Intro Micro Flashcards
Cryptococcus neoformans
Only encapsulated yeast
LPS
Found in G-ve outer membrane layer (aka endotoxin)
G+ve acids in PG layer
Teichoic acid and Lipoteichoic acid
Peptidoglycan (PG)
Aka cell wall, thick in G+ve and thin in G-ve; cross-linked NAM and NAG chains
*important target for antibiotics
Gram Staining
- Crystal violet (stains cell wall)
- Iodine (shrinks cell wall)
- Decolouriser (removes crystal violet from G-ve cell walls
- Safranin (stains cell wall of G-ve pink)
G-ve PG linkage
Peptide bond linkage, LPS in outer leaflet, portions in outer membrane (diffusion of specific low molecular weight hydrophilic compounds)
LPS (endotoxin)
Lipid A - anchors the LPS in the phospholipid layer and is assoc w/ the sx’s of toxic shock
- LPS is physical barrier to protect the G-ve bacteria
Porins
Water-filled open channels that allow passive diffusion of molecules and blocks entry of harmful substances; contributes to abx resistance by G-ve bacteria
G-ve
2 layers, LPS/lipoprotein/PG, thin cell wall (PG), periplasmic space, outer membrane, porins, less permeable and more resistant to abx
G+ve
1 layer, PG/Teichoic/Lipoteichoic acids, thick cell wall (PG), more permeable and less resistant to abx
Acid Fast Stain
used when specimen can’t be stained w/ Gram Stain
- Carbol fuschin
- Heat 🔥
- Decolourise
- Methylene Blue
* stains Mycobacterium and Nocardia
Endospore Stain
- Malachite green
- Steam bath
- Water rinse
- Safranin (same as last step in Gram Stain)
Endospore
Resistant to heat and radiation, keratin-like coat responsible for resistance to chemicals
Capsule
- aka “K antigen”
- strongly attached/difficult to remove, highly organized, antiphagocytic (important for virulence), protection against dehydration and facilitate attachment to surfaces
Slime Layer
Loosely attached/easily removed, unorganized, protection against dehydration and facilitate attachment to surfaces
Flagella
Aka “H antigen”
- cocci are rarely motile they just drift in fluids
- motility is key for bacteria causing UTIs, motility is turned on or off in response to the env
Endoflagellum
Corkscrew motility, “spirochetes” (Borrelia burgdorferi - Lime Dz, Treponema pallidum - Syphilis)
KOH prep
- 10% KOH
- Heat 🔥
- Keratin dissolves
- Fungal cells visible
Mycoplasmas
Atypical bacteria, can’t be gram stained bc no PG cell wall, sterols present in outer cytoplasmic membrane to provide rigidity, capable of independent growth
E.g. - mycoplasma pneumoniae
Actinomycetales
Aerobic: mycobacterium (tuberculosis, leprae, marinum) and Nocardia
Anaerobic: actinomyces
Mycobacterium
Mycolic acids (lipids) in CW forming a "waxy" outer coat, slow growth, limited penetration of nutrients; arabinogalactan links mycolic acids to PG E.g. - Mycobacterium tuberculosis
Chlamydia
Unusual lifecycle w/ 2 developmental forms:
- elementary bodies (EB): infections form
- reticulate bodies (RB): replicating form
Chlamydia and Rickettsia
Can’t survive outside of host cell, can’t be cultured on laboratory medium
Fungi
Ergosterol in phospholipid bilayer (target for antifungals), nuclear dsDNA circular, 80S ribosome, diploid gene structure
Cell wall: chitin - made of B(1,4)-linkage of NAGs
Yeast
Unicellular fungi that does not grow as hyphae
Mycelium
Mat of interwoven hyphae, can be septate or non-septate
Hyphae Tip Extension
Growth/extension of hyphae occurs continuously at tips
Hyphae
Threadlike, branching, cylindrical tubules composed of fungal cell attached end to end, grow by extending in length from tips
Dimorphism fungi
Can grow as either yeast or mold, depending on environmental conditions and temp (usually yeast @ body temps)
Pseudohyphae
buds grow but don’t detach; visible constriction, lack permanence/differentiation/true branches/arthrospores and chlamydospores
- e.g. Candida infections
Catalase test
- Loop of H2O2 onto slide
- Mix loop of single colony
- If “fizzing” then it is +
(+ Staphylococcus, - Streptococcus)
Saprophytic fungi
Obtain nutrients and energy from dead or decaying organic material (occasionally human tissue)
Superantigens
Aka exotoxins, cause activation/proliferation of CD4+ T-cells
E.g. - S. aureus
Cytokine Storm
Viral infection causing massive release of IL-1, IL-6, TNF-a
E.g. - SARS (IFN type I release)
Enterotoxins
Released from the microbe, so a form of exotoxins
E.g. - anthrax lethal toxin, shiga toxin, cholera toxin
Herx Reaction
Cause: rapid release of LPS endotoxin from killing bacteria too fast w/ anti-microbial tx
ROS: fever, chills, HA, hypotension, can cause death
*resembles bacterial sepsis
PANDAS
Pediatric Autoimune Neuropsychiuatric Disorders Assoc w/ Streptococcal infections
*Sydenham’s chorea
Asplenic Pt’s
Susceptibility: encapsulated organisms usually cleared through opsoinzation w/ Abs
E.g. - pneumococcal, meningococcal, and Haemophilus influenzae
*highest risk is w/in first 2 yrs s/p splenectomy
Direct Transmission
Sexual; skin-skin (MRSA), animal bites, droplets (Pertussis)
*e.g. - Gonorrhea (sexual; humans), Tetanus (soil), Rabies (animals)
Indirect Transmission
Vehicles, vectors, airborne/aerosols
*e.g. - Dengue (mosquito-human), West Nile (mosquitoes-birds)
Airborn Transmission
Droplet nuclei are suspended in the air for a long period of time; droplet nuclei = dried residue < 5 micrometers E.g. - measles
Vehicles
Food, water, blood (biological stuff), fomites (inanimate objects like door handles/clothing)
- can passively carry or provide growth environment for pathogen and its products
Propogative
Multiplies but no change/development
E.g. - bacteria
Cyclopropogative
Multiplies AND changes/develops
E.g. - Protozoa
Cyclodevelopmental
Develops but does NOT multiply
E.g. - most nematodes and trematodes
*1 larvae = 1 adult
Sanitation
Reduce #s to acceptable public health level
Sterilization
Destruction of all micro organisms
Disinfectant
Sterilization/sanitation used only on inanimate objects
*e.g. - bleach would only be used as disinfectant
Antiseptic
Sanitation/sterilization used on living tissue
Most resistant microorganisms
- Prions
- Endospores
- Mycobacteria
- Small naked viruses
* (G-ve are more resistant than G+ve)
Virulence
Damage in a susceptible host due to host-microbe interaction
*(what microbe is doing and how host is responding)
Pathogenicity
Ability to cause damage and infection, must look at virulence factors to determine pathogenicity
Acute Infection
Incubation and prodrome shorter, more severe symptoms than persistent
Persistent Infection
Longer incubation, prodrome and duration of symptoms (less severe sx’s than acute infection)
*takes body a long time to get rid of the infection
Prodromal
Nonspecific symptoms that are too vague to be able to diagnose what organism is infecting
Chronic Persistent Infection
Long duration, develops slowly, shedding continues
*more about the physical process
E.g. - typhoid fever, leprosy, syphilis
Latent Persistent Infections
Genome maintained in host in absence of microbial replication
E.g. - TB
Intoxication
Ingest food or something with toxin in it
Infection
Ingest bacterium that is actively releasing a toxin
Class I Toxins
Membrane acting/bind to host cell surface
Class II Toxins
Membrane damaging
Class III Toxins
Intracellular toxin
Tetanus Toxin
Producer: Clostridium tetani
Effect: Zn2+ dependent protease that inhibits neurotransmission at inhibitory synapses
ROS: spastic paralysis
Pertussis Toxin
Producer: Bordetella pertussis
Effect: ADP-ribosylation of G proteins, blocks inhibition of adenylate cyclase
ROS: cough
Toxic Shock Syndrome Toxin
Producer: S. aureus
Effect: acts on vascular system causing inflammation
ROS: fever and shock
Pyogenic Exotoxins
Producer: Streptococcus pyogenes
Effect: localized erythematous rxn
Hyaluronidase
Breaks down hyaluronic acid in CT and allows the microbe to be able to spread
Catalase
Breakdown H2O2
Urease
Inactivate urea to make an acidic environment more alkaline
e.g. - H. pylori
Coagulase
Converts fibrinogen to fibrin in order to form clots
Neuraminidase
Degrade sialic acid
- Why?
Vibrio cholerae Infectious Dose
Water = 10^4 - 10^6 Food = 10^2 - 10^4
Mycobacterium tuberculosis Infectious Dose
10 bacilli
Staph aureus Incubation Period
2-4 hours
*infectious dose impacts incubation period
Tetanus Incubation Period
4 days to weeks
*infectious dose impacts incubation period
Plasmodium (malaria) Incubation Period
7-30 days
*infectious dose impacts incubation period
Ways microorganisms survive transmission?
Cyst, endospore, vectors, etc.
Disinfectants useful against bacterial spores?
Hydrogen Peroxide, Formaldehyde, Chlorine
Site of entry?
usually the same as the site of exit
Pertussis - respiratory, salmonella - GI, gonorrhea - GU, trachomatis - eyes, S. Aureus - skin
True infections
Don’t require pre-existing host compromise aka can infect uncompromised host, sometimes the exposure is due to accidental contact
(*true pathogens can also be opportunistic)
Opportunistic Infection
Always requires pre-existing host compromise aka cannot infect uncompromised host, usually exposure is due to accidental contact
*opportunistic pathogens are mostly opportunistic
Components of Exotoxins?
A - for Active (enzymatic)
B - for Binding (G proteins etc.)
Adhesion of Microbes
Nonspecific or specific, can involve specialized (e.g. - pili/fimbriae) or non-specialized structures (e.g. - capsule)
Role: prevent removal
Adhesins
Ligands that help indicate tissue tropism, component on bacterial cell used for attachment to a tissue, cell or surface
(Fimbriae/pili, TA and LTA in G+ve, LPS in G-ve)
Receptors
Indicates tissue tropism, host cell molecule that bacterial adhesins attach to
Tropism of Streptococcus mutants
Bacterial adhesin: cell-bound protein
Location of relevant host cell receptor: pellicle of tooth
Tropism of uropathogenic E. coli
Bacterial adhesin: Type I or P fimbriae
Location of relevant host cell receptor: GU epithelium
Biofilm Formation
Attachment to surface, replication and microbe production of sticky expolymeric substance (EPS) coating
*default mode of growth for microbes
Advantages of Biofilm Formation
- Better resistance to antimicrobial agents
- Resists host immune response
- Acts as reservoir
Acquisition of Iron by microbes
- Surface receptors binding to iron containing compounds (OMPs of Neisseria)
- Produce siderophores to chelate iron (E. coli and K. pneumoniae)
- Reduction of Fe3+ in protein complex to Fe+ which releases gather iron by changing the affinity of the chelator (L. monocytogenes)
Siderophore
Synthesis is triggered by iron limitation conditions, has high affinity for iron, siderophore-iron complexes are taken up by surface siderophore receptors and transported into the microbe
Iron in the body? (Susceptibility)
Enhanced susceptibility (bc microorganisms need it and if you have a lot of it they’ll chill and take your iron)
Intracellular Phase for Growth
Obligate - Chlamydia trachomatis
Facultative - Salmonella
Not necessary - Vibrio cholerae
Streptokinase/Staphylokinase (“invasins”)
Converts plasminogen to plasmin (protease), used by host to dissolve fibrin clots
*in absence of streptokinase there is an abscess formed by fibrin barrier, with presence of streptokinase the fibrin barrier is broken down by plasmin enabling spread
Virulence: exotoxins
Cell damage and release of nutrients; evasion of host immune system
Virulence: Biofilm Formation
Evasion of host immune system; resistance to chemicals
Virulence: Ag variation
Evade host immune system
Virulence: Secreted Toxins
Release of nutrients; breakdown of tissue barriers; evasion of host immune system
Virulence: Dimorphism
Able to adapt to body environment
Virulence: Survival at 37C
Adaptation to body environment
Virulence: Attachment
Prevents removal
Virulence: Degradative Enzymes
Breakdown of tissue barriers; release of nutrients
Chediak-Hegashi Syndrome
Can’t traffic the engulfed microorganism to be destroyed
Chronic Granulomatous Dz
Mechanism: impaired NADPH oxidase function, pathogens are phagocytosis but not digested
ROS: infections w/ S. areus, Aspergillis and Candida
Leukocyte Adhesion Deficiency (LAD)
Defect: CD18
Mechanism: neutrophils and other cells cannot emigrate through the vessel wall to infected site
ROS: delayed separation of umbilical cord
Tx: BMT
Duncan Syndrome
*X-linked
Mechanism: functional suppression of T cells that renders them incapable of killing EBV infected B cells
ROS: no major sx’s until they get EBV
Wiskott-Aldrich Syndrome
ROS: pyogenic infections, eczema and thrombocytopenia (leads to patechiae)
Encapsulated Organisms (capsule is #1 virulence factor)
Some Killers Have Pretty Nice Slimy Capsules
- Strep pneumo
- Klebsiella
- H.influenzae
- Pseudomonas
- Neisseria meningiditis
- Salmonella
- Cryptococcus neoformans
Silent Subclinical Viruses?
CMV and EBV, causes life-long infection
