhi, Shiigella dysenteria, VIbrio cholera Faecal oral transmission - need for cleaning drinking water and sanitation for drinking, food preparation, hand washing. 58% of diarrhoeal disease due to dirty water |
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Airbourne transmission of disease |
Transmitted through droplets of saliva and mucous. Those with respiratory tract infections have bacteria/viruses in these droplets. Travel over 1 metre (100m/sec). Smaller droplets have resistant microbes in which remain airborne and travel for longer distances |
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TB as a airbourne disease |
Transmitted from person to person You inhale droplet nuclei which reaches alveoli in lungs and taken up by a macrophage. Close and frequent contact - overcrowding, damp so continuous exposure Latent infection - inactive in lungs so does not spread (1/3 of pop have this) TB disease is however infectious |
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Whooping cough as an airbourne disease Common cold and flu |
Damages cilia in airways, so you have constant cough to counteract this Common cold and flu - through droplets or inanimate objects. Infectious 1 day before illness then for 3-7 days so easily spread. Originated from humans, plants and other animals |
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Transmission through contact |
From person to person Herpes, boils, Staphyllococcus, Streptoccous Sexually transmitted diseases e.g Chlamydia or gonorrhoea Meningitus - frequent close contact Contact with object e.g. tetanus from rusty nails |
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Vector bourne transmission |
Vector bourne - insect (arthropod) or animal to human Insect bourne - common and virulent e.g. malaria (plamodium flaciparum), lyme disease (borrelia spp, bacteria) plague (yersinia pestis), sleeping sickness (Typanosomoa brucei). Often protoctists |
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Microbes and adaption to transmission |
Highly adapted to mode of transmission and infection e.g. adapted to survive outside body (faecal oral route) or evolved to live within us (direct contact) or in two different life cycles/environments (vectors) |
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Prevention of infection AVOID EXPOSURE |
Avian flu - respiratory, decrease contact TB in hospitals - single room, negative pressure (air goes out to environment not hospital), patient to wear mask Ebola - reduce contact and bodily fluid contact Common cold - discard tissue, wash hands, not sneezing/coughing over people |
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Prevention of infection DECREASE SPREAD BY CONTACT |
Concern over number of nosocomially acquired infections (acquired in hospitals) e.g. mRSA, C.difficile, Norovirus |
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Prevention of infection DECREASE RESEVOIR |
Spread dependent on number of infected individuals, probability of transmission and duration of infectious period. Effective diagnosis and treatment saved 43 millions lives between 2000 and 2015 3 million died of TB in 1990, 1.5 million in 2014 - decreasing reservoir means you decrease spread as less infection (now >70% detected and >80% cured) |
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Prevention of infection in faecal oral route - decrease reservoir and route of tranmission |
Clean water and sanitation - reduces incidence of water bourne diseases, would reduce under 5yr old deaths by 5.5% |
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How to avoid infectious disease |
Remove reservoir Prevent transmission and avoid disease |
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Define antibiotics |
Microbial products or their derivatives that kill or inhibit growth of susceptible microorganisms Bactericidal - kill bacteria Bacteriostatic antibiotics - stop growth of bacteria, let own immune system kill them |
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Penicillin G as an antibiotic |
Accidentally discovered by Alexander Fleming in 1928 Penicillum notatum inhibited growth of Staphylococcus. Fungus was producing pencillin. |
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Effect of penicillin of cell wall |
Inhibits cell wall transpeptidases, enxymes that catalyses transpeptidation reaction forming peptidoglycan cross links. Loss of integrity, forms weak spots, rapid cell lysis due to no peptidoglycan. Bextericidal antibiotics will activate autolysin which allow hydrolysis. |
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The transpeptidase reaction |
Transpeptidase (DAP) attacks sub terminal peptide bond in D-ala D-ala substrate Transient substrate-enzyme intermediate formed New peptide bond between remaining D-ala and acceptor amino acid e.g. DAP or Gly |
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Inhibition of the transpeptidase reaction |
Penicillin looks like D-ala D-ala substrate, so transpeptidase bind to the B-lactam ring instead Stabe Penicilloyl-TP intermediate with a very long half life This blocks cross linking Only bacteria have peptidocglycan so it is a good target for antibiotics |
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Access to bacteria |
Antibiotics only very effective against gram positive bacteria Gram negative bacteria outer membrane excludes many antibiotics Hydrated molecules must pass through porins Modified penicillin e.g. ampicillin is more effective against gram negative bacteria |
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The modification of penicillin to enhance activity |
Derivatives of penicillin G with different R groups - broad spectrum (active agianst G+ve and G-ve) - Resistant to B-lactamase - Increased stability in acid as taken orally (so must be able to survive in stomach acid) |
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Targets of antibiotics should be different in prokaryotes |
Cell wall synthesis - peptidoglycan unique to prokaryotes Protein synthesis - either 30S or 50S ribosomes Nucleic acid synthesis - our DNA is much bigger and so is super coiled. DNA gyrase used for super coiling and uncoiling in bacterial cells. Quinolones are new antibiotics for diseases |
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Semi synthetic antibiotics |
Chemically modified to increase resistance in body e.g. to acid. Increase resistance to degradation by pathogens and to increase sensitivity of bacteria (ampicillin is broad spectrum and penicillin G narrow spectrum) |
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Characteristics of useful antibiotics |
Selective toxicity - kill or inhibit pathogen without damaging host Therapetuic dose - drug level required to effectively stop infection Toxic dose - level at which drug becomes too toxic for patient, side effects Therpeutic index - ratio of toxic dose (low) to therapeutic dose (high) |
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How to we measure efficacy of antibiotic? |
Incubate bacteria and antibiotic over night and measure zone of inhibition compared to control Large zone = sensitive Small/ no zone = resistant Size of zone varies with diffusibility and conditions e.g. temperature |
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Antibiotic resistance |
Develops rapidly Transferred from one bacteria to another |
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Problems with bacterial resistance in antibiotics |
Alteration in target protein Antibiotic degrading enzyme (e.g. B-lactamase degrades penicillin) Antibiotic altering enzyme Efflux pump Decreased uptake |
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Define passive and active immunisation |
Passive - inject infection patient with protective antibody e.g. tetanus Active - induce a protective immune response with appropriate antigen, most vaccines |
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Different types of vaccines |
Toxoid - inactived toxin e.g. diptheria, tetanus Killed bacteria - older vaccines e.g. plague Attenuated bacteria - repeated subculture at raised growth temperature leading to mutations so decreased virulence e.g. BCG Subunit vaccine - isolate protective component e.g. HIB, Meningitus |
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Diptheria toxoid |
Toxin secreted and circulates in blood Toxin inhibits protein synthesis Toxin causes disease Formalin treated toxin induces protective immunity |
