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Quarter 3 > Microbio Exam 1 > Flashcards

Microbio Exam 1 Flashcards

1
Q

Pathogens that cause:

Otitis Media and Sinusitis

A

SMH pathogens

Strep PNA
M. Cat
H. Influenzae

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2
Q

Pathogens that cause:

Otitis Externa

A

Pseudomonas Aerug

Staph Auereus

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3
Q

Pathogen that causes Diptheria

A

Corynebacteriam diptheria

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4
Q

Pathogen that causes Whooping cough (pertussis)

A

Bordetella pertussis

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5
Q

Sx of Otitis externa

A

Otalgia (pain) and
Otorrhea (drainage)

fever greater than 38.3 indicated more than just localized involvement

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6
Q

Pseudomonas and Staph are Halophiles

A

meaning they can live on the salty skin

cause Otitis Externa

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7
Q

Pseudomonas Aeruginosa

A

Gram (-)
Pigment producer: Pyocanin (non fluorescent blue) and
Pyroverdin (fluorescent green)

Encapsulated

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8
Q

Otitis Externa

A

one cause is Pseudomonas Aeruginosa: blue and green

most strains produce Pyocyanin (blue) but nearly ALL produce pyoverdin (green!!)

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9
Q

Staph Aureus

A

another big cause of Otitis Externa

Gram (+) cocci in clusters
Coagulase (+)
B-hemolytic

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10
Q

Beta hemolytic

A

complete hemolysis, can see through

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11
Q

Tx of Otitis Externa

A

Topical: acidifying agent, topical corticosteroid, topical antimicrobial

Oral abx if fever is presnt or extension of dz

Systemic analgesics (pain)

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12
Q

Otitis Media and Sinusitis

A

SMH pathogens

Strep PNA: 50%
H. Influenza: 20%
M. Cat: 10%

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13
Q

Strep PNA

A 
Gram (+) 
Lancet shaped diplococci
Encapsulated
A-hemolysis (incomplete, cannot see thru- yellow to grayish green on plate)
Optochin sensitive
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14
Q

Strep PNA review

A 
Gram (+) 
Lancet shaped diplocicci
Encapsulated
a-hemolysis
Optochin sensitive
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15
Q

H Influenza

A

Gram (-) coccobacilli

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16
Q

M. Cat

A

Gram (-) Diplococci
Oxidase (+) !!!
B-lactamase producer

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17
Q

Otitis Media

A

Amoxicillin

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18
Q

Diptheria

A

Cutaneous (abscesses and sores) vs Respiratory

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19
Q

Diptheria

A

Gram (+) pleomorphic bacilli, often CLUB SHAPED with the “palisades” or V shaped appearance

and

Metachromatic (volutin) dark purple granules at the bottom point of the V

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20
Q

Toxigenic strains of Diptheria have a phage encoded exotoxin

A

Diptheria toxin

Exo meaning it is expelled from the pathogen

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21
Q

Diptheria toxin

A

A-B exotoxin
B: receptor binding
A: catalytic subunit

binds to heparin binding EGF receptor- exotoxin is endocyosed, vesicle acidifies, releasing A subunit and allowing it to go to cytosol

Then the A subunit inactivates EF-2 via ADP-ribosylation- halting protein synthesis

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22
Q

Cutaneous diptheria

A

most cases d/t nontoxigenic strains

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23
Q

Respiratory diphteria

A

pharyngeal colonoziation
sudden onset malaise, exudative throat, low grade fever, lymph

Formation of PSEUDOmembrane= fibrin, bacteria, WBC, and Necrotic epithelial cells

“Bullneck”

systemic comp

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24
Q

Pseudomembrane in Diptheria is what color:

A

thick grayish to black

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25
Q

Diptheria Pathogenesis

A

Adherence and prolif (2-6 days)

Localized damage d/t exotoxin- inh of protein synthesis and cell death

Leads to Local necrosis and edema OR continued exotoxin production –> Systemic toxicity (myocarditis and demyelination)

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26
Q

Diptheria is uncommon in developed countries

A

vaccinate

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27
Q

Cultures for Diptheria

A

Loeffler’s medium: supports growth and enhances formation of volutin granules (the v points)

Cysteine-tellurite agar: distinctive black to tellurite reduction (only supports growth of this pathogen)
Isolates tested for toxin production

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28
Q

Staining for Diptheria

A

Gram: club shaped gram (+) bacilli
Volutin: metachromatic (volutin) granules (the V poitn)

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29
Q

Diptheria Dx

A

Presumptive isolates should be tested for TOXIN PRODUCTION

Elek test
PCR
ELISA
Immunochromatographic strip assay- very sensitive

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30
Q

Tx/prevention of Diptheria

A

Neutralize exotoxin with Diptheria Antitoxin: the most important!!! bc exotoxin is most damaging

then,

Abx: Erythromycin

Isolate person to minimize spread

Vaccinate

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31
Q

Pertussis

aka whooping cough

A

small gram (-) coccobacilli

virulence factors: adhesins and exotoxins

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32
Q

Pertussis Adhesins

A

mediate attachment to integrins and help colonization in the respiratory epithelium

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33
Q

Four exotoxins in Pertussis

A

A-B exotoxin: inactivates Gialpha, inhibits phagocytic killing and monocytic migration: kills lymphocytes

Adenylate cyclase toxin

Dermonecrotic toxin: vasoconstriction and ishcmic necrosis

Tracheal cytotoxin: kills respiratory epithelial cells: sitmulates IL-2 release

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34
Q

overall, the toxins acting in Pertussus:

A

block the affects of the immune system

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35
Q

Pertussis pathogenesiss

A

inhalation
bacterial attachment to ciliated airway epithelium and production of toxins
bacterial multiplication, influx of neutrophils, damage to ciliated epith, mucus HYPERsecretion

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36
Q

effects of Pertussis

A

compromise small airway sesp of infants, predispose to atelectasis,c ough, cyanosis, PNA

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37
Q

Review graph for stages of pertusssis

A

draw

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38
Q

Pertussis Dx

A

Presumptive:serology
Definitive: Culture (Bordet-Gengou or Regan-Low agar)
PCR: highly sensitive!

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39
Q

Pertussis Tx

A

Erythromycin

Immunize

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40
Q

Loeffler’s medium (volutin granules)

Cysteine-tellurite agar (black)

A

Diptheria

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41
Q

Elek test, PCR, ELISA, and Immunochromatogaphic strip assay

A

Diptheria

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42
Q

Bordet-Geng and

Regan-Lowe agar

A

Pertussis

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43
Q

Presumptive dx: Serology

Definitive dx: Culture on enriched medium (Bordet-geng and Regan Lowe), and PCR- highly sensitive

A

Pertussis

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44
Q

Definitive dx for Pertussis

A

Culture on enriched

PCR

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45
Q

Gram (+) organisms

A

Staph Aureus
Strep PNA
Corny Diptheria

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46
Q

Gram (-) organisms

A

Pseudomonas
H. Influenza
M. Catt
Pertussis

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47
Q

Staph, Strep, and Corny

48
Q

All viruses are

A

obligate intracellular parasites

49
Q

Viruses replicate in a pattern that is diff from all other cellular organisms

A

one-step growth curve
“assembly line”
NO BINARY FISSION

50
Q

Lytic Virus-host interaction

A

Central goal of almost all viruses is to RAPIDLY REPLICATED NEW VIRIONS at the expense of host cell

51
Q

When virus remains with host, but genes are largely silent

A

Prophage (bacterial lysogen)

Provirus (human host cell)

52
Q

Persistent viral infection

A

infection without cell death (virus is found long term reltnship with host)
3 types

53
Q

3 types of Persistent Viral infections

A

Latent- Herpes simplex
Chronic- Hep b
Transforming- HPV

54
Q

Why is tx of viruses so hard

A

exploitation of host cells makes it hard to find a non-toxic chemo agent

55
Q

Croup

A

USUALLY caused by PIV type 1 and 2

56
Q

Croup

A

tracheal constriction below vocal cords (caused by inflammatory response)

57
Q

Croup

A

fever, hoarse, barking cough in chidren 6-18 mo of age

58
Q

PIV agent

A

Non-segmented
enveloped
4 known serotypes

59
Q

Other PIV complications

A

Otitis media- the virus sets the stage for secondary bacterial infection

Also, parotitis

60
Q

Para-influenza Epidemiology

A

seasonal upsurge with type 1 and 2
Fall-winter greatest incidence

Life long immunity is NOT observed

61
Q

Reservoir for PIV

A

adults and caregivers with minor colds are the reservoir for infant illness

62
Q

PIV Diagnosis

A

direct viral isolation from throat swabs

direct FAB test

63
Q

PIV Tx

A

Supportive

NO vaccine!

64
Q

RSV

A

annual winter outbreak

65
Q

RSV clinical manifestation

A

cough, dyspnea, cyanosis, sometimes croup (BUT REMEMBER CROUP IS USUALLY CAUSED BY PIV 1 AND 2)

66
Q

RSV clinical manifestation

A

nose, throat, and bronchi

Sx are d/t the inflammatory response to the antigen- IgE, T cells

67
Q

RSV Dx

A

Rapid antigen test

*screen infants with sx

68
Q

RSV Tx

A

Ribavirin (controversial)
Palivizumab- a Monoclonal immune globulin available for high risk pts

BUT, do not treat unless pt’s conditioin is severe!!!!

69
Q

RSV Epidemiology

A

Most common cause of LOWEr resp tract infection in children <4YO

birth season 3-4 mo before RSV szn (winter) is the worst

70
Q

The COLD (ARD)

A

typically benign, transitory, and self limited

more severe in small children

71
Q

ARD etiology

A

Rhinovirus 25%
Coronavirus 10%
Adenovirus and Unknown 30-40%

72
Q

ARD tx

A

Sx-atic

FDA says do NOT use Zicam, can cause permanent loss of smell

73
Q

Maybe >50% of URI caused by Rhinovirus but

A

no one is really certain

74
Q

Rhinovirus carrier

A

HANDS
human carrier state highly probably

immunity is only transient (18 months)

75
Q

Pleconaril

A

blocks uncoating and attachment of virus by binding into a hydrophobic pocket within the capsid

76
Q

Acute Flaccid Myelitis

A

weakness/paralysis similar to polio

most victims children

viral etiology suspected

77
Q

Influenza

A

3 types

Type A is worst

78
Q

Large number of subtypes of flu based on

A

envelop proteins

79
Q

H hemagglutinin (flu virus)

A

viral attachment

80
Q

N neuraminidase

A

viral penetration and release from infected cells

81
Q

Influenza clinical

A

short incubation 1-2 d
abrupt sx
illness lasts about a week

82
Q

Complications of Influenza

A

Pulmonary- PNA
Reyes syndrome
Guillian Barre syndrome

83
Q

Influenza dx

A

clinical finding is sufficient in epidemic situation

lab- swab. BE AWARE OF FALSE NEGATIVES if swab is taken too early in dz progression

84
Q

Amantadine and Rimantadine

A

flu tx- Type A only

stop uncoating/penetration

85
Q

Osteltamivir, Zanamavir, Peramivir

A

Type A and B

stop spreading/release of virus

86
Q

Xofluza

A

new 2018

inhibits viral cap endonuclease

87
Q

Quadrivalent flu vaccine

A

2 type A viruses and 2 type B

88
Q

name change of flu virus

A

TIV –> IIV

89
Q

High potency and adjunated forms should be given to

90
Q

Two doses of flu vaccine needed for

A

children <9 YO

91
Q

Problem with flu vaccine being made in an egg

A

virus adapts to eggs and may not match circulating forms

92
Q

Antigenic drift

A

point mutation

minor variation

93
Q

Antigenic SHIFT

A

recombination of ENTIRE genome within virion

implied MIXED INFECTIONS occur

94
Q

Flu Epidemiology

A

10-40k deaths annually

2017-18 flu szn- 80k deaths

95
Q

Flu type A can occur

A

endemic, epidemic, or pandemic
unpredictable

WINTER OCCURENCE

most children and young adults
children < 1yo rare

96
Q

Pandemics are

A

unpredictable

new pandemic virus emerged in mexico d/t unanticipated type of antigenic SHIFT

97
Q

Different about Chlamydia

A

something b/w true bacteria and virus

REPLICATE WITH BINARY FISSION

98
Q

Chlamydia life cycle

A

Energy parasites- remove ATP from host

Agent assumed two forms:
EB
RB

99
Q

Two forms of Chlamydia

A

Elementary body- infectious, non growing, dispersal

Reticulate body- growing vegetative form

100
Q

C. trachomatis

A 
Infant PNA- 3 wks after birth (rhinitis and then cough)
or Nasty eye infection
Risk factor is infected mother
Multiple serovars exist
Reiter's syndrome to follow is a risk
101
Q

C. PNA

A

single serovar known

bronchitis, PNA, sinusitis

102
Q

H. Influenzae colonizes

A

UPPER resp tract

103
Q

H. influenza has a neuroaminidase (virulence factor) that is:

A

different than influenza!

104
Q

ID-Latex Particle Agglutination Test (LAT)

A

easier to get definitive results regarding H. Influenza, relies on ANTIGEN

105
Q

Klebsiella

A

gram (-) bacillis

106
Q

Klebsiella tx

A

EMPIRIC

susceptibility testing required

107
Q

Klebsiella host aspirates microbes into the

A

Lower Respiratory Tract

108
Q

Klebsiell

A

necrotizing CAP with preference for UPPER LOBES, then the host aspirates microbes into the LOWER resp tract

109
Q

Klebsiella culture

A

done on MacConkey Agar

Gram (-) and Lactose positive!!!

110
Q

S. PNA

A

alpha-hemolytic

Optichin sensitive

111
Q

Tissue damage virulence factor

S.PNA

A

Techoic Acid and Peptidoglycan initiate inflammatory response

112
Q

Pneumolysin of S.PNA virulence factor

A

induces classical component

113
Q

Vaccines for S.PNA

A 
Pneumovax 23
Prevnar 13 (infants)
114
Q

Most dangerous type of meningitis that can lead to neuro defects and death

115
Q

Best ways to differentiate S.PNA from other types of strep

A

Heme: alpha

Bile sensitive: lysed in bile

Quarter 3 (17 decks)

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