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Microbiology Exam 2 > Lecture 10-19 > Flashcards

Lecture 10-19 Flashcards

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1
Q

What is innate immunity?

A

It is present before any exposure to pathogens and is effective from the time of birth.

It involves nonspecific responses to pathogens

Consists of external barriers plus internal cellular and chemical defenses

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2
Q

What is acquired immunity?

A

Adaptive immunity, develops after exposure to agents such as microbes, toxins, or other foreign substances.

Specific response to pathogens

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3
Q

What are the chemical mediators in innate immunity?

A

Defensins, lysozymes, complement

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4
Q

Cells and tissues of the innate immune system are

A

Granulocytes, macrophages, dendritic and NK cells.

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5
Q

Acquired or specific immune systems involve what factors?

A

Cells, tissues
Memory
Discrimination, self/no self

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6
Q

Where do T cells mature?

A

Thymus

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7
Q

Where do B cells mature?

A

Bone marrow

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8
Q

What is the ultimate result of antigen presence?

A

B cell activation which leads to production of antibodies

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9
Q

What are some physical barriers involved in the innate immune system?

A 
Epidermis
Mucous membranes
Mucous
Lacrimal apparatus
Saliva
Hairs
Cilia
Epiglottis
Urine
Vaginal secretions
Peristalsis, defecation, and vomiting
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10
Q

What are some chemical factors involved in innate immunity defense?

A 
Sebum
Lysozyme
Saliva
Gastric juice
Urine
Vaginal secretions
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11
Q

Why is skin an inhospitable environment for microbes?

A

Salty, acidic, and dry

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12
Q

Functions of lysozyme as an antimicrobial secretion

A

Hydrolyzes bond connecting sugars in peptidoglycan

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13
Q

Function of lactoferrin as an an antimicrobial secretion in mucous membranes

A

Secreted by activated macrophages and PMNs and sequesters iron from plasma

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14
Q

Function of lactoperoxidase as an antimicrobial secretion in mucous membranes

A

Produces superoxide radicals

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15
Q

What are two areas of the body that should be completely FREE of microbes?

A

The lower respiratory tract and the bladder

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16
Q

What are the innate functions of the respiratory immune system?

A

Mucociliary blanket, alveolar macrophages, and ciliary escalator

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17
Q

What are the innate functions of the gastrointestinal immune system?

A

Gastric acid in the stomach

Pancreatic enzymes, bile, GALT, normal microbiota, and peristalsis in the intestines

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18
Q

What makes the genitourinary tract an unfavorable environment for foreign microbes?

A

Acidity

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19
Q

What are some aspects of the innate immune system in the eye?

A

Lysozyme, lactoferrin, and secretory IgA in tears

Lacrimal apparatus for flushing, eyelashes as barrier

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20
Q

Bacteriocins

A

Antimicrobial peptides that are produced by normal flora; toxic proteins that are lethal to other strains of the same species in closely related bacteria

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21
Q

Three major activities of the complement system

A

Defend against bacterial infections

Bridging innate and adaptive immunity

Disposing of wastes

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22
Q

Opsonization

A

Microbes are coated by serum components (opsonins) in preparation for recognition/ingestion by phagocytic cells; binds to microbial cells, coating them for phagocyte recognition

Antibody and complement C3B together enhance phagocytosis

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23
Q

As a pathogen, which complement would you inactivate first in order to inactivate the complement system?

A

C3, followed by C5

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24
Q

What activates the classical pathway of complement system?

A

Antigen: antibody complexes (pathogen surfaces)

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25
Q

What activates the Lectin pathway of complement system?

A

Mannose-binding lectin binds mannose on pathogen surface

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26
Q

What activates the alternative pathway of complement system?

A

Pathogen surfaces - activation of C3 forms MAC

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27
Q

Name the three potential pathways for activation of the host complement system

A

Classical pathway, MB-Lectin pathway, and alternative pathway

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28
Q

How do bacteria evade the host complement system?

A

Capsules prevent C activation

Surface lipid-carbs prevent MAC formation

Enzymatic digestion of C5a

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29
Q

Soluble proteins or glycoproteins that are released by one cell population that act as intercellular mediators or signaling molecules. These must bind to specific receptors on target cells

A

Cytokines

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30
Q

Autocrine function of cytokines

A

Affect same cell responsible for their production

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31
Q

Paracrine function of cytokines

A

Affect nearby cells

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32
Q

Endocrine functions of cytokines

A

Spread by circulatory system to distant target cells

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33
Q

Chemokines

A

Specialized cytokines that stimulate chemotaxis and chemokinesis, thus directing cell movement

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34
Q

Monokines

A

Cytokines released from mononuclear phagocytes

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35
Q

Lymphokines

A

Cytokines released from T lymphocytes

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36
Q

Interleukins

A

Cytokines released from one leukocyte and act on another leukocyte

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37
Q

Colony Stimulating Factors (CSFs)

A

Type of cytokine that stimulates growth and differentiation of immature leukocytes in bone marrow

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38
Q

Which cytokine increases immunity to viral infection and upregulates cytolytic function?

A

IFN-alpha

Innate resistance

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39
Q

Which type of cytokine enhances differentiation, enhances antibody synthesis, activates phagocytic function, and enhances antigen processing and presentation?

A

IFN-gamma

Adaptive immunity

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40
Q

Which type of cytokine upregulates coagulation response, stimulates production and release of acute-phase proteins, and activates phagocytic functions?

A

TNF

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41
Q

IFN-alpha and IFN-beta are interferons that do what?

A

Cause cells to produce antiviral proteins that inhibit VIRAL replication

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42
Q

IFN-gamma is an interferon that does what?

A

Causes neutrophils and macrophages to phagocytize BACTERIA

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43
Q

What innate immune defense kills infected target cells by releasing granules that contain perforin and granzymes? In other words, helps protect cells that have not been able to produce “self” tag?

A

Natural Killer (NK) cells

Phagocytes then kill the infected microbes

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44
Q

Neutrophils

A

Stain at neutral pH, lobed nuclei

Highly phagocytic

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45
Q

Basophils

A

Stain bluish-black or purple with basic dyes

Produce histamine

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46
Q

Eosinophils

A

Stain red with acidic dyes, may appear orange

Kills parasites using lytic factors and perforin

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47
Q

Monocytes

A

Phagocytosis

Later mature into dendritic cells or macrophages

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48
Q

Natural killer cells

A

Destroy target cells, large in size

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49
Q

T-cell function

A

Cell-mediated immunity (cell-mediated response)

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50
Q

B cell function

A

Produce antibodies (humoral response)

Have receptors for unique antigens

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51
Q

Platelet function

A

Blood clotting, small in size

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52
Q

Contains specialized cells including Langerhans cell and intraepidermal lymphocytes

A

Skin Associated Lymphoid Tissue (SALT)

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53
Q

Specialized immune barrier that have a “training ground” for immunity responses. Includes gut-associated lymphoid tissue, bronchial-associated lymphoid tissue, and urogenital system.

A

Mucosal-Associated Lymphoid Tissue (MALT)

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54
Q

Name the two mechanisms of phagocytosis

A

Opsonin-independent recognition
Opsonin-dependent recognition

Phagocytosis can be greatly increased by opsonization

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55
Q

Which phagocytosis mechanism involves non-specific pathogen component recognition, with a signaling mechanism involved. May recognize peptidoglycan, flagella, and other surface characteristics.

A

Opsonin independent mechanism

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56
Q

What are the four main forms of opsonin-independent mechanisms?

A
  1. Lectin-carbohydrate interactions
  2. Hydrophobic interactions
  3. Protein-protein interactions
  4. Detection of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRR)
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57
Q

What are PAMPs?

A

Pathogen-Associated Molecular Patterns

Unique to microbes, not present in host

Examples: LPS of gram-negative bacteria, peptidoglycan of gram-positive bacteria

Recognized by PRRs in phagocytic cells

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58
Q

What are Toll-Like receptors (TLRs)?

A

class of pattern recognition receptors that function exclusively as signaling receptors; recognize and bind unique PAMPs of viruses, bacteria, or fungi

The binding triggers signal which is then communicated to host cell nucleus, initiating host response

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59
Q

Autophagy

A

Highly conserved process that tags internal microbes for destruction using monoubiquitination

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60
Q

What might a PAMP (pathogen-associated molecular pattern) be in a virus?

A

Capsid proteins, viral RNA, etc.

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61
Q

During intracellular digestion, the phagosome fuses with lysosome to form ______ that will expose the bacteria to hydrolytic enzymes

A

Phagolysosome

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62
Q

How do Streptococcus pyogenes and Streptococcus pneumoniae evade phagocytosis?

A

Inhibition of adherence: M protein, capsules

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63
Q

How does Staphylococcus aureus evade phagocytosis?

A

Killing phagocytes: Leukocidins

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64
Q

How does Listeria monocytogenes evade phagocytosis?

A

Lysis of phagocytes via membrane attack complex (MAC)

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65
Q

How do Shigella and Rickettsia evade phagocytosis?

A

Escaping the phagosome

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66
Q

How do HIV and Mycobacterium tuberculosis evade phagocytosis?

A

Prevention of phagosome-lysosome fusion

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67
Q

Define inflammation

A

Innate, nonspecific response to tissue injury caused by pathogen or physical trauma; it is the immediate response of the body to injury or cell death

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68
Q

What are the cardinal signs of inflammation?

A 
Redness
Warmth
Pain
Swelling/edema
Altered function
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69
Q

What chemical mediators are involved with acute inflammatory responses and what are their functions?

A

Selectins: cell adhesion molecules on activated capillary endothelial cells

Integrins: adhesion receptors on neutrophils

Chemotaxins: chemotactic factors released by injured cells

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70
Q

Describe an acute inflammatory response

A

Damaged tissue releases inflammatory chemicals called chemokines (kalikrein) - recruit macrophages

Dilation and increased permeability of capillaries brings blood to the area, may result in swelling

Various processes occur: margination, diapedesis, and extravasion

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71
Q

What are advantages of fever?

A

T-cell production increases due to increase in IL-1

Increase transferrins (iron scavenging)

Speeds up repair process

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72
Q

What are some disadvantages of fever?

A

Tachycardia

Acidosis due to increased metabolic rate

Dehydration

Death above 44-46 celsius (112-114 F)

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73
Q

What is the result of histamine release by damaged cells?

A

Vasodilation, increased permeability of blood vessels

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74
Q

What is the result of kinins release by damaged cells?

A

Vasodilation, increased permeability of blood vessels

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75
Q

What is the result of prostaglandins release by damaged cells?

A

Intensify histamine and kinin effect (vasodilation and increased permeability of blood vessels)

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76
Q

What is the result of leukotrienes release by damaged cells?

A

Increased permeability of blood vessels, phagocytic attachment

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77
Q

What are the two types of adaptive immunity?

A

Humoral: antibody-mediated

Cell-mediated: based on action of T lymphocytes

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78
Q

Naturally acquired active immunity

A

Type of specific immunity a host develops after exposure to a foreign substance (consequence of prior infection)

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79
Q

Naturally acquired passive immunity

A

Transfer of antibodies, e.g., mother to fetus across placenta, or through breastfeeding

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80
Q

Artificially acquired active immunity

A

Intentional exposure to a foreign material (vaccination)

Goal is to stimulate antibody production

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81
Q

Artificially acquired passive immunity

A

Preformed antibodies or lymphocytes produced by one host are introduced into another host

Goal is to give antibodies directly

For example: immune globulin therapy

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82
Q

What is a hapten and when is it used?

A

Antigen combined with carrier molecules; used when the antigen is too small to illicit an immune response on its own, but when combined with a carrier molecule the body will recognize it

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83
Q

Where are MHC-I molecules found and what type of processing do they use?

A

MHC class I are found on almost all types of nucleated cells (so not RBCs because they don’t have nucleus)

Utilize endogenous antigen processing

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84
Q

Where are MHC-II molecules found and what type of processing do they use?

A

MHC class II molecules are found only on Antigen Presenting Cells (APCs) which are macrophages, dendritic cells, and B-cells

Utilize exogenous antigen processing

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85
Q

MHC class I molecules utilize endogenous antigen processing, meaning what?

A

Class I bind to antigen peptides that originate in the cytoplasm. They then present the antigen to CD8+ T cells (cytotoxic T lymphocytes)

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86
Q

MHC class II molecules utilize exogenous antigen processing, meaning what?

A

Class II binds to antigen fragments that come from outside the cell and present them to CD4+ T cells (Helper T cells)

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87
Q

Identify the cells that can function as APCs (antigen presenting cells)

A

Macrophages
Dendritic cells
B cells

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88
Q

What type granular leukocytes destroys cells that don’t express MHC I?

A

Natural killer cells

These also kill virus infected and tumor cells, as well as attack parasites

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89
Q

In terms of Cluster of Differentiation Molecules (CDs), what is the MHC class II coreceptor on T cells, monocytes, and macrophages?

A

CD4

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90
Q

In terms of Cluster of Differentiation Molecules (CDs), what is the MHC class I coreceptor on cytotoxic T cells?

A

CD8

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91
Q

Describe T cell receptor structure and function

A

TCRs are found in plasma membrane surface and contain an antigen binding site

They recognize and bind fragments of antigens presented by APCs

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92
Q

Describe B cell receptors structure and function

A

BCRs are immunoglobulin receptors for specific antigen that will activate that particular B cell

Consist of two light chains and two heavy chains connected with disulfide bonds

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93
Q

Explain molecular events resulting in Helper T cell activation

A
  1. APC encounters and ingests microorganism. Antigen is enzymatically processed into short peptides, which combine with MHC class II molecules and are displayed on the surface of APC
  2. A receptor on helper T cell binds to the MHC-antigen complex. If this includes a Toll-like receptor (TLR), APC releases costimulatory molecules. These two signals activate helper T cell which produces cytokines
  3. Cytokines cause helper T cell to proliferate and develop its effector functions
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94
Q

Explain molecular events resulting in cytotoxic T cell activation

A
  1. Response is triggered by abnormal cell (cancer, virus infected, etc.)
  2. Abnormal antigen is presented on cell surface in association with MHC-I molecules. CD8+ T cells with receptors for the antigen are transformed into cytotoxic T lymphocytes
  3. CTL induces destruction of virus infected cell by apoptosis
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95
Q

Explain molecular events resulting in B cell activation through the T dependent pathway

A

T dependent requires 2 signals before B cell differentiates into plasma cell and memory cell:

Antigen-BCR specific interaction
Activated T helper 2 binds B cell presented antigen and secretes B cell growth factors

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96
Q

Explain molecular events resulting in B cell activation through T independent pathway

A

T independent involves polymeric antigens with large number of identical epitopes (i.e., LPS)

Less effective than T dependent pathway
Antibodies produced have low affinity for antigen
No memory cells are formed; overall weaker immune response

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97
Q

Antibodies are also known as immunoglobulin, which are made by activated B cells (plasma cells). What are the 5 immunoglobulin classes?

A 
IgG
IgM
IgA
IgD
IgE
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98
Q

Describe IgG in terms of its valence, abundance, where it is found, and function

A

Monomer - bivalent (2 binding sites)
80% of serum antibodies
Capable of complement fixation and crossing the placenta
Found in blood, lymph, and intestine
Enhances phagocytosis, neutralizes toxins and viruses, and protects fetus and newborn

**second antibody to appear in response to infection (M is first)

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99
Q

Describe IgM in terms of its valence, abundance, where it is found, and function

A 
Pentamer - (10 binding sites)
5-10% of serum antibodies
Capable of complement fixation
Found in blood, lymph, and on B cells
Agglutinates microbes, first antibody introduced in response to infection
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100
Q

Describe IgA in terms of its valence, abundance, where it is found, and function

A

Dimer (4 binding sites)
10-15% of serum antibodies
Found in secretions
Functions in mucosal protection

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101
Q

Describe IgD in terms of its valence, abundance, where it is found, and function

A

Monomer (2 binding sites)
0.2% of serum antibodies
Found in blood, lymph, and B cells
Functions in initiation of immune response on B cells

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102
Q

Describe IgE in terms of its abundance, where it is found, and function

A

0.002% of serum antibodies
Found on mast cells, on basophils (histamine), and in blood
Functions in allergic reactions; lysis of parasitic worms, opsonization

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103
Q

What is “class switching” in terms of antibody kinetics?

A

Change in antibody class secreted by plasma cells under the influence of T helper cells (i.e., may switch from IgM to IgG); event unfolds with time

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104
Q

During primary antibody response, there is a lag period of several days to weeks where there is no antibody detectable in blood. After B cell differentiation into plasma cells, the antibody is secreted. How is an antibody titer calculated?

A

The titer is the measure of serum antibody concentration

It is the reciprocal of highest dilution of antiserum that gives positive reaction

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105
Q

What are the characteristics of a secondary antibody response

A

B cells mount a heightened memory response:

Shorter lag phase
More rapid log phase
Longer persistence
Higher IgG titer and production of antibodies with higher affinity for the antigen

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106
Q

What is combinatorial joining?

A

The segments clustered separately on same chromosomes have exons that code for constant regions and exons that code for variable regions.

Exons for constant region are joined to one segment of the variable region via RAG-1 and RAG-2 recombination enzymes

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107
Q

What is the clonal selection theory?

A

States that each lymphocyte has membrane-bound immunoglobulin receptors specific for particular antigen and after the receptor is engaged, proliferation of the cell occurs such that a clone of antibody producing cells is produced

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108
Q

What is the clonal deletion theory?

A

The elimination of certain T cell populations in the thymus that have specificity for self-antigens (forbidden clones)

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109
Q

Name the 5 consequences of antibody binding of an antigen

A 
Agglutination
Opsonization
Complement activation
Neutralization
Antibody-dependent cell-mediated cytotoxicity
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110
Q

Define agglutination, one of the consequences of antibody binding of antigen

A

Agglutination reduces number of infectious units to be dealt with by sticking together

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111
Q

Define opsonization, one of the consequences of antibody binding of antigen

A

Coating antigen with antibody, enhancing phagocytosis

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112
Q

Define complement fixation, one of the consequences of antibody binding of antigen

A

Addition of complement causes inflammation and cell lysis

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113
Q

Define antibody-dependent cell-mediated immunity, one of the consequences of antibody binding of antigen

A

Antibodies attached to target cell cause destruction by macrophages, eosinophils, and NK cells

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114
Q

Define neutralization, one of the consequences of antibody binding of antigen

A

Blocks adhesion/attachment of bacteria, viruses, or toxins to mucosa

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115
Q

Describe the function of cytotoxic T lymphocyte (CTL)

A

Destroys target cells on contact; generated from T cytotoxic (Tc) cell

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116
Q

Describe the function of an activated macrophage

A

Enhanced phagocytic activity; attacks cancer cells

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117
Q

Describe the function of Natural Killer (NK) cell

A

Attacks and destroys target cells; participates in antibody-dependent cell-mediated cytotoxicity

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118
Q

Which of the cytokines promotes inflammation?

A

TNF-alpha

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119
Q

Which of the cytokines inhibits humoral immunity and activates TH1 cellular immunity?

A

Interleukin-12 (IL-12)

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120
Q

Which of the cytokines responds to viral infection and interferes with protein synthesis?

A

IFN-alpha and IFN-beta

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121
Q

Which of the cytokines stimulates macrophage activity?

A

IFN-gamma

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122
Q

How does Coxiella burnetti escape phagocytosis?

A

By surviving in the phagolysosome

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123
Q

What processes occur in the acute inflammatory response?

A

Margination
Diapedesis
Extravasion

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124
Q

What are the chemicals that are released by damaged cells?

A

Histamine
Kinins
Prostaglandins
Leukotrienes

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125
Q

What are the two types of acquired immunity?

A

Humoral response

Cell mediated response

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126
Q

Define the humoral response

A

Antibodies defend against infection in body fluids

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127
Q

Define cell-mediated response:

A

Cytotoxic lymphocytes defend against infection in body cells

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128
Q

Compare and contrast innate and acquired immunity

A

Innate: recognition of trait shared by broad ranges of pathogens using a small set of receptors. Rapid response
Acquired: recognition of traits specific to particular pathogens, using a vast array of receptors. Slower response

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129
Q 
All of the following are involved in keeping the lower respiratory tract free of microorganisms except:
A. Ciliary escalator
B. Epiglottis
C. Alveolar macrophages
D. Lacrimal apparatus
A

D. Lacrimal apparatus

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130
Q 
Which of the following pathways for complement activation is generally dependent upon the formation of antigen-antibody complexes?
A. The classical pathway
B. The alternative pathway
C. The lectin pathway
D. All of the above
A

A. The classical pathway

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131
Q 
Which leukocytes function to produce toxins against certain parasites?
A. Lymphocytes
B. Basophils
C. Eosinophils
D. Neutrophils
A

C. Eosinophils

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132
Q 
Which host defense is more effective against gram positive bacteria than gram negative bacteria?
A. Mucus
B. Sebum
C. Gastric juice
D. Lysozyme
A

D. Lysozyme

Because of thicker layer of peptidoglycan, it will have a greater impact – gram negative are protected by outer membrane

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133
Q

Natural killer cells specifically kill which of the following?
A. Gram positive
B. Gram negative
C. Fungi protozoa
D. Tumor cells and cells infected by microorganisms

A

D. Tumor cells and cells infected by microorganisms

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134
Q 
Each of the following is an effect of complement activation, except:
A. Opsonization
B. Increased phagocytic activity
C. Interference with viral replication
D. Increased blood vessel permeability
A

C. Interference with viral replication

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135
Q 
Eosinophils defend against protist and helminth parasites by:
A. Phagocytosis
B. Complement activation
C. Antibody production
D. Releasing perforin and lytic enzymes
A

D. Releasing perforin and lytic enzymes

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136
Q

Which of the following is INCORRECTLY matched?
A. PAMP - peptidoglycan
B. TLR - stimulation of the inflammatory response
C. Histamine - vasodilation
D. None of the above

A

D. None of the above

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137
Q

Class II major histocompatibility complex molecules are found on all of the following except:
A. B cells
B. T cells
C. Dendritic cells
D. None of the above, all have MHC class II molecules

A

B. T cells

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138
Q

What is the difference between normal microbiota and transient microbiota?

A

Normal microbiota permanently colonize the host

Transient microbiota may only be present for days, weeks, or months

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139
Q

Define the symbiotic relationship: Commensalism and give an example

A

One organism benefits while the other is unaffected/unharmed

Example: Staph Aureus in your nose

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140
Q

Define the symbiotic relationship: Mutualism and give and example

A

Both organisms benefit

Example: E. Coli in the gut benefit from rich nutrients, while they produce vitamins B & K for host benefit

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141
Q

Define the symbiotic relationship: Parasitism and give an example

A

One organism benefits at the expense of the other (host is harmed)

Example: H1N1

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142
Q

Define microbial antagonism

A

Competition between microbes

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143
Q

What are 3 ways that normal microbiota protect the host?

A

Occupying niches that pathogens might occupy

Producing acids

Producing bacteriocins

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144
Q

What are opportunistic pathogens?

A

Members of normal microbiota that produce disease under certain circumstances, such as when they are misplaced to an area they are not normally found

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145
Q

Where might you find the following normal microbiota:
Staphylococci (S. epidermidis)
Micrococci (M. luteus)
Diphtheroids (aerobic Corynebacterium xerosis and anaerobic Propionibacterium acnes)
Acinetobacter
Malassezia furfur

A

Skin

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146
Q

What is the predominant bacterium found on the conjunctiva of the eye?

A

Staphylococcus epidermidis

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147
Q

What normal flora might you find in the external ear?

A

Similar to skin flora as well as fungi

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148
Q

Where might you find the following normal microbiota:

S. mutans
Lactobacillus

A

Mouth

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149
Q

How do oral bacteria remain in place and what purpose do they serve as normal microbiota?

A

Oral bacteria such as S. mutans and Lactobacillus are very sticky, so they adhere to gums and teeth

They suppress pathogens by competitive inhibition in the upper respiratory system

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150
Q

What are the predominant normal microbiota in the nostrils?

A

Staphylococcus aureus and S. epidermidis

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151
Q

Where might you find the following gram positive normal microbiota:

Staphylococci (S. epidermidis)
Micrococci (M. luteus)
Diphtheroids
Streptococci (both alpha and beta-hemolytic)

A

Pharynx and trachea

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152
Q

Where might you find the following potentially pathogenic microbiota in low numbers:

Streptococcus pneumoniae
Neisseria meningitidis
Haemophilus influenzae
Mycoplasmas

A

Nasopharynx

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153
Q

What areas of the body are normally free of microbiota?

A

Lower respiratory tract, kidneys, ureter, and bladder

154
Q

Where would you find the largest and most diverse microbial population in the body, and what type of microbes live there?

A

Large intestine (colon)

Most of the microbes present are anaerobes

155
Q

Where might you find the following microbiota:

E. Coli
Bacteroids
Fusobacterium
Lactobacillus
Enterococcus
Bifidobacterium
Enterobacter
Citrobacter
Proteus
Klebsiella
Candida (fungus)
A

Large intestine

156
Q

What normal microbiota dominate the female genital tract, and what do they produce in order to keep anaerobic bacteria at bay?

A

Acid-tolerant lactobacilli, which produce H2O2

157
Q

What type of bacteria (gram negative or gram positive) primarily colonize the gut?

A

Gram negative

158
Q

What type of bacteria (gram negative or gram positive) typically colonize the respiratory tract, eyes, and ears?

A

Gram positive

159
Q

Describe the function of type 1 T helper Cell (TH1)

A

Activates cells related to cell-mediated immunity: macrophages, Tc cells, and natural killer cells

160
Q

Describe the function of type 2 T helper Cell (TH2)

A

Stimulates production of eosinophils, IgM, and IgE

161
Q

Pathogenicity

A

Ability to cause disease

162
Q

Primary pathogen

A

Causes disease by direct interaction with healthy host

163
Q

Opportunistic pathogen

A

May be part of normal flora and causes disease when it has gained access to other tissue sites or host is immunocompramised

164
Q

What is a zoonose and give examples

A

Infections passed from animal to human

SARS (bats), tuberculosis (horses, cattle), typhus fever (rats)

165
Q

Natural environmental location in which the pathogen normally resides (can be animate or inanimate)

A

Reservoir

166
Q

Organisms that spread disease from one host to another, for example: arthropods, mosquitos, and other biting insects

A

Vectors

167
Q

What is the difference between signs and symptoms?

A

Signs are measurable/objective changes in body like blood pressure, pulse, temperature, etc.

Symptoms are subjective changes experienced by patient like nausea, fatigue, body aches, etc.

168
Q

Period after pathogen entry, before signs and symptoms

A

Incubation period

169
Q

Onset of signs and symptoms but not clear enough for diagnosis

A

Prodromal stage

170
Q

Period of time where disease is most severe, ongoing signs and symptoms

A

Period of illness

171
Q

Period of time when signs and symptoms of disease begin to disappear

A

Convalescence

172
Q

Virulence factors

A

Allow a pathogen to outcompete host defense and resist their defenses

173
Q

Virulence

A

Degree or intensity of pathogenicity; determined in part by the pathogen’s ability to survive outside the host

174
Q

Major virulence factors on large segments on chromosomal or plasmid DNA

A

Pathogenicity islands

175
Q

What are common sequence characteristics of pathogenicity islands?

A

Insertion like sequences for mobility

G+C content different from bacterial genome

Several open reading frames

Can be spread through horizontal gene transfer

176
Q

What is an example of a parenteral route portal of entry?

A

A break in the barrier system, such as a contaminated needle

177
Q

If the portal of entry is the skin, what is the likely portal of exit?

A

The skin!

178
Q

What are adhesins?

A

Special molecules that mediate adherance; they act as ligands which bind to receptors on host cells

Examples:
Glycocalyx
Fimbriae/pili
M protein

179
Q

Streptococcus pyogenes causes a sore throat, what is its adhesion mechanism?

A

Protein F which binds to a protein residue on the host’s upper respiratory tract cells

180
Q

Penetration of an infectious agent can be active or passive, which type is the following?

Attack of the extracellular matrix and basement membranes of integuments and intestinal linings

Degrade carbohydrate-protein complexes between cells

Disrupt host cell surface

A

Active

181
Q

Penetration of an infectious agent can be active or passive, which type is the following?

Spread through skin lesions, insect bites, or other wounds to deeper tissues involving the production of specific products and/or enzymes that promote spreading

A

Passive

182
Q

Describe exotoxins in terms of their source, metabolic product, chemical make-up, ability to cause fever, ability to be neutralized by antitoxin, and magnitude of LD50

A

Source: mostly gram-positive
Metabolic product: by-products of growing cell
Chemistry: protein (soluble, heat-labile)
Fever? NO
Neutralized by antitoxin? YES
LD50: small (among the most lethal substances known)

183
Q

Describe endotoxins in terms of their source, metabolic product, chemical make-up, ability to cause fever, ability to be neutralized by antitoxin, and magnitude of LD50

A 
Source: gram-negative
Metabolic product: present in LPS of outer membrane 
Chemistry: lipid
Fever? YES
Neutralized by antitoxin? NO
LD50: relatively large
184
Q

Describe AB exotoxins

A

Composed of 2 subunits:

A subunit is responsible for toxic effect (active subunit)

B subunit is responsible for binding to specific target cell

185
Q

What type of exotoxin stimulates ~30% of T cells of the immune system, causing overexpression of T cells and release of cytokines?

A

Superantigens

Result in failure of multiple host organs, allowing time for microbe to disseminate

186
Q

What are the effects of biofilm development?

A
  • may cause chronic infection
  • increased virulence
  • resistance to antibiotics or disinfectants
  • “frustrates” phagocytes
187
Q

What does the cell wall component: M protein do in terms of resisting host defenses?

A

Resists phagocytosis

188
Q

What does the cell wall component: Opa protein do in terms of resisting host defenses?

A

Inhibits T helper cells

189
Q

What does the cell wall component: Mycolic acid do in terms of resisting host defenses?

A

Mycolic acid is a waxy lipid that resists cellular digestion

190
Q

How does the production of decoy proteins resist a host’s defenses?

A

Decoy proteins bind available neutralizing antibodies

191
Q

How to lengthened O-chains resists a host’s defenses?

A

Lengthened O-chains prevent host detection or lysis

192
Q

What component of a host cell may a pathogen use to eject itself from cell to cell?

A

Actin

193
Q

What do capsules do in order to resist host defenses?

A

Prevent phagocytosis

194
Q

What does the coagulase enzyme do in terms of resisting host defenses?

A

Coagulates fibrinogen which forms a wall so phagocytes can’t get there

195
Q

What do kinase enzymes do in terms of resisting host defenses?

A

Digestion of fibrin clots which is important for invasiveness (spreading to other tissues)

196
Q

What does the hyaluronidase enzyme do in terms of resisting host defenses?

A

Hydrolyzes hyaluronic acid (found in connective tissue)

197
Q

What does the collagenase enzyme do in terms of resisting host defenses?

A

Hydrolyzes collagen which allows pathogen to use amino acids

198
Q

What do IgA protease enzymes do in terms of resisting host defenses?

A

Destroy IgA antibodies

199
Q

What is phase variation?

A

Mutations that change antigenic sites or alter expression of antigens as a way of resisting host defenses

200
Q

Are pathogens that are spread through direct contact thought to be more or less virulent?

A

Less

201
Q

Are vector-borne pathogens thought to be more or less virulent?

A

Highly virulent in human host, but relatively benign in vector

202
Q

Define tropism

A

Pathogen must make contact with the appropriate host tissue (determined by specific cell surface receptors) for infection to occur

203
Q

Name the 5 main modes of pathogen transmission

A
  1. Airborne
  2. Contact
  3. Vehicle
  4. Vector-borne
  5. Vertical
204
Q

What is a vehicle in terms of vehicle transmission?

A

Inanimate materials or objects involved in pathogen transmission

205
Q

What is a fomite in terms of vehicle transmission?

A

Common vehicles such as surgical instruments, bedding, and eating utensils

206
Q

What are the 2 categories of vector-borne transmission?

A

External (mechanical) - pathogen on body of vector, no growth of pathogen during transmission

Internal - carried within a vector

207
Q

Define vertical transmission

A

Occurs when unborn child acquires a pathogen from infected mother resulting in congenital infection

Examples: gonorrhea, herpes, german measles, toxoplasmosis

208
Q

What two factors determine host susceptibility?

A

Defense mechanisms of host (innate vs. acquired immunity)

Pathogenicity of pathogen

209
Q

All gram negative bacteria contain:

A. Exotoxins
B. Endotoxins
C. Siderophores
D. IgA protease

A

B. Endotoxins

210
Q

C. Tetani causes the disease Tetanus by producing a(n)

A. Capsule
B. Endotoxin
C. Exotoxin
D. Enzyme

A

C. Exotoxin

211
Q

Septic shock can result from using antibiotics to treat

A. Fungal infections
B. Viral infections
C. Protozoan infections
D. Gram negative bacterial infections

A

D. Gram negative bacterial infections

212
Q

Arthropods provide a portal of exit for microbes in:

A. Skin
B. Blood
C. Respiratory tract
D. Genitourinary tract

A

B. Blood

213
Q

Which of the following releases histamine?

A. Mast cells
B. Basophils
C. Plasma cells
D. Mast cells and basophils

A

D. Mast cells and basophils

214
Q

Which of the following would you not find as normal flora in the nasopharynx?

A. Streptococcus pneumoniae
B. Escherichia coli
C. Neisseria meningitidis
D. Haemophilus influenza

A

B. Escherichia coli

215
Q

Which of the following areas of the human body is/are NOT normally free of microorganisms?

A. Upper respiratory tract
B. Intestinal tract
C. Eyes
D. All of the choices

A

D. All of the choices

216
Q

An inanimate object that may be contaminated with a pathogen is called a:

A. Vector
B. Fomite
C. Zoonose
D. Commensal

A

B. Fomite

217
Q

True or false: Generally, exotoxins tend to be more heat stable than endotoxins

A

False

Exotoxins tend to be more heat LABILE because they’re made up of protein

218
Q

Antibody molecules that are produced by a single hybridoma clone are called:

A. Human antibodies
B. Monoclonal antibodies
C. Hybrid cells
D. Identical antibodies

A

B. Monoclonal antibodies

219
Q

Why aren’t culture based techniques used for parasites?

A

Because they need a host

220
Q

What type of media do fungi prefer?

A

Acidic or low pH

221
Q

What type of antibody is produced by a hybridoma cell as an “immortal” cancerous B cell fused with an antibody-producing normal B cell?

Hint: these recognize a single epitope

A

Monoclonal antibodies

222
Q

What type of immunofluorescence involves unknown antigen added to antibody labeled with fluorescent dye resulting in visible fluorescence?

A

Direct, because the antibody is binding directly to the pathogen

223
Q

What type of immunofluorescence involves known antigen tested in different serums to see if there is fluorescence that occurs?

A

Indirect

224
Q

What is the best method for classification of bacteria and why?

A

Ribotyping (16S rRNA analysis)

Because the ribosome is stable; it has stayed the same despite transfer of material

225
Q

What method is used for identification of bacteria based on number of plasmids and their molecular weight?

A

Plasmid fingerprinting

226
Q

What type of serological test detects antigens from patient sample?

A

Direct

227
Q

What type of serological test detects antibodies in patient serum?

A

Indirect

228
Q

What would you assume had happened if a patient was not producing antibodies at one time, but two weeks later they were?

A

They underwent seroconversion

229
Q

Would a mat formation or a pellet formation be an indicator of agglutination?

A

Mat

230
Q

When using hemagglutination testing, what is the positive result and why?

A

A positive result would be NO agglutination, meaning that the antibodies are present and preventing agglutination

231
Q

What is the indicator for complement fixation testing?

A

RBCs (hemolysis)

232
Q

Is complement fixation test direct or indirect?

A

Indirect, because looking for the presence of antibodies

233
Q

What is a positive result in the complement fixation test?

A

No hemolysis, because the complement is tied up in the antigen-antibody reaction

234
Q

What is the indicator for the ELISA test?

A

Peroxidase enzyme, reaction is visualized by addition of chromogen (color change)

(ELISA = Enzyme-Linked Immunosorbent Assay)

235
Q

What is adsorbed to the bottom of the well in the first step of a direct ELISA? What about an indirect ELISA?

A

Direct ELISA: antibody is adsorbed to the well

Indirect ELISA: antigen is adsorbed to the well

236
Q

What occurs in the fluorescent-antibody technique?

A

Antibodies are linked to fluorescent dye

237
Q

What indicates a positive result during a neutralization test?

A

Indicator is cell damage; if antitoxins bind, they will be neutralized and we will see undamaged cells which is a positive result

238
Q

Sporadic disease

A

Occurs occasionally and at irregular intervals

239
Q

Endemic disease

A

Maintains a relatively steady low-level frequency at a moderately regular interval

240
Q

Hyperendemic disease

A

Gradual increase in occurrence frequency above endemic level but not to epidemic level

241
Q

Epidemic

A

Sudden increase in frequency above expected number

Index case is the first case in an epidemic

242
Q

Pandemic

A

Increase in disease occurrence within large population over wide region (usually worldwide)

243
Q

Outbreak

A

Sudden, unexpected occurrence of disease usually in a focal or limited segment of population

244
Q

Morbidity rate

A

Incidence rate measuring number of new cases in a specific time period per unit of population

245
Q

Prevalence rate

A

Total number of individuals infected at one time (depends on both incidence rate and duration of illness)

246
Q

Mortality rate

A

Number of deaths from a disease per number of cases of the disease

247
Q

Communicable disease

A

A disease that is spread from one host to another (a contagious disease is one that is EASILY spread)

248
Q

Noncommunicable disease

A

A disease that is not transmitted from one host to another (for example: botulism)

249
Q

Acute disease

A

Symptoms develop rapidly

250
Q

Chronic disease

A

Disease develops slowly

251
Q

Subacute disease

A

Symptoms between acute and chronic

252
Q

Latent disease

A

Disease with a period of no symptoms when the causative agent is inactive

253
Q

What is a nosocomial infection and what is the most common type?

A

Hospital acquired infection often due to normal flora of patient or caregiver acting as opportunistic pathogens

Most common is urinary tract infection

Others include: surgical site infections, bloodstream infections (IVs), pneumonia (artificial airways)

254
Q

What are the three possible sources of nosocomial infections?

A

Endogenous: brought into hospital by patient or acquired when patient is colonized after admission

Exogenous: microbiota other than the patient’s

Autogenous: caused by an agent derived from microbiota of patient despite whether it became a part of the patient’s microbiota following admission

255
Q

What is the #1 way to control nosocomial infections?

A

Education of healthcare professionals and frequent handwashing

256
Q

What type of immunity is stimulated by vaccinations/immunizations?

A

Artificially acquired active immunity

257
Q

What type of organism is contained in an attenuated vaccine?

A

Live but avirulent

258
Q

What type of organism is contained in an inactivated vaccine?

A

Dead

259
Q

What is a disadvantage to the attenuated polio vaccine given in other countries?

A

It is possible to get vaccine-derived polio due to reversion mutation from live organism

260
Q

Define adjuvant and give the most commonly used one

A

Substance mixed with antigens in vaccines to enhance the rate and degree of immunization

One of the most common is Aluminum

261
Q

What is a DNA vaccine?

A

DNA is directly introduced into host cell via gene gun, where DNA is taken into nucleus and pathogen’s DNA fragment is expressed so that host immune system can respond

262
Q

What are some characteristics that favor the use of biological agents as weapons?

A

Invisible, odorless, tasteless

Difficult to detect

Take hours/days before awareness that they have been used

Fear and panic associated with anticipation that they were used

263
Q

What are two possible key indicators of a bioterrorism event?

A

Sudden increased numbers of sick people, especially with unusual diseases for that place and/or time of year

Sudden increased number of zoonoses, diseased animals, or vehicle borne illnesses

264
Q

What is the most common type of nosocomial infection?

A. Lower respiratory infections
B. Postoperative infections
C. Bacteremia infections
D. Urinary tract infections

A

D. Urinary tract infections

265
Q

Which of the following measures is NOT used to prevent nosocomial infections?

A. Aseptic technique
B. Frequent handwashing
C. Increased use of antibiotics
D. Education of staff

A

C. Increased use of antibiotics

266
Q

What organism is the most important reservoir for the Borrelia burgdorferi?

A. Tick
B. Rabbit
C. Squirrel
D. Field mouse

A

D. Field mouse

267
Q

In what stage of syphilis do gummas develop?

A. Primary
B. Secondary
C. Tertiary
D. Latent

A

C. Tertiary

268
Q

Which urinary tract bacteria can cause headaches, fever, and possible kidney failure as a complication?

A. Escherichia coli
B. Staphylococcus saprophyticus
C. Leptospira interrogans
D. Neisseria gonorrhoeae

A

C. Leptospira interrogans

**E. Coli can cause UTIs but it is not a urinary tract bacteria

269
Q

What class of pathogen lacks a cell wall, is the smallest bacteria capable of self-reproduction, operates as an obligate intracellular parasite, contains less than 1000 genes, and grows on agar with “fried-egg” appearance?

A

Mycoplasmas

270
Q

Describe metabolism of mycoplasmas

A

Relies on host cells; they are chemoorganotrophs

  • most have urea transporter for catabolism
  • utilize an ATPase to generate a gradient driving ATP synthesis through urea hydrolysis
271
Q

What are two important mycoplasma pathogens?

A

Mycoplasma pneumoniae - primary atypical pneumonia in humans

Ureaplasma urealyticum - UTIs, premature birth, neonatal meningitis, and pneumonia

272
Q

Describe Phylum Chlamydiae

A

Gram-negative, nonmotile, coccoid

Obligate intracellular parasites with unique developmental cycle

273
Q

Describe Chlamydial metabolism

A

Cannot catabolize carbs

Cannot synthesize ATP or NAD+

Reticular bodies have biosynthetic capabilities in host
Elementary bodies seem to be dormant forms

274
Q

Describe the developmental cycle of Genus Chlamydia

A

EB attaches to host cell

RB reproduction by binary fission

Differentiate back into EB, lyses cell

275
Q

Describe Phylum Spirochaetes

A

Gram-negative, chemoheterotrophic

Long and slender with flexible helical shape

Creeping motility due to axial filaments (corkscrew)- good for viscous environments

Symbiotic with termites, mollusks, mammals

276
Q

What is the causative agent of Lyme Disease?

A

Borrelia burgdoferi

277
Q

What is the primary reservoir and vectors associated with Lyme Disease?

A

Primary reservoir: field mouse

Vector: deer tick

278
Q

What are the three stages of Lyme Disease?

A

Localized: Bull’s eye rash
Disseminated: irregular heartbeat, encephalitis
Late stage: arthritis and demyelination of neurons

279
Q

How is Lyme Disease diagnosed?

A

Serological testing (Lyme ELISA or Western blot)
Isolation of spirochete from patient (fluorescence)
Detection of Borrelia DNA (PCR)

280
Q

What is the primary treatment for Lyme disease?

A

Antibiotic therapy - must be given early to be effective

281
Q

Describe Relapsing Fever in terms of etiological agent, reservoir, and vector

A

Causative agent: Borrelia spp. (Spirochete)
Reservoir: rodents
Vector: ticks

*Successive relapses are less severe

282
Q

What is the causative agent of Syphilis and how does it invade a host?

A

Treponema pallidum which invades mucosa or through skin breaks

283
Q

What are two variations of Syphilis (in terms of transmission)?

A

Venereal: sexually transmitted
Congenital: acquired in utero

284
Q

What are the 3 stages of Syphilis characterized by?

A

Primary: chancre (small, painless, reddened ulcer) at infection site that contains spirochetes

Secondary: highly variable skin rash + palms & soles

Tertiary: formation of gummas (degenerative lesions) in skin, bone, and nervous system

285
Q

What are some methods for diagnosing Syphilis?

A

Taking clinical history, microscopic examination, and serology

Direct diagnosis by staining with fluorescent-labeled monoclonal antibodies

Indirect rapid screening and confirmation testing

286
Q

What is the primary treatment for Syphilis?

A

Antibiotic therapy - must be given early on for maximum effectiveness

287
Q

Describe Leptospirosis in terms of causative agent, reservoir, and transmission

A

Causative agent: Leptospira interrogans
Reservoir: dogs and rats
Transmission: skin/mucosal contact from urine-contaminated water

288
Q

What are the symptoms and possible complications of Leptospirosis?

A

Headaches, muscle aches, fever

Possible complications: kidney failure, meningitis, liver failure, respiratory distress (bleeding in lungs), or death

289
Q

How is Leptospirosis diagnosed?

A

Serological testing: growing bacteria from blood sample, finding antibodies or microbial DNA in the blood

290
Q

What is the treatment for Leptospirosis?

A

Doxycycline

291
Q

Describe Genus Rickettsia

A

Very small, gram-negative, non-flagellated, diverse morphology

Most species are parasitic, growing in vertebrate erythrocytes, macrophages, or vascular endothelial cells. May also live in blood-sucking arthropods

292
Q

Which type of pathogen might the mitochondria have originated in?

A

Rickettsia

293
Q

Describe Rickettsia metabolism

A

They lack a glycolytic pathway, must oxidize glutamate and TCA cycle intermediates

Typically take up and use ATP from host cell

294
Q

Describe Epidemic typhus in terms of causative agent, reservoir, vector, and transmission

A

Causative agent: Rickettsia prowazekii
Reservoir: rodents
Vector: lice
Transmission: louse feces rubbed into bite wound

295
Q

Back pain, delirium, high fever (40 C), joint pain, low blood pressure, light sensitivity, rashes, headaches, and muscle pain are symptoms of which type of Typhus?

A

Epidemic typhus

296
Q

Describe endemic murine typhus in terms of causative agent, reservoir, and vector

A

Causative agent: Rickettsia typhi
Reservoir: rodents
Vector: flea

297
Q

Abdominal pain, back ache, dull red rash (begins in middle of body and spreads), extremely high fever (41 C), hacking dry cough, severe headaches, joint pain, muscle pain, and vomiting are all symptoms of which type of Typhus?

A

Endemic murine typhus

298
Q

Describe the reproduction of Rickettsia

A

Enters host by phagocytosis

Escapes the phagosome

Reproduces in cytoplasm

Host cell bursts

299
Q

What is the causative agent of Rocky Mountain Spotted Fever?

A

Rickettsia rickettsii

300
Q

What are the two primary ways that Rocky Mountain Spotted Fever is transmitted?

A

Transmitted by ticks by:

Transovarian passage: transmission of bacteria from generation to generation of ticks through their eggs

Passage by tick feeding or by defecation of tick and rubbed into skin

301
Q

What two types of cells do Rickettsias reproduce in?

A

Endothelial cells and macrophages

302
Q

In which two diseases does the rash appear on the palms and soles?

A

Rocky Mountain Spotted Fever and Syphilis

303
Q

Vasculitis (destruction of blood vessels) in heart, lungs, or kidneys

Sudden onset of headache, high fever, chills, and skin rash are possible signs/symptoms of what disease?

A

Rocky Mountain Spotted Fever

304
Q

How is Rocky Mountain Spotted Fever diagnosed?

A

Observation of signs and symptoms and serological testing

305
Q

How is Rocky Mountain Spotted Fever usually treated/controlled?

A

Antibiotic therapy (Doxycycline) and symptomatic/supportive therapy

Tick control and avoidance of ticks

306
Q

What type of bacteria are nonmotile, gram-negative cocci that most often occur in pairs with adjacent sides flattened? They also may have capsules and fimbriae

A

Neisseria

307
Q

What two diseases are caused by variations of Neisseria?

A

Gonorrhea and Meningitis

308
Q

Meningitis may be an endogenous infection (normal biota); How might you diagnose meningitis?

A

A bacterial form may be diagnosed by gram stain of cerebrospinal fluid which may or may not work

309
Q

How is meningitis transmitted?

A

Respiratory droplets

310
Q

Initial respiratory illness or sore throat followed by vomiting, headache, lethargy, confusion, and stiffness in the neck and back may be signs of what disease?

A

Meningitis

311
Q

What are the virulence factors of Neisseria Meningitis?

A

Capsules and fimbriae

312
Q

What bacteria causes gonorrhea?

A

Neisseria gonorrhoeae

313
Q

What are the virulence factors associated with gonorrhea?

A

Fimbriae and Opa proteins which prevent CD4 T cell proliferation

314
Q

What condition, when left untreated, may lead to Endocarditis, meningitis, arthritis, or ophthalmia neonatorum?

A

Gonorrhea

315
Q

Which pathogen blocks C3 of the complement activation and exhibits antigenic variation in producing soluble pilli?

A

Neisseria gonorrhoeae

316
Q

What are the symptoms of gonorrhea?

A

Men: painful urination and discharge of pus
Women: few symptoms but possible complication of PID

317
Q

How would you diagnose gonorrhea?

A

Gram stain, ELISA, or PCR

318
Q

What treatment is typically used for Gonorrhea?

A

Fluoroquinolones

319
Q

Which type of bacteria is gram-negative coccobacilli, some with capsules that are nonmotile

A

Genus Bordetella

320
Q

Which disease involves toxins producing nitric oxide that may lead to stopping protein synthesis (such as cytokine production)

A

Pertussis

321
Q

What are the clinical manifestations of Pertussis?

A

7-14 day incubation with initial coldlike symptoms/inflamed mucous membranes

Followed by prolonged coughing sieges with inspiratory whoop

permanent or long-lasting immunity develops

322
Q

What are the 3 stages of Pertussis?

A

Stage 1: Catarrhal stage, like common cold
Stage 2: Paroxysmal stage – violent cough
Stage 3: Convalescence stage

323
Q

How would you diagnose Pertussis?

A

Bacterial culture, fluorescent antibody staining, and serological testing

324
Q

Which type of bacteria produces a characteristic blue/green discharge on surgical wounds or burn wounds?

A

Pseudomonas

325
Q

What is the causative agent of Legionnaire’s disease (and Pontiac Fever)

A

Legionella pneumophilia - a fastidious gram negative rod harbored by free-living amoeboae and ciliated protozoa

326
Q

Which type of bacteria’s life cycle involves replicative form differentiating into mature intracellular form (infectious/dormant form) which is resistant to antibiotics?

A

Genus Legionella

327
Q

Legionnaire’s disease produces what to cause localized tissue destruction?

A

Cytotoxic exoprotease

328
Q

What are the clinical manifestations of Legionnaire’s disease?

A

Fever, cough, headache, neuralgia, and bronchopneumonia

These may be severe in immunocompromised patients

329
Q

What is one important aspect of controlling Legionnaires disease?

A

Eliminating nosocomial spread

330
Q

What virulence factor contributes to Legionnaire’s resistance to antibiotics?

A

Beta-lactamase

331
Q

What is the causative agent of Cholera?

A

Vibrio cholerae - comma shaped gram-negative bacteria acquired by ingesting food or water contaminated by fecal matter from patients or carriers

332
Q

What is a natural reservoir of Cholera?

A

Shellfish

333
Q

Which disease involves production of rice-water stools and rushes of peristalsis?

A

Cholera

334
Q

How would you diagnose Cholera?

A

Culture from feces with subsequent identification by agglutination reactions

335
Q

True or False: M protein enhances the virulence of streptococcus by preventing phagocytosis

A

True

*M proteins function in attachment AND prevention of phagocytosis

336
Q

A nosocomial infection is:

A. Always caused by medical personnel
B. Always caused by pathogenic bacteria
C. Always present, but is not observed in times of hospitalization
D. Acquired during the course of hospitalization

A

D. Acquired during the course of hospitalization

337
Q

True or False: An endemic disease is constantly present in a population

A

True

338
Q

Which item is from the patient in a direct ELISA test?

A. Substrate for the enzyme
B. Antigen
C. Antihuman immune system
D. Antibodies against the antigen

A

B. Antigen

339
Q

Purified protein from Bordetella pertussis is used in a(n):

A. Attenuated whole-agent vaccine
B. Nucleic acid vaccine
C. Subunit vaccine
D. Toxoid vaccine

A

C. Subunit vaccine

340
Q

What is the function of an O antigen?

A

LPS

341
Q

What is the function of an H antigen?

A

Flagellar proteins

342
Q

What is the function of a K antigen?

A

Capsule proteins

343
Q

What are some virulence factors of pathogenic E.coli?

A

Fimbriae for attachment to intestinal cells

Production of toxins

Aggregation

344
Q

What are the symptoms, diagnosis, and treatment for Enterotoxigenic, enteroinvasive, or enteraggregative E.coli (traveler’s diarrhea)?

A

Symptoms: watery diarrhea
Diagnosis: isolation of bacteria
Treatment: oral rehydration

345
Q

Is traveler’s diarrhea an infection or an intoxication?

A

Infection via endotoxin

346
Q

What are the symptoms, diagnosis, and treatment for Siga-toxin-producing E.coli?

A

Symptoms: Shigella-like dysentary, hemorrhagic colitis, and hemolytic uremic syndrome

Diagnosis: isolation of bacteria

Treatment: quinolones; cephalosporins

347
Q

Is Shiga-toxin-producing E.coli (STEC) an infection or an intoxication?

A

Infection via Shiga exotoxin

348
Q

Which type of E.Coli produces one or both enterotoxins responsible for diarrhea and is distinguished by its heat stability (ST and LT?)

A

Enterotoxigenic E.coli (ETEC)

349
Q

Which type of E.Coli multiplies within the intestinal epithelial cells and may produce a cytotoxin and an enterotoxin?

This type also has invasiveness gene on large plasmid which can be determined by plasmid fingerprinting

A

Enteroinvasive E.coli (EIEC)

350
Q

Which type of E.coli causes effacing lesions caused by destruction of brush border microvilli on intestinal epithelial cells?

A

Enterohemorrhagic E.coli (EHEC)

351
Q

What is the reservoir associated with Salmonella?

A

Poultry and cattle

352
Q

What are possible symptoms, diagnosis, and treatment of salmonellosis?

A

Symptoms: Abdominal pain, cramps, diarrhea, nausea, vomiting, and fever

Diagnosis: isolation of organism from food or patient’s stools

Treatment: fluid and electrolyte replacement; good food handling practices, proper refrigeration, adequate cooking

353
Q

Name the pathogen, symptoms, diagnosis, and treatment of Typhoid Fever due to salmonella

A

Pathogen: Salmonella typhi (infection via endotoxin)
Symptoms: high fever, significant mortality
Diagnosis: isolation of bacteria; serotyping
Treatment: quinolones, cephalosporins

354
Q

What is the reservoir for shigellosis?

A

Humans

355
Q

What are some virulence factors in Shigellosis?

A

Endotoxin, exotoxins (Shiga toxin), type III secretion system for delivery into epithelial cells

356
Q

Name the symptoms, diagnosis, and treatment of Shigellosis

A

Symptoms: watery stools often containing blood, mucus, and pus, tissue damage, dysentary

Diagnosis: biochemical characteristics; serology

Treatment: antibiotics (quinolones), prevention by good personal hygiene and clean water supply

357
Q

What is the reservoir and vector of yersinia pestis (plague)?

A

Reservoir: rats, ground squirrels, and prairie dogs (rodents)

Vector: fleas

358
Q

What are the 3 types of plague?

A

Bubonic - bacterial growth in blood and lymph

Septicemia plague - septic shock due to bloodstream infection

Pneumonic plague - bacteria in the lungs (high mortality rate)

359
Q

What are virulence factors associated with the plague?

A

Proliferation in phagocytes, type III secretion systems deliver yersinal outer membrane proteins which shut down cell defense mechanisms

360
Q

What are the symptoms, diagnosis, and treatment for the plague?

A

Symptoms: subcutaneous hemorrhage, fever, buboes

Diagnosis: made in reference labs which use direct microscopic examination, culture, serological tests, and PCR

Treatment: antibiotics, ectoparasite and rodent control, immunizations for those at risk

361
Q

Describe Campylobacter fetus in terms of its effects on animals vs. humans

A

Causes reproductive disease and abortions in cattle and sheep

Septicemia and enteritis in humans

** may also lead to Guillain Barre syndrome triggered in molecular mimicry

362
Q

Describe the diagnosis and treatment of Campylobacter jejuni

A

Diagnosis: culture in low oxygen, high CO2 atmosphere

Treatment: symptomatic/supportive therapy, antibiotics in severe cases

363
Q

What virulence factor in Helicobacter pylori allows it to grow at its optimal pH?

What are other virulence factors?

A

Secretion of urease which converts urea to ammonia and CO2, which raises pH to 4.5

Other virulence factors: surface fimbriae (adhesins), inflammation due to proteases, phospholipases, cytokines, and cytotoxins

364
Q

How is Helicobacter peptic ulcer disease diagnosed and treated?

A

Diagnosis: urea breath, bacterial culture

Treatment: antimicrobial drugs

365
Q

Bacillary dysentery is caused by:

A. Staphylococcus
B. Shigella
C. Salmonella
D. Clostridium

A

B. Shigella

366
Q

What is the main reservoir for Yersinia pestis?

A. Deer
B. Rodents
C. Small mammals
D. Rabbits

A

B. Rodents

367
Q

C. tetani causes the disease Tetanus by producing a(n):

A. Capsule
B. Endotoxin
C. Exotoxin
D. Enzyme

A

C. Exotoxin

368
Q

Which urinary tract bacterium can cause headaches, muscle aches, fever, and possible kidney failure as a complication?

A. Escherichia coli
B. Staphylococcus saprophyticus
C. Leptospira interrogans
D. Neisseria gonorrhoeae

A

C. Leptospira interrogans

369
Q

What is the etiological agent for the disease that has catarrhal, paroxysmal, and convalescence stages?

A. Borrelia
B. Streptococcus
C. Mycobacterium
D. Bordetella

A

D. Bordetella

370
Q

List the Etiological agent, disease, virulence factors/ unique characteristics for Mycoplasma

A

Etiological agent: Mycoplasma pneumonia or Ureaplasma urealyticum

Disease: atypical pneumonia

Virulence factors: lack cell walls, contain sterols**, use gliding motility and have adhesion molecules

371
Q

List the Etiological agent, the disease, the unique characteristics and the virulence factors of Chlamydia

A

Etiological agent: Chlamydia

Disease: Chlamydia

Characteristics: Gram neg cocci, obligate intracellular parasite, has a unique developmental cycle:
-EB (elementary body): the infectious/ dormant form
-RB (reticulate body): reproduction by binary fission
Virulence factor: endotoxin

372
Q

List the etiological agent, disease, morphology, vector, reservoir, and virulence factor for Borrelia

A

Etiological agent: Borrelia burgdoferi

Disease: Lyme Disease

Morphology: Spirochete

Vector: tick

Reservoir: Rodents

Virulence factor: antigenic variation

373
Q

List the Etiological agent, disease, reservoir, and morphology of treponema

A

Etiological agent: Treponema pallidum

Disease: Syphillis

Reservoir: humans

Morphology: spirochete

374
Q

List the Etiological agent, reservoir(s), mode of transmission, characteristics and symptoms of leptospira

A

Etiological agent: Leptospira interrogans

Reservoir: Dogs and Rats

Transmission: skin/ mucosal contact from urine contaminated water

Symptoms: Headahces, muscular aches, fever, kidney failure (possible). Can lead to meningitis, liver failure, respiratory distress

Characteristics: Gram neg spirochete

375
Q

List the Etiological agent, the disease and stages, the characteristics, and the virulence factors of Bordetella

A

EA: Pertussis

Disease: Whooping cough

Stages: Stage 1: Catarrhal, Stage 2: Paroxysmal, Stage 3: Convalescence

Characteristics: gram neg coccobacilli

Virulence factors: capsule, Pertussis toxin (ADP ribosylation=> mucous)

376
Q

List the Etiological agent, symptoms, disease, vector, virulence factors and characteristics of Rickettsia

A

EA: Rickettsia rickettsi

Disease: Rocky Mountain spotted fever

Symptoms: sudden onset of head ache, vasculitis, rash on palms and soles

Vector: ticks

Virulence factors: intracellular parasites, escape phagosome

377
Q

List the Etiological agent, the disease, and the main symptom, and vector with regards to epidemic or endemic Rickettsia

A

EA: prowazekii (epidemic), typhi (endemic)

Disease typhus fever

Symptom: High fever

Vector(s): lice and fleas

378
Q

List the Etiological agent(s), characteristics, and virulence factors associated with Neisseria

A

EA: Neisseria gonorrhoeae and Neisseria meningitis

Chacrteristics of Neisseria: gram neg cocci

Virulence factors of Neisseria gonorrhea: fimbrae, opa protein, capsule, S pili
Of Neisseria meningitis: capsule and fimbrae

379
Q

List the eitiological agent, symptoms/ causes, chacrteristics, and virulence factors of pseudomonas

A

EA: pseudomonas aeruginosa

Symptoms: post-burn infections, otitis externa

Chacrteristics: Pyocyanin produces blue green pus, gram negative, one or more polar flagella

Virulence factors: efflux pumps

380
Q

List the etiological agent, disease, chacrteristics, reservoirs, and normal host of Legionella

A

EA: legionella pneumophila

Disease: Legionnaires disease

Characteristics: gram neg, Reproduction cycle: replicative form (non virulent/ replicative) and the Mature Intracellular Form (virulent/ dormant)

Virulence: Mature intracellular form (virulent and dormant)

Normal host: Amoeba

Reservoirs: Environmental reservoirs: soil, aquatic, AC systems, Shower stalls

381
Q

List the Etiological agent, characteristics, reservoir/ carriers, virulence factors, and symptoms of the disease of Vibrio

A

EA: V. Cholerae ( causes cholera)
V. Parahaemolyticus (causes gastroenteritis)

Characteristics: gram neg, CURVED ROD,

Virulence factors: cholera toxin, adheres to small intestine and mucosa.

Carriers: contaminated foods and water

Symptoms of cholera: Rice water stool

382
Q

List the etiological agent, characteristics, symptoms and virulence factors of shigella

A

EA: Shigella spp.

Microbiology Exam 2 (2 decks)

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