Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
371 Cards in this Set
- Front
- Back
|
What bacteria is the most common inhabitant of the gut and makes up 95% bacteria in stool?
|
bacteroides fragilis
|
|
|
Bacteroides fragilis
gram stain and respiration/fermentation |
gram - rod
anaerobe |
|
|
where is bacteroides fragilis found?
|
mainly gut
also upper respiratory and upper GI tract |
|
|
What is bacteroides fragilis main benefit for us?
|
synthesizes Vit K
|
|
|
When can bacteroides fragilis cause complications?
|
abdominal surgery when it escapes from colon
|
|
|
Bacillus anthracis
gram stain and respiration/fermentation |
gram + rod
aerobe |
|
|
What is the only spore-forming aerobic pathogen
|
bacillus anthracis
|
|
|
where do bacillus anthracis spores germinate
|
blood, tissues, eschars
|
|
|
what is the first pathogen seen under microscope
|
bacillus anthracis
|
|
|
what is the first microbe to be grown in pure culture
|
bacillus antracis
|
|
|
what is the first microbe used by L. Pasteur for classic immunization experiments
|
bacillus anthracis
|
|
|
Why can't anyone go on the island of Gruinard?
|
Churchill in WWII bombed the island w/ bombs carrying anthrax spores
|
|
|
When and where were the two outbreaks of anthrax in the US
|
1957 Manchester, NH in sorting wool in mill
2001 US postal service |
|
|
What caused outbreak of anthrax in Sverdlovsk, Russia in 1979
|
research: accidental release of spores from bioweapons plant
(Russians had said it was from tainted meat) |
|
|
What does it mean that Bacillus Anthracis is epizootic?
|
infects humans and livestock
(cows, sheep, pigs, horses) |
|
|
Where is Bacillus anthracis endemic?
|
parts of US, Russia, Europe
|
|
|
What makes Bacillus anthracis truly dangerous
|
secrecy (don't know if you have it)
|
|
|
What are the three forms of Bacillus Anthracis
|
pulomonary, external, intestinal
|
|
|
what is the most dangerous form of pathogenicity of bacillus anthracis?
|
pulmonary form
wool-sorter's disease |
|
|
what are the steps in pulmonary pathogenicity of bacillus anthracis
|
inhale spores
bloody stool liver, spleen extensive hemorrhaging blood clotting toxins prevent macs from functioning death from circulatory collapse |
|
|
what are the steps in external pathogenicity of bacillus anthracis
|
external pustule where contact w/ spores
germinate on skin black, necrotic lesion (Eschar) regional lymph nodes blood toxins edema/septicemia prevent macs from functioning death from circulatory collapse |
|
|
what are the steps in intestinal pathogenicity of bacillus anthracis
|
contaminated meat
spores germinate toxin septicemia prevent macs from functioning death from circulatory collapse |
|
|
how quick can bacillus anthracis cause circulatory collapse
|
5-6 days after infection
|
|
|
why is it hard to stop pulmonary form of bacillus anthracis
|
3 days and you can die
early symptoms just like the flu |
|
|
Anthrax spore germinate at ______ rates
|
different (some as long as 98 days)
|
|
|
what are the four steps in confirming someone has bacillus anthracis
|
1.) take sample from suspected sites
2.) look for bacteria under microscope for characteristics shape/stain/spore 3.) culture specimen on agar w/ medium of vits/minerals +/- 48 hours 4.) addition run lab tests |
|
|
what are fomites
|
any agent, as clothing or bedding, that is capable of absorbing and transmitting the infecting organism of a disease.
|
|
|
how do you test for bacillus anthracis in letters
|
use manmade DNA, heat it to open its strands
take suspected anthrax DNA open its strands and hybridize the two together look to see if any samples glow |
|
|
what are anthrax cards and are they a good tool
|
they take to site coated w/ anti anthrax solution, not reliable
|
|
|
how do you prevent bacillus anthracis
|
vaccinate
|
|
|
are antibiotic helpful in treating bacillus anthracis
|
only if given immendiately.
otherwise bacteria has already multiplied and produced massive amounts of circulating toxin |
|
|
what are the three treatments of bacillus anthracis
|
antibiotics
|
|
|
antisera
|
experimental: use another antitoxin to block entry of anthrax toxin into cells
|
|
|
how many proteins are in the toxin produced by bacillus anthracis and what are there names
|
3
protective Ag (PA) edema factor (EF) lethal factor (LF) |
|
|
what is purpose of PA protein in Bacillus anthracis toxin
|
binds to surface of human cell, forms 7 copies of itself into a ring on cell surface
captures EF and LF and transports them into cell |
|
|
what is purpose of EF protein in Bacillus anthracis toxin
|
upsets ion/water flow across cell membranes causing swelling
prevents phagocytosis in macrophages |
|
|
what is purpose of LF protein in Bacillus anthracis toxin
|
cleaves cell proteins
inactivates MAPKK protein (vital for many cellular pathways) in macs |
|
|
clostridium
gram stain and respiration/fermentation |
gram + spore-forming rod
anaerobes |
|
|
what is the lethal weapon for clostridium family
|
toxin rather than # bacteria
|
|
|
what are clostridium normally when they are not pathogenic?
|
saprophytic anaerobes in soil, mouth
|
|
|
what are the three things present in infection of clostridium tetani
|
1. spores are present
2. spores germinate when environment is anaerobic 3. necrotic tissue: anaerobic |
|
|
portal of entry dangerous in clostridium tetani
|
deep puncture wound
|
|
|
what is tetanus neonatorum
|
tetanus in the newborn
happens in Africa where cow dung is rubbed on umbilicus cord |
|
|
What happens if clostridium tetani enters through mouth
|
usually not harmful just goes through digestive track
|
|
|
what are the toxins produced by clostridium tetani and what does it do
|
tetanospasmin: prohibits action of cholinesterase so 2 opposing muscles contract (tetany)
tetanolysin: destroys rbcs and affects heart |
|
|
What is risus sardonicus and what bacteria causes it
|
clostridium tetani
jaws lock together, corner mouth turns up, eyebrows peak |
|
|
incubation time needed for clostridium tetani depends on what two things
|
1. time takes toxin to reach CNS
2. anaerobic condition at wound |
|
|
describe short form of clostridium tetani
|
3d-2wks incubation
wounds near brain higher mortality |
|
|
describe long form of clostridium tetani
|
4-6wks incubation
wounds on appendages lower mortality |
|
|
prophylactic
|
defending or protecting from disease or infection
|
|
|
what is process for preventative measures against clostridium tetani
|
active immunization w/ tetanus toxoid (DPT) 3X after birth
booster shots throughout life |
|
|
6 steps for treatment if suspected clostridium tetani infection
|
1. active tetanus toxoid: stimulate host to knock out toxin
2. passive antiserum: knows out toxin 3. antibiotics: kill cells 4. clean up wound: remove necrotic tissue 5. treat w/ barbiturates if toxin reaches CNS 6. soak wound in H2O2 |
|
|
barbituates
|
Any of a group of barbituric acid derivatives that act as central nervous system depressants and are used as sedatives or hypnotics.
|
|
|
foods associated w/ clostidium botulinum
|
olives, tuna, liver paste, beans, caviar, smoked foods, tamales, asparagus, pork, spaghetti sauce, potato salad, 3-bean salad, vichyssoise, venison, jerky, moldy tomatoes w/ high pH
|
|
|
do stomach acids prevent pathology of clostridium botulinum
|
no they kill the bacteria but can't deactivate toxins
|
|
|
intoxication
|
not infection as bacteria are not mutiplying: toxins give pathology
ex. clostridium botulinum |
|
|
how many toxins does clostridium botulinum form?
|
two
neurotoxins A and B |
|
|
what are the two parts of neurotoxins A and B and what bacteria are they present in?
|
clostridium botulinum
1. binds to host neuron and internalizes toxin into cell 2. changes host proteins so cells can't function |
|
|
what would a can of food look/smell/taste like if infected w/ clostridium botulinum
|
look: puffy
smell: bacteria is odorless taste: bacteria is tasteless |
|
|
what activates toxins in clostridium botulinum
|
intestinal trypsin
|
|
|
What are toxins of clostridium botulinum effect on CNS
|
inhibit release of acetylcholine from presynaptic neuron so muscles can't contract
|
|
|
what is the cause of death after 3-7 days of ingestion of clostridium botulinum
|
respiratory failure
flaccid paralysis: like stroke |
|
|
what bacteria causes Infant floppy doll syndrome
|
clostridium botulinum
|
|
|
what are symptoms of infection from clostridium botulinum
|
nausea, vomiting, no fever, not contagious, double vision, thickness of speech
|
|
|
How do you prevent clostridium botulinum
|
proper canning
autoclaving to kill spores boil foods 15 minutes to inactivate toxin chill until ready to serve to prevent putrefaction/molds to raise pH |
|
|
how do you treat clostridium botulism infections
|
passive antitoxins vs. toxin types A, B, E
respirator drug to augment release of acetylcholine in synapse |
|
|
what bacteria causes 75% of gas gangrene
|
clostridium perfringens
|
|
|
where does clostridium perfringens normally live
|
human/animal intestines
|
|
|
what are 6 main places to get clostridium perfringens
|
gunshot wounds
traumatic wounds surgical procedures birthing processes dental extraction body piercing |
|
|
what are 4 steps to gas gangrene
|
wound doesn't heal properly
partly damaged tissue remains lysosomes release enzymes and digest surrounding healthy tissue autolysis continues and digestion spreads acceleration of tissue destruction |
|
|
What happens if Cl perfringens gets into wound as spores
|
spores germinate and release exotoxine
toxins cause dying cells to ferment CH2O gas production in tissues to putrefy proteins toxin lecithinase dissolves cell membranes |
|
|
what problems does the production of CO2 gas by gas gangrene cause
|
presses on bld vessels and obstructs flow
forces cells away from blood supply oxygen deficiencies cause cell death bubble up and tear tissue apart |
|
|
what is progression of wound color due to gas gangrene
|
red, green, blue, black
|
|
|
what are a few symptome of gas gangrene
|
skin ruptures, delirium, apathy, disorientation, death b/c of invasion of vital organ by toxin
|
|
|
5 treatments for gas gangrene
|
1. remove dead tissue, drain wound, or amputate
2. antibiotics 3. hyperbaric oxygen to force oxygen into wound 4. passive antitoxin 5. hydrogen peroxide |
|
|
who has most problem w/ clostridium difficile
|
patients on antibiotics post abdominal surgery
|
|
|
what are symptoms of clostridium difficile
|
toxins cause antibiotic associated diarrhea/pseudomembranous colitis (fibrin membrane on mucosa)
|
|
|
Corynebacterium diptheriae
gram stain respiration/fermentation |
gram + bacilli
aerobic |
|
|
where do corynebacterium diptheriae congregate and what do they look like?
|
throat
look like clubs form a leather covering |
|
|
Do corynebacterium diptheriae produce an endotoxin or exotoxin?
|
exotoxin
|
|
|
what does the exotoxin produced by corynebacterium diptheriae do?
|
prevent protein synthesis in throat cells by inhibiting elongation factor 2 that allows ribosome to move along mRNA codon
|
|
|
Where is fibrous exudate produced and what bacteria is associated w/ it?
|
produced on tonsils, uvula, soft palate, larynx, nose lining
corynebacterium diptheriae |
|
|
Why is the fibrous exudate produced in the presence of corynebacterium diptheria a problem?
|
it traps rbs, wbc, bacteria, dead epithelial cells to form tough membrane anchored to tissue below
|
|
|
What is the problem with
a.) removing the fibrous exudate produced by corynebacterium diptheria b.) not removing the fibrous exudate |
a.) expose bleeing, raw tissue and new membranes form
b.) suffocation |
|
|
what are four things that corynebacterium diptheria cause over time
|
1. paralysis of soft palate
2. heart muscle weakened 3. bronchopneumonia 4. kidney and adrenal cortex affected |
|
|
what are the two classifications of carriers for corynebacterium diptheriae
|
1. individual that carries bacilli longer than a week after membrane disappears
2. non-sick person in contact w/ patient who picks up bacilli |
|
|
How is disease caused by corynebacterium diptheriae prevented?
|
immunize w/ DPT in infants and give booster shots to caretakers
|
|
|
Is passive immunity good to use in corynebacterium diptheriae, why or why not?
|
no because it can cause anaphylaxis
|
|
|
main characteristic of actinomycetes
|
look like fungi
|
|
|
what 2 bacteria are classified as actinomycetes
|
1. mycobacterium tuberculosis
2. mycobacterium leprae |
|
|
why is mycobacterium tuberculosis resistant to many drugs
|
thick waxy coat makes it impermeable (acid fast stain)
|
|
|
what bacteria caused the white plague in 1689
|
mycobacterium tuberculosis
|
|
|
what disease/bacteria is leading cause of death world wide (18.5% adult deaths)
|
tuberculosis/mycobacterium tuberculosis
|
|
|
What fraction of world's population harbors mycobacterium tuberculosis
|
1/3
|
|
|
What caused mycobacterium tuberculosis's resistance to drugs that once worked well?
|
transiet populations who don't follow 6-18 mon. regime for taking drugs against the bacteria
|
|
|
What is the Bacillus Clmette Guerin (BCG) vaccine and what is the problem w/ it
|
benign mycobacterium tuberculosis
can be anywhere b/w 0-80% effective |
|
|
how do most patients acquire mycobacterium tuberculosis
|
non-intimate contact
contagion low but just 1 bacterium can cause infection |
|
|
Three major ways of getting mycobacteria tuberculosis
|
1. sputum
2. contaminated fomites 3. milk |
|
|
What two types of TB are there and what is the difference
|
1. primary TB (childhood)
more involvement w/ lymphnotes 2. Chronic TB (reinfection) |
|
|
In primary TB how does Bacillus get into body
|
inhaled (most)
ingested |
|
|
once bacillus for TB has entered body how long are do you test + for TB
|
for the rest of life
|
|
|
where does bacilli in TB go in primary TB once its in body
|
regional lymph nodes
ingested: mesenteric lymph nodes always involved Hilar lymph nodes (lung area) |
|
|
what does body form in response to mycobacterium invasion
|
tubercules
|
|
|
what are tubercles made out of?
|
1. tubercle bacilli
2. macs coalesced together 3. fibrous tissue 4. other wbcs |
|
|
what is caseation and what disease is it associated w/
|
transformation of tissue into a soft cheeselike mass
mainly chronic TB but also primary TB |
|
|
what does TB form and how does this become a problem
|
cavities
become infected w/ strep/staph and hemorrhage |
|
|
what are the symptoms of TB
|
cough, hemorrhage, fever, chest pain, wasting, die
|
|
|
Besides pulmonary TB what other TB exists and what are two ways it can be caused by
|
TB of intestines
II from pulmoary or I from milk |
|
|
where do tubercles and caseous foci form in intestines
|
peyer's patches
|
|
|
what are the three main tests for TB
|
1. traditional tuberculin skin tests
2. sputum smear test 3. culture w/ antibiotics test |
|
|
what are the four types TB tests
where do they test which one is the least reliable |
1. vonpirquet test, mantoux, vollmer's test, tine test
2. arm 3. tine test |
|
|
if one of the TB tuberculin skin tests are + what is the next step
|
X-ray
|
|
|
what are traditional tuberculin skin tests based on?
|
that a person infected w/ tubercle bacillus is allergic to the microbe and its products so tests will cause allergic reaction
|
|
|
what other problem is TB often tied with
|
HIV
|
|
|
what are 4 main reasons for increase in M. tuberculousis and especially the resistant strains
|
increase in # of
1. homeless 2. HIV patients 3. illegal IV users 4. prisoners |
|
|
what is XMDR-TB
|
extensively multidrug R' TB
|
|
|
what does today's genetically engineered BCG produce and how does this help against TB
|
makes its own cytokines
stimulates human host to make an enhanced RX vs. TB proteins |
|
|
What is regimen for curing non R' TB
|
4 different antibiotics for 6 months
(rifampin + isoniazid + 2 others) |
|
|
What is regimen for people w/ MDR-TB
|
6 or more drugs + injections for 2 years
supervised by WHO |
|
|
what are DOTS
|
direct observed therapy
|
|
|
What disease does mycobacterium leprae cause?
|
Hansen's disease (leprosy)
|
|
|
how is Hansen's Disease transmissible?
|
only person to person by touching lesions
|
|
|
what is the incubation time for mycobacterium leprae
|
5-15 years
|
|
|
what are the two forms of hansen's disease
|
1. tuberculoid
2. lepromatous |
|
|
what happens in tuberculoid stage of hansen's disease
|
bacteria multiply inside peripheral nerves
causes skin anesthesia |
|
|
what happens in lepromatous stage of hansen's disease
|
tumor-like overgrowth of skin and mucous membranes
more serious than other stage |
|
|
lepromin
|
killed M. leparea that are injected in a skin test
|
|
|
what drug can you take to prevent M. leprae
|
bacteriostatic drug dapsone
|
|
|
what are the four main side affects of M. leprae
|
psychological
deformity ostracism loss of pain nerves and with it sense of self |
|
|
Pseudomonas aeruginosa
gram stain respiration/fermentation |
gram -
aerobe |
|
|
what is pseudomonas aeruginosa's main food source
|
dead organic matter
it's a saprophyte |
|
|
What does p. aeruginosa produce where the infection occurs
|
blue-green pigment and blue pus
|
|
|
when does first infection of p. aeruginosa occur
|
when R' is low like in sick and infants
|
|
|
where is pseudomonas aeruginosa a big problem and why
|
nosocomial infection
b/c it lingers when antibiotics kinow out first line of microbes |
|
|
what are 9 main cuases of p. aeruginosa infections?
|
otitis media
abscesses UTI wound infections sinus infections sepsis in severe burns bronchopneumonia G-Shock whirlpool bath rash |
|
|
Bordetella pertussis
gram stain respiration/fermentation main disease |
gram -
aerobe whooping cough |
|
|
is whooping cough contagious
|
very
|
|
|
where do bordetella pertussis aggregate during infection
|
among cells lining trachea and bronchi
Don't invade bloodstream |
|
|
What does tracheal cytotoxin and endo toxins in b. pertussis do
|
causes neighboring cells to produce nitric oxide
|
|
|
what does nitric oxide do in a b. pertussis infection
|
kills ciliated cell causing inflammation of respiratory tract
mucous then accumulates causing cough |
|
|
what can whooping cough lead to
|
bronchopneumonia, TB
|
|
|
how long are you immune after having the whooping cough?
|
lifetime
|
|
|
how do you prevent bordetella pertussis
|
DTaP Acellular Pertussis vaccine
|
|
|
why don't you use a whole cell for a B. pertussis vaccine
|
whole cell produces too much endotoxin
|
|
|
Francisella tularensis
gram stain respiration/fermentation |
gram -
aerobe |
|
|
how is F. tularensis transmitted
|
zoonoses
rabbits, dogs, rodents, sheep, hides/carcasses insects: ticks, lice, horseflies |
|
|
What is the portal of entry for francisella tularensis
|
any
food/drink inhalation injectino contact |
|
|
what are the four clinical types of F. tularensis
|
I: ulceroglandular
II: oculoglandular III: glandular IV: typhoid |
|
|
Ulceroglandular in F. tularensis infection
|
ulcer at infection site and lymph node infected
|
|
|
oculoglandular in F. tularensis infection
|
conjunctive infected
|
|
|
glandular in F. tularensis infection
|
like I (ulceroglandular) just no ulcer
hard to diagnose |
|
|
typhoid in F. tularensis infection
|
high fever
instines invaded abdominal pain |
|
|
what is immunity like after F. tularensis infection
|
permanent
|
|
|
Legoinell pneumophilia
gram stain respiration/fermentation |
gram -
aerobe |
|
|
what disease was discovreed when American Legionnaire's at convention in a hotel were struck sick b/c of bacteria in cooling system/shower spray
|
legionaries Disease
|
|
|
what bacteria causes Legionaries Disease
|
Legionella pneumophilia
|
|
|
what is the pathology of L. pneumphilia
|
starts as influenza then goes to pneumonia and shock
|
|
|
what is the less severe form of Legionaries Disease
|
Pontiac Fever
|
|
|
what is major problem of gram- bacilli (enteric bacilli)
|
drug R' b/c of antibiotics in animal feed
most affected food=eggs |
|
|
salmonella
gram stain group respiration/fermentation and main characteristic of all types |
gram -
enteric bacilli facultatively aerobic flagellated |
|
|
what does salmonella typhi cause?
|
typhoid fever
|
|
|
what are symptoms of typhoid fever
(7) |
1. abdominal pain w/o diarrhea
2. headache 3. continuous fever of 104 4. rose spots (bacilli in skin) 5. enlarged spleen 6. leukopenia 7. toxemia |
|
|
where does s. typhi first effect and what does it do
|
Peyers Patch in intestines
swells, necrotic, slough causes ulcer |
|
|
what does an ulcer caused by s. typhi microbes lead to
|
perforated bowel which causes hemorrhave and infects mesenteric lymph nodes
|
|
|
what is the order of organs infected by s. typhi
|
1. intestinal wall
2. mesenteric lymph nodes 3. thoracic duct 4. blood 5. heart |
|
|
what do s. typhi microbes do in the blood
|
microbes are lysed and release endotoxins
|
|
|
what do the endotoxins released by s. typhi do to the heart
|
cause myocardial degeneration
heart attack |
|
|
what is a Type I carrier of s. typhi
|
s. typhi multiplies in gallbladder, released in feces
|
|
|
what is a Type II carrier of S. typhi
|
s. typhi multiplies in kidney, exreted in urine
|
|
|
main ways to prevent S. typhi in the community
|
pasteurization
sewage and pure water tests contain carriers destroy flies vaccinate food handling life straws |
|
|
what are life straws
|
10" long and 1" diameter filters that kill bacteria on contact
|
|
|
main ways to prevent S. typhi in more personal ways
|
wash hands
isolation protocol on patient |
|
|
when are antibiotics not ok to use in a S. typhi infection
|
when microbes go to gall bladder
you have to remove gall bladder to stop person from being a carrier |
|
|
Shigella
gram stain group respiration/fermentation |
gram- bacilli
enteric bacilli facultative aerobic |
|
|
where does major pathology of shigella occur
|
colon
|
|
|
what are two main bacteria included in shigella group
|
shigella dysenteriae
e. coli |
|
|
what do endotoxins of Shigella dysenteriae do?
|
pseudomembrane covers ulcers
diarrea w/ blood mucus abdominal pain severe dehydration |
|
|
what do the exotoxin of Shigella dysenteriae do?
|
affect nervous system to paralyze host
|
|
|
does shigella dysenteriae produce endo or exo toxins
|
both
|
|
|
E. coli infections are usually classified as
|
nosocomial
|
|
|
7 main problems caused by E. coli
|
1. UTI
2. peritonitis 3. pyelonephritis 4. meningitis 5. infantile diarrhea 6. travelers diarrhea 7. endotoxin shock |
|
|
what is one possible reason for dysentery-causing toxin in Shigella being in E. coli
|
somehow DNA for this has become incorporated into E. coli
|
|
|
what is 0157:H7
|
major strain of E. coli that is pathogenic and responsible for many food poisonings
|
|
|
What two forms of E. coli cauase traveler's diarrhea
|
ETEC and EPEC
|
|
|
what are the 3 strategies for E. coli virulence
|
1. use flagella to swim to mucosa
2. penetrate mucin layer 3. use pili to attach to intestinal cells |
|
|
pathology of ETEC
|
produce LT or ST toxin to lock intestinal cell adenylate cyclase in on position to increase cAMP which pump huge amounts of water out of tissue
|
|
|
pathology of EPEC
|
attach to host cytoskeleton and damage mucosal cells' ability to take up water
cause inflammation |
|
|
pathology of EHEC
|
produce Shiga toxin (enterotoxin) that damages blood vessel cells
especially in kidney |
|
|
2 reasons antibiotics aren't used to treat E. coli diarrhea
|
1. disease is self-limiting
2. antibiotics might increase amount fo Shiga toxin |
|
|
how do you treat E. coli diarrhea
|
rehydration and kidney dialysis
|
|
|
Vibrio cholerae
gram stain group fermentation/respiration |
gram -
facultative aerobic enteric bacilli comma shaped |
|
|
where do vibrio cholerae microbes mutliply
|
bowel
|
|
|
what toxins do the 2 genes on vibrio cholera make?
|
CT cholera toxin
TCP toxin regulated pilus made by phage |
|
|
what happens when CT binds to lining of bowel?
|
violent vomiting, rice water diarrhear, fluid loss huge
|
|
|
what does massive fluid loss in vibrio cholerae cause?
|
skin becomes dry, cold, wrinkled
blood thinkens slow flow of blood to brain>coma>death |
|
|
is vibrio cholera easy to treat?
|
yes antibiotics
|
|
|
what disease was spread by drinking water from the Thames river in 1848
|
vibrio cholera
|
|
|
Haemophilus influenzea
what does the I cause |
meningitis in youth, upper respiratory tract infection
|
|
|
Haemophilus influenzae
when does II take place |
after virus has caused influenza
|
|
|
What does Haemophilu ducreyi cause
|
STD w/ a chancroid
|
|
|
Haemophilus vaginalis=gardnerella vaginalis
what does it mainly cause and what might this bacteria be |
might be a STD
vaginal odor |
|
|
Yersinia pestis
what is the main thing it caused |
bubonic plague, black death
|
|
|
what was main carrier of yersinia pestis
|
rats
|
|
|
what are the three clinical types of y. pestis
|
1. bubonic
2. septicemic 3. pneumonic |
|
|
trace the pathology of bubonic infection
|
get flulike symptoms
lymph nodes inguinal (where microbes multiply) form buboes burst blood septicemia hemorrhages=black splotches organs fail |
|
|
septicemic pathology in y. pestis
|
massive hemorrhaging
patient dies before buboes form lungs congested w/ bacilli |
|
|
pneumonic pathology in yersinia pestis
|
100% fatality
inhale from infected person |
|
|
what does toxin in yersinia pestis do
|
a. disrupts mitochondrial membranes of cells to foul up cellular respiration
b. disrupts cellular cytoskeleton of huan cells c. disrupts internal communications among human cells |
|
|
what are the three clinical types of y. pestis
|
1. bubonic
2. septicemic 3. pneumonic |
|
|
trace the pathology of bubonic infection
|
get flulike symptoms
lymph nodes inguinal (where microbes multiply) form buboes burst blood septicemia hemorrhages=black splotches organs fail |
|
|
septicemic pathology in y. pestis
|
massive hemorrhaging
patient dies before buboes form lungs congested w/ bacilli |
|
|
pneumonic pathology in yersinia pestis
|
100% fatality
inhale from infected person |
|
|
what does toxin in yersinia pestis do
|
a. disrupts mitochondrial membranes of cells to foul up cellular respiration
b. disrupts cellular cytoskeleton of huan cells c. disrupts internal communications among human cells |
|
|
how is treponema pallidum transmitted
|
kissing, sexual, oral, anal, intercourse, skin, mouth, vagina, penis
|
|
|
does wearing a condom prevent treponema
|
no b/c it is motile
|
|
|
what are symptoms of treponema pallidum
|
ulcers on skin
bone lesions |
|
|
if in a hot/humid climate what disease can treponema pallidum cause
|
yaws guyana disease: raspberry eruptions not open sores
|
|
|
if in hot/dry climate what disease can treponema pallidum cause
|
pinta: endemic syphilis damp parts of bodoy
|
|
|
if in temperate climate what disease can treponema pallidum cause
|
epidemic syphilis
|
|
|
incubation period for syphilis
|
10D to 3 months
|
|
|
what is a chancre like in syphilis
|
size of pea, dull red bump, open sore w/ gray/yellow crusty scab
painless don't bleed untreated it heals by itself |
|
|
what is the I stage of syphilis
|
1 month, chancre symptom
|
|
|
what is II stage of syphilis
|
rash symptoms
|
|
|
what are the five types of rashes cause by syphilis
|
type 1: flat rash
type 2: bumpy rash may have rings type 3: condylomata lata rash: volcano-looking, contagious, break open w/ oozing type 4: gray-white patch w/ dull red border ulcer type 5: rash located on mucous membranes |
|
|
what are thh three main symptoms in stage II of syphilis
|
rash
rubbery lymph nodes ill health |
|
|
what is stage III of syphilis
|
syphilis mimics another disease
tissue destruction |
|
|
what are the four different things that syphilis can immitate during stage III
|
1. cardiovascular
2. neurosyphilis: meninges damaged 3. tabes dorsalis: muscular coordination/sensory disturbed degredation of spinal cord 4. general paresis encephalitis: insanity paralysis and death |
|
|
main form of treatment for syphilis
|
antibiotics
|
|
|
what are three congenital syphilis symptoms
|
1. dead
2. alive no symptoms til wks/mos later 3. alive w/ syphilis |
|
|
Treponema vicenti causes what disease
and what category of bacteria does it fall into |
Vincent's Angina=trench mouth
spiral |
|
|
what are the symptoms of treponema vicenti
|
foul odor bad tase, ulcers on gums, soft palate, tonsils
|
|
|
how do you treat vincent's angina/trench mouth
|
antibiotics, paint mouth w/ gentian violet
|
|
|
category of Borrelia burgdorferi
|
spirochaete
|
|
|
who carries borrelia burgdorferi and what disease does it cause
|
tick, deer, birds, rodents, human
lyme disease |
|
|
when is the most likely season to catch lyme disease
|
may-mid July
|
|
|
how long toes it take from time of bite for microbes to infect human from tick feces in lyme disease
|
36 hours
|
|
|
what is the first stage of Lyme Disease
|
bull's eye rash
Bells' palsy (facial paralysis) |
|
|
what is second stage of Lyme disease
|
flu-like symptoms, memory loss
cardiac arrhythmia possible depression |
|
|
who carries borrelia burgdorferi and what disease does it cause
|
tick, deer, birds, rodents, human
lyme disease |
|
|
when is the most likely season to catch lyme disease
|
may-mid July
|
|
|
how long toes it take from time of bite for microbes to infect human from tick feces in lyme disease
|
36 hours
|
|
|
what is the first stage of Lyme Disease
|
bull's eye rash
|
|
|
what is second stage of Lyme disease
|
flu-like symptoms, memory loss
|
|
|
what is third stage of lyme disease
|
microbes spread in blood and organs causing Bell's palsy, cardia arrhythmia, and possibly depression
|
|
|
what is fourth stage of lyme disease
|
joint inflammation
|
|
|
why is it controversial to give antibiotics to treat lyme disease
|
killing large # of spirochetes release lipopolysaccharides which cause inflammatory Rx
|
|
|
what category does Helicobacter pylori fit into and what is the main problem it causes
|
spirals
ulcers |
|
|
what is the world's most common bacterial infection
|
helicobacter pylori
|
|
|
how does helicobacter pylori survive stomach
|
digs into wall of stomach
makes bicarbonate to neutralize itself from stomach acid |
|
|
how id helicobacter pylori transmitted
|
oral, anal
|
|
|
how do you treat helicobacter pylori
|
antibiotics and acid blockers
|
|
|
Campylobacter jejuni
gram stain respiration/fermentation |
gram- spiral
low oxygen preferring |
|
|
what is the main source of campylobacter jejuni
|
improperly cooked chicken
|
|
|
how does helicobacter pylori survive stomach
|
digs into wall of stomach
makes bicarbonate to neutralize itself from stomach acid |
|
|
how id helicobacter pylori transmitted
|
oral, anal
|
|
|
how do you treat helicobacter pylori
|
antibiotics and acid blockers
|
|
|
Campylobacter jejuni
gram stain respiration/fermentation |
gram- spiral
low oxygen preferring |
|
|
what is the main source of campylobacter jejuni
|
improperly cooked chicken
|
|
|
what symptoms are cause by rickettsiae
|
rash and high fever
|
|
|
what disease does Rickettsia prowazekii cause
|
typhus fever
|
|
|
what anthrood transmits rickettsia prowazekii
|
lice deficating
|
|
|
what is the immunity like in rickettsia prowazekii
|
if you recover, immune to all types of typhus
|
|
|
where do chlamydiae's multiply
|
cytoplasm
avoid lysosomes by getting into host cell vacuoles |
|
|
what does the peptide that mimics a portion of heart muscle protein created by chlamydiae do
|
causes T cells to attack heart muscle and cloggs artery
|
|
|
what disease does chlamydia trachomatis cause
|
trachoma (Gr-rough)
|
|
|
what are the two infection caused by chlamydia trachomatis
|
1. STD
2. Conjunctival infection |
|
|
what is the bacteria that causes one of the leading STD in US
|
Chlamydia trachomatis
|
|
|
what is the leading cause of infertility
|
Chlamydia trachomatis
|
|
|
where does conjenctival infection occur
|
lining of cornea
creates scar tissue and causes blindness |
|
|
what are the 5 treatments for Trachoma
|
1. topical cream
2. device vaccine to pump up Ab 3. identify proteins made by Chlamydia 4. Find drugs to disable Chlymydia's ability to ward off lysosomes 5. use drugs to kill infected cells before bacterium has chance to convert to form that invade uninfected cells |
|
|
What disease does Chlamydia psittaci cause
|
psittacosis (parrot fever)
RESPIRATORY INFECTION FROM HANDLING BIRDS |
|
|
What causes cat scratch fever
|
chlamydiae
|
|
|
what is cat scratch fever
|
purulent lesion at site of cat attack, mild disease
|
|
|
What are prions
|
proteinaceous infections particles (proteins)
misfolded versions of normal glycoprotein no nucleic acids hard to kill |
|
|
How do prions arise
|
no one is sure three posiibilities
1. as an infection 2. spontaneously 3. genetically |
|
|
Who causes Transmissible Spongiform Encephalopathies
|
associated w/ prions
|
|
|
How long is TSE incubation time
|
5-10 years
|
|
|
Where does TSE infect
|
brain
|
|
|
What are the two types of TSE
|
Scrapie: pass from one sheep to another
Kuru: laughing death |
|
|
What are symptoms of TSE, Kuru
|
speech slurred, emotions inappropriate, violent, uncontrollable
|
|
|
Who causes Creutzfeldt-Jakob disease
|
prions
|
|
|
What is Creutzfeldt-Jakob disease
|
fatal neurodegenerative disease w/ progressive dementia
|
|
|
Who does the new form nvCJD (creutzfeldt-Jakob) effect
|
teenager, young 30's
|
|
|
What are some symptoms of Creutzfeldt-Jakob disease?
|
ataxia, dizziness, behavioral/psychiatric distrubances, insomnia/hallucination, short term memory loss
|
|
|
What makes you susceptivle to vCJD
|
two copies of PrPsc gene
maybe 7 other genes people w/ variant genes coding for MHC receptors |
|
|
What is the path of prions causing Creutzfeldt-Jakob disease
|
gut, nodes, spleen, brain
|
|
|
What disease is linked to Mad Cow Disease
|
Creutzfeldt-Jakob
|
|
|
What cells carries the infecting agent of Creutzfeldt-Jakob disease
|
B cell
|
|
|
What are some symptoms of Creutzfeldt-Jakob disease?
|
ataxia, dizziness, behavioral/psychiatric distrubances, insomnia/hallucination, short term memory loss
|
|
|
What makes you susceptivle to vCJD
|
two copies of PrPsc gene
maybe 7 other genes people w/ variant genes coding for MHC receptors |
|
|
What is the path of prions causing Creutzfeldt-Jakob disease
|
gut, nodes, spleen, brain
|
|
|
What is special about the blood needed for blood transfusion of vCJD people
|
they need to have wbcs taken out
|
|
|
What cells carries the infecting agent of Creutzfeldt-Jakob disease
|
B cell
|
|
|
Who causes BSE and what does BSE stand for
|
Bovine Spoingiform Encephalopathy
prions |
|
|
what are symptoms of BSE
|
shake/tremble, balance impaired, cows are jumpy and rub bodies against things
|
|
|
what is the incubation time of BSE
|
5 years
|
|
|
What part of meat that humans eat are prions found in
|
brain/spinal cord, muscle, espcially hind muscle
|
|
|
how would vegetarian get TSE
|
protein content in things: really is crushed up cow brains
|
|
|
How do cows and other farm animals get it?
|
practive canabalism
|
|
|
How did disease initally pass from animal to human in Britain
|
stopped using chemical formalin that probably killed infective agent b/c it was deemed unsafe
|
|
|
What are some measure taken by Britain to stop Mad Cow Disease
|
ban MBM (Meat Bone Meal)
Herd Slaughter Policy |
|
|
5 general characteristics of viruses
|
1. tiny at molecular level
2. obligate parasites 3. no antibiotic treatment for most 4. identify the viral type by appearance of inclusion bodies (in infected cells) 5. disease themselves not usually deadly |
|
|
4 ways to classify Viruses
|
1. by host they infect
2. Major Biological Properties 3. Size 4. Epidemiology |
|
|
three stages of virus can be in
|
1. lytic
2. persitient (type of lysogenic) 3. latent |
|
|
what happens in persistent stage of virus life
|
cells survive w/ viruses slowly releasing viral particles and cells continue to divide
|
|
|
what happens in latent stage of virus life
|
wiral genes integrated into host DNA, hard to detect
|
|
|
What type of viruses mutate the most
|
RNA viruses
|
|
|
WHy do RNA viruses mutate more often than DNA viruses
|
1. RNA less stable
2. Enzymes reproducing RNA don't have proofreading capability of enzymes reproducing DNA |
|
|
What is hepatities
|
describes many causes of inflammation in liver
|
|
|
What types of hepatitis cause 97% of acute hepatitis cases in U.S
|
A, B, C, D, and E
|
|
|
What is Hepatitis A caused by
|
RNA virus
|
|
|
What is Hepatitis B and Delta caused by
|
DNA virus
|
|
|
What is hepatitis C caused by
|
RNA single stranded
|
|
|
How is Hepatitis A transmitted
|
oral-anael
|
|
|
How is Hepatitis B and Delta transmitted
|
Blood, Semen Saliva
|
|
|
How is Hepatitis C transmitted
|
Blood
|
|
|
What is incubation time for
1. Hepatits A 2. Hepatitis B and D 3. Hepatits C |
1. 4 wks
2. 1-6 mondths 3. weeks/months (vague) |
|
|
How do you detect Hepatitis
|
look for antibodies for A and C
lood for Ag for B and D |
|
|
What is the least dangerous form of Hepatitis
|
A
|
|
|
What are symptoms of Hepatits A
|
Onset: acute malaise, fever, Nausea, muscle aches, Brown urine
jaundice |
|
|
What are symptoms of Hep. B and D
|
low fever, coma in hrs, liver shrink, fatigue, nausea, blood can't clot, jaundice
|
|
|
What form of Hep. is 2nd largest cause of death
|
C
|
|
|
What are symptoms of Hep. C
|
none for weeks then fever sweat, vomiting, fatigue, anorexia
|
|
|
Are there carriers for every form of hep.
|
no not A
|
|
|
How do you treat Hepatitis
|
gamma interferon and ribavirin
|
|
|
What is most common reason for Liver Transplant
|
Hepatitis
|
|
|
What is a risk of treatment of hepatitis
|
can cause autoimmune Rx
|
|
|
What is Papilloma Virus and is it a DNA or RNA virus?
|
warts
DNA |
|
|
What is the most commonly sexually transmitted infection in US/Eur
|
Papilloma virus
|
|
|
What are 95% of cervical cancers caused by
|
Papilloma virus
|
|
|
How does Pailloma virus cause cancer
|
makes E6 and E7 proteins that attach to 2 imp cell div. inhibitors: p53 and RB
viral infected cells multiply out of control |
|
|
What are symptoms of Papilloma virus
|
symptomless
chronic condition |
|
|
Do condoms prevent Papilloma virus
|
no
|
|
|
How do you test for Papilloma virus
|
Pap smear (imprecise) miss 20-40% infected women
|
|
|
Why is a thin-prep pap test more accurate than normal pap smear
|
it suspends sample in liquid, monolayer easier for technician to read
|
|
|
What does molluscum contagiosum cause and what is a DNA or RNA virus
|
DNA
pox family virus warlike things that yield milklike sybstances |
|
|
how do you treat molluscum contagiosum
|
griseofulvin drug
|
|
|
what does herpes simplex serotype 1 cuase
|
cold sores
|
|
|
what does herpes simplex serotype 2 cause
|
STD
|
|
|
What category does cytomegalovirus fall into and what disease does it cause
|
herpes, cytomegalic inclusion disease
|
|
|
what does varicella zoster virus cause and what category does it fall into
|
herpes family
chicken pox, shingle |
|
|
What does Epstein Barr virus cause and what category does it fall into
|
herpes family
infectious mononucleosis, maybe Burkitts lymphoma, Hodgkins disease, leukemia |
|
|
What family is the Kaposi's Sarcoma virus from
|
herpes
|
|
|
what are 4 things all herpes viruses have in common
|
1. letent infection
2. recu in % pop. immun defenses of person 3. some link w/ cancer 4. Lipshutz bodies |
|
|
Where does Herpes simplex multiply
|
nucleus of infected cells
|
|
|
Symptoms of Type 1 herpes
|
fever blister/cold sores, corneal lesions, ulcers on pharynx and tonsils
herpes encephalitis (really bad) |
|
|
Symptoms of Type 2 herpes
|
1st infection not usually seen
infants: fever, throat lesion blisters on external genitalia or anus yel-grey secrection in cervix |
|
|
two complication caused by herpes simplex
|
1. cancer: mainly #2
2. infection of newborn: need to do C section |
|
|
How does Herpes simplex cause infection
|
only theory: pH becomes alkaline in mucous during sex
|
|
|
what should a diet consist of for herpes simplex treatment
|
high lysin: meat, fish, milk, eggs
Low Arginine: don't eat nut, raisin, seeds, whole wheat |
|
|
what are some chemicals that help treatment of herpes 2
|
acyclovir
intervir-A capsaicin: damages sensory neurons |
|
|
what does the first encounter w/ varicella zoster cause
|
chicken pox
|
|
|
what is one distinct feature of chicken pox
|
they crust at different stages
some drying out while others are coming out |
|
|
what is Reyes syndrome
|
occurs after chicken pox or influenza especially if you take aspirin
symptoms: unprovoked shouting, abusive language, vomittin, brain dysfunction, disorientation, liver filled w/ fat leads to death if in brain |
|
|
how do you treat Reyes syndrome
|
control brain pressure by removing flaps of skull to reduce it
give glucose |
|
|
What is the portal of entry for Epstein Barr virus
|
mouth/respiratory tract, not highly infections
|
|
|
what is the incubation and infection period of Epstein Barr virus
|
incubation: 4-7 weeks
infection 1-4 weeks |
|
|
Symptoms of Infectious Mononucleosis
|
fever, tonsillitis, swollen lymph nodes, enlarged liver spleen, sore throat
slef-limiting leukemia: wbcs multiply abnormally |
|
|
What causes Burkitts Plymphma
|
Epstein Barr virus
|
|
|
what is Burkitts Lymphma
|
cancer where chromosome 8 translocated to chrom 14 and vice versa
|
|
|
What are symptoms of I infection from Cytomegalovirus
|
like mono # lymphocytes increase, enlargement of spleen
Lipshutz bodies (inclusions) brain deformaties |
|
|
What are symptoms of II infection of cytomegalic inclusion disease
|
may complicate preexisting disease, immunosuppressed
|
|
|
Who mainly gets Kaposi's Sarcome
|
male homosexuals w/ HIV infection
|
|
|
What is Variola
|
Small pox virus
|
|
|
Clinical symtpoms of Small pox virus
|
pox all at same stage of aging
|
|
|
incubation of small pox
|
10D to 2 wks
|
|
|
First symptoms of small pox
|
fever spike, backache, vomitin, red spots, odor of rottin flech w/ no pus
|
|
|
Later symptoms of small pox
|
pustules enlarge w/ opalescent pus
skin splits lose ability to speak |
|
|
How are small pox transmitted
|
explosively contagious airborne, even just talking can transmit disease
|
|
|
how was small pox eradicated
|
humans were only host, strictly quarantined people
|
|
|
what is vaccine for small pox made of
|
live cowpox vaccinia
|
