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MSII Unit II > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is difference between bacteremia and sepsis?

A

Bacteremia: the presence of bacteria in blood—>might be asymptomatic—>immune system can clear it out
Sepsis: has clinical presentation

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2
Q

What is the relationship between SIRS and sepsis?

A

SIRS (may or may not caused by an infection) + proof of bloodstream infection = sepsis

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3
Q

SIRS can be the result from ___?

A

Cytokine storm

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4
Q

What is the role of TLR4 play in SIRS?

A

TLR4 recognizes LPS from gram - bacteria—>inflammation

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5
Q

What are the clinical presentations of sepsis?

A

Fever/high BR/chill/very low temp/change in mental status (elderly pts)

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6
Q

What is severe sepsis?

A

Sepsis plus organ dysfunction/HoTN that can be reversed by fluid

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7
Q

What are some of the complication that sepsis/septic shock cause?

A

DIC/ARF/ARDS

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8
Q

What does TLR2 do?

A

Recognizes gram + bacteria

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9
Q

What happens when the bacteria change the number of acyl chain at the lipid A end of the LPS?

A

It can downregulate the immune response from the host

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10
Q

What are the 2 natural modulators for countering sepsis induced DIC?

A

Activated protein C and antithrombin

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11
Q

Progression of infection?

A

Infection—>SIRS—>sepsis—>severe sepsis—>shock

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12
Q

What is reticuloendothelial system?

A

Liver and spleen

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13
Q

What is transient bacteremia?

A

Last for mins to a few hours/teeth brush, biopsy and what not

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14
Q

What is the most common cause of bacterial endocarditis ?

A

Mouth floral settles onto heart valve lesion

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15
Q

What do we give pts with heart murmur before a dental procedure?

A

Antibiotics

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16
Q

What is intermittent bacteremia?

A

Recurring bacteria presence in the blood/often from abscesses

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17
Q

What is the most common cause of continuous bacteremia?

A

Endocarditis

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18
Q

What are the causes of primary BSIs?

A

Infective endocarditis/mycotic aneurysm/thrombophlebitis/CABSI

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19
Q

What is the amount of bacteria in blood that can cause shock?

A

1 in 10ml. Long lasting endocarditis can be around 1 in 100ml—>need to draw multiple (3) samples of blood to confirm

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20
Q

What causes mycotic aneurysm?

A

Damage to the endothelial cells lining the arteries

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21
Q

What is the common cause of thrombophlebitis?

A

IV leaving in the pt for too long

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22
Q

What are some common causes of CABSI?

A

coagulase negative staph/S. aureus/candida

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23
Q

What route does extravascular BSI spread?

A

documented portal of bacterial entry and spread through lymphatic system

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24
Q

Why do we draw less blood from kids to detect bacteremia?

A

Kids can tolerant more bacterias in their blood stream

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25
Q

Elevated PCT is associated with?

A

Bacterial pneumonia and sepsis

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26
Q

What is the level of PCT that has risk for sepsis?

A

Over 0.5 ng/ml—>PCT is also used to see the effectiveness of a treatment

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27
Q

What are the common parasites (protozoan) that cause malaria?

A

Plasmodium falciparum (most deadly)/vivax/malariae (longest time for symptoms to appear)/ovale

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28
Q

What are some genetic protection against malaria?

A

Gene for HbC/lack of Duffy antigen (protection for P. vivax)/thalassemia

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29
Q

What is the progression of malaria symptoms?

A

Cold stage (RBCs rupture)—>hot stage (immune response to circulating protozan)—>sweating stage (protozan infect more RBCs)

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30
Q

What is the difference between faciparum and other species?

A

Its symptoms doesn’t appear in a cycle like others but has a continuous fever

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31
Q

What is recrudence and relapse regarding malaria infection?

A

Recrudence (falciparum)—>parasite remain dormant inside RBCs and then reoccur (fall below detectable level)
Relapse (vivax and ovale)—>parasite goes back to the liver and remain dormant

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32
Q

What clinical symptoms does falciparum cause?

A

Anemia/hypoglycemia/respiratory distress/metabolic acidosis

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33
Q

Falciparum binds to RBCs via __?

A

PfEMP-1 antigen (present on all RBCs—>reason why falciparum is deadly)

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34
Q

How is cerebral malaria of falciparum caused?

A

The infected RBCs sticks to the blood brain barrier—>poor oxygenation of the brain

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35
Q

Which 2 receptors can stick with falciparum parasitized RBCs?

A

CD36 (microvasular endothelial cells) and chondroitin sulphate A (placenta—>caused birth defect and what not)

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36
Q

What is the only brand of RDT approved in the US?

A

Binax NOW

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37
Q

What bug transmit Trypanosomiasis (Chagas disease caused by Trypanosoma cruzi)?

A

Reduviid bugs (need to attach to you for an hour)

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38
Q

What is the sign for Chagas infection?

A

Romana’s sign (bugs bite around eyes—>cause inflammation)

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39
Q

What does chronic Chagas disease cause?

A

Megacolon/megaoesophgus/cardiomyopathy

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40
Q

Sand fly bit you and threw up on you cause?

A

Lesihmaniasis—>cause lesion/ulcers

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41
Q

Cats poops out ___ can transit ___ to people

A

Oocyst (infectious form of Toxoplasma gondii)/toxoplasmosis

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42
Q

What is the leading cause for foodborn illness?

A

Toxoplasmosis

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43
Q

Most people with toxoplasmosis remain ___?

A

asymptomatic—>reactivate when immunosuppressed

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44
Q

The classic triad of congenital toxoplasmosis is?

A

Chorioretinitis/hydrocephalus/intracranial calcification (mental deficit)

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45
Q

Which trimester has the highest risk of transmitting toxoplasmosis to the fetus? and does the previous infection matters?

A

3rd/no (only primary infection)

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46
Q

When immunosuppressed, T gondii enters ___ and cause ___?

A

Across the blood brain barrier and cause nuerotoxoplasmosis (HIV pt is susceptible)

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47
Q

Recurrence of Toxoplasmosis can affect eye and cause?

A

eye pain/photosensitivity/tearing/blurry

Can spot white fluffy patches in the eye

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48
Q

Increase in IgM titers of Toxoplasmosis indicate a ___ infection?

A

Acute

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49
Q

P falciparum cause organ damage in the brain/lungs/kidneys by ___?

A

adhesion of infected RBCs in the capillaries that impair microcirculation

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50
Q

How does tick need to attach to the human to transmit lyme disease?

A

24-48 hrs

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51
Q

Does reinfection occur for lyme disease?

A

Yes (antibodies are not protective)

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52
Q

What is the progression of lyme disease?

A

Stage 1 (bullseye rash is the minority/flu like symptoms)—>stage 2 (cardiac and neurologic involvement)—>stage 3 (arthritis/chronic CNS disease)

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53
Q

Is seropositivity testing useful for lyme disease?

A

No

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54
Q

How long do we treat early lyme disease (stage 1)?

A

Doxycycline (alt ceftriaxone) for 10-30 days and no longer than that

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55
Q

What are the 2 bacterias that have human as their natural reservoirs?

A

Relapsing fever/epidemic typhus (vector is body louse—>bacteria eventually kills the vector)

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56
Q

What is typical of all spirochetes?

A

Immediate access to blood

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57
Q

What is the disease progress of relapsing fever?

A

Bacteria invade the blood—>strong IL-10 response and clear the bacteria (fever)—>bacteria vary their surface antigen and evade immune system—>disease resume—>immune clears again (fever)—>repeat

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58
Q

What are the number of average relapses for louse-born and tick-born relapsing fever?

A

1/3 (tick-born cause pregnancy complications)

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59
Q

What to use to diagnose relapsing fever?

A

Peripheral blood smear (during fever) or culture

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60
Q

Treatment for relapsing fever?

A

tetracycline/doxycycline
use erythromycin for children and prego
louse borne takes 1 dose/tick borne 7-10 days

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61
Q

What is the characteristics of richettsia?

A

small short rod/obligate intracellular replication/hard to stain

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62
Q

What are the reservoir for Rocky Mountain Spotted Fever?

A

Mouse and dog ticks

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63
Q

Where do lyme and relapsing fever (the bacteria) replicate?

A

Extracellular in the bloodstream

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64
Q

How is the rash in RMSF caused?

A

Bacteria infect and reproduce in the vascular endothelium—>cell to cell infection—>cells break—>blood comes out
(rash begins in the extremities and spread to trunk)

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65
Q

How to test for RMSF?

A

Immunochemical staining

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66
Q

What drug to use for spotted fever?

A

Doxycycline (even for prego sometime)—>poor prognosis associated with old age (>40) and delayed treatment

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67
Q

How is MSF compares with RMSF?

A

MSF is characterized by eschar at the bite site/less severe than RMSF/treatment is the same

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68
Q

What is the characteristics of typhus rash?

A

Start around the trunk and then spread to extremities (opposite of RMSF)

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69
Q

What is Brill-Zinsser disease?

A

Recrudescent typhus/less severe than the initial course

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70
Q

What are murine and scrub typhus?

A

Find in warm weather. Murine (rat fleece)/scrub (chiggar)

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71
Q

What lab to use to confirm typhus?

A

IF assay/immunoassay/PCR

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72
Q

Treatment for typhus?

A

Doxy and chloramphenicol (doesnt work for HME)

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73
Q

What are the characteristics of ehrlichia?

A

gram -/obligate intracellular/replicate in WBC/form morulae

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74
Q

Does HME (human monocytic ehrlichiosis/ehrlichiosis) often symptomatic/asymptomatic?

A

Asymptomatic

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75
Q

Where does HGA (human granulocytic anaplasmosis) grow?

A

In neutrophils

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76
Q

Difference between HME and HGA?

A

HGA is more severe

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77
Q

What is used to treat HME and HGA?

A

Doxycycline/chloramphenicol doesnt work

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78
Q

All the arboviruses are DNA or RNA viruses?

A

RNA (high mutation rate)

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79
Q

Important factors too look for in history for arboviruses

A

Season/travel history

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80
Q

Tell me about Eastern Equine Encephalitis

A
  1. Bird virus (mosquito feed on birds, 10% of pt develop encephalitis)—>transmitted by mosquito
  2. It is one of the 4 alphavirus: the other 3 are WEE/VEE/Everglades.
  3. No treatment for it.
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81
Q

Tell me about Japanese Encephalitis

A
  1. transmitted by culex mosquito (vector) that feeds at night
  2. natural host is pig
  3. IXIARO (vaccine)—>need 28 days to work
82
Q

Tell me about yellow fever

A
  1. Yellow fever vaccine can cause viscerotropic disease of yellow fever
  2. Endemic In south america and africa
  3. Hemorrhagic fever—>throw up blood/renal failure
  4. jungle cycle leads to urban cycle
83
Q

Tell me about Dengue virus

A
  1. Petechiae
  2. Endemic in Key West now
  3. Hemorrhagic—>shock (treat with fluid resuscitation)
84
Q

Features of Group A strep?

A

gram +/catalase -/beta-hemolytic/bacitracin-sensitive

85
Q

2 way of diagnosing Strep A?

A

Antibody assay/culture (not sensitive)

86
Q

Strep A sore throat can cause?

A

peritonsillar abscess (Quinsy)/Ludwig’s angina (infect floor of the mouth)—>blocking airway/middle ear infection (need to drain middle ear)/scarlet fever

87
Q

What is a complication from middle ear infection from Strep A?

A

Mastoiditis

88
Q

What caused scarlet fever?

A

Erythrogenic toxin from Strep A—>skin and tongue rash (strawberry tongue) (skin is not infected, just toxin)

89
Q

What kinds of M-protein of Strep A leads to Rheumatic fever?

A

M3/5/13

90
Q

Progression of Rheumatic fever?

A

Sore throat—>recovery—>fever/arthritis/endocarditis (abnormal heart sound) (autoimmune—>no bacteria anywhere)

91
Q

What test to use to diagnosis rheumatic fever?

A

look for IgM anti-streptolysin O antibody/endarteritis/Aschoff bodies/heart lesion

92
Q

Does rheumatic fever reoccur?

A

Oh yes

93
Q

What is the result of rheumatic fever on heart?

A

Distortion of endothelium—>bacteria settles—>bacterial endocarditis

94
Q

Features of viridian strep

A

Gram +/catalase -/alpha hemolytic/optochin resistant

95
Q

How does viridian strep cause dental caries?

A

Metabolize sugar into high molecular weight sugar—>sticky—>dental caries
Breakdown sugar—>make acid—>decalcification of teeth

96
Q

Long standing dental caries with viridian strep can cause?

A

Abscesses (invade soft tissue)—>unilateral swollen

Or endocarditis

97
Q

Bacterial endocarditis can cause?

A

metastatic abscess and hemorrhage (vegetation breaks off)

98
Q

Periodontal disease progression

A

Gingivitis—>create a pocket by the teeth—>teeth lost

99
Q

What is periodontal disease caused by?

A

Gram - bacteria

100
Q

Feature of Corynebacterium diphtheriae?

A

Gram + rod/infect pharyngeal mucous membrane/spread by droplet/toxin cause necrosis of heart muscle/not all are toxic—>need culture and then PCR to determine/have toxoid vaccine

101
Q

What is pseudomembrane?

A

Diphtheria kills the epithelium—>leaving a lot of dead tissues at the back of the throat

102
Q

Bacteria responsible for bacterial endocarditis are?

A

Viridian and group A strep

103
Q

Can you get sick from touching subjects (doorknob/keyboard and what not) that a S. aureus infected pt has touched before?

A

Da (S. aureus can transport either direct or indirect)

104
Q

What is the fraction of the population that is carrying S. aureus?

A

1/3

105
Q

Which antibiotic is used to treat surface/abscess S. aureus infection?

A

Mupirocin/cephalosporin

106
Q

Which bacteria cause infection at piercing/catheter site?

A

Staph epidermidis (S. aureus can infect the catheter site of immunosuppressed pts)

107
Q

How to treat piercing/catheter site infection?

A

Take out the piercing or catheter

108
Q

Feature of scabies?

A

Mite that lay eggs on places like wrists/really itchy/treat with permethrin

109
Q

What are the 4 kinds of skin abscesses (follicle and gland infection)? And what bacteria usually cause them?

A

Furunculitis (sweat gland and hair follicle of the skin)/carbuncle (multiple abscesses fused)/stye (eyelid)/acne
S. aureus

110
Q

What is important about infection of S. aureus treatment?

A

Need to test antibiotic sensitivity and prevent resistant/also need to remove dead tissue (provide nutrients for staph)

111
Q

What is exfoliatin toxin and what does it cause?

A

Toxin from S. aureus/cause exfoliation/no bacteria in there

112
Q

What is scaled skin syndrome?

A

Bad case of widespread exfoliation caused by exfoliatin toxin

113
Q

What bacteria usually cause subcutaneous skin infection?

A

S. pyogenes (group A strep)

114
Q

Difference between S. aureus and S. pyogenes in terms of spreading?

A

S. aureus doesn’t and S. pyogenes spreads

115
Q

Difference between erysipelas/cellulitis/necrotizing fasciitis?

A

All are deep skin infection. Erysipelas and cellulitis are the same. Necrotizing fasciitis is deeper.

116
Q

Treatment for erysipelas/cellulitis/necrotizing fasciitis?

A

Penicillin or cephalosporin for erysipelas and cellulitis. Amputation for NF

117
Q

How to avoid post surgical infection?

A

Eliminate staph carrier state

118
Q

What causes post strep nephritis?

A

Happens after strep infection—>autoimmune reaction

119
Q

What is thermal dimorph?

A

Fungus—>room temp grow as mold/body temp grows as yeast

120
Q

Dermatophytoses only infect ___ and transmitted through ___?

A

superficial keratinized structures/fomites

121
Q

What causes hypersensitive dermatophytid reaction (vesicles on fingers)?

A

Circulating fungal antigen (vesicles do not contain fungus)

122
Q

What is the exam for dermatophytoses?

A

Scraping/treat 10% KOH/microscope

123
Q

Best way to prevent dermatophytoses?

A

Keep dry and cool

124
Q

Difference between dermatophytoses and tinea veriscolor?

A

Infection vs. overgrowth

125
Q

What is the route of transmission for tinea nigra?

A

spores in soil enter injury

126
Q

Azole is a ___ drug?

A

anti-fungal

127
Q

How does sporotrichosis transmit? and what does it present?

A

By thorn puncture/painless pustule or ulcer (hand)

128
Q

Which is better for diagnosing sporotrichosis, biopsy or culture?

A

Culture

129
Q

Which 2 fungal infection have dark hyphae?

A

Chromomycosis and tinea nigra

130
Q

How does chromomycosis transmit?

A

Soil in the tropics enters through puncture (feet)

131
Q

What kind of stain is used for mycetoma?

A

Silver stain

132
Q

How to treat mycetoma?

A

Surgical excision of abscesses

133
Q

Common candidiasis?

A

Diaper rash/vaginitis/thrust or esophagitis (immunosuppressed)

134
Q

What follows systemic candidemia?

A

disseminated candidiasis (organ invasion)

135
Q

Neutropenia is a risk for ___ infection?

A

Fungal

136
Q

Chronic HSV keratitis and zoster in the face can cause ___?

A

Vision loss

137
Q

What is herpetic whitlow?

A

HSV1/2 on the hands/reoccurrence on the hands

138
Q

Zoster is usually uni or bilateral?

A

Unilateral

139
Q

Oral hairy leukoplakia is caused by?

A

EBV (immunodeficiency)

140
Q

CMV causes ___ rash?

A

petechial

141
Q

Roseola is caused by ___?

A

HHV 6/7 infect CD4+ T cells

142
Q

Roseola progression?

A

3 day fever followed by a faint rash on the trunk

143
Q

Features of CMV?

A

Rash and jaundice (liver enzyme elevated)

144
Q

What does coxsackie infect?

A

Throat/eye/hand, foot and mouth disease (painful blisters)

145
Q

Live smallpox vaccine (vaccinia virus) is dangerous because?

A

Contraindicated for ppl with eczema/immunosuppressed/ppl who scratch the injection site

146
Q

When rubella infect pregnant women, it causes?

A

Congenital defect

147
Q

Difference between septic shock and severe septic

A

Septic shock: HoTN can not be reversed by fluid

148
Q

HLA is the human form of ___?

A

MHC

149
Q

The diversity of HLA subtypes prevent ___?

A

Tumor from passing from person to person (only the same strand of HLA tumor can be grew on another person)

150
Q

Can our immune system target the antigens of tumor?

A

Ya e.g. HER2

151
Q

How does tumor cells that don’t express MHC II gets targeted by immune system?

A

Tumor antigen is picked up by antigen presenting cells—>stimulate CD4—>then CD8—>kill tumor cells

152
Q

3 examples for tumor cells to avoid being killed

A

Down-regulate MHC I/recruit Treg to protect it/lack co stimulatory protein like B7

153
Q

What is the cytokine that is responsible for Treg activation?

A

TGF-beta

154
Q

How does BCG works?

A

Inject into bladder with bladder cancer—>BCG infect bladder cancer cells (highly immunogenic)—>immune system get rid of them

155
Q

Why blocking CTLA-4 (using antibody) is a treatment for tumor?

A

CTLA-4 inhibit immune response

156
Q

CTLA-4-Ig ___ immunity?

A

Blocks

157
Q

PD1/PD1-L ___ the function of T cell?

A

inhibit (so blocking PD1/PD1-L can enhance immunity)

158
Q

ADCC recognizes ___ and then kill the tumor cell

A

Monoclonal antibodies on the tumor cells

159
Q

___ and ___ can be conjugated to monoclonal antibodies?

A

Toxin (tumor cells take it in—>die)/radionuclide (tumor cell die from radiation)

160
Q

What is adoptive T cell therapy?

A

Isolate T cells from a person—>grow it—>put them back (enhance immunity)

161
Q

CAR expressing T cell

A

Trained to recognize certain tumor antigens

162
Q

How do we use listeria to target tumor cells?

A

Listeria target dendritic cells naturally—>make listeria to express tumor antigen—>the more immune to listeria you are, the more listeria you take up—>better against tumor

163
Q

CTLA-4 is on ___ cell?

A

Treg cells

164
Q

Hygiene theory on type I hypersensitivity?

A

Kids nowadays are not allowed to play in the dirt—>immune system is exposed less to normal organism—>immune system don’t learn how to respond appropriately

165
Q

Process of allergen sensitization in type I hypersensitivity (no reaction)

A

Allergen bind to B cell—>B cell presents it to Th2 cells—>B cell become IgE secreting—>IgE bind on mast cells

166
Q

What happens to subsequent exposure to allergen?

A

Mast cells degranulation—>immediate (histamine) and late phase (cytokines like TNF/enzyme)

167
Q

Basophils and eosinophils comes in after mast cell degranulation, they need to be ___ to express IgE

A

activated by mast cells

168
Q

More diffuse swelling of urticaria is called?

A

angioedema

169
Q

For allergic asthma, Th2 cells makes ___ that activates ___?

A

IL13/eosinophils

170
Q

The child is atopic if the father/mother is atopic?

A

Mother

171
Q

What is the mechanism of desensitization of type I hypersensitivity?

A

IgA and IgG block IgE from cross linking with mast cells

172
Q

How does type II hypersensitivity works?

A

IgG binds to antigen on a cell—>activate complement to kill the cell/phagocytize the cell

173
Q

ABO incompatibility/Rh hemolytic disease of newborn/graft rejection are type __ hypersensitivity?

A

Type II (IgG mediated)

174
Q

What is Arthus reaction?

A

Type III—>localized injected antigen—>antibody-antigen bind to mast cells—>mast cell degranulate—>local inflammation—>attract neutrophil and macrophages—>tissue damage

175
Q

Serum sickness

A

Type III: antibodies against large amount of foreign protein

176
Q

Delayed type IV hypersensitivity?

A

Antigen in subcutaneous tissue—>activate Th1 cell—>recruit T cells—>2 days later—>flare (TB test)

177
Q

Contact type IV hypersensitivity?

A

Poison ivy + skin protein=foreign protein—>CD4 T cell sensitive—>memory T cells—>subsequent exposure—>dermatitis (latex sensitivity also)

178
Q

Difference between transplant rejection and graft vs. host ?

A

Both type IV: T cell attack the transplant organ in transplant rejection
T cell from the transplant attach the host in graft vs. host

179
Q

How to trigger autoimmunity?

A

Genetic susceptibility—>infection that activate self-reactive lymphocytes—>autoantibodies production

180
Q

AIRE present ___ to T cell in the ___?

A

self-antigen to T cell in the thymus

181
Q

Requirement of costimulation for B and T cell help controls ___?

A

the activation of self reactive B and T cells in the periphery

182
Q

Defect in FoxP3 gene affect?

A

Treg—>autoimmune disease

183
Q

What is molecular mimicry?

A

Pathogen derived peptide is similar to self antigen—>cause autoimmune disease

184
Q

What can cause the release of sequestered antigen that cause autoimmune symptoms?

A

Trauma

185
Q

What is the mechanism of Grave’s disease?

A

Autoantibodies (TSH analog) bind to TSH receptor on thyroid gland—>increase release of T3 and T4—>hyperthyroidism

186
Q

IgG mediated autoimmune disease can be transmitted to ___?

A

Fetus (plasmaphresis to remove the antibodies)

187
Q

Examples of type IV hypersensitivity autoimmune diseases?

A

Type I diabetes (target GAD)/RA/MS

188
Q

The toxin of C. tetani is called?

A

Tetanospasmin (this is what causes all the symptoms)

189
Q

What are the 4 types of C. tetani?

A

Neonatal/cephalic/local/generalized

190
Q

C. tetani toxin is travelled by ___ in the CNS?

A

Retrograde axonal transport

191
Q

Babies ingestion C. botulinum in the form of ?

A

spores (preformed toxin for adults)

192
Q

___ inactivate the botulinum toxin?

A

Cooking

193
Q

Botulinum toxin is targeting ___ nervous system

A

peripheral motor

194
Q

What is the definition of zoonoses?

A

Disease that cycles in animals jump to humans

195
Q

How can we detect Gram + cocci?

A

culture

196
Q

Endocarditis can be from Strep pyogenes?

A

Rheumatic fever—>distortion of endothelium—>bacteria lodges there—>endocarditis

197
Q

DNAse is positive for ?

A

S aureus

198
Q

Glomarular nephritis of strep follows ?

A

Skin infection

199
Q

S aureus is ___ hemolytic

A

Beta

200
Q

What does MCV lesion look like?

A

Pearly/umbilicated (school age children)

201
Q

Symptoms of rubeola (measels)?

A

Koplik’s spots/cough/conjunctivitis/fever/rash (red with bluish center)

202
Q

Primary CMV infection can lead to ?

A

congenital CMV syndrome

MSII Unit II (8 decks)

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