Ch 1 - Bacteria, Viruses, Fungi Flashcards
Bacterial ribosome
70S (50S & 30S)
Bacterial intracellular components
- Bacterial chromosome –> single circular chromosome of double-stranded DNA, plasmids
- Ribosomes –> 70S (50S & 30S)
- peptidoglycan
- no endomembrane system or subcellular organelle
- Flagella are submicroscopic single repeating peptide
Bacterial Flagella medical significance
Chemotaxis–> motility in response to sensing their environment.
H antigen–> aids in serological identification of bacteria
Common Pili (Fimbriae) medical significance
Bivalence factor: adherence, anti-phagocytic, motility.
Medical significance of Sex Pili:
–> Conjugation
Transmission of genetic material
Ex: antibiotic resistance
Capsules/ Slime layers/ Exopolysaccharide
–> K antigen
Composition: usually polysaccharide polymers consisting of A, B, or C:
A. Repeating units of a sugar molecule. Example: dextran or levan
B. Repeating units are complex polysaccharides consisting of sugar, sugar alcohols, amino sugars, sugar asses, etc.
C. Repeating units of D – glutamic acid (form a polypeptide; bacillus anthracis)
A protected structure of bacterial cells/micro colonies enmeshed in mucoid hydrated Exopolysaccharide adhering to a wet surface:
Biofilms
The CDC estimates that more than one half of human bacterial infections involve __________
Biofilms
Biofilms undergo a ___________ _______ that allows them to persist in the presence of antimicrobial agents that they are normally susceptible to.
Phenotypic change
What is the medical significance of capsules and biofilms?
three things
A. adherence (virulence) to host tissues and surfaces surface colonization.
–>(Biofilms enable bacteria to grow/thrive in moving solutions)
B. Antigen used to identify the agent in serodiagnosis. Example: K antigen w/ biofilms
C. Action against phagocytosis, serum factors, anti-bodies, antibiotics.
Unlike eukaryotes prokaryotic cell membranes contain no _______
Sterols
Mycoplasma, Heliobacter, Ehrlichia, Anaplasma
The ____________ layer in the gram positive cell wall is much thicker than the Gram negative cell wall
peptidoglycan
Polysaccharides are __________ _______ to the peptidoglycan layer in the gram-positive cell wall, NOT in the Graham negative cell wall.
covalently linked
In what type of cell are LPS molecules present?
Gram-negative bacteria
What is the function/significance of the cell walls (peptidoglycan)
of both gram-positive and negative bacteria?
- Interaction of bacteria with environment
- Site where differential staining occurs during gram staining of bacteria.
- Shield agents against environmental changes.
- bacteria which lacks peptidoglycan
E.g. Mycoplasma (penicillin not effective)
The peptidoglycan acts like a backbone or fabric shell encasing the cell and is present in both ________&_________
Gram-negative and gram-positive bacteria
Is the major function of periplasm?
Osmotic protection peptidoglycan is in the periplasm.
Other functions include nutrient uptake, sensory (chemo taxis) mechanism, degradative enzymes.
What is the major function of the outer membrane of bacteria?
To protect from some dyes, detergents, and hydrolytic enzymes like lysozyme.
The outer membrane is a lipid bilayer
What type of bacteria lack an outer membrane?
Gram-positive bacteria
–>hence, they are susceptible to dyes, detergents, & hydrolytic enzymes.
What is endotoxin O antigen?
LPS - lipopolysaccharide
What constitutes the outer membrane structure?
- Lipid bilayer - not a phospholipid bilayer (it is differentially permeable)
- proteins and lipoprotein
- LPS
Toxicity of LPS is primarily associated with _______
Lipid A
Properties and characteristics of LPS:
A. Structural component of the outer membrane.
B. Chromosomally encoated.
C. Broad specificity- effects many organ systems in a susceptible host: pyrogenicity – exogenous pyrogen. Ability to activate both alternative and classical complement pathways. Activator of Hagemann factor XIII. Induces a systemic inflammatory response syndrome SIRS pathway
D. Heat stable
E. Does not form toxoids
Mechanism of action and clinical significance of LPS
Induces a systemic inflammatory response syndrome (SIRS) –> macrophages, PMNs, etc –> hypovolemic shock
Endotoxin initiates SIRS, by binding to ___________
LBP - LPS bonding protein
Which interacts w/ CD14 on T-cells.
LPS-CD14 bunds to a LPS- signal transducer receptor protein (TLR) which communicates to the nucleus.
Soluble CD14 receptor present in serum, then binds to endothelial cells.
Effect of LPS endotoxin on patient:
- Endothelial cell dysfunction –> hypotension
- TNF-alpha, IL-1, IL-6, endogenous mediators
- Release of arachadonic acid metabs.
- Release of bradykinin
- Activation of both the alternative and classical pathway of complement.
- Release of histamines from mast cells and basophils.
- Release of nitric oxide from endothelial, vascular smooth muscle, cardiac smooth muscle cells, macrophages.
- Activates Hageman factor which activates the clotting system (fibrin deposition) & fibrinolysis–> disseminated intrvascukarvcoagukatiob –> multi organ failure, put prix skin lesion
- Release of free radicals, esp superoxide anions.
- Immunosuppression
SIRS
Systemic inflammatory response syndrome:
Two or more of the following:
- Temperature greater than 38°C or less than 36°C
- Tachycardia greater than or equal to 90 bpm
- Tachypnea >20 breaths per minute
- Leukocytosis >12,000/mmor leukopenia <4000/mm
SIRS –> Sepsis –> septic shock (refractory hypotension)
These are effects of:
LPS endotoxin
Sepsis is the presence of both:
- Proven infection (example pneumonia, UTI, bacteremia)
2. SIRS
Severe sepsis is defined by the presence of both:
- Sepsis
2. organ failure (AKA organ dysfunction, multi-organ dysfunction, multi-organ failure)
Septic shock is defined as the presence of both:
- Severe sepsis
2. Refractory hypotension
clinical manifestations of Distributive shock (hypovolemic shock):
- Fever or hypothermia
- Chills
- Leukopenia or leukocytosis (abnormally high levels of WBCs)
- Tachycardia and tachypnea
- Disseminated intravascular coagulation (DIC)
- Hypotension and shock, which can cause multi organ failure (MOF) or multi organ dysfunction (MOD) or organ dysfunction.
Gram Positive cells have NO________ OR _______
No outer membrane & No LPS/endotoxin
Structure of gram + cell wall:
A. Peptidoglycan: present in large amounts–> reason for differential staining.
–> Can induce prod of TNF-alpha, IL-6, hypotension shock/ distributive shock
B. Additional polymers:
- Lipoteichoic acid –> adherence ; anti phagocytic
- Teichoic acids –> produces endotoxin like shock
What infectious agents can cause DIC?
Disseminated intravascular coagulopathy
Gram-positive, gram-negative, fungal, and viral agents
Human body can detect infection by TLR are receptors (10 total) that are specific for ________
pathogen associated molecular patterns PAMP
PAMP’s consist of:
A. Peptidoglycan from certain bacteria. B. Teichoic acid polymers from certain bacteria
C. N- formyl-methionine-leucine-phenylalanine the 1st 3 aa of many bacterial proteins.
D. CpG nucleotides (unmethylated at the 5’ position) are normal components of bacterial DNA and DNA vaccines.
E. LPS
What Generra form bacterial endospores?
- Bacillus
2. Clostridium
Properties of bacterial spores (endospores):
Endoscopes are Highly heat, desiccation, and chemical resistant structures which are formed in response to adverse conditions. Sports can remain dormant for decades.
Bacteria divide by:
Binary fission
What genetic material can bacteria have?
Both DNA and RNA
Unlike bacteria viruses require cells to be _________
Living
Some bacteria do not require living cells.
What’s pathogen to these characteristics belong to?
- submicroscopic entities
- obligate intracellular parasites capable of infecting specific specific living cells and overproducing in such cells only.
- Consist of nucleic acid (DNA or RNA) and protein, some process an envelope
- Possess definite structure
Viruses
Capsomeres
Protein subunits of the capsid.
–> viral
Capsid
The protein shall, or cold, that encloses the Core of the NA genome (viral) plus any associated proteins. repented of polypeptide subunits arranged and symmetric patterns.
Nucleocapsid
Protein associated with the viral NA genome. The capsid together with an 18 and plus any associated proteins.
Peplomer
Spikes.
Viral glycoproteins that form spike-like projections on the surface of the envelope and play a role in attachment.
Tegument
(Matrix protein)
Amorphous layer between nucleoplasmid & envelope that mediates the interaction between the capsid & the envelope of a virus.
Viroid
Naked RNA virus
Prion
Infectious protein. Causes disease in the CNS.
Not a virus.
the six steps of replication of a virus:
A. Attachment B. Penetration--> the virion enters the cell C. Uncoating D. Macromolecular synthesis E. Assembly F. Release
Describe the attachment for a virus.
Virus ligand binds to a specific receptor site. The specificity of attachment determines both the host range of the virus and the tissue tropism (where in the body the virus locates).
Describe macromolecular synthesis RNA viruses:
A. Positive sense (+) ssRNA
(+) ssRNA serves as mRNA but they must encode for an RNA (-) dependent polymerase to make the antisense RNA to produce multiple (+) ssRNA (the viral genome)
Exception is retroviruses
B. Negative sense (-) ssRNA and ds RNA –> virions must contain functional proteins (an RNA dependent polymerase) to make mRNA as well as possess the gene that codes for the protein.
Methods of viral entry:
A. aerosol- most difficult to control and most common means of entry.
B. Direct contact
C. Ingestion- Second most difficult to control and second most common means of entry.
D. Injection
E. Transplacental
What is the infectious dose of virus required to cause infection?
Low – 1 to 10 virons
Primary replication:
Is at or near the portal of entry
Tissue tropism
–> The specificity of the virus for a particular host tissue.
Virus-receptor interactions are a major determinant of infectivity.
Productive infections:
A. Non- lethal alteration of cells & their functions –> sustained release in absence of lysis (ex rhinovirus)
B. Cell damage/death –> lytic- viral replication results in cell death via viral modifications/damage of host cells.
Methods of viral Cell damage:
A. Inhibition opt shutdown of host cell biosynthesis.
B. Cytopathic Effect of viral proteins on host cells (toxic to cell)
C. Inclusion bodies & cell fusion (synctia) –> giant multi uncleared cell
D. Chromosomal alterations can cause oncogenesus/malignant transformation
E. Induce apoptosis
Latent – persistent infections:
Intermittent acute episodes of disease between which there is an absence of infectious particles (example herpes)
Chronic – persistent infections:
Continued presence of virus, however, disease may be absent (example hepatitis B), Or is associated with late immunopathologic disease (example HBV–>cirrhosis of the liver or primary hepatocellular cancer)
Slow – persistent infections:
Following a long incubation period, a slowly progressive, lethal disease occurs (subacute sclerosing panencephalitis SSPE.)
No infectious virion may be detected.
Malignant transformation:
Oncogenesis
Transformation is the conversion of a cell from restricted growth to unrestricted growth, which is characteristic of tumors.
Describe the characteristics of a malignantly transform cell:
A. Loss of contact inhibition – unregulated cell growth, unrestricted growth.
B. Appearance of new antigens – ex: tumor specific antigens.
C. Other changes – Ex: metabolic and genetic
Viral agents associated with malignant neoplasms:
A. RNA tumor viruses –> human T cell leukemia viruses, lymphotrophic retroviruses. (HTLV-1)
B. DNA tumor viruses: HPV, EBV (Epstein barr virus), HBV (hep B virus)
C. Viral agents of benign neoplasms: warts (verruca, condyloma acuminatum) , pox virus (molluscum contagiosum)
Immune response to viral infection:
A. Physical barriers and phagocytes.
B. Cellular immunity
C. Humoral immunity
D. Nonspecific mechanisms
Cellular immunity
T lymphocytes, lymphokines and NK cells.
CMI is curative to viral infections!!!!!!
Humoral immunity to viruses:
- Virus neutralization via antibody to receptors on virus particle.
Prevents virus from attaching.
Antibodies are virus specific NOT host specific (passive immunization)!!!!!!!!!
- Complement and/or antibody dependent lysis of virus-infected cells.
Non-specific mechanisms for immune response to viral infection:
Interferons –> anti-viral agents. National cell Products that stimulate antiviral resistance by interfering with virus specific protein synthesis.
Interferons are host specific NOT virus specific!!!!
Specificity of Interferons for viruses:
Interferons are host specific!!!!
Specificity of antibodies for viruses:
Anti-bodies are viruses specific!!!!
Passive immunization
Cellular characteristics of fungi calling:
Eukaryotic - nucleus, nuclear membrane, and cytoplasmic organelles.
Method of reproduction a sexual or asexual spores.
Fungi imperfecta:
Sexual stage not yet discovered.
Cause diseases in humans (mycoses).
Yeast
Unicellular
Asexual reproduction
Mycelial fungi
Mold form.
Growth occurs by elongation of high fade to four mycelium.
Sexual and asexual spores formed.
Hyphae and mycelium.
Hyphae
Mycelial fungi cells are branching cylindrical tube’s +- Septa or crosswalls.
Mycelium
Mycelium – massive intertwined hyphae.
in fungi
Dimorphism
Ability to grow as a mycelial form at room temperature and a yeast form at 37°C
Types of asexual spores:
Blastospores
Macroconidia
Microconidia
Arthrospores
Microconidia
Asexual fungal spores small enough to get to alveoli when inhaled and are the infectious form for certain fungi
Macroconidia
Infectious form for fungi that infects skin (dermatophytes)
Fungal cell structure components
- Capsule
- Chitin
- Ergosterol in membrane
Type of immunity is essential for the control of systemic mycotic infections and the successful resolution of mycotic infections?
Cell mediated immunity
Factors that predispose to fungal infections:
A. environment
B. Host factors: age , gender/hormonal status, metabolic abnormalities such as diabetes steroids or obesity, and immunosuppression, pregnancy, oral contraceptives, trauma, and burns
Symbiosis
A close association of two different organisms
Mutualism
A beneficial association to both individuals
Commensalism
A beneficial Association for one individual without affecting the other
parasitism
Beneficial association for one and detrimental for the other
Structure of parasites
Eukaryotic – animal kingdom. Lack cell walls. May have walls on cyst forms, flexible cuticles, or chitinous exoskeletons.
Rhizopods (amoebas)
Parasites Motile by means of cytoplasmic extensions–> pseudopodia
Flagellates
Parasites motile by means of flagella
Ciliates
Parasites motel by means of cilia
Sporozoans
Parasites with complex lifecycles and asexual and sexual stages
Helminths
Worms. Adults mostly macroscopic, eggs microscopic. Mostly monoecious male and female sex organs in the same individual.
Platyhelminthes
- -> flatworms
1. Trematodes: the flukes
2. Cestodes: tapeworms
Nemathelminthes
Round worms; nematodes
–> adults macroscopic, eggs microscopic, larval form is generally microscopic.
Dioecious –> Separate male and female worms
Arthropods
Chitinous exoskeletons.
Ex: lice, mites, tics, etc
Definitive host life cycles for parasites:
Host harbors adult or sexual stage of the parasite
Intermediate host lifecycles for parasites:
Hosts in which a sexual stages occur.
Icosahedral
Capsomeres are arranged in triangles that form a symmetric figure. –> viral
