Pathogenesis: development of disease in the host - Norwalk virus; Fecal – oral, diarrhea
Disease: altered state of health, host body is changed, upset of homeostasis
Microbiology – Chapter 13
Epidemiology: Science of the study of how diseases are acquired and spread in a population
Outside assignment 3: Note that the last question has been changed to focus on MDR bacterial infections. Be sure to get a copy of the last page from instructor
** You may have to do some research ato answer all of the questions. Use other Micro. Books or other research tools. ***
Commensalism – One organism benefits; the other unaffected; can be opportunistic infector
Mutualism: both benefit; E. coli makes us Vit. K; We provide nice environment and food
Microbiology – Chapter 13
Parasitism: One benefits at the other’s expense; tapeworm or leach
Virulence: potency; how quickly they infect, spread, cause tissue damage or disease symptoms Influenza A H5N1, very virulent form of flu, or encapsulated pneumococci
Virulence factors: factors that cause disease or aid in spread of disease quickly in host or to other hosts (more later)
Microbiology – Chapter 13
Pathogen: actual agent of disease, MRSA – S. aureus
BACTERIAL, VIRAL, FUNGAL, HELMINTH
Carrier: Infected healthy individual, no symptoms (asymptomatic), or very mild form of disease, yet they both can spread disease to others – many bacterial and viral pathogens
Classic case was typhoid Mary (look it up)
Microbiology – Chapter 13
Reservoir: Where pathogen is maintained , can be in an organism (animal), in the environment (stagnant water - Legionella), or even in soil (Clostridia)
Vector: Agent that spreads pathogens from host to host
1. Arthropod: flea; mosquito, tick
2. Inanimate: things, toys, dirty hands, needles, (sometimes called “fomites”)
Microbiology – Chapter 13
Nosocomial infections: hospital acquired infections – see table in text and know it
Next slide******
MRSA both HA and CA
Pseudomonas - respiratory impaired, burn patients
E. coli and Proteus – UTI; long term catheter patients
Fig. 13.13
Review Koch’s postulates
Microbiology – Chapter 13
Nine routes of infection
**** Know this; be able to list and give an example of each****
Perinatal: at birth, STD like gonorrhea and syphilis, even Chlamydia blindness
Microbiology – Chapter 13
Virulence factors
Virulence factors – factors that aid or enhances the microbes ability to invade and spread within the host (know for test) Ex. List the categories of “virulence” factors in microbes; explain each category, and give an example of a disease causing agent for each category.
Adherence: In order for a microbe to cause disease it first must adhere to a host surface. Some microbes produce materials or structures that allow them to adhere (stick) to membranes or surfaces, and thus escape defenses
Pili (fimbriae) – Neisseria gonorrhea, if a strain has no pili it is not pathogenic. The chemicals that allow such attachment are called “adhesins” – They are often glycoproteins or protein that bind to receptors on host cell surfaces.
Glycocalyx – The capsule again is a tightly bound polyscaccharide material on the outside of certain bacterial cells (part of a bacterial envelope). Streptococcus pneumoniae is good example. Virulent strains are encapsulated; non-virulent strains are not. Recall the classic “Griffith experiment” from chapter 9? Transformation?
Spikes – Viral envelopes of some viruses, Influenza a, H5N1
Fig. 13.4
Microbiology – Chapter 13
Other adhesions
N. menigitidis (bacterial meningitis agent) produces protein a, a surface adhesion on the pili
Mycoplasma pneumonia (atypical bacterial pneumonia) has a surface adhesion that binds to receptor on mucus membrane lining of the respiratory tract
Other Adhesions
SEM of Pseudomonas, Gram (-)
Microbiology – Chapter 13
Toxins – Poisonous microbial bypoducts that are produced by the microbe and diffuse into tissues causing damage/ enhance invasion/ avoid defenses
Exotoxins – excreted outside of cell, both Gram+ and Gram – bacteria produce some of these highly destructive proteins.
Staphylococcus aureus - Staph exotoxin that causes FBI
Another causes “SSSS” Staph Scalded Skin Syndrome (exfoliate)
C. botulinum – most powerful neurotoxin, - a taste can kill you
Streptococcus pyogenes - has several tissue destroying toxins; Necrotoxin of flesh eating Strep would be a good example.
Endotoxin – Released by many Gram (-) bacteria when cells lyse, Examples:
Lipid A, lps in many pathogenic enteric bacteria like Shigella, can cause high fevers and even shock.
Endotoxin - Lipid A – raises fever, and shock in Gram (-) pathogens
Fig. 13.6
Microbiology – Chapter 13
Enzymes that help invasion
Collagenase – breaks down collagen, the protein holding cells together, thus allows spreading. Clostridia that invade tissue can produce these proteases to digest connective tissue elements (C. perfringens)
Hyaluronidase – breaks down hyaluronic acid, the polysachharide that may hold some cells together, S. pyogenes produces such an enzyme
Causes necrosis and blackening of tissue (inches of progression in hours)
Coagulase – Affects the fibrin in blood causing it to clot, Staph aureus produces one and maybe prevents phagocytosis.
Hemolysin – This exotoxin is an enzyme and lyses RBC. S. pyogenes
Evading defenses – Once in tissue some organisms can “evade” the natural defense of a host.
Capsule – Phagocytes can’t engulf the pathogen – S. pneumoniae
Surface proteins – Proteins prevent phagocytosis (leukostatin, leukocydins of Staph and Strep)
Survive inside phagocyte – Get a free ride and spread (Tubercle bacillus, Listeria bacillus, and others)
Evade immune response - Genetic variability occurs and the result is that antibodies lose effectiveness quickly – genetic shift/drift of the antigenic nature of the Influenza A virus, (FDA today is meeting to SWAG for next years vaccine)
