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Flashcards in exam 2 Deck (88):

What are the general challenges and physiological conditions microbes face whenever they colonize a host site (first part of lecture on Skin Microbiota)? How do microbes live (form colonies-or not) in their hosts?

-They must be able to adhere to some substratum and not get flushed out- adhere to human cell directly, extracellular matrix, molecule secreted by another microbe
- they must satisfy nutritional needs and growth requirements-not always trivial
-must withstand host defense- a moving target
-must withstand changes in environment caused by other microbes- may actually be an asset
-microcolonies- usually enclosed in polymer
-biofilm- teeth, crypts `of tongue
-intracellular colonization- epithelial cell of mucosa
-planktonic- free, least common


What are the predominant biological determinants that affect the ability of the microbiota and pathogens to colonize a site?

Physiochemical determinants:
-temperature- most organisms must be able to grow at 37 degrees C, may affect eye flora and some diseases like leprosy (33 degree optimum)
-pH (1.5-8)
-atmospheric composition- aerobic, microaerobic, anaerobic
-water activity- relates to NaCl levels too
Water availability: areas like some parts of the skin are very dry. If <60, microbes can’t grow
High salt can reduce water activity
Many other parts of body are bathed in fluids
Secretion of lipid-rich substance
-light-UV exposure


Autogenic succession

microbes affect the environment, may be competitive or synergistic- so bacteria that initially colonize an area make it habitable for others who otherwise would not be able to


skin: Face, forehead, behind ear, back, sides or nostril

Face, forehead, behind ear, back, sides or nostril

Environmental factors
-high density of sebaceous glands, hair and eccrine glands
Environmentally exposed

Antimicrobial Defenses
Physical and chemical barriers:
-air flow across surface prevents microbes from settling on skin
-intact stratum-prevents access
-desquamation-shedding-removes adherent microbes
-pH, dry, antimicrobials, lysozyme

Innate immunity:
Neutrophils, nitric oxide, toll-like receptors

Acquired immunity: SALT (skin associated lymphoid tissue), dendritic cells, cytokines, lymphocytes, mostly IgA secreting

Main types of bacteria in each area


Dry (palm)

Structure/Parts: Dry (palm)
Environmental factors: Thick stratum corneum
High density of eccrine gland

Antimicrobial Defenses: - IL1 complement, TH17
Main types of bacteria in each area: -Propionibacterium
-Firmicutes: streptococcus,
-A few gram neg


Moist (axilla)

Environmental factors:Apocrine glands present
High density of hair
Occluded, humid environment

Main types of bacteria in each area: -staphylococci occupy aerobic niche, use urea as nitrogen source
-corynebacteria- play big role

Antimicrobial Defenses: antimicrobial peptides- IL1 complement, TH17


4. What are some features that contribute to the large variation in Skin Microbiome?

Host physiology- sex, age, site
Environment- climate, geography, location
Immune system- previous exposures, Inflammation
Host genome- susceptibility genes such as filaggrin
Lifestyle- occupation, hygiene
Pathobiology- underlying conditions such as diabetes


Defenses of the Skin

Physical and Chemical
• Flow of air across surface,
prevents microbes from
settling on skin
• Intact stratum-prevents
• Desquamation-sheddingremoves
• pH, dry, antimicrobials,
Innate Immunity
• neutrophils, Nitric
Oxide, Toll-like
Acquired Immunity-
SALT (Skin-
Associated Lymphoid
Tissue), dendritic
cells, cytokines,
lymphocytes, mostly
IgA secreting


What are the dominant bacterial phyla found and 3 dominant bacterial genera? Are there non-bacterial genera present-what is the most common one? Make sure you know these four genera.

4 dominant
– Actinobacteria (52%)
– Firmicutes (24%)
– Bacteroidetes (16.5%)
– Proteobacteria (6%)
Dominant bacteria:
-Corynebacterium: gram positive bacilli 8/59 species typically found, non-encapsulated, non-motile, unusual cell wall containing mycolic acid, facultative or aerobic, some don’t produce their own lipids.

-Propionibacterium: gram positive, accounts for ½ of skin microbiota, cause acne, hydrolyze troglycerides and release fatty acids, obligate anaerobe or microaerophilic

-Staphylococcus: 17/35 species found on skin, gram positive, halotolerant, important opportunistic pathogens, ferment sugars to lactic acid

Non-prokaryotic inhabitants:
-Malassezia: dominant of skin fungal populations, dominant in most places expect foot
-Many phage, animal viruses: human papillomas, Polymavirus, retroviruses


6. What factors can lead to skin dysbiosis?

Dysbiosis (is a term for a microbial imbalance or maladaptation on or inside the body, such as an impaired microbiota)
Mechanisms by which skin microbacteria may initiate or amplify skin disorders:
-genetic predisposition-barrier defect
Increased microbial density
Contextual pathogens-pathobionts
Increase in defined bacteria- inflammatory


7. What is the correlation between acne and atopic dermatitis to the skin microbiome?

Atopic dermatitis- makes skin red and itchy- long term- skin can flare up, patients are colonized with S. aureus, causes eczema
Acne: propionobacter acnes, causes activation of complement


9. What are features of S. aureus that contribute to its environmental resilience?

Salt tolerant, dessication tolerant
Most have protein A: binds Fc region (activate immune system) of IgG
Have tremendous genetic diversity- transduction, conjugation and transformation


8. For Staphylococcus aureus of the skin pathogens know:
a. Basic biology and contribution of this to disease
b. Reservoir and mechanism of transmission
c. Major sites of colonization
d. Major sites of disease – are they the same or different than colonization sites
e. Main diseases
f. Major virulence factors
g. Main disease symptoms (if applicable)

Gram positive firmicute coccus
Facultative-areobic respiration and fermentation
Salt and dessication tolerant
Produce coagulase A (primary indicator used to identify it)
Main reservoir: humans, present transiently on companion animals
Transmission is direct or indirect:
-direct-skin to skin, resp secretions
Transmitted via fomites (towels, sponges)- viable for weeks outside host
Introduced into food
Nose, hands, chest skin, ankles, arms
Invasive infections in almost every organ in the body:
-bacteremia-bloodstream infection
-septic shick
-toxic shock syndrome
-endocarditis (heart)
-meningitis (brain)
Skin and soft tissue infections (SSTI): pimples, boils etc
Ulcers- open sores or craters, folliculitis- hair follicle
-Antibiotic resistance to methicillin and vacomycin is a huge problem
-Has protein A which binds the Fc region of IgG
-MecA which is methicillin, vancomycin etc resistant
-Has adhesions, enzymes that are degradative: facilitate tissue degradation- ex: nuclease- degrades NETs, protease- degrades structural proteins
-Toxins: alpha- forms pores, gamma- also pore forming, exfoliative toxins- serine proteases that destroy adhesion between cells in the epidermis, toxic shock syndrome toxin-1 is a cytotoxin and superantigen
Immune evasion (innate, complement, adaptive, intracellular)
Antibiotic resistance

Maintain skin health
Increased monitoring of populations
Public health practices to decease transmission
Antibiotic resistance is a problem, no vaccines


Mycobacterial leprae
a. Basic biology and contribution of this to disease
b. Reservoir and mechanism of transmission
c. Major sites of colonization
d. Major sites of disease – are they the same or different than colonization sites
e. Main diseases
f. Major virulence factors
g. Main disease symptoms (if applicable)

Gram pos
Slow growing
Preference for cooler regions
Bacterial tropism for macrophages and schwann cells

Chronic granulomatous infection skin and peripheral nerves

Nerve damage- mediated by cellular immune response and inflammation
Chronic inflammation

Get taken up by Schwann cells, grows slowly
Host genetic factors effect development of disease and patterns

Macrophages, not the causative M. leprae initiate host nerve demyelination and axonal damage
Large hypo pigment on skin


Mycobacterium ulcerans know:
a. Basic biology and contribution of this to disease
b. Reservoir and mechanism of transmission
c. Major sites of colonization
d. Major sites of disease – are they the same or different than colonization sites
e. Main diseases
f. Major virulence factors
g. Main disease symptoms (if applicable)

Emergind disease
Associated with wetlands in tropical wetlands
Neglected but treatable disease
Very similar to M. marinum which is a fish pathogen
Transmitted by insect bites
Reservoirs are insects, humans

Infection leads to progressive destruction of skin
Painless, mobile swelling of skin or diffuse swelling of limbs
No pain or fever, often not treated, may lead to massive ulcers sometimes bone deformities
Mycolactone: is a toxin
Is cytotoxic by unknown mechanism at high concentrations- causes localized necrosis
Is immunosuppressive at lower concentrations
-inhibits production of TNF by macrophages,
-suppresses dendritic cell activity
-inhibits macrophages, B cells, T cells
-inhibits IL production

Painless, mobile swelling of skin or diffuse swelling of limbs


leishmaniasis know:
a. Basic biology and contribution of this to disease
b. Reservoir and mechanism of transmission
c. Major sites of colonization
d. Major sites of disease – are they the same or different than colonization sites
e. Main diseases
f. Major virulence factors
g. Main disease symptoms (if applicable)

Neglected tropical disease
Type of disease depends on host and pathogen:
-cutaneous: localized, diffuse
Mucocutaneous: visceral
Transmitted through bite of sand fly
Obligate intracellular pathogen- mostly macrophages but other cells- neutrophils

Prevents phagolysosome fusion
Also affects antigen presentation and hamper ability of CD8+ T cells to kill infected cells

Skin sores that heal very slowly
Stuffy nose, runny nose, nosebleeds, swallowing difficulty, ulcers and wearing away in the mouth, nose and inner nose


9. What are features of S. aureus that contribute to its environmental resilience?

Salt tolerant, dessication tolerant
Most have protein A: binds Fc region (activate immune system) of IgG
Have tremendous genetic diversity- transduction, conjugation and transformation


Be able to give one example of the degradative enzymes, adhesins, toxins and anti‐immune functions that are used by S. aureus. What are three possible roles of adhesins in disease?

Also use immune evasion and antibiotic resistance- not all strains produce all factors
Adhesins: extracellular matrix binding protein, elastin binding proteins, Protein A, collagen binding protein, clumping factor A etc
Toxins: cytotoxins- taget leukocytes,


What is a MSCRAMM?

Microbial Surface components recognizing adhesive matrix molecule
adhesin proteins mediate the initial attachment of bacteria to host tissue, providing a critical step to establish infection


12. What is the mechanism of resistance seen in MRSA strains? Vancomycin? What is different about Community Acquired MRSA (compared to Hospital Acquired)?

MRSA: methicillin resistant
Have the MecA gene which allows bacteria to be resistant to antibiotics like methicillin, penicillin and other penicillin-like antibiotics
Mechanism: PBP2 (penicilin binding protein) is a PG peptidase (catalyzes amino acid transfer- allowing cell wall synthesis) and is a target for Beta-lactams (antibiotics). MacA gene (encodes PBP2) which beta-lactam drugs can't bind to
Vancomycin binds D-ala-D in crosslinks (resistance bacteria have D-ala, D-lac), but resistant strains don’t let it bind.

There are multiple independent origins:

CA-MRSA: community associated-
-have chromosomal genetic elements: mecA- so have B-lactam resistance
-Secreted toxins and factors
-Global gene regulators- ex: ag, sarA which upregulate many virulence factors
-efflux pumps: prodive fitnass advantage
-vancomycin resistant

HA-MRSA: hospital associated


13. How are virulence genes regulated in staphylococci, how does this related to the relationship between colonization and disease?

The accessory gene regulator (agrA) locus of Staphylococcus aureus encodes a two-component signal transduction system that leads to down-regulation of surface proteins and up-regulation of secreted proteins during in vitro growth
-it regulates other genes
Adhesins, invasins and evasins lead to colonization, which leads to toxin production, which promotes disease and transmission


14. What are some features of M. leprae that makes it difficult to study this pathogen?

Occurs in resource poor countries, tropics and warm temperate regions (so resource rich countries like the U.S won’t study it)
Cannot be grown in vitro
Prefers cooler regions
has a small genome, and many pseudohenes


15. What is one feature of M. leprae biology that limits its ability to cause systemic disease?

It prefers cooler regions- so usually occupies limbs which are cooler in temperature


16. What are the two poles of leprosy disease manifestation and how do they differ? How does this relate to the hosts immune response-specifically?

The two poles are tuberculoid pole or lepromatous pole
Exposure to leprae can either cause no disease or end in indeterminate leprosy(ill-defined, hypopigmented skin lesions)-> this can lead to either spontaneous healing or the patient enter a clinical spectrum where it can lead to TB (which involves more cell-mediated immunity) or lepromatous (which involves less cell-mediated immunity)
In tuberculoid- poor Th1 responses and strong Th2 responses, so make strong antibody response and impaired macrophage activation= is an aggressive disease
In lepromatous- strong Th1 response and low levels of Th2 antibodies= limited progression disease


17. What cell types are targeted by M. leprae and how does this contribute to pathogenesis and disease symptoms?

Machrophages and schwann cells- In macrophages- nerve damage mediated by cellular immune response and inflammation, causes chronic inflammation, cell wall contrains important targets for host immune response-infect progenitor cells->grows in them-> recruits and transfers bacteria to macrophages-> granuloma formation-> release of infected macrophages
Macrophages and not the causative bacterium M. leprae, initiate host nerve demyelination and axonal damage
In schwann cells (cells that cover the nerve fibers in the peripheral nervous system): grow slowly, host genetic factors effect development of disease and
Pattern->causes infected smooth muscle and infected skeletal muscle


18. What is the relationship between M. marinum and M. ulcerans

M. ulcerans has an almost identical genome to M. marinum which is a fish pathogen- only difference s that M. ulcerans replicates more slowly, has no pigments, gained important macrolide cytotoxin mycolactone- toxin


19. What is the main virulence factor of M. ulcerans, what disease does it cause, and what are the biological activities of this factor?

May be transmitted by insect bite
Infection leads to progressive destruction of skin
Painless, mobile swelling of skin or diffuse swelling of limbs
No pain or fever, often not treated
May lead to massive ulcers sometimes bone deformities
Has mycolactone which is cytotoxic by an unknown mechanism, it caises localized necrosis
It is immunosuppressive at lower concentrations- inhibits production of TNF by macrophages, suppresses dendritic cell activity, inhibits macrophages, B cells, T cells, inhibits IL production


20. What is the causative agent of Leshmanisis and what are the general features of this microbe? What is the role of the insect?

Causative agent: Leishmania spp.
It is protozoan
Transmitted through bit of sand fly
Obligate intracellular pathogen- mostly macrophage but also others
Prevents phagolysosome fusion through LPG-modified lipid microdomains which block the fusion
Causes a variety of diseases- cutaneous is our focus
Type of disease depends on host and pathogen:
-cutaneous: localized, diffuse
-post: dermal
-mucocutaneous: visceral
Skin sores that heal very slowly, stuffy nose, runny nose, and nosebleeds
Difficulty swallowing,
Ulcers and wearing away (erosion) in the mouth and nose and inner nose
Breathing difficulty


21. In which type of host cells can it reside and what are two ways it can accomplish its survival in these cells?

It is an obligate intracellular pathogen- mostly lives in macrophages but also neutrophils
Has a lot of mechanisms to live intracellularly- avoids phagolysosome acidification by preventing phagolysosome fusion
Also affects antigen presentation and hampers ability of CD8+ T cells to kill infected cells


Cheeks, lips, palate

Antimicrobial Defenses Main types of bacteria in each area
Desquamation (skin shedding)
Saliva Low diversity
Streptococcus predominates
Some periodontal pathogens persist by invading buocal cells


Environmental factors Antimicrobial Defenses Main types of bacteria in each area

Environmental factors Antimicrobial Defenses Main types of bacteria in each area
Stagnant sites: food impaction possible Saliva influences this Diverse microflora, site variation
Many obligate anaerobes
Veillonella, fusobacteria, prevotella, Treponema, unculturable organisms



Highly papillated surface
Has some anaerobic sites
Diverse microflora
Facultative and obligate anaerobes
Stepto, actinomyces, Rothia, Neisseria, some gram neg anaerobes


4. What are the 4 main bacterial phyla found in the oral cavity? How, in general does the oral cavity differ than other sites?



5. What is a biofilm? Know the relationship between the microbes in saliva, tongues and in plaque

Each tooth is an island-hard surface, near constant presence of liquid
Sites on same tooth are variable
Biolfilm is a cluster of bacteria
There are some microbes that are present in saliva, tongue and plaque such as streptococcus


6. Know the terms adhesion, coadhesion, and coaggregation and how they play into the formation of a biofilm on teeth. What has current research on oral biofilms revealed about the spatial organization of the biofilm?

Adhesion-microbes can recognize specific sites to adhere to- ex: streptococci can recognize receptors in salivary pellicle
Coadhesion- planktonic microbes can adhere to genetically distinct microbes
Coaggregation- bonding of 2 distinct microbes suspended in fluid phase

Plaque formation is dependent on signals- nothing is random
Autoinducer 2 is a universal intergeneric signal
Time and spatial relationships are critical for plaque formation
Signaling across even across domain
And nutrients and DNA are exchanged
spatial organization: a cauliflower structure, using tooth side and base between teeth, or in plaque or corncob


7. What “activities” are happening in a biofilm, not so much who is doing what, but general activities

Signaling and DNA exchange


8. What is the role of the Autoinducer 2 (AI2)?

A12 is made by commensal bacteria and pathogens
As the commensal bacteria biomass increases, this improves communication among trancition bacterial species
When AI2 concentrations are the highest, the pathogens are favored for growth and join the developing biofilm communities


9. What is the concept of the functional core microbiome? What have we learned about differences in the microbiome in healthy vs. diseased (periodontisis) mouths?

Functional core microbiome: we have 4 phyla that dominate
Healthy and diseased teeth have the same 4 abundant phyla but their proportions are different
Baacteriodetes is more abundant in disease than healthy
Actinobacteria and proteobaceria incread in periodontal health plaque
Proteobacteria and firmicues were most abundant phylum of periodontal health


ow do we classify Streptococcus? Make sure you know terms Viridans and Group A Strep.

Streptococcus is classified by whether it is alpha/ gamma hemolytic or beta hemolytic
Viridans Strep- oral, causes endocarditis (inflammation)
Group A strep- usually found in throat or on skin


11. What are the main virulence mechanisms of Streptococcus mutans? What disease does it cause frequently other diseases that may result from an unresolved infection? What is happening in endocarditis?

It has metabolic diversity, glycan formation, is acid tolerant
Strep. Mutans attaches using gluvosylatransferases to the tooth pelical
Accumulation of these leads to sucrose which leads to glucosyltransferase to make extracellular glucans
S mutans produces acid which can cause demineralization of the tooth structure which is the third event in the formation of dental plaque and results in a carious lesion= dental carries
Endocarditis- defined as inflammation of the lining of the heart chambers and valves, can be acutre or sub-acute. Result of a systemic infection, introduced during a medical or dental procedure,
-can occur in healthy individs, but more often in individs with risk factors such as rheumatic heart disease, heart valve problems, other heart diseases, but not always
-Bacteria can break away from the mouth and make their way to the heart and start growing, they form plaque or vegetation, streptococcus makes up great than 50% of the bacteria involved, staphylococcus makes up about 25%. Can cause strokes etc
-mechanism: strep has specific surface antigens important in attaching to surfaces, also bind heart and form biofilms, and specific protein antigens induce cytokines


12. What is periodontitis and what is the Mixed Red Complex (which microbes)?

Periodontitis is a polymicrobial disease
It is bacterially induced chronic inflammatory disease of periodontium, leads to bone loss around tooth
It has various stages: healthy teeth and gums (low biomass, resolving inflammation) -> gingivitis (incipient dysbiosis, high biomass, nonresolving inflammation)-> periodontitis (frank dysbiosis-pathogenic biofilm, high biomass, failed resolution of inflammation-> advanced pariodontitis

Mixed red complex: trigger for initiation of disease is presence of complex biofilms. A group fo 3 bacterial species found in late biofilms are recognized as most important in adult periodontitis: Porphyomonas gingivalis, Treponema denticola and Tannerella forsythis (formally bacteriodes)- they work cooperatively to cause disease


13. How do these bacteria interact to amplify disease? What is the Keystone Pathogen Theory?

Bacteria work together to cause disease- they have synergistic virulence mechanisms- porphyromons SerB inhibits IL-8, Lipid A of Porphyromonas inhibits TLR4 to other bacteria
The “keystone pathogen” hypothesis holds that certain low-abundance microbial pathogens can orchestrate inflammatory disease by remodeling a normally benign microbiota into a dysbiotic one


14. What are the basic characteristics of Aggregatibacter and what disease can it cause?

it causes a different form of periodontitis
it is a gram eng bacteria, colonizes oral cavity, in a small number of adults it causes localized aggressive periodontitis, affects central incisors and first molars
affects different populations at different rates, can cause endocarditis


15. What are several virulence factors of Aggregatibacter in particular what is the LTX? How might it be used-for the good?

It has many virulence factors similar to Mycobacterium tuberculosis
Factors: adherence proteins- late colonizer, biofilm polysaccharide, LPS, toxins- cytolethal toxin, leukotoxin A, RTX-family
All these have a combined effect on human cells
-responsible for binding Ca ions which are needed for activity. Once Ca is bound-structural changes occurs, plays role in binding to host cell surface.
It is secreted and dectected in lipid vesicles, and regulated by level of fermentable sugars, modified by fatty acids, regulated by iron levels-blocks secretion.
-its primary role is immune evasion
-may lyse Red blood cells when grown on certain media, but not specific,
-affect immunologically relevant cells
-at high dose cause pore formation
-at low dose cause apoptosis
-it has a potential therapeutic use- LFA-1 (recruits cells to site of infection) is upregulated in many leukemia’s, and treating with LTXA can increase survival rate
-LTXA binfs to LFA-1, and can cause cell death


16. What are some chronic diseases that may be “caused” by periodontisis? What are several mechanisms that are believed to be at play?

Can cause atherosclerosis and coronary ehart disease, related to repeated exposure to proinflammatory cytokines, and related to changes in blood factors


17. What are the two different main locations for S. pyogenes in the body and what are the two main classes of disease? What are some possible long-term complications of S. pyogenes infection?

Locations: throat, skin
Can cause:
-throat infections- strep throat
-post-infection complications such as kidney damage (from skin or throat infections)


18. What are some important virulence factors of S. pyogenes in pharyngitis? How does growth in human saliva contribute to disease?

Virulence factors: adhere to pharyngeal epithelium, it uses carbon sources and maltodextrin (smaller saccharide) from saliva and uses them for evergy
It can attach to pharyngeal epithelial cells and has proteins on the surface of its hyaluronic acid capsule that prevent phagocytosis, degrade NET and inhibit antimicrobial peptides,


19. What are some important virulence factors in invasive S. pyogenes infections and what is one possible mechanism that may explain the transition to invasive disease?

Virulence factors: immune evasion and host cell adherence
It transitions to different host environments, as it has a distinct transcriptome
One possible mechanism for spread is that it mutates and spreads


1. What are the major antimicrobial defenses of the urinary system and what have we learned about its microbiota?

Shedding, mucus, urine flow, pH and osmolarity of urine, urea, glycoproteins and proteins, sIgA, environmental determinants- pH 5.7-6.1, aerobic, sugars, amino acids, and nitrogen sources
Microbiota: urine is definitely not sterile, varies regardless of sex
Differences in gender and age (differences attributable to method of collection- specimen collection with elderly is an issure
Takes greater than 2 months to reestablish core after antibiotic treatment
Females and Males: Lactobacillus, Streptococcus, Staphylococcus, most others are different


2. Name unique immunological challenges of the female reproductive system?

Must protect host from variety of pathogens but must also allow development of the fetus (biggest parasite)
Estradiol (an estrogen made in ovaries) or progesterone (steroid hormoe that stimulates uterus to prep for pregnancy) regulate directly all aspects of immunity- these fluctuate


3. What are the main barriers that protect females from infection within the reproductive tract. What genus of bacteria plays a very important role-especially in the vagina?

Multiple layers of protection:
Barrier: epithelial cells
Chemicals: mucin, antimicrobial peptides
Normal microbiota: lactic acid bacteria
Immunity: innate and adaptive
Many defenses similar to skin
Vagina and cervix-mucus associated, affects of hormones and IgA and IgG
Antimicrobial peptides and proteins
After puberty, Lactobacillus acidophilus is domiant- ferments glycogen to lactic acid


4. What is the dominant phyla of microbes in the Urinary Tract?
a. How much variably is there between individuals?

Firmicutes, Proteobacteria, Actinobacteria, Bacteriodetes

a. How much variably is there between individuals?
Variable regardless of sex and age, differences in gender and age


b. What are several factors that affect the microbiota of males?

Lenth of male urethra impacts ability of microbes to colonize- only distal 6 cm colonized
Affected by sexual maturity, circumcision, sexual activity, gender of partners, frequency and number of partners, nature of birth control used
Circumcision has large influence on composition of male microbiome- uncircumcised penis has sig more anaerobes, many of these species are associated with bacterial vaginosis (disease of vagina caused by excessive bacterial growth


c. How do antibiotics affect the microbiota-especially in the elderly?

It takes more than 2 months to reestablish core microbiota after antibiotic treatment
Specimen collection with the elderly is an issue


5. Why are agents that cause STIs restricted to sexual transmission?

Are only found in body fluids from genitourinary tract- they are usually very sensitive to drying and other environmental stresses


6. What are the three most common STIs in the US today? What is the trend in STIs today?

Trend: STI’s have been increasing in the country- 3rd year in a row
Gonorrhea went up after birth control pills were creaed in the 1960s but decreased by 2000s
Chlamydia has been increasing
They remain a major public healh challenge in US
Physicians are required o report chlamydia, gonorrhea and syphilis,
Common STI’s like HOV ad genital herpes are not reported to CDC but surveyed
CDC estimates there are about 20 million new STDs each ear costing healthcare system $16.4 million annually, and cost individs more in terms of acute an long-term health consequences
Social factors:
-1/3 STDs in teenagers with multiple partners,
-many have minor symptoms
-socially stigmatic/problematic
-large disparities in racial and socioeconomic groups
Most common: chlamydia, gonorrhea and syphilis

STI’s have been decreasing in Europe, but increasing in US- attributed to education and access to healthcare for everyone in Europe


Neisseria gonorrhea
a. The main characteristics of each agent.

Gram neg, b-Proteobacteria, non-spore forming
Obligate anaerobe
Very sensitive to environmental stresses
Humans only natural host
Conjugative lasmid
Is an obligate pathogen


Gonorrhea b. The main diseases it causes.

Diff in males and female
Female: primary site is cervix- if untreated can cause pelvic inflammatory disease
Can cause mild vaginitis
Males: painful urethral infections
Heart valve problems in men
Fetus/newborn: stillborn births, premature delivery, eye infections


c. The potential complications of untreated infections- gonorrhea

Pelvic inflammatory disease in women
In either gender, it can spread if left untreated
Cause of purulent arthritis in adults


e. Treatment challenges- gonorrhea

It is becoming antibiotic resistant- mutations in 16S and 23s rRNA, topoisomerase, etc


f. What is the role of pili and its antigenic variation? gonorrhea

Pili allow attachment to host cells
-provide resistance to killing
-variable region –carboxy terminal- is exposed and the conserved region is hidden
-allows for antigenic variation


g. What is the Gonococcal Genetic Island and what is its role? gonorrhea

Codes for T4SS which secreted ssDNA out of cell for biofilm formation. It is also effective at natural transformation, which explain a lot of antibiotic resistance. It seems to be important in intracellular survival, and for iron acquisition


h. What are peptidoglycan fragments and what is their role in the pathology of the disease? in gonorrhea

As the cells grow, they nick PG to add to the existing layer. Most bacteria recycle these fragments. Neisseria recycle smaller amounts but instead release large and small fragments.
Large fragments: for depletion of complement, cause arthritis in ats
Small fragments-PGCT: induce strong proinflammatory cytokines, and causes death and shedding off of cilated fallopian tube cells


i. What is the state of antibiotic resistance against Neisseria gonorrhea? What factor(s) contribute to this?

Antibiotic resistance is becoming a big deal- it is becoming resistant. There are mutations in its 16S and 2S rRNA, mutation in topoisomeae, mutation in PB1 and 2, reduced permeability, efflux pumps, plasmids with penicillinase, mutation in tetM


9. For Chlamydia make sure to know:
a. The main characteristics of each agent.

Obligate intracellular pathogen
Gram neg
Has peptodoglycan
2 forms: elementary bodies (inactive, infective form), and reticulate bodies (metabollically active but non-infectious)
Diff species replicate in different hosts from amoeba to humans
2 biovars (strains) in humans: trachoma and lymphogarnuloma venereum (LGV)


b. The main diseases it causes

Lesions from in lymph nodes near primary site
Granuloma formation- inflammation, necrosis
Adscesses, tissue damage
Ocular trachoma(affects eyes) (LVG)
Infant pneumonia (LVG)
Inflammation, pain, mucopurulent discharge


Chlamydia c. The potential complications of untreated infections.

Pelvic inflammatory disease
Ectopic pregnancies-potentally fatal
Sexual dysfuntion
Women with chlamydia 3-5x more likely to contract HIV
Men: epididymitis and prostatitis
May attach to sperm and help transmission


Chlamydia d. What populations are most at risk

More prevalent in women- women more at risk


Chlamydia e. Treatment challenges

Evasion of host immune system: replication within inclusions, inhibit apoptosis
Resistance to nitric oxide
Reduced inflammatory LPS
Antigenic variation
Cytoplasmic secretion of proteases that degrade TSC factors (regulator) needed for MHC1 and 2 expression
Infection doesn’t confer long-lasting immunity
Subsequent infections may lead to more tissue damage


10. Chlamydia
a. What are the two life forms of Chlamydia? What is the difference between their roles in infection/disease?

Elemental bodies (RB): inactive, infective form
Reticulate bodies (RB): metabolically active but non-infectious
has lipopolysaccharaide but lacks peptidoglycan.


b. What is the role(s) of T3SS and effectors they deliver?

Different effectors are present at different stages
They facilitate entry into host as elementary body
T3SS effectors are injected into hosts for remodeling. They redirect vesicles for nutrient acquisition
It differentiates into Reticulate body (RB), proliferates and produces other effectors


Chlamydia c. What is unique about its cell wall structure?

Unique cell wall inhibits phagolysosome fusion


chlamydia d. What does Chlamydia do to insure its own survival?

It replicates within inclusions
Inhibits apoptosis
Resistance to nitric oxide
Reduced inflammatory LPS
Antigenic variation
Cytoplasmic secretion of protease that degrade TSC factors (regulator) needed for MHC1 and 2 expression


11. Human Papilloma Virus (HPV), make sure to know:
a. The main characteristics of each agent.

5 genera: alpha, beta, gamma, mu and nu-PVs
Infects basal epithelial cells of skin and mucosa


HPV b. The main diseases it causes.

A fraction of cases can turn into cancer of cervix, penis or anus and rectum
Men most lkely to get throat cancer-causes almost all cervical and throat cancers
DNA virus- papillomaviruses


HPV pops most at risk

d. What populations are most at risk
Women and men
Most men don’t have problems but can cause genital warts and may contribute to cancers of penis, anus and oropharyns although uncommon
Gay and bisexual men 17x more likely to get genital warts


HPV complications if left untreated

cervical and vulvar cancer may develop


HPV e. Treatment challenges

Condoms don’t prevent transmission, no drugs stop infection


f. What type of virus is HPV? Know what we mean by E genes and L genes and
how it relates to viral replication? What is an episome?

It is small, nonenveloped dsDNA, types are tissue specific. E genes are early, L are late. In dividing cells, only E genes are expressed. In differentiated cells E and L viral genes are expressed
In virus laden cells ready for desquamation and infection of naïve individuals- L genes are expressed
An episome is: a unit of genetic material (DNA) in bacteria, such as a plasmid, that can either replicate independently or can be integrated into the host chromosome.
E genes are oncogenic, involved in viral replication, assembly and release
L genes are capsid proteins (contain genetic material of virus)


g.HPV Which strains are of major concern and why is it such a big problem?

HPV16 annd HPV18 are of most concern- associated with cervical cancer


i. HPV- What types of cancer does it most commonly cause in women? In men?

Men most likely to get throat cancer, women cervical cancer


h. Where is its port of entry and what is required for HPV to go through its productive life cycle?

Gets in through open wound, abrasion in skin, needs perturbed Gets in through open wound, abrasion in skin,
It has a differentiation dependent life cycle, with a begitative life cycle and malignant progression- which causes invasion and metastasis, and loss of polarty
has a differntiation dependent life cycle


i. How does HPV lead to cervical cancer or other genital cancers?

Causes loss of polarity in cells in infected cells,
Causes metastasis (tumor growth far from primary site of cancer)
it invades the squamocolumnar junction and then invades the squamous cells and the columnar cells


i. What is the role of the proteins E5, E6, and E7 in viral replication and progression to cancers? HPV

HR E6 targets the tumor suppressor p53
E7’s role is to bind and de-activate a protein called “retinoblastoma protein” or pRB which would normally cause cells to stop dividing when a problem is deected
E5 turns E6 and E7 on


j. When and for whom is vaccination recommended? HPV

Girls and boys should be vaccinated at 11-12 yearsold


5. What did the study with Staphylococcus LTA tell us about the role the normal Staphylococcus have regarding the innate immune response? How does the immune system affect the microbiota?

It is an opportunistic pathogen
LTA (lipoteichoic acid) inhibits TRAF (TNF receptor Tumor necrosis factor (TNF, tumor necrosis) is a cell signaling protein (cytokine) involved in systemic inflammation and is one of the cytokines that make up the acute phase reaction.) inhibits TLR2 (toll-like receptor), inhibits inflammation
In mice that don’t control their inflammatory response in response to LTA, they are more susceptible to Staphylococcus


Por protein (protein 1)

promotes intracellular survival (prevents phagolysosme fusion


gonorrhea virulence factors

-iron-aquisition proteins
-IgA protease
-Antibiotic resistance

Opa protein (protein 2)
opacity protein- mediates attachment

Rmp protein (protein 3)- reduction- protects surface proteins and LOS from bactericidal antibodies

LOS-Lipooligosaccharaide- and endotoxin activity

iron-aquisitions proteins- complete with human cells, bind host transferrin,

IgA protease- destroys IgA

antibiotic resistance- efflux pumps, b-lactamase (penicilin resistance)