Principles Of Infectious Disease

Front 1

One organism can supply the needs of another without itself being harmed

Back 1

Commensal relationship

Front 2

Each organism supplies the needs for the other without harm to either

Back 2

Symbiotic relationship

Front 3

One organism will obtain its needs at the expense of another organism

Back 3

Pathogenic relationship

Front 4

How is clinical disease due to tissue injury defined in terms of microorganisms?

Back 4

When a microorganism evokes sufficient anatomic and/or functional damage to the host in the course of obtaining the necessary requirements for its survival.

Front 5

What is the bodies first line of defense?
What do they provide?

Back 5

- Intact skin and mucosal surfaces
- Provide physical barriers and produce antimicrobial substances

Front 6

What mechanical barriers does the skin provide?

Back 6

- Keratinized skin is a physical barrier to exogenous organisms
- Organisms shed as keratin exfoliates
- Acidic pH of the skin and sebaceous secretions unfavorable to many microorganisms.

Front 7

What is the micro environment of surfaces with high flow rate and secretions?

Back 7

Sterile
(lower respiratory tract, urinary tract, biliary system, etc)

Front 8

What is the micro environment of surfaces with low flow rate and secretions?

Back 8

Develops flora which under normal circumstances is in equilibrium w/ its environment and does not invade below surface epithelium
(upper respiratory tract, colon).

Front 9

How is pH an effective chemical barrier?

Back 9

- Most organisms can only survive within a narrow pH range.
- Gastric acid very good at sterilizing ingested organisms (particularly bacteria)

Front 10

How is Mucin an effective chemical barrier?

Back 10

- Secreted by various body membranes
- Can trap organisms before they can reach the epithelial cell surface

Front 11

This immunoglobulin is elaborated by various mucous membranes and can neutralize microorganisms before they get a chance to invade tissue

Back 11

Secratory IgA

Front 12

What are the two enzymes commonly thought of as chemical barriers?

Back 12

Lysozyme
Peroxidase

Front 13

An enzyme found in almost all tissue but has a high concentration in tears, saliva, and intestinal mucus

Back 13

Lysozyme

Front 14

How does Lysozyme act as a chemical barrier?

Back 14

Kills bacteria by dissolving their cell walls

Front 15

This is a circulating protein in the plasma which will activate the alternative complement pathway leading to the production of protective chemical complexes

Back 15

Properdin

Front 16

This is a protein that will inhibit viral replication and which can be produced by most cells in response to appropriate stimulation.

Back 16

Interferon

Front 17

What are the three types of host inflammatory response?

Back 17

1) Acute
2) Chronic
3) Granulomatous

Front 18

What are the two types of host immunologic response?

Back 18

1) Humoral
2) Cell-mediated

Front 19

Infectious disease is ultimately due to what?

Back 19

Failure of host defense mechanisms to exclude microorganisms from internal tissues
or
Failure to eliminate/ neutralize harmful effects of organisms in their attempt to grow & replicate

Front 20

What is the severity of disease related to?

Back 20

- Number of infective organisms
- Virulence (aggressiveness) of those organisms
- Status of the host defense mechanisms

Front 21

What are the factors which can interfere with host defense mechanisms, thereby increasing the susceptibility of the host to infectious disease?

Back 21

- Hereditary
- Acquired Immunodeficiency diseases
- Drugs (steroids or other immunosuppressants, antibiotics, alcohol)
- Acute or chronic debilitating disease
- Old age, etc.

Front 22

Indicates the potential of an organism to induce disease

Back 22

Virulence

Front 23

- Find a portal of entry
- Attach to epithelial surface
- Invade the tissue
- Resist host defense mechanisms
- Elaborate toxic products
- Induce hypersensitive reactions

Back 23

Factors which determine the virulence of an organism

Front 24

How do microbes enter a host generally?

Back 24

Inhalation, ingestion, sexual transmission, insect or animal bites, or injection.

Front 25

What is the most common means of a microorganism penetrating into the body?

Back 25

Through breaks in the skin:
- Superficial pricks (fungi)
- Wounds (staphylococci)
- Burns (pseudomonas)
- Diabetic and pressure-related foot sores (numerous bacteria)

Front 26

How can hospital IV's be used as a portal of entry?

Back 26

Cause bacteremias and septicemias

Front 27

How can needle sticks be used as a point of entry?

Back 27

Can lead to transmission of HBV, HCV, or HIV

Front 28

How can bites be used as a point of entry?

Back 28

- Insect bites transmit numerous infectious diseases
- Animal bites result in some zoonotic diseases.

Front 29

How do organisms attach to epithelial surfaces?

Back 29

- Use pili coated with adhesions to attach to receptors on host cell membranes. (Gram Negative)
- Contain sites that facilitate binding to host cells.

Front 30

How is it that organisms facilitate invading a hosts tissue?

Back 30

Use extracellular enzymes (aggressins) which facilitate invasion.

Front 31

These are enzymes which act to neutralize or destroy the phagocytic macrophages and neutrophils.

Back 31

Leukocidins

Front 32

These allow some organisms to cluster together so that higher concentrations of leukocidins are built up.

Back 32

Clumping factors

Front 33

How do clumping factors work?

Back 33

- Coagulase converts fibrinogen to fibrin
- Fibrin clots in surrounding blood vessels sealing off area from circulating antibodies
- Tend to result in local infection w/ abscess formation

Front 34

These enable some organisms to disseminate rapidly creating a fluid environment that tends to inhibit phagocytosis.

Back 34

Spreading Factors

Front 35

How does Hyaluronidase act as a spreading factor?

Back 35

Dissolves tissue ground substances

Front 36

How does Kinase act as a spreading factor?

Back 36

Aids in fibrinolysis

Front 37

How does collagenase act as a spreading factor?

Back 37

Dissolves collagen

Front 38

What are the structural properties that allows a microorganism to resist the host defenses?

Back 38

- Creates capsules that inhibit the contact of leukocytes
- Some phagocytized but resist intracellular destruction

Front 39

What are the functional properties that allows a microorganism to resist the host defenses?

Back 39

Alter the structure of native antigens rendering the immune response ineffective.

Front 40

What are the immune evasion properties that allows a microorganism to resist the host defenses?

Back 40

1) Growth/ replication in site with no immune response (lumen of the intestine or gall bladder)
2) Varying antigens they express resulting in lots infectious agents
3) Evading immune defenses by escaping phagocytic cells and using capsules
4) Impairment of T-cell responses by specific or nonspecific immunosuppression

Front 41

These are produced by living organisms, are released into the circulation, and can cause cellular and tissue damage at sites far distant from the site of infection.

Back 41

Exotoxins

Front 42

These are lipopolysaccharides of the cell wall of gram-negative bacteria that are released when the bacterium dies.

Back 42

Endotoxins

Front 43

What happens when endotoxins are absorbed into the blood stream?

Back 43

Can activate both the complement and coagulation cascades producing severe systemic effects (fever, shock, DIC)

Front 44

Some organisms are adept at triggering immune _____reactions which can cause _____ _____.

Back 44

hypersensitivity, tissue damage

Front 45

The nature of the disease that a specific organism can produce depends greatly on that organism's what?

Back 45

Requirements for growth and replication.

Front 46

These organisms are capable of surviving outside of the host cells and usually evoke an acute inflammatory response and a humoral immune response.

Back 46

Extracellular parasites

Front 47

These organisms usually evoke a chronic inflammatory response and a cell-mediated immune response.

Back 47

Intracellular parasites

Front 48

What are facultative intracellular parasites?

Back 48

Organisms capable of living either inside or outside host cells

Front 49

What are obligate intracellular parasites?

Back 49

Organisms that require the intracellular environment to survive and reproduce

Front 50

When organisms live inside a host cell, they are also more resistant to _____ _____.

Back 50

antibiotic drugs

Front 51

What does it mean for an organism to be species specific?

Back 51

Some organisms are able to live and reproduce in only one species of host.

Front 52

What does it mean for an organism to be tissue specific?

Back 52

Some organisms are able to live and reproduce in only certain types of tissue (trophism).

Front 53

With all infectious diseases, there is a time lag between invasion & development of clinical symptoms. This varies w/ etiological agent and is specific for that agent.

Back 53

Incubation period

Front 54

What are the local reactions of an infectious disease?

Back 54

Classical signs of inflammation:
- Swelling, heat, pain, redness, loss of function.

Front 55

What are the systemic reactions of an infectious disease?

Back 55

- Malaise
- Increased Fatigue
- Muscle aches and pains
- Decreased blood volume
- Fever/ chills

Front 56

What happens with decreased volume due to infectious disease?

Back 56

- Fluid leaks into tissues from circulation during inflammatory response
- Results in increased HR (tachycardia), increased breathing (tachypnea), and decreased urine output (oliguria).

Front 57

What are some of the clinical signs associated with fever/ chills in infectious diseases?

Back 57

- Increased metabolic demands/ Increased catabolism results in: loss of nutrients & loss of weight.
- Increased water loss via sweating (diaphoresis), tachypnea, etc

Front 58

What are the characteristics of Prions?

Back 58

- Intracellular pathogens composed of abnormal forms of host protein, termed prion protein (PrP)
- Protease-resistant PrP promotes conversion of normal protease-sensitive PrP to abnormal form that is potentially infectious.

Front 59

Where is abnormal PnP usually found?
What kind of damage does it do?

Back 59

- Neurons
- Damage characterized as spongiform encephalopathy (kuru, Creutzfeldt-Jakob disease, scrapies in sheep, mad-cow disease, etc).

Front 60

What are viruses dependent on?

Back 60

Obligate intracellular pathogens
that depend on the host’s cell metabolic machinery for their replication

Front 61

- Consist of nucleic acid genome (RNA or DNA) surrounded by protein coat (capsid).
- Classified by:
nucleic acid content
shape of capsid
presence- absence of lipid envelope
mode of replication
preferred cell type for replication (tropism)
type of tissue damage

Back 61

Structure and classification of a virus

Front 62

What is it called when viruses aggregate within the cells they infect?

Back 62

Inclusion bodies
*many viruses do not produce inclusion bodies.

Front 63

What are the different types of inclusion bodies?

Back 63

- Intranuclear (mostly DNA viruses except poxviruses)
- Intracytoplasmic (poxviruses and most RNA viruses)
- Both (paramyxoviruses).

Front 64

What are the characteristics of a short term virus?

Back 64

Transient illnesses and are eliminated from the body (colds, influenza, etc.).

Front 65

Persist within cells for years continuing to multiply (HBV)
or
survive (chronic productive infection)
or
Non-replicating form (chronic latent infection) that is reactivated later (herpesviruses).

Back 65

Characteristics of long term viruses

Front 66

To what extent can viruses cause transfomations?

Back 66

Transform host cells (transforming infection) into benign or malignant neoplasms (HPV and EBV).

Front 67

What is the viral injury mechanism?

Back 67

Direct damage to host cells by entering and replicating at host’s expense.
Viral receptors on host cells determine tissue tropism for certain viruses.

Front 68

Kill cells by preventing synthesis of host macromolecules, DNA, RNA or proteins; by producing degradative enzymes and toxic proteins; or by inducing apoptosis (produce proteins that are pro-apoptotic).

Back 68

Direct viral cytopathic effect

Front 69

What are some examples of direct viral cytopathic effect?

Back 69

Poliovirus, HSV, and HIV

Front 70

Viral protein on the surface of the host cell is recognized by the immune system and cytotoxic T lymphocytes (CTL) attack and destroy the virus-infected cells.

Back 70

Antiviral immune response

Front 71

What are examples of Antiviral immune response?

Back 71

CMV and HBV

Front 72

True/ False: the Cytotoxic T Lymphocytes can avoid significant tissue injury by destroying viral infected cells.

Back 72

False: During the antiviral immune response the cytotoxic T lymphocytes can pose a significant threat to tissue injury while destroying the viral cells (Example: HBV)

Front 73

Infected cells change into benign or malignant tumor cells through mechanisms including expression of viral-encoded oncogenes, anti-apoptotic strategies, or insertional mutagenesis (the normal function of host genes is altered by viral genes inserted into the host genome).

Back 73

Viral Transformations

Front 74

What are some examples of viral transformations?

Back 74

HTLV-1 (retrovirus-induced), HPV, EBV, HBV, and HCV.

Front 75

What are acute (transient) viral infections?

Back 75

RNA viruses:
- measles (rubeola)
- mumps
- poliovirus
- West Nile virus
- viral hemorrhagic fevers (Ebola, Marburg, Lassa, etc.)

Front 76

What are chronic productive viral infections?

Back 76

Mainly consist of the Hepatitis B Virus (HBV).

Front 77

What are chronic latent viral infections?

Back 77

DNA herpesviruses:
- Herpes Simplex Virus (HSV)
- Varicella-Zoster Virus (VZV) (chickenpox/ shingles)
- Cytomegalovirus (CMV).

Front 78

What are transforming viral infections?

Back 78

- Epstien-Barr Virus (EBV)
- Human Papillomaviruses (HPV)
- Hepatitis B Virus
- Human T Lymphocyte Virus (HTLV-1).

Front 79

- Cell membrane/wall consisting of peptidoglycan
- Lack membrane-bound nuclei and membrane-enclosed organelles (prokaryotes)
- Thick cell walls retain crystal-violet stain (gram-positive)
- Thin cell wall sandwiched between two phospholipid bilayer membranes (gram-negative).
- Either spherical (cocci) or rod-shaped (bacilli)
- Aerobic or anaerobic
- Most synthesize own DNA, RNA & proteins, but depend on host for favorable growth conditions.

Back 79

Distinguishing physical characteristics of bacteria

Front 80

What do some bacteria posses that allow them to attach to host cells or extracellular matrix?

Back 80

pili

Front 81

What does damage from bacteria depend on?

Back 81

Ability of bacteria to:
- Adhere to host cells
- Invade cells and tissues
- Deliver toxins.

Front 82

Pathogenic bacteria contain _____ that _____ proteins to confer virulence.

Back 82

genes, encode

Front 83

Bacteria adhere to host cells through _____ and _____.

Back 83

adhesins, pili

Front 84

Bacteria can invade host cells by multiple mechanisms that include _____ and _____ _____ _____.

Back 84

- phagocytosis (tuberculosis)
- complex secretion systems (gram-negative bacteria)

Front 85

What are the two types of bacterial toxins that contribute to illness?

Back 85

Endotoxins
Exotoxins

Front 86

From where do endotoxins arise from?

Back 86

The outer membrane of gram-negative bacteria

Front 87

- Secreted proteins in the form of enzymes that can degrade proteins
- Toxins that alter intracellular signaling or regulatory pathways
- Neurotoxins resulting in paralysis
- Superantigens that stimulate large numbers of T lymphocytes

Back 87

Exotoxin characteristics

Front 88

Gram-positive bacteria include...(8)

Back 88

Staphylococcus
Streptococcus
Entercoccus
Corynebacterium
Listeria
Bacillus
Nocardia
Actinomyces.

Front 89

Gram-negative bacteria include... (9)

Back 89

Bordetella
Pseudomonas
Yersinia
E. coli
Salmonella
Shigella
Hemophilus
Neisseria
Klebsiella

Front 90

Mycobacteria include...

Back 90

M. tuberculosis (human and bovine) M. leprae (leprosy)
M. avium-intracellulare complex (AIDS patients especially).

Front 91

These are gram-negative and include Treponema pallidum (syphilis), Borrelia recurrentis (relapsing fever), and Borrelia burgdorferi (Lyme disease).

Back 91

Spirochetes

Front 92

These primarily include Clostridium infections such as C. perfringens, C. difficle, C. botulinum, and C. tetani.

Back 92

Anaerobic bacteria

Front 93

Obligate intracellular bacteria include _____ and _____organisms that replicate inside membrane-bound vacuoles in the epithelial and endothelial cells, respectively.

Back 93

chlamydial, rickettsial

Front 94

Chlamydia trachomatis is a small _____ _____ _____. What is it often associated with?What is it best known for?

Back 94

- gram-negative bacterium
- urogenital infections (lymphogranuloma venereum) & inclusion conjunctivitis.
- Represents most common STD in the world.

Front 95

- Ehrlichiosis w/ intracytoplasmic inclusion (morulae) formation
- Typhus & rocky mountain spotted fever (RMSF).
*Most are vector-borne (arthropods).

Back 95

Rickettsial infections

Front 96

What damage does Typhus and rocky mountain spotted fever do?

Back 96

Injure endothelial cells resulting in hemorrhagic vasculitis w/ cutaneous rash formation being most prominent with RMSF.

Front 97

A special group of extracellular bacterial pathogens that do not have a cell wall.

Back 97

Mycoplasma

Front 98

What cell type are fungi and what is their outer membrane like?

Back 98

- Eukaryotes
- Possess a thick chitin-containing cell wall and ergesterol-containing cell membranes

Front 99

In what forms do fungi grow when they replicate?

Back 99

Either as rounded yeast cells
or
Small filamentous hyphae (molds): - Septate (cell walls separating individual cells) or aseptate.

Front 100

True/ False: Some pathogenic fungi exhibit thermal dimorphism and can grow as hyphal forms at room temperature or as yeast forms at body temperature.

Back 100

True

Front 101

How do yeasts reproduce?
Molds?

Back 101

- Yeasts reproduce by budding
- Molds consist of hyphae that grow and divide at their tips producing conidia

Front 102

Fungal infections are referred to as what?
What are the four types?

Back 102

- Known as mycoses
- Four types are:
Superficial and cutaneous
Subcutaneous
Endemic
Opportunistic

Front 103

Usually limited to the superficial/keratinized layers of the skin, hair and nails.

Back 103

Superficial and cutaneous mycoses (dermatophytes)

Front 104

Involve the deeper layer of skin, subcutis and lymphatics (only rarely become systemic).

Back 104

Subcutaneous mycoses

Front 105

Caused by dimorphic fungi and often produce severe systemic disease in healthy hosts.

Back 105

Endemic mycoses

Front 106

Cause life-threatening systemic diseases in primarily debilitated or immunosuppressed hosts (Pneumocystosis in AIDS patients).

Back 106

Opportunistic mycoses

Front 107

What type of pathogens are Protozoa?

Back 107

Extracellular
Facultative intracellular
Obligate intracellular

Front 108

What are the characteristics of the parasitic forms of protozoa?

Back 108

- Single-celled eukaryotes
- Transmitted by insects or fecal-oral route
- In humans, mainly reside in the blood or intestines

Front 109

What are the two separate forms of Protozoa?

Back 109

(1) motile trophozoites
(2) immobile cysts

Front 110

What type of pathogens are Helminths?

Back 110

(metazoan parasites)
Extracellular and intracellular pathogens

Front 111

What are the characteristics of the parasitic forms of Helminths?

Back 111

- Highly differentiated multicellular - Complex life cycle requiring both definitive & intermediate hosts.
- Contracted by consuming parasite (undercooked meat, or direct invasion of the host through the skin or via insect bites)

Front 112

What are examples of endoparasites?

Back 112

Nematodes (round worms)
Cestodes (tapeworms)
Trematodes (flukes).

Front 113

What are ectoparasites?

Back 113

Insects (lice, bed bugs, fleas), Arachnids (mites, ticks, spiders)
*attach to and live on or in the skin.

Front 114

What are the techniques for identifying infectious agents?

Back 114

Gram Stain
Acid-fast Stain
Silver Stains
Mucicarmine Stain
Antibody and DNA Probes

Front 115

Most bacteria (either gram-positive or gram-negative)

Back 115

Gram stain

Front 116

Mostly mycobacteria (tuberculosis, leprosy, avium-intracellulare complex).

Back 116

Acid-fast stain

Front 117

What dose a Silver stains (GMS) and periodic acid Schiff (PAS) detect?

Back 117

Mostly fungi.

Front 118

What does a Mucicarmine stain detect?

Back 118

Cryptococcus primarily.

Front 119

What does an Antibody and DNA probe (such as PCR) detect?

Back 119

Most all classes of organisms

Front 120

- Pus-producing bacteria that induce a purulent exudate rich in neutrophils
- Liquefactive necrosis w/ abscess formation can occur resulting from neutrophilic lysosomal enzyme release
- Severity of the tissue destruction depends on the location and organisms involved.

Back 120

Suppurative (purulent) response to inflammation

Front 121

- Acute infiltrates primarily in response to viruses, intracellular bacteria or intracellular parasites.
- Chronic response usually towards mycobacteria & fungi, spirochetes (syphilis) and helminths.

Back 121

Granulomatous (mononuclear) response to inflammation

Front 122

What are the cellular responses of granulomatous inflammation?

Back 122

lymphocytes, plasma cells (especially syphilis), macrophages, epithelioid cells and giant cells.

Front 123

What are the Cytopathic-cytoproliferative reactions of inflammation?

Back 123

- Produced by viruses resulting in lesions characterized by cell necrosis or cell proliferation.
- Inflammatory response may be minimal.

Front 124

How do the Cytopathic-cytoproliferative viruses replicate?

Back 124

- Replicate w/in cells & create viral aggregates visible as intranuclear and/or intracytoplasmic inclusions.
- May also replicate within cells & induce them to fuse & form multinucleated (syncytial) cells referred to as polykaryons (paramyxoviruses/measles).

Front 125

How is tissue necrosis induced?
What is the most common type of bacteria to do this?

Back 125

- By bacteria that secrete powerful toxins causing rapid & severe tissue damage resembling gangrenous necrosis
- Clostridial bacteria that can result in either wet or gas gangrene.

Front 126

What are definitive examples of chronic inflammation and scarring?

Back 126

- Cirrhosis of the liver by HBV.
- Fibrosis of the liver and/or urinary bladder by schistosomal eggs.