antibiotics quiz Flashcards
the 3 things that target bacteria
disinfectant, antiseptic, antibiotic
disinfectant
used to sterilize the surface of inanimate objects
disinfectants are typically very
very strong, and destroy many features of bacteria
antiseptic
used to sterilize body surfaces, these are not as strong as disinfectants
antibiotic
used to kill bacteria internally through ingestion or injection
antibiotics are the
gentlest, they should not harm human cells
what makes antibiotics good
broad-spectrum
minimal side effects
broad-spectrum
effective against many different types of bacteria
why is broad-spectrum good
many times, growing a culture will take too long
minimal side effects
little toxicity or host damage
what makes good antibiotics bad
resistance
attack normal flora
why does resistance make good antibiotics bad
makes harmful normal flora bacteria grow resistance, could become harmful or trade genes with harmful ones
why does attacking normal flora make good antibiotics bad
killing off normal flora can lead to bad things
killing off normal flora can lead to……
- increased risk of yeast infection
- increased risk of normal flora infection
- vitamin deficiency
- GI issues
examples of yeast infections caused by antibiotics attacking normal flora
yeast, vaginitis, thrush
examples of normal flora infections caused by antibiotics attacking normal flora
CDiff, MRSA/VRSA
examples of vitamin deficiencies caused by antibiotics attacking normal flora
B, B12, K
examples of GI issues caused by antibiotics attacking normal flora
antibiotic-associated diarrhea.. probiotics
thrush
an overgrowth of the fungus Candida albicans on the tongue
thrush causes
a white slimy layer on top of tongue
yeast vaginitis
an overgrowth of the fungus Candida albicans on the vaginal walls
like in chemotherapy, antibiotics
should damage “bad” cells, while doing as little collateral damage as possible
how do antibiotics avoid collateral damage
- peptidoglycan Synthesis
- protein Synthesis
- DNA/RNA Synthesis
- metabolism (bacteria often have different metabolic pathways)
why do we target peptidoglycan synthesis with antibiotics
no cell walls in human cells
why do we target protein synthesis with antibiotics
ribosome structure is different
why do we target DNA/ RNA synthesis with antibiotics
bacteria use different enzymes to facililatet
why do we target metabolism with antibiotics
bacteria often have different metabolic pathways
________ are defined by the presence of a
beta-lactams are defined by the presence of a beta-lactam ring
how do beta-lactams work
they block one of the last steps of the synthesis of peptidoglycan … BETTER ON GRAM POSITIVE
what is one of the last steps of the synthesis of peptidoglycan that is blocked by Beta-lactams
when transpeptidases and carboxypeptidases build cross-linkages between peptidoglycan strands
transpeptidases and carboxypeptidases together are known as
PBPs
PBPs
penicillin-binding proteins
examples of beta-lactams
- penicillin
- amoxicillin
- methicillin
- cephalexin
antibiotic classes that are beta-lactams (by popularity)
- penicillins
- cephalosporins
- beta-lactams (increased activity)
antibiotic agents that are beta-lactams (by popularity)
- amoxicillin
- amoxicillin, clavulanic acid
- cephalexin
1 antibiotic in india and us
Amoxicillin (beta-lactam)
antibiotics can be protein synthesis inhibitors because
the ribosomes in animal cells and human cells are different
ribosomes
site of protein synthesis
ribosomes are sorted according
to the Svedberg rate of sedimentation (S)
what is the Svedberg rate of sedimentation
how fast the particle settles to the bottom after centrifuge
for the Svedberg rate of sedimentation for ribosomes
the Svedberg rate of 2 subunits of ribosome are added
50s + 30s, 60s + 40s
70s , 80s
in bacteria the size of ribosomes are
smaller an lighter : 70s
inhumans the size of ribosomes
80s
what are the major classes of drugs that take advantage of the different sizes of ribosomes of bacteria and humans
- tetracyclines
- macrolides
Tetracyclines
bind and inhibit the 30s subunit of bacterial ribosomes
tetracylines are very common, ecspecially
very common, especially doxycycline
tetracyclines always come with
with 4 connected rings
Macrolides
bind to and inhibit the 50S subunit of bacterial ribosomes
Macrolides are the ______ most-common type of antibiotic prescribed in the US
2nd
examples of common macrolides
- erythromycin»_space;> ery-pack
- azithromycin»_space; z-pack
4 th most popular drug in india and example of tetracyclines
doxycycline
2 antiboitic class us
macrolides
2 antibiotic US
azithromycin
5 most popular antibiotic drugs in india
macrolides
what antitbiotics stop DNA or RNA synthesis
Fluoroquinolones
Fluoroquinolones
are a class of antibiotic that target and block the bacterial form of DNA topoisomerase II
DNA topoisomerase II
creates small nicks in DNA to relieve torsinal stress
without DNA topoisomerase , bacteri
becomes tightly twisted and DNA and RNA synthesis will stop
main fluoroquinolone
ciprofloxacin
4th most commone antibiotic class , …
fluoroquinolone
3rd most common antibiotic in india, fluoroquinolone
contrimoxazole
purines (needed for replication)
A and G
to make purines the body needs
tetrahydrofolate (THF)
how to make THF
the body uses folic acid reductase on folic acid
how is folic acid acquired in humans
through diet
bacterial cells getting tetrahydrofolate
cannot rely on diet to make THF, instead, make their own
what is used to address THF in bacteria???
sulfa drugs
what do sulfa drugs do
interfere with an ezyme necessary for bacteria to build THF from precursors
good place to look for more antibiotics
bacteria building THF pathway
sulfa drugs always contain
sulfur
example of sulfa drug
sulfamethoxazole
sulfa drugs interfere in THF pathway from
the enzyme that acts on PABA to convert precursor 1 to precursor 2
what is often perscribed w/ sulfa drugs
trimethoprim
trimethoprim interferes in the THF pathway from
dihydrofolate to tetrahydrofolate
mechanisms of antibiotic resistance
- pushing antibiotics out
- stopping antibiotic entry
- target modification
- inactivation of antibiotic
pushing antibiotics out is achieved by
inheriting or overexpressing an efflux pump
efflux pump
transmembrane pump that moves the antibiotic out
stopping antibiotic activity is achieved through
mutation in the shape of a porin can stop entry of antibiotics, can’t do their job
antibiotics often enter cells through
porins
inactivation of antibiotics is achieved through
inheriting a gene that codes for an enzyme that cuts the antibiotic
many bacteria have inherited a gene for
a beta-lactamase , which cleaves beta-lactam containing compounds
pushing antibiotics out is not usually seen
not common with beta-lactams, but often for others
how does bacteria achieve target modification
mutation to the structure that an antibiotic attacks
example of target modifications `
most MRSA infections as a result of mutant PBP structures
mutant PBP structures means that in MRSA
that beta-lactam antibiotics no longer bind to them (and thus, don’t work)
many types of of beta-lactamases
YES
Escherichia are gram what?
gram-negative
Escherichia shape
bacilli
what temp do Escherichia like
mesophilic
do Escherichia form spores
No
Escherichia relationship with oxygen
facultative anaerobes
Escherichia make up what % of human GI flora
0.1 %
what is the “claim to fame” of Escherichia
conversion of digested K1 into K2
Vitamin K2 is
it’s active form in humans
how many species in the Escherichia genus
5-6 known
Escherichia can divide in
just 20 minutes
a newborn’s intestine will typically be colonized with Escherichia within
40 hours of birth
who discovered Escherichia
Theodor Escherich in 1886
E. coli is most linked to what categories of disease
- infection of GI tract
- Urinary Tract Infection
- Meningitis
E. coli cause infection of the GI tract gist
colonization of virulent strain in GI tract can cause bad things
what bad things can colonization of virulent strains of E. coli in GI tract cause
diarrhea and dysentery
dysentery
diarrhea with blood
E. coli is responsible for how much of UTIs
about 85%
how does E. coli cause a UTI
passed from the fecal/oral route to the urethra or bladder
E. coli is how much more commen in girls
14x … urethra is shorter
Meningitis caused by E. coli is usally only commono in
neonates, requires entry into the bloodstream plus the K1 antigen
what does the K1 antigen help E. coli do in meningitis
helps it pass through the BBB (brain blood barrier) into the meninges
how does E. coli spread
through the fecal-oral route
what does it mean that E. coli spreads through the fecal-oral route
feces of fecal matter infected materials must enter the mouth of someone
how does the fecal-oral route usually spread
dirty water or inadequate hand-washing after using the bathroom
E. coli spread is closely linked to what food
ground beef
most important species of Escherichia is
Escherichia coli
E. coli comes in many different
serotypes
serotypes
different strains catalogued by their surface antigens (think lancefield)
Escherichia coli serotypes are grouped based on what surface antigens
Oligosaccharides
Flagellal structure
Capsule
Escherichia coli serotypes are grouped based on what surface antigens KNEUMONIC
O- Oligosaccharides
H-Flagellal structure
K - Capsule
Oligosaccharides as a surface antigen of E. coli
structure of sugar chains at the outer tip of LPS
how many LPS structures known in E. coli
173
how many unique flagellal structures known of E.coli
53
Capsule E.coli
he structure of the protein on the outermost layer of E. coli
how many unique structure known capsule e. coli
60
serotypes of E. coli are another example of
antigenic variation
leading disease-causing stereotype of E. coli
E. coli O157 : H7
and K antigen does not matter in this case
O antigen is
Oligosaccharides, somatic `
E. coli, being negative…. have
many fimbriae
most important type of fimbriae that E. coli have
type I fimbriae
type 1 fimbriae
ecspecially sticky to cells that line the small intestine and/or bladder
type 1 fimbriae allow
bacteria to stick to cells that line the small intestine and/or bladder
once E.coli sticks to cells that line the small intestine and/or bladder
secrete an exotoxin
which exotoxins would E.coli secrete once attached to cells that line small intestine and or bladder
LT, STa, or STb
E.coli secreting exotoxins LT, STa, or STb»» would
increase levels of cGMP in the intestine
when levels of cGMP are increased in the intesine by E coli
- stopping water absorption in the intestines,
- leaving more fluid in the intestinal lumen and triggering diarrhea.
one dominant virulence factor of very bad E coli
Stx
Stx
shiga toxin
Virulent E. coli express that shiga toxins
Stx1 or Stx2
Stx2 compared to Stx1
400 times as potentt
what an exotoxin agin???
secreted proteins
what do Stxs first do when release
receptors on human intestinal endothelial cells to enter the cells
the receptors on intestinal endothelial cells that Stxs bind to
NOT FOUND IN ANIMALS
since the the receptors on intestinal endothelial cells that Stxs bind to are not found in animals
allows virulent strains to grow in animals harmlessly before humans consume them
when shiga toxin enters human intestinal endothelial
one part of a shiga toxin binds to and cleaves an important part of ribosomes in those endothelial cells, halts function
if endothelial cells have no functioning ribosomes
no proteins»> cell death
what receptors do shiga toxins bind to….maybe
GB3
most dangerous E. coli strains like O157 : H7 are called
enterohemorrhagic
what does it mean to be enterohemorrhagic
disrupt the GI tract and cause hemorrhage (bleeding)
what sometimes causes E. coli to be enterohemorrhagic
cell death from Shiga toxin
other times, what causes E. coli to be enterohemorrhagic
protein enterohemolysin
enterohemolysin
breaks apart blood, only acts in intestines
REALLY BAD E. COLI STRAINS
can carry both the genes for a Shiga toxin and enterohemolysin
some E. coli strains re linked to what syndrome
hemolytic uremic syndrome
in hemolytic uremic syndrome there is
broken down blood (from hemolysins) and/or tissue (from shiga toxins
hemolytic uremic syndrome broken down blood and or tissue leads too
mini-clots forming, traveling, and eventually and clogging capillaries
clots from hemolytic uremic syndrome
clots spread through the body usually have the biggest impact on kidneys
clots from hemolytic uremic syndrome effect on kidneys
begin to fail and die
end result of hemolytic uremic syndrome
blood in the urine that onsets 5-10 days after initial E. coli onset
E. coli causes what % of UTIs
85%
in UTIs caused by E. coli, bacteria
get into the urinary tract
when E. coli enters the urinary tract…
problems begin if they hit the bladder
E. coli in the urinary tract can move even
further upstream to the ureters or kidneys
symptoms of UTI caused by E. coli
- strong urge to urinate
- unproductive urination
- cloudy urine
treatment E. coli
antibiotics.. but resistance is becoming a problem…
myocobacterium genus gram
?
myocobacterium shape
long skinny bacilli
myocobacterium relationship with oxygen
obligate aerobes
myocobacterium spores
don’t form them
myocobacterium flagella
aflagellate
myocobacterium temp
mesophilic
aflagellate
no flagella
myocobacterium generation time
SLOW … hard to culture
myocobacterium PARASITE??!!
obligate parasites
obligate parasites
can only grow in humans
M. leprae cannot even be cultured unless
human macrophages are plated with it
since Mycobacterium species are not categorized as gram positive or gram negative
called acid-fast
acid-fast
that all initial dyes are retained instead of washed away
acid-fast means gram stain
bad idea sis
Mycobacteria cell wall
thick and waxy, composed of mycolic acid
mycolic acid
lipid-like compound which holds in dyes
mycolic acid is the
primary virulence factor of mycobacteria
why is Mycolic acid is also the primary virulence factor of Mycobacteria
because it stops phagosome/lysosome fusion.
most clinically relevant mycobacterium species
Mycobacterium tuberculosis
Mycobacterium tuberculosis where does it infect
many places, most commonly the lungs
what percentage of Mycobacterium tuberculosis infections are in the lungs
90% ish
why are most tuberculosis infections in the lungs
bacterial dependence on oxygen
how much of population has a tuberculosis infection (TB)
1/3
tuberculosis infections can be categorized as
-latent infection
active infection
latent infection of TB is
LTBI
active infection of TB is
ATBI
latent tuberculosis infection
- bacteria have colonized but do not cause obvious symptoms
- maybe people never progress beyond this stage.
active tuberculosis infection
Only about 10% of people with LTBI will develop ATBI (unless HIV-positiv
mortality rate if ATBI
over 50% if not treated
spread of TB is
entirely human to human
how is TB PASSED
aerosols from:
- speaking
- singing
- coughing
- sneezing
one sneeze from TB person
40,000 droplets
infections dose of TB
SMALL»> only 10 bacteria
TB is the ___ cause of death
2nd, to HIV»> NOW IT 1 DOE
how much of US population tests positive
5-10%
in some Asian and African countries, TB rates can be as high as
80%
to work at a healthcare facility….. a person in the US must pass
PPD test
PPD test
purified protein derivative test
what happens in PPD test
mall amounts of M. tuberculosis antigens are injected to see if the body reacts and forms a bump
if PPD test is positive
you must go through extra testing to ensure you will not pass your TB on to patients`
after initial infection of TB symptoms
flu-like symptoms
f TB progresses to ATBI, the predominant symptoms will be:
- chest pain
- night sweats/fever
- persistent (3+ week) and productive cough
- weight loss
- loss of appetite
where can M. tuberculosis survive
inside the phagosome of a macrophage
why can M. tuberculosis can survive inside the phagosome of a macrophage
mycolic acid coat prevents destruction by lysosom
mycolic acid cause the M. tuberculosis in the phagosome to
reproduces until it eventually kills the host macrophage.
what happens after M. tuberculosis kills the macrophage
more macrophages come, consume the dead ones, and fuse their contents together.
cycle of M. tuberculosis growth
repeats and repeats until formation of Langhans giant cell
Langhans giant cell
giant, multinucleate cell called a Langhans
A Langhans giant cell is a multinucleate cell with a
characteristic horseshoe shape
after the formation of a Langhans giant cell by M. tuberculosis in macrophages the response is
large cellular mass»»> granuloma
granuloma (TB)
a layer of T cells, B cells, and calcium
(TB)when there is granuloma it is
is a latent infection (LTBI)
in many cases, the granuloma *TB)
holds the bacteria for life (YAY)
sometimes the granuloma (TB)
liquifies and the bacteria escape
if the M. tuberculosis stay in the lungs after escaping the granuloma
causes ABTI
if M. tuberculosis invade bloodstream after escaping granuoma
miliary tuberculosis
miliary tuberculosis
granulomas forming across the body
miliary tuberculosis ends in
death if untreated
tuberculosis treatment
antibiotics
tuberculosis antibiotic treatment length
minimum of six months of multi-antibiotic treatment to clear all granulomas
many people with TB in developping countries
do not complete their antibiotic courses
result of people in developping countries not completing TB treatment
- MDR-TB
- XDR-TB
MDR-TB
multi-drug resistant TB
XDR-TB
extensively-drug resistant TB
how much to clear regular TB
$440
treatment for MDR-TB
140, 000
treatment XDR-TB
430,000
what causes leprosy
Mycobacterium leprae
leprosy other name
Hansen’s disease
leprosy is in BIBLE
but is rare, lepers were probs people with bacterial or fungal skin infections
leprosy comes from
granulomas in the connective tissue below the skin or nerve cells
granulomas in the connective tissue below the skin causes
boils
granulomas in nerve cells
neurodegeneration
leprosy latency period
LONG AF….. long as 20 years
about how many people with leprosy develop symptoms
5%
primary symptoms of leprosy
lumps on the skin
if leprosy hits active form……
sheds original granulosas and colonize Schwann cells
which Schwann cells do M. leprae colonize
Schwann cells wrapped around axons of neurons
resulting damage from leprosy sheding their original granulosas and colonizing Schwann cells wrapped around the axons of neurons
resulting damage and inflammation»> irreversible nerve damage»» death
M. leprae spreads much better in parts of the body
with lower temperatures
places where M. leprae spreads good
eyebrows, face, fingers, elbows, and scrotum
It is thought that M. leprae underwent
reverse zoonosis
reverse zoonosis M. leprae
from humans to armadillos
why did leprosy go to armadillos
ow body temperature made them excellent reservoirs for leprosy`
armadillos
now probably pass leprosy back to humans
what causes chlamydia
chlamydia trachomatis
what causes trachoma
chlamydia trachomatis
what causes Gonorrhea
Neisseria gonorrhoeae
what causes Syphilis
Treponema pallidum
gram stain Chlamydia trachomatis
negative, no peptidoglycan
gram stain Neisseria gonorrhoeae
negative
gram stain Treponema pallidum
negative, no LPS
size Chlamydia trachomatis
.3 micrometers
size Neisseria gonorrhoeae
.6-1.0 micrometers
size Treponema pallidum
5-15 micrometers
morphology Chlamydia trachomatis
coccoid
coccoid
elongated sphere
morphology Neisseria gonorrhoeae
diplococci
morphology Treponema pallidum
spirochete
spirochete
spiral
what is the most common STD
C. trachomatis (chlamydia)
how many reported cases of chlamydia reported daily
100 million +
how many US cases of chlamydia in 2015
1.5 million
why does chlamydia spread so easily …..
75% of infected females
50% of infected men
are……ASYMPTOMATIC BUT CONTAGIOUS
why is c. trachomatis an interesting species
gram-negative ISH
why is C. trachomatis gram-negative ISH
no peptidoglycan at all
why does it mean if there is no peptidoglycan at all in C. trachomatis
peptidoglycan-targeting antibiotics will not work
how many serotypes of chlamydia exist
at least 15
what does it mean if chlamydia has many serotypes
you can get it over and over again
C. trachomatis can be described as an
obligate intracellular parasite
why is C. trachomatis an obligate intracellular parasite
it can only grow inside human cells because it cannot produce its own ATP
what does C. trachomatis usually target
epithelial cells in the urinary tract or conjunctiva
conjunctiva
inner surface of eyelids
in infants, when inhaled, C. trachomatis can cause
pneumonia
does C. trachomatis invade WBCs
no
two forms C. trachomatis comes in
- reticulate body
- elementary body
reticulate body C. trachomatis
larger, less dense, divides quickly
elementary body C. trachomatis
small and dense, acts like an exposure
elementary bodies of C. trachomatis are very very
very hardy, very small
smallest elementary body of C. trachomatis
(small as .25 micrometers)
like exospores, elementary body of C. trachomatis can
- survive harsh external conditions
- form back into a reticulate body after invading cell
in females, C. trachomatis infections begin
in the cervix, cause
- pain
- fever
- abnormal menstruation
- discharge
if C. trachomatis goes untreated, (in females)
can spread, move far up the reproductive tract and cause inflammation
in what percentage of cases do C. trachomatis in females do they move very far up the reproductive tract and cause inflammation
40 % of cases
when C. trachomatis bacteria moves up the reproductive tract and causes inflammation it is called
PID
PID
pelvic inflammatory disease
symptoms of PID vary from
none to severe
women with extensive PID can develop
- infertility (20%)
- high risk of ectopic pregnancy for life (9%)
ectopic pregnancy
when a fertilized zygote implants in the fallopian tube instead of the uterus and starts growing there
leading cause of maternal death in pregnancy
ectopic pregnancy
in most cases of chlamydia in men»_space;>.
in infects the urethra
if chlamydia in men goes untreated…. it can
spread to the testes, leading to inflammation
if chlamydia in men spreads to the testes it can cause
- random discharge
- cloudy or painful urination
- epididymitis
epididymitis in men is
inflammation of the epididymis, causes sperm damage RARELY»> infertility
why are men better at spreading chlamydia
it attaches to sperm, C. trachomatis is aflagellate
rates of chlamydia are higher
much higher in women than men
chlamydia infection in conjunctiva can be caused when
C. trachomatis travels from the reproductive tract to eye, or eye to eye
result of C. trachomatis in the eye
swelling of the eyelid called trachoma
trachoma from C. trachomatis slowly
scratches the cornea of the eye
trachoma and it scratching the cornea leads to
- permanent vision problems
- sometimes blindness
tracho is the number 1
number 1 cause of blindness in the world
trachoma is estimated to be responsible for how many cases of blindness worlwide
1.3 million and 8 million
when does WHO hope to eradicate trachoma
by 2020
life cycle
EB attaches, enters» becomes RB»> binary fission»» reorganize to EBs, lysis and release of EBs» Attachment
gonorrhea is commonly called
- the clap
- sometimes gonorrhoea
gonorrhea is caused by
N. gonorrhoeae
Gonorrhea is a close second for
most common STD in the world, still 100 million + cases a year
Gonorrhea in USA,
less common , 400,000 cases a year
is gonorrhea spread easily
YES
how many females infected with gonorrhea are asymptomatic
80% asymptomatic
how many males infected with gonorrhea are asymptomatic
10% asymptomatic
what are N. gonorrhoeae’s main for the immune system
their pili
… N. gonorrhoeae have how many different pili observed indifferent serotypes
over 1 million
since N. gonorrhoeae have many pili observed in different serotypes
you can get reinfected a LOT
infection of N. gonorrhoeae is often called
gonococcal infection
facultative intracellular pathogens are
like living inside host epithelial cells, but can survive outside as well
does N. gonorrhoeae invade WBCs
no (…maybe sometimes)
in the first step of invasion, N. gonorrhoeae uses
type IV fimbriae to pull bacteria towards epithelial cells
N. gonorrhoeae use type IV fimbriae to pull bacteria towards epithelial cells in the
- reproductive tract
- rectum
- eyes
- parts of pharynx
in the first step of invasion, N. gonorrhoeae uses _______ to stop
uses proteases and mucinases to stop mucus along the cells from breaking them down
once N. gonorrhoeae arrive at epithelial cells
use endocytosis to pass into epithelial cells
once N. gonorrhoeae enters the epithelial cells, some bacteria
- lie dormant and grow
- or pass through the bottom of the epithelial cell deeper into the body
what comes to kill N. gonorrhoeae
neutrophils, nut most are repelled
because neutrophils aren’t working….to kill N gonorrhoeae
the body send more to an area, resulting in lots of pus
LPS in gonorrhea
also causes inflammation
N. gonorrhoeae infections very closely
resemble C. trachomatis infections
symptoms of N. gonorrhoeae and chlamydia (women)
are the same, both can cause PID if travel to far in reproductive system
PID from both Gonorrhea and chlamydia
can lead to infertility or ectopic pregnancy
one big difference of symptoms of gonorrhea and chlamydia
how fast it is
gonorrhea onsets within how many days of sex
2-5 DAYS
chlamydia infections onsts within how long after sex
1-3 WEEKS
how to tell chlamydia and gonorrhea apart
swap then culture
gonorrhea and chlamydia pathologies in males
nearly the same , gonorrhea onsets faster
gonorrhea symptoms in males
almost always shows them
most notable symptoms of gonorrhea in males
discharge of a mixture of mucus and pus
because of its symptoms, gonorrhea in men almost always gets
treated before it moves deeper in the tract
if gonorrhea in men moves further in the tract
can also cause epididymitis
very important (gonorrhea?) to distinguish
epididymitis from testicular torsion
testicular torsion
a twisting of the testes leading to immediate ischemia and necrosis thereafte
ischemia
not enough blood to tissues
testicular torsion
similar symptoms, but is considered a medical emergency
testicular torsion is NOT
not bacterial
N. gonorrhea in the eye
- symptoms are less severe than chlamydia
- pink eye
Gonorrhea that enters the bloodstream
latches onto joints and causes gonococcal arthritis
gonococcal arthritis
most common type in juveniles and young adults,
in 5-10% of gonorrhea infections
gonococcal arthritis symptoms
include pain and swelling, usually subside once treated w/ antibiotics
gonococcal arthritis may require
drainage
Treponema
genus of disease causing bacteria many species
most significant species of Treponema
Treponema pallidum
Treponema pallidum can be broken
into 4 subspecies
what subspecies of Treponema pallidum causes syphilis
T. pallidum, subspecies pallidum
other Treponema pallidum subsidies cause
rare skin diseases
Treponema bacteria are gram and shapes
gram-negative (ish)spirochetes, spiral shaped
Treponema bacteria are gram-negative ish because
they do not have LPS like others
T. pallidum cannot be cultured , no obvious
without human cells, no obvious virulence factors
four stages of syphilis
- primary
- secondary
- latent
- tertiary
which stages of syphilis are contagious
primary, secondary, tertiary
primary syphilis
3-5 days after expsosure
secondary syphilis
6-24 weeks after exposure
latent syphilis
no outward symptoms for 1-45 years
tertiary syphilis
Rarely progresses this far
tertiary syphilis is less than what % of cases
less than 30% and only when it goes untreated w/antibiotics)
only symptoms primary syphilis
formation of a chancre or multiple chancres
chancre (syphilis)
painless wart-like lesions where the bacteria are burrowed inside
where do chancres occur» ON THE
ON THE
- penis
- vagina
- anus
where do chancres occur INSIDE THE `
INSIDE THE
- mouth
- cervix
- anus
chancres are EXTREMELY
extremely contagious
chancres usually subside
within 2 months
secondary syphilis comes from when the
bacteria enter the blood stream
when T. pallidum, subspecies pallidum enters the bloodstream
attach throughout the body and cause a variety of symptoms
secondary syphilis is difficult to
tricky to diagnose because the symptoms are so varied and widespread
syphilis is often called
the great imitator
in latent syphilis the body slowly
develops more and more B- and T- cells to fight off T. pallidum
eventually, in latent syphillis, the B cells and T cells are
ble to keep the infection at bay.
during latent syphilis, since the infection has
has spread to practically all body structures, it is still present in the body but dormant
during latent syphilis, each time the infection “breaks ou”
typically tackled quickly and no symptoms develop
why is the latent stage of syphilis latent
body has the infection under control (although not cleared).
many cases of latent stage syphilis
do not progress
people in latent syphilis
not contagious
what usually causes a persons immune system to weaken when they have syphilis
aging or HIV
if a persons immune system with latent syphilis weakens
progress into tertiary syphilis
tertiary syphilis usually presents as
gummata
singular gummata
gumma
what are gummata
type of ineffective granuloma formed by the immune system
in the tertiary stage, gummata can form almost
almost anywhere in the body
-depends on where the bacteria are replicating
gummata are VERY
very contagious
tertiary syphilis often damages the
walls of blood vessels, causing aneurysm and eventually hemorrhage
aneurysm
weakening of vessel
hemorrhage
rupture of vessel
tertiary stage syphilis can damage blood vessels running to
the brain or other organs
if tertiary syphilis damages blood vessels running to the brain
impaired mental function
impaired mental function
causes organ necrosis
most sever and common form of damage to walls from tertiary stage syphilis
damage of the wall of the aorta, causes aortic swelling
if tertiary syphilis damages of the wall of the aorta, causes aortic swelling
eventually lead to aortic rupture
tertiary syphilis can cause the aorta to
SWELL
chladmydia , gonorrhea , syphilis are treated by
antibiotics, becoming resistant :(
what is T. pallidum becoming resistant to
azithromycin
what is gonorrhea becoming resistant to
cipro
chlamydia is becoming resistant to
multiple drugs
