Exam one: L1-L4 Flashcards
L1:Who developed single lensed microscopes?
Robert Hooke and Antoni Van Leeuwenhoek
L1: What did Edward Jenner do?
reports cowpox vax against smallpox
L1: Florence Nightingale found:
hygiene is a great way to avoid infection
L1: Pasteur and Koch found:
microbes are causative agents of disease
L1: Hans Christian Gram did:
Gram Stain
L1: Alexander Flemming
Penicillin
L1: Chain and Florey
purification/production
L1: Avery, Macleod, McCarty
DNA is a transforming principle
L1: Watson, crick and Franklin
DNA structure
L1: Roberts
restriction enzymes
L1: Boyer and Cohen
recombinant DNA
L1: Kary Mullis
PCR
L1: morphology: how big are spheres and rods, and what microscope can you use to see them?
spheres are 0.2-2 µm diameter, rods are 0.2-2 µm wide. Can be seen with a light microscope
L1: What is the composition of a bacterial cell?
90% similarity to euks.
55% protein, 20% RNA, 3% DNA, 5% carb, 6% phospholipid
L1: What is the only envelope type found in mycoplasma?
cytoplasmic membrane
L1: What is present in the GP envelope?
capsule, pilli/flagella, PG, Techoic acids, cytoplasmic membrane
L1: What is present in the GN envelope?
capsule, pilli/flagella, LPS, PG, Periplasm, cytoplasmic membrane
L1: What part of the LPS is recognized by the immune system? What recognizes it and what does it activate?
lipid A tail is recognized by TLR 4 and induces immune response via Il2, Il3 and TNF-a.
L2: What is the origin of the normal microbiota? What is it dependent on?
Birth canal, is dependent on the route of delivery, who is present during birth, environment
L2: What factors determine the nature of the microbiota?
Local physiology and ecology, diet, microbial attributes, competition
L2: What is the microbiome of the skin?
Staph. epidermidis, cutibacterium
L2: What is the normal microbiota of the conjunctiva?
S. epidermidis and non-pathogenic corynebacteria
L2: What is the normal microbiota of the mouth?
s. mutans on teeth, neisseria and moraxella in throat, anaerobes and microaerophillic organisms in gingival crevice
L2: What is the normal microbiota of the stomach and small intestine?
sparsely inhabited bc too acidic
L2: Normal microbiota of the colon?
90% anaerobes: bactericides and fusobacterium
10% facultative anaerobes: E.coli, other enterobacteria
L2: What was found in the microbiota of breast-fed infants?
Increased bifidobacterium
L2: Normal microbiota of the nose?
mostly staph aureus and s. epidermidis
L2: Normal bacteria of the nasopharynx?
Similar to mouth but with strep pneumonia, neisseria meningitidis, haemophilus
L2: Normal microbiota of larynx, below mid ear and sinuses?
none, protected by mucociliary escalator
L2: Normal microbiota of the urinary tract?
scanty microbiota but contamination from perineum in first bit of urethra
L2: Normal Microbiota of the vagina through time?
Before puberty/after menopause: mixed, non-specific from skin, colon and perineum
during child bearing Yeats: lactobacillus, anaerobic GNRs, GPCs, mycoplasma, ureaplasma
L2: What is the role of microbiota in disease?
opportunists can cause disease and genetic attributes
L2: What are the four main beneficial effects of the microbiota?
- Priming the immune system
- exclusionary effect as demonstrated by antibiotic treatment
- nutritionally via digestion, malabsorption, vitamin k
- normal function of organs/systems
L3: What are the steps of patient diagnosis?
history, physical exam, imaging
L3: What are the steps of specimen identification?
description, microscopy, culture, molecular, immune response
L3: What do we look for in immune response of specimens?
cells present- WBC and where?
Immunoglobulin- Igm, igG
L3: How do we identify etiological agents?
determine nature of disease, predict course and potential outcomes, tailor therapy, exclude non infectious cause of symptoms
L3: What are sterile specimens?
urine and blood
L3: What are some non-sterile specimens?
indirect: specimen collected through a site containing a normal microbiota
OR a site with a normal microbiota
L3: What are the different ways we study specimens with microscopy? Type of microscopy and what to see
Bright field: gram stain and acid fast
dark field: thin organisms and spirochetes
fluorescence microscopy: very sensitive but artifacts can cause problems
L3: How do we culture organisms?
with nutrient, selective or indicator media?
L3: What are different incubation conditions?
temperatures, aerobic, microaerophillic, anaerobic, candle jar
L3: What two important tools are required for conventional identification?
- 9 log amplification
- ability to isolate single cells on a plate
L3: What do we look at when identify microbes?
gross phenotype, biochemical characteristics, antigenic structures, toxin production, nucleic acid sequences, flow on information
L3: What is the serological detection of an infection?
identification of host immunoglobulins specifically recognizing antigens from pathogenic organisms
L3: How is humoral immune response in an immunocompromised person identified?
IgM, clonal switching, IgG.
L3: What happens over the Course of a primary response to an infection?
10 day latent period, increase in IgM before later increase in IgG, plateau phase around 15 days before decline phase.
L3: What happens over the course of a secondary infection?
after second exposure, IgM increases around day 5 then decreases while IgG increases steeply and stays high past 10 day mark
L3: When would you use a pathogen specific nucleic acid sequence?
When organisms are difficult or impossible to cultivate
L3: Can a dead pathogen cause an infectious disease or pathology?
No, infectious agent must propagate to infect people, and dead pathogen can cause pathology bc of DNA remnants
L3: What are some drawbacks of molecular detection?
- false positive results due to contamination
-contamination obscuring diagnosis
-limited ability to asses pathogen properties
L3: What are the methods of molecular detection?
1- PCR
2- PCR and sanger sequencing
3- next gen sequencing
L3: What are the sequencing platform requirements?
- accuracy for identification
-informative about phylogeny - accurate evolutionary clock
L3: PCR steps?
- extract template
- amplify target sequence
- determine DNA sequence of amplicon
- align DNA sequence with sequences obtained from phenotypically validated isolates
- establish identification
L3: What are some problematic situations for conventional approaches?
- presence of contaminating DNA
- polymicrobial infection
- infection at sites with microbiota
L3: What are the seps of next gen sequencing?
- Capture single molecule templates
- cluster formation
- immobilization, 3’ extension, bridge amplification, linearization, 3’ protection, hybridization of sequencing primers - simultaneous sequencing
L4: what is a primary pathogen?
an organism that infects a competent host
L4: What is an opportunistic pathogen?
an organism that infects a compromised host via loss of specific defense mechanisms or loss of non-specific defense
L4: What in infection and when does it occur?
occurs after colonization when multiplication is sufficient to induce damage to the host
L4: What are the 5 signs of inflammation?
rubor (redness), tumor(swelling), calor(warmth), dalor(pain), LOF
L4: what is an infectious dose?
quantity of pathogen required to establish infection
L4: what are key parameters of exposure?
proximity, time, presence/absence of barriers
L4: what is net replication?
bacterial rep-bacterial death
L4: what is a virulence determinant?
unique attributes that permit a microbe to successfully establish infection and cause subsequent disease
L4: what is virulence?
quantitive measure of pathogenicity or likelihood of causing disease
L4: What is infectivity?
quantitive mausre of pathogens ability to infect another susceptible host, aka attack rate
L4: what is the equation for attack rate?
infected/#susceptible*100
L4: what are the three keys to colonization?
- adherence via pilli
- motility via flagella and chemotaxis
- survival or fitness in an environment outside host
L4: How do bacteria sequester iron?
siderophores from enteric pathogens
lactoferrin/transferrin receptors on mucosal surfaces(gonorrheaoe)
L4: How do bacteria avoid host surveillance intracellularly?
-live in vacuole and modify or block phagolysosome
- break out of phagolysosome or live in cytoplasm
L4: How do T3 secretion systems work?
Penetrate three barriers to release effector molecules that lead to intracellular replication
L4: How do bacteria avoid host surveillance extracellularly?
-Inhibit phagocytosis via capsules, IPA proteases and binding host proteins(M-proteins)
- block complement mediated lysis
- antigenic variation
L4: How do bacteria avoid host surveillance by altering host immune response?
- exotoxin: pertussis toxin
- endotoxin: can overstimulate host=DIC
- antigenic variation
- superantigens: polyclonal T-cell proliferation
L4: What are the two types of toxins bacteria make?
Endotoxin and exotoxin
L4: What are the two types of exotoxins and what does each target?
A catalytic subunit toxin: targets ADP ribosylates G-proteins
B membrane binding subunit: translocates A subunit into host cytoplasm
RTX: homylsins
L4: What are the different endotoxins and what are they present in?
endotoxin/LPS: GN
lipoteichoic acid: GP
PG: Both GN and GP
L4: What are the three mobile genetic elements?
- carried by bacteriophages: diphtheria
- plasmids: yersinia adhesions, invasions and effectors
- transposons: drug resistance
L4: How do bacteria regulate virulence determinants?
- Alter expression of determinants in response to temp, ionic conditions, oxygen concentration, pH
- Two component regulatory systems: R S–> S senses environmental stimuli and R is the response regulator
