test 3 – Microbiology Test Answers – Flashcards
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| Acellular (noncellular) |
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| infectious agent consisting of nucleic acid (genome) enclosed in a protein coat called a capsid (virally encoded) |
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| naked virus |
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| If there is no additional covering other than capsid |
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| enveloped viruses |
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| Many viruses that infect animals and humans have lipid bilayer membrane or envelope |
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| Viral envelope is of host ceInfection typically leads toll origin |
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| acquired from cytoplasmic membrane or nuclear membrane during viral release. |
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| Viral nucleic acid (genome) |
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| can be either DNA or RNA (dsDNA, ssDNA, dsRNA, ssRNA) - but not both! |
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| monopartite genome |
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| The entire genome may consist of either one nucleic acid molecule |
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| segmented or multipartite genome |
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| several nucleic acid segments |
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| virion |
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| is the extracellular/transmissible infectious form of a virus |
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| Main function of virion/virus |
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| deliver its DNA or RNA genome into host cell so that the viral genome can be replicated (make more nucleic acid) and then the genes encoded on that nucleic acid are expressed (transcribed into mRNA and translated into protein) by the host cell to make more virus. |
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| Infection typically leads to |
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| rapid virus replication, but not always - latent phage, DNA tumor viruses transform only, slow viral infections |
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| Nonliving |
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| No cell membrane, no metabolic activity or energy generating capabilities, no ribosomes, rely on host metabolic and biosynthetic machinery to produce more viral particles |
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| cannot reproduce on their own - only reproduce inside living host cells, obligate intracellular parasites |
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| Non-living viruses |
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| Some viruses replicate in |
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| cytoplasm and some in nucleus - viral replication site in host cell is dependent upon type of viral nucleic acid |
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| Viral size range |
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| 10 nm - 400 nm |
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| Viruses differ in the following characteristics |
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| Primary criteria for taxonomic classification of animal viruses based on: |
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| Morphology (size, shape, etc); type of nucleic acid (DNA, RNA - ss, ds, linear, circular, segmented, etc.); and presence of envelope. |
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| host ranges |
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| Most can only infect specific types of cells of one host species - however, some can “jump species” and infect new hosts (ex. influenza) - these viruses are often responsible for epidemics/pandemics! |
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| host ranges are often determined by |
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| requirements for specific attachment RECEPTORS availability of cellular factors for viral multiplication |
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| proteins/glycoproteins |
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| The attachment of a virus to a host cell is a highly specific process involving the interaction of proteins/glycoproteins on surface of virus with receptors (proteins/glycoproteins) on surface of a susceptible host cell. Only after attachment has occurred can virus or its genome penetrate host cell. |
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| Viral Nucleic Acid Structure |
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| Either DNA or RNA, never both! Single-stranded or double-stranded ssDNA, dsDNA, ssRNA, dsRNA Linear or circular Some in several segments a few thousand nucleotides – 250,000 |
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| Capsid |
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| protein coat surrounding nucleic acid subunits are called capsomeres some single protein, some mosaic there are a variety of shapes |
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| Envelope |
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| only found in SOME viruses lipid bilayer with proteins & carbohydrates surrounding the capsid (lipid bilayer membrane and some proteins in it from host cell – viral glycoproteins inserted) |
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| Spikes |
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| (virally-encoded glycoproteins) - some viruses project from the envelope or capsid serve to attach virions to specific receptors on the surface of host cells change composition to evade immune system |
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| Viruses are classified on basis of their capsid structure Helical - resemble long rods ex. Ebola, Rabies, Tobacco Mosaic Virus Polyhedral - many sided, roughly spherical Icosahedron – 20 triangle faces, 12 corners ex. Adenovirus, Poliovirus Enveloped – helical or polyhedral ex. Influenzavirus, Herpes Simplex Virus Complex – complicated structures ex. bacteriophage |
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| Helical Polyhedral Icosahedron Enveloped Complex |
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| Helical |
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| resemble long rods ex. Ebola, Rabies, Tobacco Mosaic Virus |
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| Polyhedral |
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| many sided, roughly spherical Icosahedron – 20 triangle faces, 12 corners ex. Adenovirus, Poliovirus |
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| Enveloped |
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| helical or polyhedral ex. Influenzavirus, Herpes Simplex Virus |
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| Complex |
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| complicated structures ex. bacteriophage |
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| [image] |
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| Bacteriophages (phages) - Complex |
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| These viruses infect only bacteria Phage may attach to bacterial cell walls, fimbriae, or pili. Only viral nucleic acid enters bacteria, capsid remains outside Have been used as an alternative to antibiotics in foreign countries - “phage therapy” |
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| Excellent models for understanding basics of viral biology |
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| Bacteriophages: - Inexpensive - Easy to grow and study in lab |
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| Overview of Virus Life Cycle |
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| After attachment and entry into host cell, virus hijacks biosynthetic and protein synthesizing abilities of cell in order to replicate viral nucleic acid, make viral proteins and arrange its escape from cell. |
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| Differences between prokaryotic and eukaryotic cells |
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| affect how and where viruses replicate! |
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| PROKARYOTES |
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| - DNA replication, transcription, and translation occur in cytoplasm. |
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| EUKARYOTES |
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| DNA replication and transcription occur in nucleus, while translation occurs in cytoplasm |
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| prokaryotes life cycle |
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| only viral nucleic acid enters cell, in animal viruses, entire virus enters cell by endocytosis, and virus must uncoat (capsid removed) |
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| The virus life cycle can be divided into five main stages: |
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| 1. Attachment (adsorption) 2. Penetration 3. Viral synthesis 4. Assembly and packaging of new virus particles 5. Virus release |
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| 1. Attachment (adsorption) |
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| of virus to host cell |
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| 2. Penetration |
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| virus or viral nucleic acid enters host cell (this process differs between bacteriophage and animal viruses). For animal viruses - viral uncoating. |
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| 3. Viral synthesis |
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| production of viral protein and nucleic acid. How this occurs depends on whether the infecting viral nucleic acid is DNA or RNA |
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| 4. Assembly and packaging of new virus particles |
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| assembly of viral genomes, proteins, enzymes into complete progeny virions |
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| 5. Virus release |
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| from infected host cell (may or may not result in death of host cell - this process differs between bacteriophage and animal viruses - cell lysis or enveloped viruses bud off) |
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| Bacteriophage (virus that infect bacteria) |
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| injects its DNA into the bacterial cell release lysozyme to break down bacterial cell wall capsid remains outside |
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| Naked animal viruses are taken into the cell by direct penetration or by injection (less common) |
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| direct penetration or by injection (less common) |
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| Enveloped animal viruses can enter via |
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| 1) fusion (like HIV and Herpes) = virus envelope fuses with the host cell membrane & releases capsid into the cell; OR 2) endocytosis (Influenza virus) |
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| once inside the cell, animal viruses ... |
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| uncoat proteolytic enzymes from the cell break down the viral capsid |
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| DNA viruses biosynthesis |
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| DNA transcribed into mRNA which is then translated into viral proteins DNA is also replicated to make more viral genomes takes place in the host nucleus (except Poxviruses) |
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| RNA viruses (biosynthesis) |
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| some can be used directly as mRNA (+ strand) some cannot be used directly as mRNA (- strand) in some, RNA needs to be copied first into DNA by a reverse transcriptase usually takes place in the host cytoplasm (exception Influenza Virus) |
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| Bacteriophage - Lytic Phages |
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| Lytic phages infect cell Make more phages within the cell Phages burst out of the infected cell Infected cell is lysed ie. T-even Phage |
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| Lysogenic (temperate) phages |
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| infect the cells but do not kill the cells |
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| a prophage |
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| Viral DNA is incorporated into the host’s chromosome |
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| Bacteriophage - Lysogenic Phages |
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| Spontaneous event, chemicals & UV are capable of pushing prophages to becoming lytic |
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| Importance of Lysogeny |
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| Cells are immune to reinfection/superinfection with the same phage |
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| Phage Conversion |
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| host cell may exhibit new properties Prophage carries genes Many pathogens get toxins this way |
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| Transduction (specialized and generalized) |
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| Phage “mistakenly” packages bacterial DNA sequences instead of viral DNA in its capsid. Specialized transduction - phage can only package certain/select bacterial genes Generalized transduction - phage can package any region of bacterial DNA |
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| Lifestyle of ANY virus designed to |
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| maximize production of progeny virus particles! |
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| Upon entering host cell, virus must ensure that two things happen |
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| #1) Some nucleic acid must be used to make more genomic nucleic acid for packaging into new progeny virions (viral replication) #2) Some nucleic acid must be transcribed and translated into viral proteins (viral replication) |
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| Animal virus reproduction stages |
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| Attachment/adsorption Penetration Uncoating Viral synthesis - how this occurs depends on whether the infecting viral nucleic acid is DNA or RNA Assembly of capsids and packaging of new virus particles Virus release |
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| Most DNA viruses enter the nucleus where they |
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| “hijack” the host cell’s DNA replication machinery to make more virus. (Exception, smallpox, DNA virus that encodes its own DNA replication machinery and thus remains in cytoplasm). |
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| most RNA viruses replicate in the cytoplasm |
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| because the enzymes used to replicate viral RNA are virally encoded. |
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| In general, for DNA viruses: |
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| Most DNA viruses (with exception of smallpox) replicate in the nucleus and use host enzymes to replicate viral DNA. |
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| Viral genome is replicated using |
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| host cell DNA polymerase (nucleus) and transcribed by host cell RNA polymerase (nucleus). |
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| In general, for RNA viruses |
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| Most RNA viruses replicate in the cytoplasm because enzymes used to replicate viral RNA are virally encoded. *RNA viruses have higher rates of mutation! |
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| (+) strand RNA viruses |
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| the mRNA can be directly translated by host cell to make viral proteins. However, host cell cannot replicate RNA, thus, virus encodes an enzyme to replicate the ssRNA genome and host translates viral proteins for capsid. - Retroviruses carry enzyme reverse transcriptase, which copies RNA into DNA – they replicate through a DNA intermediate |
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| (-) strand RNA viruses |
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| (-) RNA strand must function as template to make a complementary strand of + RNA before any translation can occur. Host translation machinery can only make proteins from (+) strand RNA. |
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| Viral genomes contain information which: |
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| ･ ensures replication of viral genomes ･ ensures packaging of genomes into virions ･ alters structure and/or function of the host cell to a greater or lesser degree |
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| VIRAL STRATEGY |
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| Viral strategy refers to the manner in which each virus carries out the above functions. Since a virus is an intracellular parasite, it has to operate within limits imposed by the host cell, or circumvent these limitations. |
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| Antigenic shift |
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| Genome Reassortment, abrupt major change in antigenicity of virus; results from recombination of genes between different viruses. |
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| Antigenic drift |
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| minor change of antigen on surface of virus that continually happens over time - due to accumulation of mutations in viral genome |
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| Growing Viruses in the Lab |
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| Bacterial viruses (bacteriophage) have proved useful model systems because the host cells (bacteria) are easily to grow and manipulate in culture. |
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| Growing Bacteriophages In Lab |
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| In suspensions or in cultures on solid media Plaque Method – solid media Bacteriophages, host bacteria & liquid agar is poured into a petri dish Following a few cycles of infection, the bacteria surrounding the original virus are all destroyed Clear area - plaque Each plaque corresponds to one virus Concentrations given in pfu (plaque-forming units) |
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| Growing Animal Viruses in the Lab |
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| Cell lines are observed for cytopathic (damaging) effects elicited by viruses and viral neutralization studies prior to human clinical trials |
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| Viruses and Cancer |
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| Cancers are the result of a disruption of the normal restraints on cellular proliferation Viruses cause cancer by altering the normal host cellular proliferation cycles resulting in a loss of growth control |
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| Proto-oncogenes |
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| normal genes that if altered, can make a normal cell cancerous (involved in cellular proliferation) |
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| Oncogenes |
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| a proto-oncogene that has been altered and can produce a protein that makes a cell cancerous |
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| Oncogenic Viruses |
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| capable of inducing tumors |
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| PRIONS |
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| Very stable - Conventional disinfection does not inactivate prions |
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| Pathogenesis of prions |
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| Fragments accumulate forming plaques (insoluble aggregates of protein), but it still is not known how this kills cells |
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| The abnormal form of the protein |
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| acquires a different shape/conformation than normal form (PrPc), this change in shape alters function of protein! |
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| VIROIDS |
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| A single piece of RNA Smaller than viral RNA 300-400 nucleotides No protein coat Does not code for a protein Causes plant diseases |
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| pathogen |
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| microorganism capable of causing disease |
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| epidemiology |
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| the study of the cause and transmission of disease within a population An epidemiologist studies where and when a disease occurs and how it is spread in populations |
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| infection |
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| invasion or colonization of the body by pathogenic microorganisms |
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| Disease |
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| an abnormal state in which part or all of the body is not properly adjusted or incapable of performing its normal functions Infection may occur without detectable disease |
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| normal flora |
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| permanent residents; usually don’t cause disease (exception - if introduced into unusual site in body |
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| transient microbiota |
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| those present only temporarily, vast majority do not cause disease - but some do under right conditions (i.e. when host is not healthy). Skin, eyes, upper respiratory, mouth, intestines, urogenital system |
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| Normal Microbiota |
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| Although continue to add transient microbiota, most of resident microbiota initially established in early months of life. |
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| Three main types of symbiosis: |
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| mutulaism commensalism parasitism |
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| Mutualism |
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| both members benefit from interaction (ex., bacteria in your colon produce vitamins and in turn receive nutrient rich environment to live) |
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| Commensalism |
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| one benefits, the other is unaffected (ex., Staphylococcus aureus growing on skin) |
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| Parasitism |
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| one benefits, the other is harmed (ex., infection of host by microbial pathogen) |
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| Types of Microbial Pathogens: |
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| - Opportunistic - Obligate |
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| Opportunistic Pathogen |
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| microbes which do not cause disease in the healthy host But can cause disease when host has weakened immune defense or when change in normal microbiota due to antibiotic treatment opportunistic infections |
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| Exposure/Portals of entry for pathogens |
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| Skin Ears Eyes Nose Mouth Mammary glands Urethra Vagina Anus |
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| Koch’s Postulates - How to prove that a particular pathogen causes a disease: |
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| The pathogen must be present in every case of the disease -i.e., the pathogen should be found in diseased tissue but not healthy tissue. The pathogen must be isolated from the diseased host and grown in pure culture. The pathogen from the pure culture must cause the disease when it is inoculated into a healthy human or laboratory animal. The pathogen must be isolated from the inoculated human/animal & must be shown to be the original organism. |
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| Exception to Postulate 1 |
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| some pathogens are found in both healthy hosts and those with disease. |
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| Exception to Postulate 2 |
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| not all pathogens can be grown in pure culture - unique culture requirements |
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| Exception(s) to Postulate 3 |
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| a) suitable animal models are not available for all pathogens; b) how well does animal model mimic the disease in humans? |
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| Other Exceptions to Koch’s Postulates |
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| Microbiota shift diseases - diseases caused by shifts in microbial populations (ex. periodontal disease) - problems for third postulate since difficult to produce specific populations shifts in lab animals |
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| Symptoms |
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| subjective changes in body function that can be felt by patient |
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| Signs |
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| objective changes that can be observed and measured Ex. nausea, pain, headache, dizziness, and fatigue = symptoms Ex. vomiting, swelling, rash, redness, fever = signs |
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| Syndrome |
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| a particular group of signs or symptoms that usually accompanies a specific disease - ex., AIDS characterized by weight loss, malaise, loss of certain white blood cells, diarrhea, pneumonia, toxoplasmosis, and tuberculosis |
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| Infectious |
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| caused by infectious agents |
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| Non-infectious |
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| caused by any other factor besides infectious agents |
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| Communicable |
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| spread from one host to another |
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| Contagious |
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| EASILY spread from one person to another |
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| Non-communicable |
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| from normal flora or from the environment and cause disease when introduced into the body (not transmitted from one person to another) |
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| Congenital |
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| diseases present at birth |
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| Nosocomial |
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| infections obtained from hospital treatment (or other health care setting like nursing home, dental office, etc). |
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| Idiopathic |
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| cause unknown |
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| Zoonoses |
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| occur primarily in wild and domestic animals but can be transmitted to humans |
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| Incidence |
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| the fraction of the population contracting a disease per time period - i.e. # of new cases of disease in a given time period |
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| Prevalence |
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| the fraction of the population having a disease at a specified time - i.e. total number of cases, both new and already existing, in a given population at a given time. |
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| Sporadic disease |
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| occurs occasionally |
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| Endemic disease |
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| constantly present |
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| Epidemic disease |
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| large number of people acquiring a disease in a given geographical area in a short period of time - (or whenever a disease occurs at a greater frequency than is usual for an area or population). |
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| Pandemic |
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| worldwide outbreak |
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| ID50 |
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| number of microorganisms required to cause infection in 50% of experimentally infected animals or humans |
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| LD50 |
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| number of microorganisms (or the amount of toxin) required to kill half of the animals experimentally inoculated Virulence of organism Potency of toxin |
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| Indirect relationship between LD50 and virulence |
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| A lower LD50 means the organism is more virulent! i.e. it takes fewer organisms to cause disease. “Less is worse”! |
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| Pathogens have a variety of traits called virulence factors that enable them to cause disease: |
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| Adhere to host cells Enter host cells Gain access to nutrients Escape detection by immune system Some of these are secreted virulence factors |
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| multiple traits often important for the organism to cause disease |
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| Virulence is multifactorial |
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| Once inside, most bacteria attach to host tissue |
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| Adherence is necessary step for their pathogenicity - fluids may wash bacteria away if they do not adhere to host cells. |
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| Bacteria use surface molecules adhesins or ligands |
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| Bacterial surface proteins that bind to host cell surface receptors (usually glycoproteins or lipoproteins) located on pili, fimbriae, flagella or the glycocalyx (capsule) used for adhering to receptors on specific host cells |
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| Streptococcus mutans |
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| tooth decay |
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| Salmonella typhimurium |
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| intestinal disease, gastroenteritis/diarrhea |
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| Bordetella pertussis |
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| lung disease, whooping cough |
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| Escherichia coli |
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| bladder infections |
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| Pseudomonas aeruginosa |
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| biofilm infections |
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| Capsules (glycocalyx) |
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| resists phagocytosis A major virulence factor |
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| Cell wall components |
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| chemical substances Streptococcus pyogenes produces M protein |
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| coagulases |
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| promote blood clotting |
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| kinases |
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| dissolve clots |
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| hyaluronidase |
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| hydrolyzes hyaluronic acid, a polysaccharide that holds cells together (especially in connective tissue) |
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| collagenase |
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| hydrolyzes collagen which is the major protein in connective tissue |
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| IgA protease |
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| destroy IgA antibodies |
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| Antigenic Variation |
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| Some pathogens can alter their surface antigens - like changing pili composition Remember: an antigen is anything that can elicit an immune response |
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| Invasins |
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| rearrange the host cell cytoskeleton to “cradle” the bacterium into the cell - can lead to host signal transduction. |
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| Toxigenicity |
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| capacity to produce toxins May be transported by the blood toxemia |
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| toxins Produce serious, and sometimes fatal, effects |
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| Fever Cardiovascular disturbances Diarrhea Shock Inhibit protein synthesis Damage eukaryotic cell membranes |
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| Intoxication |
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| Exotoxins Found in both G+ and G- bacteria Toxins secreted from the bacterial cell - into the extracellular fluid or into host tissues Body produces antitoxins (antibodies) against the toxins |
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| CYTOXINS |
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| Toxins that attack a variety of cell types |
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| Toxins that attack specific cell types named according to cell type or organ affected: |
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| Neurotoxins - act on nervous tissue Hepatotoxins – liver cells Enterotoxins - act on enteric tissue (gut) Cardiotoxins - act on cardiac tissue |
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| Type of bacterial species that produces them or for type of disease caused |
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| diphtheria toxin (C. diphtheria), tetanus toxin (C. tetani), cholera toxin (V. cholera), botulinum toxin (C. botulinum |
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| plasmids and bacteriophages |
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| Many toxins are carried on mobile DNA elements |
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| Type I toxins |
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| bind to host cell surface,but do not enter cell. Ex., Superantigens |
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| Type II toxins |
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| Act on host cell membranes and cause host cell lysis/death |
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| Type III toxins |
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| A-B toxins, have a binding region (B) that binds specific host cell receptor (but does not enter host cell), and A portion (enzymatic portion) that enters host cell and exerts its toxic effect. |
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| Superantigens: |
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| Hallmark - Force an unnatural fit between macrophages and T cells - causes an outpouring of cytokines that triggers SHOCK. |
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| Superantigen-mediated disease |
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| - Fever, rash, desquamation, hypotension, shock, multiple organ failure |
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| Two types of Membrane Disrupting Toxins |
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| Form channels in the membrane Compromise the integrity of membrane phospholipids |
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| Endotoxin Production |
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| part of G- bacterial cell wall (ie. LPS in Gram- cell walls - lipid A is toxic portion) released into tissues when the organisms die/lyse weak toxins compared to exotoxins - but deadly in high concentrations - can cause shock |
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| Shock |
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| Any life-threatening loss of blood pressure |
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| Septic shock |
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| caused by bacteria in the blood. (Toxins in the blood can also cause shock - toxemia) |
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| Systemic reaction |
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| caused by high levels of bacteria or their products (LPS, LTA, peptidoglycan fragments) in bloodstream Triggers complement activation, cytokine release, and coagulation cascade in body |
