Micro Test 2

Front 1

permanently colonize host , does not normally cause disease

Back 1

Normal flora, protects host from niches, keeps pathogens away

Front 2

Germ free animals had less defenses than animals exposed to germs, they needed:

Back 2

underdeveloped, needed higher nutrients and needed additional vitamins

Front 3

Strep pneumonia A on skin is:
Strep pneumonia A in sputum or wound.

Back 3

fine.
infectious/risk for severe infection

Front 4

immunity- result of immune response- can be from natural infection or artificially due to administration.

Back 4

Active immunity

Front 5

occurs naturally during pregnancy- breast feeding 3-6 month immunity. no memory,once antibodies are degraded immunity is lost.

Back 5

Passive immunity

Front 6

normal flora produce:

Back 6

acids,bacteriosins-lysosomes in our tears.

Front 7

First exposed to normal flora at :

Back 7

Birth through vaginal canal.-

Front 8

strep pneumionia nose and skin normal, not normal and worrisome in:

Back 8

Sputum and wounds

Front 9

Should not have gram negative rods in:

Back 9

Respiratory system

Front 10

Should not have gram positive rods in:

Back 10

Intestinal system.

Front 11

Large intestine has normal gram negative rods:

Back 11

E-coli, Enterbacter,Klebsiella,Proteus.

Front 12

Gram positive rods that are normal in Resp. systems

Back 12

Staph,Diptheroids, Streptococcus, Haemophilis.

Front 13

Prevents growth of harmful organisms/normally will beat out abnormal flora-

Back 13

Microbial Antagonnism

Front 14

One benefits, other unaffected]Lives off our secretions, no benefit or harm.

Back 14

Corynebacterai spp. in eyes

Front 15

Benefits both organism- we will let you have our nutrients. E-Coli will produce-
Lactic Acid helps alleviate-

Back 15

Vitamin B and Vitamin K

Relieves diarrhea

Front 16

Benefits both organisms:

Back 16

Mutalism- E-Coli

Front 17

Organism benefits at expense of the other organism. Most disease causing organisms.

Back 17

Parasitism-

Front 18

organsims that are usually normal flora, but depending on situation (flora )it becomes this a pathogen. Too many antibiotics- or open lesion.

Back 18

Opportunistic
IE: E-coli- Yeast infection

Front 19

Disease not caused due to competition-pathogens for gingivitis- strep is geared for our gums/receptors. Out competes- flourish.

Back 19

Cooperation.
Receptors: for Streptococci spp.

Front 20

Exceptions to Koch Postulates: mere presence of organism does not prove causation- Need live tissue.

Back 20

Treponema pallidium(syphllis)
Mycobacterium leprae
Streptococcus pyogenes- strep throat, impetigo, flesh eating. Causes multiple of disease.

Front 21

Latent disease includes:

Back 21

Shingles. ( non-active- becomes active)

Front 22

Long lasting vaccine considered:
Life long:

Back 22

Long lasting.
Hep B

Front 23

Long lasting vaccination leads to: Vaccinate high enough percent of population-

Back 23

Herd Immunity.
Ex: small pox.

Front 24

Local infection:
Systemic:

Back 24

abcess
measles

Front 25

Local infection enters blood stream and spreads to another site:
Can lead to a toxic inflammatory condition:
Multiplication in the blood:

Back 25

Sinus infections.
Sepsis ( starts as focal)
Septicemia ( multiply in blood)

Front 26

Bacteria in blood, not always treated-
Toxins in blood-
Virus in blood-

Back 26

Bacteremia
Tetanus.
Viremia.

Front 27

Acute infection is an"

Secondary infection:

Back 27

acute infection,causing initial illness.

Opportunistic infection after primary (yeast)

Front 28

Does not cause noticable illness:

Back 28

Subclinical infection (immunocompromised pt)

Front 29

No s/s of illness- interval between initial infection and first appearance.

Back 29

Incubation period.

Front 30

Early mild symptoms-

Back 30

Prodromal

Front 31

Disease is most severe- if not treated will lead to death.

Back 31

Period of illness/ Infected stage

Front 32

Signs and symptoms subside-Pt's vulnerable to 2nd infections.

Back 32

Period of Decline.

Front 33

Convalescence stage.

Back 33

Body returns to pre-disease state.

Front 34

Humans- inapparent infections or latent diseases- (Reservoirs) Ex:

Back 34

AIDS- Gonorrhea are latent stage easily passed unaware of disease.

Front 35

Zoonoses can be transmitted to humans:

Back 35

Rabies-Lyme disease
2 big Zoonoses

Front 36

Non- living Reservoirs- soil or water

Back 36

Botulism,tetanus, cholera.( regular bacteria in soil-botulism)

Front 37

Host to host-
Human to human

Back 37

Direct transmission- no intermdiate.

Front 38

Bedding, tissues,door knobs- transmitted by:

Back 38

Indirect contact- host to non-living object.

Front 39

Transmission of airborne droplets:

Back 39

Droplets. ( 20,000) droplets in common sneeze.

Front 40

Transmission of medium is called:

Back 40

Vehicle ( food, water)

Front 41

Arthropods, fleas, ticks,mosquitos are:

Back 41

Vectors (arthropods)

Front 42

fly- is not sick- picking it up on its feet and distrubuting it through environment:

Back 42

Mechanical Vector- common house fly.

Front 43

Pathogen reproduces in vector or increases in number-(consumes pathogen-goes to host-)

Back 43

Biological ( mosquito) MALARIA

Front 44

8 legs-
4 legs-
6 legs

Back 44

Arachnida-spiders
Crustacea-shellfish
Insecta-mosquitos

Front 45

External skeletons, jointed legs, approx. 1 million species. Three main categories.

Back 45

Arthropods-

Front 46

Female needs bood meals for eggs- need protein, saliva released to prevent clotting. Most common vector:

Also, need blood meal.

Back 46

Mosquito-( Probiscus never clots)

Fleas.

Front 47

Lice blood sucking-hold onto surfaces- cannot survive long without host. Cause:

Back 47

Trench fever.

Front 48

Ticks are blood sucking,many varieties can cause:

Back 48

Rocky Mountain Spotted Fever

Front 49

Tiny, fast moving. Burrow into outer epidermis-lay eggs

Back 49

Mites-Rhicettsia pox can lead to pneumonia.

Front 50

20,000 die a year, are acquired as as result of hospital. 5-15% all pts acquire this:

Back 50

noscomial infection ( MRSA) pre-screened-

Front 51

3 things have to occur to have a nosocomial infections:

Back 51

microorganism in hospital
compromised host
chain of transmission( nurse, dr)

Front 52

Major nosocomial infection now:

Back 52

Staph (MRSA)
Gram + 60-80% of staph are resisitant.

Front 53

Compromised host- two conditions:

Back 53

Broken skin-mucous membrane. Suppressed immune system.

Invasive device- intubation.

Front 54

Sheets, linens, direct contact, things in a hosptial room. Ventilation. Areas reserved for specilaized care ( TB)

Back 54

Chain of transmission

Front 55

Majority of nosocomial infections are 40%:

Back 55

UTI

Front 56

Asceptic techniques, handeling of material, handwashing ( only 40% adhere to hanndwashing)

Back 56

Control of infection

Front 57

New strain of cholera-

Changes of weather :

Back 57

V. cholerae 0139

Hantavirus

Front 58

Import of exotic birds cause:

Ecological disaster,war, expanding human settlement:

Back 58

West Nile Virus

Coccidioidomycosis (fungal)

Front 59

Animal control measures ,tick control causes:

Back 59

Lyme disease

Front 60

Public Health Failure causes:

Back 60

Diphtheria ( diagnosed and not contained)

Front 61

Incidence of specific notifiable disease:

Deaths from notifiable disease:

Back 61

Morbidity (occured)

Mortality( deaths numbers)

Front 62

Number of people affected divided by total population in a given period of time:

Back 62

Morbidity rate

Front 63

Number of deaths from a disease divided by total population in a given time:

Back 63

Mortality Rate

Front 64

The ability to cause diesease in another organism:

Back 64

Pathogenicity

Front 65

The extent of damage caused by the pathogen.

Back 65

Virulence.

Front 66

Microbe has to have these three things:

Back 66

Portal of entry, host/invasion, portal of exit.

Front 67

Most frequently used entry of pathogen:
May also enter via:

Back 67

Respiratory

Skin, Direct deposit( surgery)

Front 68

May enter via GI tract, some that cannot be destroyed by our digestive system:

Back 68

Hep A
Amoebic dystentery

Front 69

In GU tract, you must have a cut or abrasion to gain entrance for these:

Back 69

Chlamaydia
Gonorrhea

Front 70

Skin is usually impenetrable but can gain access via:
One can bore through skin:

Back 70

Hair follicles, sweat ducts.

Hook worms.

Front 71

Parenteral Route some may be deposited into tissue, punctures,insect bites, wounds:

Back 71

Tetanus (direct deposit)
Gas gangrene

Front 72

Organism may not cause disease, needs specific portal of entry. Must enter digestive system:

Back 72

Salmonella typhi ( you have to eat/digest it to contract)

Front 73

Organism must have specific portal of entry via resp:

Back 73

Strep pneumonia has to be inhaled to become bacteria pneumonia ( if you eat it you will not get it, you have to inhlae it )

Front 74

Minimum amount of microbes needed to cause disease in healthy people in 50%-

Back 74

Infectious dose of 50 ( ID 50)

Front 75

The smaller the ID 50 have:

Back 75

Greater chance to cause disease.

Front 76

The agar plate contains:

Back 76

over 1,000,000 endospores

Front 77

Dose needed to caused death:

Back 77

Lethal dose 50 is the dose needed to kill 50% of population.

Front 78

The lower the number means:

55,000 spores equals death with this:

Back 78

More pathogenic/likely to cause disease.

Anthrax.

Front 79

Organism needs to evade defenses long enough to enter, multiply and exit.

Back 79

Mechanisms of pathogenicity.

Front 80

Goal is to spread, gain nutrients, host does not die, I can get out of host.

Back 80

Balanced pathogenicity.

Front 81

Not the organism that kills you, it is the toxin that it produces.( food poisoning)

Back 81

Clostridium botulism.

Front 82

Colonization of mucous membrane followed by toxin production (intestinal or upper respiratory tract)

Back 82

E-Coli-0157: H7 (in mucous membranes)
Hemorrhagic form-

Front 83

Invasion of host tissue, penetrates and multiple within host tissue:

Back 83

Mycobacterium tuberculosis.

Front 84

Invasion of host tissue followed by toxin prodcution:

Back 84

Shigella is in the tissue (not membrane)

Front 85

Surface molecule used for attachment called:

Back 85

Adhesins.

Front 86

Some will attract to sugaron cell wall and pass through system with sugars, attached to:

Back 86

Glycoprotein or Lipoprotein.

Front 87

Fimbrae,suckers,hooks and barbs are in:

Back 87

Glycocalyx

Front 88

Prevents phagocytosis,resists host defense encapsulated causes disease (needs capsule):

Back 88

Streptococcus pneumoniae has to have capsule to cause disease.

Front 89

Streptococcus pyogenes has this to help with attachment anb protection:

Back 89

M protein

Front 90

Fimbrae attaches to epithelial cells:

Back 90

Neisseria gonorrhoeae

Front 91

Has waxy lipid layer which protects it and helps replicate within phagocyte.

Back 91

Mycobacterium tuberculosis.

Front 92

Protects form phagocytosis in this bacteria using coagulase:

Back 92

Staphylococcus spp.

Front 93

Removes blood clots in heart attacks. Helps digest blood clots. This is:
Species:

Back 93

Kinase.
Streptococcus pyogenes.

Front 94

Holds together cells in connective tissue-may lead to blackening-gas gangrene-helps spread drugs through body:

Back 94

Hyaluronidase- breaks apart our connective tissue. Causes black gangrene.

Front 95

Breaks down collagen:

Back 95

Collagenase- breaks down clostridus spiridium species

Front 96

Prevents attachment to to mucosal surfaces-destroys antibodies: 2 species LOVE this:

Back 96

IgA protesases-
Neisseria gonorrhoeae
Neisseria meningitidis

Front 97

Alteration of surface antigen, so antibodies do not recognize me, able to alter antigens as needed: 2 love this-- ( it changes strains)

Back 97

Anti-genic Variation
Influenza
Neisseria gonorrhoeae

Front 98

Once host defenses are overcome, it then causes direct damage, toxin production, using host nutrients. Species living in host:/ damaging host?

Back 98

Allergic reactions, related to hypersensitivity.

Front 99

Pathogen pockets nutrients, pathogen consumes iron.

Back 99

Siderophores-

Front 100

Direct damage, causing cellular rupture, so all nutrients are relaeased in my environment.

Back 100

DAMAGE CELL-DIRECT DAMAGE

Front 101

Poisons produced by microbes, primary pathogenic property known as:
What species:

Back 101

Toxigenicity.
Streptococcus- toxic shock syndrome, botulism, tetanus.

Front 102

Produced within the cell-excreted from the cell-enzymatic activity, easily diffuse in blood (gram + and gram -)

Back 102

Exotoxins
EXO=Exiting the cell

Front 103

Most lethal toxins are:

Back 103

Exotoxins

Front 104

Attacks nerves:

Entererotoxins:

Cytotoxins:

Back 104

Nerve cells

Attack GI

Attack many cell types

Front 105

Three types of exotoxins,based on structure and function:

Back 105

A-B Toxins
Membrane Disrupting Toxins
Superantigens

Front 106

1 mg Botulism can kill:

Back 106

1 million guinea pigs/ same thing used for plastic surgery/to prevent wrinkles.

Front 107

Most toxins are A-B toxins.
A does:
B does:

Back 107

A cell-Alters function of host cell
inhibits protein synthesis

B cell binds to the cell

Front 108

Membrane disrupting toxins or known as:
What do they do?

Back 108

Type 2

Lyse host's cell by protein channels, disrupts phospholipid bilayer, stops things from entering or leaving cell.m Causing lysing of the cell.

Front 109

Superantigens are what kind of toxins?

What symptoms?

Back 109

Exotoxins that cause intense immune response.

Intense immune- release of cytokines from cell- causes Fever,N/V/D, shock and even death.

Front 110

Gram Negative are they endo or exotoxins?

Back 110

Endotoxins toxin within the cell wall.

Front 111

Only gram____ bacteria are within the cell, cause fever,chills,weakness, shock, death. May lead to miscarriage. EX:

Back 111

Negative.
Ex: Salmonella typhi

Front 112

Within the cell- you must consume the organism to receive the toxin-

Back 112

Dented can- organism must be in food that you consume.

Front 113

Big contributer of miscarriages:
May activate blood clotting proteins.

Back 113

Salmonella typhi- have to consume to get the toxin

Front 114

Avoid antibody response, continuous transfer between cells, can fuse to neighboring cells causing a "commune"-can modify surface antigen.

Back 114

Viruses.

Front 115

Hide within cell to avoid exposure to antibodies Vary surface antigens-

Back 115

Protozoa

Front 116

Most common portal of exits:

Back 116

Usually same as portral of entry. But, can be Resp, GI tract, Skin scales, Fecal exit, STD's, removal of blood.

Front 117

Less contact, less likely to spread. Is it a short or long incubation?

Back 117

Short Incubation.

Front 118

Contract infection-extreme spread.

Back 118

Long Incubation.

Front 119

Higher Immunity =
More likely or less likely?

Back 119

Less likely-

Front 120

When a disease cannot spread due to high number of immune individuals, cannot spread, this is called?

Back 120

Herd Immunity.

Front 121

Population characteristics.
African ancestry- with this is protected against this?

Back 121

Sickle cell anemia
Malaria

Front 122

Nothern Europeans less like to have?

Back 122

HIV

Front 123

Asian cultures more likely to eat fresh fish, at risk for?

Back 123

Parasitic infections.