week 3, lec 2 BAD Flashcards by Claire Jamieson

normal vs resident vs transient microbiota

Normal microbiota – microorganisms living inside and on the human

Resident microbiota – once disturbed, these microbes promptly reestablish themselves (specific per area and age)

Transient microbiota – only temporary inhabitants, includes commensals and pathogenic microbes

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bacterial interference is the process in which ____ microbes prevent colonization by ____ microbes

what 3 mechanisms is this done by

resident microbes prevent colonization by pathogenic microbes

compete for receptors or binding sites on host cells
compete for resources (i.e. nutrients)
mutual inhibition by metabolic or toxic product release

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microbiome in the urethra

small # of organism, same as on regional skin and perineum

healthy urine has bacteria in it (not sterile)

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vaginal microbiomes

after birth

until puberty

during puberty

menopause

what type of bacteria species and what is the pH?

after birth: lactobacilli app - acidic

until puberty- cocci and bacilli etc. - neutral pH

puberty: lactobacilli species- acidic (from glycogen metabolism) to prevent pathogens
-and also have group B streptococci
- also clostridium, listeria, gardnerella vaginalis

menopause: less lactobacilli, more mixed

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antibiotics remove which vaginal bacteria species and increase risk of colonization of yeast and pathogenic bacteria resulting in vaginitis

lactobacilli

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placenta and uterus - what bacteria>

not sterile,

commensal bacteria in placenta,

uterus microbiome quite different from vaginal or GI

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bacterial vaginosis- what are the dysbiotic changes that lead to the problem

increase gardnerella vaginalis and mycoplasma hominis (among others)

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clinical features of bacterial vaginosis

vaginal malodorous, increased white-grey discharge

possible dysuria and pruritus

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what are risk factors for bacterial vaginosis

STI, antibiotics, douching, flora imbalances

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what other microbes outside of normal STIs are transmitted via sex

Zika virus, Ebola virus, Neisseria meningitidis group C, some anaerobes associated with bacterial vaginosis

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what type of bacteria is chlamydia? what 2 morphologies>

obligate intracellular bacteria

replicate body (replicative)
elementary body (infective)

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which serotypes of chlamydia trachoma’s produce “chamydia” and with produce lymphogranuloma venereum

chlamydia= serotypes D-K

L.V= serotypes L1-L3

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how is chlamydia trachomatis transmited

sexual/mucosal

neonatal during vaginal delivery

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symptoms of chlamydia

urethritis- dysuria and no bacteriuria (bc intracellular) and female often asymptomatic

cervicitis

vaginal discharge,
post-coital bleed

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complications of chlamydia

epididymitis, proctitis

PID, neonatal conjunctivitis (vaginal delivery)

reactive arthritis (cant see, cant pee, cant dance with me)

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presentation of chlamydia trachomatis- lymphogranuloma venereum

genital ulcers,

lymphs: lymphangitis with necrosis and abscess

scar tissue (possible proctocolitis and rectal fibrosis)

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neisseria gonorrhoea is what type of bacteria

**acapsular and many plasmids

Gram negative, diplococci, obligate aerobe, many non-pathogenic species are commensals, acapsular, many plasmids (genetic variability), facultatively intracellular

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virulence factors in neisseria gonorrhoea

lipooligosacchardie (LOS)

Opa and Pilin proteins (phase variation, promote adherence)

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how is neisseria gonorrhoea transmitted

sexual/mucosa (reinfection likely bc od no immunological memory)

neonatal (vaginal delivery)

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presentation of neisseria gonorrhea

males vs females

urethritis
–> males symptomatic (discharge, dysuria, epididymitis)
–>females asymptomatic (discharge, dysuria, pruritic, discharge, cervicitis)

extra-genital: proctitis, pharyngitis, conjunctivitis, disseminated infection (septic arthritis, gonococcal dermatitis- arthritis syndrome)

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what is gonococcal dermatitis arthritis syndrome (in gonorrhoea)

Polyarthralgia, tenosynovitis, dermatitis

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which type of treponema palladium causes syphilis

spirochete

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how is syphilis transmitted

sexual/ mucosal

perinatal (congenital syphilis)

contaminated blood products

stages and features of syphilis

stage 1: painless, chancre –> ulcer

stage 2: ulcer disappears, new wart like lesion (condyloma datum) that diffuse, non pruritic rash, fever, headache, malaaise

latent stage: no sx for years

stage 3: granuloma/ gamma, neurologic (i.e. seizure, dementia, meningitis), cardiac (aortic aneurysm)

what is the tertiary stage of syphilis have (3 things)

(1) granuloma/ gumma – soft collection of bacteria, infected cells and macrophages (2) neurological: seizures, dementia, meningitis (3) cardiac: aortitis, aortic aneurysm

during pregnancy what can happen with congenital syphilis

Spontaneous abortion Stillbirth Prematurity Low birth weight

when baby Is born; how does congenital syphilis present

-Deformed bones -Severe anemia -Hepatosplenomegaly, jaundice -Brain and nerve problems: deafness, blindness -Meningitis -Skin rashes

haemophilus hücreyi where is it more common? features?

africa painful pustule --> ulcer inguinal lymphadenopathy

what is special about Mycoplasma genitalium and Ureaplasma urealyticum structure of the bacteria? sx?

no cell wall urethritis, cervicitis (PID, abortion, infertility)

bacteria that causes trichomonas vaginalis

parasite with 4 flagella transmitted via sex (can only exist in humans)

pathogenesis of trichomonas vaginalis

cytotoxin destroys epithelial cells hides from immune system by binding plasma proteins

clinical features of trichomonas vaginalis

urethritis vaginal trichomoniasis (yellow discharge, petechial on cervix/ strawberry cervis), increase vaginal pH >5

pelvic inflammatory disease is a common complication of which STIs

N. gonorrhoea, C. trachomatis,

what is pelvic inflammatory disease associated with

changes in genital flora (BV)

what can pelvic inflammatory disease lead to

chronic pelvic pain, infertility, ectopic pregnancy, bilateral tubal occlusion, miscarriage, premature birth

sx of PID

asymptomatic OR lower abdominal pain, pelvic pain, fever, cervical motion tenderness, cervical inflammation, aggravated by menses, movement and coitus

Candida albicans cahracteristics

part of normal vaginal microbiome dimorphic (yeast or hyphae) biofilm phenotypic swtiching secrete hydrolytic enzymes adapts to pH quickly

pH and candida albicans

pH < 6 then high density population- yeast form (primary form of dissemination) pH >7 then low density population- hyphae form (more invasive than yeast)

clinical features of candida albicans

vulvovaginal candidiasis (pruruitis, burning, white scanty discharge like cottage cheese)

vulvovaginal candidiasis complications

recur >4+ per year non-candid albicans species associated with diabetes, pregnancy, immunosuppression

HPV sx? clinical features?

usually asymptomatic STI, spontaneously resolves genital warts and genital cancer

HSV-2 herpes

genital herpes; cause latency in local/sacral sensory ganglia

clinical features of HSV-2

urethritis congenital and perinatal infection (from mom to baby- if early in gestation then moms IgG can protect fetus)

HIV is part of which family and what type of virus

lentivirus family; retrovirus ssRNA

what immune cells does HIV attack and destroy

CD4+ T cells and macrophages

3 ways of transmission of HIV

1. sex 2. congenital, breast milk 3. blood transfusion and needles

how does HIV do transcytosis

HIV leaves the cell and uses GP120 ligand and GP41 co-ligand to attach to the galactosyl ceramide lipid on the new host’s epithelium, enter the cell and pass through it to the basolateral side

HIV transmission

trauma (damaged epithelium) transmigration (attach to DC-SIGN on dendritic cell and get internalized into endoscope and transport to lymph) in lymph: XR4 ligands to attach to CXCR4 receptor of CD4+ or R5 ligand on CCR5 receptor on macrophage to get inside cell

which ligand and receptor on T cell and macrophage does HIV use

XR4 ligand to CXCR4 receptor on CD4+ T cell R5 ligand on CCR5 receptor on macrophage

how is HIV activated to replicate in a cell if

1. cell detects HIV antigen 2. another STI activates T-cell or macrophage

when HIV replicates what happens to T cells and macrophages

T-cells die, macrophages survive

stages of HIV

stage 1- lymphadenopathy stage 2- latent stage 3- advanced sx stage 4- AIDs- opportunist infection (lowest CD4+ count)

HIV- AIDS defining illness

from many species of parasites, bacteria (i.e. TB, salmonella), fungi (i.e. candida), virus (i.e. HSV, varicella-zoster)

malignancy from HIV AIDS

* Kaposi’s sarcoma * Non-Hodgkins lymphoma * Primary lymphoma of brain

HIV can invade the CNS and cause

encephalopathy -infected macrophages and microglia release neurotoxins -dementia

how is AIDS usually transmitted

perinatal and breast milk