week 3, lec 2 BAD Flashcards
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
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
microbiome in the urethra
small # of organism, same as on regional skin and perineum
healthy urine has bacteria in it (not sterile)
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
antibiotics remove which vaginal bacteria species and increase risk of colonization of yeast and pathogenic bacteria resulting in vaginitis
lactobacilli
placenta and uterus - what bacteria>
not sterile,
commensal bacteria in placenta,
uterus microbiome quite different from vaginal or GI
bacterial vaginosis- what are the dysbiotic changes that lead to the problem
increase gardnerella vaginalis and mycoplasma hominis (among others)
clinical features of bacterial vaginosis
vaginal malodorous, increased white-grey discharge
possible dysuria and pruritus
what are risk factors for bacterial vaginosis
STI, antibiotics, douching, flora imbalances
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
what type of bacteria is chlamydia? what 2 morphologies>
obligate intracellular bacteria
- replicate body (replicative)
- elementary body (infective)
which serotypes of chlamydia trachoma’s produce “chamydia” and with produce lymphogranuloma venereum
chlamydia= serotypes D-K
L.V= serotypes L1-L3
how is chlamydia trachomatis transmited
sexual/mucosal
neonatal during vaginal delivery
symptoms of chlamydia
urethritis- dysuria and no bacteriuria (bc intracellular) and female often asymptomatic
cervicitis
vaginal discharge,
post-coital bleed
complications of chlamydia
epididymitis, proctitis
PID, neonatal conjunctivitis (vaginal delivery)
reactive arthritis (cant see, cant pee, cant dance with me)
presentation of chlamydia trachomatis- lymphogranuloma venereum
genital ulcers,
lymphs: lymphangitis with necrosis and abscess
scar tissue (possible proctocolitis and rectal fibrosis)
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
virulence factors in neisseria gonorrhoea
lipooligosacchardie (LOS)
Opa and Pilin proteins (phase variation, promote adherence)
how is neisseria gonorrhoea transmitted
sexual/mucosa (reinfection likely bc od no immunological memory)
neonatal (vaginal delivery)
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)
what is gonococcal dermatitis arthritis syndrome (in gonorrhoea)
Polyarthralgia, tenosynovitis, dermatitis
which type of treponema palladium causes syphilis
spirochete
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
- sex
- congenital, breast milk
- 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
- cell detects HIV antigen
- 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
