Microbio Exam 1 Flashcards
1
Q
Pathogens that cause:
Otitis Media and Sinusitis
A
SMH pathogens
Strep PNA
M. Cat
H. Influenzae
2
Q
Pathogens that cause:
Otitis Externa
A
Pseudomonas Aerug
Staph Auereus
3
Q
Pathogen that causes Diptheria
A
Corynebacteriam diptheria
4
Q
Pathogen that causes Whooping cough (pertussis)
A
Bordetella pertussis
5
Q
Sx of Otitis externa
A
Otalgia (pain) and
Otorrhea (drainage)
fever greater than 38.3 indicated more than just localized involvement
6
Q
Pseudomonas and Staph are Halophiles
A
meaning they can live on the salty skin
cause Otitis Externa
7
Q
Pseudomonas Aeruginosa
A
Gram (-)
Pigment producer: Pyocanin (non fluorescent blue) and
Pyroverdin (fluorescent green)
Encapsulated
8
Q
Otitis Externa
A
one cause is Pseudomonas Aeruginosa: blue and green
most strains produce Pyocyanin (blue) but nearly ALL produce pyoverdin (green!!)
9
Q
Staph Aureus
A
another big cause of Otitis Externa
Gram (+) cocci in clusters
Coagulase (+)
B-hemolytic
10
Q
Beta hemolytic
A
complete hemolysis, can see through
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)
12
Q
Otitis Media and Sinusitis
A
SMH pathogens
Strep PNA: 50%
H. Influenza: 20%
M. Cat: 10%
13
Q
Strep PNA
A
Gram (+) Lancet shaped diplococci Encapsulated A-hemolysis (incomplete, cannot see thru- yellow to grayish green on plate) Optochin sensitive
14
Q
Strep PNA review
A
Gram (+) Lancet shaped diplocicci Encapsulated a-hemolysis Optochin sensitive
15
Q
H Influenza
A
Gram (-) coccobacilli
16
Q
M. Cat
A
Gram (-) Diplococci
Oxidase (+) !!!
B-lactamase producer
17
Q
Otitis Media
A
Amoxicillin
18
Q
Diptheria
A
Cutaneous (abscesses and sores) vs Respiratory
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
20
Q
Toxigenic strains of Diptheria have a phage encoded exotoxin
A
Diptheria toxin
Exo meaning it is expelled from the pathogen
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
22
Q
Cutaneous diptheria
A
most cases d/t nontoxigenic strains
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
24
Q
Pseudomembrane in Diptheria is what color:
A
thick grayish to black
25
Diptheria Pathogenesis
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)
26
Diptheria is uncommon in developed countries
vaccinate
27
Cultures for Diptheria
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
28
Staining for Diptheria
Gram: club shaped gram (+) bacilli
Volutin: metachromatic (volutin) granules (the V poitn)
29
Diptheria Dx
Presumptive isolates should be tested for TOXIN PRODUCTION
Elek test
PCR
ELISA
Immunochromatographic strip assay- very sensitive
30
Tx/prevention of Diptheria
Neutralize exotoxin with Diptheria Antitoxin: the most important!!! bc exotoxin is most damaging
then,
Abx: Erythromycin
Isolate person to minimize spread
Vaccinate
31
Pertussis
aka whooping cough
small gram (-) coccobacilli
virulence factors: adhesins and exotoxins
32
Pertussis Adhesins
mediate attachment to integrins and help colonization in the respiratory epithelium
33
Four exotoxins in Pertussis
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
34
overall, the toxins acting in Pertussus:
block the affects of the immune system
35
Pertussis pathogenesiss
inhalation
bacterial attachment to ciliated airway epithelium and production of toxins
bacterial multiplication, influx of neutrophils, damage to ciliated epith, mucus HYPERsecretion
36
effects of Pertussis
compromise small airway sesp of infants, predispose to atelectasis,c ough, cyanosis, PNA
37
Review graph for stages of pertusssis
draw
38
Pertussis Dx
Presumptive:serology
Definitive: Culture (Bordet-Gengou or Regan-Low agar)
PCR: highly sensitive!
39
Pertussis Tx
Erythromycin
| Immunize
40
Loeffler's medium (volutin granules)
| Cysteine-tellurite agar (black)
Diptheria
41
Elek test, PCR, ELISA, and Immunochromatogaphic strip assay
Diptheria
42
Bordet-Geng and
| Regan-Lowe agar
Pertussis
43
Presumptive dx: Serology
Definitive dx: Culture on enriched medium (Bordet-geng and Regan Lowe), and PCR- highly sensitive
Pertussis
44
Definitive dx for Pertussis
Culture on enriched
| PCR
45
Gram (+) organisms
Staph Aureus
Strep PNA
Corny Diptheria
46
Gram (-) organisms
Pseudomonas
H. Influenza
M. Catt
Pertussis
47
Staph, Strep, and Corny
Gram (+)
48
All viruses are
obligate intracellular parasites
49
Viruses replicate in a pattern that is diff from all other cellular organisms
one-step growth curve
"assembly line"
NO BINARY FISSION
50
Lytic Virus-host interaction
Central goal of almost all viruses is to RAPIDLY REPLICATED NEW VIRIONS at the expense of host cell
51
When virus remains with host, but genes are largely silent
Prophage (bacterial lysogen)
| Provirus (human host cell)
52
Persistent viral infection
infection without cell death (virus is found long term reltnship with host)
3 types
53
3 types of Persistent Viral infections
Latent- Herpes simplex
Chronic- Hep b
Transforming- HPV
54
Why is tx of viruses so hard
exploitation of host cells makes it hard to find a non-toxic chemo agent
55
Croup
USUALLY caused by PIV type 1 and 2
56
Croup
tracheal constriction below vocal cords (caused by inflammatory response)
57
Croup
fever, hoarse, barking cough in chidren 6-18 mo of age
58
PIV agent
**Non-segmented**
enveloped
4 known serotypes
59
Other PIV complications
Otitis media- the virus sets the stage for secondary bacterial infection
Also, parotitis
60
Para-influenza Epidemiology
seasonal upsurge with type 1 and 2
Fall-winter greatest incidence
Life long immunity is NOT observed
61
Reservoir for PIV
adults and caregivers with minor colds are the reservoir for infant illness
62
PIV Diagnosis
direct viral isolation from throat swabs
| direct FAB test
63
PIV Tx
Supportive
| NO vaccine!
64
RSV
annual winter outbreak
65
RSV clinical manifestation
cough, dyspnea, cyanosis, sometimes croup (BUT REMEMBER CROUP IS USUALLY CAUSED BY PIV 1 AND 2)
66
RSV clinical manifestation
nose, throat, and bronchi
| Sx are d/t the inflammatory response to the antigen- IgE, T cells
67
RSV Dx
Rapid antigen test
| *screen infants with sx
68
RSV Tx
Ribavirin (controversial)
Palivizumab- a Monoclonal immune globulin available for high risk pts
BUT, do not treat unless pt's conditioin is severe!!!!
69
RSV Epidemiology
Most common cause of LOWEr resp tract infection in children <4YO
birth season 3-4 mo before RSV szn (winter) is the worst
70
The COLD (ARD)
typically benign, transitory, and self limited
more severe in small children
71
ARD etiology
Rhinovirus 25%
Coronavirus 10%
Adenovirus and Unknown 30-40%
72
ARD tx
Sx-atic
| FDA says do NOT use Zicam, can cause permanent loss of smell
73
Maybe >50% of URI caused by Rhinovirus but
no one is really certain
74
Rhinovirus carrier
HANDS
human carrier state highly probably
immunity is only transient (18 months)
75
Pleconaril
blocks uncoating and attachment of virus by binding into a hydrophobic pocket within the capsid
76
Acute Flaccid Myelitis
weakness/paralysis similar to polio
most victims children
viral etiology suspected
77
Influenza
3 types
| Type A is worst
78
Large number of subtypes of flu based on
envelop proteins
79
H hemagglutinin (flu virus)
viral attachment
80
N neuraminidase
viral penetration and release from infected cells
81
Influenza clinical
short incubation 1-2 d
abrupt sx
illness lasts about a week
82
Complications of Influenza
Pulmonary- PNA
Reyes syndrome
Guillian Barre syndrome
83
Influenza dx
clinical finding is sufficient in epidemic situation
lab- swab. BE AWARE OF FALSE NEGATIVES if swab is taken too early in dz progression
84
Amantadine and Rimantadine
flu tx- Type A only
| stop uncoating/penetration
85
Osteltamivir, Zanamavir, Peramivir
Type A and B
| stop spreading/release of virus
86
Xofluza
new 2018
| inhibits viral cap endonuclease
87
Quadrivalent flu vaccine
2 type A viruses and 2 type B
88
name change of flu virus
TIV --> IIV
89
High potency and adjunated forms should be given to
elderly
90
Two doses of flu vaccine needed for
children <9 YO
91
Problem with flu vaccine being made in an egg
virus adapts to eggs and may not match circulating forms
92
Antigenic drift
point mutation
| minor variation
93
Antigenic SHIFT
recombination of ENTIRE genome within virion
implied MIXED INFECTIONS occur
94
Flu Epidemiology
10-40k deaths annually
2017-18 flu szn- 80k deaths
95
Flu type A can occur
endemic, epidemic, or pandemic
unpredictable
WINTER OCCURENCE
most children and young adults
children < 1yo rare
96
Pandemics are
unpredictable
new pandemic virus emerged in mexico d/t unanticipated type of antigenic SHIFT
97
Different about Chlamydia
something b/w true bacteria and virus
REPLICATE WITH BINARY FISSION
98
Chlamydia life cycle
Energy parasites- remove ATP from host
Agent assumed two forms:
EB
RB
99
Two forms of Chlamydia
Elementary body- infectious, non growing, dispersal
| Reticulate body- growing vegetative form
100
C. trachomatis
```
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
C. PNA
single serovar known
| bronchitis, PNA, sinusitis
102
H. Influenzae colonizes
UPPER resp tract
103
H. influenza has a neuroaminidase (virulence factor) that is:
different than influenza!
104
ID-Latex Particle Agglutination Test (LAT)
easier to get definitive results regarding H. Influenza, relies on ANTIGEN
105
Klebsiella
gram (-) bacillis
106
Klebsiella tx
EMPIRIC
| susceptibility testing required
107
Klebsiella host aspirates microbes into the
Lower Respiratory Tract
108
Klebsiell
necrotizing CAP with preference for UPPER LOBES, then the host aspirates microbes into the LOWER resp tract
109
Klebsiella culture
done on MacConkey Agar
| Gram (-) and Lactose positive!!!
110
S. PNA
alpha-hemolytic
| Optichin sensitive
111
Tissue damage virulence factor
| S.PNA
Techoic Acid and Peptidoglycan initiate inflammatory response
112
Pneumolysin of S.PNA virulence factor
induces classical component
113
Vaccines for S.PNA
```
Pneumovax 23
Prevnar 13 (infants)
```
114
Most dangerous type of meningitis that can lead to neuro defects and death
S. PNA
115
Best ways to differentiate S.PNA from other types of strep
Heme: alpha
| Bile sensitive: lysed in bile
