Other microbes + ANTIMICROBIAL DRUGS Flashcards
What is bactericidal?
ex:
act on cell wall, cell membrane or DNA > kills B-lactams Vancomycin Fluoroquinolones Metronidazole
What is bacteriastic?
act on protein synthesis > halts growth
-some infection such as Group A strep > toxins benefit from inhibiting protein synthesis
Trimethoprim Sulfamethoxazole Aminoglycosides macrolides clindamycin tetracyclines oxazolidinones
Mechanisms for resistance? (3)
- altered binding sites
- drug inactivation
- reduced drug accumulation
What is def of antibiotics?
- substance made by one org to destroy another org
- old term - now for drugs we use antimicrobials
When were most drugs formed?
1940s-1960s
no major development since
Naming: -cillin ceph or cef- -penem -floxacin -thromycin -micin or mycin
Penicillins Cephalosporins Carbapenems Fluoroquinolones Macrolides Aminoglycosides
What is ideal antimicrobial?
but there are none!
- kill pathogens - 100% susceptible
- safe, no sideeffects
- ignores bystanders
- does not induce resistance
- cheap
bonus: affects hosts’ bad effects (sepsis, ARDS)
What is NAM and NAG on bacteria?
- sugars forming peptidoglycan on cell membrane
- crosslinked by TRANSPEPTIDASE that connects d-ALA to D-ALA
- N-actylglucosamide
- N-acetylmuramic acid
B-lactams:
- cidal
ex: Penicillin, Cephalosporins, Carbapenems - have B-lactam ring with side chain = determine activity
- bind TRANSPEPTIDASES > prevents D-ala-D-ala chain crosslingking > bad cell wall > cell death
Resistance to B-lactams?
- drug inactivation
- altered binding site
- B-LACTAMASES from bacteria cleave ring >drug can’t bind
ex: MRSA resistant to all
Overcome B-lactamases?
- add bigger sidechains to penicllin > METHICILLIN
- use drug with B-lactamases inhibitors > CLAVULANIC ACID, TAZOBACTAM
- Ceph and -penems are resistant to B-lactamases
Penicillin?
- b-lactam
- still main drug for Group A strep and Strep pneumoniae
+B-lactamase inhibitor = broad spectrum
Amoxicillin and ampicllin?
A: oral form of penicillin
P: parenteral form
Piperacllin?
- penicillin
- broad gram-ve
Cephalosporins?
B-lactam
- Gen 1-4
- cover gram+ and gram- (usually 1=+; 3=-ve but bad system)
- not good for anerobes
Carbapenems?
- B-lactam
- broad
- stable against extended spectrum b-lactamase
ex: Doripenem, Ertapenem, Imipenem, Meropenem
What is a common problem with B-lactams?
- Allergy!
- reported vs actual
- if true, 5% chance allergy to ceph-
- most common: amox and ampi
Vancomycin?
-cidal
-glycopeptid with large tricylcic molecule
-binds directly to D-ala-D-ala to prevent crosslinking of peptidoglycan
-good for Gram+ve. too big for -ve
-weak - not as effective as B-lactams
»dosing issues. risk of renal failure
VISA and VRSA?
VISA: vanco-intermediatly susceptible Staph aureus: thickened cell wall to block drug access
*reducing drug accumulation
VRSA: vanco-resistant Staph aureus: alteration of peptidoglycan peptide terminus of D-ala-D-ala to have a D-lactate. Vanco can’t bind.
*altered binding site
Fluoroquinolones?
- most overused
- bind DNA during supercoiling process > error > repair process > damage the DNA > cell death
- Gram+: depends on activity of DNA gyrase A - causes -ve supercoiling during replication
- Gram -ve: depends on Topoisomerase IV parC
Resistance to fluoroquinolones?
- altered binding site: MUTATIONS in DNA topoisomerases
2. altered activity and reduce accumulation: EFFLUX PUMPS and ALTERED PORINS > drug doesn’t get in cell
Trimethoprim and Sulfamethoxazole?
- cidal when used together. static separately?
- block 2 steps of folic acid metabolism > affect DNA production > preventing cell synthesis
- used together = broad spectrum
Aminoglycosides?
-static + cidal
ex: GENTAMICIN, TOBRAMYCIN, AMIKACIN
side effects: nephro and ototoxicities!
-bind 30s ribsomal subunit > inhibit protein synthesis
-also bind membrane > cell leaky = bactericidal
*can’t penetrate gram+ve cell wall
Resistance to aminoglycosides?
- change drug activity: modify drug > can’t enter, can’t bind
- increase efflux
Macrolides?
- static
ex: ERYTHROMYCIN, CLARITHROMYCIN, AZITHROMYCIN - bind 50S subunit > prevent protein synthesis
sideeffect: GI intolerance, QT intervals > sudden death
Clindamycin?
- in lincosamide class
- static
- similar activity to macrolides
- bind 50S subunit > prevent protein synthesis
sideeffect: GI intolerance
Resistance to macrolides and clindamycin?
- modification of 23S RNA > change conformation> drug can’t bind the 50S
- altered binding site
Tetraclyclines?
- static
ex: TERTRACLYINE, DOXYCYCLINE, MINOCYCLINE, TIGECLYCINE - bind 30S subunit
- broad gram+ and -ve
Linezolid?
- static
- in Oxazolidinone class (pretty new)
- bind 50S
- good for gram +ve
- $, no gram-ve
side: neutropenia and neuropathy
Metronidazole
- cidal: aneorobes and some parasites!
- overused (no resistance yet)
- small, diffuses into cell > takes e > radicals
What are the main antifungals?
- Polyenes
- azoles
- echinocandins
Polyenes?
how to avoid toxicities?
-antifungals
ex: AMPHOTERICIN B
-bind ergosterol in fungal wall > holes > leaky > death
-broad spec
side: amphoterrible!
-attack host cells because sterols similar > inflammation
-cytokines > symptoms: fever, chills
-nephrotoxic
To avoid toxicity: use slow infusion or bind to liposomes < $
Azoles?
- most used antifungals
ex: CLOTRIMAZOLE, FLUCONAZOLE, ITRACONAZOLE, KETOCONAZOLE, POSACONAZOLE, VORICONAZOLE - inhibit lanosterol 14aplah-demethylase (p450 ensyme)> prevent conversion of lanosterol > ergosterol > cell membrane perm changes > growth issues and exposed toxic sterols
- static
- drug interactions
- resistance
Echinocandins?
- new antifungals
- inhibit 1,3,beta glucan synthase > inhibit cell wall production
ex: ANIDULAFUNGIN, CASPOFUNGIN, MICAFUNGIN - $, safe
what is antimicrobial stewardship?
- pt get right drug only when they need
- refers to coordinated interventions designed to improve and measure appropriate use of antimicrobials by promoting seletion of optimal antimicrobial drug regimen, dose, duration, route
How toward stewardship?
- many things we don’t know - length, use.. = research!
- restricted formulaary
- pre-authorization to some drugs
- audit and feedback of prescribers
- education
- guideliines
- de-escalation - use narrow spectrums
- use more oral drugs to save cost
-in UK: prescribers should be competent in
infection preve and control, resistance, prescribing, stewardship, monitoring, ongoing learning
What are mycobacteria
ex
- mycolic acid in cell wall
- aerobic, slow growing
- nonspore, nonmotile
- very small!
- detected via acid-fast bacilli, fluorochrome dyes
ex: M.tuberculosis complex (M.tuberculosis, M.bovis), M.avium complex, M.leprae, non-tuberculous mycobacteria (opportunistic inf from envt)
Detecting mycobacteria?
- Acid-fast bacilli stain - kinyoun stain - sputum smear
- *Culture: Mtb - slow up to 6wks; nonTM range; leprae not culturable in vitro.
- Nucleic acid amplification
- drug susceptibility testing - important for TB, MAC
Transmission of TB?
factors affecting:
- airborne
- inhale droplet nuclei that may have been there up to 2hrs before
- large droplets and surface contaminations NO risk
*susceptibility - immune of host
infectiousness - smear positive, culture positive, other disease, coughing > aerosols
envt: poor ventilation, overcroding
exposure: higher duration, prox, freq
Pathogenesis of TB:
inhalation > *1ry focus = middle and lower lung zone > macrophage ingest > lymph nodes (Ghon complex) > *2ry focus = upper lungs, nodes, vertebral bodies, meninges > lympho and mono > tubercles & caseous necrosis
Primary disease dx within months -5% > immune failures
Latent TB: 95% - + tuberculin test. fibrosis, calcification.
>5% reactivation (10% chance over lifetime. usually first 2yrs)
» Pulmonary** or extrapulmonary
**only those with pulmonary > SPREAD
(proliferate > spread to other lung sites > infectious droplets)
Latent vs Active Pulmonary TB:
Latent:
-no symptoms, no spreading, + tuberculin test, normal CXR, sputum
Active:
- symptoms, spread, +tuberculin,
- maybe normal chest x-ray
- maybe positive sputum smear and culture
How does Type 4 hypersensitivty occur with TB?
-Th1 cells activated > cytokines : IL2, IFNgamma, TNFalpha
> fever, wt loss, night sweats
-if no Th1 profile > IL10 > suppress immune > disease progression!
How does tuberculin skin test work?
-purified protein inject intracutaneously
-rxn read 48-72hrs later
-+: >10mm induration or 5mm in immunocomp
*latent or active with no pulmonary symptoms or vaccination
-2 steps: booster effect for 1st time testing
most useful for latent: sensitivty 75-90%
issues: FN - immunocompromised or immune system react deep under skin
FP: crossrxns
What is Interferon gamma release assay?
- IGRA: in vitro, T cells exposed to TB antigen and IFNgamma
- no crossrxn, 1 time test
- only good for latent
Management of TB
- at least 2 drugs: ISONIAZID, RIFAMPIN, PYRAZINAMIDE, ETHAMBUTOL 6-9months
- resistance issues; liver toxicity side effects
- DOT - direct observed treatment
- isolation
- N95 resp
for latent: ISONIAZID for 9 months
Vaccine for TB?
BCG: bacille calmetter-guerin
- live attenuated M.bovis
- DOES NOT prevent infection
- helps prevent progression and dissemination
- give to skin test -ve ppl
What is Leprosy?
- Mycobacterium leprae
- acid fast bacilli
- NOT culturable in vitro
- replicates in macrophages - escape phagocytoic killing
- likes cold T’s : mouth, nose
Transmission of leprosy?
- unclear. airborne? NOT contact
- repeated exposure
Tuberculoid vs Lepromatous Leprosy?
T: red blotchy lesions, increase sensation b/c nerve damage. Type 4 hypersensitivity.
-less freq. can be self limiting
L:
- not due to hypersensitivity
- skin, nerves, disfigurement, profuse growth of bacteria
Ex of mycobacteria
resevoir, virulence, disease, spread in human?
- M.tuberculosis. humans. high virulence > TB.
- M.bovis. animals. high virulence >TB
- M.avium complex: envt, birds. low virulence > TB like or disseminated IN AIDS. NO ppl transmission
- M. marinum: water, fish. low virulence. > skin granuloma. transmit via water not via ppl.
- M.laprae. human. high virulence. > leprosy.
Fungi
types?
-eukaryotic, uni/multicellular
-mostly asexual
-rigid cell wall: chitin, glucans, mannoproteins, ERGOSTEROL
-aerobic, requires organic carbons
Types: yeast, mould, dimorphic = yeast and mould
saprophytic vs symbiotic vs parasitic?
fungi
sap: use nonliving organic material
sym: use living - mutally beneficial
para: harming living org when using resources
Yeasts?
ex:
-single, budding
-blastoconidium - budding spores
-cultures: colonies, smooth, creamy, bacteria-like, slimy, capsule = halos
ex: Cryptococcus neoformans
Candida
Moulds?
ex?
- mycelium, filamentous
- hyphae - septae
ex; Aspergillus fumigatus, Scopulariopsis brevicaulis
Dimorphic fungi?
yeast or mould form depending on T, nutrients, O2
- yeast: in vivo or in vitro @ 37
- mould: in vitro in 22-25C
- fatal!
ex: Bastomyces dermatitidis; Histplasma capsulatum; Sporothrix schenkii
Types of fungal infections (4)
Mucocutaneous
-moisture, warmth, disrupt normal flora, decrase neutrophils, lymphocytes
ex: Candida albicans
>diaper rash
Superficial
-outermost layer of skin/nails; likes keratinized tissues
ex: Dermatophytoses: Tinea (ringworms); Microsporum, Tirchophyton, Epidermophyton
> athelete’s foot, ringworms
Subcutaneous
-on foot from envt
> Chromoblastomycosis: soil moulds> chronic nodular lesions
>mycetoma: chronic nodules, sinus trast, discahrge caused by black moulds, fungus-like bacteria
Systemic
- dimorphic mycoses: lung issues, can be fatal
- opportunistic mycoses: all fungi can cause dissemination by getting into bloodstream
ex: candida, cryptococcus, aspergillus
Blastomyces dermatitidis?
- dimorphic fungi
- endemic in ON
- inhalation of CONIDIA from envt > convert to yeast > disseminate through out body from lungs
Drugs for Fungi infections?
Polyene: binds sterol, interferes with cell membrane
use for: systemic disease, superficial candidiasis
Azole: inhibits ergosterol synthesis > cell membrane
use for: superficial candidiasis, systemic disease
Allylamine: inhibits ergosterol synthesis > cell membrane
use for: dermatophytosis
Echnocandin: inhibits glucan synthesis > cell wall
use: systemic disease
Helminths?
classifications:
- Flatworms : Trematodes (flukes); Cestodes (tapeworms)
* Roundworms: Nematodes (filarial vs non filarial)
transmission routes
- contact: through skin; faecal-oral is common
- grows in guts, lays eggs > stool > grows in envt/intermediate host > infect next
diagnostic of helminths and protozoa?
(6) ex of helminths
- Direct examination (stool helminths - look for eggs)
- culture (Strongyloides)
- Antigen (Blood flukes; filaria)
- Host Ab detection/serology (invasive worms)
- Nucleic acid amp/PCR (some)
- Radiologic (tapeworms)
How do host respond to helminths?
>cytokines >Th2 response >eosinophils and mast cells degranulation >macrophages >nitric oxide production >Ab: neutralize, enhance phagocytosis
Define infectious hosts: direct vs indirect. Intermediate.
Direct: 1 host
Indirect: >1 host
Intermediate: larval, juvenile, non-sexual stages develop in
How do helminths harm host?
- mechanical - obstruct, barrier
- compete for resources
- cytotoxicity
- inflammation
- immune-mediated injury
- malignant transformation
Ex of helminths and what they cause: Ascaris Filaria Tapeworms Hookworm Flukes
Ascaris: intestinal obstruction
Filaria: obstruct lymphatics, immune-mediated injury
Tapeworms: takes VitB12 > anemia
Hookworm: takes iron > anemia
Flukes: goes through liver tissue; inflammation, immune-mediate injury, squamous bladder cancer
Treatments for helminths? HEADS
- Herbs/Plant extracts (ex: pumpkin seeds for tapeworm)
- Endoscopic removal (ascaris in bile duct)
- Anti-parasites (all)
- Drainage (hydatid cyst)
- Surgical excision (hydatid cyst, filaria)
What is neurocysticercosis?
organism
symptoms
tx
by: pork tapeworm: Taenia solium
- parasite in CNS > mass effect, inflammation
- siezures, headaches, hydrocephalus, cysts in brain
1. -grows in guts > eggs in stool > pigs eat stool > larve grows > humans eat raw pork with the larvaes > grows up to 15 ft
2. if humans eat the stool with larvae = intermediate host»_space; CYSTICERCOSIS
tx: Antiparasitics: ALBENDAZOLE, PRAZIQUANTEL, prednisone; endoscopic removal from ventricles
What is cutaneous larva migrans?
organism
symptoms
tx
-eggs in feces from dogs/cats > hatch in envt. Worm penetrate skin of humans > pruritus
tx; Antiparasitics: ALBENDAZOLE, IVERMECTIN
Lioasis?
-type of filariasis (neomotode, roundworm)
-worm crawling around
-obstruct lympathatics
from deer fly > human > mature and moves around and makes microfilaraie in blood > deer fly bites and take micro
dx: microscopy, skin nips, blood film, antigen, ab serology, nucleic acid amp, radiologic for lymphs
tx: Doxycycline (antibiotic)
anti-parasitic: Diethylcabamazine, albendazole, ivermectin
surgery - remove from eyes
How to classify protozoa? (4)
using what?
ex
by moving mechanism
- amoebae: pseudopods (E.histolytica)
- flagellates: flagella (Trypansoma)
- ciliates: cilia (Balandidium)
- apicoplexans: gliding (Plasmodium)
How are protozoa transmitted?
contact: fecal-oral; ingestion directly
or indirectly : vector-borne
GI symptoms, diarrhea, abscess (pus in nonantomical cavity)
How do protozoa harm? ex?
- Mechanical - Giardia > barrier to fat absorption but coating wall; plasmodium infect RBC > clog vessels
- Competition for resources > plasmodium: glucose comp
- cytotoxcicity: E.histolytica: abscess in liver
- inflammation - plasmodium > cytokine storm
- immune mediated - Leishmania: activate T cells . ulcers
malignant: none we know
How to diagnose: stool protozoa Plasmodium > malaria Leishmania E.histolytica Trypanosomes Amoebic liver abscess
- Plasmodium > malaria: examine in blood; Rapid Diagnostic test for antigen
- Leishmania: culture, radiology for liver abscess
- E.histolytica: stool protein test for antigen; host Ab
- Trypanosomes: Ab
Treatment for protozoa?
ex?
- antibiotics: Giardia, Plasmodium (doxycycline)
- antifungals: Leishmania
- antiparasitics: all
- herbs/plants: quinie tree bark for plasmodium
- elements: Leishmania - antimony (Sb)
- drainage (E.histolytica abscess)
Cutaneous Leishmaniasis?
by: Leishmania - flagellate. Protozoa, vector-borne. Indirect.
-bite of sand fly > mobile form into blood > mature and mutiple > exits via fly bite
> ulcers
dx: biopsy, culture, host ab, nucleic acid amp
tx:
antibiotics: Azithromycin, paromomycin
antifungals: fluconazole, amphotericin
garlic
pentavalent antimony
What is malaria?
-Plasmodium: falciparum (deadly), vivax (most common), malariea, ovale
-protozoa, vector-borne (night-biting anopheles mosq), indirect
>odd shaped RBC, obstruct capillaries > headache, chills, abdo pain, cough, FEVER from the tropics!
-Dx: direct exam of BLOOD SMEAR with Giemsa stain (thick for diagnosis, thin for species); Rapid diagnostic test (antigen in urine stick), PCR good if smear is negative since it can detect small amounts
-Tx: antibiotics - Coxyclicine, clandamycin
antiparasitics - Choloroquine, Mefloquine
Herbs: Artemisinin, quinine (tree bark)
(meds attack erythrocytic cycle
What are common symptoms from travelers?
What are common infections? from where most often?
-fever, rash, acute diarrhea, chronic diarrhea, GI
Infections: Malaria - africa dengue - SEA, caribbean rickettsiosis - africa typhoid - south asia mononucelosis -south asia
Approach to fever in returned traveller?
- pre-travel vaccines, malaria prophylaxis: Yellow fever, Hep A, Hep B, typhoid, meingococal, Japanese encephalitis
- Itinerary of trip: urban/rural, timing, accomodations
- Exposure hx: water, flooding, insects, bites, sex, dairy
- Hx, PE
- Lab tests accordingly
Back from tropics for longer than 7 days and have fever?
NOT ___?
long incubation period = think which?
NOT DENGUE (incub period: 3-5days) think: malaria TB viral hep schistosomiasis
4 things to know to treat malaria?
- fever = assume malaria because it kills fast. if malaria, which species?
- if plasmodium falciprum, what is the load?
- Is it resistant to CHLOROQUINE?
- is it severe malaria?
Drugs for malaria
- Malarone = uncomplicated malaria
- Artsunate for severe
- chloroquine is 1st antimalarial
Dengue?
-Flavirus
-vector borne: day-biting Aedes mosquitoes
-caribbean and SEA, urban
-short incub: 3-5days!
-fever, headache, pain, nausea/vomitting, rash, hemorrhagic shock
-Dx: CBC for WBC, platelets, liver enzymes
serology, IgG, PCR
-Tx: IV fluids, antipyretics,
AVOID salicylates, NSAIDS
Typhoid?
-bacteria: Salmonella typhi (gram -ve bacillus)
-fecal-oral
-South Asia
>FEVER, headache, abdo pain, constipation, diarrhea, cough, sore throat
Dx: blood culture, gram stain, CBC, travel hx, rule out malaria
Tx:
-CEFTRIAXONE (3rd gen cephalosporin)
-Azithromycin/Cefixime
AVOID fluoroquinolones b/c of resistance
Rickettsiosis?
Tick bite fever
- R. africae; R.conorii
- southern Africa, India, Mediterr
- FEVER, adenopathy, rash, tache noire = bite looks like a cig burn)
Other common causes of fever but non-tropical?
-pneumonia, pyelonephritis, gastroenterisits, influenza, meningitis
Travel to:
South asia
fever
gram -ve bacteria
Typhoid
Travel to: South africa
fever
cig burn lesion
Rickettsiosis
Travel to:
carribean, SEA
fever within 3 days of coming back
sore muscles, better quick
Dengue
Respiratory infection cluster includes: 5 syndromes
POMPS
- pharyngitis
- otitis media
- pneumonia
- meningitis
- sinuisitis
Bugs: pneumoccus, H.influenzae, meningoccous, chlamydophila pneumoniae, mycoplasma pneumoniae, Group A strep
Intra-abdo cluster6 syndromes
DIPPDC
- diverticulitis
- abscess/periotonitis
- pyelonephritis
- pelvic inflammatory disease
- diabetic foot infection
- cholecystitis
bugs: Gram -ve bacilli aerobes
anaerobes
enterocci
Skin cluster: 3
ACE
-abscess, cellulitis, erysipelas
bug: Group A strep, Staph aureus
Organization of drugs:
3 big families: Penicillins, FQ, Cephalosporins (C)
4 pretty big families:
>2 outpatients MT: macrolides (S), tetracyclines (S)
>2 sick inp AC: cabapenems (C), aminoglycosides (S or C)
5 singles: VTNMC vancomycin (C) trimethoprim-sulfamethoxazole (C) nitrofuantoin (C or S) metronidazole - anaerobes (C) clindamycin (S)
What is bacterial meningitis?
tx?
-fever, neck stiffness, altered mental state, headache
>ICP > edema, seizures, death
-usually people have 2/4
-BRUDZINKI’s: neck flexion > knee flexion
-Kernig’s sign: hip
-due to: Strepto pneu, meningococcus, gram -ve bacilli
Tx: according to age group
-IV dexammethasone
-ampillicin, vancomycin, ceftriaxone, cefotaxime
When to LP? what is included in analysis?
LP only if no sign of mass effect. CT first!
- cell count, differential
- glucose, protein
- gram stain, culture, infectious stuff
- cell count, differential with xanthochromia
What is necrotizing fasciitis?
what causes it?
tx?
-flesh-eating: subcutaneous infection > destruction and necrosis of tissue, fascia, vasculature
Type 1: polymoicrobial - 1 anaerobe + 1 facultative anaerobe + enterobacteria
ex: bacteroides + non grou
p A strep + Ecoli
Type2: monomicrobial - *Staph pyogenes usually with staph aureus
-risk factors: drug use, DM, obesity, immunosupp, pvd
-FEVER, tachy, hypotn
>tense edema, disporptionate pain, blisters/bullae, necrosis, crepitus, subcaneous gas
Tx: Clindamycin, Pen G, IVIG, SURGERY
-prophalyxis for contacts
Meningitis in >50yrs?
by: S.pneumoniae, Listeria monocytogenes, gram _ve bacilli
tx: Ampicillin, vancomycin, ceftriaxone/cefeotaxime
or meropenem and vancomycin
Meningitis for kids and adults
by: S.pneumoniae, meningococcus, rarely H.influenzae
tx: vancomycin, cetraixone or cefotaxime +/- ampicillin
or meropenem and vancomycin
Meningitis in neonates?
by: Group B strep, Ecoli, listeria, mram -ve/gram+
ampicillin and cefotaxime or gentamycin
What 2 does penicllin cover?
Strep A
pneumococcus
What does piperacillin cover?
more gram-ve
pseudomonas
What does cloxacillin cover?
Strep A, pneumococcus
-and Staph aureus
First gen Cephalosporins?
Blactam
po: CEPHALEXIN
iv: CEFAZOLIN
- cover gram +ve aerobes (NOT enterococci)
- some gram- bacilli (ecoli, klebsiella, proteus mirabilis)
2nd gen cephalosporins?
CEFUROXIME
- cover gram +ve aerobes (NOT enterococci)
- some gram- bacilli (ecoli, klebsiella, proteus mirabilis)
- Hemophilus influenzae
3rd gen cephalosporins?
CEFIXIME
CEFTRIAXONE
*gram-ve bacilli and cocci
good for pneumococcus
3 major FQ?
CIPROFLOXACIN - gram- bacilli, esp UTI, abdo
LEVOFLOXACIN - resp, pneumonia
MOXIFLOXACIN - resp, pneumonia
Macrolides?
- gram +ve aerobe cocci
- if allergic to penicillin
- resp infections
- Azithromycin - some -ve coverage (gonorrhea, traveler’s diarr)
Erythromycin
Clarithromycin
Tetracyclines?
- ex: DOXYCYCLINE
- for resp inf, chlamydia, other usual
Aminoglycosides?
ex: GENTAMICIN, TOBRAMYCIN
- gram -ve bacilli
- seriously ill
* nephrotoxic, ototoxicity
Carbapenems?
- seriously ill pts; high resistant to others
- very broad spec
Cystitis - bladder infection. use what?
- Trimethoprim-sulfamethoxazole
- nirtrofurantoin
Metronidazole
- cdiff
- gram-ve
Vancomycin?
gram positive aerobic cocci
MRSA resistant to others; or allergies
Clindamycin?
- anerobes from above diaphragm + gram+ve aerobe (like MRSA)
- but not enterococcus
Drug for Group A strep
Penicillin
Ceph 1
macrolide
Pneumoccus
Penicillin
Ceph 2, 3
Maroclide
Enterococci
Ampicillin
Vancomycin
Staph aureus, meth-sensitive
Cloxacillin
Ceph1, Vancomycin, TMP-SMX
MRSA
Vancomycin
Clindamycin
TMP-SMX
Ecoli
Ciprofloxacin (FQ), Ceph 1,2,3
Aminoglycosides
Pseudomonas (gram-ve)
Ciprofloxacin (FQ)
Piperacillin
Aminoglycoside
Ceftazidime
H.Influenzae
Ceph 2,3
Amoxicillin
Macrolide (A, C)
RFQ
Meningococcus
Ceph 3
Chlamydia
Azithromycin
Doxycycline
Anaerobes
Metronidazole
Clindamycin
Moxifloxacin
Gonococcus
Ceph 3
Azithromycin
Legionella
Macrolide
RFQ
Which STI is reportable to PH
- gon
- chlamydia
- syphilis
- hep B
- trachomonas
