Lecture 1: Infection and Disease Flashcards
Microbiota
personal unique mix of bacterial species colonize: nose mouth, eye, upper resp. tracts, intestine and urogenital, and skin.
Deaths from infectious disease per year
15 million
one pathogen can… (3)
…cause more than one disease
-new diseases coming. old diseases re-emerging
…be used in bioterrosism (ex. anthrax)
superbugs
become resistant to antimicrobials- *awareness when rxing antibiotics
Phylogenic tree of life
is organism a Bacteria, fungus, protozoan, or virus
Proakaryoitc cells
small, no nucluear membrane of nucleoli, no membrane enclosed organells, no carbohydrates on plasma membrane, no cytoskeleton or cytoplasmic streaming, ribosomes are small
binary fission for cell division.
*think, loft/studio apartment
Eukaryotic cells
larger than prokaryotes, true nucleus with membrane and nucleoli, membrane bound organelles present, sterols and carbs on plasma membrane as receptors, cytoskeleton, larger size, mitosis
**think mansion with many rooms
Gram- negative cell wall
peptidoglycan later surrounded by outer membrane
Gram-Positivie cell wall
layers in peptidoglycan with no outer membrane
Viral Pathogens
Viruses not microbes and are not cells- they have DNA or RNA care and are surrounded by a protein coat (capsid)
Viruses cannot replicate withouth replication machinery in a host cell (obligate parasite)
Ex: SARS-coV-2, COVID-19, HIV, Hep A/B, Measles, Influenza
Fungi
- may cause human disease
- others produce useful antibiotics
- can cause food spoilage
ex) Candida albicans, aspergillus fumigatus, blastomyces dermatitis, pneumocystis jirovecii
* alexander flemming-penicillin won nobel prize
Typles of Parasites (5)
1) Flagellates- with flagella (ex. giardia, trichomonas, trypanosomes)
2) Amebae- entanomoeba, neagleria, and acanthamoeba
3) Sporozoa- cyptosporidium, toxoplasma, malarial parasies
4) ciliates- rare, only 1 human parasite
5) heminths- parasitic worms
Mutulism
symbiotic relationship that benefits both participants
Commensalism
symbiotic relationship that benefits microbe but does not affect host
parasitism
symbiotic relationship that benefits microbe and harms host
Sterile Sites
blood, CSF, internal organs, muscles bone and brain
* if site has organisms something is very wrong
Contributors to microbtiota development
breast feeding, delivery (cesarian vs. vaginal), feeding from maternal skin, hands and feet introduced to mouth, hands on floor, siblings and pets
Pathogenicity
qualitative trait referring to genetic capacity to cause disease/ liklihood that infection will results in disease
Virulence
quantitative trati: related to the extent of pathology (degree of disease) caused by microorganism.
expresses interaction between pathogen and host.
ex: cold-low virulence while ebola-high virulence
For disease to occurr…
…pathogen must come in contace with proper body part in sufficient numbers
portal of entry is the route an exogenous pathogen uses to enter body
infectious dose is number of microbes entering body
Respoiratory portal
inhalation of pathogens in air
GI portal
fecal oral
urogenital portal
sexually transmitted
parenteral
peircing skin or muccous membranes through cuts, bites, injections
translocation
organism moves from one area to another (e coli from GI to urethra to bladder)
Letal Dose
50% LD50, number of bacteria or virus particles required to kill 50% of an experimenl group of animal hosts
**Low LD50 is highly virulent
Infectious dose
50% ID50, infectious dose to colonize 50% experimental hosts
measured by determining how many microbes are required to cause disease symptoms in half of an experimental groups of hosts
not easy to measure
Primary infections
occur in otherwise healthy individuals
Secondary infections
occur in a body weakend by a primary infections
ex) post-influenze bacterial pneumonis
local disease
restricted to single area
systemic disease
disseminate to organs and systems
bacteremia
-emia in blood
transient, septicemia is proliferation of bacterial cells in blood
signs of disease
evidence/ fever, bacterial cells in blood
symptoms of disease
changes in body function, sore throat & headache
syndrome
collection of signs and symptoms
incubation period
time from contact to fisrt symptoms, replication
prodromal phase
time of mild discomfort
acute period
illness most severe
period of decline
when illness subsides
period of covalescense
return to good health
Capsules
exist on bacterial, fungal, and protistan speies
defensice structures prevent invating cells form engulfing and aid in the sucess of adhering to host cells
Pili
exist on bacterial cells
offensive structures adere to specific protein receptos sites on target host cells, aid in adhering to host cel
Spikes and capsid proteins
exist on viruses
offensive to bind to receptos on host cell in aid inhost cell adhesion
Adhesion
Virulence factor: many pathogens have adhesins that allow then to adhere to specific tissutes
*gram-neg bacterial species contain pili that can adhere to specific host cell on tissue baased on adhesions located on pili
Invasiveness
ability of pathogen to penetrate tissues and spread
some use phagocytosis by body cells to enter cells and pass through defenses
Chemical Virulence factors (3)
1) enzymes: offensive or defensive
2) toxins: exotoxins, cytotoxins, neurotoxins, enterotoxins
3) biofilms (not technically chemical virulence factos)
Enzymes as virulence factor
help pathogens resist body defenses
ex. staph produce coagulase to from blood clot to protect from phagocytosis
Hyaluronidase
Enzyme that can influence virulence: enhances pathogen penetraton through tissues, chews away at hyaluronic acid
Leukocidins
Enzyme as Vir. Fac. disintegrate neutrophils and macrophages
Hemolysins
Enzyme as Vir. Fac.
dissolve RBC
Biofilms
can enhance virulence becuase immune cells cannot reach bacterial cells
toxigenicity
ability of pathogents to produce toxins
toxemia
presence of toxins in blood
exotoxins
proteins produced during bacterial cell metabolism within cell, and sent out during lysis.
*most common in gram + bacterial
- cytotoxins kill cells
- neurotoxins interfere with nerve transmission
- enterotoxins affect intestinal tract
Antitoxins
produced by host to newutralize toxins
toxoids
toxins whose toxicity has been destroyed but still elicit immune response
-great for vaccinations, build immunity (ex. diptheria and tetanus vax)
Endotoxins
released upon disintigration of gram - cell walls
- endotoxin part of gram neg cell wall
- lipid portion of lipopolysaccharides
- part of outermembrane
- cause blood coagulation
- endotoxin shock may occur with antibiotic treatment of deseases caused by gram negative bacilli
**gram + dont have endotoxin
Reminder of disease
lasting effects of disease: paralysis from polio/ arthritis from lyme disease
Resevoir, 3 types
Resevoir= source of pathogen
1) nonhuman: ex. rabid bat for transmission of rabies
- human dead end host (no human-human transmission or human-animal)
2) Human; smallpox- humans only resevoir (all new infections acquired from people)
3) nonliving: food, soil, water
Zoonosis
disease transmitted from animal to human
Horizontal spread
person to person contact
vertical spread
mother to fetus or newborn during delivery
indirect transmisstion
results from contact with non living onjects or vectors
Fomites
inanimate object where organisms can linger
Vehicle
contaminated food, water, or air
vector-indirect
zoonotic method of disease spread (ticks, mosquitos, etc)
Mechanical
passive
biological
mathogen multiplies within insect
Epidemiologist
track how disease spreads throughout populaton
epidemic
disease occuring in excess of what is normally expected within populaiont
oubreak
more contained epidemic- contained in cetain aread
pandemic
worldwide
Mode of transmittion of HAI
patient-patient
patient-staff
indirect patient-contaminated surfaces or instruments
nosocomial infections
acuired in hospital
Skin microbiota
*primarily gram +
staphylococcus, streptococcus, corynebacterium, propionibacterium, microccocus
fungal: candida
femal reproductive microbiota
lactobacilis, staphylococcus, corynebacterium, streptococcus, enterococcus
fungal: candida
small intestine microbiota
bacteroides, lactobacillus, streptococcus
large intestine microbiota
dense and diverse microbial population
Urinary tract (female) microbiota
lactobacillis, cerynebacteriums, streptocccus, bacteroides
Male urinary tract microbiota
corynebacterium, streptcoccus
Oral cavity microbiota
streptococcus, treponema, neisseria, haemophilus, lactobacillis, staphyloccus, propionibacterium
Upper respiratory tract
diverse microbes vary by site (nose, nasopharynx, etc)
streptococcus, neisseria, haemophilis, staphylocccus
fungal-candida
phases of disease
1) incubation period
2) prodromal phase
3) acute period
4) period of decline
5) period of convalesencse
obligate parasite
parasite the relies on host cell to replicate and nourish
cytotoxins
KILL CELLS
neurotoxins
impair funfctioning of nervous system
enterotoxins
affect intestinal tract
Pathogen entry into host cell depends on cell adhesion
1) capsules
2) Pili
3) Spikes and capsid proteins
