Introduction to infectious disease Flashcards
What are ID caused by?
bacteria, viruses, pathogens, fungi
what are the ways they are spread?
pateint to patient, vector to patient,(animal to patient), environment to patient (hospital), patients own flora
Organisms that live on body concern?
no they can be harmless or even helpful, under certain conditions that may cause disease
What are pathogens?
Organism that can cause host tissue damage and intitae a immune reponse that usualy reuslts in infection
what is the basic approach to identifying ID?
- establish infection
- fever does not always mean infection
- determine sites of infection
- deternine pathogens
- select apporpriate antimicrobial therpay
how can we establish an infection?
- careful history and phsycial
- s and s
- predisposing factors
what are the signs and symptoms we can use to identify an infection?
-fever
-increased WBC
- Acute Phase reactants (ESR, CRP, Procalcitonin)
what should we know about fever? other causes? specifically drugs?
fact: lowest in the morning and highest in the evening
other causes:
- maligancy (epecailly CNS), autoimmune diseae, stress, drugs
Drugs:
- anticonvulsants, sulfa-containing compounds, antiarrhythmics, antipsychotic, beta-lactams
What should we know about WBC? other causes, and drugs
Fact: infection can cause mobilization of granulocytes and lymphocytes
Other causes:
malignancy, inflammatory disorders, stress, drugs
Drugs:
- corticosteroids
- epinephrine
- lithium
if an increase in lymphocytes indicates what?
viral infection
if an increase in neutrophils indicates what?
bacterial or fungal infection
what are acute phase reactions?
ESR - erythrocyte sedimentation rate
CRP - C- reactive protein
procalcitonin -
Expand on ESR
-can show inflammatory activity in the body
- measure the distance RBC falls in a test tube within an hour
- Further RBC have fallen the greater the inflammatory response of the immune system
Expand on CRP
- made in the liver
- levels increase when there is an inflammatory response
Procalcitonin
- biomarker release in reponse to bacterial infections
- used to distinguish etiology of infectious process
S and S mild vs severe
mild - sore throat, small sore on skin
Severe - painful cough, gross production of sputum
S and S localized vs deep-seated
localized: Skin - swelling , erythema, tenderness and purulent drainage
Deep-seated: meningitis, pneumonia - must be determined from tissue or fluid sample
What do clinicans usualy look for? then what is the next step?
determine a focus:
- cough - prob lungs
- leg sore - prob and ulcer, cut
- child pulling ear - probably inner ear canal
the next step is to determine what organisms are common for that area?
Gram-positive Cocci
Staph : S.aureus, S.epidermis
Strep : Pneumococcus, viridians
Enterococcus: E.Faecalis, E.Faecium
Gram positive bacilli
Corynebacteria
Listeria
Antimicrobial coverage for MSSA
Cloxacillin, cefazolin, Caphaleixin
hospital-acquired MRSA
Vancomycin, daptomycin, clindymin( linezolid),
Community-acquired pneumonia (penicillin-susceptible)
penicillin, ampicillin
Community-acquired pneumonia (penicillin-resisitant)
3 gen cephalosporin (not ceftazidime), a quinolone (not cipro), vancomycin
community acquired MRSA
Clindamycin, SNX-TMP, doxycycline
Enterococcus
Ampicillin or vancomycin (depending on resistance)
Gram-negative cocci
Moraxella,
Neisseria: meningitis, gonorrhea
gram-negative bacilli
a bunch
Easy to kill gram-negative
HPEK M SS
antimicrobial to kill easy to kill gram-negative
amoxicillin, amox/clavulate, 2nd gen cephalosporines for milder infections
antimicrobial to kill hard-to-kill gram-negative
SPACE
- MAFIA PCC:
meropenem, aminoglycosides, FQ (not moxi), imipenem, pip/tazo, cefepime, ceftazidime
what HTK are hard to get?
Pseudomonas and acinobacter
What are the anaerobes?
Peptococcous, Peptostreptoccoucs, bacteroides, fuscobacterium, prevotella
When treated do we need o know the pathogen right away to pick an agent?
no we can use a broad spectrum and then use a more specific one when we need more trageted therapy
Colonization def
presence of an organism without inflammatory response
Contamination def
the presence of an orgaism acquired during specimen sampling without evidence of host inflammtoyr repsonse
Infections
presence of an organism that initiates a host inflammatory response
when patients is acutley ill febrile what should we do?
do blood cultutres before antibbiotics are initiated
T>= 38.5 degress celsius
what types of results should be evaluated? useful results
blood, sputum, urine, wound, or sinus drainage
- not always useful reuslts
what can we evalute to detrmine the lilkeyl pathogen?
Blood cultutre, blood, sputum, urine, sinus darainge, wound, spinal fluid in menigitis, joint aspirations in septic joints, abcess/cullulitis drainag
what areas are heavily colonized with a variety of bacteria?
skin, oropharynx, ears, throat, and perineum
- concern if revocered from blood, venous cathether or prosthetic devices
what are some considerations for interpreting results if the sample is from the CSF?
glucose, WBC, proteins
what are some considerations for interpreting results if the sample is from the Sputum?
diffiucly to interpret, most reliable if from bronchoscopy or deep suctioning or an intubated patient
what are some considerations for interpreting results if the sample is from the urine?
cats, nitrites, polymicrobila. pyruia
MIC and types
minmum inhibtory concentration - lowest Ab dose that prevents growth after 24 hours
S - susuctible,
I - intermediate or indtermine
R - resistant
Pharmacokinetics
what body does to drug
Pharmacodynamics
what drug does to body
What info do we need from he patient’s history?
- acquitsion of infection
- previous infections or colonization
- Previous antibiotic use
- site of infection and most liley pathogen
Time-dependent killing
- above MIC by 2-4 times
- higher cocnetraion doesn’t work better
- minimla to no PA
Concentration-dependent killing
- more durg more death
- have P- need 10more then MIC AE
drug class most knonw for PAE?
Aminoglycosides
when do we prefer bacteriocidial?
- when immuncomprmises
- in sever life threatening infection ) endocarditis or meningitis)
Baterostatiic drugs?
M
T
L
Drug factors: tissue pentration
if it cannot reach the site of infection, usueless
Abscess
they can inactiavte drugs so muct be drained
meningitis
cafazolin can work against bacterila but not penetrate CNS
Moxifloxicin
low renal clearance, don’t use for UTI
Nitrofuratoin
is metabolized before reached urinary tract in poor renal failure
Daptomycin
inactivated by lung surfactant - bad for lung infection
If we are severly ill what should we be aware of?
oral absorption may be hindered
drug that can cause increase in seizures
imepenem
Aminoglycosdies SE
nephrotocityc, ototcity
Glycopetides SE
red man syndorme
Datomycin (lipopetide)
hepatoxicity
Sulfonamides and trimethoprim
HIV patients caution
When is combination therapy indicated?
- boraden spectrum of acticivty
- Synergisc effects
- when risk of failure is catastrphic (rex: resp infection in ICU with SPACE)
How can we monitor effectiveness?
- fever resolves in 24-48 hours
- patient compliants dimish
- pneumia scans will still show evdience fo damage for a while
when is IV - PO stepdown therapy indicated?
- overall improvemnt
- lack of fever for 24 hours
- decrease in WBC
- Functioning GI tract
- taking other meds by mouth
- tolerating oral diet (no nauseou or vomiting)
draugs that have better oral bioavailibilty then IV
FQ, Metronidazle, SMX-TMP, clindamycin,
Duaration of therpay for UTI Drugs
nitor- 5 d
TMP -SMX - 3 days
Fosfomycin - 1 d
febrile UTI 7-14 d
rest 7 d
Pneumoina
5-7 d
COPD
5-7 days
Streptococoal pharyangitis
10 days
acute otis media
10 days
Intraabodimal
appendicitis
Absecss infection
no more then 24 post opertaion
only before
less then 7 days
Bacteremia
7 days
osteoarticular
weeks
