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define pathogen, infection, and disease
- pathogen: micro-org that has potential to cause disease.
- infection: invasion and prolif. of pathogenic microorganisms
- Disease: infection causes damage to host tissues or function.
What are fomites?
any inanimate object that carries infection (e.g. cell phone)
What is the difference b/n empiric and specific antibiotic therapy?
empiric: given before you know what is causing the disease, usually broad spectrum
specific: given when the sensitivity and identity of the offending organism are known. Usually narrower spectrum.
Why do Abx levels testing
- 1) therapeutic index is low: (tmt conc/toxic conc)
- 2) if there is worry about Abx harming organ systems
- 3) genetic hypersensitivity to drug exists
What are the 4 cardinal manifestation of infection?
- 1) fever
- 2) leukocytosis (WBC greater than 10 or 11)
- 3) local signs and symptoms
- 4) systemic signs and symptoms
Why would you treat fever?
- 1) patient comfort
- 2) harmful secondary effects
- -febrile conulsions
- -hypercatabolic state
why would you NOT treat fever?
- 1) fever enhances immune activity: stumlates lymphocytes, and enhances their transformation.
- 2) complicates interpretation of: patient's illness, response to therapy
What are the three R's in specimen collection
- The right specimen: One that should have the pathogen (e.g. CSF for neurological symptoms)
- The Right time: while patient is still symptomatic and before Abx
- The Right way: e.g. if sterile, KEEP it sterile from your own flora
Risk factors for MRSA
- -hospitalizations: tubes, contact, multiple Abx
- -community: athletes, crowded, aboriginal, tattoos, IVDU
VRE risk factors
-hospitalization: tubes, multiple Abx, immunosuppression
List some alpha and beta hemolytic strep
- alpha: viridans, s. pneumoniae
- beta: Group A - S. pyogenes, Group B - S agalactial
List some common sites for anaerobic infection
- dental infections/abscesses
- abscesses of resp, abdo, pelvic origin
- CNS abscesses
Difference in cell wall between GNB and GPB
- GNB walls have:
- -less rigid walls
- -thinner peptidoglycan layer
- -inner and outer membrane
- -no teichoic acid
- -LOTS of lipopolysaccharide (lipid A is an endotoxin)
What are some of the complications due to the release of LPS endotoxin in GNB?
Answer the following about enterbacteraceae:
1)large gram _____ rods
2) ______ anaerobes
3) grow in presence of _____
4) All ferment ______+/- other carbs
- 1) negative
- 2) facultative
- 3) bile acids
- 4) glucose
How does MacConkey media work?
- 1) it is selective: contains crystal violet and bile acids which inhibit the growth of gram +ve bacteria
- 2) it is differential: contains a pH indicator; lactose fermenters make acid turning the media red; otherwise it stays clear
Answer the following about non-fermentive GNB
1) _______ GN rods
2) ______ aerobes
3) non _____ fermenters
4) Many are ______ to lots of Abx
5) some are ______ positive (vs. enterobactereceae)
6) Important ______ infections
- 1) Skinny
- 2) Obligate
- 3) lactose
- 4) resistant
- 5) oxidase
- 6) nosocomial
What are the 3 L's for psuedomonas
- Landscape: GNB, lactose non-fermenter, oxidase positive, found in hospitals (ventilators), burn patients,
- Landmarks: lung infections in cystic fibrosis, bacteremia in neutropenic patients
- Landmines: resistant to most Abx except gentamycin and a few others.
The 3 L's for Stenotrophomonas.
- Landscape: GNB, non-fermenter, oxidase negative
- Landmarks: treat with Septra
- Land mines: resistant to most Abx
Fill in the blanks regarding the HACEK organism:
1) Normal flora of __________
2) _________ is an important risk factor in HACEK
3) most commonly implicated in ________
- 1) Upper resp tract
- 2) periodontal disease
- 3) culture negative endocarditis
Describe the life cycle of a virus
- 1) adsorption: attach to host cell
- 2) penetration/uncoating: virus enters host cell and shoots its nucleic acid inside
- 3) gene expression: viral genes expressed to make more viruses in hijacked cell
- 4) Assembly: new intact viruses inside cell
- 5) Release: virus particles exit host cell
4 possible outcomes of viral infection
- 1) lytic (acute) infection
- 2) persistant (chronic) infection
- 3) latent infection
- 4) host cell transformation
What are 5 reasons that viruses are so hard to treat?
- 1) viral latency in recurrent infection
- 2) They are inside of cells
- 3) They use the cell's machinery to replicate
- 4) They display host antigens on exterior
- 5) Rapid mutation with rapid replication
What are the three categories of AV agents?
- 1) Virucidal: directly inactivate intact viruses
- 2) Immunomodulatory: augment or modify host response to virus
- 3) Direct Acting: inihibit viral replication on a cellular level
What are the 5 indications for IFN-alpha therapy
- 1) HBV chronic
- 2) HCV chronic
- 3) HPV infection
- 4) HIV?
- 5) non-infectious: ITP, some leukemias
6 classes of HIV antiretrovirals avail
- 1) NRTIs (nucleotide/side analogue reverse transcriptase inhibitor)
- 2) non-NRTI's
- 3) protease inhibitors
- 4) fusion inhibitors
- 5) entry inhibitors
- 6) Integrase inhibitors
How does AmpB work?
binds to ergosterol on the fungal cell membrane and causes holes
When should you use lipid AmpB?
- 1) refractory to conventional AmpB
- 2) patient intolerant to AmpB
- 3) renal dysfunction
- 4) selected difficult to treat pathologies
what is the first line treatment for candidiasis?
First line treatment in invasive aspergilliosis
4 things that are true of exotoxins but not endotoxins
- 1) must be released from cells to have toxic effects
- 2) require specific receptors
- 3) small doses are lethal
- 4) most act remotely from the site of infection
6 modes of action for exotoxins
- 1) pore formation
- 2) alteration of cytoskeleton
- 3) inhibition of protein synthesis
- 4) activate second messenger pathways
- 5) proteases
- 6) activate immune response (superantigen)
How does botulism work?
- 1) starts with cranial nerve symptoms and then descending paralysis
- 2) floppy people
- 3) Affects the SNARE proteins that are responsible for the release of ACh
- 4) irreversibly bound, need to grow new nerve terminals
- 5) most potent toxin known to man
How does tetanus work?
- 1) muscle rigidity and spasms
- 2) blocks the release of inhibitory neurotransmitters (e.g. GABA)
How does Diptheria work?
- 1) terminates protein synthesis
- 2) toxicity is conferred by a bacteriophage (need this)
- 3) causes tissue destruction (remember psuedomembrane)
How does bordetella pertussis (whooping cough) work?
- 1) there are multiple toxins at work, complicated
- 2) basically attacks the mucociliary escalator
How does cholera work?
- 1) volume depleted because of the profuse watery diarrhea
- 2) It affects the secondary messenger, causes Cl to be shunted out of the cell, the Na and H2O follow
- 3) requires bacteriophage
What are the features of untreated leprosy (lepromatous vs tuberculoid)
- Lepromatous provides little or no CMI response.
- Tuberculoid produces a vigorous CMI response.
What is the treatment of active TB?
- They are RIPE for treatment:
- R: Rifampin
- I: Isoniazid
- P: Pyrazinamide
- E: Ethambutamol
What are the 3 objectives in treating TB?
- 1) rapid killing of TB bacilli (reduce mortality, morbidity, contagousness)
- 2) prevent the emergence or existence of drug resistence
- 3) Prevent relapse after therapy and achieve cure
what is the difference between fever and hyperthermia?
fever - the setpoint of body temp has been altered
hyperthermia - you go above the setpoint of the body
What are the 4 categories of fever of unknown origin? Details. temperature
Temp for all of these is >38.3
Classical FUO: >3 wks, or at least 3 outpatient visits, or 3 days in hospital
Nosocomial FUO: 3 day of investigation with 2 days of cultures
neutropenic FUO: same as nosocomial with neutrophil count <500/ml
HIV-associated FUO: same as nosocomial with HIV, with > 4weeks duration outpatients or >3dys inpatient
What are the 5 main etologic causes of FUO in order of prevalence?
- -neoplastic causes
- -connective tissue diseases (SLE, RA, etc)
- -miscellaneous (drugs, etc)
- -no diagnosis
What are the 4 cancers that commonly present with fever (remember the 4H)
- -hypernephroma: renal cell ca
- -head: brain
What are some peripheral signs of endocarditis (6)?
- Roth spots: small ovoid hemorrhagic rings in retina
- Janeway lesions: small painless microemboli on the palms or soles
- Osler's nodes: painful, on thenar eminance
- splinter hemorrhages
- petechial rashes
what is the most common cause of native valve endocarditis?
viridians group strep
What is the most common cause of prothetic valve endocarditis?
- CONS (late)
- S. Aureus (within first 12 months)
What is the hallmark of bacterial endocarditis?
What are the clinical features of infectious endocarditis (recall the FROM JANE mnemonic)
- Roth's spots
- Osler's nodes
- Janeway lesions
- Nail bed hemorrhages (aka. splinter hemorrhages)
Out of all the GI parasites, which is the one that can make you the sickest?
Entamoeba histolytica - because it can cause symptoms outside of the gut
What three major pathological findings do you find in entamoeba histolytica?
- large flask-shaped ulcers in in the large intestine
- liver abscesses
- lung abscesses
What is the treatment for entamoeba histolytica (invasive disease and for asymptomatic cyst passers) and giardia lambia?
- invasive: metronidazole
- asymptomatic: iodoquinol (need a compounding pharmacy)
What are the three pathological flagellates?
- Giardia lamblia
- dientamoeba fragilis
- trichomonas vaginalis
What is the crucial point to know about D. fragilis?
they can parasitize helminth eggs
What are the three critical concepts in helminth infections
-worm burden: number of ADULT parasites in host
-autoinfection: completes their whole lifecycle in the host (pinworm and strongyloides only)
-systemic migration: eosinophilia, rashes, dyspnea
What are the two P's in helminth stool examination
- Preservative: submit in the correct vial
- Provide clinical justification to justify microscopy
What are the Sx you see with high worm burden?
- GI: abdo discomfort, bowel obstruction, +-diarrhea
- Diet: malnutrition, hypoproteinemia(adema, ascites)
- Mental: decreased IQ, cognitive impairment
What are the 5 parameters of the Child-pugh classification of cirrhosis?
Bili, albimin, INR, ascites, ecephalopathy
What tests would you order with asymptomatic patients with elevated liver transaminases
- Hep B surface antigen
- Hep C antibodies
- Anti smooth muscle, antinuclear Abs
- Copper studies
- alpha1 AT phenotype
What are the 4 most common respiratory viruses?
- Influenza (flu)
How can you differentiate RSV and paraflu?
- RSV: bronchiolitis, pneumonia > croup, URI
- paraflu: croup, laryngitis, URI > bronchiolitis, pneumonia
what is the incubation time for the PAIRs viruses, enterovirus, hantavirus?
- Paraflu: 2.5 days
- Adeno: 5.5 days
- Influenza: 1.5 d (A), 0.5 d (B)
- RSV: 4.5 days
- entero: 3-6 days
- hanta: usually 2-4 weeks
What is the difference between antigenic drift and antigenic shift? how does a shift happen
drift: point mutations in H or N, allows to re-infection every year
shift: Completely different H and N, no immunity at all, causes pandemics. Animal and human virus combine in pig cell to make a new virus.
What are the "common cold" viruses?
corona viruses, rhinovirus
How would you treat influenza and adeno virus? What about the rest of the rest of the resp viruses?
Influenza: neuramidase inhibitor for A or B (osetamvir, zanamivir), vaccine (2 A's and a B) for prophylaxis
Adeno: Cidofovir only in immunocompromised patients
The rest of them have no effective clinical treatment
What are the three stages of bordella pertussis (whooping cough)
- 1-2 weeks of cold symptoms
- 2-4 weeks of paroxysmal cough (+- the "whoop")
- Convalesce for 1-2 weeks: slow recovery with chance of rebound cough
What are the three major bacterial causes of acute otitis media? 4 viral causes?
bacterial: pneumoniae>H. flu>>M. Catarrhalis
viral: PAIR (paraflu, adeno, influenza, RSV)
What bugs (bacteria, viral, fungal) cause pharyngitis
- Bacterial: Group A strep, gonorrhea
- Viral: rhinovirus + PAIRs viruses + others
- Fingal: Candida albicans
What are the usual bugs involved in ludwig's angina?
Gp A strep, viridins (alpha) strep, oral anaerobes
List the 4 fastidious GNB
4 cardiac complications of endocarditis?
- 1) destruction of valve leading to free regurg
- 2) CHF
- 3) heart block
- 4) pericarditis
When should you treat B. hominis?
- 1) patient is symptomatic
- 2) no other parasites identified
- 3) lots of them seen in stool
Describe what a positive test for HBsAg, HBsAb, HBcIgM, and HBcIgG
- HBsAg: infection, either chronic or active
- HBsAb: immune, either through a past resolved infection or a vaccine
- HBcIgM: acute infection
- HBcIgG: chronic infection or immunity due to past resolved infection
How does the CURB-65 pneumonia severity index work?
- Confusion - 1 point
- Urea > 7 mmol - 1 point
- RR > 30 beats per min - 1 point
- Blood pressure low - <90 sys., <60 dia - 1 pt
- 65 or older - 1point
- 0-1: treat as outpatient
- 2: consider hosp.
- 3-5 consider ICU
Name the top 3 pathogens for both CAP and HAP
- CAP: S. pneumoniae, Mycoplasma, Chlamydophile
- HAP: enteric GN rods (e.g. e. coli), psuedomonas, S. aureus