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foundations > micro - viral/fungal/parasite pathogenesis > Flashcards

micro - viral/fungal/parasite pathogenesis Flashcards

1
Q

result from virus replication at site of virus entry

A

localized infections

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2
Q

virus traveling from stie of entry to target organ

A

systemic/disseminated infections

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3
Q

symptoms appearing shortly after viral infection characterize:

A

acute viral diseases

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4
Q

symptoms appear months to years following infections:

A

persistant/chronic viral disease

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5
Q

Do viruses have lipopolysaccharides? Exotoxins?

A

No lipopolysacchardies (endotoxins) or exotoxins!

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6
Q

Do diseases result from direct or indirect effects of virus replication in host cells?

A

Both!

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7
Q

Do viruses need to kill cells to cause problems?

A

No, may merely alter cellular physiology

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8
Q

What effects of host’s immune system play a significant role in disease?

A

inflamation

tissue damage

delayed hypersensitivity reactions

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9
Q

Where is Herpes virus latent?

A

trigeminal nerve

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10
Q

WHere do most viruses enter?

A

mucosa of respiratory or GI tract

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11
Q

Where do most viruses replicate?

A

at site of entry.

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12
Q

Which viruses produce disease at site of entry and do not spread further?

A

flu

rotaviruses

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13
Q

Are entry routes specific for viruses?

A

Yes

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14
Q

What are other entry routes?

A 
direct innoculation into blood stream,
 via needles (HBV & HIV)
 or insect vectors (arbovirsues)
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15
Q

What are 5 modes of dissemination? (virus spreading)

A
  • free in plasma (poliovirus, HBV, togaviruses)
  • Mononuclear peripheral WBC (measles virus, EBV, CMV, HSV, and HIV) (Causes transient immunosuppression)
  • RBC (colorado tick fever virus)
  • Nerve Fibers (rabies virus, HSV, VZV) (virus shielded from immune sstem)
  • Direct spread (w/in respiratory tract - influenza) ( respiratory -> GI - adenovirus)
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16
Q

What is shingles?

A

VZV suppressed by immune system - when immune system depressed, shows up

shingle vacine = upped concentration of chicken pox vaccine. cuts down on pain of shingles.

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17
Q

Epsten Bar causes….

CMV causes….

how do they travel through the body?

A

Epsten bar causes mono

CMV causes mono-like symptoms

travel through body in white cells (alter normal property of WBCs)

These PATIENTS ARE IMMUNOSUPPRESSED DUE TO VIRUS! remember!

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18
Q

Do naked or enveloped viruses cause GI tract infections?

A

NAKED.

the envelope viruses are destroyed by GI tract

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19
Q

Tissue which shows most prominent clinical symptoms:

A

TARGET ORGAN

many viruses spread from site of infection to other areas of the body; will only replicate in tissues with cells that have necessary receptors and host factors.

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20
Q

Where does chicken pox virus reside and what is its target organ?

A

lives in nerves, but target organ = skin

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21
Q

What is cytopathogenesis caused by?

A

it’s cell injury - cytoloysis caused by cytolytic viruses or immune respone and physiological alterations

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22
Q

Mechanisms of viral cytopathogenesis:

  • inhibition of cellular protein synthesis
  • inhibition and degradation of cellular DNA
  • alteration of cell membrane structure
  • Inclusion bodies
  • virion component toxicity
A

Many inhibit cell protein synthesis…

INCLUSION BODIES=aggregates of viral specific protein material - help with diagnosis!

if you see negri bodies in saliva - RABIES

COWDRY’S TYPE A = Herpes simplex virus!!!!

Only 2 have toxicity:

ADENOVIRUS
ROTOVIRUS

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23
Q

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)*

results in:

A
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24
Q

Influenza mode of transmition:

Herpes simples :

rotavirus :

mono:

Hep A

Hep B

Rabies

A

respiratory

salivary (long communicability)

alimentary

contact (long communicability)

alimentary (long comm.)

inoculation (Very long comm)

animal bite (nil comm.)

25
Q

Types of transmition:

HORIZONTAL

A
  • respiratory
  • intestinal
    (fecal - oral - hep A)
  • STD
    (mucosal contact w/susceptible individuals, usually not urine)
  • oropharynx
    (saliva - HSV, mumps virus, and CMV)

-skin and skin glands
(physical contact - HSV, VZV, HPV)

  • blood
    ( needles and arthropod bites - HIV, HBV, Dengue)

(droplets - flu)

26
Q

types of transmition:

VERTICAL

A
  • transplacental
  • perinatal
    (infected birth canal; HSV)
  • postnatal
    (milk or direct contact; CMV & HBV)

-germline
(many retroviruses)

(rubella virus, CMV, HIV, and HBV)

27
Q

types of transmition:

ANIMAL

A
  • arthropod-borne
  • vertebrates
    (arenaviruses, poxviruses, and rhabdoviruses)

(togaviruses and bunyaviruses)

28
Q

clinical signs of infection last a short period of time (days ->weeks) followed by disappearance of virus

A

ACUTE

  • Localized* (little or no viral spread, occurs at initial infection site, clinical signs due to replication there, short incubation time) think FLU
  • Systemic or disseminated* (virus must spread to target organ before clinical signs appear, primary and secondary viremia possible, longer incubation time) think MUMPS AND MEASLES
29
Q

Persistant Virus Infection signs

A
  • persistent
    (virus perssists in infections form w/continuous or intermitent shedding) Think HBV & EBV
  • slow
    (long incubation time w/no sympotoms following infection for months/years) (May follow acute disease - SSPE HIV and HTLV-1) (May not follow acute disease - Creutzfeld-Jakob disease)
  • latent
    (virus persists in latent, non-infectious form) Think HSV & VZV

- reactivation of persistent infections
(old age, pregnancy, leukemias, lymphomas, post-transplant immunosuppression, and HIV infection)

30
Q

Transforming Virus Infection info

A

many viruses transform cells in culture, but few show a strong assoc. with human cancers

there is strong evidence for EBV, HPV, HBV, HTLV-1, and HTLV-2, however

31
Q

Influenza site of implantation, route of spread, target organ, and site of shedding:

A

locally spread - all respiratory tract.

Gastroenteritis also local - all alimentary tract.

32
Q
  • anatomical and chemical barriers - skin, lactic acid, etc.
  • age and phsiological condition of the host - more sever infections in neonates and elderly
A

INNATE IMMUNITY (part of nonspecific resistance in host immune response)

33
Q

Lack of receptor sites
Non-permissive cells – actively growing cells are more permissive, e.g., small lymphs (non-permissive) and large lymphs (permissive)

A

CELLULAR RESISTANCE (part of nonspecific resistance in host immune response)

34
Q

What does Inflammation do as part of nonspecific resistance in host immune response?

A

creates unfavorable viral replication conditions

35
Q

What are interferons?

A

Polypeptide cytokines produced in cells in response to viral infection and other stimuli, e.g., endotoxin and natural or synthetic d.s. RNA

Antiviral host glycoprotein which is not virus specific, but is species specific (humans must use human interferon, but they’ll use it on all viruses)

First host defense mechanism at site of infection (nonspecific resistance)

Several different types (, β and γ) depending on cell which produces them

Induces several anti-viral proteins including 2, ‘5’ A synthetase and specific protein kinases

all cells have genetic info for interferons…they induce synthesis of anti-viral molecules.

36
Q

-Virus neutralization
Decrease virus infectivity
Inhibit viral adsorption – anti-VAP ab
Complement-mediated degradation – lesion in envelope

  • Cytolysis of virus-infected cells
  • IγM more effective than IγG*
  • Non-neutralizing antibody
  • Act as opsonins to enhance phagocytosis and degradation of virus*

What kind of immunity and type of resistance is this?

A

Specific resistance: HUMORAL IMMUNITY - antiviral antibodies

37
Q

Sensitized “T” cells
Kill virus-infected cells

NK cells
Attack cells with viral glycoprotein on their surface
Release perforin which polymerize to form pores in target cells
Release TNF-like toxins

Activated macrophages
Produce and release cytokines like IL-1

What kind of immunity and type of resistance is this?

A

Specific resistancce: Cell-mediated immunity - antiviral cells

38
Q

What is cellular immune response most important for?

A

non-cytolytic infections where the infected cell’s membranes are antigenically altered

39
Q

What host immune responses are most important for

a) cytolitic infections accompanied by viremia and
b) infections of epithelial surfaces

A

Ab and IFN (antibodies and interferons)

these come and stop from entering other cells

40
Q

What is the role of Ag-Ab complexes in disease?

A
  • skin rashes (play a role in maculopapular rashes, - measles and rubella)
  • Tisue deposition (deposits in the kidney, HBV; may initiate intravascular coagulation)
41
Q

Other host immune responses:

autoimmune antibodies

A

some viruses induce synthesis of autoimmune antibodies

42
Q

Viral Induced Immune Suppression!

A

Certain virus infect cells of lymphocyte-macrophage lineage
HIV long lasting decreases ab and decreases CMI immunosuppression
EBV, measles virus, CMV, VZV and mumps cause temporary suppression of CMI

43
Q

What are the 3 morphological forms of fungi…

A

Molds (filamentous fungi)
Composed of tubular branching filaments
May have individual walled-off cells (septate hyphae) or not (aseptate hyphae)

Yeasts
Unicellular eukaryotic cells which are usually round

Dimorphic fungi (Histoplasma, Blastomyces, & Coccidiodes)
Exist as yeast or molds depending on environmental conditions
In environment or at room temperature grow as molds, but in the body grow as yeasts

44
Q

5 Types of Fungal Infections (Mycoses)

A

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

Cutaneous – involve keratin containing epidermis and deeper layers of nails, hair and skin

Subcutaneous – involve dermis, subcutaneous tissue, muscles and fascia

Systemic – usually begin in the lungs but disseminate to other organs, particularly in immunocompromised individuals

Opportunistic – occur in individuals with compromised immune systems

45
Q

What is the following describing?

They usually live in the soil or decaying organic matter

They require preformed organic compounds for growth

They transport soluble nutrients across their cell membranes

They secrete degradative enzymes eg. cellulase, protease, etc. to obtain solute nutrients

A

Fungal growth

46
Q

What does the following describe?

Uses keratin as a source of nutrition

Don’t generate an immune response

Cause cosmetic problems (Athlete’s foot, ringworm, jock itch, etc.)

Usually characterized by itching and scaling skin problems which can become inflamed

Transmission from
Soil
Infected skin scales from humans or animals

A

Suerficial and Cutaneous Mycoses (Dermatophyoses)

47
Q

What does the following describe?

Causative agents found in soil and decaying vegetation, particularly thorns

Enter the body through cuts or punctures

Not transmissible from human to human under normal conditions

Characterized by either
Granulomatous ulcer
Warty nodules
Localized abscesses

A

Subcutaneous Mycoses

48
Q

What does the following describe?

Most agents are dimorphic fungi

Infections occur in defined geological areas where organisms live in the soil and can be aerosolized

Enter the body as airborne spores which germinate in the lung

In healthy individuals, infection is likely to be asymptomatic or mild, self-limiting pulmonary infection

A

Systemic Mycosis

49
Q

What does the following describe?

Infect debilitated or immunocompromised individuals

Cause serious lung involvement and can disseminate to other organs

Usually part of normal flora

Not dimorphic except for Candida

A

Opportunistic Mycosis

50
Q

How do you inhibit fungi?

A

Antifungal Agents

**Fungi are eukaryotic w/ a unique cytoplasmic membrane that contains a fungal sterol: ergosterol. **

The major mechanism is to inhibit ergosterol (a fungal membrane sterol) synthesis (Imidazoles) or bind to it to disrupt fungal membrane activity (Amphotericin B & Nystatin)

A second mechanism is to inhibit fungal glycan synthesis (Echinocandins); similar to bacteria β-lactams

51
Q

What are the pathogenic parasites?

A

Pathogenic protozoa:
Ameba, flagellates, ciliates, and sporozoa

Pathogenic helminths (worms):
Nematodes, cestodes, and trematodes

52
Q

Ways pathogenic protozoa move

A

Types of Helminths

53
Q

How do protozoa enter the body?

What do they do under unfavorable conditions?

what else do you know about them? :P

A

Enter the body through the eye, nasal, ingestion, sexual contact, or arthropod bite.

Live as intracellular or extracellular organisms in the blood, intestine, and urogenital system.

Intracellular organisms can ingest cell ctyoplasm and extracellular organisms can ingest host cells.

Multiply in the host.

Under unfavorable conditions, many form cysts to ensure survival.

Cysts facilitate transmission from host to host also.

Immunopathologic mechanisms contribute to the disease. (they’re very foreign to our bodies)

54
Q

Are these Helminths or Protozoa?

Most are multihost parasites (definitive and intermediate hosts).
Entry by ingestion, penetration, or arthropod bite.
Larval forms migrate to various tissues.
Do not multiply in hosts.
Cell-mediated immune responses. including allergic reactions are directed to parasite, egg, or larval antigens.
Immunopathological mechanisms contribute to the disease.
Disease severity correlates with worm load.

A

Helminths!

55
Q

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

A

Nematodes (roundworms)

56
Q

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

A

Cestodes (tapeworms)

57
Q

Except for Schistosomes, infection occurs by ingestion of freshwater fish, mollusks,or plants.

(Schistosomal certicaria penetrate the skin, spread to the circulation, and move through the body to target tissues.)

Allergic reactions contribute to pathogenesis.

A

Trematodes (Flukes)

58
Q

What are the parasitic mechanisms evade host immune response?

A

foundations (9 decks)

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