Microbiology Lecture 4 Review: Chapter 11,13

Lecture Review - By: Remy Voloshchak

Chapter 11 Diversity of Bacteria

1.     Compare properties of bacterial phyla Proteobacteria, Firmicutes and Actinobacteria – Lecture 4, Slide 2 –
Properties of Proteobacteria, Firmicutes, and Actinobacteria (phylum of bacteria)

a.     Proteobacteria is gram-negative, firmicutes is gram-positive, and actinobacteria is gram-positive or acid-fast

b.     GC content: Actino – 69-73%, proteo – 40-50%, firmi – 23-53%

c.     They can all be aerobic; firmi and action can also be obligate anaerobes

d.     Morphology:

                                               i.     Proteo – bacilli, cocci, coccobacilli

                                             ii.     Firmi – bacilli, cocci, pleoimorphic

                                            iii.     Actino – bacilli, cocci, filamentous, branching

e.     All have small colonies, but action can have large colonies too

f.      Only proteo produces endotoxins, since it’s GRAM-NEGATIVE; they ALL produce exotoxins

g.     Proteo – not antibiotic producer; firmi and action – yes antibiotic producers

h.     They are ALL human pathogens

2.     Compare the properties of bacterial genera Haemophilus and Vibrio. Name principal species that are human pathogens – Lecture 4, Slides 3, 5-7 –
Ptoreobacteria à haemophilus, vibrio, pseudomonas, legionella

a.     Haemophilus – gram-negative gamma-proteobacteria, coccobacilli, not motile, and no flagella

                                               i.     Aerobic

                                             ii.     Tolerant to stomach acid

                                            iii.     Has a capsule and forms biofilm

                                            iv.     Produces endotoxin but not exotoxin

                                              v.     Natural reservoir – humans and other animals

b.     Vibrio – gram-negative gamma-proteobacteria, curved rod, motile, has flagellum

                                               i.     Facultative anaerobe

                                             ii.     Not tolerant to stomach acid

                                            iii.     Has capsule and forms biofilm

                                            iv.     Produces exotoxin and endotoxin

                                              v.     Natural reservoir – coastal and brackish waters

3.     Describe the properties of enteric bacteria. Name principal species that are human pathogens and diseases they cause – Lecture 4, Slides 3, 8, 9 –
Properties of enteric bacteria:

a.     Gram-negative

b.     Bacilli

c.     Facultative anaerobes

d.     Associated with human and animal guts

e.     Most are flagellated

f.      Produce acid in fermentation of sugars

g.     Examples:

                                               i.     Shigella causes shigellosis

                                             ii.     E.coli can cause UTI when it enters the urinary tract

                                            iii.     Salmonella causes intestinal infections in human guts, but is part of normal flora of birds

                                            iv.     Klebsiella causes pneumonia

4.     Compare the properties of bacterial genera Clostridium and Mycoplasma. Name principal species that are human pathogens and diseases they cause – Lecture 4, Slides 10-14 –
Comparison of firmicutes important species bacteria

Clostridium · Firmicutes: low GC content · Doesn’t form endotoxins · Motile · Bacillus · Has a cell wall (gram-positive) · Forms endospores · Is sensitive to penicillin · Forms exotoxins Ex: C. perfringes: food poisoning, gangrene

Mycoplasma · Firmicutes: low GC content · Doesn’t form endotoxins · Motile · Pleiomorphic · No cell wall · Doesn’t form endospores · Not sensitive to penicillin · Doesn’t form exotoxins Ex: M. hominis: pelvic inflammation, bacterial vaginosis, male infertility

5.     Compare the properties of bacterial genera Staphylococcus and Streptococcus Name principal species that are human pathogens and diseases they cause – Lecture 4, Slides 10, 11, 15, 16 –
Further comparison. Firmicutes: low GC content, gram-positive

Streptococcus · Firmicutes: gram-positive, low GC content · Forms exotoxins · Not motile · Bacillus · Has a cell wall (gram-positive) · Doesn’t form endospores · Is sensitive to penicillin · Forms exotoxins · Cocci grow in clusters · Facultative anaerobe Ex: S pyogenes: cellulitis, impertigo, necrotizing fasciitis, toxic shock syndrome, scarlet fever, streptococcal pharyngitis

Staphylococcus · Firmicutes: gram-positive, low GC content · Forms exotoxins · Not motile · Bacillus · Has a cell wall (gram-positive) · Doesn’t form endospores · Is sensitive to penicillin · Forms exotoxins · Cocci grow in chains · Aerotolerant anaerobe Ex: S. aureus: opportunistic pathogen, normally vital in limiting skin pathogens; pneumonia, scalded skin syndrome, toxic shock syndrome, food poisoning, impertigo

6.     Compare cellular properties of Staphylococcus aureus and Streptococcus pyogenes. Name diseases they cause – Lecture 4, Slides 15, 17, 18 –
Staphylococcus aureus belongs to phylum firmicutes and is a gram-positive coccus, growing in clusters; it has golden colonies, and is alpha, beta, and gamma hemolytic on blood agar. It grows well and produces acid on mannitol salt agar; it is a facultative anaerobe, catalase-positive, and coagulase-positive.
Streptococcus pyogenes also belongs to phylum firmicutes and is a gram-positive coccus, but it grown in chains. It is beta-hemolytic, and grows in white colonies on blood agar. It does not grow on mannitol salt agar, because it is salt-sensitive. It is both coagulase-negative, and catalase-negative.

7.     Besides capsules, what are other virulence factors of S. aureus and S. pyogenes preventing killing of bacterial cells by phagocytes? – Lecture 4, Slide 18 –
Virulence factors are molecules produced by microbes that help them colonize a niche in the host, avoid being killed by the host’s immune system.

a.     Staphylococcus aureus is typically not pathogenic – part of normal flora in humans, but it is an opportunistic pathogen, which has the following virulence factors:

                                               i.     Capsule/biofilm (interferes with ingestion by phagocytes

                                             ii.     Adhesins – clumping factor A binds to fibrin, for example

                                            iii.     Protein A – binds to IgG inverted, thus making the cell invisible to phagocytes.

                                            iv.     Enzymes –

1.     penicillases that digest penicillin

2.     beta-lactamases, that digest beta-antibiotics

3.     catalase – inactivates hydrogen peroxide

4.     staphylokinase – dissolves blood clots

                                              v.     Penicillin-binding protein A – does NOT bind penicillin, making resistant

                                            vi.     Staphyloxantin – inactivated hydrogen peroxide

b.     Streptococcus pyogenes – NOT a part of normal human flora, is always pathogen

                                               i.     Calsule/biofilm – helps avoid being phagocyted

                                             ii.     Adhesins – M protein has two functions:

1.     Being and adhesin

2.     Inhibiting the activity of C3 catalase, which prevents activation of the complement system, interfering with attraction of phagocytes

                                            iii.     Protein G – binds IgG inverted (like protein A, just produced by a different bacteria)

                                            iv.     Enzymes:

1.     Hyaluronidase – breaks connections between human cells

2.     Streprokinase – dissolves blood clots

3.     C5e peptidase – digest C5a, preventing inflammation reaction and hence attraction of phagocytes to site of infection

                                              v.     Exotoxins – superantigens (non-specifically activate T-helper cells leading to cytokine storm), lipid-digesting enzymes, Streptolysin O and Streptolysin S, which form pores in cholesterol containing membranes, leading to cell lysis

8.     Describe the functions of virulence factors involved in covering the cells of S. aureus and S. pyogenes by human proteins – Lecture 4, Slides 15, 16, 18 –
Mention some virulence factors of Staphylococcus aureus (capsule/biofilm, Protein A – binds IgG inverted, staphylokinase enzyme, which dissolves blood clots, adhesin (protein A again), exotoxins. OK, now mention some for Streptococcus pyogones – capsule/iofilm, protein G (protein M, which also inhibits C3 convertase, preventing the activation of complement system, which is designed to attract phagocytes to the cell), Streptokinase enzyme (does what staphylokinase does – dissolves blood clots), superantigens, which activate T-helper cells.

9.     Compare the properties of bacterial genera Corynebacterium and Mycobacterium. Name principal species that are human pathogens and diseases they cause – Lecture 4, Slides 19-22 –
Corynebacterium and mycobacterium are general of the phylum actinobacteria (high GC content – 69-73%).

a.     Similatiries: neither produce endospores, antibiotics, or endotoxins (since they are not gram-negative).

b.     Corynebacterium – gram-positive, straight or slightly curved bacilli

                                               i.     Obligate aerobe OR facultative anaerobe

                                             ii.     Produces exotoxins

                                            iii.     C diphtheriae causes diphtheria

c.     Mycobacterium – acid-fast, slender bacilli grow in chains

                                               i.     All obligate aerobes

                                             ii.     Does not produce exotoxins

                                            iii.     M tuberculosis causes tuberculosis and M leprae causes leprosy

10.  Compare the properties of bacterial genera Mycoplasma and Mycobacterium. Name human pathogens from these genera. – Lecture 4, Slides 10, 11, 13, 14, 20, 22 –
Mycobacterium vs mycoplasma:

a.     Similarities: both are prokaryotes and source of human pathogens

                                               i.     Obligate aerobes

                                             ii.     Don’t produce endotoxins, since neither is gram-negative

                                            iii.     Don’t produce exotoxins either

                                            iv.     Don’t produce endospores

b.     Mycoplasma – firmicutes, so low GC content

                                               i.     No cell wall

                                             ii.     Pleiomorphic

                                            iii.     Exhibits gliding motility

                                            iv.     M pneumoniae is a pathogen that causes pneumonia

c.     Mycobacterium – actinobacteria, so high GC content

                                               i.     Acid-fast cells wall

                                             ii.     Slender bacilli growing in chains

                                            iii.     Usually nonmotile

M. tuberculosis causes tuberculosis

Chapter 13: Viruses

1.     Describe the universal characteristics of viruses and their architecture – Lecture 4, Slide 23 –.
Universal characteristics of viruses: no cellular organization, obligate parasites because they can’t synthesize their own DNA, so they have to hijack the host’s DNA replication machinery, very small, very host-specific, because they need to a very specific protein in the cell membrane to bind to.
Viral architecture:

a.     Genetic material – can be single- or double-stranded DRA or RNA

b.     Capsule – made of proteins, houses genetic information

c.     Envelope – optional; has a lipid membrane and hosts viral adhesins

2.     What defines the virus’ host specificity? – Lecture, Slide 24 –
The virus’ host specificity means that the virus is unique, because it can only infect the cells which it can adhere to, which are very specific.

a.     Defined by viral adhesins – proteins the virus uses to bind to the host

b.     Restriction-modification system, consisting of two proteins – restrictase and DNA modifying enzyme – this allow the virus to actually replicate. This is because typically a cell has defenses against viruses, like the restriction enzyme might recognize foreign DNA and destroy it, but restrictase protects from that. Modification enzyme can attach a methyl group to the restriction site of viral DNA, thus making it look like it’s not foreign.

3.     What is lysogenic conversion? Give two examples naming bacterial species and virus involved, toxin produced, and disease caused in humans – Lecture 4, Slide 28 –
Lysogenic conversion is when the phenotype of normal bacteria differs from the phenotype of bacteria infected by some virus. This is important because some bacteria, such as E.coli that comprise part of normal flora of humans may become pathogenic once infected with the virus.

a.     Ex: C. diphtheriae gets infected by beta-virus, which makes it produce diphtheria toxin, which causes diphtheria in humans

b.     Ex: v cholera gets infected with CTX alpha virus, which codes for cholera toxin, which the cell then expresses. This causes cholera in humans

4.     Describe replication of reverse transcribing viruses (retroviruses) in eukaryotic cell. – Lecture 4, Slide 31 –
Each retrovirus will have:

a.     dsDNA: goes to nucleus to make mRNA and DNA copies

b.     ssDNA: goes to nucleus and gets converted into dsDNA, which is used to synthesize ss (+) DNA copies used for new viral particles

c.     it replicates like this:

                                               i.     it attaches to host cell

                                             ii.     it enters the cell

                                            iii.     uncoats and releases viral genetic material

                                            iv.     if it is DNA, it goes to the nucleus for replication, if it is RNA, it replicates in the cytoplasm

                                              v.     the virus assembles

                                            vi.     the virus gets released

5.     Compare three types of persistent viral infections – Lecture 4, Slide 32 –
There are two major types of viral infections: acute and persistent.

a.     Acute viral infection usually lasts for a short time and the host likely develops long-lasting immunity. Large amounts of viral particles are made during a short amount of time and then they die

b.     Persistent viral infections occur when the virus stays insite the host for a long time, like for life. When the virus replicates, it likely buds out of the cell and the cell would usually die from the host immune system, rather than the viral infection itself there are three types of persistent viral infections:          

                                               i.     Chronic infection – virus present for a long time; symptoms develop in the beginning of the disease, but can disappear later (hepatitis B)

                                             ii.     Latent infection – the virus is present and then not detectable in the blood stream because it is dormant inside the host cells during the symptomless period. The symptoms may reappear later after reactivating the virus, and the symptoms may be different from the first time (herpes)

                                            iii.     Slow infection – the presence of infectious virus in the blood gradually increases over a prolonged period of time, and no apparent symptoms may be detectable during that period (HIV, retroviral infections)

A good website covering the various types of viruses: 
https://www.kumc.edu/AMA-MSS/Study/micro4.htm