Micro 4. Chap. 23

Front 1

Disease production in infected wounds depends on:
-How __________ an organism?
-How many organisms infect?
-Is the host _____________?
-Nature of the wound (Does it contain _________ ________, if so, it won't heal until removed.)

Back 1

Virulent
Immunocompetent
Foreign material

Front 2

An __________ wound is an incision produced by a knife or other sharp object.

Back 2

Incised

Front 3

A ___________ wound is from penetration of a sharp object.

Back 3

Puncture

Front 4

A ___________ wound is a laceration when tissue is torn.

Back 4

Laceration

Front 5

A ___________ wound is a contusion caused by a blow, so you're dealing with ___________ tissue.

Back 5

Contused
Crushed

Front 6

Wound ___________ are localized collection of pus surrounded by _______ ________.

Back 6

Abscesses
Body tissue

Front 7

Abscess formation helps to __________ __________.

Back 7

Localize infection

Front 8

To effect cure, the abscess must rupture to a body surface or be ___________ __________.

Back 8

Surgically drained.

Front 9

Common bacterial wound infections include:
1. Staphylococcal wound infections
2. Group A ___________ wound infections
3. ____________ _____________ infections.

Back 9

Streptococcal
Pseudomonas aeruginosa

Front 10

_____________ are the leading cause of wound infections. There are more than ____ strains, the two most common in humans are:

Back 10

Staphylococci
30
1. S. aureus
2. S. epi

Front 11

S. aureus causes virulence due to the production of ___________ products.

Back 11

Extracellular

Front 12

___________ causes blood clotting to evade phagocytosis.

Back 12

Coagulase

Front 13

___________ factor aids in bacterial wound colonization.

Back 13

Clumping

Front 14

___________ A hide bacteria from phagocytic cells.

Back 14

Protein

Front 15

________-_______ produces hold in host cell membrane.

Back 15

Alpha-toxin

Front 16

Systemic spread of virulence factors can lead to ___________ in other tissues. Commonly the _______ and joints.

Back 16

Abscesses
Heart

Front 17

Certain species produce toxins which in the blood act as ____________ and can lead to TSS (__________ _________ ___________)

Back 17

Superantigen
Toxic Shock syndrome

Front 18

Prevention of Staph wound infections directed at:

Back 18

Cleansing wound
Prompt closure
Pre-surgical antistaphylococcus medications

Front 19

Treatment of Staph wound infections can be hard because many strains develop _____________ to antibiotics and are resistant to _________.

Back 19

Resistance
Penicillin

Front 20

Many strains of Staph wound infections are treated anti-beta ____________.

Back 20

Lactamase

Front 21

Group A Streptococcal infections are aka _________ __________. The primary pathogen is S. ___________.

Back 21

Flesh eaters
Pyogenes

Front 22

True or False:
Group A Strep wound infections are mostly easily treated with little antibiotic resistance.

Back 22

True

Front 23

More severe infections of Group A Strep are called __________. Include ________, meningitis, puerperal (__________ fever), ____________ _________ (flesh eating disease) and Streptococcal ________ __________.

Back 23

Invasive
Pneumonia
Childbirth
Necrotizing fasciitis
Toxic shock

Front 24

Symptoms of Group A Strep infections:

Back 24

Acute pain at the site
Swelling
Fever and confusion
Shock and death without treatment

Front 25

___________ _________ is destroyed in necrotizing fasciitis. ________ tissue is also destroyed when bacteria penetrates muscle tissue.

Back 25

Subcutaneous fascia
Muscle

Front 26

Organisms multiply and produce _________ products that enter ___________ and can cause shock.

Back 26

Toxic
Bloodstream

Front 27

Cases of Group A Strep are generally __________. Small epidemics have occured, like in San Fran in 1996.

Back 27

Sporadic

Front 28

There were ~9,000 cases of S. ____________ in 2002 resulting in 1080 deaths (~12%). 135 of those were from necrotizing fasciitis.

Back 28

Pyogenes

Front 29

There is no proven prevention, urgent surgery is required due to _________ of toxic spread and amputation is sometimes required.

Back 29

Rapidity

Front 30

__________ is still an effective treatment, but it must be given early and has little to no effect on bacteria in _________ tissue and no effect on toxin.

Back 30

Penicillin
Necrotic

Front 31

P. aeruginosa is an ___________ pathogen that is a major cause of __________ infections.

Back 31

Opportunistic
Nosocomial

Front 32

Community acquired P.aeru infections:
Eye infections
Infection of foot ________
Rash and external ear infections
Heart ________ infections
Lung _________ that compromise gas exchange

Back 32

Bones
Valve
Biofilms

Front 33

Nosocomial P.aeru infections:
_______ infections
_______ infections (most common)

Back 33

Lung
Burn

Front 34

Symptoms of P.aeru wound infection:
1. Release pigments that change tissue color to _______.
2. Chills, fever, skin lesions and shock caused by bacterial infection of ___________.

Back 34

Green
Bloodstream

Front 35

Overall, the effect of P.aeru is tissue damage, prevention of healing and increased risk of _________ ________.

Back 35

Septic shock

Front 36

Some strains produce enzymes and toxins to enhance virulence:
1. ____________ S
2. ___________ A
3. ____________ C

Back 36

1. Exoenzyme S
2. Toxin A
3. Phosphlipase C (signal transduction molecule that tricks your cells into favoring infection.)

Front 37

Tetanus is aka _________.

Back 37

Lockjaw

Front 38

True or False:
Lockjaw is common in the developed world and rarely is fatal.

Back 38

False:
Not common in developed world, often fatal

Front 39

Early symptoms of tetanus:
Restlessness, irritability, difficulty ____________, contraction of jaw muscles, ___________ (particularly in children.)

Back 39

Swallowing
Convulsions

Front 40

Late symptoms of tetanus:
Increased muscle ___________ creating more pain
Difficulty breathing
_____________ of stomach contents into lungs

Back 40

Involvment
Regurgitation

Front 41

The causative agent of tetanus is ___________ ___________, an anaerobic, Gram _________ bacillus spore former.

Back 41

Clostridium tetini
Gram negative

Front 42

The C. tetini bacteria form a toxin called ____________ that is responsible for the pathogenesis.

Back 42

Tetanospasmin

Front 43

Toxin is composed of 2 chains
1. Heavy chain binds ___________ on motor neuron
2. Ligher chain taken up through ___________.

Back 43

Receptors
Endocytosis

Front 44

Tetanospasmin blocks ___________ of motor neurons, causing ___________.

Back 44

Inhibition
Paralysis

Front 45

Muscle contration is _____________, muscles do not relax.

Back 45

Uncontrolled

Front 46

______________ is the best prevention of lockjaw.

Back 46

Immunization

Front 47

The vaccine for tetanus is inactivated ________________. This is given in combo with diptheria and ___________ vaccine (DTaP)

Back 47

Tetanospasmin
Pertusis

Front 48

Treatment of tetanus includes cleaning wound and removing dead tissue, antimicrobial treatment and an Antitoxin, an __________ against ___________ (which neutralizes toxin not attached to nerve cells).

Back 48

Antibody against tetanospasmin

Front 49

Gas gangrene is the common term for _________ ___________.

Back 49

Clostridial myonecrosis

Front 50

Clostridial myonecrosis is primarily a _________ disease. The spores are found everywhere but rarely lead to this disease.

Back 50

Wartime

Front 51

The causative agent of Clostridial myonecrosis is __________. The most common offender is C. _________ which is an encapsulated, gram _______ bacillus.

Back 51

Clostridium
C. perfrigens
Gram-neg

Front 52

The two factors that foster development of clostrial myonecrosis are:
1. Prescence of ______ and dead tissue in wound
2. Long delay of treatment

Back 52

Dirt

Front 53

The bacteria of Clostridial myonecrosis produces ________ toxin taht attacks the host cell membranes. Other enzymes break down the __________ of dead tissue

Back 53

Alpha
Macromolecules

Front 54

C. perfringens are unable to grow in healthy tissue. Only survives well in dead or poorly ___________ tissue.

Back 54

Oxygenated

Front 55

Bacteria of Clostridial myonecrosis produces gas through _____________ which accumulates in tissue, contributing to spread.

Back 55

Fermentation