Week 3 - Microbiology Vial, Fungal, and Parasite Pathogensis Flashcards

1
Q

what should we know?

A

viruses - influenza virus* single stranded RNA virus with segmented genome

Whats the only diploid virus?

Retroviruses..

phsutomones (poster)

Herpes virus

Virulence factors on how bacterial cause disease

Viruses and how they cause disease

and just because infection dont necessary get a disease

injectosomes

enzymes that are secreted

toxins that are produced..

Slide on staffolacaucus.. not individual things but emphazid.. how they get there is very complex.. immune system repsonse to it.. Innoculation dose of bacteria…

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2
Q

Infection does not ALWAYS…

A

Cause disease

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3
Q

Subclinical infection

A

is the rule (only way you can tell a person has been infected is to do an antibody study*) Even if pt says they’ve had chx pox… still check antibodies..

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4
Q

Target organ

A

All viruses have a target organ

Hep B is liver
influenza is lungs

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5
Q

IMportant: the immune system can

A

play an active role in development of symptoms (rash) .. the rash is due to immune response to virus replicating in skin!

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6
Q

Vesicular rashes

A

The fluid in them contains infections virus that can be transferred

Just skin rashes do not hvae this (macular..something)

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7
Q

Localized infections

A

result from virus replication at the site of virus entry

-influenze. breath it in it targets lungs

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8
Q

Systemic or Disseminated infections

A

Take longer to take becuase the virus has to travel to target organ…

Rabies.. virus has to get from bite to the brain.. takes a while. Dont see clinical disease at bite.. see it in the brain. if bite in neck vs leg… have much longer time to treat pt if bite is in leg (neck is close to target organ!)

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9
Q

Acute viral disease

A

Symptoms occur shortly after viral infection (days to a week) Rabies

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10
Q

Persistent or chronic viral disease

A

Symptoms take months or years to occur.. Hep B

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11
Q

Steps in viral patholoties

A

No lipopolysaccharides (no endotoxins) or no exotoxins associated with viral infections

If you stop virus form multiplying - dont get diseases

Viruses only need to alter cells.. not kill cells

Bodies response to infectoin is inflammation, tissure damage… etc play significant role in severety of disease.

Latency is a common property

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12
Q

Steps continued

A

Entry and primary replication

routes are specific per virus
Most entery through mucous, resp or GI
Some inoculated into blood by needles (HIV HEPB) or insect vectors (arboviruses from moisquee or tics)
Most replicate at site of entry and some produce the disease there (flu and rotavirus) and dont spread

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13
Q

Spreading of viruses

A

free in plasma

White blood cells - sensitized T cells..
important - if have a disease like epsteen bar or measles. cause mono.. those viruses multiply and travel through body in WBC’s.. then they alter the normal properties of cells.. WBC are supposed to rid body of other infections.. so pts who have these are immunosuppressed…

RBCs

Nerve fibers
IF they are in the nerver fibers they are hidden by body. When they get to the neurons they can go latent.. body doen’t know they are there. (chicken pox - reactivated causes shingles.. )(chicken pox disease is live attenuated vaccine)(shingles vaccine is an increased level of virus in vaccine to increase immune system response). so can only repress the virus is when it in the periferial and active (like in the skin…)

Direct spread
Repiratory tract infections (flu virus) and
resperiatory TO GI infections (adenovirus)

**Naked viruses cause GI problems.. If you have enveloped virus going thorugh GI tract the envelope gets removed and the virus is killed.

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14
Q

Trophism and target organs

A

Spread from site of infecdtion to other area

Replicate only in tissue with cells having necessary receptors and host factors

*TIssue which shows most prominant clinical symptoms is the target organ.. chicken pox.. resides in neurons but rash is the clniica symptom so SKIN is the target organ.

Epstein bar causing mono.. Blood cells is target organ**

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15
Q

When virus gets to cell

A

Get cell injury

cell could lyse if naked virus
if enveloped virus will tranform cells…

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16
Q

Mechanisms of cytopathogensis

A

Add pic.

A LOT of viruses alter cell membrane structure

NET result of mechanisms is to create inclusion bodies in infected cells..

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17
Q

Inclusion bodies

A

Accumulations of virus specific proteins in the cell..

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18
Q

All herpes viruses cause

All cytomegalovirus

A

Cowdry’s typ a incluseion bodies

Owl’s eye inclusions (intranuclear)

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19
Q

Need to ask question.. :

A

Is it due to physiological issue or is it cause by an infections disease?

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20
Q

Toxicity of virion components

A

ONLY 2 viruses cause toxins…

Fibers of adenovirus

GI invection rotvirus (naked virus - they lyse cell - proteins in cell are released and one of the proteins is toxic)

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21
Q

Desease that you see?

A

and insensitive indicator of virus infection since inapparent or subclinical infections are extremeley common with some viruses

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22
Q

Circumstances and events that can result in disease from virus..

A
Inoculum size
Competence of immune system
Immune and health status of host
Genetic constitution of host
Age and nutritional condition of host
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23
Q

Hepatitis is very important to study for boards

A

… lots of questions will be on these.. and AIDS

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24
Q

Transmission Routes of viruses

A
Respiratory
Intestinal
Urogenital
Oropharynx
Skin and skin glands
Blood (tattoo needles)
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25
Vertical and animla transmission
lk
26
Acute infcection
Clinical signs of infection which last a short period of time (days to weeks) followed by the disappearance of the virus Localized: SHORT incubation time (no viremia) Systemic: LONGER incubation time.. Viremia possible (virus in blood)
27
Persistent
HEP B - persiste in infections form with continuous or intermittant shedding, EBV
28
Slow
Long incubation time, months or years... follwo acute diseasa
29
Latent
HSV VZV,
30
Reactivation of persistent infections
Old age, pregnancy, leukemias, lymphomas.. and POST-TRANSPLANT immunosuppression*, HIV AIDS - cytamegalo virus kills pt, not the aids virus..
31
Transorming
many viruses transform cells in culture.. strong association wiht human cancers.. EBV, HPV, HBV, HTLV1, HTLV2
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Host immune response to viruses
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33
Nonspecific resistence - innate immunity
age and physiological condition of the host... anatomical chemical barriers
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Nonspecific resistence - Cellular resistance
lack of receptor sites non-permissive cells - actively growing cells are more permissive (small lymphs..add
35
inflammation
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36
Interferon
AntiVIRAL host glycoprotein which is NOT virus specific bu species specific (human interfurons vs horse interfurons - different) *FIRST HOST DEFENSE MECHANISM at site of invection They induce anti-viral proteins like 2, 5 A synthetase.. and kinases
37
Know chart... 2, 5 A synthetase
Degrades viral mRNA adn inhibits protein synthesis... ***Add picture slide 21..
38
Interfuron is important**
Study it . It is an antiviral state for ALL viruses.. NON SPECIFIC RESISTANCE
39
Specific resistance
humoral immunity
40
Humoral immunity
ANTIVIRAL antibodies that sits on surface of attachmetn protein so viruses can bind and invect cells. anti VAP ab cytolysis of virus infected cells.. non0neutralizing antibody
41
Cell mediated immunity - antiviral cells
lk
42
Most important components for eliminating disease are..
antibodies... Ab adn IFN (interfuron) MOST important for cytoloytic infections accompanied by viremia and infectious of epithelial surfaces... SO smart way to control infection is destroy factory (cell) NOT the virus..
43
Role for Ab-Ag complexies
skin rashes - play a role in maculopapular rashes tissue deposition - deposits in kidney HBV -may initiate intravascular coagulation.. * negative immune response
44
Auto immune response
lkj
45
Viral - induced immune suppression
SHould no HIV, CMI, EBV, measles, CMV, VZV, CMI..
46
Molds
morphological forms of fungal infections.. molds - Yeasts - Dimorphic fungi (hisotplasma, blastomyces, coccidiodes) - exist as yeast or mold depending on environmental cond's - in body yeasts..
47
Types of fungal infections
superficial - athletes foot cutaeous subcutanious systemic opportunistic - individuals with CIS (compramized immune system)
48
Fungal growth
eukaryotic, grow in soil, secrete degredative enzymes to obtain nutreins they need
49
Superficial and cutaneous
keratine as source of nutrition.. no immune response cosmetic probs (athletes foot.. ringworm) itching scaly skin
50
Subcutaneous mycoses
found in soil and thorns enter through cuts not transmissable Granulamatous ulcer warty nodules localized abscesses
51
Systemic mycosis
dimorphic fungi geological areas aerosolized so enter body in lungs (spores) usully mild if healthy
52
Most important thing in diagnosing infection iss...
clinical history- get as much info as possible.
53
opportunistic mycosis
immunocompramized indivuduals serious lung involvement usuallyi part of normal flora all are not dimorphic except for candida
54
Antifungal agents
major mechainsm is to inhibit ergosterol synthesis Second mechansim is to inhibit fungla glycansynthesis
55
Pathogenic parasites
They are geographical.... protozoa - ameba, flagellates, ciiates, sporozoa helminths (worms) - nematodes cestodes and trematodes
56
Protozoa
df
57
Helminths
lk
58
cestodes
lk
59
Nematodes
lk
60
Trematodes (flukes
0
61
So for each parasite there is a specific way to get into host... usually by ingestion..
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