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host
supporting organism, thing providing pathogen with the environment it needs to live, grow, and reproduce
infection
invasion and multiplication of harmful microorganisms, which can lead to damage to tissues and disease
pathogen
microorganisms capable of producing a disease
opportunistic infection
cause disease in immunocompromised host
prions - what are they
protein particles that lack a genome
resistant to enzymes which normally break down proteins
normal cells tricked into producing abnormal proteins which deposit s amyloid plaques
prions - pathophysiology
slowly progressive degeneration of nerves (don’t see symptoms right away)
amyloid plaques in brain, spread throughout nervous system
prion proteins are mutant forms of normal host protein which cause disease
prions - examples
chronic wasting disease - seen in deer and elk
bovine spongiform encephalopathy (mad cow disease) - affects cattle but humans can get from eating infected meat
creutzfeld-jacob disease - humans
S/S: ataxia, dementia, wasting
*no treatment, rare
virus - thrive, replication, structure
thrive and reproduce only in a host cell (intracellular)
simple organisms w/ no organelles
basic structure contains nucleic acid protected by capsid
some enclosed within a lipoprotein envelope
virus - classification
7 classes based on presence of dna OR rna and single or double strands (viral genome), type of replication, and disease produced
virus - life
attachment to cell surface proteins, receptors
penetration
uncoating - release of nucleic acid
replication
assembly & release of new virions
virus - how body gets rid
antibodies (tagging of virus for phagocyte to eat, clumping, etc.)
cytotoxic T cells - search for infected cells presenting on MHC1
interferons - proteins inside cell that are turned on by a virus coming in, tells other cells to not let the virus in
virus - damage to cells
disrupt protein synthesis
promote apoptosis
cause infected cells to become malignant
virus - evade hosts immunity
mutate, hide, shut down immune signaling, sabotage MHC presentation, or attack immune cells directly
bacteria - basics
prokaryotic, unicellular
1 chromosome
plasmids w/ circular DNA
typically both RNA and DNA
bacteria - categorization
based on morphology, staining
cocci, bacilli - shape
gram negative or positive
attachement - pili
bacteria - staining
cell walls contain peptidoglycan
gram negative stain red - thin layer peptidoglycan, outer layer of lipopolysaccharide
gram positive stain purple - thick layer of peptidoglycan
tells us susceptibility to antibiotics
bacteria - harder to kill
gram negative bacteria are harder to kill because outer layer of lipopolysaccharide is an extra barrier thus making them harder to penetrate
bacteria - toxins (how they cause damage to cells)
when we ingest bacteria they produce toxins that cause inflammation and damage
exotoxins: both + and -, secreted proteins and enzymes that are very specific and potent
neurotoxins (nerves), enterotoxins (gut), cytotoxins (kill/damage cells)
endotoxins: gram - only specifically their lipopolysaccharide walls, released when bacteria die, cause excessive inflammation symptoms
fungi - overview
eukaryotic (have nucleus w/ rna and dna) organisms, different wall than bacteria
types: mold, yeast, dimorphic
mycosis = infection with fungus
fungi - where they grow
skin and mucous membranes because require cooler temperature than body temp so most on surface
fungi - who is most susceptible
immunocompromised or infants are most susceptible, opportunistic infection (healthy people typically not affected, but immunocompromised people are likely to be)
*need antifungal agents, antibiotics do not penetrate wall
parasites - what are they
members of the animal kingdom that infect us
helminths (parasitic worms) spread by the ingestion of eggs, or through the skin (roundworms, tapeworms, flukes)
arthropods that carry parasites = ticks, mites, lice, fleas, mosquitos
parasites - protozoa infection
eukaryotic, unicellular
spread directly by host to host (sexually) or indireclty from arthropod or food/water ingestion
example: plasmodium, the malarial parasite, transmitted by anopheles mosquito → invades liver cells → liver cells rupture → released in blood → RBCs infected → plasmodium multiply in RBCs → S/S: intermittent fever, chills, anemia, neurological damage, death
how do infections overcome the immune system
microbial adherence - attach to mucous membranes
encapsulation (thick carb/protein coat) - protects against phagocytosis
rapid replication - overwhelms immune system
mutation - constant genetic changes can alter surface proteins, leading to antibiotic resistance
enzyme/toxin production - dissolve EC matrix, prevent antibiotics from reaching
biofilm formation - form slimy protective layer on surfaces to shield from antibiotics and immune cells
intracellular survival - hide inside cells
antigenic variation - change surface antigens so antibodies don’t recognize them
coating with host antigens - disguise themselves to avoid detection
S/S of infection
related to site of infection
general: fever, malaise, increased WBC count
clinical stages of infectious disease
incubation - exposure
prodromal - in b/n stage, start to develop generalized symptoms
acute - increase in severity of symptoms + become specific
convalescence - treatment has started to kick in
atypical courses
fulminant - no prodrome
insidious - prolonged prodromal phase
subclinical/subacute - no clinical S/S
diagnosing infection
culture and sensitivity
growth of microorganisms outside body
determination of antibiotic effectiveness
gram stain
serology
measuring specific antibodies in the serum
detection of antigens
DNA and RNA sequencing of organisms