Midterm 2 (Lectures 7-11) Flashcards

1
Q

The immune system is composed of…?

A
  • Lymphatic vessels
  • Lymphatic cells
  • Lymphoid tissues/organs
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2
Q

Different types of immune cells screen the tissues of the body for __________________.

A

Foreign antigens

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3
Q

Leukocytes are also known as…?

A

White Blood Cells (WBC)

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4
Q

Where do all leukocytes arise from?

A

Bone marrow hematopoietic stem cells

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5
Q

What are the primary lymphoid organs?

A
  • Where immune cells develop:
  • Bone marrow
  • Thymus
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6
Q

What are the secondary lymphoid organs?

A
  • Where immune cells become activated:
  • Lymph nodes
  • Spleen
  • Tonsils
  • Mucosa-associated lymphoid tissue (MALT)
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7
Q

What is MALT?

A

Mucosa-associated lymphoid tissue

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8
Q

What are the 2 branches of the immune system?

A
  1. Innate Immunity
  2. Adaptive (Acquired) Immunity
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9
Q

What is innate immunity?

A

Structures, chemicals, and processes that work to prevent pathogens from entering the body.

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10
Q

What are the 4 types of innate immunity?

A
  1. Physical barriers and associated chemicals (skin, mucous membranes, and microbiome)
  2. Non-specific chemical defences (complement factors, cytokines = interferons)
  3. Phagocytic & non-phagocytic killing of pathogens
  4. Inflammation
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11
Q

What forms the body’s 1st line of defence?

A
  • Skin
  • Mucous membranes
  • Microbiome
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12
Q

The skin is a _____-layered organ.

A
  • Multi-layered organ
  • Covered with dead cells, making an impenetrable barrier for pathogens
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13
Q

Describe how the skin is a physical barrier to pathogens.

A
  • Covered with dead cells = impenetrable barrier
  • Perspiration secreted by sweat glands (salt, antimicrobial peptides, lysozyme)
  • Sebum secreted by sebaceous/oil glands (lowers skin pH to inhibitory level)
  • Secretion of small antimicrobial peptides (disrupt pathogens’ cytoplasmic membrane)
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14
Q

Lysozyme destroys…?

A

The cell wall of bacteria.

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15
Q

_______ helps keep the skin pliable, therefore it is less likely to break or tear.

A

Sebum

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16
Q

What are the 2 distinct layers of mucous membranes?

A
  1. Epithelium
  2. Lamina propria
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17
Q

Describe the epithelium of mucous membranes and its role in preventing pathogen entry.

A
  • Epithelium = thin outer covering of the mucous membranes:
  • Tightly packed epithelial cells (prevent entry)
  • Covered with layer of mucus (prevent entry)
  • Continual shedding of cells carries away microorganisms
  • Goblet and ciliated columnar cells help remove invaders
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18
Q

What type of cells found in the epithelium of mucous membranes help remove invaders?

A
  • Goblet cells
  • Ciliated columnar cells
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19
Q

Continual shedding of _________ cells carries away microorganisms.

A

Epithelium (of mucous membranes)

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20
Q

What is the lamina propria? What does it contain?

A
  • Deeper connective layer that supports the epithelium of mucous membranes
  • Contains connective tissue, blood vessels, nerves, and large number of immune cells
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21
Q

Mucous membranes also produce ________ with antimicrobial properties.

A

Chemicals

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22
Q

What physical barrier to pathogens produces and drains tears?

A

Lacrimal apparatus

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23
Q

Describe the role of the lacrimal apparatus in being a physical barrier to pathogens.

A
  • Produces and drains tears
  • Blinking spreads tears and washes eye surface
  • Lysozyme in tears destroys bacterial cell wall
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24
Q

What enzyme is found in tears that destroys the bacterial cell wall?

A

Lysozyme

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25
What is microbial antagonism?
How the normal microbiome competes with potential pathogens.
26
How is the microbiome a physical barrier to pathogens?
- Microbial antagonism: - Consumption of nutrients - Create unfavourable environment to other microorganisms - Prevent pathogen attachment to host cells - Help stimulate body's 2nd line of defence - Generate antimicrobial compounds - Provide vitamins to host (promote overall health)
27
The complement system is composed of over ___ proteins, known as ______________, which are present in blood and tissues.
- Over 30 proteins - Complement factors
28
Many complement factors are produced as...?
- Zygomens (inactive enzymes) - Get cleaved to be activated
29
What are the 3 pathways of complement activation?
1. Classical pathway 2. Alternative pathway 3. Lectin pathway
30
Activation of the complement system is triggered by the presence of...?
Pathogens in blood and tissues.
31
What antimicrobial responses does activation of the complement system trigger? Describe them.
- Direct cytolysis = killing of pathogen (membrane attack complex) - Opsonization = coating pathogen cells to induce their phagocytosis - Inflammation = recruitment of immune cells and antimicrobial processes to the site of infection
32
What are cytokines?
- Soluble regulatory proteins that act as intracellular signals for immune cells - Produced in response to infection - Regulate function of immune cells
33
Complex web of signals among cells of the immune system.
Cytokine network
34
What are the different types of cytokines?
- Interleukins (IL) - Interferons (IFN) - Growth factors - Tumor necrosis factors (TNF) - Chemokines
35
Signals among leukocytes.
Interleukins
36
Antiviral proteins that may act as cytokines.
Interferons
37
Proteins that stimulate stem cells to divide.
Growth factors
38
Describe TNFs.
- Tumor necrosis factors: - Secreted by macrophages and T cells - Kill tumour cells - Regulate immune responses & inflammation
39
What are chemokines?
Chemotactic cytokines that signal leukocytes to move (chemotaxis).
40
____________ are released by host cells to inhibit the spread of viral infections.
Interferons
41
What are the 2 types of interferons?
1. Type I = IFN-alpha and IFN-beta 2. Type II = IFN-gamma
42
How do Type I interferons provide uninfected neighbouring cells with resistance to viral infection?
- Induce expression of genes that code for antiviral proteins in cells - The antiviral proteins are activated if the cell gets infected (degrade mRNA, bind to ribosomes)
43
What immune cells are granulocytes?
- Neutrophils - Eosinophils - Basophils
44
What are some characteristics of granulocytes?
- Contain large granules in their cytoplasm - Have a multi-lobed nucleus
45
What dye are basophils stained with? What colour do they stain?
- Methylene blue (basic dye) - Stain blue
46
What dye are eosinophils stained with? What colour do they stain?
- Eosin (acidic dye) - Stain red/orange
47
What dyes are neutrophils stained with? What colour do they stain?
- Mix of acidic/basic dyes - Stain lilac
48
What are the most abundant type of leukocyte in the blood?
Neutrophils
49
What are some characteristics of neutrophils?
- Phagocytic cells - Capable of diapedesis = migrate out of blood vessels into the tissues
50
Leukocytes that do not have granules in their cytoplasm.
Agranulocytes
51
Cytoplasm appears uniform under a light microscope.
Agranulocytes
52
What immune cells are agranulocytes?
- Lymphocytes (T cells, B cells, NK cells) - Monocytes (macrophages)
53
What are the types of lymphocytes?
- T cells & B cells => adaptive immunity - Natural Killer (NK) cells => innate immunity
54
Describe monocytes.
- Migrate from the blood into tissues => mature into macrophages - Macrophages = phagocytic cells
55
Neutrophils compromise ___% of total WBCs.
40-60%
56
Lymphocytes compromise ___% of total WBCs.
20-40%
57
Monocytes compromise ___% of total WBCs.
2-8%
58
Eosinophils compromise ___% of total WBCs.
1-4%
59
Basophils compromise ___% of total WBCs.
0.5-1%
60
Rank the WBCs from most abundant to least abundant.
1. Neutrophils 2. Lymphocytes 3. Monocytes 4. Eosinophils 5. Basophils
61
When do frequencies of leukocytes in the blood change?
During an infection.
62
Why is a differential WBC count performed?
To determine the relative frequencies of different leukocytes in the blood, which can signal disease.
63
Increased eosinophils indicate...?
- Allergies - Parasitic worm infection
64
Bacterial diseases show an increase in what immune cells?
- Leukocytes - Neutrophils
65
Viral infections show an increase in what WBCs?
- Lymphocytes
66
What are the major phagocytes in blood and tissues?
- Neutrophils - Macrophages
67
What are the stages of phagocytosis?
1. Chemotaxis 2. Adhesion 3. Ingestion 4. Maturation 5. Killing 6. Elimination
68
How do eosinophils attack parasitic helminths?
- Adhere to their surface - Secrete toxic molecules that weaken or kill the helminth
69
______________ is often indicative of a helminth infestation or allergies.
Eosinophilia (increased numbers in blood)
70
Describe killing of pathogens by NK lymphocytes.
Secrete toxic molecules onto surface of virally infected cells and tumours to induce apoptosis.
71
Describe non-phagocytic killing of pathogens by neutrophils.
- Produce toxic chemicals that kill nearby invaders - Generate neutrophil extracellular traps (NETs) that bind to and kill bacteria
72
What are NETs?
- Neutrophil extracellular traps (NETs): - Extracellular fibers that bind to and kill bacteria
73
Nonspecific response to tissue damage from various causes including pathogen infection.
Inflammation
74
Difference between local vs. systemic inflammation?
- Local = restricted to site of infection/injury - Systemic = involving many organs
75
Local inflammation is characterized by...?
- Redness - Heat - Swelling - Pain
76
Inflammatory characteristics (e.g., redness, pain) are due to...?
- Increased blood flow to the area - Vasodilation - Increased blood vessel permeability - Immune cell infiltration into the tissue
77
What are the 3 main functions of inflammation?
1. Destroy the agent causing the injury 2. Limit the effect of the agent on the rest of the body 3. Repair and replace the damaged tissue
78
What are the 2 types of inflammation?
1. Acute inflammation (quick, short-lived) => typically beneficial 2. Chronic inflammation (long-lasting) => can damage tissues that will cause a disease
79
What are the 3 steps inflammation is induced in?
1. Vasodilation & increased permeability of blood vessels at the site of infection 2. Migration of WBCs into site of infection 3. Clearance of pathogen & tissue repair
80
What chemicals is vasodilation and increased blood vessel permeability triggered by?
- Chemicals produced in injured or infected tissues: - Bradykinins - Prostoglandins - Leukotrienes - Histamines
81
___________ increases blood flow to the area.
Vasodilation
82
What does increased blood vessel permeability allow for release of?
- Proteins - Antibodies - Complement factors - Blood clotting proteins - Fluids
83
Migration of leukocytes out of the blood vessels.
Extravasation
84
What steps does extravasation involve?
1. Neutrophils & monocytes delivered to site of infection (recruited by chemokines) 2. Attach to receptors and adhesion factors on blood vessels 3. Diapedesis = squeeze between cells of vessel wall and enter site of infection
85
What is diapedesis?
How WBCs (e.g., neutrophils, monocytes) squeeze between cells of blood vessel wall and enter the site of infection.
86
What facilitates tissue repair?
Delivery of nutrients and oxygen.
87
What are the steps of tissue repair?
1. Blood clot formation 2. Phagocytosis & killing of pathogens 3. Pus formation 4. Clearance of dead cells 5. Repair of damaged tissue by tissue stem cells 6. Blood clot absorption
88
What is pus made up of?
- Damaged tissue - Dead WBCs (mostly neutrophils)
89
The body's ability to recognize and defend itself against distinct invaders and their products.
Adaptive immunity
90
What are the 5 attributes of adaptive immunity?
1. Specificity 2. Inducibility 3. Clonality 4. "Self" vs. "Non-Self" Discrimination 5. Memory (immunological)
91
What are the 2 main types of lymphocytes involved in adaptive immunity?
1. B cells => humoral immune responses (antibodies) 2. T cells => cell-mediated immune responses
92
What are antigens?
- Molecules that the body recognizes as foreign => triggers a specific immune response - Include various bacterial components, and proteins of viruses, fungi, and protozoa
93
How are antigens recognized by lymphocytes?
Epitopes = 3D regions on antigens
94
What are epitopes?
3D regions on antigens (small peptides) that are recognized by lymphocytes.
95
What are the 3 types of antigens?
1. Exogenous => include components of an extracellular microbe (e.g., from cell walls, membranes, flagella, pilli, and toxins) 2. Endogenous => produced by intracellular microbes that reproduce inside a cell 3. Autoantigens => self-antigens derived from normal cellular processes
96
T cells express ______________________ that recognize specific epitopes of an antigen.
Antigen-specific receptors
97
Describe the structure of antigen-specific T cell receptors.
- Composed of 2 protein chains (dimer) that are embedded in the cell membrane - Each chain composed of 2 domains: variable and constant regions - AA of the variable region vary between different T cells = each T cell has different antigen specificity
98
What are the different types of T cells based on?
- Surface glycoproteins - Characteristic functions
99
What are the 3 types of T cells?
1. Cytotoxic T cells = CD8+ (directly kills other cells) 2. Helper T cells = CD4+ (help regulate B cells and cytotoxic T cells) 2. Regulatory T cells = CD4+ (represses adaptive immune responses as they can cause damage to tissues if active for too long)
100
What are some different types of Helper T cells?
- Depending on type of cytokine they produce: - TH1 - TH2 - TH17
101
T cells only recognize antigens that are processed and presented to them on...?
Major histocompatibility complexes (MHC) = glycoproteins found on most cells.
102
T cells receptors only bind epitopes associated with an ______ protein.
MHC (major histocompatibility complexes)
103
Only specific cells called ___________ can process and present antigens to activate T cells.
- Antigen-presenting cells (APC) => e.g., dendritic cells - Expand/increase SA so they can express antigens
104
What are the 2 classes of MHC proteins?
1. MHC class I = present on all cells except RBCs 2. MHC class II = present on antigen-presenting cells
105
CD8+ (cytotoxic) T cells recognize antigens presented on...?
MHC-I molecules
106
CD4+ (helper) T cells recognize antigens presented on...?
MHC-II molecules
107
How are endogenous antigens processed? What type of MHC are they present on?
- Processed by the cell's proteosome complex => sent to ER => packaged by Golgi bodies into vesicles => vesicle fuses with cell membrane - Presented on MHC-I molecules
108
How are exogenous antigens processed? What type of MHC are they present on?
- Are phagocytosed and processed in the endosomal compartment - Presented on MHC-II molecules
109
Describe the cell-mediated immune response.
- Mediated by CD8+ cytotoxic T cells - Respond to intracellular pathogens (viruses) and abnormal body cells (cancer cells) - T cell activation occurs in the 2ndary lymphoid organs (lymph nodes, spleen, MALT)
110
T cell activation occurs in what types of organs?
2ndary lymphoid organs (lymph nodes, spleen, MALT).
111
Describe the steps to cytotoxic T cell (CTL) activation.
1. Antigen presentation: an infected or antigen-presenting cell (APC) displays a foreign antigen on its MHC-I molecule, signalling Tc cells 2. Helper T cell differentiation: Th cells, activated by MHC-II on APCs, release cytokines like IL-2 (interleukin 2) to enhance Tc cell activation (have IL-2 receptors) 3. Clonal expansion: active Tc cells rapidly proliferate and differentiate, killing infected cells 4. Self-stimulation: Tc cells produce their own IL-2, activating even more Tc cells => takes about 1-2 weeks to mount effective immune response
112
Describe the 2 pathways that cytotoxic T cells can kill targets through.
1. Perforin-granzyme pathway: perforin forms pores in the cell membrane => allows granzymes to enter the cell and induce apoptosis 2. CD95 pathway: mediated through cell receptors that induce apoptosis in the target cell
113
B cells are found primarily in...?
- Spleen - Lymph nodes - MALT - Small % circulate in the blood
114
The major function of B cells is secretion of...?
Secretion of antibodies (immunoglobulin).
115
Describe the structure of antibodies (immunoglobulins).
- Y-shaped structure: - Made up of 2 heavy (H) and 2 light (L) protein chains - Each protein chain is composed of constant and variable domains - The variable regions of the H and L chains form the antigen-binding sites
116
The antigen-binding sites on B cells are formed by...?
The variable regions of H/L chains.
117
What do B cells express for antigen recognition?
- Antigen-specific B cell receptor (BCR) - BCRs on each B cell recognize a specific epitope
118
BCRs (B cell receptors) are _________ forms of immunoglobulins.
Membrane-bound
119
Humoral immunity is also called...?
T-dependent humoral immunity (depends on the function of helper T cells)
120
What are the 4 steps of activation of humoral immune response?
1. Antigen presentation for CD4+ T cell activation 2. Differentiation of CD4+ T cells into Helper T cells 3. Activation of B cells 4. Proliferation and differentiation of B cells into antibody-producing plasma cells
121
What are the functions of antibodies?
- Complement factor activation (through classical pathway) & inflammation - Neutralization (prevent antigen from attaching to cell receptors) - Opsonization (coating of antigens with antibody molecules recognized by phagocytes) - Agglutination (clumping of pathogens due to antibodies binding) - Antibody-dependent cellular cytotoxicity (ADCC; NK cells have receptors that recognize the antibody)
122
What are the 5 classes of antibodies?
1. IgM 2. IgG 3. IgA 4. IgE 5. IgD
123
Describe IgM antibodies.
- Monomer or Pentamer - Produced early on - Monomer can act as BCR - Pentamer involved in complement activation, neutralization, and agglutination
124
What type of antibody is most abundant?
IgG
125
Describe IgG antibodies.
- Monomer - Most abundant antibody - Involved in all antibody functions (complement activation, neutralization, opsonization, agglutination, ADCC), and oxidation
126
Describe IgA antibodies.
- Monomer or Dimer - Dimer secreted on surface of mucous membranes - Involved in neutralization and agglutination
127
Describe IgE antibodies.
- Monomer - Involved in allergic reactions
128
Describe IgD antibodies.
- Monomer - Unknown function, perhaps acts as BCR
129
The majority of T and B cells are _______(short/long)-lived.
Short-lived (die within a few days of activation)
130
Describe memory T and B cells.
- Long-lived (persist for months or years in lymphoid tissues) - Respond to subsequent antigen exposure much FASTER than the primary response - Memory (2ndary) response is more effective than the primary response
131
Primary/secondary response is more effective.
Secondary (memory => quicker, stronger)
132
Specific immunity acquired during an individual's life.
Acquired immunity
133
What are the 2 types of acquired immunity?
1. Naturally acquired: response against antigens encountered in daily life 2. Artificially acquired: response to antigens introduced via a vaccine
134
What are the 2 artificial methods of immunity?
1. Active immunization: administration of antigens so patient actively mounts an adaptive immune response (i.e. vaccination) 2. Passive immunotherapy: individual acquires immunity through the transfer of antibodies formed by immune individual or animal
135
The most efficient, cost-effective, and safe method of controlling infectious diseases.
Vaccination
136
__________ are a method of inducing immunity without causing the disease.
Vaccines
137
After vaccination, and subsequent exposure to the pathogen, what happens?
The memory B and T cells mount a strong immune response, preventing the pathogen from causing a disease.
138
What does a vaccine contain?
- Antigens - Weakened or killed pathogen - Or parts of the pathogen
139
What are some side effects of vaccination?
- Mild local inflammation resulting in pain, fever, fatigue - May trigger allergic reactions or anaphylactic shock in some individuals - Residual virulence from attenuated viruses
140
What are the 2 types of vaccines that contain whole pathogens called?
1. Attenuated (modified live) vaccines 2. Inactivated (killed) vaccines
141
What are the 2 types of vaccines that contain parts of the pathogen called?
1. Subunit vaccines 2. Toxoid (inactivated toxin) vaccines
142
What are the 2 types of vaccines that are made using recombinant DNA technology?
1. RNA and DNA vaccines 2. Recombinant vector vaccines
143
The process of treating a pathogen to make it less virulent.
Attenuation
144
What are some examples of attenuated vaccines?
- MMRV (Measles, Mumps, Rubella, Varicella) - Sabin (Oral Polio)
145
What are some advantages of attenuated vaccines?
- Mimic the pathogen, resulting in mild infection = stimulate a strong immune response - Contain a large number of antigens - Can induce life-long immunity
146
What are some disadvantages of attenuated vaccines?
- Can cause disease in immunocompromised individuals (b/c can retain residual virulence) - Not suitable for pregnant women (risk of harm to the developing fetus) - Risk of the pathogen reverting to virulent form
147
Vaccine that contains killed whole pathogen.
Inactivated vaccines
148
What are some examples of inactivated (killed) vaccines?
- Salk (inactivated Polio) - Seasonal Flu vaccines
149
What are some advantages of inactivated vaccines?
- Safer than attenuated live vaccines - Contains large number of antigens
150
What are some disadvantages of inactivated vaccines?
- Antigenically weaker; therefore administered at higher doses - May require booster dose to achieve full immunity
151
Vaccines that contain antigenic fragments of microbes instead of whole pathogen.
Subunit vaccines
152
What is an example of a subunit vaccine?
Hepatitis B vaccine
153
What is an advantage of subunit vaccines?
Safe (no infectious agent present)
154
What are some disadvantages of subunit vaccines?
- Often require multiple doses to achieve full immunity - Often contain adjuvants (chemicals added to increase antigenicity) that cause local inflammation
155
Chemicals added to (subunit/toxoid) vaccines to increase effective antigenicity.
Adjuvants
156
Chemically or thermally modified toxins used to stimulate active immunity.
Toxoid vaccines
157
Describe toxoid vaccines.
- Inactivated toxins (chemically or thermally modified) used to stimulate active immunity - Useful for some bacterial diseases: diphtheria, tetanus, whooping cough - Stimulate antibody-mediated immunity
158
What type of vaccine is useful for bacterial diseases and stimulates antibody-mediated immunity?
Toxoid vaccines
159
What are some disadvantages of toxoid vaccines?
- Require multiple doses (toxoids possess few antigenic determinants) - May contain adjuvants (cause local inflammation)
160
What is an advantage of toxoid vaccines?
High safety profile
161
Vaccine that involves simultaneous administration of antigens from several pathogens.
Combination vaccines
162
What is an example of a combination vaccine?
DTaP (Diphtheria; Tetanus; Pertussis)
163
Vaccine that combines bacterial capsule polysaccharide (not very antigenic) with a highly antigenic protein.
Conjugate vaccines
164
Conjugate vaccines induce a strong ________ immunity against polysaccharide capsules.
Humoral (antibody) immunity
165
There are conjugate vaccines against which bacteria?
- Haemophilus influenzae - Streptococcus pneumoniae
166
Attempts to make vaccines more effective, cheaper, and safer.
- Recombinant vector vaccine - mRNA vaccine
167
Future generation of vaccines.
Peptide vaccines
168
Administration of antiserum that contained pre-formed antibodies.
Passive immunization
169
What is an advantage of passive immunization?
Provides immediate protection against a recent infection or ongoing disease.
170
What are the limitations to antiserum (passive immunization)?
- Can trigger allergic reactions (serum sickness) - Antibodies of antiserum are degraded relatively quickly - Individuals NOT protected from subsequent infections
171
How are limitations of antiserum (passive immunization) overcome?
Development of hybridomas (immortalized antibody-producing plasma cells).
172
Immortalized antibody-producing plasma cells.
Hybridomas
173
Describe hybridomas (immortalized antibody-producing plasma cells).
- Produce monoclonal antibodies with defined antigen specificities - High purity of antibodies - Free of serum component (does NOT trigger allergic reactions)
174
What are the different types of serological tests?
- Precipitation tests - Agglutination tests - Neutralization tests - Complement fixation tests - Labelled antibody tests - Point-of-care tests
175
What is serology?
The determination of the presence of specific antigens or antibodies in serum.
176
Describe precipitation tests.
- Antigens and antibody mixed in the proper proportion form antigen-antibody complexes (immune complexes) - Immune complexes form a precipitate - Immunodiffusion performed in a semi-solid gel is a common precipitation technique
177
What immune complexes?
Antigen-antibody complexes ("1:1 ratio") that form a precipitate.
178
Agglutination occurs due to the...?
Cross-linking of antibodies with particulate antigens.
179
Clumping of insoluble particles.
Agglutination
180
Aggregation of soluble molecules.
Precipitation
181
Agglutination of RBCs.
Hemagglutination
182
Hemagglutination can be used to determine ____________.
Blood type
183
Describe agglutination tests (titration).
- Method to measure antibody levels in blood serum - Serum being tested is serially diluted and tested for agglutinating activity - Highest dilution of serum giving a positive reaction is the titer
184
The use of agglutination to quantify the amount of antibody in a serum sample.
Titration
185
Describe viral neutralization.
- Cytopathic effect: viruses introduced into appropriate cell cultures will kill the cells - Ability of virus to kill culture cells is neutralized when virus is first mixed with antibodies against it
186
Detects presence of viral neutralizing antibodies in the serum.
Viral neutralization test
187
Describe the viral neutralization test.
- Mixture of virus and serum added to cell culture - Absence of cytopathic effect indicates presence of antibodies against the virus in the serum - Identifies whether individual exposed to a particular virus
188
Describe the viral hemagglutination inhibition test.
- Useful for viruses that are NOT cytopathic - Based on viral hemagglutination (some viral surface proteins can clump RBCs) - A serum sample that contains antibodies against a specific virus will inhibit viral hemagglutination - Commonly used to detect antibodies against influenza, measles, and mumps
189
What serological test is commonly used to detect antibodies against influenza, measles, and mumps?
Viral hemagglutination inhibition test (type of neutralization test)
190
What are the types of labelled antibody tests?
- Indirect/direct fluorescent antibody test - ELISA (EIA) - Antibody sandwich ELISA - Western blot (immunoblot)
191
Describe labelled antibody tests.
- Use antibody molecules linked to some "label" that enables them to be easily detected - Used to detect either antigens or antibodies
192
What serological test uses antibodies labelled with fluorescent dye?
Fluorescent antibody tests
193
What are the differences between direct and indirect fluorescent antibody tests?
- Direct: the label is on the primary antibody - Indirect: the label is on the secondary antibody (anti-antibody)
194
What is ELISA or EIA?
- ELISA = enzyme-linked immunosorbent assay - EIA = enzyme immunoassay
195
Describe the ELISA antibody test.
- Uses an enzyme as the label (enzyme-linked anti-antibody) - Reaction of enzyme with its substrate produces a coloured product indicating a positive test
196
What are some advantages of the ELISA antibody test?
- Can detect either antibody or antigen - Sensitive - Quantitative - Easy to perform/automate - Relatively inexpensive
197
Describe the antibody sandwich ELISA.
- Modification of the ELISA technique - Commonly used to detect antigen - Antigen being tested for is "sandwiched" between 2 antibody molecules
198
Describe Western blotting.
- Technique to detect antibodies against multiple antigens - Used to confirm the presence of proteins
199
What are the 3 steps to Western blotting?
1. Electrophoresis separates proteins in a solution 2. Blotting transfers protein to nitrocellulose membrane 3. Probe the membrane with antibodies and detect colour where antibody has bound to proteins
200
What are some common point-of-care serological tests?
- Immunofiltration assay - Immunochromatography assay
201
What are point-of-care serological tests?
- Simple immunoassays that give results in minutes - Useful in determining a quick diagnosis
202
Describe an immunofiltration assay.
- Rapid ELISA that uses antibodies bound to membrane filters rather than plates - Reduced time (due to the large SA of the membrane filter) to complete the assay
203
Describe immunochromatography.
- Very rapid and easy-to-read ELISAs - Antigen solution flows through a porous strip and encounters labelled antibody - Visible line produced when antigen-antibody immune complexes encounter antibody against them - Used in pregnancy testing and for identification of some infections
204
Used in pregnancy testing.
Immunochromatography
205
Allergies (hypersensitivity) are immune responses against __________.
Allergens (harmless antigens)
206
Caused by immune responses against self-antigens.
Autoimmune disorders
207
What are some examples of autoimmune disorders?
- Autoimmune hemolytic anemia (antibodies against RBC) - Type 1 diabetes mellitus (cellular damage to islets of Langerhans) - Multiple sclerosis (cellular damage to myelin sheaths)
208
What are the 2 types of immunodeficiencies?
1. Primary: genetic defects that impair immune functions 2. Secondary: caused by infections, therapies, aging, malnutrition, etc.
209
AIDS
Acquired immunodeficiency syndrome
210
HIV
Human immunodeficiency virus
211
What are the signs and symptoms of AIDS?
- Severe decrease in Helper (CD4+) T cells; < 200 cells/uL blood - Seroconversion (presence of serum antibodies against HIV) - Several opportunistic or rare infections along with HIV infection
212
Presence of serum antibodies against HIV.
Seroconversion
213
Describe HIV infection.
- HIV = enveloped +ssRNA retrovirus - HIV infects Helper (CD4+) T cells; CD4 is the receptor for HIV gp120 protein - CD4 binding to gp120 mediates attachment/entry of HIV into Helper T cells
214
CD4 is the receptor for HIV _____ protein.
gp120
215
What are the 2 major types of HIV?
1. HIV-1: prevalent across the globe 2. HIV-2: mainly present in parts of West Africa
216
Describe the replication cycle of HIV.
1. Attachment 2. Entry by endocytosis 3. Uncoating 4. Synthesis of DNA (reverse transcriptase: ssRNA to dsDNA) 5. Integration of viral genome into human DNA 6. Synthesis of ssRNA and polypeptides 7. Release 8. Assembly and maturation (protease function)
217
Describe the pathogenesis of HIV.
1. Primary infection (HIV in blood, decreased Helper T cell count) 2. Clinical latency (increased antibodies against HIV) 3. Opportunistic diseases 4. Death (Helper T cell count = 0)
218
What are the modes of HIV transmission?
- Sexual contact with an infected (HIV+) individual - Intravenous drug use (sharing of contaminated needles) - Blood transfusion/organ transplant (if donor is HIV+) - Mother-to-child transmission (from an HIV+ mother to child)
219
Describe the diagnosis of HIV infection.
- Unexplained weight loss, fatigue, fever; and other signs/symptoms of opportunistic infections - < 200 Helper (CD4+) T cells/uL blood - Seroconversion (presence of serum antibodies against HIV) - PCR test for HIV RNA (definitive diagnosis)
220
Describe HAART (highly active anti-retroviral therapy).
- Cocktail of 3 or more antiviral drugs (nucleotide analogs, integrase inhibitors, protease inhibitors, reverse transcriptase inhibitors); combination therapy important to prevent drug resistance - Stops HIV replication (reduces viral titers & prevents CD4+ T cell destruction) - Treatment immediately after diagnosis of HIV infection significantly reduces the chance of developing AIDS
221
HAART
Highly active anti-retroviral therapy
222
There are NO vaccines for _____.
HIV
223
Skin is a ______________ membrane.
Cutaneous
224
What are the 2 distinct layers of the skin?
1. Epidermis (outer) 2. Dermis (inner)
225
What are some functions of the skin?
- Prevents excessive water loss - Regulates temperature - Assists in vitamin D formations - Involved in sensory phenomena - Barrier against microbial invaders
226
Describe some characteristics of the skin microbiome.
- Normally harmless microbes - Typically grow in moist areas of the skin - Compete with potential pathogens for nutrients and space - Produce chemicals that interfere with growth of other microbes - Cannot be completely removed through cleansing - Waste products cause body odor
227
Some ________ and ___________ tolerate the harsh environment of the epidermis.
- Yeasts - Bacteria
228
What are some microbes that make up the skin microbiome?
- Yeast (Malassezia) - Gram-positive bacteria (Staphylococcus epidermidis, Micrococcus, Diphtheroids like Cutibacterium acnes)
229
Small lipophilic yeast that digests sebum.
Malassezia
230
How may pathogenic microbes produce disease of the skin?
- Penetrate epidermis due to trauma (cuts, scrapes, surgery, burns, bites, etc.) - Or if immune system compromised
231
What skin diseases does Staphylococcus aureus cause?
- Folliculitis - Scalded disease syndrome - Impetigo
232
What skin diseases does Streptococcus pyogenes cause?
- Erysipelas - Cellulitis - Necrotising fasciitis
233
Acne is caused by what bacteria?
Cutibacterium acnes
234
Cat scratch disease is caused by what bacteria?
Bartonella henselae
235
Pseudomonas infection is caused by what bacteria?
Pseudomona aeruginosa
236
Spotted fever rickettsiosis is caused by what bacteria?
Rickettsia rickettsii
237
Cutaneous anthrax is caused by what bacteria?
Bacillus anthracis
238
Gas gangrene is caused by what bacteria?
Clostridium perfringens
239
What are signs and symptoms of folliculitis?
- Infection of the hair follicle; becomes red, swollen, pus-filled (often called a pimple) - Called a sty when it occurs at the eyelid base - Spread of infection into surrounding tissues can produce a furuncle (boil); large, painful, raised nodular - Carbuncles occur when multiple furuncles grow together
240
Spread of folliculitis into surrounding tissues produces this.
Furuncle (large, painful, raised nodular)
241
_________ occur when multiple furuncles grow together.
Carbuncles
242
Folliculitis is most commonly caused by what bacteria (2 common species)? Describe their characteristics.
- Most commonly caused by Staphylococcus - 2 common species in skin are S. epidermidis and S. aureus (normal microflora than can become pathogenic) => Gram-positive; facultatively anaerobic; cocci typically arranged in clusters; tolerant of salt and desiccation
243
What are the virulence factors that S. aureus (involved in folliculitis) produces?
- Coagulase (blood clotting) - Hyaluronidase (breaks down HA in tissues) - Staphylokinase (dissolves blood clot) - Lipase (digests lipids; including sebum) - β-lactamase (resistance to penicillins) - Polysaccharide slime layer & Protein A (on cell surface); inhibits phagocytosis - Cytolytic toxins (disrupts cell membrane) - Leukocidin (kills leukocytes) - Epidermal cell differentiation inhibitor (disrupts lining of blood vessels) - Exfoliating / toxic shock syndrome toxins (in more virulent strains of S. aureus)
244
Staphylococcus epidermidis lacks ________________ and is rarely pathogenic.
Lacks virulence factors
245
Describe the pathogenesis of folliculitis.
- Staphylococcus transmitted via direct contact or by fomites - Infection can spread to hypodermis (furuncle), neighbouring hair follicles (carbuncle), into the blood (bacteremia), and other organs
246
Describe the epidemiology of folliculitis.
- S. epidermidis lacks virulence factors and is rarely pathogenic - S. aureus transiently colonizes the skin or mucous membranes of most people
247
Describe the diagnosis of folliculitis.
Isolation of Gram-positive bacteria in grape-like clusters from pus that can clot blood (diagnostic of S. aureus infection).
248
Describe the treatment for folliculitis.
- Treated with topical/oral semi-synthetic penicillin - Or vancomycin (for resistant strains)
249
What is the prevention for folliculitis?
Hand antisepsis; proper procedures in hospitals to minimize methicillin-resistant S. aureus (MRSA) infections.
250
What are the signs and symptoms of Staphylococcal scalded skin syndrome (SSSS)?
- Cells of the epidermis separate from one another and from the underlying tissue - Skin becomes red and wrinkled; forms blisters filled with clear liquid (NOT pus) - Outer epidermis peels off in sheets
251
Describe the pathogens/virulence factors involved in SSSS.
- Caused by some Staphylococcus aureus strains - 1 or 2 different exfoliative toxins; causes dissociation of epidermal desmosomes (intracellular bridge proteins that hold together cytoplasmic membranes of adjacent cells)
252
Intracellular bridge proteins that hold together cytoplasmic membranes of adjacent cells.
Desmosomes
253
Describe the pathogenesis of SSSS.
- Circulation of toxins in the blood produces toxemia - NO scarring (dermis is unaffected); epidermis is restored within 7-10 days after infection is resolved - Death is rare but most often due to 2ndary infections by Candida albicans or Pseudomona aeruginosa
254
Death by SSSS is rare but most often due to 2ndary infections by...?
- Candida albicans - Pseudomona aeruginosa
255
Describe the epidemiology of SSSS.
- Disease occurs primarily in infants and young children - Can affect elderly and immunocompromised patients - Transmitted by person-to-person spread of bacteria (need cut/tear in skin, etc.)
256
Describe the diagnosis, treatment, and prevention of SSSS.
- Diagnosis: by characteristic sloughing of skin - Treatment: intravenous semi-synthetic penicillin (oxacillin) - Prevention: difficult due to widespread presence of S. aureus
257
What are the signs and symptoms of impetigo (pyoderma)?
- Red patches form on the face and limbs - Patches develop into pus-filled vesicles - Vesicles break and form a crust that causes intense itching
258
What are the signs and symptoms of erysipelas?
- Impetigo infection spreads to the lymph nodes (triggering pain and inflammation) - Reddening occurs on the face, arms, or legs - Swollen local lymph nodes, pain, fever, chills, and leukocytosis (increased WBC counts)
259
Leukocytosis refers to...?
Increased WBC counts
260
What are the pathogens that cause impetigo and erysipelas?
- Staphylococcus aureus causes most cases (80%) of impetigo - Streptococcus pyogenes causes erysipelas and some cases (20%) of impetigo
261
Group A Streptococcus.
Streptococcus pyogenes
262
What are the virulence factors that Streptococcus pyogenes produces (to cause impetigo/erysipelas)?
- M protein (membrane protein that destabilizes complement system and interferes with phagocytosis) - Hyaluronic acid capsule (to hide from phagocytes) - Pyrogenic toxins (stimulates macrophages and T cells to release cytokines causing fever, rush, and shock)
263
Describe the pathogenesis of impetigo/erysipelas.
- The bacteria invade where the skin is compromised - Acute glomerulonephritis if infection spreads to kidneys
264
What can happen if impetigo/erysipelas infection spreads to kidneys?
Acute glomerulonephritis
265
Describe the epidemiology of impetigo/erysipelas.
- Impetigo occurs mostly in children - Erysipelas occurs in children and adults - Transmitted by person-to-person contact OR via fomites (toys, clothing, bedding, towels, or hairbrush)
266
Describe the diagnosis of impetigo/erysipelas.
- The presence of pus-filled vesicles (impetigo) - Gram-positive cocci in clusters (Staphylococcus) or chains (Streptococcus) in the pus
267
Describe treatment and prevention for impetigo/erysipelas.
- Treatment: impetigo is treated with topical mupirocin, oral clindamycins, or doxycycline (and careful cleaning of infected areas); erysipelas is treated with penicillin - Prevention: proper hygiene and cleanliness
268
Describe the signs and symptoms of necrotizing fasciitis.
- Heat, intense pain, swelling, and sunburn-like rash at the site of infection - Patients develop fever, nausea, malaise, and muscle ache - Infection can destroy soft tissues causing a drop in BP, possible mental confusion, and ultimately comatos
269
Describe the pathogens (and their virulence factors) that cause necrotizing fasciitis.
- Most cases caused by Streptococcus pyogenes (streptokinase & hyaluronidase facilitate invasion of tissues; exotoxin A & streptolysin S damage cells and tissues) - Some cases are caused by Staphylococcus aureus, Clostridium perfringens, and Bacterioides fragilis
270
Describe the pathogenesis of necrotizing fasciitis.
1. S. pyogenes is passed from person-to-person and enters the body through breaks in the skin; it spreads rapidly along muscle fascia 2. S. pyogenes secrete enzymes (streptokinases, hyaluronidase) that allow the bacterium to invade body tissues (and deoxyribonucleases: break down DNA = bacteria can spread) 3. Other virulence factors include M protein (help bacterium attach to nose/throat cells, and survive phagocytosis) 4. S. pyogenes also secretes toxins (streptolysin S, exotoxin A; triggers overactive immune response) that damage tissue
271
Describe the epidemiology of necrotizing fasciitis.
- Transmission from person-to-person through breaks in the skin - Can develop following surgery, abortion, and insect bite - Increased risk in diabetes, cancer, and chickenpox
272
Describe diagnosis and prevention of necrotizing fasciitis.
- Diagnosis: difficult because early symptoms are general and flu-like - Prevention: proper hygiene and cleanliness of wounds
273
Describe treatment of necrotizing fasciitis.
- Considered surgical emergency; treated by immediate removal of dead tissue and repeated until bacterial tissue destruction is halted - Intravenous broad-spectrum antimicrobials help curb severity of the disease
274
Acne is caused by bacterial infection of the ______________.
Hair follicles
275
Describe the development of acne.
1. Normal skin: oily sebum produced by glands reaches the hair follicle (discharged onto the skin surface via the pore) 2. Whitehead: when bacteria infect the hair follicle, the inflamed skin swells over the pore (causes accumulation of colonizing bacteria and sebum) 3. Blackhead: dead/dying bacteria and sebum form a blockage of the pore 4. Pustule formation: caused by severe inflammation of the hair follicle (rupture, causing cystic acne; often resolved by scar tissue formation)
276
Describe the pathogen that causes acne.
- Commonly caused by Cutibacterium acnes (Gram-positive, rod-shaped diphtheroids) - Commonly found on the skin
277
Describe the epidemiology of acne.
- Acne bacteria are normal members of the microbiome - Typically begins in adolescence but can occur later in life
278
Describe the diagnosis of acne.
Diagnosed by visual examination of the skin.
279
Describe the treatments for acne.
- Antimicrobial drugs - Topical benzoyl peroxide cause exfoliation of dead skin cells - Accutane is used for severe acne; inhibits formation of sebum (can cause intestinal bleeding and birth defects) - UV light is also used to destroy bacteria
280
Why is long-term use of Accutane not recommended?
Can cause intestinal bleeding and birth defects.
281
Describe the signs and symptoms of cat scratch disease.
- Fever, malaise - Localized swelling at infection site
282
Describe the pathogens/virulence factors involved in cat scratch disease.
- Caused by Bartonella henselae - Endotoxin (Lipid A of LPS) is the primary virulence factor
283
Describe the epidemiology of cat scratch disease.
- Transmitted by cat bites/scratches - Or by blood-sucking arthropods
284
Describe the diagnosis, treatment, and prevention of cat scratch disease.
- Diagnosis: serological test to detect Bartonella antigens - Treatment: antimicrobials (azithromycin) - Prevention: avoid or properly clean cat scratches/bites
285
Describe the signs and symptoms of Pseudomonas infection.
- Common opportunistic infection in burn victims - Blood infection causes fever, chills, and shock - Pyocyanin (blue-green bacterial pigment) in massive infections; causes discolouration
286
Describe the pathogen that causes Pseudomonas infection.
- Pseudomonas aeruginosa (Gram-negative bacillus) - Found in soil, decaying matter, moist environments, hospital surfaces
287
What are the virulence factors that Pseudomonas aeruginosa produces?
- Fimbriae, adhesins (adhesion; biofilm formation) - Capsule (inhibition of phagocytosis) - Neuraminidase, elastase (attachment; tissue breakdown) - Endotoxin (triggers fever, inflammation, blood clotting) - Exotoxin A, exoenzyme S (inhibition of protein synthesis; cell death) - Pyocyanin (tissue damage via formation of reactive oxygen species)
288
Describe the pathogenesis of Pseudomonas infection.
- P. aeruginosa is an opportunistic pathogen (cannot penetrate intact tissues and cells) - Infection can occur in burn victims; bacteria grow under the surface of the burn, kill cells, destroy tissue, and trigger shock
289
Describe the epidemiology of Pseudomonas infection.
P. aeruginosa is an inhabitant of water and soil; can infect almost any organ or system once in the body.
290
Describe the diagnosis of Pseudomonas infection.
- Diagnosis can be difficult - Pyocyanin discolouration indicates massive infection
291
Describe treatments and prevention of Pseudomonas infection.
- Treatment: difficult because of multi-drug resistance; combination of antimicrobials and debridement of burns - Prevention: impossible to prevent exposure (P. aeruginosa is widespread)
292
What is the most severe form of spotted fever rickettsiosis?
- Rocky Mountain spotted fever - Transmitted via hard ticks
293
Describe the signs and symptoms of spotted fever rickettsiosis.
- Non-itchy spotted rash on trunk and appendages - Patients experience fever, chills, headache, muscle pain, nausea, and vomitting - Organ failure can occur in severe cases
294
Describe the pathogen that causes spotted fever rickettsiosis.
- Caused by Rickettsia rickettsii - Gram-negative, obligate intracellular pathogens (don't use glucose; oxidize AA and Krebs cycle intermediate) - Does NOT secrete any toxins (infect endothelial cells and cause damage to blood vessels)
295
Describe the pathogenesis of spotted fever rickettsiosis.
1. Infected introduces R. rickettsii by feeding on blood for at least 6 hours 2. R. rickettsii triggers endocytosis by cells lining blood vessels (endothelium); then it lyses the endosome's membrane (now in cytosol) 3. R. rickettsii divide every 8-12 hours in the cytosol; daughters escape from long cytoplasmic extensions and infect adjacent endothelial cells 4. Damage to the endothelial cells leads to leakage of blood into the tissues (results in low BP and insufficient nutrient/O2 delivery to organs)
296
Describe the epidemiology of spotted fever rickettsiosis.
- Transmitted via bite of infected hard tick (Dermacentor) - Male ticks infect female ticks during mating; female ticks trasmit bacteria to eggs forming in their ovaries - Hard ticks can survive without feeding for several years, making tick elimination in the wild problematic
297
Transmitted via bite of infected hard tick (Dermacentor).
Spotted fever rickettsiosis
298
Describe the diagnosis, treatment, and prevention of spotted fever rickettsiosis.
- Diagnosis: serological test for bacterial antigens OR detection of bacterial nucleic acid in lesion specimens - Treatment: antimicrobials (doxycycline for adults; chloramphenicol for children & pregnant women) - Prevention: use of tick repellents and avoidance of tick-infested areas
299
Describe the signs and symptoms of cutaneous anthrax.
- Localized itching - Develop into painless black lesions (eschar) within 7-10 days
300
Associated with painless black lesions (eschars).
Cutaneous anthrax
301
Describe the pathogens/virulence factors involved in cutaneous anthrax.
- Caused by Bacillus anthracis; Gram-positive endospore-forming bacilli - Virulence factors include capsule, anthrax toxins, and endospore
302
Describe the pathogenesis and epidemiology of cutaneous anthrax.
- Direct contact of endospores with wounded skin, infected animals (zoonotic disease), or contaminated animal products - Animal handlers (e.g., farmers) are susceptible
303
Describe the diagnosis, treatment, and prevention of cutaneous anthrax.
- Diagnosis: appearance (black lesions) is diagnostic - Treatment: antimicrobials (doxycycline or ciprofloxacin) - Prevention: livestock vaccination
304
How does gas gangrene come to be?
- Interruption of blood supply to tissue by a wound causes ischemia and necrosis of tissues - Creates condition of growth for anaerobic spore-forming bacteria
305
Describe the signs and symptoms of gas gangrene.
- Death of muscle and connective tissue - Blackening of infected muscle and skin - Presence of gas bubbles - Shock, kidney failure, and death can occur quickly
306
Describe the pathogens (and their virulence factors) that cause gas gangrene.
- Caused by several Clostridium species (mostly C. perfringens) - Gram-negative endospore-forming bacilli - Bacteria endospores survive harsh conditions - Vegetative bacterial cells secrete 11 toxins that lyse RBCs/WBCs, increase vascular permeability, and kill cells
307
Describe the pathogenesis and epidemiology of gas gangrene.
- Clostridium does not affect healthy tissue and is not invasive - Traumatic event (surgery, puncture wounds, gunshot wound, crushing trauma, etc.) must introduce endospores into dead tissue - Despite therapeutic care, morality rate exceeds 40%
308
Describe diagnosis and prevention of gas gangrene.
- Diagnosis: appearance is usually diagnostic - Prevention: proper cleaning of wounds
309
Describe treatment for gas gangrene.
- Rapid treatment is crucial; considered a medical emergency - Surgical removal of dead tissue - Administration of antitoxin and antimicrobials (intravenous penicillin and clindamycin) - Application of oxygen under pressure
310
What are some types of Poxviruses?
- Smallpox - Cowpox - Monkeypox
311
Various types of skin lesions are caused by what virus?
Herpesvirus
312
Chickenpox and Shingles is caused by what virus?
Varicella-zoster virus (VZV)
313
Warts are caused by what virus?
Papillomavirus
314
German measles (Rubella) is caused by what virus?
Rubivirus
315
Measles (Rubeola) is caused by what virus?
Morbillivirus
316
What Poxviruses cause human diseases?
- Smallpox - Orf - Cowpox - Monkeypox (rare in humans)
317
The first human disease to be eradicated by vaccination.
Smallpox
318
Describe the series of stages Poxvirus diseases progress through (i.e. signs and symptoms).
1. Macule (flat macules on and just below the epidermis) 2. Papule (lesions become raised sores) 3. Vesicle (lesion fills with fluid) 4. Pustule (pus forms in the lesion) 5. Crust (a dry layer forms on the epidermis) 6. Scar
319
Poxviruses are _____ (DNA/RNA) viruses.
DNA viruses
320
Poxviruses produce various ___________ that interfere with the immune response.
Proteins
321
What specific type of Poxvirus causes smallpox?
- Orthopoxvirus (variola virus) - Only infects human cells
322
Describe the pathogenesis of Poxviruses.
- Smallpox occurs by inhalation of virus (virus spread from the respiratory tract throughout the body) - Other Poxviruses are spread by direct contact
323
What are the 2 different smallpox strains?
1. Variola major 2. Variola minor (less lethal)
324
Describe the epidemiology of Poxviruses.
- Smallpox has been eradicated; but variola virus stocks maintained in US and Russian labs for research - Monkeypox cases have increased over the past decade
325
Describe the treatment and prevention of Poxviruses.
- Treatment requires immediate vaccination - Vaccination program discontinued in 1970s following disease eradication - Some military and health care personnel are vaccinated
326
Describe the signs and symptoms of Herpes infections.
- Slow-spreading skin lesions (can be painful and itchy) - Infections can occur at various body sites (oral cavity, fingers, skin, etc.) - Recurrence of lesions is common
327
Herpetic gingivostomatitis occurs in the ___________.
Oral cavity
328
What type of Herpes occurs on an infected finger?
Whitlow
329
Herpes that can occur anywhere on the skin.
Herpes gladiatorium
330
Describe the pathogens/virulence factors involved in Herpes infection.
- Caused by human Herpeviruses 1 and 2 - Both virus species can cause lesions at multiple locations - Produce various proteins that act as virulence factors
331
Compare/differentiate between Herpesvirus (HHV) 1 and 2.
- HHV-1 = 90% of cold sores/fever blisters (whitlow); HHV-2 = 85% of genital herpes cases, 10% of oral herpes cases, 70% of neonatal herpes cases - HHV-1 transmitted through close contact; HHV-2 through sexual intercourse - HHV-1 latent in trigeminal/brachial ganglia; HHV-2 latent in sacral ganglia - HHV-1 lesions on face, mouth (and rarely trunk); HHV-2 lesions on external genitalia (and less commonly: thighs, buttocks, anus)
332
Describe the pathogenesis of Herpes infections.
- Viruses may remain inactive inside infected cells for years - Painful lesions caused by inflammation and cell death - Fusion of infected cells forms syncytia
333
Fusion of infected cells forms ___________.
Syncytia (this is in relation to Herpes infection)
334
Describe the epidemiology of Herpes infections.
- Spread between mucous membranes of mouth and genital - Herpes infections in adults are not life threatening - Neonatal infections can be fatal
335
Describe the diagnosis, treatment, and prevention of Herpes infections.
- Diagnosis: made by presence of characteristic lesions; immunoassay reveals presence of viral antigens - Treatment: chemotherapeutic drugs control the disease, but do NOT cure it - Prevention: healthcare workers can wear gloves to limit exposure
336
Describe the signs and symptoms of warts.
- Benign epithelial growths on the skin or mucous membranes - Can form on many body surfaces
337
Describe the pathogens/virulence factors involved in warts.
- Various Papillomaviruses cause warts - Some strains trigger oncogenes in host chromosome
338
Describe the pathogenesis of warts (Papillomavirus).
- Warts develop several months after infection - Most warts are harmless - Papillomaviruses may precipitate some cancers
339
Describe the pathogenesis/epidemiology of warts (Papillomavirus).
1. Papillomavirus is transmitted via direct contact OR from contaminated fomites 2. Virus multiplies within cells 3. Virus invades adjacent cells 4. Rapid growth of virus-infected cells creates wart 5. Virus is shed when dead skin cells are sloughed off
340
Describe the diagnosis, treatment, and prevention of warts.
- Diagnosis: by observation - Treatment/prevention: various techniques to remove warts (new warts can develop as a result of latent viruses), vaccine available to prevent genital warts
341
Describe the signs and symptoms of chickenpox.
- Highly contagious infectious disease caused by Varicella-zoster virus (VZV) - Characterized by lesions on the back and trunk that spreads across body - VZV becomes latent within sensory nerves
342
Describe the signs and symptoms of shingles.
- Occurs following reactivation of VZV (e.g., after infected with chickenpox) - Lesions are localized to skin along an infected nerve - Pain may last after lesions have healed
343
Describe the pathogenesis of chickenpox/shingles.
1. Inhalation of Varicella-zoster virus (VZV) 2. Infected cells replicate and release virus into the blood (viremia) and lymph 3. VZVs infect liver, spleen, and lymph nodes throughout body 4. 2nd viremia spreads VZVs to skin, causing extensive rash 5. VZVs shed through respiratory droplets and fluid from skin lesions 6. Immune system eliminates VZVs from blood and most cells 7. Some VZVs become latent/dormant in nerve ganglia 8. Upon reactivation, VZVs travel inside nerve cells, down the nerve, to infect skin cells 9. Rash develops in the band of skin innervated by the infected nerve
344
Describe the epidemiology of chickenpox/shingles.
- Chickenpox occurs mostly in children; VZV infected 90% of children prior to immunization - Disease is more severe in adults - Only 15-20% of people who have had chickenpox develop shingles; risk of shingles increases with age
345
Describe the diagnosis, treatment, and prevention of chickenpox/shingles.
- Diagnosis: based on characteristic lesions - Treatment/prevention: treatment based of relief of symptoms; vaccines available
346
Describe the signs and symptoms of Rubella (German measles).
- Children develop a mild rash - Adults may develop arthritis and encephalitis - Congenital infection can result in birth defects or death of fetus
347
Describe the pathogenesis of Rubella.
- Caused by Rubivirus - Infection spreads from the respiratory tract throughout the body via the blood - The immune response to infected cells contributes to disease severity in adults
348
Describe the epidemiology of Rubella.
- Spread by respiratory secretions - Infects only humans
349
Describe the diagnosis, treatment, and prevention of Rubella.
- Diagnosis: by observation of rash and serological testing - NO treatment available - Prevention: vaccine is available (aimed at preventing Rubella infections in pregnant women)
350
Describe the signs and symptoms of Measles (Rubeola).
- Characterized by Koplik's spots (oral lesions of measles) - Numerous red lesions appear on the head and body - Sub-acute sclerosing panencephalitis is rare but deadly complication that can develop years after initial infection
351
Describe the pathogens/virulence factors involved in Measles.
- Caused by Morbillivirus - Adhesion and fusion proteins help virus avoid immune recognition
352
Describe the pathogenesis of Measles.
- Immune response to infection causes most symptoms - Disease can be fatal in children
353
Describe the epidemiology of Measles.
- Highly contagious and spread via respiratory droplets - Humans are the only host
354
Describe the diagnosis, treatment, and prevention of Measles (Rubeola).
- Diagnosis: based on signs of measles and confirmed with serological testing - Treatment: involves administration of vitamin A, antibodies against virus, and ribavirin - Prevention: MMR vaccine protects against measles
355
Describe Erythema infectiosum (type of viral rash).
- Also referred to as "fifth disease" - Caused by B19 virus - Respiratory disease that manifests as a rash - Adults may also develop anemia and joint pain
356
Erythema infectiosum is caused by what virus?
B19 virus
357
Also referred to as "fifth disease."
Erythema infectiosum
358
Describe Roseola (type of viral rash).
- Endemic disease of children - Caused by human Herpesvirus 6 (HHV-6) - Characterized by rose-coloured rash
359
Roseola is caused by what virus?
Herpesvirus 6 (HHV-6)
360
Describe the different location classifications of Mycoses (fungal diseases).
- Superficial = occur on the outer surfaces - Cutaneous (dermatophytoses) = occur in the skin - Subcutaneous = occur in the hypodermis and muscles - Systemic = affect numerous systems
361
Most common fungal infection affecting the hair, nails, and outer skin layers.
Superficial mycoses
362
What fungi causes superficial mycoses of the skin?
Malassezia furfur (normal inhabitant of human skin)
363
Describe signs/symptoms of superficial mycoses of the skin.
- Hypo- hyper-pigmented patches of scaly skin - Caused by Malassezia furfur (normal inhabitant of human skin)
364
Describe the pathogenesis and epidemiology of superficial mycoses of the skin.
- Fungi is non-invasive and produce keratinase (dissolves keratin) - Fungi are often transmitted via shared hairbrush and combs - Disease occurs most often in adolescents
365
Describe the diagnosis, and treatment of superficial mycoses of the skin.
- Diagnosis: infected skin is pale under UV light; definitive diagnosis requires microscopic examination - Treatment: topical or oral drugs
366
Describe characteristics of dermatophytoses (cutaneous mycoses).
- Cutaneous lesions caused by some fungi that grow in the skin - Caused by dermatophytes (Trichophyton, Microsporum, Epidermophyton floccosum) - Cell-mediated immune responses damage deeper tissues - Include Ringworm and Athlete's foot
367
What 3 fungi genera cause dermatophytoses (e.g., Ringworm, Athlete's foot)?
1. Trichophyton 2. Microsporum 3. Epidermophyton floccosum
368
Describe the pathogenesis of dermatophytoses.
- Fungi colonize skin, nails, and hair (use keratin as nutrient source) - Infection is rare (fungi must invade living layers of skin)
369
Describe the epidemiology of dermatophytes.
- Dermatophytes are among the few contagious fungi - Classified by natural habitat (anthropophilic, zoophilic, geophilic dermatophytes)
370
Describe the diagnosis and treatment of dermatophytoses.
- Diagnosis: by clinical observation; KOH preparation of skin/nail samples confirms diagnosis - Treatment: limited infections treated with topical agents; widespread ones treated with oral drugs
371
Describe wound mycoses.
- Some fungi grow in deep tissues but do NOT become systemic - Fungi eventually grow into the epidermis to produce skin lesions
372
What are the types of wound mycoses?
- Chromoblastomyocosis - Phaehyphomycosis - Mycetomas - Sporotrichosis
373
Caused by 4 species of ascomycete fungi.
Chromoblastomycosis
374
Describe chromoblastomycosis (type of wound mycoses).
- Caused by 4 species of ascomycete fungi - People who work barefoot in soil are at risk - Signs/symptoms: painless lesions that progressively worsen - Diagnosis: presence of golden brown bodies in skin sample - Treatment: requires removal of infected tissues and administration of anti-fungal drugs
375
Describe phaehyphomycosis (type of wound mycoses).
- Caused by over 30 genera of fungi - Acquired when spores enter wounds - Disease is variable in presentation (depends on site of fungal colonization); permanently destructive to tissues - Diagnosis: observation of hyphae in skin sample, biopsy material, or cerebrospinal fluid - Treatment: anti-fungal agents like Itraconazole (ITZ inhibits synthesis of ergosterol)
376
Describe mycetomas (type of wound mycoses).
- Caused by several genera of soil fungi (people who work barefoot in soil most at risk; pricks and scrapes introduce fungi) - Signs/symptoms: tumour-like lesions form on skin, fascia, and bones - Epidemiology: infections are prevalent in countries near the equator - Diagnosis: based on symptoms and presence of fungi in clinical samples - Treatment: involves surgical removal of mycetoma and anti-fungal therapy
377
Caused by Sporothrix schenckii (resides in the soil).
Sporotrichosis
378
Describe sporotrichosis (type of wound mycoses).
- Caused by soil fungi Sporothrix schenckii (occurs most often in gardeners/farmers; pricks and splinters introduce fungi) - Subcutaneous infection usually limited to arms/legs - Fixed sporotrichosis remains localized - Lymphocutaneous sporotrichosis occurs when the fungus enters the lymphatic system
379
Describe the diagnosis, treatment, and prevention of wound mycoses.
- Diagnosis: based on patient's history, clinical signs, and observation of fungi in clinical samples - Treatment: cutaneous lesions are treated with anti-fungal drugs - Prevention: requires wearing proper attire to avoid inoculation of the fungus
380
What 2 diseases are parasitic infestations of the skin?
1. Leishmaniasis 2. Scabies
381
What pathogen causes Leishmaniasis?
Leishmania (protozoan transmitted via female sand flies)
382
Protozoan transmitted via female sand flies.
Leishmania
383
Describe the signs and symptoms of the types of Leishmaniasis.
- Cutaneous = large, painless skin lesions - Mucocutaneous = skin lesions enlarge to encompass mucous membranes - Visceral = spread by infected macrophages throughout the body
384
Describe the pathogenesis and epidemiology of Leishmaniasis.
- Infected macrophages stimulate inflammatory responses - Leishmaniasis is endemic in parts of the tropic and subtropics
385
Describe the diagnosis, treatment, and prevention of Leishmaniasis.
- Diagnosis: by microscopic identification of the protozoa - Treatment: most cases heal without treatment, but antimicrobials are needed for severe infections - Prevention: reducing exposure to the reservoir host
386
Describe the signs and symptoms of Scabies.
- Characterized by intense itching and rash at infection site - Lesions common between the fingers; around the genitalia; and on the wrists, elbows, knees
387
Describe the pathogenesis and epidemiology of Scabies.
- Caused by Sarcoptes scabiei (mite); inflammation and damage to nerve endings occur as the mites burrow - Itching blisters occur where female mites lay eggs - Mites transmitted via prolonged body contact
388
Describe the diagnosis and treatment of Scabies.
- Diagnosis: made by observing mites, eggs, or fecal matter in the skin samples (or the characteristic burrows) - Treatment: mite-killing lotions
389
Respiratory system ________________ between the atmosphere and the blood.
Exchanges gases
390
Describe the 2 main parts of the respiratory system.
- Upper respiratory system (nasal cavity, pharynx): colonized by many microorganisms; normal microbiome limits growth of pathogens; normal microbiome may become opportunistic pathogens - Lower respiratory system (larynx, trachea, bronchi, diaphragm): microorganisms are NOT typically present
391
What are the respiratory system barriers to infection?
- Tonsils (groups of lymphoid tissue); immune cells; chemical defences - Mucus contains various antimicrobial chemicals - Phagocytic alveolar macrophages - Normal microbiota
392
What type of viruses cause the common cold?
Enteroviruses (Rhinoviruses)
393
What bacteria causes Diphtheria?
Corynebacterium diphtheriae
394
What are some infectious diseases of the upper respiratory tract, sinuses, and ears?
- Streptococcal respiratory diseases - Diphtheria - Rhinosinusitis - Otitis media - Common cold
395
Describe the signs and symptoms of the various Streptococcal respiratory diseases.
- Pharyngitis: sore throat and difficulty swallowing (pus pockets on tonsils); often accompanied by fever, malaise, headache - Laryngitis/bronchitis can occur if infection spreads to lower respiratory tract - Complications in some cases include scarlet fever (skin rush); rheumatic fever (inflammatory disease of the heart, joints, skin, and brain); acute glomerulonephritis (kidney inflammation)
396
Describe the pathogens/virulence factors involved in Streptococcal respiratory diseases.
- Caused by group A streptococci (Streptococcus pyogenes) - Variety of virulence factors: M protein, hyaluronic acid capsule, streptokinase, C5a peptidase, streptolysin O
397
Describe the pathogenesis of Streptococcal respiratory diseases.
- Disease depends on the virulence factors present - Occurs when normal microbiota are depleted, large inoculum is introduced, or adaptive immunity is impaired
398
Describe the epidemiology of Streptococcal respiratory diseases.
- Spread via respiratory droplets - Occurs most often in winter and spring
399
Describe the diagnosis and treatment of Streptococcal respiratory diseases.
- Diagnosis: often confused with viral pharyngitis - Treatment: oral penicillin
400
Describe the signs and symptoms of Diphtheria.
- Sore throat, localized pain, and fever - Presence of a pseudomembrane that can obstruct airways
401
Describe the pathogens/virulence factors involved in Diphtheria.
- Caused by Corynebacterium diphtheriae (ubiquitous in animals and humans) - Diphtheria toxin: inhibits mRNA transcription and protein synthesis, causing cell death
402
Describe how the diphtheria toxin works.
1. B subunit of diphtheria toxin attaches to human growth factor receptor 2. This triggers endocytosis 3. Subunit A is released from endocytic vesicle 4. Subunit A destroys elongation factor, preventing mRNA transcription in the nucleus of the human cell
403
Describe the pathogenesis and epidemiology of Diphtheria.
- Spread via respiratory droplets or skin contact - Symptomatic in immunocompromised or non-immune individuals - Leading cause of death among un-immunized children
404
Leading cause of death among un-immunized children.
Diphtheria
405
Describe the diagnosis, treatment, and prevention of Diphtheria.
- Diagnosis: based on presence of pseudomembrane and a positive Elek test (detects diphtheria toxin from patient samples) - Treatment: antitoxin (passive immunization) and antibiotics - Prevention: DTaP vaccine
406
Describe the signs and symptoms of Rhinosinusitis & Otitis Media.
- Malaise, headache, and inflamed nasal passages - Otitis Media results in severe pain in the ears
407
Describe the pathogens involved in Rhinosinusitis & Otitis Media.
- Caused by various respiratory microbiota - May be due to damage to upper respiratory system and auditory tube
408
Describe the pathogenesis and epidemiology of Rhinosinusitis & Otitis Media.
- Microbes in the pharynx spread to the sinuses via the throat - Middle ear is infected via the auditory tubes - Rhinosinusitis is more common in adults; Otitis Media is more common in children
409
Describe the diagnosis, treatment, and prevention of Rhinosinusitis & Otitis Media.
- Diagnosis: symptoms are often diagnostic - Treatment: antimicrobials; nasal flushing (can reduce duration of symptoms) - Prevention: NO known way to prevent Rhinosinusitis
410
Describe the signs and symptoms of the common cold.
- Sneezing, runny nose, congestion, sore throat, malaise, and cough
411
Describe the pathogens/virulence factors involved in the common cold.
- Enteroviruses (rhinoviruses) = most common cause; non-enveloped +ssRNA viruses - Numerous other viruses cause colds
412
Describe the pathogenesis of the common cold.
- Lower temperature of the nasal cavity promotes infection of cells and replication of cold virus - Cold viruses replicate in and kill infected cells
413
Describe the epidemiology of the common cold.
- Rhinoviruses are highly infective - Spread by coughing/sneezing, fomites, or person-to-person contact - Develop some immunity to serotypes over time
414
Describe the diagnosis, treatment, and prevention of the common cold.
- Diagnosis: signs and symptoms are usually diagnostic - Treatment: Pleconaril (antiviral drug) can reduce duration of symptoms and prevents acute asthma exacerbations - Prevention: hand antisepsis
415
What are some bacterial diseases of the lower respiratory system?
- Bacterial pneumonia - Legionnaire's disease - Tuberculosis - Whooping cough (pertussis) - Inhalation anthrax
416
What are some viral diseases of the lower respiratory system?
- Influenza - Coronavirus respiratory syndrome - Respiratory syncytial virus (RSV) infections
417
What are some mycoses (fungal diseases) of the lower respiratory system?
- Coccidioidomycosis - Blastomycosis - Histoplasmosis - Pneumocystis pneumonia
418
What bacteria can cause pneumonia?
- Streptococcus pneumoniae - Mycoplasma pneumoniae - Klebsiella pneumoniae
419
What bacteria causes Legionnaire's disease?
Legionella pneumophila
420
What bacteria causes tuberculosis?
Mycobacterium tuberculosis
421
What bacteria causes whooping cough (pertussis)?
Bordetella pertussis
422
What bacteria causes inhalation anthrax?
Bacillus anthracis
423
The most serious and most frequent disease in adults.
Bacterial pneumonias
424
Describe bacterial pneumonias.
- Lung inflammation accompanied by fluid-filled alveoli and bronchioles - Empyema (presence of pus) - Described by affected regions or organism causing the disease (lobar/pneumococcal, atypical/mycoplasmal, healthcare-associated)
425
The presence of pus.
Empyema
426
What are the types of pneumonia?
- Lobar or pneumococcal pneumonia - Atypical or mycoplasmal pneumonia - Healthcare-associated pneumonia
427
Describe the signs and symptoms of lobar/pneumococcal pneumonia.
- Fever, chills, congestion cough, and chest pain; resulting in short, rapid breathing - Blood enters the lungs, causing rust-coloured sputum
428
Describe the pathogens/virulence factors involved in lobar/pneumococcal pneumonia.
- Caused by Streptococcus pneumoniae (Gram-positive diplococci) - Virulence factors: adhesins, capsule, pneumolysin, secretory IgA protease
429
Describe the pathogenesis and epidemiology of lobar/pneumococcal pneumonia.
- Inhalation of bacteria causes infection; bacterial replication causes damage to the lungs - Pneumococcal secretory IgA protease destroys host secretory IgA (on surface of mucosal membranes) - Accounts for most cases of bacterial pneumonia
430
Accounts for most cases of bacterial pneumonia.
Lobar/pneumococcal pneumonia (Streptococcus pneumoniae)
431
Describe the diagnosis, treatment, and prevention of lobar/pneumococcal pneumonia.
- Diagnosis: identifying diplococci in sputum smears - Treatment: penicillin (some strains are now resistant) - Prevention: vaccination
432
Describe the signs and symptoms of primary atypical (mycoplasma) pneumonia.
- Fever, malaise, sore throat, and excessive sweating - Symptoms may last for weeks
433
Describe the pathogens/virulence factors involved in primary atypical pneumonia.
- Caused by Mycoplasma pneumoniae - Virulence factors include an adhesion protein
434
Describe the pathogenesis of primary atypical pneumonia.
- Bacteria colonize and kill epithelial cells - Mucus buildup and colonization by other bacteria
435
Describe the epidemiology of primary atypical pneumonia.
- Bacteria spread by nasal secretions - Most common pneumonia in teenagers and young adults
436
Most common pneumonia in teenagers and young adults.
Primary atypical (mycoplasma) pneumonia
437
Describe the diagnosis, treatment, and prevention of primary atypical pneumonia.
- Diagnosis: difficult to diagnose - Treatment: erythromycin or doxycyline - Prevention: difficult since infected individuals may be asymtomatic
438
Healthcare-associated pneumonia.
Klebsiella pneumonia
439
Describe the signs and symptoms of Klebsiella pneumonia.
- Bloody sputum - Chills
440
Describe the pathogens/virulence factors involved in Klebsiella pneumonia.
- Caused by Klebsiella pneumoniae - Virulence factors include a capsule - Immunocompromised patients at greater risk for infection (healthcare-associated pneumonia)
441
Describe the diagnosis, treatment, and prevention of Klebsiella pneumonia.
- Diagnosis: identifying Klebsiella in sputum samples - Treatment: antimicrobials - Prevention: good aseptic technique by healthcare workers
442
Can cause disease similar to pneumococcal pneumonia.
- Haemophilus influenzae - Staphylococcus aureus
443
Causes pneumonic plague.
Yersinia pestis
444
Causes psittacosis.
Chlamoydophila psittaci
445
What diseases does Chlamoydophila pneumoniae cause?
- Pneumonia - Bronchitis - Rhinosinusitis
446
Describe Legionnaire's disease.
- Typical pneumonia symptoms; pulmonary function can rapidly decrease - Most cases caused by Legionella pneumophila
447
Describe the pathogenesis of Legionnaire's disease.
- Legionella pneumophila lives in and kills human cells (intracellular pathogen) - Causes tissue damage and inflammation
448
Describe the epidemiology of Legionnaire's disease.
- Legionella survives in domestic water sources - The elderly, smokers, and immunocompromised individuals are at increased risk
449
Describe the diagnosis, treatment, and prevention of Legionnaire's disease.
- Diagnosis: fluorescent antibody staining or serology - Treatment: quinolones or macrolides - Prevention: controlled by reducing bacterial presence in water
450
Causes blue-colour colonies when grown on buffered charcoal yeast extract agar.
Legionella pneumophila
451
The leading disease killer in the world.
Tuberculosis (but incidence has declined in the industrialized world)
452
Describe the signs and symptoms of tuberculosis.
- Not always apparent - Initially limited to minor cough and mild fever
453
Describe the pathogen involved in tuberculosis.
- Mycobacterium tuberculosis - Presence of mycolic acid gives unique features: slow growth, protection from phagocytic lysis, intracellular growth (e.g., in macrophages), resistance to many antimicrobial drugs
454
Describe the pathogenesis of tuberculosis.
- Spread via inhalation of respiratory droplets - 3 types of tuberculosis: primary, secondary, disseminated
455
What are the 3 types of tuberculosis?
1. Primary 2. Secondary (re-activation) 3. Disseminated (spread to other parts of body)
456
What are tubercles?
Tightly packed macrophages surrounding the site of infection (by Mycobacterium tuberculosis).
457
Describe primary tuberculosis.
1. Mycobacterium infects respiratory tract (via inhalation of respiratory droplets from infected individuals) 2. Alveolar macrophages phagocytize mycobacteria (but bacterium inhibits fusion of lysosomes to endocytic vesicles) 3. Bacteria replicate freely within macrophages, gradually killing them; get released and phagocytized by other macrophages 4. Infected macrophages present antigen to T cells, which produce lymphokines that attract and activate more macrophages (form tubercles over 2/3 months: tightly packed macrophages surrounding site of infection) 5. Other cells deposit collagen fibers, which enclose the tubercles; infected cells in the center die (produces caseous necrosis) 6. A "stalemate" between the bacterium and the body's defenses develops
458
Describe secondary tuberculosis.
- Results when M. tuberculosis breaks the "stalemate" = ruptures tubercle and re-establishes an active infection - Re-activation occurs in about 10% of patients (with weakened immune systems)
459
Secondary tuberculosis occurs in about __% of patients.
10%
460
Describe disseminated tuberculosis.
Results when macrophages carry the pathogen via blood and lymph nodes to other sites of the body.
461
Describe the epidemiology of tuberculosis.
- 1/3rd of the world's population is infected - Most deaths occur in Asia and Africa
462
Describe the diagnosis, treatment, and prevention of tuberculosis.
- Diagnosis: tuberculin skin test (doesn't tell if active or not, just presence); chest X-ray (identify tubercles in the lungs) - Treatment: requires combination of drugs (there are drug resistant strains of M. tuberculosis) - Prevention: BCG vaccine available where tuberculosis is common
463
Describe the signs and symptoms of whooping cough (pertussis).
- Initially cold-like, then characteristic cough develops - Poor oxygen exchange may produce cyanosis (blue tint to skin)
464
Describe the pathogens/virulence factors involved in whooping cough.
- Caused by Bordetella pertussis - Produces numerous virulence factors (e.g., adhesins and several toxins)
465
Describe the pathogenesis of whooping cough.
- Pertussis progresses through 4 phases (incubation; catarrhal; paroxysmal; convalescent)
466
Describe the 4 phases of whooping cough.
1. Incubation (no symptoms; ~1 week) 2. Catarrhal (rhinorrhea, sneezing, malaise fever; highest titer of bacteria; ~2 weeks) 3. Paroxysmal (repetitive cough with whoops, vomiting, exhaustion; immune system highly active) 4. Convalescent (diminishing cough, possibly 2ndary complications)
467
Describe the epidemiology of whooping cough.
- Highly contagious; bacteria spread through airborne droplets (don't survive long outside the body) - Considered a re-emerging disease
468
Describe the diagnosis, treatment, and prevention of whooping cough.
- Diagnosis: symptoms are usually diagnostic - Treatment: primarily supportive - Prevention: DTaP vaccine
469
Describe the signs and symptoms of inhalation anthrax.
- Initially resembles a cold or flu - Progresses to severe coughing, lethargy, shock, and death
470
Describe the pathogens/virulence factors involved in inhalation anthrax.
- Caused by Bacillus anthracis (Gram-positive endospore-forming bacilli) - Virulence factors include a capsule and anthrax toxin
471
Describe the pathogenesis and epidemiology of inhalation anthrax.
- Anthrax NOT spread from person-to-person - Acquired by contact or inhalation of endospores
472
Describe the diagnosis, treatment, and prevention of inhalation anthrax.
- Diagnosis: based on identification of bacteria in sputum - Treatment: early and aggressive antimicrobial treatment is necessary - Prevention: anthrax vaccine is available to selected individuals
473
Describe the signs and symptoms of influenza.
- Pharyngitis, congestion, cough, and myalgia (muscle ache) - Sudden fever distinguishes flu from a common cold
474
Describe the pathogens/virulence factors involved in influenza.
- Caused by type A/B influenza virus; enveloped with segmented -ssRNA genome - Mutations in hemagglutinin and neuraminidase produce new strains; occurs via antigenic drift and shift - Concerns about appearance of new highly virulent strains
475
Mutations in genes coding for what proteins lead to new strains of influenza?
- Hemagglutinin - Neuraminidase
476
Describe antigenic drift.
1. Influenzavirus enters host cell 2. Mutations in antigen genes occur during viral replication 3. New strain of influenzavirus (differing slightly from original virus) exits the cell
477
Describe antigenic shift.
1. 2 different strains of influenza A viruses enter the same host cell 2. Genes and antigens from both viral types are incorporated (combined) into new virions 3. A new influenzavirus (can be very different from the original 2 viruses) exits the cell
478
Antigenic shift by influenza A virus occurs about __________________.
Once a decade
479
Influenza ___ virus does NOT undergo antigenic shift.
Influenza B
480
Describe the pathogenesis of influenza.
- Virus causes damage to the lung epithelium - Flu patients are susceptible to 2ndary bacterial infections
481
Describe the epidemiology of influenza.
- Infection provides some immunological protection from similar strains - Concern that changes in type A influenza viruses may cause another major pandemic
482
Describe the diagnosis, treatment, and prevention of influenza.
- Diagnosis: signs/symptoms during a community-wide outbreak are often diagnostic - Treatment: supportive care to relieve symptoms; antiviral drugs (oseltamivir & zanamivir) can be administered early in infection - Prevention: multivalent vaccine
483
What are some types of coronavirus respiratory syndromes?
- Severe acute respiratory syndrome (SARS) - Middle East respiratory syndrome (MERS) - Coronavirus disease 2019 (COVID-19)
484
Describe the signs and symptoms of coronavirus respiratory syndromes.
- High fever, shortness of breath, and difficulty breathing - Later, patients develop dry cough and pneumonia
485
Describe the pathogens involved in coronavirus respiratory syndromes.
- Coronaviruses; SARS- and MERS-associated, and SARS-CoV2 (enveloped +ssRNA viruses) - Most diseases are usually mild - SARS and MERS have higher fatalities
486
Describe the pathogenesis and epidemiology of coronaviruses.
- Coronaviruses spread via respiratory droplets - Virus spreads from the lungs to the heart/kidneys
487
Describe the diagnosis of coronaviruses.
- Based on signs/symptoms - Confirmed by detection of viral nucleic acids, isolating the virus, or detection of antibodies against the virus
488
Describe the treatment/prevention of coronaviruses.
- Treatment is supportive - Vaccine against MERS is available for young camels - Vaccines against COVID-19 available for humans
489
Most common childhood respiratory disease.
Respiratory Syncytial Virus (RSV) infection
490
Describe the the signs and symptoms of respiratory syncytial virus (RSV) infection.
- Leading cause of bronchiolitis, a major cause of pneumonia among children < 5 y/o - Fever, runny nose, cough in babies or immunocompromised individuals - Mild cold-like symptoms in older children and adults
491
What type of viral genome does RSV have?
Enveloped -ssRNA
492
Describe the pathogenesis of RSV infection.
- Virus causes syncytia (fusion of cells) to form in the lungs - Immune response to RSV further damages the lungs
493
Describe the epidemiology of RSV infection.
- Transmission via close contact with infected persons - Less frequent = spread via respiratory droplets - Prevalent in the US - 98% of children in daycare centers are infected by age 3
494
__% of children in daycare centers are infected with RSV by age 3.
98%
495
Describe the diagnosis, treatment, and prevention of RSV infection.
- Diagnosis: made by immunoassay - Treatment: supportive treatment for young children - Prevention: includes aseptic technique of healthcare and daycare employees
496
Describe the signs and symptoms of hantavirus pulmonary syndrome (HPS).
- Early symptoms include fever, fatigue, and muscle aches - Symptoms progress to cough, shock, and laboured breathing
497
Describe the pathogen involved in HPS.
- Caused by Hantavirus; enveloped, segmented -ssRNA bunyavirus (has 3 genome molecules within capsid) - Transmitted from infected mice to humans via inhalation
498
An enveloped/segmented -ssRNA bunyavirus.
Hantavirus
499
Describe the pathogenesis of HPS.
- Hantavirus spreads throughout body via the blood - Infection causes widespread inflammation leading to shock - 50% of patients die from pneumonia and shock
500
Describe the epidemiology of HPS.
- Transmitted to humans via contact with infected mice and their excrement/saliva - High rainfall and thick vegetation increases mice population = human disease more likely - High viral titers in the blood vessels of infected humans, but few viruses pass out of the lungs; person-to-person spread does NOT occur
501
Describe the diagnosis and prevention of HPS.
- Diagnosis: based on characteristic symptoms - Prevention: requires control of rodents
502
Describe the treatment of HPS.
- No pharmacological treatment is available - Treatment is supportive; pulmonary intubation, fever-reducing drugs, pain medication, and supplemental oxygen
503
Cases of mycoses have increased over the last __ decades.
Last 2 decades
504
AIDS patients are susceptible to _____ infections due to their compromised immune system.
Fungal infections
505
Also known as valley fever.
Coccidioidomycosis
506
Describe the signs and symptoms of coccidioidomycosis.
- Resembles pneumonia or tuberculosis; 60% of patients experience only mild respiratory symptoms - Can become systemic in immunocompromised persons
507
Describe the pathogens/virulence factors involved in coccidioidomycosis.
- Caused by Coccidioides immitis and C. posadasii; dimorphic soil fungus (grows as a mycelium in soil and assumes yeast-form at human body temperature) - In the soil, produces chains of asexual spores (arthroconidia)
508
Describe the pathogenesis of coccidioidomycosis.
- Arthroconidia from the soil enter the body through inhalation - Arthroconidia germinate in the alveoli into a form called a spherule (contain spores that can infect surrounding tissue)
509
Describe the epidemiology of coccidioidomycosis.
- Almost exclusively in the southwestern US and northern Mexico - Disruption of the soil can disseminate arthroconidia
510
Describe the diagnosis, treatment, and prevention of coccidioidomycosis.
- Diagnosis: presence of spherules in clinical specimens - Treatment: amphotericin B - Prevention: protective masks can prevent exposure to arthroconidia
511
Describe the signs and symptoms of blastomycosis.
- Flu-like symptoms - Systemic infections can produce lesions on the face/upper body OR purulent lesions (contain pus) on various organs
512
Describe the pathogen involved in blastomycosis.
- Caused by Blastomyces dermatitidis - Dimorphic fungus: grows as mycelium in soil (that is rich in organic material); assumes yeast-form at human body temperature
513
Describe the pathogenesis of blastomycosis.
- Enters body through inhalation of fungal spores - In the lungs, spores germinate to form yeasts and multiply - Respiratory failure and death can occur in immunocompromised patients; relapse common in AIDS patients
514
Describe the epidemiology of blastomycosis.
Endemic across the southeastern US and parts of Canada.
515
Describe the diagnosis and treatment of blastomycosis.
- Diagnosis: based on identifying fungus in clinical samples - Treatment: amphotericin B
516
Most common fungal disease affecting humans.
Histoplasmosis
517
Describe the signs and symptoms of histoplasmosis.
- Asymptomatic in most cases - Symptomatic infection causes coughing with bloody sputum or skin lesions
518
Describe the pathogens/virulence factors involved in histoplasmosis.
- Caused by Histoplasma capsulatum (intracellular parasite); dimorphic fungus found in moist soils (assumes a pathogenic yeast-form at human body temperature) - Histoplasma produces several proteins that inhibit macrophage activation and other host defences
519
Describe the pathogenesis of histoplasmosis.
1. Humans inhale airborne spores from the soil 2. H. capsulatum first attacks alveolar macrophages in the lungs 3. Infected macrophages disperse the fungus via blood/lymph 4. Patients may develop chronic cutaneous histoplasmosis (ulcers), ocular histoplasmosis (inflamed red eyes), or systemic histoplasmosis (in immunocompromised patients: enlargement of spleen/liver; death may result)
520
Describe the epidemiology of histoplasmosis.
- Prevalent in the eastern US - And parts of South America, Africa, and Asia
521
Describe the diagnosis of histoplasmosis.
Diagnosis is based on identifying fungus in clinical samples.
522
Describe the treatment of histoplasmosis.
- Infections in immunocompetent individuals typically resolve without treatment - Unresolved infections treated with amphotericin B and itraconazole - Maintenance therapy for AIDS patients is recommended
523
Describe the signs and symptoms of pneumocystis pneumonia.
- Difficulty breathing - Anemia - Hypoxia - Fever
524
Describe the pathogen involved in pneumocystis pneumonia.
- Caused by Pneumocystis jirovecii - Obligate parasitic fungus; normal member of the respiratory microbiome (but can become opportunistic)
525
Describe the pathogenesis and epidemiology of pneumocytis pneumonia.
- Transmit by inhalation of droplets containing the fungus - In immunocompromised patients, it multiplies rapidly; extensively colonizing the lungs (cysts found in lung tissue) - Common disease in AIDS patients
526
Describe the diagnosis and treatment of pneumocystis pneumonia.
- Diagnosis: based on clinical and microscopic findings - Treatment: trimethoprim and sulfamethoxazole (does not respond to anti-fungal drugs)