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Microbiology > Exam 1 > Flashcards

Exam 1 Flashcards

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1
Q

What type of environment does S. Pyogenes require

A

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

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2
Q

What type of environment does S. aureus require

A

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

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3
Q

What does strep pyogenes look like under the microscope

A

A chain of balls. Strep is a strip!

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4
Q

What does staph aureus look like under the microscope

A

clusters of grapes

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5
Q

What 6 counters/evasion strategies does strep pyogenes employ

A
  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
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6
Q

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

A

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

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7
Q

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

A
  1. local pyogenic infection 2. toxic system disease 3. Immune-sequelae’ diseases
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8
Q

What is type 2 hypersensitivity

A

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

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9
Q

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

A

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

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10
Q

What is a type 3 hypersensitivity

A

immune-complex-induced damage (innocent bystander)

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11
Q

What is the best way to prevent rheumatic fever

A

Penicillin TX of strep throat

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12
Q

What is scarlet fever

A

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

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13
Q

What are the main ways Strep infections can damage the heart

A
  1. acute bacterial endocarditis 2. rheumatic fever 3. sub-acute bacterial endocarditis
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14
Q

Why do many people develop hypersensitivity to penicillin

A

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

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15
Q

what are the main classifications of streptococcus

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

What is the classification of S. pyogenes

A

beta-hemolytic, group A

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17
Q

What is the classification and primary location of S. agalactiae

A

beta-hemolytic, group B. Lives primarily in vagina

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18
Q

What are the main pathologies caused by S. pyogenes

A

Strep throat, rheumatic fever, cellulitis, scarlet fever

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19
Q

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

A

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

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20
Q

What is the classification of S. pneumoniae

A

alpha-hemolytic, no lancefield

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21
Q

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

A

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

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22
Q

What is the classification and location of viridans type strep

A

alpha hemolytic, they live in the mouth

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23
Q

What are the main pathologies caused by viridans type strep

A

Endocarditis, dental caries

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24
Q

What are the most pathogenic stains of Staph

A

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

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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

Microbiology (4 decks)

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