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FMS 3 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are the characteristics of the gram positive bacterial cell wall?

A

-thick peptidoglycan layer with teichoic acid (cross linked with peptidoglycan)

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2
Q

What are the characteristics of the gram negative bacterial cell wall?

A
  • thinnner peptidoglycan layer

- outer membrane with lipopolysaccharide (LPS)

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3
Q

What is the structure of LPS and what does it do for the bacteria?

A
  • one Lipid A and one polysaccharide core, many repeats of O antigen
  • Lipid A: endotoxin activity of LPS, essential for bacterial viability
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4
Q

How do antibiotics inhibit synthesis of peptidoglycan?

A

action of beta lactam and vancomycin antibiotics work on the terminal d-alanine-dalanine dipeptde in precursor of peptidoglycan

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5
Q

What enzymes are the targets of beta lactam antibiotics?

A

transpeptidase carboxypeptidases, that catalyze cross linking reaction (called transpeptidation).

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6
Q

What are examples of spore forming species?

A

Bacillus and Clostridium. They can form spores under harsh conditions, vegetative state.

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7
Q

What is the structure of a spore?

A

dehydrated, multi shelled structure. contains copy of chromosome.

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8
Q

What are the 3 genera of medically important gram positive cocci?

A

Staphylococci, Streptococci, Enterococci

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9
Q

What laboratory tests can distinguish between GPC?

A
  • Catalase Test: Staphylococcus is positive, streptococcus and enterococcus is catalase negative
  • gram stain: staphylococci are clusters, streptococci are chains
  • Culture: S. aureus has golden pigment on sheep agar
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10
Q

What are the 3 most common disease causing Staphylococci?

A

Staph aureus, Staphylococci epidermidis, S. saprophyticus

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11
Q

What are the 2 most common disease causing streptococci?

A

S. pyogenes, S. pneumoniae

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12
Q

How do you confirm the ID of S. aureus?

A

-Coagulase test, only S. aureus is +

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13
Q

What are the immune modulators of S. aureus (enzymes that disable our immune defenses)?

A
  • protein A: binds Fc of IgG, protect from opsonization and phagocytosis
  • Coagulase: can build fibrin capsule around bacteria, protect from phagocytosis
  • Hemolysins: destroy RBCs, neutrophils, macrophages, platelets
  • Leukocidins: destroy leukocytes
  • catalase: breaks down H2O2 from neutrophils
  • penicillinase: destroys beta lactam ring of penicillins
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14
Q

What proteins do S. aureus have that allow penetration through tissues?

A
  • hyaluronidase: breaks down hyaluronic acid in connective tissue
  • fibrinolysin (staphylokinase): lyses fibrin clots
  • lipases:degradation of fat helps colonization of fat containing areas of body
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15
Q

What toxins do S. aureus possess?

A
  • Exfoliative toxins
  • enterotoxins
  • toxic shock syndrome toxins
  • cytotoxins
  • panton valentine leukocidin
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16
Q

What are diseases caused by Staph aureus infection?

A 
SKIN
-impetigo: small pus filled vesicles
-cellulitis: infection of deep skin
-abscess
-wound infection
BONE/JOINT
-septic arthritis: infection inside joint w/ pus
-osteomyelitis: infection of bone with destruction of bony tissue
LUNG
-pneumonia
Also, bacteremia and endocarditis
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17
Q

What are the diseases caused by Staph aureus toxins?

A
  • staphlococcal scalded skin syndrome - exfoliative toxin
  • food poisoning from enterotoxins
  • toxic shock syndrome from TSST-1
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18
Q

How is S. aureus infections treated?

A
  • resistant to penicillins
  • MRSA-multi drug resistance version of S. aureus
  • vancomycin can be helpful
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19
Q

Where is Staphylococcus epidermidis normally found?

A
  • skin and mucous membranes, can be contaminants of cultures due to poor technique
  • normally harmless
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20
Q

How does Staphylococcus epidermidis cause disease?

A

infection from indwelling medical devices like foley urine catheters or IV lines

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21
Q

What disease does Staph saprophyticus cause?

A

UTIs in young sexually active women

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22
Q

How are streptococci species classified?

A
  1. Hemolytic ability (alpha-partial, beta-complete, gamma-none)
  2. Lancefield grouping-based on cell wall antigens
  3. other biochemical properties
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23
Q

How can streptococcus progenies be identifies?

A
  1. beta hemolysis
  2. Group A strep (lancefield)
  3. bacitracin sensitive and PYR test positive
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24
Q

What are the structural components of Streptococcus pyogenes?

A
  • hyaluronic acid capsule (antiphagocytic)

- Cell wall: lipotechoic acid (adhesion), M protein (virulence), F protein

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25
Q

What are the toxins of Streptococcus pyogenes?

A
  • pyogenic exotoxins
  • streptolysin S
  • streptolysis O-blood test to detect
  • streptokinase- used as drug to lyse blood clots
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26
Q

What are the clinical syndromes associated with Strep pyogenes infections?

A
  • Skin: erysipelas (superficial), cellulitis, necrotizing fasciitis
  • strept pharyngitis (strep throat)
  • pneumonia
  • puerperal fever
  • bacteremia
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27
Q

What are the clinical syndromes caused by Strep pyogenes toxins?

A
  • Scarlet fever (strawberry tongue, sandpaper rash)
  • Stretococcal toxic shock syndrome
  • acute rheumatic fever (assoc. with preceding pharyngitis)
  • acute glomerulonephritis (follow pharyngitis or skin infection)
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28
Q

How do you tell the difference between Staph epidermidis and staph saprophyticus?

A

-S. saprophyticus is resistant to Novobiocin, S. epidermidis is sensitive.

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29
Q

What clinical syndromes are caused by viridian streptococci? What antibiotic are they resistant to?

A

GI malignancy. Resistant to optochin antibiotic.

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30
Q

What can be used to identify Strep pneumoniae?

A
  • Quellung reaction-anticapsular antibiotics added, capsule swells, can be visualized microscopically as opaque swollen ring.
  • Optochin sensitive (will be inhibited by Optochin)
  • also is diplococci, lancet shape
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31
Q

What are the clinical diseases associated with Strep pneumoniae?

A
  • pneumonia
  • otitis media (middle ear infection)
  • sinusitis
  • meningitis
  • bacteremia
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32
Q

How can enterococci be differentiated from streptococci in laboratory?

A

-enterococci can grow in 6.5% NaCl, 40% bile salts, and hydrolyze esculin

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33
Q

How can you differentiated between Neisseria Gonorrhoeae and Meningitidis?

A

Glucose tests
Gonorrhoeae oxidizes glucose
Meningitidis oxidzes glucose+maltose

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34
Q

This is a weakly gram negative, rod shaped, intracellular bacteria. Causes urethritis, epididymitis, prostratitis in men. Also causes trachoma. What is the organism that causes this disease and how would it be diagnosed?

A

Chlamydia trachomatis. Diagnosed with molecular amplification tests.

35
Q

This is the leading cause of neonatal conjunctivitis.

A

Chlamydia trachomatis.

36
Q

This causes a fever, headache, rash on trunk that spreads outwards but spares palms/soles. Exposure to louse. What is the organism and how is it diagnosed?

A

Rickettsia prowazeckii. micfo immuno fluorescence. Western blot and PCR to follow.

37
Q

Presents with fever, severe headache. Rash spreads from extremities to trunk and palms/soles. Patient might have been spending time hiking on East coast.

A

Rocky mountain spotted fever. Diagnosed by MIF, followed by Western blotting or PCR. Transmitted through tick bite.

38
Q

A slaughterhouse worker presents with mild influenza like fever with muscle pain. May lead to liver or renal failure. Does not gram stain well. obligate aerobe, corkscrew shaped with terminal hooks.

A

Leptospira interrogans

39
Q

A patient presents with erythema chromium megrims (skin lesion) with fever, headache, malaise, arthritis lyphandenopathy, myalgia. Develops Bell’s palsy and cardiac dysfunction weeks later. What organism and how diagnosed?

A

Borrelia burgdorferi. ECM skin lesion and indirect immunoflorescence assay for IgM or IgG antibodies followed by Western blot. Spread by ticks. Is a spirochete.

40
Q

What are the 5 characteristics of viruses?

A
  1. nucleoproteinic entities
  2. obligatory intracellular parasites
  3. potentially pathogenic
  4. either RNA or DNA, never both
  5. replicate directly from genetic material
41
Q

What are the characteristics of viral nucleic acids?

A
  1. either DNA or RNA
  2. single or double stranded
  3. one or several pieces
  4. represent plus or minus strand (+ strand have same polarity as mRNAs)
42
Q

Describe the structure and subunits of an icosahedron

A

shape: 20 triangular faces, 12 corners, 60 subunits (subunits are at the corner or each triangular face). Large numbers of subunits can be accommodated by dividing each triangular face into sub triangles an placing protein subunit at each corner of subunit=icosadeltahedrons.

43
Q

What are arboviruses?

A

Viruses that are transmitted by arthropods. E.g. flaviviruses and alpha viruses.

44
Q

List the steps in the life cycle of a positive stranded RNA virus

A
  1. adsorption
  2. penetration
  3. 5 Uncoating
  4. eclipse
  5. maturation
  6. release
45
Q

What is eclipse in the viral life cycle?

A

Disappearance of viral infectivity early in infection stage because viral genome has been liberated inside the cell, about to start viral replication.Viral info present in free nucleic acid form and is sensitive to enzyme degradation.

46
Q

What is the structure of the influenza virus?

A

helical capsize with envelop. A negative stranded RNA virus. Pleomorphic-can have multiple shapes and sizes. Contains:

  1. hemagglutinin (HA)-mediates adsorption and penetration
  2. neuraminidase (NA)-helps release virus from cell
  3. matrix protein M - structural function
  4. nucleocapside protein (NP)-surrounds RNA
  5. 8 different RNA segments
  6. RNA polymerase
47
Q

What is the life cycle of influenza virus?

A
  1. adsorption - involves HA proteins
  2. penetration -fusion of viral envelope with membrane of endocytotic vesicle
  3. uncoating
  4. eclipse
  5. synthesis - makes 8 monocistronic mRNAs
    6 maturation and release - each virus particle released individually continuously
48
Q

How is the replication pathway of negative stranded RNA virus different from positive stranded RNA virus?

A

In negative stranded RNA viruses:
-mRNA has to be transcribed from negative stranded RNA to make viral proteins
-positive strands are made by viral polymerase to be used as templates for progeny negative strand synthesis
-more copies of negatives are made than of positives
In positive stranded:
-a negative strand copy of parental RNA is made, and serves as template for more positive strand synthesis
-positive strands are made in excess over negative stranded RNA

49
Q

Describe genetic reassortment of influenza virus.

A

Influenza has 8 independently replicating RNA segments. If 2+ influenza viruses infect same cell, their segments will be mixed. Occurs with high frequency.

50
Q

Describe the relationship between antigenic shift of influenza virus and flu pandemics

A

Appearance of new influenza viral subtypes, results from new genes acquired by genetic exchange with other influenza viruses. New influenza A subtypes appears every 10 years, little prior immunity from past infections, results in high rates of morbidity and significant mortality worldwide.

51
Q

Describe antigenic drift of influenza virus

A

Antigenic drift= gradual antigenic change of surface glycoproteins leading to escape from neutralization by antibodies. Due to point mutations in head region of HA molecule.

52
Q

Describe the structure of adenovirus.

A

Naked, icosahedral, medium.
linear dsDNA
capsid: Penton base, Hexon, Fiber
core: DNA genome (covalently linked to Terminal Protein (TP) and DNA-associated proteins

53
Q

How does adsorption/attachment to host cell occur in adenoviruses?

A

Two stages

  1. fiber protein interacts with cellular receptors, e.g. MHC class I and coxsackievirus-adenovirus receptor
  2. penton base binds to integrin family–>receptor mediated endocytosis
54
Q

Describe gene expression in adenoviruses?

A

3 temporally distinct phases

  1. immediate-early genes: E1A proteins - regulatory factors required for subsequent phases of gene expression
  2. Early genes: required for viral RNA replication - pTP (precursor terminal protein) and DBP (ssDNA binding protein)
  3. late genes: structural proteins
55
Q

What diseases are caused by adenoviruses?

A

Adenoviruses are a frequent cause of acute upper respiratory tract (URT) infections. Pharyngitis in infants. Severe in immunocompromised.
Less common are a number of other types of infections (acute hemorrhagic cystitis, gastroenteritis, hepatic disorders, pneumonia).

56
Q

Understand the mechanism for DNA replication in adenovirus.

A

Takes place in nucleus

  1. Viral genome is coated with the virally encoded DNA binding proteins (DBP) –not shown in figure-.
  2. pTP (precursor Terminal Protein) and pol (DNA Polymerase) are recruited to the initiation complex.
  3. A covalent link is formed between deoxycytidine triphosphate (dCTP) and a serine residue in pTP (dCMP-pTP). This act as the primer for the synthesis of the nascent DNA strand.

Second strand of DNA forms pan handle while not being replicated

57
Q

Describe the structure of parvovirus

A

small, non enveloped, icosahedral
linear ssDNA
NS: non structural proteins required for DNA rep
CAP: structural proteins for viral capsid

58
Q

What are the diseases caused by parvovirus?

A
  1. fifth disease: “slapped cheek” rash appearance
  2. polyarthropathy syndrome- sudent onset of symmetric polyarthralgia or poly arthritis
  3. transient aplastic crisis- severe anemia, life threatening if host already has low RBC
  4. spontaneous abortion, intrauterine fetal death

First phase is viremia and flue like symptoms, second phase is immune related. Biphastic

59
Q

What are important points to remember about parvovirus life cycle?

A

Receptor molecule is erythrocyte P antigen. Occurs in nucleus. Ends of genomes have palindrome sequences which form hairpins-The double-stranded DNA version of the viral genome is required for transcription and replication.

60
Q

Describe the structure of herpes virus.

A

large, enveloped, icosahedral
dsDNA
-tegument- protein filled region between envelop and capsid
-core- toroidal shape with large DNA genome

61
Q

Describe gene expression in the herpes virus lifecycle.

A

3 temporally distinct phases, same as adenovirus
1. alpha - immediate early
2. beta - early
3 . gamma - late

62
Q

What are the diseases caused by Herpes virus?

A
  1. HSV 1+2: oral and genital herpes
  2. varicella zoster virus VZV
  3. Epstein Barr EBV - mononucleosis
  4. cytomegalovirus CMV - usually symptomatic or mild except in AIDS, Immunosuppressed, baby
  5. HHV6 -fever and respiratory tract
  6. HHV 7 - similar to HHV6
  7. HHV8 - kaposi’s sarcoma
63
Q

What is latency?

A

virus can enter silent phase of infection that allows virus to escape immune response. Reservoirs can be neuronal ganglia, b lymphocytes, t cells, macrophages

64
Q

List the commensal anaerobic bacteria by anatomical site.

A

skin: propionibacterium (+B)
vagina: lactobacillus (+B)
oropharynx: prevotella (-B) and Veillonella (-C)
GI Tract: Bacteroides (-B)

65
Q

A patient with a penetrating wound in the past week presents with cellulitis, suppurative myositis, and myonecrosis. When you press on her skin, you feel a crackling sensation, like gas underneath. What is the bacteria, and how do you diagnose it? What is another infection that this bacteria causes?

A

Clostridium perfringens. Gram positive anaerobic bacilli, spore forming. culture and gram stain.
Also causes gastroenteritis.

66
Q

You see a floppy baby with constipation and flaccid paralysis. What caused this and how would you diagnose it?

A

Clostridium botulinum. Diagnosed with presence of toxin in food or patient serum/feces. Anaerobic gram + spore forming rod.

67
Q

What is the virulence factor(s) behind Clostridium botulinum infections?

A

Caused by botulinum toxin (BoNT) with an A domain (inhibits exocytosis of neurotransmitter vesicles) and B domain (inhibits AcH release at skeletal neuromuscular junctions)–>flaccid paralysis.

68
Q

A patient presents with lockjaw, drooling, sweating, irritability, back spasms. He develops cardiac arrhythmias and profound sweating later. What causes this and how would you diagnose? Explain the mechanism behind the toxin.

A

Clostridium tetani. Diagnosed by determining toxin in food or patient serum/feces.
-caused by tetanus toxin (TeNT) with
A domain: inhibits vesicular exocytosis
B domain: inhibits release of inhibitory GABA or Gly in skeletal muscle–>muscular rigidity.

69
Q

A patient that has been undergoing antibiotic therapy develops severe chronic diarrhea and colitis. A colonoscopy finds a pseudomembrane colitis. What organism causes this? How is this diagnosed?

A

Clostridium dificile. Caused by ToxA (enterotoxin) and ToxB(cytotoxin–>cardiac edema). Diagnosed with immunodetection of Tox A and Tox B in feces. This organism is commensal in GI tract.

70
Q

I have severe, voluminous watery diarrhea that looks like rice water, but no abdominal pain. I am colorless on a MacConkey plate and aerobic, oxidase positive. What am I?

A

Vibrio cholerae

71
Q

List the gram negative bacilli that are commensal and their anatomical sites.

A

Oropharynx: Haemophilus, Prevotella
GI: Bacteroides

72
Q

I ate rice out for half a day and eat it and now I have nausea and vomiting and stomach discomfort. Later symptoms may be diarrhea. What can cause this food poisoning? How is it diagnosed?

A

B cereus infection. Spores can survive harse conditions and germinate in moisture/nutrients.
Diagnosis: motile, aerobic, spore forming, gram positive rod. serology tests for enterotoxin, presence of serotype in feces/vomit and food samples. Note: diagnosis usually note performed.

73
Q

A pregnant woman ate some feta cheese. After she gave birth (vaginally), her neonate presented with meningitis (after 5 days post partum). What can cause this and how is it diagnosed? What are the virulence factors?

A

Listeria monocytogenes. Diagnosis: blood culture using cold temperatures, beta hemolytic, Cat +. Virulence factors are: hemolysis that is heat labile and antigenic, and exotoxin LLO (lysteriolysin O)

74
Q

How is the poliovirus capsid assembled?

A
  • Precursor VP0 cleaved into VP1,2,3,4 at end of maturation
  • 5S protomer assembled: has VP0, VP3, VP1
  • 14S pentemer: 5 protomers
  • 73S procapsid: made of 12 pentemers
  • 73 S procapsid+progeny RNA=provirion
  • VP0 cleaved to VP2 and VP4—> 155 S infectious form
75
Q

What are the most common causes of neonatal meningitis for <1 month?

A

E. coli and Group B strep, then Listeria monocytogenes

76
Q

What are two types of infections that can be caused by C. perfringens?

A

Enteric infection: from food poisoning associated with raw meats
soft tissue infection: penetrating wounds

77
Q

What is the most common cause of meningitis from 6months to 6 years old children?

A

Strep Pneumoniae. Listeria is most common among 0-6mo and the elderly.

78
Q

What are the commensal bacteria on skin?

A

Propionibacterium
corynebacterium
Staphylococcus

79
Q

What are the commensal bacteria in the oropharyx?

A 
Corynebacterium
H. Influenza
Streptococcus
Prevotella
Veilonella
80
Q

What and how do Diphtheria toxins work?

A

Binary toxin with ADP ribosylating activity that inhibits protein synthesis by inactivating EF2

81
Q

Which bacteria are alpha hemolytic?

A

S. Pneumoniae and viridians

82
Q

Which are bacteria are beta hemolytic?

A

Strep pyogenes and Group B Strep

83
Q

Which bacteria are gamma hemolytic?

A

Enterococcus

FMS 3 (8 decks)

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