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Infectious Disease > Week 2 > Flashcards

Week 2 Flashcards

1
Q

MacConkey agar

A

inhibits gram + bacteria, lactose fermenters become pink/purple

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2
Q

EMB agar

A

methylene blue inhibits gram + bacteria, lactose fermenters become dark purple/black (E. coli is green)

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3
Q

Salmonella

oxidase \_\_\_\_\_
gram \_\_\_\_\_\_\_
ferments \_\_\_\_\_\_
Lac \_\_\_\_\_
Invasive or noninvasive?
infects what part of GI tract?
A

oxidase -
gram -
ferment glucose
Lac -

INVASIVE
Small intestine

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4
Q

Typhoid fever

A

Caused by salmonella Typhi infection

1) enteric fever, systemic disease, fever
2) Human adapted - Colonizes gall bladder → carrier state or intestinal perforation
3) Constipation or inflammatory diarrhea –> Stepwise increase in temperature to high fever

4) 1-3 weeks incubation
- Can continue for 6-8 weeks

5) Can kill immunocompetent people
6) Has a capsule that helps with immune evasion

TX = abx

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5
Q

Non-typhoidal salmonella infection

A

Fecal-oral transmission from poultry, eggs, contaminated fresh produce

Febrile food poisoning 24-48 hrs after ingestion

Nausea, vomiting, headache, chills, fever, cramps, watery diarrhea

High neutrophils

Self-limited - no abx required

Can cause disseminated disease in HIV patients

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6
Q

Salmonella

Toxins/Virulence Factors

A

TYPE III SECRETION SYSTEM

1) Invasion via M cells with type III secretion system → transient bacteremia
2) Uptake by phagocytes (macs) via different type III secretion system → salmonella multiply

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7
Q

Typhoid vaccine

A

purified Vi polysaccharide (adults and children > 2 yrs)

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8
Q

Shigella

gram \_\_\_\_\_\_
oxidase \_\_\_\_\_
ferment \_\_\_\_\_\_
Lac \_\_\_\_\_\_\_
Invasive or noninvasive?
Infects what part of GI tract?
A 
Gram -
Oxidase -
Ferment glucose
Lac -
INVASIVE
Large intestine
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9
Q

What is the infective dose of shigella?

A

Requires SMALL infective dose (very acid resistant)

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10
Q

Shigella diarrhea

A

inflammatory diarrhea, dysentery

Fever, malaise, vomiting, watery diarrhea → frank dysentery (frequent small stools with blood/mucus, cramps, tenesmus)

Humans are only known reservoir → fecal-oral from person to person (Food, fingers, feces, flies)

Can cause HUS (S. dysenteriae)

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11
Q

Incubation time for Shigella

A

Incubation 1-4 days

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12
Q

Shigella

Toxins/Virulence Factors: (2)

A

1) ENTEROTOXIN –> produce watery diarrhea

2) TYPE III SECRETION SYSTEM

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13
Q

Type III secretion system in Shigella mechanism of invasion and spread

A

ntry via M cells, uptake by macrophages → induce apoptosis and inflammation (IL-1/IL-8)

Invade basal side of epithelial cells, lyse vacuole, grow in cytoplasm, spread directly into neighboring cells

Only S. dysenteriae (type 1) make cytotoxic Shiga toxin

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14
Q

E. Coli

gram \_\_\_\_
shape?
Ferment \_\_\_\_\_
Oxidase \_\_\_\_\_
Lac \_\_\_\_\_
A 
Gram -
rod
ferments glucose
oxidase -
lac +
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15
Q

ETEC (Enterotoxigenic)

Diarrhea

A

traveler’s diarrhea, severe watery, no blood/pus, abdominal cramps, vomiting

Toxigenic, NONINVASIVE

Infects small intestine

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16
Q

ETEC (Enterotoxigenic)

Toxins/Virulence factors (3)

A

1) Heat labile enterotoxin
2) Heat stable enterotoxin
3) Fimbrial adhesins → colonize small intestine

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17
Q

ETEC (Enterotoxigenic)

Treatment

A

supportive, fluid replacement

Do NOT use abx

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18
Q

Heat labile enterotoxin

A

Present in ETEC

similar to CHOLERA TOXIN but binds to different gangliosides (different B-subunit) than cholera → target different populations

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19
Q

Heat stable enterotoxin

A

Present in ETEC

small peptide toxin, activates guanylate cyclase → increased cGMP → increase fluid secretion

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20
Q

EHEC: Enterohemorrhagic

Diarrhea

A

bloody, hemorrhagic colitis, dysentery

INITIAL WATERY diarrhea → grossly BLOODY

Fever can be seen

Fecal leukocytes uncommon **

Primarily toxigenic - NONINVASIVE

Infects large intestine

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21
Q

EHEC: Enterohemorrhagic

Infectious dose?
Incubation period?
Possible complications?

A

Requires only small infectious dose (acid stable)

3-9 days of incubation

Can cause Hemolytic Uremic Syndrome (HUS)

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22
Q

EHEC: Enterohemorrhagic

most common serotype

A

O157:H7 serotype = colorless colonies on sorbitol-MacConkey media (does NOT ferment sorbitol)

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23
Q

EHEC: Enterohemorrhagic

Treatment

A

supportive
NO abx

abx → increase risk of HUS by increasing expression of shiga-like toxin

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24
Q

EHEC: Enterohemorrhagic

Toxins/Virulence Factors:

A

1) Attaching and effacing

2) Shiga-like cytotoxins Stx-1 and Stx-II

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25
Q

Shiga-like cytotoxins Stx-1 and Stx-II

A

chromosomally encoded by lysogenic toxin-converting bacteriophages

Stx binds Gb3 sphingolipids of enterocytes and renal endothelial cells

Stx-A subunit → binds rRNA → inhibit protein synthesis → tissue damage

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26
Q

EPEC: Enteropathogenic

Diarrhea

A

watery, persistent diarrhea in infants (<1yr), no blood/mucus, no tissue invasion, vomiting, low grade fever, prolonged, can have relapse

NON INVASIVE

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27
Q

EPEC: Enteropathogenic

Treatment

A

rehydration, responsive to abx

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28
Q

EPEC: Enteropathogenic

Main toxin/virulence factor

A

Attaching and effacing (AE)

-TYPE III SECRETION SYSTEM

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29
Q

Attaching and effacing toxins

A

Present on EHEC and EPEC

1) Adhere to enterocyte surface
2) **Type III secretion system secretes intimin receptor → microvilli destruction, pedestal formation → interferes with absorption

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30
Q

Yersinia spp:

Gram _____
Oxidase ____
ferment _____
Infects what part of GI tract?

A

Gram -
Oxidase -
Ferment glucose
Infects small intestine

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31
Q

Yersinia spp:

disease

A

Associated with eating undercooked pork, dairy products

Disease: low grade fever, watery diarrhea + some blood + fecal leukocytes

Infects terminal ileum
RLQ pain → MIMIC APPENDICITIS

Can cause reactive arthritis (especially in HLA-B27)

ABX not very effective

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32
Q

Vibrio cholerae

Gram _____
Oxidase ____
Invasive or noninvasive?
Infects what part of GI tract?

A

Gram -
Oxidase +
NONINVASIVE
Infects SMALL INTESTINE

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33
Q

Vibrio cholerae

Diarrhea

A

Non invasive diarrhea - profuse, watery, “rice water”

Caused by ENTEROTOXIN (primarily toxigenic)

2-5 day incubation period

Abrupt onset diarrhea, abdominal cramps, vomiting - NO FEVER

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34
Q

Vibrio cholerae

Treatment

A

fluid replacement + abx (can shorten infection)

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35
Q

Vibrio cholerae

A

1) Enterotoxin - Cholera Toxin

2) TCP Pilus

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36
Q

Cholera Toxin

A

BACTERIOPHAGE (CTX) conversion is important, uses TCP pilus to transfer toxin gene

Has A-B type toxin

Cytotonic (does NOT kill the cell)

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37
Q

A-B type toxin

A

Cholera toxin

B-subunit: binds to cell surface receptors (ganglioside GM 1) of enterocytes

A-subunit: enters cell cytoplasm, transfers ADP-ribose from NAD to G-protein → constitutive activation of adenylate cyclase → increase cAMP → Cl- secretion → fluid loss

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38
Q

TCP Pilus

A

Cholera toxin

surface-expressed adherence factor (toxin coregulated pilus)

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39
Q

Transmission of cholera

A

Fecal-oral transmission (water, contaminated foods, shellfish)

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40
Q

Vibrio parahaemolyticus

A

in salt water

Gastroenteritis, wound infections, septicemia

Associated with raw/undercooked shellfish

Can produce bloody stools → produces hemolysin

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41
Q

Vibrio vulnificus

A

gastroenteritis/wound infections from contaminated seafood (oysters) and extraintestinal infections in immunocompromised

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42
Q

Campylobacter

gram \_\_\_\_
size and shape?
oxygen requirement?
Temperature requirement?
Oxidase \_\_\_\_
Catalase \_\_\_\_\_
Ferment \_\_\_\_\_
A 
Gram -
small, curved rod
microaesophilic
Grows best at 42 C
Oxidase +
Catalase +
Ferments glucose
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43
Q

Dose requirement for Campy infection?

A

Low dose required for infection

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44
Q

Campylobacter

diarrhea

A

diarrhea, fever, abdominal cramping, +/- bloody stools +/- fecal leukocytes

Invades terminal ileum and proximal colon

Food borne gastroenteritis (poultry, milk, water, pets)

Most common cause of gastroenteritis in Western world

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45
Q

Complications of Campylobacter infection (2)

A

1) Guillain-Barre syndrome - molecular mimicry between LPS antigen and GM1 ganglioside = ASCENDING paralysis
2) Reiter’s syndrome (autoimmune reactive arthritis) possible (especially HLA-B27)

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46
Q

Treatment of Campylobacter

A

fluid replacement, abx in severe cases (erythromycin, quinolones)

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47
Q

Helicobacter

Gram \_\_\_\_
shape?
Motility?
oxidase \_\_\_\_
urease \_\_\_\_
ferment \_\_\_\_\_\_
Oxygen requirements
Isolated on \_\_\_\_\_\_\_ agar
A 
gram -
curved, rod
highly motile
oxidase -
Urease +
Ferments glucose
Microaerophilic

Isolated on Campy agar

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48
Q

Helicobacter

Disease

A

gastritis, gastric/duodenal ulcers, gastric adenocarcinoma, MALToma

MOST common human bacterial pathogen

Colonizes mucous layer of stomach - does NOT invade

Causes mucosal inflammation, epithelial cell damage, and neutrophil infiltration

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49
Q

Helicobacter

Treatment

A

Triple therapy: PPI + amoxicillin + clarithromycin x 14 days

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50
Q

LPS (lipopolysaccharide)

A

in outer membrane of all gram neg bacteria

Made up of Lipid A + core polysaccharides + O antigens

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51
Q

Lipid A

A

toxic part of LPS (endotoxin), outer layer

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52
Q

Core polysaccharides

A

constant region of LPS within a genus

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53
Q

O antigens

A

repeating subunits of oligosaccharides, variable, used for species identification

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54
Q

H antigens

A

flagella (motile organisms only)

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55
Q

K antigens

A

capsular polysaccharide (increases virulence, not in all strains)

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56
Q

Watery diarrhea

symptoms
what part of GI tract affected
4 bugs

A

copious, watery, no blood or pus, no tissue invasion, in small intestine

Small intestine disease usually secretory diarrhea

→ ETEC, EPEC, Campylobacter, Vibrio cholerae

57
Q

Dysentery

symptoms
what part of GI tract affected
4 bugs

A

scant volume, blood/pus/mucus present, tissue invasion

in large intestine

→ Shigella, Entamoeba histolytica, EIEC, Campylobacter

58
Q

Protracted diarrhea

A

lasting > 14 days

→ EPEC

59
Q

Bloody, watery diarrhea

symptoms
what part of GI tract affected
3 bugs

A

copious, some blood/pus, invasion

in Ileum or colon

Salmonella, Campylobacter, Yersinia

60
Q

Hemorrhagic colitis

symptoms
what part of GI tract affected
1 bug

A

copious, like liquid blood, no leukocytes/ invasion, in large intestine

→ EHEC

Large intestine infection typically inflammatory

61
Q

2 bugs that require high infectious dose

2 bugs that require low infectious dose

A

More sensitive to acid → requires higher infective doses
Vibrio, ETEC

Resistant to acid → requires low infective dose
Shigella, Salmonella

62
Q

4 bugs that cause noninvasive diarrhea

A

V. Cholera, ETEC, EHEC, EPEC

63
Q

3 bugs that cause invasive diarrhea

A

Shigella, Salmonella, S. Typhi

Produce inflammatory diarrhea + frequent/low-volume/mucoid/bloody stools + tenesmus + FEVER + abdominal pain + MANY LEUKOCYTES

Sheets of leukocytes in stool indicative of colonic damage

64
Q

Zipper model

A

tight interaction between bacterial cell surface ligands and host cell receptors → host cell surface closes around bacterium

65
Q

3 bugs that use the zipper model

A

1) Parasite induced phagocytosis (Listeria)
2) Receptor-mediated phagocytosis of macrophages (TB)
3) Coiling phagocytosis (Legionella)

66
Q

Trigger model

+ two bugs that use this

A

bacterial products induce cell surface to take up bacteria

Type III secretory systems cause this (Salmonella, Shigella)

67
Q

Listeria

gram \_\_\_\_\_\_
Shape?
Catalase \_\_\_\_\_
Spore forming?
Hemolysis?
Motility?
Intracellular or extracellular?
A 
Gram + Rod
Catalase +
Non-spore forming
B-hemolytic
TUMBLING motility extracellularly
Facultative intracellular
68
Q

Listeria grows at what temperatures? What things can you eat that are associated with Listeria?

A

Grows at refrigerated temperatures → poorly pasteurized milk/cheeses, deli meats, raw vegetables

69
Q

How does listeria enter the body?

A

Uses “Zipper Mechanism” - penetrates GI mucosa, invades phagocytes → grows/spreads intracellularly

70
Q

How does listeria replicate?

A

spreads cell to cell without exposure extracellular environment using actin-based cellular contractile mechanism (actin rocket)

NO exposure to antibodies, complement or neutrophils with cell-to-cell spread → Cell mediated immunity critical

71
Q

2 main virulence factors of Listeria

A

1) Produces an endotoxin - only gram + organism with endotoxin
- Has tropism for nervous tissue → meningitis

2) Listeriolysin O bacterial toxin: digests phagosome allowing Listeria to infect target cell

72
Q

How is listeria transmitted? (3)

A

Ingestion of bacteria in food
Placental transmission
Vaginal transmission

73
Q

Susceptible populations for severe Listeriosis (meningitis and sepsis)

A

Susceptible populations = pregnant women, neonates, elderly, AIDS patients due to deficiency cell-mediated immunity

74
Q

Consequences of Listeria bacteremia in pregnancy

A

3rd trimester amnionitis, preterm labor, spontaneous abortions, stillbirths

75
Q

Granulomatosis infantiseptica

A

placental transmission of Listeria to infant → early onset sepsis, granulomas throughout body, rash

76
Q

Listeria Infection in Immunocompetent person causes what?

A

febrile gastroenteritis

77
Q

Treatment of Listeria

A

ampicillin, penicillin G, TMP-SMX +/- Gentamicin

78
Q

Legionella

Gram \_\_\_\_\_
shape?
Special stain?
Intracellular or extracellular?
Oxidase \_\_\_\_\_
Grows on what special agar? 2 important cofactors...
A 
Gram negative rod (weak gram stain)
Silver stain
Facultative intracellular
Oxidase +
Grows on charcoal yeast extract with IRON and CYSTEINE
79
Q

Transmission of Legionella

A

aerosols from environmental water sources (air conditioning, hot water tanks)

80
Q

Two diseases caused by legionella infection

A

1) Legionnaire’s Disease

2) Pontiac fever

81
Q

Legionnaire’s Disease

A

severe pneumonia, lobar

Nonproductive cough

Confusion, DIARRHEA

Signs of kidney damage (proteinuria, microscopic hematuria)

HYPONATREMIA - due to SIADH or renal tubulointerstitial disease impairing sodium reabsorption

Diagnosed by presence of ANTIGEN IN URINE

82
Q

Pontiac fever

A

mild flu-like illness (fever, chills, fatigue, malaise, headache) WITHOUT respiratory symptoms

83
Q

Treatment of Legionella infection

A

Macrolides (Azithromycin) + Fluoroquinolones (Levofloxacin)

84
Q

How does legionella invade and replicate?

A

Enters respiratory tract, taken up by macrophages → inhibits phagosome-lysosome fusion → intracellular replication

85
Q

Obligate intracellular organisms (5)

A

cannot reproduce outside cell

Chlamydia
Coxiella burnetii
Ehrlichia
Mycobacterium leprae
Rickettsia
86
Q

Facultative intracellular organisms

A

capable of both intra and extracellular growth

1) Bartonella
2) Brucella
3) Francisella
4) Legionella
5) Listeria
6) Mycobacterium
7) Nocardia
8) Salmonella
9) Shigella

87
Q

Aminoglycosides vs. Tetracyclines for treatment of intracellular organism infections:

Aminoglycosides (gentamicin): enters into cells via ________ → ___________ → accumulates in _________

Tetracyclines: enter into cells via ________ → action in ________

A

Aminoglycosides (gentamicin): enters into cells via PINOCYTOSIS → phagosomes fuse with lysosomes → accumulates in lysosomes

Tetracyclines: enter into cells via DIFFUSION → action in cytosol

88
Q

Signs and symptoms of VIRAL gastroenteritis

A

ACUTE onset WATERY diarrhea (no blood/mucus) +/- vomiting

Nausea, intestinal cramping, muscle aches, low grade fever

89
Q

Epidemiology of VIRAL gastroenteritis

incubation and duration?
shedding phase length?
transmission how?

A

Short incubation and duration of symptoms with prolonged asymptomatic shedding phase

Transmitted on surfaces, food, and water (STABLE)
Seasonal transmission
Person-to-Person or Fecal-Oral

90
Q

Pathophysiology of viral gastroenteritis infection (4)

A

1) LOCAL infection of intestinal epithelial cells
2) MALABSORPTION due to virus killing mature enterocytes
3) Local VILLUS ischemia
4) Viral ENTEROTOXIN → transepithelial fluid loss

91
Q

What is the best way to diagnose viral gastroenteritis?

A

Multiplex RT-PCR detection of viral nucleic acids in stool = most sensitive

RIA or ELISA for ab can tell if exposure occurred, not if there is active infection

92
Q

Calciviruses (2)

A

1) Norovirus

2) Sapvirus

93
Q

Norovirus

size?
enveloped?
genome? (DNA vs. RNA, etc.)
shape?

A

Small
non-enveloped
ssRNA (+ sense)
Cup shaped (chalice-like) indentations (golf ball)

94
Q

Norovirus has ______ and _______ which causes antibody to only give short-term protection

A

strain diversity and antigenic shift

95
Q

Individuals homozygous ____________ are highly resistant to norovirus infection

A

Individuals homozygous non-secretors of FUT2 are highly resistant to norovirus infection

96
Q

Disease caused by Norovirus

A

⅓ infected are asymptomatic and shedding virus

Vomiting, watery diarrhea, nausea, cramping, malaise, headaches, myalgias, low grade fever

Quick on, quick off

97
Q

Incubation, duration, and shedding of Norovirus infection

A 
Incubation = 15 hrs - 2 days
Duration = 1-2 days
Shedding = up to 8 weeks
98
Q

Norovirus infections are associated with which locations?

how is it spread?

A

Cruise ships, hospitals, nursing homes

Fecal-oral person-to-person transmission

Year round outbreaks (less seasonal as rotavirus)

99
Q

Rota virus:

genome?
Shape?
Envelope?
Season of most infections?

A

11 genome segments of dsRNA + RNA-dependent RNA-polymerase (each encodes ssRNA that makes 1 protein)

Rota = Wheel

Non-enveloped

WINTER

100
Q

Rotavirus protein shell is made up of what 3 layers?

A

1) Outer capsid layer: VP7 with VP4 spikes → acid stability, induces neutralizing antibody
2) Inner capsid layer: VP6
3) Innermost core: VP2

101
Q

When two different rotaviruses infect the same cell, what happens?

A

Reassortment of genome when two different rotaviruses infect same cell

102
Q

Rota virus virions are not infectious unless activated by _________

A

Trypsin

103
Q

Rota virus causes what disease

A

Infects small intestine and replicates in villus epithelial cells → villous shortening and stunting

High viral titers shed in stool

Abrupt onset fever, vomiting, then diarrhea (explosive, nonbloody, watery)

104
Q

Rota virus

incubation
duration
shedding

A

Incubation period: 1-3 days
Duration: 4-8 days, self-limited
Shedding can occur for > 3 weeks

105
Q

Treatment of Rotavirus

is it preventable?

A

REHYDRATION

Preventable by vaccination

106
Q

Rotavirus vaccine

A

RotaTeq: Pentavalent live bovine rotavirus vaccine

Rotarix: monovalent live human rotavirus vaccine

Associated with increased risk of intussusception

107
Q

Diagnosis of Rotavirus

A

ELISA Rotazyme identification

108
Q

Enteric Adenoviruses:

eveloped?
shape?
genome?

A

Non-enveloped
Icosahedral
dsDNA virus

109
Q

Enteric Adenoviruses:

Diseases (2)

A

1) URI symptoms (conjunctivitis, pharyngitis, pneumonia, hemorrhagic cystitis) + gastroenteritis (serotypes 40 and 41)
2) Watery diarrhea, then vomiting lasting 5-12 days (longer than Nora/Rota) - persistent, but less severe

110
Q

Astroviruses

size?
envelope?
genome?
shape?

A

Small, non-enveloped
ssRNA (+ sense)
Star shaped capsomers

111
Q

Astroviruses

CAN be grown in cultures of _____________
Requires ________ to activate virus infectivity

A

CAN be grown in cultures of human intestinal epithelial cells
Requires trypsin to activate virus infectivity

112
Q

HPV

main features

A

papillomavirus

Small, non-enveloped, icosahedral DNA virus

113
Q

Two main structural proteins of HPV (late genes) and what they are used for

A

Major capsid protein L1 → basis of vaccine, outer part of virus

Minor capsid protein L2 → required to produce infectious virus particles

114
Q

HPV Lifecycle/Invasion

A

Invades only undifferentiated proliferating basal cell layers in epithelium → Infect epithelium of skin, anogenital tract, and oropharyngeal mucosa

Replicates upon epithelial differentiation

Releases virus particles from fully differentiated skin layers

115
Q

HPV

Transmission

A

sexual contact oral/genital and mother-newborn (vertical transmission)

116
Q

Risk factors of HPV infection:

A 
Early onset intercoars (before age 20)
Multiple sexual partners
History of genital warts
Immunosuppressive disorders (HIV/AIDS)
Failure to receive regular Pap test screening
Long term use of oral contraceptives
117
Q

Persistence of HPV infections

A

80% of HPV infections transient and cleared within 1-2 years

10% get persistent infection - persistence of high-risk HPV type is required for cancer development AND maintenance → <1% develop cancer

118
Q

6 diseases caused by HPV

A

1) Common wart (verruca vulgaris)
2) Plantar wart (verruca plantaris)
3) Anogenital wart: (condyloma cumintaum)
4) Respiratory papillomatosis
5) Epidermodysplasia verruciformis
6) Squamous cell carcinoma

119
Q

Common wart (verruca vulgaris)

caused by HPV ____ or ____

A

small, rough tumor, on hands/feet

HPV2, HPV7

120
Q

Plantar wart (verruca plantaris)

caused by HPV ____, ____, or ________

A

on sole or toes of foot

HPV1, HPV2, HPV4

121
Q

Anogenital wart: (condyloma cumintaum)

caused by HPV ____ or ____

A

sexually transmitted

HPV6 and HPV11

122
Q

Respiratory papillomatosis

caused by HPV ____ or ____

A

warts on larynx or in respiratory tract

HPV6 and HPV11

123
Q

Epidermodysplasia verruciformis

A

rare AR disease, increased susceptibility to HPV

124
Q

Squamous cell carcinoma caused by HPV

5 types of HPV that can cause this?

A

Cervical cancer or head/neck cancer

HPV16, HPV18, HPV31, HPV33, HPV45

125
Q

Cervical cancer is typically caused by _____ and arises where?

A

HPV

arise within transformation zone (squamocolumnar junction)

Especially associated with HPV 16 and 18

126
Q

High risk HPV: (6)

A

HPV16, HPV18, HPV31, HPV33, HPV45, HPV58

These are covered by current vaccine

127
Q

Low risk HPV: (2)

A

HPV6, HPV11

128
Q

HPV oncoproteins

A

cancer regresses when E6 and E7 are blocked

E6 protein: binds and degrades p53

E7 protein: binds phosphorylated-RB → release E2F transcription factor → activate cell replication and cell cycle progression

HPV can integrate into host chromosome → uncontrollable expression of E6/E7

129
Q

HPV Vaccine

A

want to vaccinate before sexually active

Gardasil: contains 6, 11, 16, and 18

Cervarix: contains 16 and 18

Gardasil-9: contains 6, 11, 16, 18, 31, 33, 45, 52, 58

*How vaccine is made: HPV L1 protein only, an empty virus → immune response without risk of infection

130
Q

Screening and diagnosis of cervical cancer

A

HPV pap smear / HPV test → positive, then test cytology, if negative, test again in 3-5 years → positive cytology then do colposcopy

131
Q

Cause of acute endocarditis

A

Staph aureus

Most common sites: mitral > aortic > tricuspid > pulmonic

132
Q

Causes of subacute endocarditis (3)

A

Viridans strep, Strep bovis, Enterococci (faecalis)

133
Q

What are predisposing factors to developing subacute endocarditis?

A

pre-existing cardiac lesion → turbulent, non-laminar blood flow, endothelial trauma, and fibrin deposition

134
Q

Cause of prosthetic valve endocarditis

A

coagulase negative staph (S. Epidermidis)

135
Q

Local complications of endocarditis?

A

effect integrity of heart valves → valvular insufficiency, CHF, myocardial and valve ring abscesses, pericarditis, conduction system disturbances

136
Q

What are embolic complications of endocarditis? (7)

A

EMBOLI released from valve vegetation

1) Stroke or PE
2) Splinter hemorrhages
3) Petechiae, subconjunctival hemorrhages
4) Janeway lesions: nontender flat lesions on digits
5) Osler’s nodes: tender, purplish raised papules on digits
6) Roth Spots: retinal flame-like hemorrhagic
7) Septic emboli to kidneys

137
Q

What are immune complex deposition complications of endocarditis? (3)

A

1) Glomerulonephritis
2) Osler’s nodes (small vessel vasculitis)
3) Roth spots

138
Q

Presentation of Necrotizing Fasciitis (4)

A

1) Presents with signs of systemic toxicity (hypotension, tachycardia, fever, leukocytosis)
2) Poorly defined area of erythema + pain out of proportion to physical exam
- Very tender in areas that are not erythematous → suggest deep tissue involvement
- Get thrombosis of small vessels and destruction of superficial nerves
3) Spreads along facial planes
4) Later findings: skin breakdown + bullae + anaesthesia

139
Q

Bugs with a type 3 secretion system? (5)

A 
EHEC
EPEC
Shigella
Salmonella (typhoidal, and non-typhoidal)
Yersinia

Infectious Disease (9 decks)

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