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477 Cards in this Set
- Front
- Back
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what family is the rhiniovirus
|
picorna
small naked ichosohedral |
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what are the two major causes of gastroenteritis
|
roto and noro virus
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what are the characteristics of the rhinovirus
|
115 serotypes, acid labile, cytopathic, optimum replciation at 33 vs37 C
limited to upper respiratory infections. |
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what are the intestinal normal flora
|
e. coli
klebsiella proteus enterococcus candida |
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What does the high number of serotypes of rhinovirus mean
|
that even if u gain immunity to one ur still vulnerable to others this is why people get colds so often
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what class of virus is roto
|
reoviridae
sgmented DsRNA naked icosohedral capsid fecal oral |
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what is the characteristics of the cornavirus
|
+ssRNA lipid enveloped
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what is the leading cause of lower resp. inf.
|
step pneumo
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what are the two major causes of the common cold
|
rhino virus
corona virus |
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what does Rotavirus look like
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wheel with spokes
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should you prescribe antibiotics for the common cold
|
no, the vast majority are caused by viruses
group B strep is the only one that causes cold like symptoms and only account for 10% of infection |
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what is the predominant cause of UTI
|
e. coli
|
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how is the virus transmitted
|
human to human vir respiratory secretions
2-3 day incubation |
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what is rota the major cause of
|
vomiting and diarrhea in children
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when is the rhiniovirus most common
what about corona |
rhino year round
corona winter |
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what are the three most common human parasites
|
ascaris lumbricoides
hookworms trichuris trichiura |
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what is the treatment for common cold
|
antihistimes over the counter not very good mainly just have to live with it
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how are vacines made for rota
|
animal human reasortment create live attenuated
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what is needed for e. coli to invade the blood stream
|
capsule espeacially K1
|
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is there any immunity to virus
|
not really secretory IgA protects but is not life long
this is why there are no vaccines for virus |
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what is the season peak for roto
|
winter spring
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what are the properties of the adenoviruses
|
naked icosahedral capsid
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what does strep pneumo cause
|
pneumonia
menegitis otitis media |
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how are adenoviruses transmited
|
rispiratory and fecal oral
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how is roto diagnosed
|
ag capture ELISA done only in the winter and spring
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what are the symptoms of the infection in adenovirues
|
GI tract infection is asymptomatic but infection of respriatory tract is symptomatics
|
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what is the most common cause of bacterimic sepsis
|
e. coli
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what does adenovirus cause
|
acute respirtitory disease
mild upper respiratory tract syndromes(tonsils and adenoids of children) |
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what are the main symptoms of roto
|
diarrhea, fever , vomiting
1-3 day incubation |
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what are some characteristics of the acute respirtatory disease cause by adenovirus
|
two types 4, and 7
most common in winter, and military type 14 common in young adults causes penmonia severe and sometimes fatal in childrean |
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what class are mycobacterium tuberculosis
|
rod shaped aerobic
ACID FAST(red on blue background) |
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what adeno virus types cause what
|
acute respiratory disease-type 4,7,14
pnemonia- type 3, 7(kids) 4,7 (adults) mild upper respiratry tract syndomes-1,2,5,6 pharyngoconjuctiveal fever-summer infection kids, types 3,7 |
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how long is roto infective
|
about 11 days starting 1 day before symptoms and lasting till about 5 days after symptoms end
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what are the nonrespiratory adenoviral syndrome
|
epedimec keratoconjuctivitis: types 8, 37 and 19
acute hemorrhagic cystitis: young boys types 11, 21 cervicitis and urethritis: type 37 gastroenteritis: infants types 40, 41, and 31 pediatric transplant recipients: adenovirus infection associated with higher rate of complicasion and organ rejection |
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where can e. coli infect
|
GI- unique strain EHEC ETEC
UTI-normal flora blood- leads to systemic skin- can infect wounds |
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what does paramyxoviridae cause
|
measles
mumple respiratory syncytial virus parainfluencza |
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what is the second leading cause of gastroenteritis in children
|
noroviruses, major cause in older children and adults
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what is a unique formation in the paramyxociridae
|
syncytia formation
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what type of hemolysis does strep pneumo cause
|
alpha hemolysis
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how are measle mumps rubella spread
|
respiratory route droplet spread and contaminated surface
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what is the major infection caused by foodborne illness
|
norovirus
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when is the peak time for measles mumps rubella
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winter/spring
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how do u diagnose ecoli UTI
|
nitrite
luiikocyte esterase gram stain culture sometime just treat them based on probablity |
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can measles mumps rubella be prevented
|
yes there are vaccines(live attenuated) and one time getting the disease provide life long immunity
6months immunity in newborns |
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what are the symptoms of norovirus
|
30% asyomptomatic
acute onset vomiting non bloody diarrhea incubate 24-48 hours abdominal cramps nausea, fever headache can occur any time of the year in any age group |
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what are the 4 Cs of measles
|
cough
coryza,-rash on face that coelese conjunctivitis Kopliks spots -grains of sand in mouth diagnostic |
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what is the most common parasite in the US ranked 1 -6
|
1.pinworms
2 toxoplama-can pass to fetus problems in eye 3. trichomonas vaginalis, femal venereal disease 4. head lice 5. Giardia-diarrheal diease 6. inetestinal amoeba, can cause dysentery |
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what are some complications of measles
|
fatal pneumonia
otitis media post infectino encephalomyelitis subacute scelersing panencephalitis(rare) |
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what is the treatment for norovirus
|
usually clears on own
fluid and electrolyte therapy |
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what are the symptoms of mumps
|
swollen salivary glands
|
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how do u treat e. coli
|
extended specturm beta lactamases allow e. coli to be resistant to beta lactams and even 3rd gen cephalosporins
sensitive to carbapenems and beta lactamase inhibitiors UTI-first line treatment is TMP-SMX(20% resistant) sepsis/menigitsi- 2nd and 3rd gen cephalosporins antisepsis drugs like CXigis |
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what are the complication of mumps
|
orchitis
oophoritis meningitis hearing loss arthritis acute pancreatitis |
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how is norovirus diagnosed
|
RT-PCR on stool or emesis not commonly used
most often not diagnosed |
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what does RSV cause
|
bronchiolitis pneumonia
winter spring |
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Viridans strep can cause what when spread to the blood stream
|
endocraditis
prosthetic join infection abscesses, brain, liver, lung, abdomin |
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parainfluenza types 1 and 2 cause flue when
|
around fall
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what is the second most common cause of UTI
|
Klepsiella pneumonaie
also can cause pneumonia |
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how is RSV, parainfluenza and adenoviruses diagnosed
|
antigen detection kit assay
RT-PCR and PCR based test of respiratory specimen to detect |
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what can lead to hepatitus other than Hep A B C D E in immunocomprimised
|
human herpers viruses espeacially CMV
|
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how is measles treated
|
vit A
|
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what is a common symptom in klebsiella pneumoniae
|
red jelly like sputum
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what are the properties of rubella
|
lipid enveloped icosahedral capsid with + ssRNA
humna to human transmission |
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what is the morphology of strep pneumo
|
lancet shaped gram pos diplococci
|
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what are the symptoms of rubella
|
mild measle like symptoms rash on face spotty
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what is kelbsiella resistant to
|
extended spectrum beta lactamase
Carbapenase resistant |
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what is the major risk of rubella
|
congenital rubella syndrome
deafness visual defects congental heart defects |
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what is the diffent types of host
|
definitive host-sexually mature adult parasite lives here
intermediate host- parasites lives in host at some point in its life cycle accidental host- infection by a parasite that normally lives in something else |
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how is congenital rubella syndrome diagnosed
|
anti rubbella IgM antibody capture ELISA from newborn serum
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what bacteria is often causing kidney stones
|
proteus
|
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what are hemaglutinin and neuraminidase
|
membrane glycoprotiens that are used for vaccines and constantly undergo antigenic drift
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what are teh virulence factors of strep pneumo
|
cellular antigens
-peptidoglycan -teichoic acid -lipteichoic acid Major virulence factor is antiphagocytic CAPSULE 83 different types pneumolysin IgA protease |
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what are the 3 types of influenza
|
type A-(many subtypes)in human, mammals and birds causes seasonl epidemcis almost every year
Type B- only in human, causes epidemics type C - infects human but not clinically important |
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what are some bacteria other than e. coli and klebsilla that cause UTI
|
enterobacter
providencia serratia citrobacter |
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what are the only types of influenzae A that are transmited human to human
|
H1-H3
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what are some diseases caused by mycobacterium
|
TB and leprosy
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what is the major cause of serious lower respiratory dieases
|
influenza A and B
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what is the vaccine target for strep pneumo
|
the caspsule
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what are the symptoms of influenza brought on by
|
TNF - alpha inflammatory
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what is a generality about intracellua and extracellualr parasites
|
extracellualr compete for nutreint
intraceltual kill cells |
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what are the major symptoms of influenza
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fever, chills, aches, pnemonia
NO NAUSA |
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what is pneumolysin
|
oxygen-labile hemolysin that kills phagocytes produced by s. pneumo
|
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how is influenza diagnosed
|
nucleic acid specific assays
rapid antigen capture ELISA useful for defining antiviral treatment. |
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Gp120/gp41
|
they bind to the cells to cause the infection
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what is the peak month for influenza
|
february
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what is the transmission of s. pneumo
|
human to human
in lungs goes to ear aspiration |
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what are the major antivirals used for influenza
|
amantadine and rimantadine block uncoatin and nuclear transport
neuramindidase inhibitors(prophalaxis) block the final stages of virion budding |
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how is parasites diagnosed
|
microscopic exam of feces
pt history serological test-toxoplamsa,a dn trichomonas PCR-plasmodium falciparum |
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who should not get flu vaccine
|
6mo younger
egg allergy really bad |
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what makes one vulnerable to encapsulated bacteria
|
asplenia
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what are upper resp. symptoms
lower? |
upper-sneezing, coughing,
lower- wheezing |
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what species of mycobacterium cant be grown on agar
|
m. laprae
|
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when is the most common time for respriratory disease
|
dec, jan, feb
mainly RSV |
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what is the most common cause of otis media and adult menigitis
|
s. pneumo
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6 mo URI with FEVER and wheezing ?
|
bronchiolitis probably RSV
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treatment for parasites is
|
metronidizole
benzamidazoles |
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two yo with barking cough URI spasmodic cough
|
laryngotracheobronchitis
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rusty sputum is indicative of what
|
s. pneumo
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12 yo with sudden fever headache, myalgias cough
|
acute influencza virus
|
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which hepatitis viruses have RNA genomes
|
A
C D E |
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what are some complication of pneumonia
|
plural effusion(empyema pus)
bacteremia with menignitis endocarditis pericarditis specit arthritis tissue infection |
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what is intestinal ameoba
|
entamoeba histolytica- causes amoebic dysentery
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what is the two most common causes of URTI, pneumonia, menigitis
|
s. pneumo
Haemophilus influenzae |
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where are mycobacteria found
|
transmission from the environment
grow in macrophages in host |
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how is s. pneumo diagnosed
|
sputum, blood, CSF
gram stain antgen detection kits fro urine culture on blood agar shows alpha hemolysis mucoid colonies capsule serotyping |
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what is atrial amoeba
|
naegleria fowleri-ameci menigoencephalitis
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how is s. pneumo treated
|
penicillins
some are resistant then treat with vancomycin |
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is salmonella normal flora in humans
|
no
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how is the s. pneumo vaccine made
|
purified capsule from 23 most common strains -pnoumovax
prevnar is a conjugate vaccine that is used in infants to 5 yrs. |
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What are the unique features of the amoeba
|
have two forms adult trophozoite and the environmental stabel cyst
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what class is haemophilus
|
gram neg coocobacilii
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how long does it take for m. tuberculossis to grow on agar
|
weeks
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why is haemophilus uncommon now
|
conjugate vaccine has wiped it out almost completley
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E. histolytica has wat virulence factro
|
secretes multiple proteinases and granuloysins lik enzymes that degrades cells
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where is h. haemophilus
|
normal flora
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which hep viruses are naked icosahedral
|
picorna hep a
calici like hep E |
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what is another bacteria other than strep pneumo that is a twin of haemophilus in that it causes URI , otitis media and meningitis in children
|
moraxella catarrhalis
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how are ameoba transmitted
|
cysts ingested from food or water
fecal oral |
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what makes h. influenczae difficult to diagnose
|
doesnt grow in regular blood agar
much use special media xfactor hemin and vfactor choclate agar requires increased CO2 |
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what are the characters of nocardia
|
filiments long rods with branching
ACID FAST intracellular in macrophages |
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what are the virulence factors of H. influenczae
|
no O antigen
has fimbraie CAPSULE major virulence factor exo-enxymes -IgA protease -beta lactamase |
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what does e. histoyltica cause
|
amoebic dystentery
Inflammatory bowel diease |
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what serotype of H. influenczae is most virulent
|
type B
|
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what does tat and rev do
|
RNA synth. and trans to cytoplasm
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how is H. influenzae transmitted
|
normal flora human to human transmission
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how is e. histolytica diagnosed
|
present with radual weeks of bloody diarrhea abdominal pain and tenderness
rarely fever revent travel to tropical place direct microscopic observation shows ingested RBCs in the ameoba |
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why is the window of susceptabilty to H. influenzae 6mo. to 2 yrs
|
transplacent antibody at first and then takes about 2 yrs to develope own antibodies
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what does nocardia cause
|
TB like disease
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what does H. influenzae cause
|
URT
otitis media sinusitis conjuncivitis chronic bronchitis |
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how is N. Fowleri diagnosed
|
sudden headache altered taste and perception can progress to fatal coma in 4 to 6 says usually in spas and sauna
examin for neutrophils in cerebrolspinal fluid and amoeba with absence of bacteria by gram staining |
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what type of h. influenzae did the vaccine make uncommon
|
type b
that caused pnemnia cellulitis epiglotitis septicemia |
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which hep virus is lipid enveloped
|
hep c
|
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how is H. influenzae diagnosised
|
gram stains-gram neg baccilicoccis
culture -with special agar |
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How are ameobas treated
|
E. histolytica -metronidizole
N. fowerli-amphotericin B |
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hwo is H. influenzae treated
|
use 3rd gen cephalosporins
bc of the beta lacrimase |
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what is the character of rhodococcus qui
|
short rods and cocci
ACID FAST causes TB like disease |
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what class are mycoplasms
|
small prokaryotes with no cell wall
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what is ascaris lumbricoides aka
|
common round worm the most common parasite worldwide
|
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what is the hard part in diagnosing mycoplasm
|
takes a long time to culture and need speacial augars and requrie sterols
|
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what is cryptococcus and pneumoscytis associated with
|
immunocomprimised and AIDS
|
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what is indicitave of mycolplasms
|
fried egg colonies small
|
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how do u diagnose worm infections
|
high eosinophilia, ground itch, cough, fever, muscle pain, fatigue
serology can take months microscopic exam of perianal area on scotch tape |
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what is an atypical pneumonia
|
any pnemonia that does not grow on normal agar
|
|
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what are the characteristics of m. tuberuclosis
|
slender, straight or crved rods, filamnets
ACID fast stain |
|
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what are the virulence factors of mycoplasms
|
cards toxins-cause vacules
|
|
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how is pin worm treated
|
mebendazole
petrolium jelly |
|
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what age group is mycoplams most common in
|
school age to adult
|
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how long after exposure do u show symptoms of hep A
|
1 to several months
|
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|
clincical manifestation of mycoplasm
|
pharyngitis that spreads to treacheobronchitis
|
|
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what are the virulence factors of the round worms
|
extremely hard to kill eggs
|
|
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what does the xray look like in mycoplasm pneumonia
|
patchy infiltrate
|
|
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what are the virulence factors fo m. tuberculosis
|
obligate aerobe
intracellular growth in macrophages |
|
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how is mycoplams diagnosided
|
throat swab has neg routine culture
PCR is best fastest |
|
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what are some symptoms of round worm infection
|
insomnia, abdominal pain
malnutrition |
|
|
what is the treatment of mycoplasm
|
erythromycin, azithromycin, clarithromycin
|
|
|
what is nef protien
|
important for pathogenicity
|
|
|
what is the diferential for pharyngitis
|
strep pyogenes
mycoplamsm pneumonia bordetella pertussis netseria gonorrheae |
|
|
how is diagnosed round worm
|
eggs or even adult worms found in vomit and feces
|
|
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what class are bordetella
|
small gram neg coccobacili
|
|
|
what is the PPD
|
purified protien derivative that u develop antibodies to if u have TB
|
|
|
why is boretella hard to diagnose
|
requires special media for initial growth and grow slowly
|
|
|
how hook worm transmitted
|
larvae enter through skin typically foot causeing itching migrate fhrough blood to lungs
|
|
|
why bordetella rare now
|
whooping cough is now vaccinated
|
|
|
how do u diagnos hep A
|
antibody capture ELISA/EIA to detect serum anti -HAV IgM indicative of current/recent infections
|
|
|
what causes whooping couph
|
b. pertussis
|
|
|
how is hook worm diagnosed
|
eggs in stool not seen til 5 -7 weeks of infection
|
|
|
what are teh virulence factors of b. pertussis
|
endotoxin
fimbrial hemagglutinin -essential for colonization and addherence to epithelias surface pertussis toxin-most important toxin tracheal cytotoxin adenylate cyclase toxin-also inhibts monocyts and neutrophil by incresing cAMP |
|
|
what make mycobacterial acid fast
|
the long chain glucocarbohydrate acids
|
|
|
what does pertussis toxin do
|
inhibits moncyte and neutrophil activation and killing by increaseing cAMP
causes lymphocytosis* diagnostic |
|
|
how is hook worm treated
|
mebendazole
anemia treated with iron suppliment |
|
|
how is whooping cough transmitted
|
human to human via droplets
|
|
|
what does salmonella typhimurium and enteritidis cause
|
gastroenteritis
|
|
|
what are the two stages of whooping cough(b. pertussis)
|
cartarrhal stage- 7-10 day incubation period with mild symptoms of uncomplicated URTi, highly infectious
paroxysmal stage- repeated cough without breathing within inspiratinoal whooping when breath is taken can lead to anoxia in infants |
|
|
what are the clinical manifestatino of whip worm
|
hatch instide the small intestine burrow into the villus
4 year life span abdominal pain, distention bloody or mucous filled diarrhea severe infectino can lead to rectal prolapse growth retardation, weight loss, nutrional deficiencies, and anemia |
|
|
what is the clinical presentation
|
whooping cough
no gram staining PCR rapid is best culture can be done with special media but takes a long time |
|
|
how is TB transmitted
|
person to person by inhalation of droplets, survives for long periods in air and surfaces
|
|
|
what is the treatment of b. pertussis
|
TMP-SMX(erythromycin
|
|
|
how do u diagnos whip worm
|
stool exam colonoscopy
|
|
|
what is in the DTP
|
diphtheria
tetanu aP-acellular pertussis vaccine is effective till teen years need to take Tdap to boost as an adult. |
|
|
what is antiviral IgG indicative of
|
past infection
|
|
|
how do u treat whip worm
|
combined mebendazole with ivermectin
treatment with imodium increases amount of drug contact with the parasites |
|
|
what are the clincal aspect of TB
|
primary infectino-latent asymptomacit
spreads to lymph nodes then to blood to spleen and liver still asymptomatic immune system kicks in then granulomatous inflammations occurs everywhere TB is located in the body. |
|
|
what is the most likely to encounter parasite in kentucky and tennessee
|
the threadworm
strongyloides stercoralis |
|
|
pol does what
|
encodes reverse transcriptase major target of NRTIs
|
|
|
what are three other types of nematodes other than the most common ones
|
toxocara-mainly in animals
trichinella-cysts in pigs consumed wuchereria bancrofti- tropical areas with 1 year incubation comes from misquitoes |
|
|
what is reinfection TB
|
the causeating granulomas filled with TB burst and respread the infection
|
|
|
what is the most common tape worm
|
taenia solium gotten by eating uncooked meat
diagnosed by find worm seg in stools requires surgical excisino |
|
|
hep A is what type of immunization
|
active immunization with inactiveated virus
passive immunization with normal human IG for post exposure protection |
|
|
what are the 3 blood fluke
|
mansoni, japonicum, haematobium
colonized by a form called cercariae |
|
|
what are symptoms of TB
|
fever fatigue, anorexia, cough,
|
|
|
what do the blood flukes cause
|
schistosomiasis causes immune response which causes bad tissue damage
diagnosed with eggs in stool prazquantel can treat it highly fatal disease |
|
|
what bacteria infect the stomach
|
H. hylori
|
|
|
what is miliary TB
|
when the TB spreads everywhere brain, menegies etc.
|
|
|
what type of virus is hep E
|
small nakes icosohedral
|
|
|
diagnosis of M. tuberculosis
|
first check for acid fast
culture-take weeks PPD checks immune status quantiferon-TB dont have to come back PCR used to confirm after acid fast test |
|
|
what is the primary receprto for attachment of HIV1
|
CD4
CCR5 |
|
|
what is the treatment for TB
|
1. isoniazid, rifapmin, pyrazinamid
2. fluorquinolones, aminoglycosides MDRstrain- resistan to at least 2 first ling xDR strains- resistant to 2nd line |
|
|
where is hep E common
|
parts of africa, latin america, asia
|
|
|
prevention of TB
|
isoniazid prevention prophalaxis
|
|
|
what causes typoid fever
|
s. typhi
s. paratyphi |
|
|
what is the key diagnostic test for Hep B
|
HBsAg
|
|
|
how is immune to HIV
|
mutant CCR5
usually european whites |
|
|
what is anti-HBc IgM
|
acute infection
|
|
|
wat is cyrptococcus classified as
|
yeast
encapsulated |
|
|
what indicates chronic hep B infection
|
+IgG with - IgM in the presence of HBsAg
|
|
|
HIV was cured once how
|
bone marrow transplant from a person with CCR5 mutation
|
|
|
what is the presence of HBeAg mean
|
high level of infectivity
|
|
|
what does s. cholerastis cause
|
septicemia
|
|
|
what does anti-HBs IgG indicate
|
indicates past infection if there is anti-HBc IgG
or immunization if no anti-HBc IgG |
|
|
how is HIV diagnosed
|
antibody capture ELISA to detect antiHIV antibody detects IgG but takes time to get that in the blood so u have to wait a while before u can find out, must wait 2 too 14 weeks
western blot is used to confirm because ELISA can give false pos. this test will not work on newborns of infected mothers PCR to detect proviral DNA in peripheral blood cells in new borns nucleic acids test can be used to find disease 12 days after exposure |
|
|
nucleic acid based assays and polymerase chain reactinos or branched chain DNA assays are used to do what?
|
quantitate viral DNA genome to deteremine viral load in a person with known hep B this will guide choice to undergo therapy or not.
|
|
|
what class are the pseudomonas
|
gram neg rods
obligate aerobes motile with flagella |
|
|
what is the immunization for hep B
|
active immunization with recombinatn HBsAg
passive immunization with HBIG for post exposure prophylaxis for non immune or for people who immunization doesnt work |
|
|
what is quantititive RT-PCR used for
|
used to measure viral load for treatment
|
|
|
how do you diagnose hep C
|
antibody capture ELISA/EIA to detect anti HCV
confirm with RIBA |
|
|
how is salmonella transmitted
|
ingestional of food contaminated by animal feces
eggs |
|
|
what is the therapy for HBV and HCV
|
inferon alpha reccommended for chronic B and C
pegylated IFN-alpha longer lasting and requires only one injection/ week instead of 3 NRTIs from chronic HBV lamivudine ribavirin in combination with IFN alpha fro chronic HCV |
|
|
transmission of HIV ?
|
blood, needle sharing, tattoing
blood transfusino semen vaginal seretions breast milk |
|
|
what are the main characteristics of HAV-HEV
|
majoritey of infections are asympotmatic or mild without jaundice
jaundine in only 20-50% |
|
|
what are the major forms of cryptococcus
|
c. neoformans
c. gattii |
|
|
what is the preicteric phase
|
3-10 days malaise and weakness, follwoed by anorexia, nausea and vomiting dull pain in right upper quadrant
|
|
|
what is used to preven mom child transmission
|
nevirapine
short term combination therapy |
|
|
what is the icteric phase
|
1-3 wekks juandice and or dark urine dramitic increase in aminotransferases
|
|
|
what is the incubation otime for salmonella
|
12-36 hours
|
|
|
when are you infective with hepatitis
|
in incubation
precteric and first week or two of icteric phase |
|
|
what is the definition of AIDS
|
HIV infection and less than 200 CD4 t/mm
|
|
|
what is the convalescent phase
|
malaise and weakness may persist for weeks with relapse or prolonged illness up to six months with HAV
|
|
|
what bacteria infect the small intestine
|
vibrio cholerae
e. coli ETEC slamonella enteritidis salmonella typhi campylobacter |
|
|
what is the major cause of mortality in acute viral hepatiitis
|
fulminant hepatitis rare
|
|
|
who are long term non progressors
|
HLA-b57
|
|
|
what types of hep C are most common in the US
|
1a and 1b which are the one that are least responsive to treatment best treatment is rebetron plus protease inhibitor
|
|
|
what are the symptoms of gastroenteritis
|
nausea, vomiting, FEVER, diarrhea, abdominal pain.
|
|
|
what is the most common killer in HIV
|
pneumocystis jirovici-fungal disease caused pneumonia
esophageal candidissis-generally not life threatening Kaposi sarcoma oral hairy leukoplakia cytomegalovirus retinitis mycobacterium avian complex TB herpies JC polyomaviris-fatal brain disease molluseumcontagiosum virus B cell lymphomas invasive cervical carcinoma |
|
|
what is the virulence of cryptococcus
|
capsules
|
|
|
what are the treatments for HIV
|
protease inhibitors
NRTIs Fusion inhibtors integrase enzyzme inhibitors CCR5 attachment inhibitors |
|
|
what cell types does salmonella prefer
|
invades and replicates in epithelial cells
replicates in macrophages as the prefered host. no spread into blood typically |
|
|
what vaccines can be used in HIV pt
|
any vaccine that is inactivated
|
|
|
what bacteria make up the anaerobes
|
bacteroides
peptostreptococcus actinomyces veillonella |
|
|
what is a related disease that comes after gasteroenteritis
|
reiters syndrome-autoimmune
cant see, cant pee, cant bend the knee inflamed conjunctiva, urethritis, arthritis of large joints |
|
|
what does c. gattii cause
|
pneumonia
meningitis |
|
|
what is treatment for salmonella gastroenteritis
|
none in mild
ciprofloxacin in severe cases |
|
|
what bacteria infect the larg eintestines
|
shigella dysenteriae
e. coli. EHEC vibrio parhaemolyticus c. diff |
|
|
what is the major virulence factor in serotyping for S. typhi
|
k antigent -Vi
|
|
|
what is c. neoforumans cause
|
aid associated meningitis
|
|
|
what is the typical transmission for typhoid fever?
|
person to person transmission via fecal oral route
|
|
|
what is the population that is targeted by the pseudomonas and legonella
|
immunocomprimised
|
|
|
what is a factor that increases susceptibilty to typhoid fever?
|
hemolytic anemias
|
|
|
which cryptococci can affect normal people
|
c. gattii
|
|
|
what is the moa of typoid fever
|
infection begins in intestines with no diarrhea, replicates in macrophages then invades into the blood stream and colonizes spleen and bone marrow
|
|
|
what is the class of helicobacter
|
gram neg, spiral rod
|
|
|
what are the symptoms of typhoid fever
|
sustained bacteremia with high fever
dissemination to kidney gall bladder peyers patches skin, rose spots on abdomen eventually sepsis in severe cases |
|
|
how is cryptococcus transmitted
|
air born sexual spores'
soil decaying trees pigeon droppings*- neoformins eucalyptus, douglas firs- gattii |
|
|
how is typhoid fever diagnosed
|
culture from stool
|
|
|
what class are mycobacterium tuberculosis
|
rod shaped aerobic
ACID FAST(red on blue background) |
|
|
how is typhoid fever treated
|
ciprofloxin
two vaccines |
|
|
how is cryptococcus diagnosed
|
india ink
brown pigment in culture |
|
|
what are vibrio, camplylobacter, helicobacter classified as
|
enteric gram negative bacilli
bacilli-curved or spiral shaped |
|
|
what does helicobacter cause
|
gastritis
|
|
|
what does vibro cause
|
cholera
caused by Vibrio cholerae |
|
|
what is the incubation period of C. gattii
|
2-10 months
|
|
|
what serotype causes cholera
|
Oantigen - O1 or O139
non O1 is associated with mild diarrhea |
|
|
wounds contaminated by fresh water often get infected by this
|
aeromonas hydrophila that can spread systemically
|
|
|
what is the moa of V. cholerae exotoxins
|
affects adenylate cyclase to permanently turn on this increases cAMP which leads to constant fluid secretion in the intestinal epithelial cells.
|
|
|
what is the disease progression for cryptococcosis
|
starts in lung often assymptomatic
in gattii can have necrotizing or fibrosing granulomas CNS is the major time its symptomatic meningitis/mengioencephalitis (confusion, headache, lethargy) cryptococcoma lesions fatal withouth therapy skin conditions bone issues |
|
|
what is the target area for cholera
|
the small intestine
|
|
|
what is the virulence factor of H pylori
|
flagella allows penetration through gastric mucus
adhesisn mediate binding to host cells cagA protein -surface pilus needle like injects CagA protein into host cells which is lethal associated only with more virulent strains stimulates inflamation Urease-nuutralizes gastic acid Acid inhibitory protein Mucinase -degrades gastric mucus Vacuolating cytotoxin-induces vacuolation and cell death in epithelial cells stims neutrophil migration and inflamation |
|
|
What are the symptoms of cholera
|
massive diarhea and fluid loss
NO FEVER bc NO INVASION |
|
|
what is the treatment for c. gatti
|
fluconazole or itraconazole
|
|
|
what is transmission of campylobacter
|
fecal oral often on beef chicken and pork
|
|
|
what class are bacteroides
|
gram neg rods
|
|
|
what is the incubation period of campylobacter
|
3-5 days
|
|
|
what is the diagnosis
|
CSF
blood Direct antigen test indi ink stain for capsule |
|
|
what is the symptoms of campylobacteria
|
diarrhea,
persistant high fever colonized small intestine |
|
|
what is the transmision of H pylori
|
human human fecal oral
|
|
|
what are two associated conditions that are brought on by camplyobacter infection
|
rieters syndrome-cant see, pee, bend knee
guillain barre syndrome-flacid paralysis |
|
|
what does pneumocystis cdause
|
pneuocystis pnemonia
|
|
|
how is camplyobacter diagnosed
|
difficult to diagnose
isolate on special media difficult to culture |
|
|
what wound infection produces purple colonies when cultured
|
chromobacterium violaceum
|
|
|
how is camplyobacter treated
|
fluoroquinolones or erythromycin in severe cases
|
|
|
what makes pneumocystis hard to kill
|
no ergosterol which is the major target of antifungals
|
|
|
How is campylobacter prevented
|
proper hygine during food prep
NO VACCINES |
|
|
how is h pylori diagnosed
|
biopsy
ureas breath and blood test |
|
|
what are the two enteric gram neg rods
|
shagella
e-coli |
|
|
how is pneuocysitis transmitted
|
person to person
normal flora only comes out in immunocomprimise |
|
|
what are the TSI results for psudomonas aeruginosa?
|
glu-neg
lac-neg gas-neg H2S-neg |
|
|
what are some diseases caused by mycobacterium
|
TB and leprosy
|
|
|
what are the TSI results for shigella sonnei
|
glu - pos
lac-neg gas-neg H2S- neg |
|
|
how is pneumocystis diagnosted
|
look for cysts in microscope
immunoflourence stains PCR is main way its found NO CULTURE possible |
|
|
what are the TSI results for salmonella typhi
|
glu-pos
lac-neg gas-neg H2S-pos |
|
|
what is the treatment of h pylori
|
proton pump inhibitor for symptoms
sequential therapy step 1 rabeprazole +amoxicillin 5 days step 2 rabeprazole + clarithromycin+ tinidaxole 5 days |
|
|
what are the TSI results for E coli
|
glu-pos
lac-pos gas-pos H2S- neg |
|
|
how is pneumocystis treated
|
no azoles
TMP-SMX works well even though that is an antibiotic |
|
|
what are the TSI results for Proteus mirabiis
|
Glu-pos
lac-pos gas-neg H2S-pos |
|
|
what wound pathogen has emerged recently in combatant from Iraq and is now found in hospital water supply causes pneumonia
|
acinetobacter baumannii
|
|
|
what is O antigen
|
carbohydrate LPS repeat surface of bacteria
|
|
|
what diseases are caused by aspergillus
|
allergies
mycotoxicosis |
|
|
what is the H- antigen
|
flagella
|
|
|
what class is listeria
|
gram pos rods or coccbacilli
|
|
|
what is the K antigen
|
capsule
|
|
|
what is aftatoxin
|
liver tox, liver cancer, immune deficiences.
caused by aspergillis |
|
|
what are the O, H , K antigens used for
|
serotyping to find out what species of bacteria is there
|
|
|
what class are peptostreptococcus
|
gram pos cocci
|
|
|
where does E coli come from
|
normal flora of the intestina
|
|
|
what type of fung is aspergillus
|
fillimentous fungi
growth as a mold COLORLESS HYALINE and SEPTAIE |
|
|
What are the two types of ways ecoli causes disease
|
normal flora that escapes from teh intestinal tract and colonize other body sites
exogenous strain that pick up new virulence factors and can infect the intestines |
|
|
how is listeria transmitted?
|
food borne
|
|
|
what do E coli use pili for
|
adherence to mucosal surfaces
in disease E. coli picks up new types of pili that allow them to adhere in places they normally would and in amounts that they normal wouldnt be able to achieve which causes the disease. |
|
|
what tempurature is the optimum for aspergillus
|
45degrees
can survive at 37 |
|
|
what are some virulence factors for e.coli
|
enterotoxins
|
|
|
how do u treat acinetobacter baumannii
|
carbapenems
|
|
|
Heat labile toxin is what
|
a cholera like toxin that activates adenylate cyclase which leads to fluid secretion only it is made by a disease causeing strain of E. Coli
|
|
|
what is the virulence factors of aspergillus
|
aflatoxin
enzymes |
|
|
what is heat stable toxin
|
stimulates guanylate cycles to lead to fluid secretion/diarrhea. in ecoli
|
|
|
what are the distinctive factors of listeria
|
tumbling motitliy
facultative anaerobe likes cold temps can grow in refig |
|
|
what is shiga like toxin
|
found in e. coli enterohemorrhagic colitis
leads to bloody diarrhea bc it actually kills cells identical to shiga toxins associated with hemolytic uremic syndrome can cause renal endothelias cell death does it by inhibiting protien synthesis found in EHEC strains of E. coli |
|
|
where is aspergillus found
|
molds on food, and water damage housing
dust in farms |
|
|
how are e. coli classified
|
by their virulence factors and pathology
|
|
|
what species of mycobacterium cant be grown on agar
|
m. laprae
|
|
|
what is EHEC e. coli
|
enterohemorrhagic
|
|
|
aspergillus is most common in people with
|
neutropenia
immunocomprimised |
|
|
what is ETEC e. coli
|
enterotoxigenic
|
|
|
what are the virulence factors
|
listeriolysin
-hemolytic toxin-beta hemolysis ActA -polymerizes actin that push it into another cell |
|
|
what is EPEC e. coli
|
enteropathogenic
|
|
|
what happens in allergic bronchopulmonayr aspergillosis
|
allergic reaction to aspergillus that is growin in the tracheobronchial mucosa.
asthmas symptoms lung damage |
|
|
what is EIEC e. coli
|
enteroinvasisve
|
|
|
what are the environmental pathogens
|
pseudomonas aeruginosa
bukholderia cepacia stenotrophomonas multophilia acinetobacter baumannii aeromonas hydrophila chromobacterium violacceum chrysabacterium meningosepticum |
|
|
what is EAggEC e. coli
|
enteroaggregative
|
|
|
what is an aspergilloma
|
aspergillis colonates a preexisting cavity.
found on xray / CT |
|
|
which type of ecoli is spread animal to human
|
EHEC
|
|
|
what is a unique transmission mode of listeria
|
transplacental
|
|
|
What additional virulence factor other than the toxi do EHEC and ETEC have
|
new fimbre that allow adherence in the intestinal tracts
|
|
|
chronic necrotizing aspergillius pneumonia does what
|
similar to aspergilloma except its forms the cavity can be hard to tell the diffience. more dangerous and grow faster
|
|
|
what is EHEC associated with
|
bloody diarrhea and kidney failure
HUS |
|
|
what class are actinomyces
|
gram pos rods
|
|
|
what serotype is most common with EHEC
|
O157:H7
|
|
|
invasive pulmonary aspergillosis(IPA)
|
widspread forming necrotic lesions
fever cough chest pain total lung destruction |
|
|
what is the implications of O104:H4
|
aquired additional fimbre
double shiga toxin production |
|
|
what is the usual symptoms of listeria
|
healthy adult-asymptomatic-mild flu
immunocompromised/elderly- severe invasive disease with meningitis, encephalitis, septicemia pregnant woomen-flu like illness can lead to septic abortion, premature delivery, stillbirths neonates- early onset tsepticemia and pneumonia |
|
|
what is the incubation period of E. Coli
|
1-10 typically 2-5
|
|
|
IPA with bloodstream dissemination
|
it can spread to the blood and high fatality
can spread to brain, skin etc |
|
|
symptoms of EHEc
|
watery diarrhea first
then leads to bloody diarrhea no invasion no fever no pus eventually kidney failure and HUS |
|
|
what are characteristics of the environmental pathogens
|
gram neg
found only in immunocomprimised source is usually water or dirt often antibiotic resistant |
|
|
sorbital pos is diagnositic of what
|
EHEC e. coli
|
|
|
what is the diagnostic for aspergillus
|
45 DEGREE angle septae
found on biopsy can be cultured slowly |
|
|
What is the treatment of EHEC
|
NO ANTIBIOTICS
MAKE HUS WORSE dialysis as needed ShigamAB mAB that inactivates shiga toxins no vaccines |
|
|
what is the pathogenesis of listeria
|
ingestion invasion in epithelia, replication in macrophages like salmonella.
can get into the bloodstream and spread to meninges or across the placenta |
|
|
where is shigella foudn
|
not normal flora
only found in humans with disease |
|
|
how is aspergillus treated
|
Voriconazole
any azole caspofungin if immune to azole |
|
|
what antigens does shigella have
|
O antigen
no H no K invasive plasmid Ag |
|
|
where are mycobacteria found
|
transmission from the environment
grow in macrophages in host |
|
|
what are the two types of shigella
|
S. dysenteriae- most severe
S. sonnei, S. flexneri, and S. boydii most common in U.S. leads to shigellosis |
|
|
what is the major diffierence btw zygomycetes and aspergillus
|
zygomycetes are immune to azoles
90 degree SEPTAE *** most common in uncontrolled diabetes with ketoacidosis |
|
|
what is the symptoms of shigellosis
|
1-3 incubation
watery diarrhea usually fever colonization of colon and replication in epilthelial cells |
|
|
how is listeria diagnosed
|
monocytosis in the peripheral blood and CSF
gram stain of CSF culture of CSF or blood |
|
|
what are teh symptoms of dysentery
|
bloody diarrhea
painful straining to pass stools FEVER ulceration of intestinal mucosa |
|
|
zygomycetes aka
|
rhizopus
|
|
|
what is diagnosis of shigella
|
stool culture
|
|
|
what is the virulence factors for p. aeruginosa
|
flagella
CAPSULE-antiphagocytic -slime layer -mucoid capsule secretes alot of toxins -several antiphagocytic toxins -some kill RBCs as well elastase - degrades host antiproteases which leads to lung damage |
|
|
treatment
|
ciprofloxin
timethroprim-sulfamethoxazole dialysis hand washing no vaccine |
|
|
what all can zygomycosis cause
|
rhinocerbelos-facial damage
pulmonary cutaneous gastrointinal basically just degrades and breaks down the tissue really really bad |
|
|
how is listeria treated
|
ampicillin/penicillin
TMP-SMX, erythromycin resistant to cephalosporins |
|
|
how is zygmycets treated
|
antifungal
-amphotericin B aggressive surgical debridment |
|
|
where are bacteroides found
|
normal flora
diseases caused by invasion overgrowth or immunocompromise |
|
|
vorcanazole can be used in prophalaxis for what
|
aspergillus
NOT zygomycetes |
|
|
what are the animal to human food borne diseases
|
campylobacter
e.coli salmonella |
|
|
what are the characteristics of histoplasma, blastomyces, coccidiodes
|
soil fungi
respirtatory tract spread systemically CAN INFECT NORMAL PEOPLE yeast in body mold in soil |
|
|
what is diagnostic of p. aeruginosa
|
changes the color of the agar to blue or green
|
|
|
where is histo plasmosis endemic
|
ohio and mississippi river valley
|
|
|
what are the seafood derived food borne diseases
|
cholerae
|
|
|
where is blastomyces endemic
|
ohio, missipii, missouri and arkensas
|
|
|
how long does it take for m. tuberculossis to grow on agar
|
weeks
|
|
|
histoplasma capsulatum is carried by what
|
birds droping and bat dropings
|
|
|
what are the human to human transmission food bourne disease
|
staph aureus
e. coli salmonella shigella listeria |
|
|
where is coccidiodes endemic
|
southwestern US
CA, AZ, NM, TX |
|
|
what does p. aeruginosa cause
|
pneumonia
wound infection uti dermatitis corneal infection endocarditis only happens in immunocomprimised |
|
|
where is paracoccidioides found
|
south america
|
|
|
what disease are caused by ingestion of preformed toxins
|
clostridium perfringens
staph aureus bacillus cereus |
|
|
where is penicillium marnefi found
|
southeast asia
|
|
|
where are anaerobes usually found
|
abscessses- main
peritonitis wound infection dental oral infecion decrotizing pneumonia pelvic inflammatory disease bite wounds |
|
|
virulence of histoplasmosis
|
spores
|
|
|
what class are the clostridiums
|
large gram pos rods
spore forming(heat resistant) anaerobe |
|
|
which of the histo, blasto, coccidio is not a yeast in the body
|
coccidio
|
|
|
what are the two types of pneumonia that are caused by p. aeruginosa
|
nosocomial pneumonia
cyctic fibrosis pneumonia |
|
|
what is histoplasmosis like
|
tubuculosis
|
|
|
what is the disease caused b clostridiums
|
enterotoxins
|
|
|
what is a difference in presentation with blasto and histo
|
blasto tends to show skin conditions before respirtatory
more acute/purulent less granulomatous |
|
|
what are the characters of nocardia
|
filiments long rods with branching
ACID FAST intracellular in macrophages |
|
|
what is the presentation of coccidioides
|
most common of the these fungals to affect normal people
asymptomatic infection mild flue like syndrome resembles pneumonia very few cavaties and nodules fever, weight loss, flu like |
|
|
what is produced by clostridium perfiringens
|
CO2 and H2 gas
very smelly |
|
|
what is the most serious complication of coccidioides
|
mengitis
|
|
|
what is the characteristics of p. aeruginosa nosocomial pneumonia
|
immunocomprimised
acute pneumonia bloodstream invasino high mortaltiy slime capsule usually caused by aspiration |
|
|
where does coccidioidomcosis attack
|
1.lung
2. skin 3. meninges |
|
|
what does c. perfringens cause
|
gas gangrene(alpha toxin creates invasion)
anaerobic celluitis(localized) can cause enteritis if u get the type that has enterotoxins not as serious or as common |
|
|
how is histo/blasto/coccido diagnosed
|
microscopic examination
imaging for granulomas look for yeasts or sphericles culture non culture detection assay antigen detection in serum and urine serology of IgM serotypes |
|
|
what are the predisposing factors to infection
|
reuction in tissue Eh(oxidation reduction potential)
trauma with loss of blood supply growth of facultatvie bacteria to use up the oxygen disruption of epithelial barriers comprimiesed host defense preveious antimibrobial therapy |
|
|
what is the treatments of the histos/blastos/coccidio
|
azoles and amphotericin B
long term therapy voriconazole prophylaxis |
|
|
what type of toxin is produced in most human strains of C. perfringens
|
alpha toxin
kappa toxin theta toxin enterotoxins |
|
|
what is unique amount candida
|
it is the only normal flora fungi found in URT, skin , GI, Vagina.
|
|
|
what are the characteristics of p. aeruginosa cystic fibrosis pneumonia
|
defective mucocilliary clearence
chronic progressive lung destruction no blood stream invasion bc stops toxins production and makes lots of mucus often the cause of death in CF |
|
|
what is the most important lifethreatening fungi
|
candida
|
|
|
what is alpha toxin
|
phospholipase C-breaks down membranes
dermonenecrotic hemolytic-beta hemolyisis |
|
|
what are the two different strains of candida
|
c. albicans- most common
c. glabrata- resitant to azoles and amph. B |
|
|
what does nocardia cause
|
TB like disease
|
|
|
what are the factors that determine whether a fungi will be yeast or mold
|
tempurature in most fungi
tempurature and medium for candida |
|
|
how is C. perfringens transmitted
|
exogenous(soil in wound)
endogenous(escape from normal flora in the intestine can be traumatic like surgury or nontraumatic-tumors) |
|
|
what is a difference that aides in diagnosis of candida
|
they have hypae in the body most fungi do not
|
|
|
what is the course for for burn wound infection with p. aeruginosa
|
large area burns
spreads to blood stream causes septicemia GREEN PUSS DIAGNOSTIC |
|
|
what does candida cause
|
thrush- newborns/AIDS
tracheobronchitits-AIDS diaper rash/face/nails- newborns/AIDS, any wet area onychomycosis- nail infection chronic mucocutaneous- really bad nail infection vulvovaginitis GI blood sepsis-candidemia hepatosplenic pneumonia-abscesses endocarditis endophthalmitis renal arthritis/osetomyelitis |
|
|
how is c. perfringens diagnosised
|
gram stain of tissue
shows gram pos rods |
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how is candida diagnosed
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microscopic-yeast and hyphae/psuedohyphe
culture-2-7 days must distinguised from normal flora non culture detection assay antigen |
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what the appropriate and inappropriate forms of diagnostic sampling
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acceptable
-aspirated pus -tissue -bod fluids(cerebrospnial, pleural, pericadial, synovial) -transtracheal aspirate inappropriate-bc already anaerobes present -throat, gingival or vaginal swabs sputum feces, gastic contents, urine |
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what is the treatment for candida
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azoles topically
fluconazole amphotericin B 4-6 weeks of therapy for sever systemic infections |
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what is the treatment of c. perfringens
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debridment of necrotic tissue
aggresive treatment with penicillins hyperbaric oxygen |
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what are the characteristics of UTI psudomonas
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only found in cathaters
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what are the virulence factors for c diff
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Toxin A and toxin B
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what is the character of rhodococcus qui
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short rods and cocci
ACID FAST causes TB like disease |
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how does toxin A and B work in c diff
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covalen glucosylatino of cellular Rho GTPase interfering with intracellular signaling triggers fluid secretion and cell death and inflammation
toxin be is 100x more cytotoxic than toxin A |
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where do u get aeruginosa dermatitis from
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hot tubes
often diabetes |
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what is the NAP1 strain of c. diff
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20x more toxins produced
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what are properties of anerobe samples
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foul smell
gas production |
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how is c. diff transmitted
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overgrowth of normal flora due to antibiotic use
can be acquired via fecal oral route nosocomial |
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who gets psudomona endocarditis
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iv drug use
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how is C. diff treated
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c. diff is sensitive to vancomycin, metronidazole, fidazomicin
probiotics or fecal transplant to restore normal flora treatment with flouroquinolins can cause c. diff by killing of normal flora |
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what are the characteristics of m. tuberuclosis
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slender, straight or crved rods, filamnets
ACID fast stain |
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what is yellow pseuodomenbrane indiciative of.
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c. dificile inflamation
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how is psudomonas diagnosed
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gram stain, and culture are both good
need antibiotic sensitivity testing |
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how is c. diff diagnosed
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yellow pseudomembran
3 unformed stolls per 24 hour day culture antigen detection stool kit for toxin A and B and GDH PCR if unsure |
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what are the gram neg rods
|
bacterioides
porphyromanas prevotella |
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what is the treatment against psuedomonas
|
anti pseudomonas antibiotics
monotherapy unless really serious infection |
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what are the virulence factors fo m. tuberculosis
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obligate aerobe
intracellular growth in macrophages |
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how is legionalla transmited
|
arersol found in most fresh water
drinking and then aspriating no person to person |
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where is bateroides found
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intestines
vagina |
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wat class is leginella
|
gram neg rods
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what is the PPD
|
purified protien derivative that u develop antibodies to if u have TB
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why is leginalla hard to diagnose
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hard to culture need charcole
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where is phorphyromonas
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oral
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what does legonella cause
|
legionnaires disease-acute pneumonia
2-10 day incubation, fever heachache chlls cough eventually respiratory failure pontiac fever- mild respiratory disease. |
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what make mycobacterial acid fast
|
the long chain glucocarbohydrate acids
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how is legonella diagnosed
|
urine antigen test
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prevotella is found where
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oral
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how is legonella treated
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erythromycin, azithromycin, clarithroycin(macrolides)
best is fluroquinolones in severe cases use both |
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how is TB transmitted
|
person to person by inhalation of droplets, survives for long periods in air and surfaces
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what does porphyromonas cause
|
p. gingivialis
periodontal disease |
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what are the clincal aspect of TB
|
primary infectino-latent asymptomacit
spreads to lymph nodes then to blood to spleen and liver still asymptomatic immune system kicks in then granulomatous inflammations occurs everywhere TB is located in the body. |
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what does prevotella cause
|
gingivitis -main
lung abscesses, genital infections |
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what is reinfection TB
|
the causeating granulomas filled with TB burst and respread the infection
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what is the major virulence factor in bacterioids fragilis
|
polysaccharide capsule helps with invasion
|
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what are symptoms of TB
|
fever fatigue, anorexia, cough,
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what does bacterioides fragilis cause
|
abdominal abscess
peritonitis diarrhea any abscess bc its the most common anaerobe |
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what is miliary TB
|
when the TB spreads everywhere brain, menegies etc.
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what are some properties of bacteroides fragilis
|
moderate anaerobe -can stand some oxygen
intestine |
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diagnosis of M. tuberculosis
|
first check for acid fast
culture-take weeks PPD checks immune status quantiferon-TB dont have to come back PCR used to confirm after acid fast test |
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what is the treatment for baaceroides fragilis
|
metronidazole
carbapenems combo beta lactam with beta lactamase inhibitor 3rd gen cephalosporins |
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what is the treatment for TB
|
1. isoniazid, rifapmin, pyrazinamid
2. fluorquinolones, aminoglycosides MDRstrain- resistan to at least 2 first ling xDR strains- resistant to 2nd line |
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what is bacteroides fragilis resistant to
|
penicillin-has beta lactamase
aminoglycosides tetracycline, erythromycin vancomycin |
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prevention of TB
|
isoniazid prevention prophalaxis
|
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what class is fusobacterium
|
gram neg rod
fusiform |
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what does fusobacterium cause
|
acute necrotizing ulcerative gingivitis
|
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what class is peptostreptococcus
|
gram pos cocci
|
|
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where is peptostreptococcus found
|
anywhere normal flora is found
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what can peptostreptococcus
|
decubitus skin ulcers
diabetic foot ulcers human bite wounds pelvic inflammatory disease peritonitis and intra abdominal abscces any abcess 2nd most common anaerobe |
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what class is actinomyces
|
gram postivie fiamentous branching bacilli
|
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what can be found in actinomyces that is diagnostic
|
yellow sulfur granules
|
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where is actinomyces found
|
mainly oral
also in intestines and vagina |
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|
what does actinomyces cause
|
chronic suppurative and granulomatoous infections
cervicofacial lesions abdominal lesions salpingitis related to intrauterine contraceptive device. |
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|
what doe human bite wounds usually have
|
bacteroides, fusobacterium, peptostreptococcus
eikenella, s. aureus, viridans strep |
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|
what class is eikenella corrodens
|
gram neg bacilli
facultative anaerobe |
|
|
what can eikenella corrodens cause
|
endocarditis
menigitis sinusitis |
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|
where is eikenella found
|
oral, upper resp.
|
|
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how is eikenella corrodens treated
|
sensitive to most antibiotics, including penicillins.
|
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|
how are bite wound generally treated
|
must treate anaerobes and aerobes.
|
|
|
what is pasteurella usually found in
|
animal bites
|
|
|
what class is pasteurella
|
small gram neg coccobacilli or rods
|
|
|
what is the major virulence factor in pasteurella
|
a capsule
|
|
|
what is the clincial manifestation of pasteurella
|
cellulitis
ostemyelitis respiratory tract infetion systemic infection |
|
|
what is the diagnosis of pasteurella
|
clincal picture and cultures
|
|
|
what is the treatment and prevention for pasteurella
|
penicillin or other antibiotics
no vaccine |
|
|
what is the key to understanding bite wound treatment
|
must cover aerobes and anaerobes
penicillins cover most of the aeorbes pasteurella, eukinella, but does not work for bacteroides |
