Micro Exam 2

Front 1

describe the characteristics of viruses

Back 1

Obligate intercellular parasites
No indipendent metabolism
Small Size (15-300nm)
Progeny made in assembly like fashion
One step growth Curve
Special techniques are requited to observe and quantify

Front 2

Describe viral structure

Back 2

Nucleic acids and protiens in a lipid containing envelope

Front 3

What are Capsomeres?

Back 3

the small protein subunits typically composed of several small
proteins that combine in groups to form the capsid

Front 4

What are Capsid (nucleocapsid)?

Back 4

-- Protein covering surrounding core of nucleic acid and
(sometimes) enzyme

Front 5

What are the f two basic patterns of the nucleic acid genome formation in virus?

Back 5

1. Extended nucleic acid form
2. Condensed nucleic acid form

Front 6

What is a virion?

Back 6

the complete (infectious) virus particle

Front 7

What is the viral envelope made out of?

Back 7

Combination of host membrane with some virus proteins
Host membrane is studded with viral proteins and progeny virions acquire
during budding out process

Front 8

What are peplomeres?

Back 8

Spikes:
virus proteins embedded in envelope that project from surface; the are associated with enzymatic activity

Front 9

Describe the virus genome

Back 9

Nucleic acid – the viral genome, may be DNA or RNA
Many forms have been observed (double stranded, single stranded,
segmented)

Front 10

What does RNA virus “polarity” mean?

Back 10

Positive (+) stranded -- can serve as mRNA directly, i.e., they may
be directly translated by host ribosomes into proteins

Negative (-) stranded – cannot be directly translated, must first be
transcribed by a virus-encoded RNA dependent RNA polymerase
to get a strand of + polarity that can act as mRNA and be
translated by ribosomes

Front 11

How are virusus classified?

Back 11

1. Physical features , ex
Nature and physical form of nucleic acid genome, Capsid structure and symmetry, Helical or Icosahedral,
Presence/absence of envelope,
Countable or measurable features of virion, Size, Number of capsomeres (icosahedral)
Helix diameter (helical)


2. Biological Properties

Host range
Transmission mechanism
Tissue tropism
Pattern of replication

Front 12

What is the goal of nearly all viruses?

Back 12

to replicate virus at the expense of the
host cell

Front 13

What are the stages of Animal Cell Virus Replication?

Back 13

Attachment
Penetration
Uncoating
Early synthesis- Genome
Late Synthesis- Viral maturation and capsid
Burst or release of progeny virions

Front 14

In gengeral, where do DNA virus replication and maturation to occur?

Back 14

Host nucleus

Front 15

What are the modes of penetration for a virus?

Back 15

Surface eclipse: Direct fusion of capsid with host membrane

Membrane-membrane fusion

Receptor-mediated endocytosis:
Uptake in clathrin coated pits, or
Fusion with lyosomes, removal of capsid

Front 16

If DNA replication is a tightly controlled process in the host cell and viruses frequently infect cells that are not actively dividing and producing DNA, how are they able to get their DNA made?

Back 16

DNA viruses disrupt host cell cycle control functions p53
and Rb and nudge the host into something akin to S phase to
replicate
OR they
supply their own host cell-independent DNA replication
functions.

Front 17

In general, where do you expect RNA virus replication and maturation to occur?

Back 17

host cell cytoplasm.

Front 18

Although structurally diverse, all RNA genome viruses face what common
problems?

Back 18

1) RNA is comparatively unstable and molecules must be copied
rapidly in the infected cell
2) Host cells don't have RNA copying enzymes so virus must bring those wiith them or synthesize them from their genome

Front 19

What is the hallmark of retrovirus replication?

Back 19

reverse transcription and integration
These pseudo-diploid RNA viruses first convert their RNA genome to DNA (reverse transcription). The DNA is incorporated into the hose DNA becoming a provirus and that DNA can be trascribed into RNA
RNA->DNA->RNA->Proteins

Front 20

What viruses have a strong risk for cancer development?

Back 20

Human papilloma virus types 16 and 18 (cervical/oral cancer)

Hepatitis B and C viruses (liver cancer)

Epstein-Barr virus (Burkitt’s lymphoma, nasopharyngeal cancer and
others)

Human herpes virus type 8 (Kaposi’s sarcoma with HIV)

Human T cell lymphotropic virus type 1

Front 21

What causes rheumatic fever?

Back 21

Strep pyogenes

Front 22

What are the sx of rhumatic fever?

Back 22

SPEECulation
Subcutaneous nodes
Polyarthrits
Erythema marginatum
Chorea
Carditis

Front 23

What bugs can be pathogenic in URI?

Back 23

Staphylococcus aureus (G+) 
Streptococcus pyogenes (G+)  
Streptococcus pneumoniae (G+) 
Moraxella catarrhalis (G –) 
Neisseria meningitidis (G –)   
Haemophilus influenzae (G –)   
Bacteroides fragilis (G –) 
Candida albicans (Yeast/Fungus) 

Front 24

What are the general characteristics of the genus Streptococcus? 

Back 24

Cells are arranged as chains or pairs and are gram‐positive, catalase negative and nonmotile 
grows on Chocolae Agar
Lancefeild Groups A-U

Front 25

What is the source molecule that is the basis for the Lancefield scheme of classification? 

Back 25

antigenicity of a cell wall carbohydrate   C substance or group carbohydrate antigen   
    GAS = NAG + rhamnose  

Front 26

What is Lancfelid Group, Hemolysis type and main pathogenicity area of S. Pyogenes?

Back 26

Group A Beta Hemolytic
Acute pharyngits and skin infections

Front 27

What 3 compoments to cell envelope in GABHS give virulence?

Back 27

1)M-Protein:
2) Protein F and LTA 
3)Capsule 

Front 28

S pyogenes Virulence Factors, Describe Hyaluronic Acid Capsule 

Back 28

Inhibits phagocytosis 

Front 29

S pyogenes Virulence Factors, Describe Lipoteichoic Acid (LTA) 

Back 29

Adhere to pharyngeal epithelium 

Front 30

S pyogenes Virulence Factors, Describe M protein 

Back 30

Interferes with phagocytosis; responsible for sequelae 

Front 31

S pyogenes Virulence Factors, Describe Protein F 

Back 31

Responsible for attachment to fibronectin on host cells 

Front 32

S pyogenes Virulence Factors, Describe Streptolysins O and S 

Back 32

β‐hemolysis; Lyse leukocytes and erythrocytes; 

Front 33

S pyogenes Virulence Factors, Describe Streptodornase;  

Back 33

Enhance spread of bacteria; breakdown DNA of host cells 

Front 34

S pyogenes Virulence Factors, Describe C5a peptidase 

Back 34

Inhibits attraction of phagocytes by destroying C5a 

Front 35

S pyogenes Virulence Factors, Describe Streptokinase 

Back 35

Activates plasminogen to plasmin; Dissolves blood clots 

Front 36

What is the effect of Streptococcal Pyrogenic Exotoxins (Spe A, B, C)  

Back 36

  SpeA functions as superantigen 
      Massive cytokine release  
Results in tissue damage 
  Only lysogenized strains produce SpeA 
Responsible for 
  STSS ‐ Streptococcal TSS (toxic shock syndrome)  
  Scarlet fever 

Front 37

Describe the Epidemiology of GAS Pharyngitis 

Back 37

Most Common Bacteria
HUMANS ONLY RESIVOIR
Prominent in winter and spring
Peak ages kids 1-15

Front 38

How id GAS Pharyngits spread?

Back 38

Respiratory droplets and person‐to‐person contact, NOT fomites

Front 39

What are the 3 Pathogenic mechanisms for GABHS?

Back 39

1.Pyogenic inflammation – pharyngitis 
2. Toxin-mediated – Scarlet fever – Scarletina 
3.Immunologic disease – Acute rheumatic fever (ARF) and Poststreptococcal acute  
      Glomerulonephritis (AGN) 

Front 40

What is required to get scarlett fever?

Back 40

Requires infection with a lysogenized strain ‐ releases the pyrogenic exotoxin (SpeA) 

Front 41

What are the characteristics of scarlett fever?

Back 41

Pastia’s lines
Sandpaper skin/rash with possible desquamation of hands and feet wehre rash spared
circumoral pallor and “strawberry tongue” in mouth

Front 42

What are Pastia’s lines?

Back 42

 accentuated petechial lesions on flexor skin creases/folds 

Front 43

Rheumatic Fever (RF) is what type of hypersensitivity?

Back 43

Type II

Front 44

What are Aschoff bodies?

Back 44

perivascular granulomas in myocardium that are evidenced as they are   Replaced by scar tissue 
Indicative of Scarlett fever

Front 45

Describe Poststreptococcal Acute Glomerulonephritis – (AGN) 

Back 45

Type III Hypersensitivity
Commonly preceded by cutaneous infection. 
 
Nephritogenic M Protein types are associated with disease 

Front 46

A child presents to your office with Puffy face – fluid retention/kidney damage 
Hematuria – dark urine – blood 
  Possible hypervolemia – secondary to fluid retention 
After a severe skin infection. What is the dx and cause?

Back 46

Post strep glomerularnephritis

Front 47

What are the diagnostic tests with key features for strep?

Back 47

Rapid Antigen Detection Test (RADT) -Fast but not sensitive, need to culture negatives
Bacitracin sensitivity - only group A inhibited, other groups not
PYR‐positive test 

Front 48

What is preferred tx for strep?

Back 48

10 day penicillin VK
then Macrolides if B-latam sensitivity or clyndamycin is there is macrolide resistance suspected

Front 49

Most common bacteria implicated in in otitis externa?

Back 49

Pseudomonas aeruginosa
Staphylococcus aureus

Front 50

Characteristic signs of otitis externa?

Back 50

otalgia -Pain
otorrhea - discharge

Front 51

What is the morphology of Pseudomonas aeruginosa?

Back 51

gram-negative encapsulated bacillus
pigment producers – pyocyanin & pyoverdin

Front 52

What does Pyocyanin look like?

Back 52

nonfluorescent bluish pigment

Front 53

What does Pyoverdan look like?

Back 53

fluorescent green pigment

Front 54

Describe the morphology of Staphylococcus aureus...

Back 54

gram-positive encapsulated coccus, coagulase- positive organism, β-hemolytic on blood agar.

Front 55

What is the preferred tx for otits externa?

Back 55

Topical antibacterial agents

Front 56

What are the bugs associated with otits media?

Back 56

Streptococcus pneumoniae
Haemophilus influenzae:
Moraxella catarrhalis:

Front 57

How does otitis media typically present?

Back 57

inflammation of the middle ear, including the tympanic membrane.
Often associated with a buildup of fluid in the middle ear space. Common in children

Front 58

What is the recommended tx for otitis media?

Back 58

DOC is amoxicillin
for chronic infections tympanic tubes may be plced

Front 59

What is the morphology of Streptococcus pneumoniae?

Back 59

e: gram-positive, encapsulated, lancet-
shaped diplococcus; exhibits α-hemolysis on blood agar.

Front 60

What is the morphology of Haemophilus influenzae:?

Back 60

gram-negative coccobacillus; the nontypeable
strains are often involved in otitis media and sinusitis.

Front 61

What is the morphology of Moraxella catarrhalis?

Back 61

gram-negative diplococcus; oxidase-positive
organism; β-lactamase producer and non-fermenter of carbohydrates (to
allow differentiation from Neisseria species).

Front 62

What organisms typically cause sinusitis?

Back 62

The same as middle ear
Strep pneumoniae
Haemophilus influenza
Moraella catarrhalis

Front 63

What is the causitive agent of diptheria and what is its morphology?

Back 63

Corynebacterium diphtheriae
gram-positive
pleomorphic bacillus; often club-shaped. Has a “Chinese letter” appearance

Front 64

What characteristics of diphtheria aid in its dx microscopically?

Back 64

metachromatic (aka volutin) granules

Front 65

Describe phage-encoded exotoxin

Back 65

AKA diphtheria toxin.
The diphtheria toxin is an A-B exotoxin and functions by binding to heparin-
binding EGF receptors, causing an inactivation of EF-2. This results in
inhibition of eukaryotic protein synthesis and the cells die.

Front 66

What are the two forms of diptheria?

Back 66

Cutaneous diphtheria
Respiratory diphtheria

Front 67

Describe Cutaneous diphtheria:

Back 67

the organism is inoculated into broken skin; a papule
develops, progressing to an ulcer that does not heal.

Front 68

Describe Respiratory diphtheria:

Back 68

respiratory droplets or direct contact transmits bug to pharynx where it incubates 2-4 days and excretes exotoxin. The toxin is absorbed into the mucous membranes, causing destruction of the
epithelium and a superficial inflammatory response. Gray "pseudomembrane" in throat is characteristic

Front 69

What is the epidemiology of diptheria?

Back 69

Found worldwide, especially in poor urban areas where vaccine-induced immunity is low... Person to person contact

Front 70

Bull Neck & “club-shaped” refernce what bacteria?

Back 70

Diptheria

Front 71

What cultures would you use if you suspected diptheria?

Back 71

Culture on blood agar, cysteine-tellurite agar, and Loeffler’s medium
 Blood agar will help to rule out hemolytic strep
 Loeffler’s medium reveals typical colony morphology
 Black colonies on cysteine-tellurite agar

Front 72

What 4 ways should C. diphtheriae isolates should be tested for toxin production?

Back 72

Elek immunodiffusion test
PCR
ELISA
Immunochromatographic strip assay

Front 73

What is the treatment for diptheria?

Back 73

DOC is erythromycin or penicillin
Neutralize the exotoxin using antitoxin to reducemortality

Front 74

What is the morphology of Bordetella pertussis?

Back 74

aerobic gram-negative
coccobacillus

Front 75

What are the adhesive Bordetella pertussis virulence factors?

Back 75

 Pertactin = P69
 Filamentous hemagglutinin (FHA)
 Fimbriae (significant in in vitro studies; role in vivo unknown)

Front 76

What are the exotoxin Bordetella pertussis virulence factors?

Back 76

Pertussis toxin = an A-B exotoxin
Adenylate cyclase toxin:
(Both increase cAMP)
Tracheal cytotoxin: causes ciliostasis and stimulates IL-1 secretion.
Dermonecrotic toxin:

Front 77

How do macrophages contribute to pertussis infection?

Back 77

Localized proliferation and phagocytosis by macrophages occurs. The bacteria
inhibit intracellular killing mechanisms and can survive/replicate intracellularly.

Front 78

What bug causes lymphocytic leukocytosis?

Back 78

pertussis by inhibitin WBC extravization

Front 79

What are the three stages of pertussis infection?

Back 79

Catarrhal stage: inflammation of mucous membranes
Paroxysmal stage: attacks or spasms
Convalescent stage: recovery

Front 80

Describe the epidemiology of pertussis

Back 80

Strictly a human disease; often considered a pediatric disease but adults are infected as well. Disease is more serious in children.

Front 81

How do you get a definitive dx for pertussus?

Back 81

culture on Bordet-Gengou or Regan-Lowe agar, PCR

Front 82

What is the treatment for pertussus?

Back 82

Macrolides and Immunuzation

Front 83

What are the typical CAPs?

Back 83

S. pneumoniae,
H. influenzae, some
K. pneumoniae, and
S. aureus

Front 84

What are the 3 zoonotic (atypical pneumonia) pathogens?

Back 84

•  Chlamydia psittaci (psittacosis)
•  Francisella tularensis (tularemia)
•  Coxiella burnetii (Q fever)

Front 85

What are the 3 NON-zoonotic (atypical pneumonia) pathogens?

Back 85

•  Chlamydia pneumoniae
•  Mycoplasma pneumoniae
•  Legionella pneumoniae

Front 86

Describe the presentation of Typical Bacterial Pneumonias...

Back 86

Suddenly Ill
High Fever
Chills
Shaking
Productive ciugh
Consolidated cxr
Chest pain & SOB

Front 87

Describe Streptococcus pneumoniae

Back 87

Gram-positive, lancet-
shaped diplococcus
•  Alpha-hemolytic colonies
–  Greenish colonies
•  Optochin sensitivity
•  Encapsulated strains are
virulent

Front 88

Describe the following virulence factor for Pneumococci: Capsule

Back 88

; it inhibits phagocytosis
by interfering with C3 activity;

Front 89

Describe the following virulence factor for Pneumococci: Pneumolysin

Back 89

interacts with the target cell membrane, and
forms transmembrane pores with resulting host cell lysis.
This lysis event results in the activation of the complement
system.

Front 90

Describe the following virulence factor for Pneumococci: Peptidoglycan-teichoic acid complex

Back 90

s a potent
immunomodulator; the heightened response may be
destructive to host tissues.

Front 91

What bacteria has IgA protease which disables host IgA?

Back 91

Streptococcus pneumoniae

Front 92

What bacteria besides influenza has Hyaluronidase and neuraminidase?

Back 92

Streptococcus pneumoniae

Front 93

Where is Autolysin found?

Back 93

S. Pneumoniae
has importance in the release of pneumolysin and neuraminidase from the cytoplasm of the bacterium.

Front 94

What adhesion facots does strep. pneumoniae have that let it bind to respiratory epithelium?

Back 94

Pilli and choline binding proteins

Front 95

Pneumococcus is responsible for what diseases initially?

Back 95

– Bacterial meningitis
– Otitis media
– Sinusitis

Front 96

If pneumococcus disseminates, what other diseases can it cause?

Back 96

•  Bacteremia
•  Meningitis
•  Arthritis
•  peritonitis

Front 97

When is the Quellung reaction used?

Back 97

to observe the capsule in s. pneumonia

Front 98

What is the DOC for pneumonia?

Back 98

penicillin G

Front 99

What are the vaccine recommendations for S. Pneumoniae currently?

Back 99

23-valent capsular polysaccharide vaccine for those 65 and older (covers most adult infections)
  7-valent capsular polysaccharide vaccine for those 6 years and younder

Front 100

What does Haemophilus influenza cause?

Back 100

haEMOPhilis
Eppiglottis
Meningitis
Otitis media
Pneumonia
NOT THE FLU!

Front 101

What is the morphology of H. influenza?

Back 101

small gram - coccobacillary rod

Front 102

What culture do you use for Haemophilus influenza?

Back 102

When you have the "flu" mom goes to the five-(V) & dime-(X) store to get some chocolate:
Grows on choclate agar but needs factors V (NAD) and X (Hematin) for growth

Front 103

What vaccine and invasive disease is predominantly capsular type B?

Back 103

H. influenzae

Front 104

What is the major virulence factor for H. influenzae?

Back 104

  Polyribosylribitol phosphate (PRP)
capsule is major virulence factor
–  Renders resistant to hagocytosis by PMNs
•  All virulent strains produce
neuraminidase and an IgA protease

Front 105

What is preferred tx for H. Influenzae?

Back 105

Treated typically with β-lactams
(amoxicillin/clavulanic acid)

Front 106

What population is Klebsiella pneumoniae most frequently seen?

Back 106

alcoholics and persons suffering from diabetes mellitus; frequently in homeless... Source of both CAP and Nosocomial Pneumonia

Front 107

Describe the morphology of Klebsiella pneumoniae ...

Back 107

Non-motile, Gram-negative bacillus
•  Coated by a thick, mucoid (slimy) capsule

Front 108

Where is Klebsiella pneumoniae seen physiologically in the body?

Back 108

Found in normal flora of
mouth, skin and
intestines

Front 109

What are the virulence factors of Klebsiella pneumoniae?

Back 109

Primary virulence factor- polysaccharide capsule
LPS
Adhesins

Front 110

What type of infection does this indicate:
•  Patients have an acute onset of high fever and a productive cough with a thick, blood tinged sputum
(Currant jelly sputum)
•  Infection leads in many cases, to abscess formation,
cavitation, pleuritic chest pain

Back 110

Klebsiella pneumoniae

Front 111

What is the mortality rate of -Klebsiella pneumoniae?

Back 111

Mortality rate is 50%
regardless of treatment

Front 112

how do you treat Klebsiella pneumoniae?

Back 112

Combinations used for
treatment:
•  Aminoglycosides
•  3rd generation
cephalosporins
•  Fluoroquinolones

Front 113

Why is suseptibility testing required for Klebsiella pneumoniae?

Back 113

some produce beta-lactamase

Front 114

What are the typical nosocomial infections?

Back 114

S. aureus with Predominantly gram-negative aerobes
Klebsiella pneumoniae;
Pseudomonas aeruginosa

Front 115

What is the second leading cause infection in burn patients?

Back 115

Pseudomonas aeruginosa

Front 116

What opportunisitc pathogen can be fatal to CF patietns?

Back 116

Pseudomonas aeruginosa

Front 117

What causes Necrotizing Pneumonia?

Back 117

Staphylococcus aureus G+

Front 118

What does Protein A in Staphylococcus aureus do?

Back 118

binds to Fc of IgG
interferes with phagocytosis and complement activation

Front 119

What is Clumping factor?

Back 119

Clumping factor A, or ClfA, is a virulence factor from Staphylococcus aureus (S. aureus) that binds to fibrinogen; causes plasma to clump
different than coagulase