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1

What type of environment does S. Pyogenes require

It is aerotolerant or microaerophilic, and so requires just a small bit of oxygen

2

What type of environment does S. aureus require

It is facultative, and so can grow with or without oxygen

3

What does strep pyogenes look like under the microscope

A chain of balls. Strep is a strip!

4

What does staph aureus look like under the microscope

clusters of grapes

5

What 6 counters/evasion strategies does strep pyogenes employ

1. Protective outer coat that blocks complement 2. Coats itself with host fibrinogen 3. produces a hyaluronic acid capsule similar to the host extracellular matrix 4. strain variation of M protein 5. Cytolytic exotoxins and enzymes that kill defensive leukocytes and destroy clots 6. facilitates colonization with M protein and F protein that cross link pili to host fibronectin on host epithelial cells, etc

6

What are some of the main disease that strep (mainly pyogenes) causes

strep throat, scarlet fever, rheumatic fever, childbirth fever, endocarditis neonatal sepsis, pneumonia, meningitis, ear infections

7

What are the three mechanisms by which S. pyogenes damages the host

1. local pyogenic infection 2. toxic system disease 3. Immune-sequelae' diseases

8

What is type 2 hypersensitivity

Damage that results from the direct binding of an antibody to a host epitope

9

What is the main type 2 hypersensitivity disease caused by S. pyogenes

Ab made against S. pyogenes cross reacts with heart tissue epitopes, thus damaging the heart and causing one of the severe outcomes of rheumatic fever

10

What is a type 3 hypersensitivity

immune-complex-induced damage (innocent bystander)

11

What is the best way to prevent rheumatic fever

Penicillin TX of strep throat

12

What is scarlet fever

System-wide inflammation and dysfunction including rashes fever and shock. Caused by S. pyogenes pyrogenic super antigen

13

What are the main ways Strep infections can damage the heart

1. acute bacterial endocarditis 2. rheumatic fever 3. sub-acute bacterial endocarditis

14

Why do many people develop hypersensitivity to penicillin

Because it has a very active beta lactim ring that will bind to host proteins

15

what are the main classifications of streptococcus

1. Hemolysis 2. Lancefield 3. Natural cluster 4. 16S rna sequences

16

What is the classification of S. pyogenes

beta-hemolytic, group A

17

What is the classification and primary location of S. agalactiae

beta-hemolytic, group B. Lives primarily in vagina

18

What are the main pathologies caused by S. pyogenes

Strep throat, rheumatic fever, cellulitis, scarlet fever

19

What are the main pathologies caused by S. agalactiae and its main virulence factor(s)

neonatal sepsis, mom sepsis. Main virulence factor is a capsule

20

What is the classification of S. pneumoniae

alpha-hemolytic, no lancefield

21

What is the main virulence factor(s) and pathologies caused by S. pneumoniae

uses a capsule. Causes pneumonia, ear infections, and meningitis

22

What is the classification and location of viridans type strep

alpha hemolytic, they live in the mouth

23

What are the main pathologies caused by viridans type strep

Endocarditis, dental caries

24

What are the most pathogenic stains of Staph

S. aureus, S. epidermidis, and S. saprophyticus

25

Why does staph remain infectious for weeks

because it is non-fastidious: grows in up to 10% NaCl, resists drying for weeks or months, resists heating up to 60C for 30 minutes, and resists pH changes.

26

What is a big problem with Staph

They are frequently multi drug resistant and have multiple virulence factors, mostly because they are promiscuous conjugators. Additionally, they have a high carrier rate.

27

What pathogen secretes catalase and what does it do

Staph secretes catalase which converts H2O2 to water which protects them in phagolysosomes

28

Where is S. saprophyticus normally found and what is its appearance

S. saprophyticus is found in the colon and vaginal mucosa. It forms a white colony

29

Where is S. epidermidis normally found and what is its appearance

S. epidermidis is found on the skin or other dry epithelium and forms a white colony

30

Where is S. aureus normally found and what is its appearance

S. aureus is essentially the only bug that inhabits nasal mucosa. It inhabits moist skin surfaces, and often the GI tract. It forms a yellow colony and is coagulase positive.

31

What are the virulence factors in S. aureus

Protein A, secrete many enzymes and toxins, drug resistance

32

What are the virulence factors in S. epidermidis

Capsule, drug resistance

33

What are the main pathologies caused by S. aureus

Food poisoning, TSS, nosocomial infections, skin infections like abscesses and impetigo

34

What are the main pathologies caused by S. epidermidis

Catheter and prosthetic implant infections

35

What is the main pathology of S. saprophyticus

UTI in young women

36

What does protein A do

neutralize IgG antibodies by binding to the Fc region

37

What are the 5 main virulence factors of S. aureus

1. Fibrin-binding proteins on the cell to help colonize 2. Protein A 3. Enzyme (spreading factor) secretion 4. cytolytic exotoxins to kill PMN 5. super antigen exotoxins

38

What is the function of coagulase

Produces local fibrin deposition that helps to wall off the infection. This makes a nice little home for S. aureus, and is also why abscesses can be pressurized.

39

What's the best way to deal with an abscess

Lance and drain the abscess and let in lots of oxygen

40

What are the main local pyogenic diseases caused by Staph

1. Local skin infections like abscesses (boil, furuncle, stye) or impetigo 2. Deep localized infections like osteomyelitis, spleen liver or kidney abscess, and septic arthritis 3. acute endocarditis 4. pneumonia after an illness like influenza

41

What are the major systemic toxic diseases caused by Staph

1. Scalded skin syndrome from exfoliative toxin 2. Food poisoning from enterotoxins 3. Toxic shock syndrome from super antigen TSST-1 4. Staph caused enterocolitis

42

what is a nosocomial infection and why do they happen

hospital acquired infection. They happen because hospitals are full of immune-compromised individuals. Staph is an opportunist so goes unnoticed on healthy personnel who then spread it from patient to patient.

43

What is the foreign body effect

essentially, a foreign body in the skin can act as a microbe highway. 100,000,000 bacteria w/o suture vs 100 with a suture can cause an abscess

44

What type of bacteria are Strep and Staph? what color does that mean they are?

gram positive which means they are purple

45

What is the difference between dysentery and diarrhea

Diarrhea is frequent, runny stool whereas dysentery is blood, mucus, and pus in diarrhea

46

What are the 5 'F's

Foods, fingers, fluids, flies, feces. The first 4 are really just a means for the 5th to reach your mouth.

47

What is the major group of enteric gram- rods?

enteric bacilli (mainly from enterobacteriaceae) that constitute the principle gut flora

48

What is one of the most important characteristics of enteric bacilli

They love sharing virulence factors with other pathogenic as well as commensal flora

49

What types of diseases can enteric gram- cause

GI infections, food 'poisoning', UTI, sepsis and bacteremia, ulcers and gastritis

50

What type of environment do enteric gram- rods like

They are facultative anaerobes and so like very little oxygen. Normally they are in human and animal GI tracts

51

What enteric gram - rods are major parts of normal human flora

Escherichia coli, Klebsiella, Proteus, Bacteroides

52

What is the main transmission route for enteric gram- rods

Oral-fecal (the 5 F)

53

What are H, K, and O antigens

H = flagella, K = capsule, O = endotoxin

54

What is antigen variation

The ability of a bacterium to switch between genes for an antigen for the purpose of evading the immune system

55

What is phase variation

The ability of a bacterium to express or not express an H,K, or O antigen. In other words, a bacteria can get rid of its fimbrae or flagella to evade antibodies

56

What are the main enteric gram- virulence factors

Adhesive factors, endocytosis into host cell for intracellular growth, macrophage taxis, capsules, antigenic and phase variation, antibiotic resistance, toxins

57

How does EPEC E. coli cause pathology

It attaches to gut endothelial cells and alters the microvilli structure, causing malabsorption

58

How does EIEC E. coli and Shigella cause pathology

Bacterial-directed endocytosis into mucosal epithelium of the colon where they live until the cell dies or is killed

59

What does LPS activate

macrophages, Hageman factor, Platelets, Complement pathway

60

What are the main symptoms of sepsis

hypovolemic shock, disseminated coagulation, multiple organ shutdown, acute respiratory distress syndrome

61

What type of exotoxin is most common in pathogenic enteric gram- bacteria

A-B exotoxins

62

How does one figure out the disease causing potential of any microorganism

(virulence)(dose)/host resistance

63

Shigella likes to live in the colon; how does it get there

It is very acid resistant and so survives the stomach. This means it has a small infectious dose

64

What are the main strains of Shigella

Shigella dysenteriae, S. flexneri, S. sonnei

65

How does Shigella cause dysentery

They live in the mucosal epithelium, and so host cells must be killed by the immune system to get to the bacteria, causing mucosal abscesses

66

What makes S. dysenteriae particularly pathogenic

It releases AB exotoxin shiga which cleaves rRNA in epithelial cells. However, if shiga gets in the blood, it attacks glomerular endothelial cells, causing HUS

67

What is EHEC

Entero-haemorrhagic E. coli which has a shiga-like toxin 0157:H7

68

What are the main strains of Salmonella

Salmonella enterica, S. typhimurium, S. typhi

69

What allows Salmonella typhi to become a systemic infection

The use of macrophage taxis

70

How does Salmonella normally infect people

Via contaminated food products

71

How does Salmonella get past the stomach

Because it is sensitive to stomach acid, it relies on a large dose to start an infection in the small intestine

72

What causes typhoid fever

The symptoms are largely in response to the LPS on S. typhi that have invaded the bloodstream

73

What is ETEC

Enterotoxigenic E. coli. It acquired V. cholera exotoxin gene and causes watery diarrhea

74


What is EHEC



Enterohemorrhagic E. coli. It has a shiga-like exotoxin and causes dysentery and HUS (0157:H7) It's found in cows!


75

What is EPEC

Enteropathogenic E. coli. It acquired shigella exotoxin gene and an adherence gene. It causes diarrhea

76

What is EIEC

enteroinvasive E. coli. It has invasive genes and causes dysentery

77

How does one get a UTI

uropathogenic strains of E. coli originate in the colon or on a catheter, contaminate the urethra and make their way upward. Normally bacteria are flushed out, but these strains have specialized adhesives.

78

What is Helicobacter pylori

H. Pylori is a primary cause in many ulcers and cancers of the gut. It produces urea, which raises the stomach pH, along with some toxins and proteases

79

What is Pseudomonas aeruginosa

bacteria that chronically infects cystic fibrosis ppl and responds poorly to many abx

80

What is Campylobacter jejuni

Major cause of diarrhea and colitis with shiga-like toxins. Mostly from undercooked chicken meat, guts

81

What is Bordetella pertusis

(Whooping cough) B. pertusis binds ciliated bronchial and tracheal epithelium

82

what is the main transmission route for Yesinia pestis

From its small rodent reservoir to humans via flea vector. Human to human via pneumonic transfer

83

What antibodies are part of passive immunity

IgA from breast milk, and IgG crosses the placenta

84

How does passive immunity protect the most vulnerable population from cholera

Breast fed babies get immunity from mom (if she had cholera) since cholera doesn't invade cells, but rather stays on the mucosa. IgA can prevent it from adhering and neutralize its toxins

85

What is the window of opportunity

3-5 months of age when mom-acquired IgG is dropping and baby's IgG production is still low