Test 3 Chap 23 Flashcards Preview

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Flashcards in Test 3 Chap 23 Deck (39):
1

Competition

Process in which normal flora protects us from microbes

2

Microbial interactions

Mutualism =both host and microbe benefit
Commensalism= microbe causes n damage to host
Parasitism= microbes causes damage to host
All of the above are symbiotic

Pathogenic relationship=microbe (pathogen) causes damage to host; this pathogen is called microbial parasite
Normal Flora= microorganism normally found in or on the body, no disease
Synergistically= capable of working together, produce host response greater than the sum of effects they produce alone
Communicable= able to transmit between host

3

Disease reservoir

Natural source of disease agent. Reservoirs could include sick patients, asymptomatic carriers, animals, recovered patients, environmental sources

4

Laten infection

Some infections that go form symptomatic to asymptomatic and later reappears.

Ex. Herpes, Shingles, Chickenpox

5

Primary versus second infection

Infection cause by pathogen is followed by a second infection cause by a second pathogen

Ex. Mid respiratory infection caused by virus may be followed by bacterial pneumonia

6

Asymptomatic disease

Called subclinical
Patient unaware of disease due to no symptoms
Carriers: are person colonized but does not have disease

7

Comité

Inanimate object capable of transmitting microbe

Hospital equipment; patient’s bedding and gowns; latex gloves; eating and drinking utensils.

8

Pathogens

Organisms that live on or in a host organism, causing damage to the host, are called parasites.

Microbial parasites are called pathogens.

9

Pathogenicity (Virulence)

The outcome of host is based on this.

This is the ability of the parasite to cause damages on the host and on the resistance or susceptibility of the host to the paradise

VIRULENCE: measure of pathogenicity i.e. degree of pathogenicity
Quantitative measure of the degree of pathogenicity

Virulence- resistance always changing

EX. Streptococcus progenies=strep throat
Candida (commensal-no damage) can become virulent cause thrush

10

Opportunistic Pathogens

Vaginal yeast- flora killed by antibiotic

Pneumocystis Carinii pneumonia common in AIDS patients

Aspegillis niger eye infection in cancer patients

C.difficile can grow excessively when using too many antibiotics
Cause a pseudomembrane

Some can be benign in some other parts of the body, virulent in others
NEisseria-meningitis
Strep- pneumonia

11

OCmpromised host

Host with lowered resistance to infection and disease
Can be cause due to:
Malnutrition, alcoholism
Trauma from surgery or an injury
Cancer leukemia
Diabetes
Immunosuppressant Medication, HIV virus or SCID (genetic)
Altered flora due to antibiotic
Stress

12

Infection and Disease

Refers to any situation in which microorganism normally not present is established and growing in or on a host regardless of whether or not host is harmed

Disease= is damage or injury to host and impairs host functions

Infection not synonymous with disease, normal flora can sometimes cause disease

INFESTATION: presence of organism not necessarily growing and reproducing

13

Normal Flora in humans

SLIDE 12

A lot found on skin (10^12)-Fungi is commons

Internal tissue such as brain, blood, cerebral spinal fluid, muscles should have NO bacteria

Stomach has los pH around 2 which serves as barrier. Mycobacterium & salmonella are resistant. H. Pylori also resistant and causes ulcers

Colon also has a lot. About 50% of poop is due to bacteria degradation. B12 and K is produced in colon.

14

Normal Flora continued

GU tract (kidneys, ureters, bladders) should be free of microbes.

Upper respiratory (nasal passages, oral cavity, larynx, pharynx)= restricted # of colonies

Lower respiratory tract (trachea, bronchi, bronchioles, alveoli) NO bacteria.
Mucous traps move it up and out (excrete in saliva and nasal secretions)

15

Steps to Disease

Portal of Entry
Adherence
Invasion
Colonization and growth
Virulence factor produce damage (toxins and invasive factors)
Disease

16

Portals of entry

Food and water: outbreaks usually caused by sewege contamination in water (vibrio cholera, salmonella, shigella (dysentery))
Exhalation droplets: coughing and sneezing (mycobacterium, tuberculosis) Viruses such as glum chickenpox and measles
Direct Contact: Mono, Syphilis, Herpes, HIC, Chlamydia
Indirect Contact: Mono, Flu, Cold virus, hand to hand contact or hand to eye
Animal Bite or Scratches: actually part of parenteral
Rabies, Cat scratch fever (mild) Bartonella, Lyme disease, Rocky mt Fever dengue Zika, bubonic plague, malaria
Parenteral: wound or puncture penetration of skin or mucus membrane (clostridium tetani)

17

Classification of port of entry

Mucus membrane- exhalation droplets
GI track- food and water
GU- direct contact
Skin- hair follicles and sweat glands or also wounds (parenteral)

18

Adherence

Microbes adhere to epithelial cells on mucus membranes, using adhesin (located on pili or fimbriae) this process is highly selective and it dictates which tissue to attach

19

Tissue selectivity

Gonorrhea adheres more strongly to urogenital epithelium (its specific)

Microorganism that infect humans bind better to human epilithial cells than say rats

20

Adherence factors

Capsule (well defined layer)/ slime layer(loose network of polymers)
Adherence proteins
Lipoteichoic acid
Fimbriae (pili)- bacteria surface protein structures that function in attachment Ex, EColi enterotoxic strains that adhere to small intestine

SLIDE 24

21

Invasion & colonization and growth

Pathogen has to grow to produce disease
When it invades (penetrate through small breaks or lesions or even intact mucosal surface) it establishes itself, grow and multiply which can lead to disease via:

Toxicity-toxin effect local or system
Invasiveness- further growth of original and distant sites

22

Resistance

Acquired or induced immunity

Humoral:mediated by antibodies
Cellular: mediated bu Tcells

Natural resistance
Cells:macrophages
Mechanical barriers: skin mucus
Chemi: interferon, fatty acids on skin
Microbial: normal flora competition

23

Virulence Factor
Hyaluronidase

Spreading factor, catalases breakdown of hyaluronic acid, which cement human tissue cells together and allows bacteria to spread causing cellulitis

24

Coagulase

Catalyzes conversion of fibrinogen to fibrin with resultant clot formation

25

Fibrinolyson

Catalyzes con versión of plasminogen to the fibrinolytic enzyme plasmin. So it acts opposite of coagulase.

26

Lipase

Production of excessive Lipase allows bacteria to penetrate fatty tissue cause abscesses

27

Collagenase

Catalyzes degradation of collagen, fund in tendons, ligaments, cartilage, nails and hair

28

Leukocidins

Cause lysis of white blood cells

29

Lecithinase

Destroys red blood cells and other tissue

30

Hemolysis

Lyse red blood cells

31

Capsule

Carbohydrate or protein coat adherence (attach) & antiphagocytic (hide)

32

Pili and fimbriae

Attachment to surface receptors on host cells
UTI

33

Flagella

Motility

34

C3b

Binds to receptor on phagocygotic cells and prevent sit phagocytosis

35

Measuring Virulence

Can be estimated with leathal dose 50 study’s (LD50)

LD50 is the dose of an agent that kills 50% of the animals in test group

LOWER LD50 =MORE VIRULENT

36

Properties of ENDO and EXOTOXINS

SLIDE 45

37

Exotoxins

Cytolytic toxins: damage cell membrane causes cell lysis and death
AB toxins: B promotores specific binding of a toxin to host cell receptor, and allows A (toxic part) across the membrane (ANTHRAX)

Superantigen toxins: stimulate large numbers of immune lymphocytes and causes systemic as well as inflammatory response

38

Exotoxins site of action

Cytotoxin: inhibit cel function and causes cell death (Corynebacterium diphteriae)

Neurotoxin: inhibit nerve transmission (tetanus, botulism)

Enterotoxin: interstitial epithelium (staph, cholora)

39

Endotoxins

Gram neg bacteria produc lipopolysaccharides as part of the outer layer of their cells. Lipid A portion responsible for toxicity.

Called endo because they are cell bound and are released in large amounts when cell dies

Can cause septic shock
Not as toxic as exotoxins