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Exam 3 > Ziegler- Viral, Fungal and Parasite Pathogenesis > Flashcards

Ziegler- Viral, Fungal and Parasite Pathogenesis Flashcards

1
Q

What are the clinical symptoms of virus replication?

A
  1. Infection does not always result in disease; SUBCLINICAL INFECTION is the rule for some viruses (only way to tell is through antibody study)
  2. The immune system can play an active role in the development of some symptoms, e.g., rashes (clinical sign of some diseases, maculopathic have no virus, vesicles in chicken pox have active virus that can be transferred to someone else)
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2
Q

What are localized infections?

A

Virus replication at the site of virus entry (incubation time shorter)

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3
Q

What are systemic or disseminated infections?

A

Virus traveling from the site of entry to a target organ (incubation time longer)

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4
Q

What is acute viral disease?

A

Appearance of symptoms relatively shortly following viral infection (Rabies–target organ is brain, exception)

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5
Q

What is persistent or chronic viral disease?

A

Symptoms appear months to years following infections (AIDS)

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6
Q

What are general aspects of viral pathogenicity?

A
  1. No lipopolysaccharide (endotoxin) or exotoxins
  2. Disease results from direct or indirect effects of virus replication in host cells
  3. Viruses do not need to kill cells, but may merely alter cellular physiology ex. viroporins to cause problems
  4. Inflammation, tissue damage, and delayed hypersensitivity reactions due to host’s immune system play a significant role in disease
  5. Latency in host cells is a common property of some viruses (Herpes, latent in triseminyl ganglia)
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7
Q

What is the first step in viral pathogenesis?

A
  1. Entry and primary replication
  2. Routes are specific for viruses–most enter through the mucosa of respiratory or GI tract, some inoculated directly into blood stream by needles (HBV and HIV) or insect vectors (arboviruses)
  3. Most replicate at the site of entry, some produce disease there (flu and rotaviruses) and don’t spread further (localized infections)
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8
Q

How do viruses spread?

A
  1. Free in plasma
    Poliovirus, HBV and togaviruses
  2. Mononuclear peripheral WBC
    Measles virus, EBV, CMV, HSV and HIV, Cause transient immunosuppression (CMB multiplies and travels throughout the body in white blood cells, alter normal properties of cells that are supposed to suppress infections, those pts are more susceptible to other infections)
  3. RBC–
    Colorado tick fever virus
  4. Nerve fibers
    Rabies virus, HSV, VZV, Virus shielded from immune system, get to neurons and can go latent and survive until stimulus makes them come out (VZV is shingles, immune system as you get older gets weaker, virus travels down nerve fibers, disease manifests along dermatome)
  5. Direct spread
    Within respiratory tract (influenza virus), respiratory to GI (adenovirus–cause respiratory and GI infections) **all viruses that cause GI infections are naked

**Shingles shot, cuts down on virus replication in skin

**structure of virus determines what disease you see

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9
Q

What is tissue trophism and what are target organs?

A
  1. Viruses spread from the site of infection to other areas of the body
  2. Viruses replicate only in tissues with cells having necessary receptors and host factors
  3. Target organ–shows most prominent clinical symptoms (Hep B-liver, Chicken pox-Rash, Herpes1-coldsores, Mono–WBC)
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10
Q

What is cell injury (cytopathogenesis)?

*Occurs when virus gets to cells

A
  1. Cytolysis by cytolytic viruses or immune response
  2. Physiological alterations–due to take over of biosynthetic machinery (naked–kills cell)
  3. Mechanisms of viral cytopathogenesis:

a. Inhibition of cellular protein synthesis
b. inhibition and degradation of cell DNA
c. alteration of cell membrane structure
d. Inclusion bodies–help with diagnosis, accumulations of viral specific proteins (Rabies, cytomegalovirus, herpes)
3. toxicity of virion components–adenovirus fibers and rotavirus proteins

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11
Q

What does disease indicate in viral pathogenesis?

A
  1. An insensitive indicator of virus infection since inapparent or subclinical infections are extremely common with some viruses, e.g., EBV and HPV (EBV mono–can get from someone without sympt)
  2. Results from a complex series of circumstances and events: Inoculum size, Competence of immune system, Immune and health status of host, Genetic constitution of host, Age and nutritional condition of host
  • *Common cold, short incubation, moderate subclinical infections, spring/autumn
  • *Diarrhea
  • *Hepatitis A/B–high incidence of subclinical infections
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12
Q

What is transmission in viral pathogenesis?

A
  1. Horizontal: Respiratory, DROPLETS – influenza
  2. Intestinal: FECAL/ORAL – hepatitis A
  3. Urogenital (STD): Most not spread by urine, most spread by mucosal contact with susceptible individuals, e.g., HSV
  4. Oropharynx: SALIVA – HSV, mumps virus and CMV
  5. Skin and skin glands: PHYSICAL CONTACT – HSV, VZV and HPV
  6. BLOOD: Needles and arthropod bites – HIV, HBV and Dengue, tattooing needles
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13
Q

What is vertical transmission?

A
  1. Transplacental: rubella virus, CMV, HIV and HBV
  2. Perinatal (infected birth canal): HSV
  3. Postnatal (milk or direct contact): CMV and HBV
  4. Germline: Many retroviruses
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14
Q

How does transmission occur through animals?

A
  1. Arthropod-borne: Togaviruses and bunyaviruses

2. Vertebrates: Arenaviruses, poxviruses and rhabdoviruses

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15
Q

What are the steps in viral pathogenesis?

A
  1. Entry and primary replication
  2. Viral spread
  3. Tissue trophism and target organs
  4. Cell injury (cytopathogenesis)
  5. Disease
  6. Transmission
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16
Q

What are the types of infection?

A
  1. Acute
  2. Persistent
  3. Transforming
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17
Q

What is acute infection?

A
  1. Clinical signs of infection which last a short period of time (days to weeks) followed by the disappearance of the virus
  2. Localized:
    -Occurs at the initial site of infection
    -Little or no viral spread
    -Clinical signs due to replication there
    -Short incubation time
    Example - influenza
  3. Systemic or disseminated
    -Virus must spread to target organ before clinical signs
    -Primary and secondary viremia possible
    -Longer incubation times
    Examples - mumps and measles
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18
Q

What is persistent infection?

A

Types of persistent infection:
1. Persistent: Virus persist in infectious form with continuous or intermittent shedding
Examples – HBV and EBV
2. Slow:Long incubation time with no symptoms for months or years following infection, May follow acute disease – SSPE, HIV and HTLV-1, May not follow acute disease – Creutzfeld-Jakob disease
3. Latent: Virus persists in latent, non-infectious form
Examples – HSV and VZV
4. Reactivation of persistent infections:
Old age, pregnancy, leukemias and lymphomas, post-transplant immunosuppression and HIV infection (cytomegalo virus often kills HIV patients, likes to replicate in WBC)

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19
Q

What is a transforming infection?

A

Many viruses transform cells in culture, but few show a strong association with human cancers
Strong evidence for EBV, HPV, HBV, HTLV-1 and HTLV-2

20
Q

What are the different types of host immune response?

A
  1. Nonspecific Resistance
  2. Interferon
  3. Specific Resistance
  4. Cell mediated immunity
21
Q

What is nonspecific resistance?

A
  1. Innate immunity
    Anatomical and chemical barriers – skin, lactic acid, etc., Age and physiological condition of the host – more severe infections in neonates and elderly
  2. Cellular resistance:
    Lack of receptor sites, Non-permissive cells – actively growing cells are more permissive, e.g., small lymphs (non-permissive) and large lymphs (permissive)
  3. Inflammation:
    unfavorable viral replication conditions
22
Q

What is an interferon? (Don’t occur with bacteria) How does it work?

A
  1. Polypeptide cytokines produced in cells in response to viral infection and other stimuli, e.g., endotoxin and natural or synthetic d.s. RNA
  2. ANTIVIRAL host glycoprotein which is not virus specific, but is species specific
  3. FIRST HOST DEFENSE MECHANISM at site of infection
  4. Several different types (alpha, β and γ) depending on cell which produces them
  5. Induces several anti-viral proteins including 2, ‘5’ A synthetase and specific protein kinases

How does it happen?

  1. Virus induces synthesis of interferon
  2. Interferon binds to uninfected celll, induces synthesis of 2,5 A syntehtase (degrades viral RNA) and enzyme that inhibits protein synthesis
  3. IFN induces synthesis of antiviral molecules
23
Q

What is specific resistance?

A
  1. Humoral immunity – production of antiviral antibodies
    a. Virus neutralization: Decrease virus infectivity, Inhibit viral adsorption – anti-VAP ab, Complement-mediated degradation – lesion in envelope
    b. Cytolysis of virus-infected cells: IγM more effective than IγG
    c. Non-neutralizing antibody: Act as opsonins to enhance phagocytosis and degradation of virus
24
Q

What is cell mediated immunity (anti-viral cells?)

A 
1. Sensitized “T” cells
Kill virus-infected cells
2. NK cells
Attack cells with viral glycoprotein on their surface
Release perforin which polymerize to form pores in target cells
Release TNF-like toxins
3. Activated macrophages
Produce and release cytokines like IL-1
25
Q

What is the importance of the immune response?

A
  1. Ab and IFN most important for a) cytolytic infections accompanied by viremia and, b) infections of epithelial surfaces (antibodies sit on virus and neutralize it, interferon sitson neighboring cells)
  2. Cellular immune response most important for non-cytolytic infections where the infected cell’s membranes are antigenically altered (Infected cell is a factory producing viruses, smart way to control infection is to control factory and not viruses, cytolytic–control and neutralize individual viruses)
26
Q

What is the role for AG-Ab complexes in disease? (Bad effects of antibodies)

A
  1. Skin rashes: Ag-Ab complexes play a role in maculopapular rashes, e.g., measles and rubella
  2. Tissue deposition: Deposits in the kidney, e.g., HBV–May initiate intravascular coagulation
27
Q

What are negative aspects of immune response?

A
  1. Autoimmune antibodies: Some viruses (e.g., Coxsackie B virus) induce the synthesis of autoimmune antibodies
  2. Skin rashes
  3. Tissue deposition
28
Q

What is viral induced immune suppression?

A
  1. Certain virus infect cells of lymphocyte-macrophage lineage
  2. HIV long lasting decreases ab and decreases CMI immunosuppression
  3. EBV, measles virus, CMV, VZV and mumps cause temporary suppression of CMI
  4. Medical students should know viruses causing immunosuppression
29
Q

What are molds?

A
  1. Filamentous fungi
  2. Composed of tubular branching filaments
  3. May have individual walled-off cells (septate hyphae) or not (aseptate hyphae)
30
Q

What are yeasts?

A

Unicellular eukaryotic cells which are usually round

31
Q

What are dimorphic fungi?

A
  1. Histoplasma, Blastomyces, & Coccidiodes
  2. Exist as yeast or molds depending on environmental conditions
  3. In environment or at room temperature grow as molds, but in the body grow as yeasts
32
Q

What are the types of fungal infections (mycoses)?

A

SSSCO
1. Superficial – involve keratinized outer layers of nails, hair and skin

  1. Cutaneous – involve keratin containing epidermis and deeper layers of nails, hair and skin (athletes foot)
  2. Subcutaneous – involve dermis, subcutaneous tissue, muscles and fascia
  3. Systemic – usually begin in the lungs but disseminate to other organs, particularly in immunocompromised individuals
  4. Opportunistic – occur in individuals with compromised immune systems
33
Q

What do fungi need to grow?

A
  1. They usually live in the soil or decaying organic matter
  2. Require preformed organic compounds for growth
  3. Transport soluble nutrients across their cell membranes
  4. Secrete degradative enzymes eg. cellulase, protease, etc. to obtain solute nutrients
34
Q

What are the characteristics of superficial and cutaneous mycoses (dermatophyoses)?

A
  1. Uses keratin as a source of nutrition
  2. Don’t generate an immune response
  3. Cause cosmetic problems (Athlete’s foot, ringworm, jock itch, etc.)
  4. Usually characterized by itching and scaling skin problems which can become inflamed
  5. Transmission from: Soil, Infected skin scales from humans or animals
35
Q

What are the characteristics of subcutaneous mycoses?

A
  1. Causative agents found in soil and decaying vegetation, particularly thorns
  2. Enter the body through cuts or punctures
  3. Not transmissible from human to human under normal conditions
  4. Characterized by either
    Granulomatous ulcer
    Warty nodules
    Localized abscesses
36
Q

What are the characteristics of systemic mycosis?

A
  • *SYSTEMIC
    1. Most agents are dimorphic fungi
  1. Infections occur in defined geological areas where organisms live in the soil and can be aerosolized
  2. Enter the body as airborne spores which germinate in the lung
  3. In healthy individuals, infection is likely to be asymptomatic or mild, self-limiting pulmonary infection
37
Q

What are the characteristics of Opportunistic Mycosis?

A
  1. Infect debilitated or immunocompromised individuals
  2. Cause serious lung involvement and can disseminate to other organs
  3. Usually part of normal flora
  4. Not dimorphic except for Candida
38
Q

What are anti-fungal agents?

A
  1. Major mechanism is to inhibit ergosterol (a fungal membrane sterol) synthesis (Imidazoles) or bind to it to disrupt fungal membrane activity (Amphotericin B & Nystatin)
  2. A second mechanism is to inhibit fungal glycan synthesis (Echinocandins); similar to bacteria β-lactams

**Eukaryotic cells have unique cytoplasmic membrane with fungal specific ergosterol, synthesis of this compound is inhibited by some antifungal agents

39
Q

What are pathogenic parasites?

A
  1. Pathogenic protozoa:
    Ameba, flagellates, ciliates, and sporozoa
  2. Pathogenic helminths (worms):
    Nematodes, cestodes, and trematodes
40
Q

What are the characteristics of Protozoa in terms of entry and existence(1)?

A
  1. Enter the body through the eye, nasal, ingestion, sexual contact, or arthropod bite.
  2. Live as intracellular or extracellular organisms in the blood, intestine, and urogenital system.
  3. Intracellular organisms can ingest cell ctyoplasm and extracellular organisms can ingest host cells.
41
Q

How do protozoa replicate?

A
  1. Multiply in the host.
  2. Under unfavorable conditions, many form cysts to ensure survival.
  3. Cysts facilitate transmission from host to host also.
  4. Immunopathological mechanisms contribute to the disease–foreign to body so get huge immune response to them
42
Q

What are helminths (Entry and replication)?

A
  1. Most are multi-host parasites (definitive and intermediate hosts).
  2. Entry by ingestion, penetration, or arthropod bite.
  3. Larval forms migrate to various tissues.
  4. Do not multiply in hosts.
43
Q

How do Helminths create disease?

A
  1. Cell-mediated immune responses. Including allergic reactions are directed to parasite, egg, or larval antigens.
  2. Immunopathological mechanisms contribute to the disease.
  3. Disease severity correlates with worm load.
44
Q

What are Nematodes (Roundworms)?

A
  1. Major parasites of humans.

2. Acquire infection by ingestion of eggs or soil larval forms which then penetrate the skin.

45
Q

What are cestodes (Tapeworms)?

A

Ingestion of larval forms from raw or poorly cooked meat or fresh water fish is the most common route of entry.

46
Q

What are trematodes (flukes)?

A
  1. Except for Schistosomes, infection by ingestion of freshwater fish, mollusks,or plants.
  2. Schistosomal certicaria penetrate the skin, spread to the circulation, and move through the body to target tissues.
  3. Allergic reactions contribute to pathogenesis.

Exam 3 (12 decks)

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