Summer Micro 3

Front 1

What is transmission?

Back 1

organism has to get to you in order to cause disease

Front 2

What is portal of entry?

Back 2

it has to get into you in the correct way in order to cause disease

Front 3

What is the period of incubation?

Back 3

-the organism needs time to grow, or increqase the load

Front 4

How ius invasiveness a dmonstration of virulence?

Back 4

when the organism grows through your tissues and damages them. Sometimes the organism even digests your tissues—(ex: syphilis)

Front 5

How is production of toxin a demonstration of virulence?

Back 5

some organisms produce toxins which harm you, but are not invasive at all (ex: tetanus, botulism)
o Still others are both invasive and toxin producing

Front 6

What are signs and symptoms?

Back 6

your reactions to the growth of the organism (fever, diarrhea, headache, rash, death)

Front 7

What is the portal of exit?

Back 7

the organism leaves your body. In terms of portal of exit there are two concerns:
o How does the organism exit? Possibilities include blood, feces, saliva
o When does the organism exit? Sometimes a disease can leave your body before you even show symptoms, such as in the case of AIDS

Front 8

What is a vector? Examples? passive vs active?

Back 8

anything that can carry the organism
o The “4 F’s” are the 4 traditional vectors for transmission of microbial infections.
 1. fingers
 2. flies
 3. fomites
 4. food
o There are 2 others in addition to the 4
 5. phlegm
 6. fun
o Passive/mechanical vectors = only sources because the organism is carried without the vector having the disease
o Active vectors = carrier has the disease

Front 9

How are fingers a vector? Nasal secretions? oral secrctions? open sores? feces? How is it active?

Back 9

o Food industry, healthcare (hospitals)
o Fingers = usually passive / nothing grows on it
 Nasal secretions (mucous) – streptococci
• Nose = active because it has the infection
 Oral secretions (saliva) – staphylococci
 Open sores – MRSA
• Pus
• Touching an open sore, such as a bed sore infected with staph, or popping pimples
 Feces - viruses
• Feces -> fingers -> mouth
• Feces -> fingers -> food -> mouth
E. Coli, Salmonella
Sometimes fingers can be active vectors Syphilis sores on fingers
These sores can transmit the disease

Front 10

How are flies a vector? Passive? Active?

Back 10

o Refers to biologics, or living vectors (including flies)
 Flies, roaches, mice, rats, bats
o Drying in sunlight decreases virulence by decreasing the number or load

o Passive Biologic Vectors
 Not as dangerous as active biologic vectors
 In the example of flies, flies may land on fecal matter and then spread the organisms. But, this is not quite as dangerous as active because as the feces are exposed to the environment the load and the virulence of the organisms are being decreased. By the time it makes its way into a person, via food for instance, the organism, if alive, may have lessened virulence
o Active biologic vectors (a.k.a. Reservoirs of Infection)
 More dangerous than passive
 The microbe grows inside of the organism
 Example: bats and rabies or mosquitoes and malaria
 Is more dangerous because if the microbe grows inside of the vector, the load and the virulence both increase

Front 11

What is a reservoir of infection?

Back 11

allows transmission of disease but also provides a place for growth of the organism & survival too.

Front 12

How is a formite a vector? Source?

Back 12

o Inanimate objects = RESERVOIR OF INFECTION (organisms can grow and survive on it)
 Soil harbor the growth of athlete’s food and anthrax
• Diseases is passed on to humans
 Ganges River in India harbors the growth of cholera in the waters
 VIRBRIO in salty waters
 MOST inanimate objects are simply sources
o SOURCE: passive/mechanical way of transmission
 Needles can have hepatitis B on them
 Sponges can pass microbes, food utensils, and money, bed sheets, toilet seats
 In the case of money, there exists both paper and coin money. Properties of each, interestingly enough, help to inhibit the growth of microbial organisms
 Paper money has dyes on them which inhibit the growth of G+ bacteria
 Coins have a property known as oligodynamic properties, in which the metal is slowly released. This inhibits the growth of the organisms
 Toilet seats = not really a problem unless there’s wetness
 Handkerchiefs = dirty
 Thongs—increase in UTI’s, especially in females because shorter urethra

Front 13

How is food a vector?

Back 13

o Can act as a reservoir
o Examples include milk and water

Front 14

How is phlegm a vector?

Back 14

o Sneezing can project mucous up to 10 feet with micro aerosol
 Creates micro aerosol (stay in air for a while)
 Can stay up in the air for up to 1 hour
 Droplet infections are passed
o Coughing also creates aerosol that can stay in the air for 30 minutes
o Talking creates aerosol that can stay in the air for 6 minutes
 94-96% = non-pathogenic
 4-6% = pathogenic
 Also, even though some are pathogenic, you must keep in mind that there exists a minimum concentration of bacteria for diseases in order for the disease to get transmitted. This is called the ID50 – infectious dose required to infect 50% of the population
• TB is 10 bacilli
• Each droplet has 1-3 of these
 You also need a patient with pre-disposing factors.
• Compromised individual (aids, diabetes, advanced age)

Front 15

How is sex a vector?

Back 15

o Humans = reservoirs
o STD’s (sexually transmitted Diseases)
o Kissing, intercourse
o STD’s are especially dangerous sometimes because they are passed through direct person to person contact, with very little, if any, decrease in the load and virulence of the organism

Front 16

What are the various methods in control of tranmission of infections?

Back 16

eliminate reservoirs
break the link in transmission
immunizing biologics

Front 17

How do you eliminate reservoirs in control of transmission of infections?

Back 17

o Small pox = people vaccinated against
o Insecticides have been used to kill mosquitoes (malaria, west Nile virus)
o Rodents (rats, prairie dogs, etc.) are eliminated in various ways because they carry the plague

Front 18

How do break the link in transmission to control infectious diseases?

Back 18

o Cows can be a source of TB in their milk
 Pasteurize the milk to get rid of the pathogenic organisms
o Feces can spread E. Coli and salmonella
 wash your hands and chlorinate water to stop their spread
o AIDS
 Prophylactics, such as condoms, help to stop the spread
 Abstinence

Front 19

How are immunizing biologics (vaccines) usd in control of infectious diseases?

Back 19

o If the other methods of controlling the transmission, there are always vaccines.
o Tetanus
 everywhere around us, so there is a vaccine against it
 transmitted by cuts
 spores
o Hepatitis B

Front 20

How is tetanus an example of portal of entry? Typhoid fever?

Back 20

o Tetanus is caused by clostridium tetani, which has a portal of entry into the skin through a puncture wound (nail). If it is ingested is has no effects.
o Typhoid fever caused by salmonella typhi, causes severe disease if ingested thru digestive tract, but if it is gotten through a puncture wound, only a minor infection results—no typhoid fever.

Front 21

How is skin a portal of entry? Examples?

Back 21

o Defense Mechanism
o Interlocking layers of the epidermis and dermis help to make the skin a good border against most microbes.
o DERMATOPHYTES (fungi) can still gain access through the skin through the hair follicle
 Examples: include molds (ringworm, athletes foot) and staph
o STREP PYOGENES is usually in your nasopharynx
 If your skin becomes compromised (burns, blisters/chicken pox, needles, bite skin around nails, cuts, scrapes, IV drug users, mosquito—malaria, W.Nile) it can get into your body thru opening and cause disease
• Childbirth, broken skin

Front 22

How is the respiratory tract a portal of entry? Examples?

Back 22

o One main entry portal for most diseases
o Droplet infections (coughing, sneezing, talking)
 Bacteria: TB, haemophilis, pneumonia
 Viral: flue (bird flu, chicken flu), cold, small pox (supposedly wiped out, but CDC has some in freezer in USA & Russia), German measles (Rubella), measles (Rubeola)

Front 23

How is the digestive tract a portal of entry? examples?

Back 23

--one main entry portal for most diseases
o Food, water can be contaminated, especially by way of feces.
 E. Coli, Salmonella (food poisoning, milder strain), Dysentery (caused by shigella), cholera (lots of fluid comes out—50% mortality rate)
 Hepatitis A—feces spread
 Polio—feces spread, CDC no longer recommends oral vaccine because when it comes out, it is more pathogenic and therefore easily transmitted.

Front 24

How is th genito-urniary tract a portal of entry? examples?

Back 24

o Venereal diseases (STD’s)
 Syphilis, gonorrhea, Chlamydia
 Viruses: AIDS, herpes
o Can also get non STD infections
 Streptococci—childbirth fever, staphylococci—TSS, nasal/oral secretions
o Inanimate
 Bubble baths can transmit infections into the vagina. They are also thought to change the pH (making them alkaloid), helping the spread of infection. For this reason bubble baths are not recommended for young girls. (pseudomonas aeruginosa)
 Catheters for urinating can become contaminated
 UTI – toilet paper with improper wiping, and thongs can both cause feces to gain entrance into the vagina and cause an E.Coli UTI

Front 25

How is the placenta a portal of entry? Examples?

Back 25

o Some organisms can cross the placenta and infect babies if the mother has the diseases. (there is an acronym to remember this.: STORCH)
o S – Syphilis (bacterial STD)—can affect unborn baby, can go years without knowing you are infected
o T – Toxoplasmosis (Protozoal infection passed through cat feces), can cause mental retardation/death in/of unborn baby
o O – Others (AIDS, hepatitis B, Chlamydia)—can cross BBB
o R – Rubella (German measles)
o C – Cytomegalovirus: can be deadly to unborn baby in placenta
o H – herpes simplex 1 and 2 (1 causes cold sores/fever blisters, 2 is the STD/genital herpes)

Front 26

How is nature of organism affect period of incubation?

Back 26

o Cold and flu incubate in 24-48 hrs—VERY short
o Most acute childhood infections are 1-3 weeks (chicken pox, measles, mumps, etc.)
o TB is 6 months
o Leprosy is 2-5 years (usual range), although it has been seen up to 40 years
o AIDS is 2-15 years, though the average is 9.8 years (old) NOW: average=8 years

Front 27

How does th virulence of organisms affect period of incubation?

Back 27

o If the virulence is high, the incubation period decreases
 it can increase during an epidemic
 In an epidemic of chicken pox (type of herpes), for example, the incubation period at the beginning is anywhere from 1-3 weeks (10-21 days). As the disease gets spread from child to child (1st kid may take the longest to get sick), the virulence of the organism heightens due to increased strength. The incubation period, at the height of the epidemic, may therefore only be 1 week.

Front 28

How does resistance of host affect period of incubation?

Back 28

o If a host is more resistant, the incubation period is longer
o Bell-shaped curve, some will show no symptoms, some will die, and MOST will fall somewhere in the middle
o With a lot of diseases, if the host has increase resistance and the pathogen has decrease virulence, that person will not show serious symptoms or any symptoms at all. This is called a sub-clinical dose in which the person can still transit the disease although they appear healthy (healthy carrier)—actual people who spread the disease ex: strep throat, flu, fever

Front 29

How does distance from entrance to focus of action affect priod of incubation?

Back 29

o Rabies incubates for 1-2 months, so if someone is bitten on the ankle, it has to grow up to the brain (death). This obviously takes a longer period of time than if someone was bitten on the neck—shorter incubation period. **focus of action is the brain**

Front 30

How does amount of infectious agnt affct period of incubation?

Back 30

o LOAD—more organism exposed to, more chance you’ll get infection
o ID50 (infectious dose)– minimum infectious dose
 TB -10 bacilli, 100 people exposed—50% would get TB, 1,000 bacilli—shorter incubation period; so ID50
• In each droplet of a cough, there could be anywhere from 1-3 bacilli
 Salmonella – 100,000
• ID50=105 bacilli
• Main source=chicken, 1/3 package of chicken has salmonella on it—can be avoided when properly handled
 The higher the dose, the lower the incubation period
 Anthrax—8,000 to 10,000 spores: inhale, get pulmonary form, which is VERY deadly—die within a few hours of inhalation.

Front 31

What does virulence depend upon? Examples?

Back 31

o Dependent upon 2 factors:
 Invasiveness – ability to spread/can an organism spread throughout your body?
 Toxogenicity – can/does the organism produce toxins/poisons that can damage your cells?
o Syphilis – tremponema pallidum STD is very invasive, spreads through your entire body—bones, brain; but it is not very toxic at all. Untreated, it could take 20-30 years to kill you. (long, slow death)
o Tetanus – clostridium tetani is not invasive at all but is highly toxic
 Streptococcus pyogenes – strep sore throat, typical pneumonia. It can be dangerous, because it both produces a toxin and is invasive—can kill within 24 hours sometimes

Front 32

What is exaltation?

Back 32

increase the virulence of an organism by passing it from one susceptible host to another

Front 33

What is attenuation? example?

Back 33

decrease in virulence, done by exposure to adverse conditions such as increase in temperature, drying, chemicals (formaldehyde), grow organism on lab media (decreases virulence) i.e.—TB in lab is attenuated

Front 34

What is acute? Exampels?

Back 34

quick, short onset lasts a short time. Examples include flu, cold, Hepatitis A

Front 35

What is chronic? Examples?

Back 35

slow, long onset, long incubation period, lasts a long time
• AIDS—not an automatic death sentence, just a chronic infection as long as drugs can be afforded
• Leprosy
• TB—treatment is 6-24 months
• Hepatitis B and C

Front 36

What is systemic?

Back 36

affects the whole body
• similar infections—syphilis (STD, can spread throughout body), Lyme disease (tick bite, bulls eye ring, spreads throughout entire body)

Front 37

What is a local infection? Examples?

Back 37

confined to one area
• boil (pimples) caused by staphylococcus aureus
• TB localized to lung when first transmitted—primary TB is pulmonary TB, extrapulmonary TB is spread throughout the entire body
• Tetanus

Front 38

What is a focal infection? Examples?

Back 38

once local, it then spreads to other parts of the body
• boils – staph can spread
• TB can leave your lungssecondary TB or extra pulmonary

Front 39

What is septicemia? Examples?

Back 39

pathogenic organisms in your blood
• bacterenemia – bacteria in your blood
• virunemia – viruses in your blood (HIV positive)

Front 40

What is pyemia? Examples?

Back 40

pus (white bld cells called neutrophils) producing (pyogenic) organisms in your blood
• Staphylococcus, streptococcus

Front 41

What is toxemia?

Back 41

any organism that can produce a toxin, such as tetanus and diphtheria (toxins damage heart, and results in death), toxins in blood!

Front 42

What is sapremia? Examples?

Back 42

saprophytes growing in you (they live off the dead materials (tissues) inside of you—live host
• Sometimes a doctor may fail to remove all of the placenta after childbirth, so the mother can get a saprophytic infection
• Gas gangrene—frostbitten, dead tissue, grows saprophytes

Front 43

What enzymes of microbes affect invasiveness?

Back 43

Hyaluronidase
-collagenase
-lecithinase
-streptolysins
-leucocidan
-kinases

Front 44

What is Hyaluronidase? Examples?

Back 44

 Part of our “cement” (hyaluronic acid)
 Organism can move between cells and therefore spread because they’re able to breakdown the “cement”
 Enzyme that breaks down hyaluronic acid
 Ex: clostridium perforinges: in intestinal tract, Gram positive rod, anaerobic, can spread during surgery, cancer, accident, etc.—can produce gas gangrene (tissue dies—rots in place)
 Ex: streptococcus pyogenes—causes strep throat, and many others, causes tissue death-nephrotizing fascitis, kills flesh by destroying oxygen and rotting tissue

Front 45

What is collagenase? Examples?

Back 45

proteolytic enzyme
 Breaks down protein (collagen)
 In connective tissue
 Any organism with this enzyme can spread through our connective tissue
 Ex: clostridium perforinges: anaerobic, so ideal; connective tissue do not have good vascular protection

Front 46

What is lecithinase?

Back 46

: phospholipid
 Breaks down lecithin (found in cell membranes, phospholipids)
 Destroys cell membranes, causing cells to burst and die, especially RedBldCell’s because unnucleated and therefore can’t do repairs
 Hemolysin—toxin that destroys RBC
• Can do 2 things
o cause anemia
o decrease amount of oxygen to cells (anoxia/hypnoxia)

Front 47

What are streptolysins?

Back 47

 Hemolysin
• Anemia
• Anoxia
 Made by streptococci
 Streptococcus pyogenes is capable (why serious toxin)

Front 48

What is leucocidan? Examples?

Back 48

 Cidan=kill, leuco=white
 Enzyme that kills WBC’s
 Staphylococci and streptococci

Front 49

What are kinases? Examples?

Back 49

 Streptokinase
 Staphylokinase
• Dissolves fibrin (involved in clots)
 Ex: boils
• Staphylococci gets into hair follicle with WBC’s (pus) which are trying to kill staph which is actually killing WBC which then makes clot (boil)

Front 50

What is an endotoxin? Examples? Gram negative shock?

Back 50

 Gram negative bacteria—outer membrane: LPS (lipopolysaccharides)—where endotoxin is
 Part of cell wall, therefore in ALL gram negative bacteria
 Released when bacteria die, and THEN poisonous
 Not poisonous when bacteria are alive
 Low doses: causes fever, pyrogen
• Pyrogen=causes fever (not same as PYOgen which is pus forming)
 Mix antibiotics with sterile water (sterile can still be poisonous) autoclave-sterile, still toxic
 Not heat labile (not broken down by heat)
 Gram negative shock
• Patient with large number of gram negative bacteria in blood—septicemia & bactericemia
• Given antibiotics—quickly kills organisms
• Normally happens in compromised patients (diabetics)
• Get fever and hypotension (low heart beat, low blood pressure, and respiratory rate—slow breathing and circulatory collapse—go into shock and die)
 NONSPECIFIC!!!

Front 51

What are exotoxins? Examples?

Back 51

 Most poisonous
 Determine ID50
 SPECIFIC
 Very different for all bacteria
 Ex: tetanus, made by clostridium tetani which produces tetanosporin (neurotoxin)
 1 mg purified exotoxin can kill 10 mice
 Example: streptococcus pyogenes
• Arithrogenic toxin
• Super allergen—will make lots of antibodies and no disease to fight
o Hypersensitive reaction
 Rash
 Skin falls off—exfoliation
 Example: staphylococcus aureus
• Gram positive
• Make lots of toxins
• Enterotoxin—vomiting and diarrhea, affects GI Tract
 Salmonella—gram negative rod, can also make endotoxins, and enterotoxins
 Shigella—can make enterotoxin and endotoxin, gram negative rod
 Cholera—exotoxin, can make enterotoxin, can also make endotoxins

Front 52

What is a sign?

Back 52

quantitative, therefore can be measured and is objective ex: fever, swelling, paralysis

Front 53

What is a symptom?

Back 53

qualitative, not easily measured, subjective, ex: pain, malaise (nausea)

Front 54

What is syndrome?

Back 54

any group of signs and symptoms used to define an illness ex: flu syndrome, cold syndrome—dr. won’t take a sample, too expensive, instead go thru signs and symptoms ex: AIDS—caused by HIV Virus, need insurance to pay for drugs

Front 55

Whata re various forms of ways that an organism can use for a portal of exit?

Back 55

-feces
-urine
-sputum
-secretions
-blood

Front 56

How is feces a portal of exit? Examples?

Back 56

G.I. tract, had to eat/drink something containing feces
o Example: typhoid, e-coli, salmonella, shigella, hepatitis A, polio

Front 57

How is urine a portal of exit? Example?

Back 57

some penetrate epithelial cells and can get into urinary tract (typhoid)

Front 58

How is sputum a portal of exit? Examples?

Back 58

droplets from cough, microaerosol, ex: cold and flu, measles, German measles, TB, pneumonia,
o NOT AIDS! generally won’t pass thru saliva

Front 59

How are secretions a portal of exit? examples?

Back 59

lesions, mucus membranes,
o ex: gonorrhea—pus drips out of urethra, a.k.a.—“the drip”
o syphilis—rash & lesions, transferred by rash
o Herpes—USE condoms!
o Fungal infections—MRSA, little boils/pimples, transmitted by pus
o Chicken pox
o Leprosy—takes long contact time

Front 60

How is blood a portal of exit? examples?

Back 60

many organisms transmitted this way
o hepatitis B and C
o AIDS (main way of transmission)
o malaria

Front 61

What are various genetic defensze mechanisms against diseases?

Back 61

-species immunity/barrier
-racial immunity
-individual immunity

Front 62

How does species immunity/barrier affect genetic defense mechanisms against disease?

Back 62

o Smallpox—humans only, WHO & CDC vaccinated the world
o Typhoid—salmonella typhi, humans only
o Hand, foot, and mouth—humans: Coxsackie’s virus, enteric (intestinal) spread by feces, chicken pox like blisters
o Hoof and mouth—cows, can’t eat-die.
o 250 diseases transferable between humans and animals
 salmonella food poisoning
 rabies

Front 63

How is racial immunity a factor in genetic defense mechanisms against disease?

Back 63

o TB
 high incidence in American Indians
 not due to race at all
 poor nutrition=main reason
o Malaria
 racial differences
 mosquitoes are more abundant in certain countries
 some people are resistant die to sickle cell anemia mutation
• pigment in blood is hemoglobin
• RBC’s aren’t spherical, instead are crescent/sickle shaped
• Malaria can’t develop in sickle cells
 Duffy Factor
• Most people have
• Some people have mutation and are missing Duffy Factor
• If no Duffy factor, malaria can’t get in, and can’t develop
• On surface of RBC’s

Front 64

How does individual immunity affect genetic defense mechanisms against disease?

Back 64

o Athlete’s foot
o MS
 human herpes virus # 6 (everyone has)
• causes roseola—rash and fever (age 1-2)
• MS has a correlation with this roseola
 similar to odds of Rheumatic Fever from strep throat (only 3% of the population

Front 65

How is age a factor for indivdual and health in defense against diseases?

Back 65

o Very young < 2 years old, because haven’t been exposed to diseases yet, so no subclinical doses
o Therefore, no antibodies and low levels of complement (helps antibodies identify bacteria and virus as foreign, complements are proteins in serum)
o Very old, develop underlying disease, don’t eat right/exercise or smoke and drink too many sweets, develop diabetes, therefore more susceptible to disease and have decreased antibody production

Front 66

How is gender a factor in defense mechanisms against diseases?

Back 66

o Females
 more UTI’s because shorter urethra
 STD’s—gonorrhea and syphilis, more benign (unknown to have) in females—healthy carriers

Front 67

How is mental state a factor in defense mechanisms against disease?

Back 67

o Attitude can affect symptoms due to endorphins or hormones

Front 68

How do living conditions affect defense mechanisms against disease?

Back 68

o Upper-class: educated, wash hands, cleaner, more careful, but not exposing self to pathogens so get disease full-blown

Front 69

How does occupation affect defense mechanisms against disease?

Back 69

o Firefighters: exposure to hepatitis C thru blood which can be dormant for 20-30 years, affects liver

Front 70

How does fatigue affect defense mechanisms against disease?

Back 70

o Sleep deprivation
o Cold sores, start appearing—herpes I
o Infectious mononucleosis—could fight-off if not tired

Front 71

How does poor nutrition affect defense mechanisms against disease?

Back 71

o Alcoholics, drink instead of eating properly

Front 72

What are the various first lines of defense against diseases?

Back 72

-skin
-mucous membranes
-gastrointestinal system
-eyes
-genitourinary system

Front 73

how is skin a first line of defense against diseases?

Back 73

o Interlocking layers—THICK! Protects against most infections
o Very few pathogens get thru
o Through hair follicles
 Dermatophytes, staphylococci
o SHEDS (ex. Dandruff)
 Horny layer, stratum corneum sheds alot
 Constantly sloughed off
 Loaded with microorganisms
o Acid-Mantle
 pH—acidic=4-6.5
 Most organisms prefer neutral pH
residents & transients: residents are organisms that get on ur skin but are normal flora; transients are organisms that get on but are NOT normally on ur skin
 Only grows resident flora (plants)
 Transients—any one microorganism passing thru-CANT get thru
 Residents flora: take up space, secrete fatty acids, antimicrobial

Front 74

How are mucuous membranes a first line of defense against disease?

Back 74

o Mucous traps anything we inhale other than air
o Lines nose, etc.
o Also have cilia
 flapping hairs, push mucous into GI Tract
 swallow about 1 pint daily
o Good line of defense!

Front 75

How does the gastrointestinal system act as a first line of defense against disease?

Back 75

o Stomach
 Produces HCl, which results in a pH of 1-3 in the stomach.
 This inhibits the growth of most microbes.
 It also has thick walled mucous to act as a defense
o The small intestine
 Secretes sodium bicarbonate to neutralize the HCl, and this also helps to protect. **duodenum secretes sodium bicarbonatealkaline**
 Bile(anionic) in the small intestine acts as an emulsifying agent for lipids, but acts as an anionic detergent
 1st section of small intestine is duodenum
o The large intestine (colon)
 Favorable for micro-organism growth, which is usually removed in the feces.
 Thin walled mucous layer offers a small amount of protection

Front 76

How do eyes act as a first line of defense?

Back 76

o Tears act as mechanical flushing for protection
o In tears, immunoglobulin (IgA) (type of antibody) helps to protect. It is also found in saliva and mucous membranes
o This protects against recurring infection
o Tears also have lysozymes in them which is more effective than G+ than G- (because it breaks down the NAM-NAG bonds within the murein of the cell walls)
o Lysozymes are also found in saliva, perspiration, some WBC’s (white bld. cells)

Front 77

How does the genitourinary system act as a first line of defense?

Back 77

o Lubricated by mucous, offers some protection

Front 78

What are general facts about the 2nd lien fo defense against disease?

Back 78

• = Innate (we are born with them)
• = Non-specific
• Skin = protect against everything

Front 79

Whata re the various examples of the 2nd lien fo defense against disease?

Back 79

-leukocytes
-inflammation
-antimicrobial substances
-lacroferrin and transoferrin\
-lysozyme

Front 80

What is the relationship b/t red blood cells and white blood cells?

Back 80

o RBC # = 5 million per microliter (primary purpose = carry O2)
o WBC # = 5 – 10 thousand per microliter

Front 81

What are the 3 types of granulocytes that act as a 2nd lien fo defense against disease?

Back 81

-neutrophils
-eosinophils
-basophils

Front 82

How do neutrophils act as a 2nd line of defense against disease?

Back 82

MOST PHAGOCYTIC CELL
 55-90% of WBC count
 Responsible for most of phagocytosis that occurs
• Dead/waste materials in body
 PUS = dead microbes + neutrophils

Front 83

How do eosinophils act as a 2nd line of defense against disease?

Back 83

 1-3% of WBC count
 Contains lysozymes
 Rarely phagocytize
 Major function = produce toxins against large parasites
• Eukaryotes (fungi and helminthes infections)

Front 84

How do basophils act as a 2nd line of defense against disease?

Back 84

 < 1% WBC count
 Histamines and heparin are in granules
• Histamines = basil dilators
o Dilate/Increases the diameter of blood vessels
o Increases permeability of blood vessels
o Allows for more blood flow to an area and for more liquids to be released (swelling)
• Heparin = anti-coagulant (prevents blood from clotting)
 Involved in allergic reactions and inflammation
 In mucous connective tissues
• Mast cells have histamines and have similar function as basophils in produce of histamines BUT NOT A TYPE OF GRANULOCYTES

Front 85

Whata re two types of agranulocytes that act as a 2nd lien of defense against disease?

Back 85

-monocytes
-lymphocytes

Front 86

how do monocytes act as a 2nd line of defense against disease?

Back 86

o MONOCYTES
 Phagocytosis
 3-8% of WBC
 aka MACROPHAGES
• Monocytes enlarge when they phagocytize
• “Wandering Macrophages” = stay in blood and continues to circulate until a disease is encountered (phagocytosis)
• “Fixed Macrophages” = histocytes
o Go into tissues, specifically the RES (reticulo endothelial system)
o RES (aka MPS, mononuclear phagocytic system) = lymph drainage system

Front 87

How do lymphocytes act as a 2nd line of defense against disease?

Back 87

 20-30% of WBC count
• B LYMPHOCYTES = responsible for humoral (blood) immunity, in which antibody production results
• T LYMPHOCYTES = responsible for cell mediated immunity, which regulates the amount of antibodies
o Can increase/decrease production

Front 88

What are the various changes in White blood cell count during disease?

Back 88

o ↑ in leukocytes = leukocytosis
o ↑ in neutrophils = neutrophilia
 occurs with most acute bacteria infections, such as staph and strep (pyogenic cocci)
o ↑ in easinophils = eosinophilia
 fungal, helminthes infections
o ↑ in lymphocytes = lymphocytosis
 viral infections, such as infectious mononucleosis
o Counts can also DECREASE
 Leukopenia/Leukocytopenia
 Neutropenia
• Caused by:
o Typhoid, TB, Influenza, Measles - (MITT)
o Radiation, some drugs (sulfa drugs, chloramphenical)
 Lymphopenia /Lymphocytopenia
• AIDS (HIV) is characterized by a decrease in the number of CD4 T-helper cells/lymphocytes
• 500-1000 / microliter is normal
o 200/ microliter is considered to be the point at which an individual is diagnosed with AIDS

Front 89

What are the various cardinal signs of inflammation? how does it act as a 2nd line of defense against disease?

Back 89

o Redness, swelling, heat, pain, loss of normal function, increased fluids
o Redness – results from histamines dilating blood vessels (vasodilators) and increasing the blood flow to a particular area.
o Swelling (edema) – results from the histamines increasing the permeability of the blood vessels so the liquids leave the vessels and enter the surrounding tissues
 Classification of Edema:
• Serous = clear (for recent wounds, helps to dilute toxins)
• Purulent = pus (keeps infection from spreading)
• Fibrinogen = a lot of fibrinogen is produces, which produces clots
o Heat – warmth occurs because of increased blood flow to a localized area
o Pain – results when the edema/swelling presses against neurosensors
o Loss of normal function due to pain
o Increased fluid to an area –
 Serous - dilutes any toxins that might be present.
 Purulent, WBC are coming to fight an infection and destroy bacteria at the site.
 Fibrinogen forms clots, which creates a barrier around a wound or infection, tries to contain it in one area

Front 90

How do antimicrobial substances act as 2nd lines of defense against diseases?

Back 90

• Inflammation also brings antimicrobial substances to an area such as:
o Complement =
 Serum proteins that help antibodies fight infection by attaching to the bacteria or virus
 Helps body recognize it as foreign
o Interferons (alpha, beta, gamma)
 Are proteins with uncertain function and quantity
 Antiviral medsMS
 Suppress/inhibit the expression of some cancer genes
 Also have many other functions:
• Alpha (type I) interferons help activate natural killer cells
• Beta (type I) interferons help in the maturation of B and T lymphocytes.
• Gamma (type II) interferon activates macrophages
• Others:
o Type III tamda
o Type I: omega epsilon

Front 91

How do lacroferrina dn transoferrin act as 2nd lunes of defense against diseases?

Back 91

• ACTIVE BARRIER
• Proteins that hold iron in solution by binding to the iron.
o Prevent bacteria from using iron and act as a growth inhibitor/barrier in this way

Front 92

How do lysozymes act as a 2nd line fo defense against diseases?

Back 92

• Enzyme that breaks down murein (G+):effective against G+
o NAG and NAM bonds

Front 93

What are general characteristsics of the thrid lien of defense against diseases?

Back 93

-not innate
-nonspecific

Front 94

How are aquired resistance antibodies act as a third line of defense?

Back 94

• Are adaptive, which means that we much acquire them.
• For instance, if someone has never been exposed to TB, they do not possess the antibodies for the TB bacterium. Antibodies are also highly specific.
• Bergy’s 2nd Edition

Front 95

What is the mycobacteria in general?

Back 95

• Actinobacteria Phylum
o Cell walls consisting of high G+ (gram nonreactive)
o High G + C (guanine and cytosine) ration

Front 96

What is tuberculosis?

Back 96

-mycobacterium infection
characterized by symptoms mostly involving the lungs
o TB = primarily a lung infection that can spread elsewhere

Front 97

What is the etiology of mycobacterium?

Back 97

o Mycobacteria Tuberculosis – humans are the host for this organism (a.k.a. tubercle bacillus)
o Mycobacterium--M. Bovis – cows are the reservoirs of infection for this organism
o MOTT – Mycobacteria Other Than Tubercle bacillus (a.k.a. NTM – non-tubercle mycobacterium)
 M. Kansasii = unsure of reservoir
 M. Aviam = intracellular complex— from birds.
 These two
• Normally do not cause infection in competent individuals, but can cause problems in immunocompromised patients
• Can be more resistant than non-mott TB, so it requires identification if it is present.
• Sometimes surgical removal of the infected part of the lung is necessary

Front 98

What are the characteristsic sof mycobacterium? how do you culture it?

Back 98

o Gram non-reactive (don’t stain, due to waxy covering), acid fast organism
o Grows on Lowenstein-Jensen media
 Selective – a dye called malachite green inhibits the growth of G+ organisms (Staph & Strep) and selects for the TB
 Enriched – contains eggs and potato starch
 Mycobacterium grows very slowly, takes about 2-4 weeks to grow out
o Colonies appear dry and crumbly & waxy

Front 99

What is the morbidity of mycobacterium?

Back 99

o There are 20,000 active cases in the US each year
o 8 million active cases per year worldwide
o A large percentage of the population has the latent bacteria in them, which can stay in the body for up to 15-30 years without causing disease.
 15 million people in the US are latent carriers
 1/3 of the world’s population are latent carriers

Front 100

What is the mortality rate of mycobacerium?

Back 100

o Up until the early 1900’s, TB accounted for the most deaths out of any infectious agent. They called it the white plague, and 20-30% of deaths were from TB
o For roughly 80 years the world saw a decline in the instances of TB, but then in 1984 there was another increase in the cases due to increase IV drug use, increased cases of AIDS, increase homelessness and increased drug resistance
o There are 2000 deaths a year in the US, 1.5 million worldwide
 TB is still the most common cause of death worldwide by an infectious agent

Front 101

How is mycobacerium transmitted? ID50? primary site of infection?

Back 101

o Generally, it is non-white males over the age of 30 and non-white females over the age of 60
o It is a droplet infection spread by microaerosols from coughing
 Each droplet can contain anywhere from 1-3 bacilli
o USE TO BE: by way of milk, but NOW that most people drink pasteurized milk
o ID50 = 10 bacilli
o Primary site of infection is the lungs (alveoli

Front 102

Whata re predisposing factors of mycobacterium?

Back 102

o Advanced age—older, immune system is more worn down
o Poor nutrition
o Chronic alcoholism
o Poor economic status
o Prolonged stress

Front 103

What si the demonstration of virulence of mycobacterium? pulmonary? Mililay? Extrapulmonary? Osseous?

Back 103

o Primary site=lungs
o RES 1-3mm
o Tubercle fig.19.16
o Body builds tubercle (tissues) around bacteria to contain it, but organism isn’t dead
 Stays confined and latent
 Healthy = no signs or symptoms
 If patient meets criteria (pre-disposing factors) then bacteria will break-out and cause TB to digest lungs=Active TB
o Primary (pulmonary) TB—in lungs, most common. Spreads through lymphatic system
o Miliay TB – lesions on the skin resembling millet seeds
o Extrapulmonary TB (spread from your lungs and may spread to your bones)
 TB enters blood stream and can travel to other body parts
• Causes lesions on organs and body
o Osseous TB – TB in the bones. This is rare and only accounts for 5% of the cases because it has to be left to go long enough to get to this stage

Front 104

What is the incubation period of mycobacterium?

Back 104

- 6 months

Front 105

What are clinical symptoms of mycobacterium?

Back 105

O Pleurisy (fluid build up in the chest cavity surrounding the lungs characterized by vague chest pains)
O Coughing – a TB patient coughs up both the organism and sometimes blood in a stringy mucous mixture.
O Periodic fever
O Fatigue
O Weight loss – this is why they used to call TB “consumption”—organism digests lung tissue

Front 106

What are the various stratigies to diagnose mycobacterium infections?

Back 106

-sputum smear
-culture
-x-rays
-skin tests
-mantaux test

Front 107

How do you diagnose mycobacterium infections by sputum smear?

Back 107

 Sample of saliva (usually very stringy) is placed on a slide and acid fast stained
 If acid fast bacilli (AFB) are present from sputum smear, the patient has an active case of TB
 This test does only shows active cases (where patients are coughing up bacteria)
• Does NOT show latent

Front 108

How do do you diagnose mycobacterium infections by culturing?

Back 108

 Sputum smear = followed by a culture using Lowenstein Jensen media
• Cultures = incubated until growth is seen up for 30 days
• No growth after 30 days = negative test result
 This will only show active cases, not latent
 Grows out in 2-4 weeks, but must keep culture for 30 days
 This test is more sensitive than acid fast

Front 109

How do you diagnose mycobacterium infections by x-rays?

Back 109

 In the x-ray, you are looking for tubercles in the lungs
 This can diagnose both active and latent cases of TB
 Used for high risk patients
 Can be used to detect latent patients (advantage)

Front 110

How do diagnose mycobacterium infections my tine tests?

Back 110

-skin test
• Older test that was done for TB
• 4 prongs with Old Tuberculin (OT) protein or PPD (Purified Protein Derivative) on them
• PPD = more accurate and more effective than the Old Tuberculin (only used on animals in vets now) but is more expensive
• These proteins act as ANTIGENS in our bodies that try to detect for the presence of antibodies against TB
• The CDC no longer recommends this test to be done for TB
• PPD is recommended but you don’t get antibodies

Front 111

How do you diagnose mycobacterium infections by Manteux test?

Back 111

-skin test
• Newer test done for TB
• Requires an ID (intradermal) injection of antigens into the dermal layer
o Injection contains .1 ml of water with .0001 mg of PPD or 0.1ml
o After 3 days the results are checked to see varying degrees of indurations (raised, hardened areas surrounding the injection)
• In all cases, erythma (redness of the skin) and indurations result—part of inflammation response or where the skin hardens.
• This test also takes into account certain risk factors to help determine what sized indurations (hardenings) are considered to be a positive TB test.
• Test is palpable (can be felt): it can be measured: diameter of bump measured, results depend on risk factors.
• 5 mm (anywhere from 5-9mm); considered positive
o Immuno-compromised (AIDS)
o Household contact of a person with active TB
• 10mm (anywhere from 10-14mm)
o foreign born from Asia, Africa or Latin America
o IV drug user
o Resident of a long term care facility
o Diabetic
• 15 mm (anything 15 or higher)
o no risk factors

Front 112

How do you interpret skin tests for diagnoses of mycobacterium infections?

Back 112

O Positive TB test shows the presence of antibodies against TB in body
 Does not necessarily show an active case of TB
 At various age groups the likelihood of the antibodies being in your body vary:

Age %
>40, (>60) 80-90%
30-40 30%
7-30 5% (rare)
<7 0.3% (very rare)

o If the test is positive, do sputum smear and culture.

o There is a possibility with the skin test for a false negative due to tuberculin anergy, in which the tuberculin doesn’t attract the attention of the antibodies in the patient due to the antibodies actively fighting TB bacteria.
o False Positive is due to other bacteria in immuno-compromised patients or if patient is vaccinated (not absolute positive); ASK patients if they are vaccinated yet!
o Gene Probes, PCR
 Doesn’t give false negatives, is more accurate but is more expensive, quicker—(TB takes 2-4 weeks to grow-out)

**If you are in the >40, >60 age group and you test positive with no risk factors, doctors will look for patients with NEGATIVE results because that means that you don’t have any antibodies and so you are more susceptible to infection

Front 113

How do you use direct objerve therapy for treatment of mycobacterium infections?

Back 113

 One of the biggest problems with TB patients is non-compliance, either by belligerence or forgetting to take their meds
 DOT = patients are directly observed during course of therapy to ensure compliancy
• Higher cure rate than self-administered because patients usually stop taking medications after they are feeling better (bad idea)
 DOT is sometimes important because
• There are always multiple drugs that are given to a patient
• The treatment time can go anywhere from 6 months to 24 months
o During this time, resistance can develop.
• By using more than 1 drug the odds of the therapy being ineffective due to acquired bacteria immunity is less
 A higher dose of meds is used at the beginning of diagnosis to quickly lessen the load
 INH, Isoniazid, is the DOC (6-12 months) and is the only drug given by itself as a prophylaxis-chemoprophylaxis (preventative measure) A lower dose can be used because it is strictly preventative. (if a hospital employee gets coughed on by a patient with active TB) and is also in latent cases in high risk individuals like AIDS.

Front 114

How do you use empiric intial treatment for treatment of mycobacterium infections?

Back 114

for drugs, done immediately after diagnosis
 This treatment is done during the first 2-4 weeks of diagnosis while drug susceptibility tests are done on the bacilli. AFB—confirm with culture. A combination of 4 drugs are usually given


Isoniazid
Rifampin combined into 1 pill: RIFATER
Pyrazinamide MOST effective combo.

this drug is good because it is the only one that can attack the bacteria if it is inside of the
mitochondria (WBC’s)
 Ethambutol or Streptomycin
 That is a total of 4 drugs

Front 115

How do you treat suspectible organisms of mycobacterium infections?

Back 115

 Once the susceptibility tests come back and the bacilli are identified to be susceptible to the drugs, the therapy is lessened
 Rifater = first 2 months (no ethambutol)
 Test sputum during this 2 months
• Negative AFB result = continue on Rifimate (INH + Rifampin) for the next 4 months (total 6 months of therapy)
• Positive AFB result = continue Rifimate for 7 months (total 9 months of therapy)
 Resistance to drugs can occur, in which case the therapy must be modified.
 The drug that TB is especially resistant to is INH, because it is the longest used of the drugs for TB.
• If INH resistance is identified, Rifampin, Pyrazinamide and either Ethambutol or streptomycin are given for 6 months (total of 3 drugs for 6 months

Front 116

How do you treat multiple drug resistant tuberculosis during mycobacterium infections?

Back 116

 = INH & Rifampin
 The treatment for MDR TB is 4-7 drugs to which the organism is susceptible.
• This regiment is given for 18-24 months and daily DOT is recommended.
• AFB and culture done once a month for 12-18 months.

Front 117

How do you conduct retreatment of mycobacterium infections?

Back 117

o Sometimes retreatment is needed due to resistance or non-compliance
o There is a 7% chance of resistance developing mostly due to pt. non-compliance

Front 118

How do you prevent mycobacterium infections?

Back 118

o Quarantine/Isolation: isolate people who are infected w/ TB
o Education: educate pt w/ TB
o INH as a chemoprophylaxis—treat latent cases (especially AIDS patients) (can cause hepatitis also)
o BCG Vaccine – Bacillus of Calmetle + Guerin
 Mycobacterium bovis – live vaccine
 Given in the right arm because small pox is given in the left arm
 Lasts 5-15 years
 80% success rate in children,
 20-50% success rate in adults

Front 119

What is the etiology of Diphtheria infections?

Back 119

Corynebacterium diphtheria

Front 120

What is the incubation time of diphtheria infections?

Back 120

-1-10 days
-acute infection

Front 121

What are the symptoms of diptheria infections?

Back 121

o Forms a pseudo membrane in the throat (local infection), nasopharynx,
 Can get thick enough that it causes suffocation
o Produces a toxin that can cause heart problems and eventually lead to death
 Toxemia

Front 122

How do you diagnose diphtheria?

Back 122

o Gram stain of isolated sample from pseudo membrane
o G+, rods
o Metachromatic granules ( o o o )
o Exotoxin
o Look like “x’s and y’s”
o Palisade arrangement (rods line up side by side)
o Have metachromatic Granules (granules of various colors)
o The toxin used to be isolated and tested, but now that we have PCR we have a much more efficient and accurate way of identifying diphtheria

Front 123

How are diptheria infections transmitted?

Back 123

o Droplet infection (throat area) – healthy carriers
o Very hearty organism that can live on surfaces (fomites) NOT sensitive to environment
o Easy to get so important to get vaccinated

Front 124

What are the predisposing factors of diptheria infections?

Back 124

o Poor nutrition (#1 Reason)
o Nose and throat operations
o Children who are un-immunized. In the US, children are immunized

Front 125

How do you prevent diptheria infections?

Back 125

o The vaccine used to immunize US children is called DTP – Diphtheria Tetanus Pertussis vaccine
 This vaccine consists of ANTIGENS so a child produces antibodies against them.
 This is called active immunization (the antigen is directly put into the person so they can produce their own Antibodies)
 DTaP: acellular Pertussis, given to kids under 7 years old, less side effects
• Keeps body from overreacting

Front 126

How do you treat diptheria infections?

Back 126

o DOC Erythromycin – this kills the organism
o DAT – Diphtheria Anti-Toxin – this destroys the toxin that is present in blood of patient.
 DAT is actually diphtheria antibodies (come from horse), which destroy the toxins, and are then subsequently destroyed by the patients own immune system (short-term).
 The placement of antibodies into the patient is called passive immunization

Front 127

What is the etiology of staphylococcus infections?

Back 127

• FIRMICUTES
o Low G & C ratio
o G+
 Cell-wall chemistry consistent with being G+
 Does NOT necessarily stain G+
O STAPHYLOCOCCUS AUREUS
 G+ cocci
 Clusters
 Beta Hemolytic
 Tests + for coagulase (95% = positive)

Front 128

What are predisposing factors of staphylococcus infections? Primary reservoir?

Back 128

• NOSOCOMIAL INFECTIONS (OPPORTUNIST, takes advantage of compromised patients)
o Not a primary invader because staph is already on the skin
o Some people = persistently colonized
o Some people = never colonized
o Some people = intermittently colonized
• The primary reservoir is the anterior nares in the nose.
o In all, 40% of the population has staph aureus in their nares.

Front 129

What is the morbidity rate of staphylococcus infections?

Back 129

• Causes about 20% of nosocomial infections, because staph aureus is an opportunist

Front 130

What are the various diseases that are caused by staphylococcus infections?

Back 130

-toxic shock syndrome
-staph food poisoning
-abscess
-osteomyelitis
-contagious impetigo
-staph scalded skin syndrome

Front 131

What is toxic shock syndrome? symptoms?

Back 131

o Associated with nose/vaginal area:
 Highly absorbent tampons
 Absorbent padding stuff in noses after nose surgery
o In order to cause toxic shock syndrome, the staph aureus must be of the strain that produces TSST1 (Toxic Shock Syndrome Toxin 1), which is an exotoxin
 Exotoxins are produced by G+, endotoxins are produced by G-
 This toxin produces a fever, diarrhea, vomiting, myalgia, hypotension (low blood pressure),
 Patient can go into shock and eventually die.
 Penicillinase resistant, MSSA: use oxicillin, cloxicillin, or cephalosporin
o This strain could be growing and not causing a problem.
 But, the highly absorbent materials absorb Mg from blood
 The low Mg levels promote the development of the TSST1 toxin
o Most strains of staph have B-Lactam resistance, so you have to use a B-lactamase resistant drug

Front 132

What is staph food poisoning? symptoms? Prevention?

Back 132

food toxicity
 Typically infected foods = potato salad, macaroni salad (not due to the mayonnaise, but rather the starches in the potato and macaroni), hams and custards
 Toxin produced is an exotoxin, which acts as an enterotoxin (which causes problems in the intestines)
 The toxin only needs 3-8 hours to be in a high enough quantity to cause illness.
 The SYMPTOMS have a quick onset, anywhere from 1-6 hours after infection.
• For most people it is self-limiting, meaning it goes away without treatment (NO antibiotics) by itself, usually within 24 hours.
• The very young and the very old (especially heart patients) are a special case, as they can die from the loss of electrolytes and fluids from the vomiting and diarrhea. (a.k.a. 2 bucket syndrome: vomiting and diarrhea) Need electrolytes and fluids.
quick consumption and proper refrigeration is the only way to prevent it
• Staph can still grow but are inhibited in refrigerator
• Toxin is not heat labile (would need to heat at 100C for 30 mins.)
• So once present on the food, it can’t be heated up to destroy it

Front 133

What is staphyloccous abscess?

Back 133

o Boils, carbuncles, furuncles
o Staph get into the hair follicles, kills your neutrophils with leukocytin and destroys the fibrinogen with kinase
o Bacteria-leucocidin, staphylokinase

Front 134

What is a food infections?

Back 134

(e.g.: salmonella) = when the microbe is growing on the food and then the food is consumed, spreading the infection to the consumer

Front 135

What is food toxicity?

Back 135

= when a microbe grows and releases toxins on the food (now it can die, don’t need to ingest live), and then when the food is consumed the toxins make the consumer sick. Botulism is caused like this—food toxicity.

Front 136

How doy ou diagnose staphylococcus infections?

Back 136

• Beta-hemolytic
• Coagulase test (+)

Front 137

How do you treat staphylococcus infections?

Back 137

• When MSSA does not work, switch to MRSA
• Most staph are B-Lactam/Penicillinase resistant.
o Treatment is usually done with oxicillin or cloxacillin
o If it is resistant to these (MRSA), vancomycin is the DOC.
o If it is resistant to the vancomycin (VRSA), zyvox can be used.
o VISA (vancomycin intermediate staph aureus) VISA & VRSA are still susceptible to trimethoprim & sulfamethoxazole & linezolid (zyvox)

Front 138

What is osteomyelitis?

Back 138

 Staph aureus causes most cases (80%) of this disease, which is in the bones

Front 139

What is the etiology of group A streptococci?

Back 139

streptococci—STREP PYOGENES
• 80 different serovars, art of nasopharynx

Front 140

What are the various diseases of streptococci group A infections?

Back 140

-streptococcal pharyngitis
-scarlatina (scarlet fever)
-puerperal sepsis
-late non-suppurative sequelae
-contagious impetigo
-necrotizing fascitis

Front 141

What is streptococcal pharyngitis? symptoms?

Back 141

o Strep sore throat in tonsils and pharynx/throat
o Droplet infection
o Incubation: 1-3 days
o Symptoms: high fever, swollen (edema) throat, pus (purulent), cervical lymph nodes
o Can also get rhinitis or sinitis (dripping running nose

Front 142

What is scarlatina (scarlet fever)? Predisposing factors? symptoms? complications? prevention?

Back 142

-streptococcus infection
o 1830-1850, killed many
o Predisposing factors
 Need strain that produces erythrogenic toxin (exotoxin)
• Super antigen that stimulates a large immune response
• Immune system ends up attacking your own tissues
o Lysogenic conversion
o Symptoms
 High fever, sore throat, red rash
 Desquamations—massive exfoliation
o Complications
 Mastoiditis (behind the ear) = mucus goes back up nose from blowing too hard
 Nephritis = kidneys
 Otitis media = middle ear infection, hearing loss
 Streptococcal Toxic Shock Syndrome (STSS)
• Spread by milk and runny noses
• Bacteremia (bacteria in blood)
• Multiple organ failure
• 30% mortality rate with treatment
o Prevention
 Quarantine/isolation
 Pasteurize milk
 Cleanliness

Front 143

What is puerperal sepsis?

Back 143

-streptococcus group A infection
-o aka childbirth fever (very deadly)
o Mother (not the child) gets this and many organisms cause it (mainly strep pyogenes)—usually in the nasal area; colonizes vagina if MD’s hand was contaminated by the infected mucous
o During childbirth, skin tears, and strep pyogenes gets into skin and causes bacteremia which can result in the death of the mother

Front 144

What is late non-suppurative sequelae?

Back 144

o Late, 1-2 weeks following infection
o Non suppurative=no pus
o Sequelae= consequence

Front 145

What is rheumatic fever? prevention?

Back 145

starts as strep sore throat
 1-2 weeks, goes away, hypersensitivity reaction
• Causes high fever, polyarthritis, and possible heart damage
 Antibody (produced against your own proteins) attack proteins in your heart causing a connective tissue build-up around the valves (especially mitral valves) and could need valve replacement
• Aschoff bodies—large nodule formations
 If person gets in once there’s a 50% chance that they’ll get it again
• Use pf prophylactics (PREVENTION)
o Benzathine Pen. G—monthly injection
o PCN V—take orally once a month
o Sulfisoxazole—if allergic to PCN, once a month

Front 146

What is glomerulonephritis?

Back 146

 AGN (Acute GlumeruloNephritis)damage kidneys
 Strep pyogenes attacks kidneys

Front 147

What is contagious impetigo?

Back 147

 Staph aureus or strep pyogenes
 Crusty sores around mouth

Front 148

What is necrotizing fascitis?

Back 148

 Flesh eating disease; not really flesh eating but rather causes flesh to rot; fascitis refers to connective tissue
 Strep has enzymes that stop oxygen from going to tissues

Front 149

How do you treat group A streptococci infections?

Back 149

-sensitive to penicillin G

Front 150

What is the etiology of Group B Streptococci?

Back 150

-Strep Agalactiae

Front 151

What are the various life thretening diseases caused by Group B streptococci? In newborns and other opputuinistic strep?

Back 151

-pneumococcal strep (pneumonia and meningitis and haemophilus influenza)
-strep mitior
-strep mutans
enterococcus faecalis

Front 152

what is the morbidity rate of life threatening diseases in newborns caused by Group B Streptococci? Predisposing factors? Early onset form? late onset form? treatment? prevention? Also occurs in?

Back 152

o Morbidity 4% of all births
25% of all women have this as part of their normal genital flora
o Predisposing factors—premies (premature babies <3lbs)
o Common form
 Come out of birth canal
 Early onset form
• Child sick within a few days, gets pneumonia & septicemia
• 50-80% mortality rate without treatment
 Late onset form
• Few weeks after birth
• Meningitis SX
• Less mortality rate, but causes mental retardation, blindness, deafness, and cerebral palsy
o Treatment--Strep agalactiae sensitive to PCN G and ampicillin
o Prevention—C-section, or treat baby with antibiotics immediately after birth
o Other: immunocompromised, diabetics

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What is pneumococcal strep?

Back 153

streptococcus pneumoniae
• Seen in nasopharynx
• Causes no problem—5-500% of normal flora
• Bacteria that usually causes pneumonia (60% of all)
- includes pneumonia, meningitis, and haemophilis influenza

Front 154

What is the predisposing factors of pneumonia? Prevention?

Back 154

o Predisposing Factors
 Age, hospital stay
 Gets in lungs and eats lung tissue, causes death
o Prevention
 Vaccine: PPV23 Pneumococcal vaccine polyvalent
 23 serovars of pneumonia (active vaccine)
 60-70% effective
 Given to target groups, old

Front 155

What is meningitis?

Back 155

o Streptococcus pneumonia (#1 cause (and of otitis media also))
o Neisseria Meningitis (#2 cause)—communicable *dorms* VERY deadly.

Front 156

what is haemophilus influenza?

Back 156

-streptococcus pneumonia (#3 cause)(used to be #1 cause)
o Causes otitis infection – ear, middle ear, infection
o Treatment
 DOC: PCN G (if at least intermediate)
 MIC should be done
• <0.1ug/mL susceptible, use PCN G sensitive/PCN V
• 0.1-2ug/mL intermediate, use PCN G thru IV
• >2ug/mL resistant, aggressive treatment
o Resistant—vancomycin & cephalosporin (ceftriaxone or cefotaxime

Front 157

What is streptmitior?

Back 157

a.k.a.— viridans
o found in oral cavity
o can cause Endorcarditis
 Damage heart/valves
 75% of cases is endocarditis

Front 158

What is strep mutans?

Back 158

o Lesser cause of Endorcarditis
o Turns sweet into acid also dental cavities

Front 159

What is enterococcus faecalis?

Back 159

• ENTEROCOCCUS FAECALIS
o Live in GI (feces)
o More resistant to vancomycin
o Can cause Endorcarditis, also UTI
o G+ spore forming rods
• G+ cocci, chains in broth

Front 160

Whata re the characteristsics of the firmicates phylum?

Back 160

Mycoplasms, G+ spore forming rods—exotoxins
Clostridium & Bacillus species: both G+, both form spores, Clostridium Is anaerobic but bacillus is aerobic

Front 161

What is the etiology of botulism? Diseases that it causes?

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-mycoplasma
-clostridium botulinum
-food poisioning
-wound botulism
-infant botulism
-unclassified

Front 162

What is food poisoning botulism? symptoms? treatment? prevention?

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(20% of all cases)
 Food intoxication (not infection)
• Toxins in food, organism may already be dead
• Main poison = botulinum type A; most powerful
= it is a neurotoxin (NOT enterotoxin which affects GI system causes vomiting & diarrhea);
affects nervous system;
usually in cans (most likely people who do home canning)
• Canned food/jars, does NOT grow in high acid foods
o High acid foods
 Carbonated (soda, beer)
 Tomato sauces
 Citrus
 Vinegar
o Low acid foods—ideal.
 String beans
 Potatoes
 Corn
• Typical Food poisoning/infection
o Would have to cook at 121.5C for 15-30 mins.
 To destroy spores (pressure-cooker)
o Toxins heat and age labile = toxin will be destroyed with time
 Lasts for 6 months
 Killed in 10 mins. (boiling)
 Doesn’t alter taste
o Symptoms
 18-36 hours
 No vomiting/diarrhea (not enterotoxin)
 Blurred vision
 Paralyzes muscles--can’t breathe (affects diaphragm)
o Treatment
 Respirator: toxins wear off in 24-48 hours
 Antitoxin—CDC provides trivalent
• Have to get early before toxin binds to nerves
• Passive (from horses—equine)
• Treats types A, B, and E
 No antibiotics needed; b/c no organism is in you, just its toxins
 Death rate<10% due to quick treatment
o Prevention: try to wash it out
 High enema: bag with hose and flush soapy water up the rectum
• May perforate feces/intestines
 Catharctic
 Laxative

Front 163

What is wound botulism?

Back 163

(8%): causeblack tar heroin
 Mostly won’t happen
 Local infection, but toxin spreads
 Pen G.

Front 164

What is infant botulism?

Back 164

(60%--most common)
 Seen in 1976 when making baby food
• Honey
• Corn syrup
• Honey & corn syrup infected w/ spores
 Baby doesn’t have normal flora to fight infection
 Baby dies of toxin, looks like SIDS(sudden infant death syndrome)—only 4% of cases

Front 165

What is unclassified botulism?

Back 165

(12%)
 Can’t find cause
 Like NONE of the above

Front 166

What is the etiology of tetanus? Where is it found? What toxin does it produce?

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• Etiology: clostridium tetani
• Commonly found in feces, soil, etc. – can get into a deep wound
• Toxin = TETANOSPASMIN
o Exotoxin  dead, G+ (as powerful as botulism)
o Neurotoxin, very powerful
o Will only grow locally
o Causes involuntary violent contractions of voluntary muscles
 Lockjaw
 Hits diaphragm, stop breathing

Front 167

What is the morbidity rate of tetanus?

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o No immunity
o People over 50 years old
o Young usually vaccinated every 10 years
o Only about 50 cases a year in USA
o Over 1 million cases yearly worldwide (usually babies)

Front 168

How do you treat tetanus? DOC?

Back 168

o Respirator
o Muscle relaxants
o Antitoxins
 TIG (Tetanus ImmunoGlobulin)
• Human origin
• Preferred
• Less side reactions
 TAT (Tetanus AntiToxin)
• Horse origin (equine)
• More likely to have side reactions
• Only given when TIG isn’t available
o DOC: Flagyl (metronidazole) antibiotic for tetanus

Front 169

How do you prevent tetanus? Various vaccines?

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o Vaccination:
 DPT (diphtheria and tetanus toxoids and pertussis vaccine absorbed)
• Absorbed (less soluble, longer antibody stimulation)
• Toxoid= antigen
o Partially destroyed toxin, so body can make antibodies without destroying it completely; NOT the toxin; toxoid will not kill you
• Pertussis = dead bacteria
• Active vaccine (antigens)
• Capitalized b/c it’s high dose
 DPaT (diphtheria and tetanus toxoids and aceullar pertussis vaccine absorbed)
• Given to children under 7; too high of a dose for adults
• Not given to adults
o Body cant handle high dose of diphtheria
• Memory cells become activated causing a pertussis hypersensitivity reaction

 Tdap (tetanus and diphtheria toixoids absorbed)
 TD (tetanus diphitheria toxoids absorbed)
• Less diphtheria toxin for adults to take and no pertussis
o 11-12 adolescents
 Persistent cough
 Pertussis vaccine doesn’t last long
• Every 10 years
• If wounded:
o Clean, only give shot if do not know if taken in last 10 years
• Dirty, give shot only if not given in last 5 years
 DT (Diphtheria & Tetanus toxoids absorbed)
• Some kids can’t handle pertussis of DPT (may cause death)
• Wait to see how sensitive to pertussis kids are
• Used in kids under 7

Front 170

What is the etiology of gas gangrene? What diseases can occur?

Back 170

• Etiology: clostridium perforinges
o Anaerobic
o Come out with feces (part of GI)
o Produces gas which causes tissues to rot
-anaerobic cellulites
-myonecrosis

Front 171

What is anaerobic cellulites?

Back 171

-caused by gas gangreen (clostridium perforinges)
o Rotting, black tissues
o Local, not deep or spreading, more superficial
o Necrotic tissue helps growth of organism

Front 172

What is myonecrosis? DOC?

Back 172

-caused by gas gangrene
-o Can spread rapidly, more dangerous form
o Rotting away of muscles
o Surgical removal of dead tissue
 Allows oxygen to penetrate and kill anaerobes
 Antibiotics: DOC=PCN G

Front 173

What is antibiotic associated colitis? Bacteria involved? Treatment?

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ANTIBIOTIC ASSOCIATED COLITIS
• Inflammation of colon
• Broad spectrum antibiotics (ampicillin)—kills part of normal flora in intestinal tract
• Clostridium difficile is resistant to it, grows and irritates bowels causing diarrhea
• Treatment
o Mild: stop antibiotics
o Severe: take Flagyl (metronidazole)
o DOC was vancomycin, but stopped due to fear of developing resistance

Front 174

What is the etiology of anthrax? forms?

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• G+ rod
• Etiology: bacillus anthracis
o Spores in soil (reservoir)--farm animals eat grass, get anthrax
o People handle animals, and infected meat and get anthrax
-cutaneous
-pulmonary

Front 175

What is the cutaneous form of anthrax?

Back 175

 Looks like gas gangrene
 Necrotic tissue
 Not as deadly as pulmonary

Front 176

What is the pulmonary form of anthrax? DOC?

Back 176

 DOC = ciprofloxacin
 Breathe anthrax into lungs
 Die within a few hours of onset of symptoms
 VERY deadly

Front 177

How do you prevent anthrax?

Back 177

o Cremation/deep burial
o Vaccination
 Humans—bad reactions
 Cows—not long lasting
o Antibiotics--ciprofloxacin

Front 178

What is the etiology of mycoplasma? What does it cause? DOC?

Back 178

• No cell wall- G- (based on DNA)
• Mycoplasm pneumoniae
o Causes walking pneumonia (mild, not bed-ridden)
o DOC's
 Erythromycin
 Azithromycin
 Tetracycline