Microbiology

microbio w Beaton!

What are the factors that determine whether we remain healthy or get sick?

both innate and adaptive (acquired) immunity keeps us healthy.

microbial illness happens when defense fails because:

• there are too many organisms for the immune system to handle

• organisms evade host defense

• organisms gain access through previously unavailable location through an injury/break in the skin/membrane

• dysbiosis: an imbalance in the normal microbial community may cause (or exacerbate) disease (ex. antibiotic use)

What functions does the human microbiome have in keeping us healthy?

the human microbiome may determine whether a substance is sequestered, excluded, or metabolized before accessing our cells. the microbiome can affect drug potency and chemical toxicity. fecal transplants have been used to overcome resistance to antibiotics and treat gut diseases.

importance of “seeding” at birth so the immune system “learns” the difference between: safe vs harmful and self vs non-self.

How does normal resident flora protect us?

it is mutually beneficial

normal flora inhibits pathogens by:

• producing metabolic products that inhibit pathogen growth

• blocking pathogen binding sites on host cells

• competing for and depleting nutrients essential for pathogen growth

• non-specifically stimulating the immune system

Indiscriminate use of antibiotics can result in

infections caused by opportunistic, antibiotic-resistant, normal flora.

How does the immune system distinguish friend from foe?

To differentiate friend from foe, Pattern Recognition Receptors (PRRs) on cells recognize Pathogen Associated Molecular Patterns (PAMPs) on bacteria.

Pattern Recognition Receptors (PRRs) are found on phagocytic cells, lymphocytes, endothelial cells and epithelial cells. the largest family of Pattern Recognition Receptors (PRRs) are Toll-Like Receptors.

What are the main components of the innate immune system and what are their functions?

cells:

• Natural Killer (NK) cells: much faster immune reaction than CD₄ and CD₈ T cells; produces cytokines such as IFN-y, key to antibacterial immune defense

• Macrophages: phagocytose → kill with lysosomes; facilitate communication

• Neutrophils: phagocytose → kill via Reactive Oxygen Species and hydrolytic enzymes

proteins:

• cytokines: chemical messengers: interferons, interleukins, chemokines; released from one cell and affects the actions of others by binding to receptors on their surface

• complement: OIL → opsonization, inflammation, lysis

  • opsonization: coating/binding of a microbe by complement (or an antibody) that results in enhanced phagocytosis

  • inflammation: complement induces histamine release from mast cells and basophils, causing blood vessel dilation and leakage

  • lysis: complement induces bacterial lysis

What are the main components of the adaptive immune system and what are their functions?

humoral immunity: how do antibodies work to protect us?

• neutralization: block attachment of pathogens and toxins

• opsonization: coat bacteria for increased phagocytosis

• activation of complement via the classical pathway (antigen-antibody complex formation) → formation of Membrane Attack Complex and cytolysis.

• previous exposure to a pathogen results in a quicker response due to memory cells primed to recognize that organism

cell-mediated immunity: CD4 T cells and CD8 T cells

• CD₄ T cells: recognize MHC II peptide complexes

  • activate B cells, macrophages, and CD₈ T cells

• CD₈ T cells: recognize MHC I bacterial-peptide complexes, not intact pathogens

  • destroy cells by inducing apoptosis by utilizing perforins and granzymes

  • can kill several infected target cells in succession

  • can become memory CD₈ T cells, allowing a quicker response on second exposure to the same pathogen

What is the difference between pathogenicity and virulence?

pathogenicity: the ability of the organism to cause disease

virulence: the degree of pathology caused by the organism

• differences between strains of the same species

• can change as organisms acquire different mobile genetic elements

What is the difference between colonization and infection?

colonization: the presence of bacteria on a body surface (skin, mouth, intestines or airway) without causing disease

infection: invasion of pathogens leading to the development of illness

colonization involves the presence of bacteria WITHOUT it causing disease, while infection implies disease-causing bacteria

What are the different types of bacterial virulence factors?

• motility: promotes contact and invasion of host cells and dissemination

• attachment: adherence factors aid in adhesion and evasion of host cell immune response

• invasion: allows access to a ready supply of nutrients. the invasion of phagocytes neutralizes their “killing ability,” turns them into a “safe haven” for bacterial replication

• spread: bacterial enzymes degrade extracellular matrix proteins making it easier for bacteria to disseminate

• competition for iron: e.g. bacteria siderophores

• ability to resist immune response:

  • develops resistance to antibacterial peptides (like defensins), antibodies, and surface variations (e.g. changing the tips of pili and other surface proteins)

  • general resistance to phagocytosis: carbohydrate capsules and slime layers → interferes with ability of PRRs on host cells to recognize PAMPs, interferes with complement and opsonization, and forms biofilms.

  • induces autoimmune responses: antibodies to bacterial antigens cross-react with epitopes on host cells and damage them (rare case); abs to bacterial antigens and can form immune complexes that damage tissues

• toxins: exotoxins and endotoxins

What is an exotoxin and what are the targets of type I, type II, and type III bacterial exotoxins?

Exotoxin: proteins secreted by bacteria that can damage cells or tissues; low molecular weight proteins (~25 kd)

• type I toxins: cell surface active

  • many enterotoxins are type I exotoxins. they bind to receptors on the host cell surface and affect intracellular signaling pathways

  • superantigens bypass normal t cell specificity by simultaneously binding to t cell receptors and MHC molecules on APCs → leads to the activation of an inordinate number of t cells

    • provoke intense, excessive immune responses

    • promotes excess cytokine secretion

    • example: Toxic Shock Syndrome Toxin (TSST-1)

• type II toxins: membrane disrupting

  • disrupts cell membranes and cause cell lysis

    • pore-forming toxins, lipid-modifying enzymes, detergent-like peptides

• type III toxins: intracellular targeting

  • two different subunits: “A-B” toxins

    • B subunit binds to cell surface receptor

    • A (active) subunit enters the cell and disrupts intracellular metabolism, interferes with translation, fluid/electrolyte balance, and intracellular communication

What is an enterotoxin?

An enterotoxin is an example of a type I exotoxin. They are small heat-stable peptides release extracellularly from bacteria as they grow. By definition, they cause monkeys to vomit. They binds to receptors on the host cell surface and affect intracellular signaling pathways.

What is the difference between exotoxin and endotoxin?

exotoxins: proteins secreted by bacteria that can damage cells or tissues with a low molecule weight

• relatively high potency and high degree of specificity

endotoxins: intrinsic component of gram-negative bacterial cell wall = lipopolysaccharide

• high molecular weight (>100kd), heat stable

• binds to specific receptors on macrophages and B cells, results in the outpouring of cytokines (IL-6, IL-1, prostaglandins)

• activates inflammatory responses, vasodilation and induces fever (IL-1)

• relatively low potency and low degree of specificity

What is the difference between bacterial intoxication and necrosis?

intoxication: ingestion of preformed bacterial products (toxins); live bacteria are not necessary to harm tissue or cause disease

necrosis: tissue destruction by bacterial enzymes that are metabolic by-products that can lead to bacterial spread

What are the different morphologies of bacteria?

• cocci: spherical shape

• rod/bacillus

• vibrio: comma-shaped

• spiral

What are the components of a prokaryotic cell?

external structures:

• glycocalyx: capsule and slime layer

  • capsule if strongly adherent to cell wall. otherwise, slime layer

• flagella: motility

• pili: attachement

internal components:

• cytoplasm: home to DNA, RNA , enzymes, amino acids, ribosomes, carbohydrates, lipids, inorganic ions, and many low molecular weight compounds

  • site of synthesis for DNA, RNA, and proteins

• nucleoid: DNA-containing region where the genetic material is located and organized but is not enclosed by a membrane

  • bacteria have haploid genomes: 1 circular molecule of double stranded, helical, supercoiled DNA

• extrachromosomal DNA: plasmids

  • extrachromosomal circles of DNA

    • replicate autonomously

    • extra pool of genes/mobile genetic elements that encode toxins and antibiotic resistant genes

• ribosomes: protein synthesis

  • 50s and 30s subunits → 70s ribosome complex

  • protein synthesis is concomitant with RNA synthesis due to lack of nucleus in prokaryotic cells.

• endospores: in gram + bacteria only

  • not reproductive structures, dormant survival forms

  • very resistant to high temperatures (including boiling), most disinfectants, low energy radiation, drying

  • they can survive long periods until conditions permit germination

What is a biofilm?

biofilms form when microorganisms adhere and proliferate on a surface, producing extracellular polysaccharides that promote adhesion and matrix development.

bacteria in a biofilm:

• communicate with each other by “quorum sensing” → “count themselves”

  • quorum sensing enables bacteria to act as a coordinated group rather than individual cells and is crucial for pathogenicity symbiosis

  • virulent bacteria use "quorum sensing” to detect when to secrete toxins

  • mechanism to avoid host’s immune defense

• interact and adapt to their environment as a population

• resist antibiotics, immune response

• show rapid genetic diversification and increased mutations

examples of biofilms:

• dental plaque

• infections: inner ear, bladder, prostate

• films on medical devices such as replacement heart valves, IUDs, catheters

• can form on contact lenses and/or cases

role of biofilms in virulence:

• virulence: the disease-producing capabilities and mechanisms of a microorganism and also the inherent potential of an infection to cause harm

• quorum sensing allows the bacteria in biofilms to evade the host immune response → crucial for pathogenicity and symbiosis

What is the function of flagella, pili, and slime layer/capsule?

flagella: motility

• made of flagellin protein. while its main function is motility, it may also play a role in attachment

• in terms of virulence and pathogenicity, the motility and chemotaxis that flagella allows help pathogens move through mucous layers and attach to cells.

pili: adhesion

• short, rigid proteins composed of pilin, mostly not involved in -taxis

• more common on gram negative bacteria than gram positive bacteria

• conjugation: F pilus

• receptors for extracellular DNA uptake → transformation

• early steps in biofilm formation

• twitching motility: translocation over moist surfaces

capsule/slime layer: immune evasion and adhesion

• protective, sticky layer composed of complex carbohydrates and proteins that sit outside the bacterial cell wall

• immune evasion: resists phagocytosis by white blood cells

• adhesion: to environmental surfaces (rocks, root hairs, teeth, etc.) → results in colonization and resistance to flushing

• antigenic determinants (some vaccines are directed against them)

What is the gram stain and how does it differentiate between types of bacteria?

gram stain: laboratory technique that differentiates bacteria based on the components of their cell walls (cell wall properties), classifying them as either gram positive or gram negative bacteria

• gram stain divides bacteria into two types of categories: gram + and gram -

How do the cell walls of gram positive and gram negative bacteria differ?

bacterial cell walls: a semi-rigid structure of interlocking chains of identical peptidoglycan monomers; common to all bacteria (except mycoplasmas!)

peptidoglycan: prevents osmotic lysis

• NAG polymerizes to form chitin

• during bacterial growth, autolysins break the peptidoglycan

  • transgylcosidases: attach new monomers to the growing end of the bacterial cell wall

  • transpeptidases: cross-link peptidoglycan chains to form rigid cell walls

gram positive cell wall:

• has a thick peptidoglycan layer

  • thick cell wall (15-80 nanometers)

• the peptidoglycan is cross-linked with teichoic acid

  • techoic acid is found in gram + cell walls ONLY. it helps provide rigidity and links various layers of peptidoglycan

gram negative cell wall:

• relatively thin → 10 nm; single layer of peptidoglycan surrounded by an outer membrane

• periplasmic space: houses enzymes that are responsible for breaking down nutrients and binding proteins that facilitate nutrient transport across the cytoplasmic membrane

• gram - bacteria have the outer membranes (NOT gram +) → the outer membrane is the major permeability barrier

• LPS is outer membrane → three components: Lipid A, core polysaccharide, o-specific antigen

  • Lipid A: innermost layer of LPS, hydrophobic, anchors LPS to outer membrane

    • retains biologic activity when heated and is responsible for much of toxicity of gram - bacteria

  • Core Polysaccharide: highly variable among different bacteria

  • O-Specific Antigen: outermost domain of LPS

    • major serologic determinant of gram negative bacteria

• in humans, LPS signals that bacteria are present and trigger an innate immune response

  • can also induce lethal septic or endotoxic shock

What is the function of the bacterial cell wall?

primary function: maintain cell shape and provide structural support

bacterial cell walls: a semi-rigid structure of interlocking chains of identical peptidoglycan monomers; common to all bacteria (except mycoplasmas!)

peptidoglycan: prevents osmotic lysis

• NAG polymerizes to form chitin

• during bacterial growth, autolysins break the peptidoglycan

  • transgylcosidases: attach new monomers to the growing end of the bacterial cell wall

  • transpeptidases: cross-link peptidoglycan chains to form rigid cell walls

bacterial cell wall composition divides bacteria into two major classifications: gram - and gram +

What are bacterial secretion systems and why are they important?

bacterial secretion systems: protein complexes that bacteria use to transport substances across their cell membranes

• they enable pathogens to invade or colonize host cells

• play crucial roles in virulence, nutrient acquisition, cell-cell communication, and DNA transfer

• found in both gram - and gram + bacteria

  • 11 → gram negative specific

  • 4 → gram positive specific

  • 2 → both - and +

What are the components inside a bacterial cell and how do they differ from their eukaryotic counterparts?

both prokaryotic and eukaryotic cell membranes have phospholipid bilayers embedded with proteins. however, unlike eukaryotes, the prokaryotic bilayer has NO sterols.

• exception: mycoplasms → have sterols but lack a cell wall

prokaryotic cells lack specialized organelles, so certain functions → energy production, housing bases of bacterial flagella, removing waste, functioning in DNA and cell wall ynthesis, formation of endospores → all occur within the prokaryotic cell membrane.

What are some of the differences between bacteria and eukaryotic cells that we can take advantage of with respect to specifically treating bacterial infections?

there are fundamental differences between prokaryotes and eukaryotes that explain selectivity of antibiotics:

• antibiotics target:

  • differences in protein synthesis. prokaryotes have the 70S ribosomal complex, while eukaryotes have the 80S ribosomal complex.

  • can target prokaryotic topoisomerase/dna gyrase

  • the differences in RNA synthesis: inhibits RNA synthesis initiation

  • the cell walls in prokaryotes that are absent in eukaryotes

Describe the bacterial growth curve including when a semilog plot is used.

bacterial growth is exponential/logarithmic.

when looking at a semilog plot, it is divided up into four sections:

• the lag phase: bacteria are gearing up to prepare for division

• the log phase: exponential growth of bacteria

• the stationary phase: the number of bacteria dying = the number of bacteria growing/dividing

• the death or decline phase: losing viable bacteria, more bacteria is dying

What are the different types of metabolism used by pathogenic bacteria?

• fermentation

• respiration

• autotrophy: photosynthetic bacteria that utilize CO₂ as a carbon source; not clinically significant

What needs to be supplied so that bacteria can grow?

bacterial nutrient requirements:

• prototrophs: grow on minimal media consisting of a simple carbohydrate with inorganic sources of all other nutrient requirements

• auxotrophs: mutant microorganisms that require >/= 1 complex organic nutrients such as amino acids, nucleotides, or enzymatic cofactors for growth.

  • require growth factors (organic carbon sources) to grow

• organisms that require many growth factors and have complex nutritional requirements are fastidious

• microbes require sources of

  • Nitrogen → for proteins and nucleic acids

  • Phosphorous → for compounds such as ATP, nucleic acids, coenzymes

  • Mg²⁺, Fe: cytochromes, peroxidases

  • Sulfur, Potassium, Sodium, Calcium

  • Trace amounts of Fe, Zn, and Co

What are the ways that bacteria can be identified?

• phenotypic identification:

  • “old fashioned” observational techniques

    • what does it look like on agar plates?

    • what does it look like microscopically?

      • cell size, shape, staining; presence/absence of special structures

  • biochemical tests: e.g. catalase, fermentation of sugars, drug sensitivities

• immunological tests:

  • antibody/antigen interaction

  • often easier than testing for the microbe itself

  • ex: rapid strep tests

• genotypic testing:

  • rapid diagnostic tests: PCR, DNA sequencing

  • advantage: speed and accuracy

  • disadvantage: cost

What is selective media used for?

has >/= 1 components that inhibit the growth of some species, while promoting the growth of the desired species.

What is differential media used for?

A type of growth medium that distinguishes between bacteria based on their biochemical properties.

What has to be done to isolate a pure culture from a mixed population of bacteria?

utilizing the streak-plate method → spread a small, diluted sample of bacteria across a sterile agar-based nutrient medium using a sterilized inoculating loop in a four quadrant pattern

What is the genetic makeup of bacteria?

bacterial growth → cell division/binary fission

identical genomes are passed on

• bacterial genomes = ~3-5 × 10⁶ base pairs

• DNA is configures as a single, circular chromosome that encodes ~2-4000 proteins

What are plasmids and why are they important?

• optional, extra-chromosomal, small, circular DNA molecules that replicate autonomously and code for non-essential genes

• plasmids are important because

  • they carry many antibiotic resistant genes (R genes)

  • carry many virulence genes

  • fertility or F plasmids contain genes that make conjugation possible

• plasmids can be genetically engineered to enable bacteria to produce needs proteins, degrade pollutants, and as tools for studying gene expression.

What are the different ways that bacteria exchange genetic information with each other and why is this important?

genetic exchange allows bacteria to acquire new genes rapidly, facilitating their adaptation to changing environmental conditions.

bacteria exchange genetic information in four ways:

• transformation: uptake of naked DNA from the environment

• conjugation: DNA transfer between bacterial cells

• transduction: a bacterial virus (phage) carries bacterial DNA into a new bacteria

• transposition: movement of bacterial DNA within a cell

  • transposable elements (TNs) are discrete DNA segments that move within a genome using non-homologous recombination.

    • most encode a transposase that breaks and rejoins the DNA

    • insertion of transposable element into a new site alters host DNA

What are some of the ways antibiotic resistant bacteria spread?

conjugation, transduction, transposition, transformation are the mechanisms by which antibiotic resistance and virulence genes are spread.

What kind of activities do some antibiotic resistance genes encode?

mechanisms of antibiotic resistance:

resistance results from genes that:

• encode enzymes: that destroy or inactivate the antibiotic

• alter the receptor (for the antibiotic): reduce or block antibiotic binding and entry

• act as an efflux pump: actively transport the antibiotic out of the bacterium

• alter porins: reduce uptake of antibiotics in gram -

• target bypass: increase production of targeted bacterial enzyme or express alternative enzymes

How are antibiotic resistance/sensitivity tests carried out?

susceptibility testing: determines whether bacterial are inhibited by an antimicrobial

• Minimal Inhibitory Concentration (MIC):

  • lowest concentration that prevents visible growth of a microbe

  • depends on the microorganism, the affected human being (in vivo only), and the antibiotic; determined experimentally

• Kirby Bauer disk diffusion assay:

  • sensitive: if growth is inhibited by a concentration that is easily and safely achieved in a patient’s bloodstream, a positive clinical response is anticipated

What are some of the best practices with respect to use of antibiotics?

CDC recommends 4 core strategies to limit antibiotic resistance:

• prevent infections

• track antibiotic-resistant infections

• improve prescribing of antibiotics

• develop new drugs, diagnostic tests and vaccines

How do you differentiate Staph from Strep?

Microscopic morphology is the key to identification. After gram staining and viewing under microscopic conditions, Streptococcus appears in pairs or chains, while Staphylococcus has the appearance of grape-like clusters. Completion of the Catalase test can differentiate between Staph and Strep. Staphylococci test positive on the Catalase test, indicating that they possess the enzyme catalase that can rapidly breakdown Hydrogen Peroxide (H₂O₂) into water (H₂O) and oxygen (O₂). Streptococcus, however, test negative on the Catalase test, indicating the absence of the catalase enzyme. 

How do you differentiate Staph aureus from S. epidermidis from S. saprophyticus?

By performing the Coagulase test. Staph aureus has the coagulase enzyme, meaning it can cause blood plasma to clot. Other Staph species, such as Staph epidermidis and Staph saprophyticus, do not possess the coagulase enzyme, and consequently, will produce a negative result on the Coagulase test. Staph aureus, having the coagulase enzyme, will produce a positive response on the Coagulase test, effectively differentiating it from other species of Staphylococcus. 

What virulence factors of S. aureus allows it to form abscesses?

The prototypical lesion of Staphylococcus aureus is an abscess, which is a confined pocket of pus in tissues, organs, or spaces inside the body. The necrotic center contains fluid (pus), dead bacteria, and polymorphonuclear cells (PMNs). The enzyme Coagulase is a virulence factor that builds a fibrin wall and allows the bacteria to persist in the host tissue. Staphylocoagulase combines with prothrombin (a proprotein involved in clotting) to form the Stpahylo-thrombin complex. This complex then converts fibrinogen (a precursor)  to the active form fibrin, which is the clotting protein that makes up the wall that encases the bacteria and allows it to remain in the host tissue. 

What virulence factors of S. aureus allows it to spread?

Fibrinolysin is a proteolytic enzyme that plays a crucial role in the breakdown of fibrin, which is the protein that allows for clot formation. Fibrinolysin allows the bacteria to escape the the abscess and spread to other areas. Hyaluronidase is an enzyme that breaks down hyaluronic acid, which is found in the skin, joints, and other tissues. More specifically, hyaluronidase dissolves the connective tissue ground substance, which is hyaluronic acid.

What virulence factors of S. aureus allows it to cause:
- Gastroenteritis?
- TSS?

Type I toxins are a virulence factor of Staph aureus. They bind to receptors on the cell surface, which stimulates intracellular signaling pathways. There are two types:

• Enterotoxins → which are exotoxins that cause emesis. Ingestion of a pre-formed enterotoxin results in intoxication.

  • heat stable, resists gastric acid hydrolysis 

  • e.g. Staphylococcal food poisoning → Staph present in a food source secretes the enterotoxin, someone eats the food and gets gastroenteritis.

• Superantigens → they do not require processing by APCs and can bind directly to MHC class II molecules and T cell receptors. This leads to the activation of an inordinate number of T cells.

  • Superantigens trigger non-specific activation of T-cells, which can lead to the release of large amounts of cytokines and T cell mediators.

    • During normal antigen presentation, 0.01% of T cells are stimulated. Superantigens activate up to 20% (range is 2% - 20%) of circulating T cells, which can result in Toxic Shock Syndrome (TSS).

How is it that the same enterotoxin cause gastroenteritis in some cases and toxic shock
syndrome in other cases?

When ingested, enterotoxins A-E cause diarrhea and vomiting and are responsible for Staphylococcal food poisoning (an intoxication). Gastroenteritis does not result in Toxic Shock Syndrome because enterotoxins are poorly absorbed across the intact mucosa. But during an infection, when an organism secretes toxins systemically, Toxic Shock Syndrome can result. Toxic Shock Syndrome Toxin 1 (TSST-1) is responsible for ~75% of TSS, including all menstrual cases.

• Simply ingesting the toxin will only cause gastroenteritis. If the live organism replicating has access to your blood supply and is secreting the toxin, allowing it to systemically spread throughout your body, it will then result in TSS. 

What virulence factors of S. aureus allows it to evade the immune response?

Type II toxins disrupt membranes, which causes cell lysis. Examples of cytolytic proteins/toxins include Alpha Toxin and Leukocidins.

• Alpha toxin: potent membrane-damaging toxin that causes leakage and release cytokines leading to inflammation.

• Leukocidins: increases the permeability of leukocytes, leading to their rupture

This allows for Staph aureus to evade the immune system → “immune evasion strategy”

What are the virulence factors of S. epidermidis?

Cell wall-anchored proteins that had a role in biofilm formation. Biofilms are hard to get rid of once they are formed. Staph epidermidis also has a capsule which inhibits phagocytosis.

What are the virulence factors and epidemiology of S. saprophyticus?

Staph saprophyticus is a bacteria associated with urinary tract infections (UTIs) primarily in young women.

• Transmission: normal flora of the skin and vagina, related to sexual intercourse

• Pathogenesis: adhesins for uro-epithelial cells. urease damages the uroepithelium.

How do you differentiate S. pyogenes (GAS) from S. agalactiae (GBS)?

Some Streptococci are serotyped into Lancefield groups, based on the Group C carbohydrate antigens found in their cell walls. [~20 Lancefield groups (A-U)]

• Strep pyogenes: group A (GAS) 

• Strep agalactiae: group B (GBS)

What is the most important virulence factor of S. pyogenes and what is its function?

The M protein is the most important virulence factor (for Group A bacteria) 

• Major surface antigen

  • >100 M serotypes; makes it challenging to develop a vaccine

• Anti-phagocytic 

• Fosters immune evasion 

• Can trigger auto-immunity 

Why can you get multiple instances of strep throat, but get scarlet fever only once?

Strep pyogenes is the bacteria known to cause strep throat. It is a Group A bacteria that possesses the M protein that has more than 100 M serotypes. This is the reason you can get strep throat more than once. You can get infected with different M types, which means you can get strep throat multiple times. 

Scarlet fever is caused by a Group A bacteria that causes strep throat but has also acquired a mobile genetic element - a bacterial virus - that encodes an erythrogenic toxin. You typically only get Scarlet fever once because once you have been exposed to the toxin, which lacks varying antigenic types, your body produces antibodies to it, making it difficult to be reinfected. 

What demographic is most at risk from infection by GBS?

Pregnant Women → in the 1970’s, GBS emerged as the 2^nd most common cause of neonatal sepsis/meningitis with an attack rate of 1/1000 births. 

• increase in obstetrical complications i.e. premature rupture of membranes 

What are the possible consequences/sequallae of an untreated S. pyogenes infection and how can they be avoided?

What is the most important virulence factor of S. pneumoniae and what is its function?

For which of the gram+ cocci are there vaccines?

Compare and contrast 2 species of gram negative cocci:

• virulence factors

• ability (or not) to be normal flora

• pathogenesis

• prevention

the two species of gram negative cocci: 

What are the main virulence of E. coli?

What is a parasite and explain how does it differ from a commensal organism?

A parasite is an organism that lives on or in a host organism and gets its food from or at the expense of the host. Pathogenic parasites harm the host.

A commensal organism benefit from the host without causing any harm.

What are the two major categories of parasites based on cellular structure?

1. Protozoa → unicellular parasites

• mastigophora 

• sarcodina (ameboid)

• sporozoa 

• ciliata 

2. Metazoa (Helminths) → multicellular worms

• Cestodes

• Trematodes

• Nemahelminthes (roundworms)

Which blood test result is commonly associated with parasitic infections?

What are the two forms of protozoa and their characteristics?

Which protozoan group uses flagella for locomotion? Give two examples.

What is the only ciliated protozoan that infects humans.

What are the two forms of protozoa and their characteristics?

Which protozoan group uses flagella for locomotion? Give two examples.

Which parasite causes trichomoniasis and how is it transmitted?

What vector transmits Trypanosoma brucei and what disease does it cause?

How is Chagas disease acquired and what organ is commonly affected in chronic infection?

Which protozoan is known as the “brain-eating amoeba” and how is it acquired?

What ocular infection is commonly associated with Acanthamoeba?

What are the different genome types for RNA viruses and how does that affect their gene expression?

single stranded

• positive polarity (mRNA sense)

• negative polarity (complementary to mRNA)

• segmented or non-segmented

double stranded

enveloped or non-enveloped

single stranded, positive polarity, non-enveloped:

• picornavirus

• norovirus

single stranded, positive polarity, enveloped:

• rubella

• hepatitis C

• corona

• arboviruses: west nile, dengue, yellow fever, zika, chikungunya

double stranded (DS)

• rotavirus

single stranded, negative polarity, enveloped

• influenza

• rabies

• measles

• mumps

• rsv

• parainfluenza

• ebola

• marburg

• hantavirus

• nipah

What is the route of acquisition for polio and how/why is that different from where it causes pathology?

fecal-oral acquisition

it infects primates only - receptor = CD155, involved in intercellular adhesion

→ CD155 is expressed during embryogenesis in structures that evolve into spinal cord anterior horn motor neurons