TBL 3 Flashcards
examples of helical shaped viruses
advantage of shape
Examples: Influenza, Measles, Mumps, Rabies, Ebola
REMIM
Advantages: only one type of capsid protein is required less free energy to assemble than a capsid composed of multiple proteins
examples of icosahedron-shaped viruses
advantage of shape
parvo B 19, Hepititis, Dengue, Norwalk, Polio virus, rhinovirus, adenovirus
far more common
naked virus examples
poliovirus
enveloped viruses
envelope comes from the host, examples are HIV HERPES
Gram – bacteria have ______ and are recognized by _____
Gram-negative bacteria can also induce pro-inflammatory cytokines by:
Lipopolysaccharides (LPS) endotoxin is recognized by TLR4
LPS is a key mediator of sepsis and septic shock
gram + bacteria have ___ and are recognized by _____
Gram-positive bacteria can also induce pro-inflammatory cytokines via bacterial components such as:
Teichoic acid and lipoteichoic acid are both recognized by TLR2 and TLR6
Acid-fast bacteria:
The hydrophobic composition of _________ impairs recognition by immune receptor
mycolic acid, glycolipids, and lipoarabinomannans
Bacterial flagellin is recognized by ______
Peptidoglycan is recognized by ______
Unmethylated CpG nucleotides in bacterial DNA are recognized by _____
Bacterial flagellin is recognized by TLR5
Peptidoglycan is recognized by TLR2
Unmethylated CpG nucleotides in bacterial DNA are recognized by TLR9
simple viral replication steps
what virus have ssRNA and what does that mean?
Influenza and Ebola
because they have ssRNA they use RNA pol which makes a lot of errors and becomes advantage when invading the immune response
antigenic drift vs antigenic shift
Viral genetic material is recognized by the innate immune receptors:
Double-stranded RNAs make up the genomes of some viruses and are generated during the life cycle of most viruses recognized by _______
TRL3
Single-stranded viral RNAs recognized by ____, _____,______,_____
TRL7, TLR8, RIG-I, MDA-5.
Viral DNA with unmethylated CpG nucleotides recognized by ______.
Triggers antiviral state by inducing _____
what is inhibited by this molecule?
TLR9
Interferon 1
what are the main mechanisms we are able to get of virus-infected cells?
cytotoxic T cell toxicity is the main
crytococcus neoformans ( yeast) vs Aspergillus fumigatus (mold)
clinical significance
______ is the main cause of fungal infections?
what are the different areas that can be affected?
what are the PRR that recognize the fungal antigens? what are the PAMP that is recognized)
TLR-4 and TLR-2
describe the immune response of a yeast infection
dendritic cells present PAMP Olinked mannan or phospho-lipomannan lipoproteins on their MHC II receptor to the T cells
Th17 secrets IL 17 and activates neutrophils to kill infection
helper T2 activates B cells
Helper Th, activates macrophages through INF gamman and TNF alpha
characteristics of fungi
characteristics of protozoa
Giardia duodenalis vs plasmodium falciparum
nematodes vs tapeworms vs flukes
Helminths and protozoa such as Plasmodium spp., Toxoplasma gondii, and Cryptosporidium spp predominantly recognized using _______on dendritic cells
TLR-2 and TLR – 4
protozoa are recognized by TLR 11
main players of immune response against the parasites
macrophages secrete NO, neutrophils secrete hydrogen peroxide and eosinophils release lots of enzymes
Kuru vs CJD
dysbiosis
imbalance of microbiota can lead to infection
ex, if taking antibiotics can kill lactobacillus in the vagina which will allow for opportunistic infection of candida albicans(yeast infection)
exogenous infection comes from ____________ and examples are_______
influenza virus (flu)
neisseria gonorrhoeae( gonorrhea)
clostridium tetani (tetanus)
treponema pallidum (syphilis)
endogenous infections comes from _____ and examples are_____
s. viridans found in the oral cavity all the way down to GI
strict pathogens are _____and example is _____
the majority of infections are ______
How are pathogens able to disrupt the normal microbiota in the gut and become infectious? how does our own microbiome try to compensate?
bacteria that is part of our gut?
E. coli, Enterococcus spp.
bacteroides spp., clostridium spp.
Ecoli BEC spp
EE make need O2 so C. diff cant grow here
BC make buteric acid and salmonella doesnt like that
what are the different virulence factors
what are some examples of virulence factors?
what are some virulance factors for used for invading the immune system??
evading (hiding):
what inflicts disease?
what are biofilms and why are they a problem?
capsular polyssacharides can be made antigens for vaccines of streptococcus pneumonia and haemophilus influenzae
what are the different parts of LPS (endotoxin) and where are they found?
Lipopolysaccharides (LPS) are made up of a lipid domain (lipid A), a core oligosaccharide, and a distal polysaccharide (O-antigen). The lipid A is a hydrophobic anchor that is the main virulence factor of LPS.
describe the two immune responses that can be produced by LPS (endotoxin)
antigen-specific is proper for host
the non-specific acts as mutagens elicit an oligoclonal expansion and is bad for host!!!
what are superantigens ?
type of mutagen
results in oligoclonal activation of T cells
what are the bacterial that can cause disease in the upper respiratory tract?
neisseria meningitides,
Clostidium diphtheriae,
bordetella pertussis
what are the normal microbiota of the GI? (5)
99% are anaerobic genera such as:
Bacteroides, Bifidobacterium, Eubacterium, Peptostreptococcus, and Clostridium
These genera proliferate and occupy most available niches
They help produce metabolic waste products such as acetic, butyric, and lactic acids
The strict anaerobic conditions, physical exclusion and bacterial waste products are factors that inhibit the growth of other bacteria in the large bowel
what are the normal microbiota of the GU?
STAGES OF INFECTIONS:
PUT THEM IN ORDER
DECLINE, PRODROMAL, ILLNESS, CONVALESCENCE, INCUBATION. what does each stage mean?
what is the communicability period? latency? carrier state?
clinically important encapsulated bacteria?
gram positve and gram negative
