Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
32 Cards in this Set
- Front
- Back
|
Parasites |
Helminths (nematodes , Trematodes , Cestodes) , lice, mites, protists |
|
|
Mutualism |
Both members benefit |
|
|
Commensalism |
One benefits |
|
|
Pathogenicity |
The ability to cause disease |
|
|
Virulence |
Measure of Pathogenicity |
|
|
Describe the Process if Infection Tansmission |
Passes between host Entry: Attach to and enter host Establishment: Survive the host’s antimicrobial defences Disease: Disperse within host and causes disease Evolution |
|
|
Methods of Controlling Disease |
Block transmission (sanitation , vector control) Prevent entry ( sanitation , bed nets and safe-sex) Boost antimicrobial defences (vaccines) Kill the pathogens (drugs) |
|
|
Factors Affecting Disease |
Pathogenic potential of infectious agent Susceptibility of host Way in which they encounter Species Genetics Age Gender Nutritional status Immune status |
|
|
Portals if Entry |
Mucosal Surfaces: Respiratory tract, GI Tract and Genitourinary Tract Skin: Bites , wound contamination , contact , direct invasion |
|
|
Obstacles to Attachment and Colonisation |
Competition w/ normal flora: Nutrients and attachment sites Specific adhesion mechanisms to host receptors: combat protective and cleansing mechanisms of body Evade and survive barriers: acid stomach |
|
|
Define Localised and Generalised/Systemic Infection |
Localised infection: Establishment phase followed by dissemination Generalised/systemic infection or toxin spread from localised site |
|
|
Describe Means by Which a Pathogen Can Damage Host |
Direct damage by infectious agent Multiplication within and destruction of host cell Extoxins Indirect damage via inflammation Overactivity of immune system can damage host tissues E.g. endotoxin (lipopolysaccharide) , rheumatic fever |
|
|
Confounding Factors in Controlling/Eliminating Transmissible Diseases |
Drug and vaccine developments Human behaviour Social disruption and warfare Alternative/traditional medicines Pathogen ingress to human species from animals Pathogen evolution Climate/environmental change Politics/ sociology , religion etc. |
|
|
How Can Antibiotics Cause Issue with Gut Micro-flora |
There is limited recolonisation of gut microflora after infection |
|
|
Issue with vaccine and pathogen evolution |
Evolve faster to circumvent immune system/drugs/vaccines Over time vaccines may increases virulence of the wild circulating pathogens. |
|
|
Describe Airborne Transmission Of Pathogens |
Many microorganisms spread in droplets Some inactivated by rapid drying/light, Close contact is needed for transmission - influenza virus, meningococcus Others are more hardy and survive much longer in air or in dust - Corynebacterium, Mycobacterium |
|
|
Human Respiratory Defences |
Filtration system (only small particles reach alveoli) Mucociliary circuit Coughing |
|
|
Alveolar Macrophage |
Primary defence of lungs- effector cells Phagocytic and microbicidal activities Antigen presenting cells –induction of acquired T-cell responses |
|
|
Describe the Alveolar Inflammatory Response |
Influx of neutrophils (phagocytic and microbicidal) into the alveoli (diapedesis) in response to chemotactic factors such as complement to combat the infection |
|
|
Describe some Adaptive Immune Response to Airborne Infection |
IgG and C - opsonins (promote phagocytosis) Lymphoid tissue providing T and B cells |
|
|
Describe some Humoural Immune Responses to Airborne Infection |
IgA antibodies predominant in upper airways More IgG in the lungs. mainly dimer form S-IgA,interacts with the mucin prevents attachment of microorganisms neutralisation of toxins |
|
|
What Other Defences Are There? |
Lung surfactant - may enhance bactericidal activity of macrophage and complement -Lysozyme - digests bacterial peptidoglycan Transferrin and lactoferrin - bind available iron |
|
|
Epidemiology of Diphtheria |
Common in poor areas 10-15% mortality - 5000 deaths pa Mainly in under 5s |
|
|
Is corynebacteria diphtheria: Sporing or non-sporing Gram +ve/-ve Where does it grow? Is it extracellular or intracellular? |
Non-sporing, aerobic Gram-positive bacillus Humans are only known reservoir Grows in the upper respiratory tract Extracellular and does not invade the tissues |
|
|
Describe the pathogenesis of Diphtheria |
Toxin mediated IgA protease - cleaves IgA Pili for mucosal colonization Inflammatory response forms leathery pseudo-membrane of bacterial cells, dead inflammatory cells and fibrin Cord factocell wall component, toxic for phagocytes |
|
|
Describe the Effects of Diphtheria Toxin |
Carried on bacteriophage ADP ribosyltransferase for EF2 (elongation factor 2) Transfers ADP-ribose from NAD to EF2 Inhibist protein synthesis Death caused by partial suffocation and tissue-destroying effects of the toxin |
|
|
Treatment |
(Horse) antitoxin - neutralises toxin Antibiotics - must be given early (Penicillin, erythromycin) Triple vaccine DTaP formalin-treated diphtheria toxin (toxoid) (D) + tetanus toxoid (T) and pertussis acellular vaccine(aP) |
|
|
TB Epidemiology |
1993:WHO declares that TB situation is a global emergency 9m new cases p.a with approx 1.7m deaths 1/3 of population infected in some countries |
|
|
Who Discovered Mycobacterium Tuberculosis |
Rober Koch in 1882 |
|
|
Mycobacterium tuberculosis Slow or fast growing? Gram +ve/-ve? Sporing or non-sporing? Coccus or bacillus? Acquired by? Hardy? |
Slow growing, non-sporing, aerobic, Gram-positive bacillus Acquired by inhalation Tubercle bacilli survive for long periods in air or dust |
|
|
Pathogenesis |
Primarily a lung disease but may affect any organ Damage is not due to a toxin but to host immune response trying to combat this persistent organism Inhalation of bacteria Bacteria enters lungs and infects macrophage and reproduceLesion forms (caseous necrosis) |
|
|
Describe the Two Paths By Which |
|
