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SP14 - Micro Immuno Exam 2 > sp14_-_micro_immuno_exam_2_20141210195220 > Flashcards

sp14_-_micro_immuno_exam_2_20141210195220 Flashcards

1
Q

A ______ is a mixture of ______ and a ______ made up of ______.

A
  • biofilm- microbes- matrix- extracellular polymers
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2
Q

______ form complex structures within a ______.

A
  • bacteria- biofilm
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3
Q

Most biofilms are mixtures of ______.

A

different species of bacteria

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4
Q

Biofilms can include ______.

A

other micro-organisms than bacteria

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5
Q

Biofilms have complex structures that ______ and ______.

A
  • give accessibility to nutrients- removal of waste products
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6
Q

Bacteria in biofilm are more ______ to ______ and ______.

A
  • resistant- antibiotics- host attacks
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7
Q

Most bacteria form ______ in an environment where ______.

A
  • biofilms- there is liquid flowing
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8
Q

Wild bacteria have ______ attached to their surface that allow them to ______.

A
  • extracellular polymers- bind to surfaces of other bacteria
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9
Q

Biofilms are associated with many diseases such as ______ and ______.

A
  • periodontal disease- caries
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10
Q

Many bacterial diseases (including oral infections) are ______ where ______ are involved.

A
  • polymicrobial- several species
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11
Q

______ is the communication between bacteria.

A

quorum sensing

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12
Q

There are two general mechanisms for quorum sensing. One that ______ and one that ______.

A
  • recognizes similar bacteria (same species)- recognizes all bacteria
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13
Q

______ have mechanisms for quorum sensing.

A

essentially all bacteria

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14
Q

Quorum sensing mechanisms produce a response when ______.

A

a certain threshold concentration of secreted molecules is reached

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15
Q

______ is an essential process in ______.

A
  • quorum sensing- biofilm formation
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16
Q

______ must have oxygen to grow. ______ cannot tolerate oxygen. ______ can grow with or without oxygen.

A
  • strict aerobes- obligate anaerobes- facultative anaerobes
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17
Q

DNA that enters a bacterial cell can be ______, ______, or ______.

A
  • degraded- integrated into the host chromosome- integrated into a plasmid (extrachromosomal element
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18
Q

______ (or ______) are used by bacteria to degrade ______.

A
  • restriction endonucleases- restriction enzymes- foreign DNA
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19
Q

______ is the uptake of naked DNA by “______.”

A
  • transformation- competent cells
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20
Q

______ is the transfer of DNA between bacteria through a virus.

A

transduction

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21
Q

______ is the transfer of DNA through cell to cell contact using a ______.

A
  • conjugation- sex pilus
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22
Q

Mutations in DNA can causes ______. Mutations can be the result of ______, ______, ______, ______, or ______. ______ are less likely to cause ______.

A
  • antibiotic resistance- base changes- deletions- insertions- duplications- rearrangements- deletions- antibiotic resistance
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23
Q

Bacteria remove ______ from the cell by converting them to ______ with ______. ______ is converted to ______ and ______ with ______.

A
  • oxygen radicals- hydrogen peroxide- superoxide dismutase- hydrogen peroxide- water- oxygen- catalase
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24
Q

Bacteria that do not have ______ and ______ will not tolerate ______; they are ______.

A
  • superoxide dismutase- catalase- oxygen- anaerobic
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25
Q

______ is the most numerous members of the normal flora of the human colon.

A

Bacteroides

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26
Q

Spillage of intestinal material into the peritoneal cavity typically results in a ______: ______ followed by ______.

A
  • biphasic disease- acute inflammation- localized abscesses
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27
Q

There are a large number of bacterial species present during the ______ with only a few species that predominate in ______.

A
  • acute phase- abscesses
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28
Q

______ is the most common isolate from intra-abdominal abscesses.

A

Bacteroides fragilis

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29
Q

The ______ on the surface of B. fragilis is ______ unlike other gram ______ bacteria.

A
  • LPS- not toxic- negative
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30
Q

Of the hundreds of species that are introduced into the peritoneal cavity by spillage from the colon, those (including ______) that have a ______ survive ______ by the host.

A
  • B. fragilis- polysaccharide capsule- phagocytosis
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31
Q

______ abscesses caused by ______ or other bacteria can lead to ______ and ______.

A
  • intra-abdominal- B. fragilis- bacteremia- septic shock
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32
Q

______ is the presence of bacteria in the ______, with or without the presence of ______.

A
  • bacteremia- blood- an illness
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33
Q

______ is a severe systemic illness marked by ______ and ______.

A
  • sepsis- hemodynamic derangement- organ malfunction
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34
Q

Treatment of ______ with ______ is important, but can be difficult because ______.

A
  • sepsis- antibiotics- the dead bacteria can release toxins that initially cause more damage
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35
Q

______ are widespread in nature, but few cause disease.

A

spirochetes

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36
Q

The corkscrew-like movement of ______ is facilitated by a ______.

A
  • spirochetes- periplasmic flagella
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37
Q

______, the causative agent of ______, has been difficult to study because ______.

A
  • Treponema pallidum- syphilis- it cannot be grown in the laboratory
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38
Q

When ______ enters the body, it becomes systemic almost immediately by ______.

A
  • T. pallidum- traveling through the lymphatic channels to the systemic circulation
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39
Q

The ______ formed by ______ heals spontaneously, but the infection is ______.

A
  • primary chancre- T. pallidum- already systemic
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40
Q

About __% of the patients who do not receive treatment enter ______.

A
  • 50%- the secondary stage of syphilis
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41
Q

The ______ produced by ______ is often mistaken for other problems.

A
  • rash- secondary syphilis
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42
Q

______, if left untreated, can progress to the ______, causing ______, ______, ______, ______, and ______.

A
  • tertiary syphilis- CNS- ataxic gait- paresis- blindness- dementia- death
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43
Q

______ is one of the easiest ______ to control. There are good ______ and ______ is available and inexpensive.

A
  • syphilis- STDs- diagnostic tests- treatment
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44
Q

______ is the causative agent of Lyme’s disease.

A

Borrelia burgdorferi

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45
Q

Like syphilis, ______ progresses in stages from ______ to ______.

A
  • an acute and local skin infection- a chronic disease of the CNS and joints
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46
Q

B. burgdorferi is transmitted by ______.

A

ticks

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47
Q

There are ___-___ bacterial species found in the oral cavity from a wide variety of phyla.

A

500-1000

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48
Q

Different bacteria occupy different ______. Subgingival bacteria are generally ______. Supragingival bacteria are generally ______.

A
  • environmental niches- proteolytic- saccrolytic
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49
Q

Factors that promote colonization in the oral cavity include ______, ______, ______, ______ and ______.

A
  • adherence properties- synergistic bacteria- nutritional substrates- temperature- moisture content
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50
Q

Factors that inhibit colonization in the oral cavity include ______, ______, and ______.

A
  • the antimicrobial properties of saliva- mechanical shearing- antagonistic bacteria
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51
Q

There are many bacterial species associated with ______ while few species are associated with ______.

A
  • periodontitis- periodontal health
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52
Q

Shifts in ______ occur in periodontitis, however no bacterium is found that ______.

A
  • microbial composition- is in all patients with periodontitis and never found in healthy subjects
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53
Q

The ______ that occurs during periodontitis is mainly the result of ______.

A
  • tissue damage- host response
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54
Q

There is a small shift from ______ to ______ during periodontitis.

A
  • gram positive- gram negative
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55
Q

The ______ increases during periodontal disease.

A

complexity of the microbial community

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56
Q

There is a slight shift to more ______ in periodontitis.

A

uncultivated bacteria

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57
Q

______ declines in caries.

A

microbial diversity

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58
Q

There is a progression of ______ as caries progresses.

A

dominant species

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59
Q

Each location in the oral cavity has its own ______. However, there is overlap of ______.

A
  • associated microbial composition- species
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60
Q

What is the difference between primary/congenital immunodeficiencies and secondary/acquired immunodeficiencies?

A
  • primary immunodeficiencies - genetic defects that result in an increased susceptibility to infection; frequently manifested in infancy and childhood- secondary immunodeficiencies - develop as a consequence of malnutrition, disseminated cancer, treatment with immunosuppressive drugs, or infection of cells of the immune system
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61
Q

True or false: Integrity of the immune system is essential for defense against infectious organisms and their toxic products.

A

true

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62
Q

What is the significance of Toll-like Receptors in immunodeficiencies?

A
  • TLRs are conserved across widely diverse species- any loss-of-function mutation affecting a TLR has negative consequences for survival
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63
Q

What cells/proteins in the immune system may be affected in primary immunodeficiences?

A
  • T or B lymphocytes- natural killer cells- phagocytic cells- complement proteins
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64
Q

Defects in what 2 processes may lead to primary immunodeficiencies?

A
  • defects in leukocyte maturation/activation- defects in effector mechanisms of innate and adaptive immunity
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65
Q

What is the principal consequence of an immunodeficiency?

A

an increased susceptibility to infection

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66
Q

How can the type of immunodeficiency be predicted?

A

by using the type of recurring infection (viral, bacterial, etc.)

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67
Q

A patient with deficient humoral immunity will usually have an increased susceptibility to what type of infection?

A

infection by pyogenic bacteria

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68
Q

Describe the immune system of someone suffering from X-linked Agammaglobulinemia (XLA).

A
  • all antibody isotypes are low (not even IgM or IgD)- circulating B cells are usually absent- pre-B cells are present in reduced numbers in the bone marrow
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69
Q

Why are boys suffering from X-linked Agammaglobulinemia (XLA) healthy for the first 6-9 months of their lives?

A

because they still have maternal IgG antibodies in their system

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70
Q

What is the cause for the lack of B cells in a patient with X-linked Agammaglobulinemia?

A

loss of function of Bruton Tyrosine Kinase that is important for pre-B cell expansion and maturation into Ig-expressing B cells

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71
Q

Describe the immune system of someone suffering from X-linked Immunodeficiency with hyper IgM.

A
  • very low serum IgG, IgA, and IgE- markedly elevated concentration of polyclonal IgM
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72
Q

What is the difference in symptoms between patients with XLA and hyper-IgM?

A

patients with hyper-IgM have lymphoid hyperplasia

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73
Q

What defect is responsible for hyper-IgM disease?

A
  • loss of function of the CD40 ligand that is expressed on helper T cells- loss of this molecule prevents the T cell from co-stimulating antigen-specific B cells- B cells are NOT SIGNALED by the T cell to go through ISOTYPE SWITCHING and only produced IgM
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74
Q

What type of treatment is used for humoral immunodeficiencies?

A

prophylactic antibiotics and/or gamma-globulin therapy

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75
Q

Patients who have deficient cell-mediated immunity are usually more susceptible to what diseases?

A

viruses and other intracellular pathogens

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76
Q

How does the treatment of cell-mediated and humoral immunodeficiencies differ?

A
  • humoral immunodeficiencies can be treated routinely- cell-mediated immunodeficiencies have few, if any, treatments available to help with deficient T cell responses; in patients with absolute defects in T cell function, it is rare to survive past infancy/childhood
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77
Q

What causes DiGeorge’s syndrome?

A
  • thymus does not develop- the percentage of T cells is variably decreased and as a result, there is a relative increase in the percentage of B cells
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78
Q

What is the typical outcome of a patient with DiGeorge’s syndrome?

A
  • most infants die from infections, cardiovascular defects, or seizures within the first 2 years of life- patients who survive infancy are usually mentally retarded
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79
Q

Describe the immune system of a patient with X-linked Severe Combined Immunodeficiency Disease (XSCID).

A
  • few or no T cells or NK cells- elevated percentages of B cells (but B cells do not produce immunoglobulin normally)
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80
Q

What are the 2 aims of treatment of immunodeficiencies?

A
  1. to minimize and control infections2. to replace the defective or absent components of the immune system by adoptive transfer and/or transplantation
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81
Q

What type of treatment is used for Severe Combined Immunodeficiency Disease (SCID) patients?

A

bone marrow transplant

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82
Q

HIV is what type of immunodeficiency?

A

secondary/acquired immunodeficiency

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83
Q

How does HIV bind to the cell?

A

binds to a chemokine receptor

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84
Q

What are the cellular reservoirs of HIV? Which is responsible for the majority of the plasma virus? Which is responsible for the longevity of the disease?

A
  • activated CD4+ T cells: 93-97% of plasma virus- macrophages and dendritic cells- resting/memory CD4+ T cells: have half life of more than 50 years
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85
Q

Describe the progression of HIV disease in the body.

A
  • primary infection of the cells in blood/mucosa- infection established in lymphoid tissues- acute HIV syndrome; spread of infection throughout the body (viremia)- immune response (partial control of viral replication)- clinical latency (establishment of chronic infection; virus trapped in lymphoid tissues by folicular dendritic cells; low-level viral production)- increased viral replication- destruction of lymphoid tissue; depletion of CD4+ T cells (AIDS)
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86
Q

Over the course of an HIV infection, describe the number of CD4+ cells. Describe the amount of HIV viremia (viruses in blood).

A
  • CD4+ T cells decrease slowly over time- viremia is high in initial infection, then very low during latency, and then becomes high again as CD4+ T cell numbers lower and it progresses to AIDS
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87
Q

Define hypersensitivity.

A

exaggerated or aberrant immune response to an antigen resulting in inflammation and tissue damage

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88
Q

Define hypersensitivity diseases.

A

disorders that are caused by aberrant immune responses

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89
Q

What type of antibody is associated with Type I hypersensitivity? What type of antigen?

A
  • IgE- soluble antigen
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90
Q

What is the effector mechanism of Type I hypersensitivity?

A

mast cell activation

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91
Q

What are the 5 IgE mediated allergic reactions?

A
  • systemic anaphylaxis- acute urticaria (wheal-and-flare)- allergic rhinitis (hay fever)- asthma- food allergy
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92
Q

For systemic anaphylaxis, what is the route of entry and response?

A
  • route of entry: intravenous (either directly or following oral absorption into the blood)- response: edema, increased vascular permeability, tracheal occlusion, circulatory collapse, death
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93
Q

For acute urticaria (wheal-and-flare), what is the route of entry and response?

A
  • route of entry: through skin- response: local increase in blood flow and vascular permeability
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94
Q

For allergic rhinitis (hay fever), what is the route of entry and response?

A
  • route of entry: inhalation- response: edema of nasal mucosa, irritation of nasal mucosa
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95
Q

For asthma, what is the route of entry and response?

A
  • route of entry: inhalation- response: bronchial constriction, increased mucus production, airway inflammation
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96
Q

For food allergies, what is the route of entry and response?

A
  • route of entry: oral- response: vomiting, diarrhea, pruritis (itching), urticaria (hives), anaphylaxis (rarely)
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97
Q

What type of hypersensitivity is known as the immediate hypersensitivity?

A

Type I

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98
Q

True or false: Type I hypersensitivity occurs within minutes after exposure to an antigen/allergen.

A

FALSE. It occurs within minutes after REexposure to an antigen/allergen.(you can’t have a Type I response until after you develop antibodies to it)

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99
Q

What is the most common disorder of the immune system?

A

Type I hypersensitivity

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100
Q

What is sensitization in Type I hypersensitivity?

A

initial exposure to antigen and production of IgE antibodies

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101
Q

What is the general sequence of events of a Type I hypersensitivity reaction?

A
  1. initial exposure to antigen and production of IgE antibodies (sensitization); TH2 cells secrete ILs; TH2 cells CD40L binds to B cell CD402. binding of IgE antibody to Fc receptors on mast cells3. cross-linking of bound IgE upon reexposure to allergen4. release of mast cell mediators -> BIPHASIC RESPONSE5. immediate effects: dilation of blood vessels, increased vascular permeability, smooth muscle contraction6. late response: inflammation
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102
Q

What occurs during the immediate response of mast cell degranulation?

A
  • vasoactive amines (histamine and serotonin) and proteases are activated- synthesis and secretion of lipid mediators (prostaglandins and leukotrienes made from arachidonic acid)
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103
Q

What are the effects of prostanglandins?

A
  • vasoconstriction in the lungs or dilation in vascular smooth muscle- constriction or dilation of bronchioles- cause aggregation or disaggregation of platelets
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104
Q

What are the effects of leukotrienes?

A
  • powerful inducer of bronchoconstriction- increased vascular permeability- increased secretion and accuumulation of mucus- inflammatory cell infiltration into airways
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105
Q

What occurs during the late-phase reaction of mast cell degranulation?

A
  • synthesis and secretion of cytokines (TNF-alpha, IL-4, IL-5, GM-CSF) and chemokines (MIP-1alpha)- infiltration of eosinophils, monocytes, and neutrophils (eosinophils release granules containing ROS, major basic protein, prostaglandins, and leukotrienes)
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106
Q

What are the most common asthma signs and symptoms?

A

coughing, wheezing, and shortness of breath

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107
Q

What are the common triggers of asthma?

A
  • airborne allergens such as pollen, animal dander, mold, cockroaches, and dust mites- respiratory infections such as the common cold- physical activity (exercise-induced asthma)- cold air- air pollutants and irritants such as smoke
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108
Q

How is an allergic response triggered by dust mite allergens? What protein is associated with this?

A
  • tight junctions normally seal the barrier of the airway epithelium- the enzyme Der p 1 cleaves occludin in the tight junction- Der p 1 is taken up by dendritic cells for antigen presentation and TH2 priming- Der p 1-specific IgE binds to mast cells; Der p 1 triggers mast cell degranulation
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109
Q

What are the 5 treatment strategies for asthma?

A
  • inhaled corticosteroids(): long-term control to relieve inflammation/swelling of airways- inhaled long-acting beta2 agonists: open airways- leukotriene modifiers(): block chain reaction that increases inflammation- cromolyn: prevent mast cell degranulation- theophylline: opens airways(*) = highlighted in notes
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110
Q

True or false: The dose and routes of entry of allergens determine the type of IgE-mediated allergic reaction that results.

A

true

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111
Q

What is the most severe form of immediate hypersensitivity?

A

anaphylaxis

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112
Q

What causes anaphylaxis in the body? What occurs as a result of anaphylaxis? What is used to treat anaphylaxis?

A
  • response driven by the systemic release of vasoactive amines and lipid mediators from mast cells- causes life-threatening drop in blood pressure accompanied by severe bronchoconstriction- treated with epinephrine (vasoconstrictor and bronchodilator) and antihistamine
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113
Q

In Type I hypersensitivity, what are the events that occur as a result of mast cell activation?

A
  1. mast cell degranulation2. synthesis and secretion of lipid mediators3. cytokine release (recruitment of neutrophils and eosinophils)
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114
Q

What type of antibody is associated with Type II hypersensitivity? What type of antigen?

A
  • IgG- cell or matrix-associated antigen or cell-surface receptor
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115
Q

What is Type II hypersensitivity?

A
  • antibodies produced by the immune response bind to antigens on our own cell surfaces (primarily IgG and IgM); host antibody binds foreign antigen on cell surfaces or binds self antigen- can activate complement resulting in membrane attack complex formation (leads to destruction of cells, inflammation, or interfere with normal cellular function)
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116
Q

What are the 5 diseases associated with Type II hypersensitivity?

A
  • autoimmune hemolytic anemia- myasthenia gravis- Graves’ disease (hyperthyroidism)- hemolytic disease of the newborn- blood transfusion reactions
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117
Q

In autoimmune hemolytic anemia, what is targeted as an antigen? What occurs as a result? How does this manifest clinically?

A
  • erythrocyte membrane proteins- opsonization and phagocytosis of erythrocytes- hemolysis and anemia
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118
Q

In myasthenia gravis, what is targeted as an antigen? What occurs as a result? How does this manifest clinically?

A
  • acetylcholine receptor- antibody inhibits Ach binding- muscle weakens because it is not stimulated to contract
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119
Q

In Graves’ disease, what is targeted as an antigen? What occurs as a result? How does this manifest clinically?

A
  • thyroid-stimulating hormone receptor- antibody-mediated stimulating of TSH receptor- hyperthyroidism
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120
Q

What occurs in hemolytic disease of the newborn?

A

maternal antibodies target fetal RBCs for destruction

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121
Q

What occurs in blood transfusion reactions?

A

host anti-blood group antibody’s target transfused RBC’s for destruction

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122
Q

What are the therapeutic strategies used for the Type II hypersensitivity diseases?

A
  • autoimmune hemolytic anemia: prednisone or blood transfusion- hemolytic disease of the new born: anti-Rh antibodies- Graves disease: radioactive iodine, anti-thyroid drugs, or thyroid removal- myasthenia gravis: cholinesterase inhibitors and corticosteroids
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123
Q

What is the antibody associated with Type III hypersensitivity? What type of antigen?

A
  • IgG- soluble antigen
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124
Q

What is Type III hypersensitivity?

A

antigen-antibody complexes clump and deposit in blood vessels or tissues attracting an acute inflammatory reaction

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125
Q

What is the difference between large and small aggregates in Type III hypersensitivity?

A
  • larger aggregates: fix complement and are cleared from the circulation by phagocytes- small aggregates: form in antigen excess and deposit in vessel or tissue; ligate Fc receptors on leukocytes, leading to activation and tissue damage
126
Q

How long after exposure does Type III hypersensitivity usually take place?

A

3-10 hours after exposure

127
Q

Is Type III hypersensitivity caused by endogenous or exogenous antigen?

A

both

128
Q

Where do aggregates usually deposit in Type III hypersensitivity?

A
  • at sites where antigen is localized- at sites of turbulence- at sites of high pressure
129
Q

What are the 3 mechanisms through which immune complexes trigger inflammation during Type III hypersensitivity?

A
  1. mast cell activation2. macrophages release TNF-alpha and IL-1 that induce the inflammatory cascade3. C3a, C4a, and C5a stimulate mast cells to release more histamine, serotonin, and chemotactic factors and attract monocytes, neutrophils and other leukocytes
130
Q

What is the arthus reaction?

A
  • Type III hypersensitivity triggered in the skin by IgG- immune complexes form and complexes bind to Fc receptors on mast cells and other leukocytes- local inflammation with vascular permeability so fluid and cells enter the site; C5a activates leukocytes
131
Q

What are the symptoms of the arthus reaction? How long does is usually take for them to appear? What is the treatment for the arthus reaction?

A
  • swelling, induration, severe pain, edema, hemorrhage, and occasionally necrosis (which can lead to gangrene)- usually within a few hours after exposure- anti-inflammatory agents
132
Q

What is the classic example of transient systemic immune complex-mediated syndrome?

A

serum sickness

133
Q

What is serum sickness? How long does it take for symptoms to show?

A
  • caused by an injection of a foreign protein which leads to the formation of immune complexes which deposit in small blood vessels and activate complement and phagocytes- symptoms occur within days or weeks after injection (chills, fever, rash, etc.)
134
Q

What are the 4 causes of serum sickness?

A
  • antivenin: serum from horses immunized with snake venom given to treat people with poisonous snake bites)- anti-lymphcyte globulin: immunosuppressive agent for transplant recipients- antibiotics- streptokinase: bacterial enzyme used to treat heart attach patients
135
Q

What is Systemic Lupus Erythritosis?

A
  • have IgG antibodies against self antigen in all nucleated cells- large amounts of small complexes deposit in blood vessels, kidney, joints, etc.- phagocytes activated by Fc receptors- auto-reactive T cells also become involved (more antibodies produced)- damage can lead to death :(
136
Q

What therapies are used for the 3 main diseases of Type III hypersensitivity?

A
  • arthus reaction: avodiance or anti-inflammatory agents- serum sickness: drug avoidance, antihistamines, corticosteroids, etc.- lupus: NSAIDs, corticosteroids, immunosuppressive agents, etc.
137
Q

What is Type IV hypersensitivity?

A

mediated by antigen-specific T cells which induce macrophage infiltration in a sensitized individual; delayed-type hypersensitivity to injected or absorbed antigen (occurs within 2-3 days)

138
Q

What type of hypersensitivity is also known as delayed-type hypersensitivity? How long does the reaction take to develop?

A
  • Type IV- 2-3 days
139
Q

Which type of hypersensitivity isn’t antibody-mediated?

A

Type IV hypersensitivity

140
Q

What cells are important effector cells in the delayed-type hypersensitivity response?

A

macrophages, CD8 T cells, and NK cells

141
Q

What are the types of Type IV hypersensitivity?

A
  • tuburculin type hypersensitivity- contact dermatitis- chronic asthma- gluten-sensitive enteropathy- graft rejection
142
Q

What are haptens?

A

small molecules that must become bound to a larger carrier molecule in order to illicit an immune or inflammatory response

143
Q

What is a tuberculin test?

A
  • Type IV hypersensitivity used as a test- small amounts of tuberculin are injected intradermally- within 24-72 hours, a local T cell-mediated inflammatory reaction evolves in individuals previously exposed to TB; response is mediated by TH1 cells
144
Q

What is contact dermatitis?

A
  • highly reactive small molecules (hapten) complex with skin proteins and become internalized by APCs in the skin (especially due to itching)- can be elicited by either CD4 or CD8 T cells- inflammation occurs as a result of the inflammatory response initiated by T cells
145
Q

What are the 2 phases of contact hypersensitivity? Describe them.

A
  • sensitization: occurs during first exposure to antigen; takes 10-14 days to develop; Langerhans’ cells in skin take up antigen and present it to T cells to form CD4+ memory T cells specific to antigen- elicitation: upon reexposure to antigen; develops within 24-48 hours; APCs present antigen to memory T cells at the site of entry; T cells release IFN-gamma and pro-inflammatory cytokines that recruite macrophage, CTL, NK, and other effector cells
146
Q

What is a common example of contact dermatitis?

A

poison ivy

147
Q

What is chronic asthma?

A
  • mast cell degranulation leads to TH2 and eosinophil influx- eosinophils activate and degranulate to damage tissue and recruit more cells- chronic inflammation can cause irreversible damage and death
148
Q

What is granulomatous inflammation/Crohn’s disease?

A
  • chronic inflammation of the bowel mucosa/submucosa- thought to be due to unresolved delayed-type hypersensitivity- initial presentation may be in oral cavity and pharynx- 6% present with oral lesions at some time
149
Q

What therapies are used for Type IV hypersensitivity?

A
  • TB test injection: self-limiting- contact hypersensitivity: limit exposure, corticosteroids, antihistamines, etc.- chronic asthma: corticosteroids, bronchodilators, cromolyn, etc.- Crohn’s disease: corticosteroids, immunosuppressants, etc.
150
Q

What are strict aerobes? Obligate anaerobes? Facultative anaerobes?

A
  • strict aerobes: must have oxygen to grow- obligate anaerobes: cannot tolerate oxygen- facultative anaerobes: can grow with or without oxygen (most medically important bacteria)
151
Q

Which type of bacteria is the most medically important bacteria?

A

facultative anaerobe

152
Q

What are oligotrophs?

A

bacteria that can grow with limited nutrients

153
Q

What are microaerophiles?

A

bacteria that require some oxygen, but lower levels of oxygen

154
Q

What are mesophiles?

A

bacteria that grow well in mild temperatures (15-45 *C)

155
Q

What color do gram positive cells stain in a gram stain? Gram negative cells?

A
  • gram positive: purple- gram negative: pink
156
Q

What is the difference in the envelope structure of a gram positive cell vs. a gram negative cell?

A
  • gram positive: has a thick layer of murein (peptidoglycan), teichoic acids, and lipoteichoic acids- gram negative: thin layer of murein (peptidoglycan), outer membrane, and lipopolysaccharides
157
Q

What two sugars make up murein? What links them?

A
  • N-acetylmuramic acid (NAM)- N-acetylglucosamine (NAG)- peptide bond
158
Q

What are the similarities and differences between the composition of murein of a gram positive and gram negative cell?

A
  • gram positive: links lysine to alanine with 5 glycines (?)- gram negative: links DAP to alanine
159
Q

Describe the locations of the biosynthesis of murein.

A

synthesis of NAG and NAM is in the cytoplasm and then they are linked in the periplasmic space

160
Q

Which envelope (gram positive or negative) has LPS? Which has teichoic acids?

A
  • LPS: gram negative- teichoic acids: gram positive
161
Q

What is the difference between teichoic and lipoteichoic acids? What is their purposes?

A
  • teichoic acids just attach to NAG/NAM while lipoteichoic acids also attach to the membrane- they maintain the rigidity of the membrane (cross support)
162
Q

What is the composition of lipopolysaccharides?

A
  • lipid A: fatty acids attached to a phosphorylated disaccharide- polysaccharide core: very similar between gram negative bacteria but have sugars that are somewhat unique to bacteria- O-antigen: highly variable repeating sugar subunit
163
Q

What is the main reason for the different antigenic specificities among gram negative bacteria?

A

the O-antigen of the LPS

164
Q

What term is used to describe an LPS? What can LPS lead to?

A
  • endotoxin- LPS induces TNF-alpha and can lead to septic shock at high levels
165
Q

What are LPS and teichoic acids considered? Why is this significant?

A
  • pathogen associated molecular patters (PAMPs)- cells of the immune system can recognize PAMPs using pattern recognition receptors (PRRs)
166
Q

What receptor recognizes LPS? Peptidoglycan? Teichoic acids?

A
  • LPS: toll-like receptor 4- peptidoglycan: toll-like receptor 2- teichoic acids: toll-like receptors 2 and 6
167
Q

Other than teichoic acids and LPS, what are other extracellular structures?

A
  • pili (fimbriae)- flagella- glycocalyx
168
Q

What is the purpose of fimbriae?

A

involved in the attachment of bacteria to cells and other surfaces; have adhesins on the tips

169
Q

What are adhesins?

A

specialized proteins that are more specifically developed for adherence

170
Q

What is a sex pilus used for?

A

to transfer DNA from one microbe to another

171
Q

What is the term used to describe a bacteria with one flagella? A few flagella? Many flagella?

A
  • one flagella: monotrichous- a few flagella: lophotrichous- many flagella: peritrichous
172
Q

Describe the general structure of a flagella.

A

filament protein has a hook that is connected to the rod that is embedded in the lipid bilayer surrounded by many rings

173
Q

What type of movement is produced by a clockwise-turning flagella? A counter-clockwise-turning flagella?

A
  • clockwise: “tumbles”- counter-clockwise: forward “run”
174
Q

What is the term used to describe directed flagella movement?

A

taxis

175
Q

What are the 4 types of taxis?

A
  • chemotaxis- aerotaxis- osmotaxis- thermotaxis
176
Q

What is a glycocalyx? What are the two types of glycocalices?

A
  • a substance that surrounds a cell- capsule: a glycocalyx that is well organized and firmly attached; usually made of polysaccharides- slime layer: a glycocalyx that is not well organized or firmly attached
177
Q

Why would capsules be beneficial to pathogens?

A
  • necessary virulence factor- makes it harder to phagocytose- makes it harder to recognize
178
Q

How can the immune system recognize a bacterium that has a capsule?

A
  • TLR 5 can recognize flagella- sometimes the capsular polysaccharide can be recognized
179
Q

What does the serological designation O stand for? H? K?

A
  • O: O-antigen- H: flagella- K: capsule
180
Q

What are the 2 broad classes in which bacterial pathogens can be classified? Describe each.

A
  • opportunistic: rarely cause disease in individuals with intact immunological and antimicrobial defenses; normally found on the body- primary: capable of establishing infection and causing disease in individuals with intact immune defenses; contain virulence determinants that allow them to adhere, colonize, invade, and induce damage
181
Q

What are the 2 types of adherence?

A
  • nonspecific: reversible; docking (Brownian movement, electrostatic interactions, interactions with glycocalyx or extracellular matrices)- specific adherence: primary pathogens need this; irreversible; anchoring; involve adhesins
182
Q

What type of adherence involves adhesins? Where are they found?

A
  • specific adherence- found on fimbrae often, but also capsules or cell surface
183
Q

What bacteria causes caries?

A

Steptococcus mutans

184
Q

What adhesin is commonly not found on fimbrae?

A

fibronectin (in plasma and on mucosal surfaces)

185
Q

What is the limiting factor in colonization?

A

nutrient availability

186
Q

What are the 3 ways that bacteria can take up nutrients?

A
  • carrier-mediated diffusion (facilitated)- phosphorylation-linked transport (group translocation)- active transport (energy dependent)
187
Q

How can enteropathogenic E. coli induce tissue pathology?

A
  • colonization leads to actin polymerization- actin polymerization causes structural rearrangement of the host cell- structural changes to host cell leads to loss of function of the host cell
188
Q

What are the 2 most prominent mechanisms to invade host tissue?

A
  • secretion of hyaluronidase: will degrade hyaluronic acid which is a component of the extracellular matrix- secretion of collagenase: will degrade collagen (which is a component of connective tissue)
189
Q

What are the two types of bacterial toxins?

A
  • endotoxin: not secreted; on the surface of the bacteria- exotoxin: diffusable proteins that are secreted
190
Q

What are the 3 classifications of exotoxins?

A
  • type I: membrane acting; bind surface receptors and stimulate transmembrane signals- type II: membrane damaging; directly affect host cell membranes (create pores, etc)- type III: intracellular effectors; get into the host cell and induce enzymatic activity
191
Q

What 4 abilities make a microbe a pathogen?

A
  • ability to adhere to the host- ability to colonize the host- ability to replicate within a given niche- ability to cause damage (invasion, production of toxin, and activation of the immune system)
192
Q

What occurred in the history of antibiotics in 1920? In 1940?

A
  • 1920: Alexander Fleming described the potential usefulness of penicillin- 1940: Ernst Chain and Howard Flory demonstrated the safety and effectiveness of penicillins in humans (changed the scope of WWII)
193
Q

What are the two modes of action of antibiotics?

A
  • bactericidal: kills bacteria- bacteriostatic: stops bacterial growth
194
Q

What are the attributes of an ideal antibiotic?

A
  • broad spectrum of activity- would not induce resistance- high therapeutic index (ratio between toxic dose and effective dose; if the ratio is 1, then you need a toxic dose in order to eradicate the microbe)- selective toxicity
195
Q

What is high therapeutic index?

A
  • ratio between toxic dose and effective dose- if ratio is 1, then you need a toxic dose in order to eradicate the microbe
196
Q

How can selective toxicity be achieved?

A

by acting against things that are unique to microbes like:- cell wall- enzymes for replication, transcription, and translation- essential metabolites- ribosome structure

197
Q

What are the 5 ways in which antibiotics inhibit bacteria?

A
  • inhibition of cell wall synthesis- disruption of cell membrane function- inhibition of protein synthesis- inhibition of nucleic acid synthesis- action as antimetabolites
198
Q

How does penicillin disrupt cell wall synthesis?

A
  • bacteria have an enzyme that cleaves off the terminal D-Ala to make peptidoglycan- enzyme rather cleaves penicillin than D-Ala- penicillin is cleaved into a more toxic form that kills bacteria in an unknown mechanism
199
Q

What type of antibiotic is penicillin?

A

beta lactam ring

200
Q

What compound is used to disrupt cell membrane function? How does it do it?

A
  • polymyxin B sulfate- disrupts cell membrane by binding to phospholipids
201
Q

How do antibiotics inhibit protein synthesis?

A

block the ribosome cycle at multiple points (for example, block binding groove of ribosome, can’t recognize the mRNA site, etc.)

202
Q

What are the 3 common ways antibiotics inhibit nucleic acid synthesis?

A
  • directly bind DNA: most are too toxic but (metronidazole is inert but is activated by anaerobic microbes)- affect DNA gyrase: nalidixic acid and quinolones- inhibit RNA polymerase: rifamycin
203
Q

What is the way discussed in lecture that antibiotics act as antimetabolites?

A

healthy bacteria uses para-aminobenzoic acid (PAB) to make folic acid to make amino acids; antibiotic acts with sulfanilimide instead of PAB so there is a decrease in amino acids

204
Q

Who/what contributes to antibiotic resistance?

A
  • agricultural use- physician misuse- pharmacist misuse- patient misuse
205
Q

What are the steps of the action of antibiotics?

A
  • drug penetrates the envelope (unless they are acting on it)- transport into the cell- drug binds to target
206
Q

What are the 3 mechanisms of drug resistance?

A
  • synthesis of enzymes that inactivate the drug- prevention of access to the target site (inhibiting uptake and increasing secretion of the drug)- modification of the target site
207
Q

What is the example discussed in class of an antibiotic resistance based on synthesis of enzymes to inactivate the drug?

A

beta-lactamases cleave a bond in the beta-lactam ring of beta-lactam antibiotics

208
Q

What are the two ways discussed in class that a bacteria can develop antibiotic resistance by preventing access to the target site?

A
  • change the structure of the porin (resistance to tetracyclines and quinolones)- efflux pumps to pump the antibiotics out (resistance to tetracycline)
209
Q

What are the two ways discussed in class that a bacteria can develop antibiotic resistance by modifying the target site?

A
  • modify enzyme affinity (have the enzyme have a higher affinity for normal substrate than antibiotic)- alteration of a metabolic pathway (depends on other precursors)
210
Q

What are the 3 ways that antibiotic resistance may spread?

A
  • chromosome-associated resistance- plasmid-mediated resistance- rapid spread of resistance (because selective pressures are placed upon them)
211
Q

Why must you continue to take an antibiotic for the full length of time prescribed?

A

the antibiotic may kill the more susceptible bacteria quickly but it takes a longer time to kill the more resistant ones so if you stop taking it early, all you will have left is the more resistant bacteria

212
Q

What are the 3 different types of antibiotic relationships?

A
  • synergism: antibiotics work together- antagonism: antibiotics work against each other- indifference: antibiotics neither work together nor against each other
213
Q

What are the drawbacks to administering an antibiotic cocktail?

A
  • failure to eliminate pathogen has an increased likelihoood of superinfection- syngergistic toxicity
214
Q

Are antibiotics effective against all microbes?

A

NO! (not against viruses or various other microbes)

215
Q

Is Streptococcus gram positive or negative? Aerobic or anaerobic? Catalase test result? What does it commonly infect?

A
  • gram positive- facultative anaerobe (can grow with/without oxygen)- catalase negative- infects humans and animals
216
Q

What is the basis of the Lancefield group classification of Streptococcus?

A
  • serological classification based on major cell-wall carbohydrate antigens- use an agglutination test with latex particlaes coated with group-specific antibodies in which a positive result occurs when agglutination occurs
217
Q

What are the 3 ways to classify Streptococcus?

A
  • hemolysis pattern- lancefield group- species (metabolic reactions in culture media)
218
Q

What does an alpha result look like during a hemolysis test? A beta result? A gamma result?

A
  • alpha: partial hemolysis and green discoloration of hemoglobin- beta: clear zone of complete hemolysis- gamma: no zone of clearing
219
Q

What type of hemolysis pattern does Group A Streptococcus exhibit?

A

beta

220
Q

What is the bacteria discussed in lecture as a Group A Streptococcus?

A

S. pyogenes

221
Q

What diseases discussed in class are associated with Group A Streptococcus?

A
  • streptococcal acute pharyngitis (strep throat)- scarlet fever (strep throat with a red skin rash)- acute rheumatic fever (ARF)- acute post-streptococcal glomerulonephritis (APSGN)
222
Q

Where does an Acute Rheumatic Fever infection occur? What symptoms will occur?

A
  • site of infection: pharynx- primary results are strep throat- nonsuppurative sequelae (non-pus forming secondary results): inflammation of heart and joints, polyarthritis, carditis, severe valvular scarring, all but carditis usually resolve over time
223
Q

How is Acute Rheumatic Fever treated?

A
  • infection invokes immune system response and it is that response that causes the secondary results of the infection- can be prevented by treating strep throat with penicillin since S. pyogenes are susceptible
224
Q

What is Acute Post-Streptococcal Glomerulonephritis (APSGN)?

A
  • active inflammation in the glomeruli of the kidneys- urine smoky due to proteins, lukocytes, and erythrocytes- caused by only a few types of Group A Streptococcus
225
Q

How does Acute Post-Streptococcal Glomeruonephritis differ from Acute Rheumatic Fever?

A
  • APSGN can follow pharyngitis or pyodermal infections- APSGN susceptibility is more common- recurrent attacks are rare in APSGN- APSGN is not reliably prevented by penicillin
226
Q

How are Group A Streptococcus encountered?

A
  • live on skin and mucous membranes (nasopharynx)- person-to-person transmission (infected respiratory droplets, hand-to-hand-to-mouth, food, skin/wound, towels, shed skin)
227
Q

How can Group A Streptococcus enter the body?

A

cannot penetrate intact skin; bites, wounds, lesions (chicken pox), cuts, abrasions

228
Q

How does Group A Streptococcus enter cells?

A
  • bacteria bind to epithelial cells using adhesins- lipoteichoic acid: makes streptococci sticky; binds to fibronectin on epithelial cell surfaces- protein F: high affinity fibronectin binding protein- M protein: keratinocytes adhesin
229
Q

How do Group A Streptococci spread within the body?

A
  • infection on skin/mucous membranes: remains localized- infection of deeper tissues: rapid spread; bacteria produce digestive enzymes like proteases, hyaluronidase, DNases, streptokinase, and streptolysins S and O
230
Q

What is the function of streptokinase?

A

disrupts clot formation so that the host cannot wall of bacteria; allows spread of bacteria

231
Q

How does Group A Streptococcous avoid phagocytosis?

A
  • M protein: most important; rod-shaped molecule; central to pathogenesis and required for virulence- hyaluronic acid capsules: mucoid capsule- C5a peptidase: inactivates phagocyte chemotaxin
232
Q

What are the functions of the M protein? Which bacteria has M protein?

A
  • binds several host serum proteins (fibrin, etc.)- forms dense coating on bacteria’s surface- blocks complement from binding cell- binds host complement control proteins (inhibits formation of opsonins)- Group A Streptococcus
233
Q

What is the purpose of the hyaluronic acid capsule? Which bacteria have a hyaluronic acid capsule?

A
  • makes bacteria slippery which interferes with phagocyte attachment- cannot have capsule to attach to epithelial cells so have on/off switch in vivo
234
Q

What are the exotoxins associated with Group A Streptococcus? What do they do?

A
  • streptococcal pyrogenic exotoxins (SPEs)- superantigens that can mimic the effects of endotoxins (activated T cells release of cytokines); responsible for the red rash of scarlet fever
235
Q

Which streptococcus are more common: Group A or Group B?

A

Group B

236
Q

Where are Group B Streptococci usually found?What do they cause?

A
  • inhabit lower GI and female genital tracts- neonatal sepsis, meningitis, cellulitis, and arthritis
237
Q

What type of capsule does Group B Streptococcus have?

A

polysaccharide capsule that is antigenic; unlike hyaluronic acid capsule of Group A

238
Q

What type of hemolysis does Group B Streptococcus exhibit?

A

beta

239
Q

What type of hemolysis does Group D Streptococcus exhibit?

A

alpha or gamma

240
Q

Where are Group D Streptococci usually found? What is genus does many of them belong to?

A
  • normal flora of the GI and genitourinary tracts (low virulence, usually accompany other bacterial infections)- enterococci and nonenterococci
241
Q

What bacteria is known as “World’s Toughest Pathogenic Bacteria”? Why? How is it treated?

A
  • enterococci (Group D Streptococci)- grows in high salt concentrations and in detergents; inhibited but not killed by penicillin; resistant to most antibiotics- antibiotic synergism
242
Q

What is the most common nonenterococcal Group D Streptococcus? What can this genus of bacteria affect?

A
  • S. bovis- affects abnormal heart valves and colonic lesions
243
Q

How do enterococci and nonenterococci differ?

A
  • nonenterococci do NOT grow in high salt- nonenterococci ARE killed by penicillin
244
Q

What is the Group D Streptococcus bacteria found in the oropharynx? What can it cause?

A
  • Viridans (“greening”) streptococci (gets its name from being alpha hemolytic)- subacute bacterial endocarditis (affects abnormal heart valves) and CARIES (S. mutans)!
245
Q

What bacteria is responsible for causing caries? How?

A
  • Streptococcus mutans- surface proteins bind salivary glycoproteins on teeth; bacteria thrive on sucrose and ferment sugar to lactic acid which demineralize enamel (and they remain metabolically active at a low pH)
246
Q

Are staphylococcus gram positive or negative? Aerobic or anaerobic? Spore-forming?

A
  • gram positive- facultative anaerobes (predominantly)- non-spore forming
247
Q

What is the species of Staphylococcus that causes the highest burden of disease in people? Is it coagulase positive or negative?

A
  • Staphylococcus aureus- coagulase positive
248
Q

What diseases can be caused by S. aureus?

A
  • integumentary and wounds- bacteremia (organ abscesses, endocarditis, embolic pneumonia, septic arthritis)- aspiration pneumonia- UTI- toxic shock syndrome- scalded skin syndrome- food poisoning
249
Q

How are Staphylococcus usually encountered?

A
  • live on and around people (found on muco-cutaneous junctions); commensal- survive well in the environment (clothing, surfaces)
250
Q

How do Staphylococcus usually enter the body?

A
  • damage to skin/follicles (wounds, burns, insect bites)- damage to mucosal surfaces
251
Q

What does the multiplication/spread of Staphylococcus in the body depend upon?

A
  • bacterial inoculum (how much bacteria)- host immunocompetence- location of infection
252
Q

Who is at a higher risk for infections with Staphylococcus?

A
  • young children/elderly- diabetics- individuals on immunosuppressive therapy (autoimmune diseases, cancer chemo, long-term corticosteroids)- HIV+- dialysis patients- IV drug users
253
Q

What factor does Staphylococcus have that enhances its ability to colonize and invade?

A

MSCRAMMs (Microbial Surface Components Recognizing Adhesive Matrix Molecules)

254
Q

What are some examples of MSCRAMMs?

A
  • fibronectin-binding protein: helps attach Staphlyococcus to host cell’s fibronectin- collagen binding protein (CNA): binds in cartilage, CT, bones, joints- clumping factors that bind fibrinogen
255
Q

What type of damage is inflicted by Staphylococcus?

A
  • acute suppurative inflammation (accumulation of pus which is made up of neutrophils)- abscesses- ROS damage by neutrophils
256
Q

What occurs in an abscess during a Staphylococcus infection?

A
  • PMNs (neutrophils) are the first to show up- PMNs phagocytose bacteria and release ROS (reactive oxygen species)- PMNs also release cytokines to call more white blood cells
257
Q

What are the virulence factors of S. aureus?

A
  • polysaccharide capsule: blocks phagocytosis- protein A: blocks antibody function- pore-forming toxin: pop PMNs (neutrophils) and other cells which leads to more damage/inflammation (ex. Panton-Valentine Leukocidin)
258
Q

What is the pore-forming toxin that is very toxic to neutrophils? What bacteria releases it?

A
  • Panton-Valentine Leukocidin- S. aureus
259
Q

What occurs during Staphylococcal Scalded Skin Syndrome? What causes it?

A
  • exfoliative toxins are proteases with high-specificity for desmosomal proteins in the skin; toxins break down desmosomes which causes the layers of the epidermis to separate- exfoliative toxins A and B
260
Q

What is the definition of a superantigen?

A

cause an unregulated inflammatory response by activating high numbers of CD4+ T cells

261
Q

What is the superantigen of Staphylococcus? What does it do?

A
  • TSST-1- cross-links the T-cell receptor with the MHC-II surface molecule of antigen presenting cells to create a cytokine storm
262
Q

What does the cytokine storm induce in a patient with Toxic Shock Syndrome?

A
  • IL-1: fever- TNF alpha and beta: hypotension and capillary leakage- IFN gamma and IL-2: rash
263
Q

What contaminates the food in Staphylococcal food poisoning?

A

bacteria in food form toxins so heating the food will kill the bacteria but not the toxins that they have formed

264
Q

What types of toxins are secreted by S. aureus?

A
  • enterotoxins (A, B, C, D, and E, but A is the most common)- superantigens: cause intense peristalsis
265
Q

What are the functions of penicillin binding proteins? What inhibits them?

A
  • make the crosslinks in peptidoglycan- beta-lactam antimicrobial agents (antibiotics)
266
Q

How does Methacillin Susceptible S. aureus differ from Methacillin Resistant S. aureus?

A
  • MSSA (susceptible): has penicilin binding proteins (PBP) 1, 2, 3, 3’, 4, and 5- MRSA (resistant): has same proteins, but also PBP2a which can still do its job of assembling the cell wall, even in the presence of penicillin
267
Q

What are the 2 ways S. aureus can be resistant to beta-lactam antibiotics?

A
  • presence of PBP2a (resistant to many beta-lactam antibiotics)- blaZ penicillinase enzyme (resistant to only some beta-lactam antibiotics like penicillin)
268
Q

True or false: MRSA frequently carry resistance genes to other drug classes.

A

true

269
Q

What antibiotic is frequently used to treat MRSA? How are some MRSA becoming resistant to it?

A
  • vancomycin- vancomycin-resistant MRSA have the VanA resistance gene that was probably transferred from Enterococcus faecium via conjugative transposon
270
Q

What percent of the population carries MRSA? What percent of healthcare professionals?

A
  • less than 1% of the population- 5-15% of healthcare professionals
271
Q

What is the most effective tool to prevent the spread of Staphylococcus?

A

washing hands

272
Q

Is Streptococcus pneumoniae gram positive or negative? Aerobic or anaerobic? Spore-forming? Encapsulated?

A
  • gram-positive- aerotolerant anaerobe- non-spore-forming- encapsulated
273
Q

What bacteria is the main cause of community-acquired pneumonia?

A

Streptococcus pneumoniae

274
Q

What hemolytic pattern is exhibited by Streptococcus pneumoniae? Is it catalase positive or negative? What is it susceptible to which is a “dead giveaway”?

A
  • alpha hemolysis- catalase negative- optochin
275
Q

How is Streptococcus pneumoniae usually encoutered? (Who are the carriers and how is it transmitted from person to person?)

A
  • young children are major reservoirs; usually in the nasopharyngeal mucosa- transmission via respiratory secretions/hands
276
Q

How does Streptococcus pneumoniae usually enter the body?

A

access through lower airway (usually cleared by barrier/innate immunity)

277
Q

What are the risk factors that may increase the establishment of an infection of Streptococcus pneumoniae?

A
  • viral infection (especially influenza)- smoking- loss of consciousness (aspiration)- edema (fluid) in the lungs for any reason- high risk comorbidites, age, and demographics- seasonality (winter/spring)
278
Q

What are the 4 stages of pathogenesis of Streptococcus pneumoniae?

A
  1. alveoli fill with fluid2. early consolidation phase: suppurative (neutrophils) inflammation3. late consolidation phase: alveoli and airways are packed with neutrophils; affected tissue is solid instead of spongy4. recovery phase: macrophages phagocytose debris; normal architecture is re-established
279
Q

What are the other disease manifestations of Streptococcus pneumoniae?

A
  • otitis media in children- pleural effusion (fluid outside the lungs) in adults- bacteremia (meningitis)
280
Q

How is Streptococcus pneumoniae diagnosed?

A
  • gram-stained sputum- culture
281
Q

What is used as therapy for Streptococcus pneumoniae infections?

A
  • penicillins and other beta-lactam antibiotics (resistance is a concern)- macrolides- fluoroquinolones
282
Q

What is the vaccine of Streptococcus pneumoniae composed of? Who is suggested to receive the vaccine?

A
  • polysaccharide antigens (capsular) from multiple strains of Streptococcus pneumoniae- children and adults (over the age of 65)
283
Q

Is Legionella pneumophila gram positive or gram negative? Aerobic or anaerobic? What is its identifying characteristic?

A
  • gram negative- obligate aerobe- cysteine requirement is its identifying characteristic
284
Q

How is Legionella pneumophila encountered by humans?

A
  • contaminated water (parasite of protozoa in biofilms; thermotolerant)- environmental aerosols (NOT spread by cough)
285
Q

How does Legionella pneumophila spread within the body?

A
  • bacteria in alveoli are phagocytosed by alveolar macrophages- virulent strains multiply within autophagosomes- inflammation (acute bronchopneumonia): suppurative (neutrophils), recruitment of more macrophages, abscess formation
286
Q

How does the immune system react to a Legionella pneumophila infection?

A
  • cell-mediated immune response: secretion of INF-gamma; iron sequestration (decreases replication of bacteria)- virulence/proinflammatory mechanisms: survival in macrophages; LPS has some cytotoxic effects; flagellin enhances inflammation via innate immune system
287
Q

What is used as therapy for Legionella pneumophila infections?

A
  • antimicrobial drugs with good intracellular penetration- penicillins are not effective because they do not achieve therapeutic concentrations in the macrophages
288
Q

Are Bordetella pertussis and parapertussis gram positive or negative? Aerobic or anaerobic?

A
  • gram negative- obligate aerobe
289
Q

What does Bordetella pertussis and parapertussis cause? Is it contagious?

A
  • cause of whooping cough- VERY contagious
290
Q

How is Pertussis usually encountered by humans? Where and how does it enter the body?

A
  • adults are believed to be reservoir- nasopharynx is where it is colonized; organism accesses trachea/bronchi and has ciliary adherence via proteins
291
Q

What is similar between the damage produced by B. pertussis and P. parapertussis? What is different?

A
  • similar: adenylate cyclase/hemolysin; both upregulate host cAMP (decreased neutrophil function and increased capillary permeability which results in edema); endotoxin- different: B. pertussis produces pertussis toxin while P. parapertussis does NOT
292
Q

What are the three stages of a Pertussis infection?

A
  • catarrhal stage- paroxysmal stage- convalescent stage
293
Q

What occurs during the catarrhal stage of a Pertussis infection?

A
  • really runny nose- organisms are spreading down the respiratory tract- extremely contagious!
294
Q

What occurs during the paroxysmal stage of a Pertussis infection?

A

fits of coughs followed by a “whoop” sound

295
Q

What occurs during the convalescent stage of a Pertussis infection?

A

gradual recovery; susceptible to other respiratory infections

296
Q

How is Pertussis diagnosed?

A
  • fewer organisms shed in paroxysmal stage so it is tricky- deep nasal swab (bacterial culture)- nasal flush (PCR)
297
Q

What does the Pertussis vaccine consist of? Who receives it?

A
  • acellular pertussis- babies receive dTaP (Diphtheria, Tetanus, and Pertussis); adults receive Tdap (lower doses of Diptheria and Pertussis)
298
Q

What is the “animal version” of Pertussis?

A

Bordatella bronchiseptica (part of “kennel cough complex”)

299
Q

What bacteria is responsible for the highly contagious tuberculosis? The contagious leprosy?

A
  • Mycobacterium tuberculosis- Mycobacterium leprae
300
Q

What type of bacteria are Mycobacterium? Are they aerobic or anaerobic? Spore-forming?

A
  • acid-fast bacteria- obligate aerobes- non-spore formers
301
Q

Why are Mycobacterium TB considered acid-fast bacteria?

A

they have a thick, waxy cell wall of mycolic acid which binds carbol fuscin dye so it can be stained by acid (gram stain won’t stick)

302
Q

How are Mycobacterium TB encoutered by humans? Where do they localize in the body? How do they spread throughout the body?

A
  • inhalation or ingestion- localized in the intestine or as a primary lesion in the lung- the organism is killed by activated macrophages and forms a granuloma -> latency -> reactivation (secondary TB) occurs with dissemination within the lung or intestine and spreads to other organs
303
Q

What special structure is formed by Mycobacterium TB? How?

A
  • forms granulomas- Mycobacterium multiplies in the macrophages- CD4+ (TH1) cells are activated and there is clonal TH1 expansion- there is a cytokine profile of IFN-gamma, IL-12, and IL-2- recruitment of more macrophages eventually forms a granuloma
304
Q

What is a granuloma?

A

a multi-nucleated giant cell made by Mycobacterium, epithelial cells, and T cells

305
Q

What are the 4 ways that Mycobacterium TB is diagnosed?

A
  • intradermal skin test: uses killed antigen “tuberculin” (PPD); relies on delayed type hypersensitivity in which there is activation of CD4+ cells and localized inflammation at site of injection- acid-fast sputum exam- culture (very slow growing)- PCR
306
Q

Which of these bacteria form granulomas: M. tuberculosis or M. leprae? Which prefers lower temperatures?

A
  • both!- M. leprae
307
Q

How is M. leprae spread?

A

via respiratory route

308
Q

What are the two forms of M. leprae? Describe each.

A
  • tuberculoid leprosy: milder form; may be self-limiting; very few bacteria present in lesions- lepromatous leprosy: severe and disfiguring; many organisms in lesions; cell-mediated immunity is significantly decreased
309
Q

What animal carries M. leprae?

A

armadillos

310
Q

True or false: M. leprae is culturable in vitro.

A

FALSE. It is NOT culturable in vitro.

SP14 - Micro Immuno Exam 2 (1 decks)

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