Week 3 - Microbiology Vial, Fungal, and Parasite Pathogensis Flashcards
what should we know?
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…
Infection does not ALWAYS…
Cause disease
Subclinical infection
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..
Target organ
All viruses have a target organ
Hep B is liver
influenza is lungs
IMportant: the immune system can
play an active role in development of symptoms (rash) .. the rash is due to immune response to virus replicating in skin!
Vesicular rashes
The fluid in them contains infections virus that can be transferred
Just skin rashes do not hvae this (macular..something)
Localized infections
result from virus replication at the site of virus entry
-influenze. breath it in it targets lungs
Systemic or Disseminated infections
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!)
Acute viral disease
Symptoms occur shortly after viral infection (days to a week) Rabies
Persistent or chronic viral disease
Symptoms take months or years to occur.. Hep B
Steps in viral patholoties
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
Steps continued
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
Spreading of viruses
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.
Trophism and target organs
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**
When virus gets to cell
Get cell injury
cell could lyse if naked virus
if enveloped virus will tranform cells…
Mechanisms of cytopathogensis
Add pic.
A LOT of viruses alter cell membrane structure
NET result of mechanisms is to create inclusion bodies in infected cells..
Inclusion bodies
Accumulations of virus specific proteins in the cell..
All herpes viruses cause
All cytomegalovirus
Cowdry’s typ a incluseion bodies
Owl’s eye inclusions (intranuclear)
Need to ask question.. :
Is it due to physiological issue or is it cause by an infections disease?
Toxicity of virion components
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)
Desease that you see?
and insensitive indicator of virus infection since inapparent or subclinical infections are extremeley common with some viruses
Circumstances and events that can result in disease from virus..
Inoculum size Competence of immune system Immune and health status of host Genetic constitution of host Age and nutritional condition of host
Hepatitis is very important to study for boards
… lots of questions will be on these.. and AIDS
Transmission Routes of viruses
Respiratory Intestinal Urogenital Oropharynx Skin and skin glands Blood (tattoo needles)
Vertical and animla transmission
lk
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)
Persistent
HEP B - persiste in infections form with continuous or intermittant shedding, EBV
Slow
Long incubation time, months or years… follwo acute diseasa
Latent
HSV VZV,
Reactivation of persistent infections
Old age, pregnancy, leukemias, lymphomas.. and POST-TRANSPLANT immunosuppression*, HIV
AIDS - cytamegalo virus kills pt, not the aids virus..
Transorming
many viruses transform cells in culture.. strong association wiht human cancers..
EBV, HPV, HBV, HTLV1, HTLV2
Host immune response to viruses
w
Nonspecific resistence - innate immunity
age and physiological condition of the host… anatomical chemical barriers
Nonspecific resistence - Cellular resistance
lack of receptor sites
non-permissive cells - actively growing cells are more permissive (small lymphs..add
inflammation
w
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
Know chart… 2, 5 A synthetase
Degrades viral mRNA adn inhibits protein synthesis… ***Add picture slide 21..
Interfuron is important**
Study it .
It is an antiviral state for ALL viruses.. NON SPECIFIC RESISTANCE
Specific resistance
humoral immunity
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
Cell mediated immunity - antiviral cells
lk
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..
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
Auto immune response
lkj
Viral - induced immune suppression
SHould no HIV, CMI, EBV, measles, CMV, VZV, CMI..
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..
Types of fungal infections
superficial - athletes foot
cutaeous
subcutanious
systemic
opportunistic - individuals with CIS (compramized immune system)
Fungal growth
eukaryotic, grow in soil, secrete degredative enzymes to obtain nutreins they need
Superficial and cutaneous
keratine as source of nutrition.. no immune response
cosmetic probs (athletes foot.. ringworm)
itching scaly skin
Subcutaneous mycoses
found in soil and thorns
enter through cuts
not transmissable
Granulamatous ulcer
warty nodules
localized abscesses
Systemic mycosis
dimorphic fungi
geological areas
aerosolized so enter body in lungs (spores)
usully mild if healthy
Most important thing in diagnosing infection iss…
clinical history- get as much info as possible.
opportunistic mycosis
immunocompramized indivuduals
serious lung involvement
usuallyi part of normal flora
all are not dimorphic except for candida
Antifungal agents
major mechainsm is to inhibit ergosterol synthesis
Second mechansim is to inhibit fungla glycansynthesis
Pathogenic parasites
They are geographical….
protozoa - ameba, flagellates, ciiates, sporozoa
helminths (worms) - nematodes cestodes and trematodes
Protozoa
df
Helminths
lk
cestodes
lk
Nematodes
lk
Trematodes (flukes
0
So for each parasite there is a specific way to get into host… usually by ingestion..
er
