Microbiology – Chapter 13

Microbiology – Chapter 13

Pathology: Science of study of disease

Etiology: Cause of disease; often microbial

Flu – etiological agent, Influenza virus

Tb – M. tuberculosis

Pathogenesis: development of disease in the host - Norwalk virus; Fecal – oral, diarrhea

Disease: altered state of health, host body is changed, upset of homeostasis


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. ***


Relationship between organisms:

Normal flora: normal inhabitants of the host

ex. S.epidermidis on skin, E.coli in intestine

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


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)


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)


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, tick2. Inanimate: things, toys, dirty hands,

needles, (sometimes called “fomites”)


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


Nine routes of infection

**** Know this; be able to list and give an example of each****

1. Respiratory droplets: cough sneeze, air born droplets

Flu, colds, Strep throat even Staph infections of wounds

Fig. 13.12


2. Fomites

Inanimate objects that spread disease agents

Shared drinking cups, baby toys in a nursery, contaminated sharps

** add pictures**


3. Direct body contact- Oh what fun!!

Person to person:

STD,

Impetigo


4. Fecal – OralFeces contamination of food water, even dirty hands (hands are a vector, or even a house fly or roach)

Enteric diarrheal disease;Helminth

Protozoans: Giardia, Balntidium


5. Arthropod Vectors

Flies, fleas, mosquito, tick

Fig. 13.11


6. AirborneParticles suspended in air (dry; dust), travel long distances; tb, anthrax spores (potential for WMD), Respiratory fungal infections (Histoplasma)


7. ParenteralDirect transmission via blood: universal precautions

HIV, HVB, HVC


8. Deep Wound traumaGas gangrene and tetanus, even wound botulism

Beaman’s world infant tetanus


9. Horizontal: Mother to infant

Prenatal: across the placenta; HIV

Perinatal: at birth, STD like gonorrhea and syphilis, even Chlamydia blindness


• 9. Horizontal: Mother to infant

• Perinatal: at birth, STD like gonorrhea and syphilis, even Chlamydia blindness


Virulence factorsVirulence 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


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 AdhesionsSEM of Pseudomonas, Gram (-)

Virulence Factors


Toxins – Poisonous microbial bypoducts that are produced by the microbe and diffuse into tissues causing

damage/ enhance invasion/ avoid defensesExotoxins – 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 youStreptococcus 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

Endotoxin - Lipid A – raises fever, and shock in Gram (-) pathogens

Fig. 13.6


Enzymes that help invasionCollagenase – 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

Alpha and Beta Hemolysis of the Strep.

Virulence Factors

• Enzymes: Collagenase, Hyaluronidase

Virulence Factors

• Enzymes: Hemolysin – lyse RBC


Evading defenses – Once in tissue some organisms can “evade” the natural defense of a

host.Capsule – Phagocytes can’t engulf the pathogen – S.

pneumoniaeSurface 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)

Virulence Factors

• Evade defenses: Capsule – resisting phagocytosis, Strep.

Virulence Factors

• Adherence: Glycocalyx (capsule)

Virulence Factors

• Surface proteins : Leukocydin, S. aureus

• (MRSA) – Attacks WBC’S

M. tuberculosis inside lung macrophage

Virulence Factors

• Survive inside phagocyte, tubercle bacillus

•

Evading immune response• Influenza

Virulence Factors

• Evade immune response : Influenza A

• H5N1 – “Bird Flu”

•


Iron binding – Iron is tightly bound in our bodies and microbes need it to grow,

Those organisms that can acquire it have and advantage and can spread faster;

more virulent – Cholera is an example, HIB (H. influenza B)

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Microbiology – Chapter 13