Bugs And Drugs Flashcards
These bacterial toxins are encoded by a lysogenic phage:
Group A strep erythrogenic toxin (think scarlet fever), Botulinum toxin, Cholera toxin, Diphtheria toxin, Shiga toxin
Morphology of Moraxella catarrhalis
GN cocci
Respiratory GNRs
Bordetella pertussis; Burkholderia; Haemophilus (HiB or NTHi); Legionella (Legionella doesn’t gram stain super well but can be visualized with silver stain)
Why don’t Treponema pallidum and Leptospira gram stain well?
They are too thin to be visualized
Morphology of common bacterial causes of diarrhea
Campylobacter, Shigella, Salmonella, E.coli… These are GNRs
Morphology of a bacterial species associated with food poisoning from cantaloupe and cottage cheese
Listeria - GPR
These antibiotics are generally ineffective against anaerobes because they require O2 to enter into the bacterial cell walls:
Aminoglycosides: gentamicin, tobramycin
GP rods with spores
Clostridium
Asplenics are at particular risk of infection from these pathogens:
Encapsulated bacteria: the capsules serve as an anti phagocytes virulence factor. Asplenics have decreased ability to opsonize bacteria, leading to a decreased ability to clear these infections. Major ones are S.pneumoniae, HiB, N.meningitidis (these three are ones for which we have vaccines), Klebsiella pneumoniae, Salmonella, E.coli, Group B strep, Pseudomonas.
Pathogen that causes watery diarrhea in developing countries and pathogen associated with shellfish and shark bites: morphology
Vibrio species (V.cholera; V.vulnificans): comma-shaped GNRs
This bacteria produces biofilms and is implicated in otitis media quite frequently.
NTHi
Morphology of Neisseria (N.meningitides, N.gonorrheae)
GN cocci
Define transformation.
Ability of bacteria to take up free DNA (often generated by cell lysis). S.pneumo, HiB, and Neisseria can do this.
These bacteria don’t have cell walls, so they don’t gram stain
Mycoplasma, Ureaplasma
Mechanism for vaccines against encapsulated bacteria
Polysaccharide capsule conjugated to carrier protein, which enhances immunogenicity by promoting T cell activation, leading to class-switching on B cells. Examples are the PCV (pneumococcal conjugate vaccine), HiB vaccine, and meningococcal vaccine.
Why don’t these bugs gram stain well? Legionella, Rickettsia, Chlamydia, Bartonella, Ehrlichia, Anaplasma
Primarily intracellular
These bacterial toxins cause toxic shock syndrome.
Super antigens from Staph aureus (Toxic shock syndrome toxin - TSST-1) and Strep pyogenes (Exotoxin A). They bind to MHC class II molecules and to TCRs outside of the usual binding site, causing overwhelming release of pro-inflammatory cytokines.
Important aerobic bacteria
Nocardia, Pseudomonas aeruginosa, Mycobacterium tuberculosis
This bacteria produces biofilms and is frequently implicated in infective endocarditis following dental procedures.
Viridans strep (strep mutans)
This bacteria produces a blue-green pigment.
Pseudomonas aeruginosa
This bacteria produces biofilms and is frequently implicated in catheter and prosthetic device infection.
Staph epidermidis
Define specialized transduction.
Lysogenic phage infects a bacterium and incorporates its DNA into the bacterial chromosome. When the viral DNA is excised, parts of the surrounding bacterial DNA are taken with it as well, and those can be transferred to another bacterium.
Catalase-negative and/or SOD-negative anaerobes, which are generally foul-smelling due to short-chain fatty acid production
Clostridium, Bacteroides, Fusobacterium, Actinomyces
Obligate intracellular bacteria
Rickettsia, Chlamydia, Coxiella
Key spirochetes
Borrelia, Leptospira, Treponema pallidum
This bacteria produces biofilms and is frequently a major culprit in respiratory colonization in cystic fibrosis patients, as well as in contact-lens-associated keratitis.
Pseudomonas aeruginosa
What bacterial species expresses protein A, and what does protein A do?
Staph aureus. Protein A binds the Fc region of IgG, preventing opsonization and phagocytosis.
These bacterial exotoxins cause watery diarrhea: what are they, and how do they work?
ETEC heat-labile and heat-stabile toxins; Vibrio cholerae Cholera toxin. These over-activate adenylate cyclase, increasing cAMP, leading to increased Cl- secretion in the gut, causing H2O efflux and watery diarrhea. Heat-stabile toxin over-activates guanylate cyclase, increasing cGMP, and leading to decreased resorption of NaCl and H2O, also causing watery diarrhea.
Why don’t Mycoplasma (TB, etc) stain well on gram stain?
No cell wall
Define conjugation.
F+ plasmid contains the genes required for a sex pilus and conjugation. It will cause a sex pilus to form, which contacts the F- bacterium, leading to transfer of plasmid DNA across that bridge.
GP cocci, aerobic, catalase-positive, coagulase-positive
Staph aureus
Treatment for intertrigo
clotrimazole or nystatin, can also use barrier paste like zinc oxide
What bacterial species expresses M protein, and how does that help in pathogenesis?
Group A strep (S.pyogenes): M protein is an antiphagocytic factor with similar epitopes to various human proteins, which is what causes the autoimmune response that occurs in rheumatic fever.
Fungus that stains well with India ink
Cryptococcus neoformans
Diagnostic technique for scabies infection
Mineral oil prep: look for mites, poop, eggs. Presence of any is diagnostic, although you may treat empirically with a high index of suspicion.
Spore-forming bacteria
Bacillus, Clostridium
GP anaerobic branching filaments, not acid-fast
Actinomyces
Skin pain and erythema starting and the head and going across the body, with flaccid bullae that desquamate in sheets
Staph Scalded Skin Syndrome - due to toxin. Treat inpatient with IV antibiotics and supportive care
A bacterial endotoxin leads to tissue factor activation. What complication can occur?
This can activate the coagulation cascade, leading to DIC.
GP cocci in chains, beta-hemolytic
Group B strep agalactiae, Group A strep pyogenes
This bacterial exotoxin is clinically important because antibodies against it can be used to diagnose rheumatic fever. What is it, and how does it work?
Streptolysin O, released by Strep pyogenes. It degrades cell membranes, leading to hemolysis.
This bacterial exotoxin causes hemolytic-uremic syndrome.
Shiga toxin (Shigella) or Shiga-like toxin (EHEC). It inactivates 60S ribosome by removing adenine from rRNA. This leads to bloody diarrhea (febrile in Shigella, non-febrile in EHEC) and can cause HUS due to enhanced cytokine release.
Define transposition.
Segments of DNA can jump between plasmids and chromosomes. These are called transposons. If they jump from a chromosome to a plasmid, they can become incorporated into other bacterial genomes. This is what led to the development of vancomycin-resistant S.aureus after a plasmid containing a vancomycin resistance transposon was transferred from VRE.
This exotoxin is a phospholipase that causes tissue degradation. What is it and what does it lead to?
Clostridium perfringens alpha toxin, causes gas gangrene.
What are the main effects of bacterial endotoxins?
Endotoxins are LPS on the outer membrane of gram-negative bacteria. Their three main effects are macrophage activation via TLR-4, complement activation, and tissue factor activation.
Treatment of pityriasis versicolor
Give oral fluconazole, exercise till sweating, then rinse off after 4 hours, and repeat in a week
Secondary staph aureus infection in a pre-existing skin lesion
Impetiginized
GP aerobic bacillus: what could it be?
Listeria, Bacillus, Corynebacterium
This bacterial toxin causes flaccid paralysis and “floppy baby” - what is it, and how does it work?
Botulinum toxin, from Clostridium botulinum: a protease that cleaves SNARE proteins, preventing release of stimulatory neurotransmitters (ACh) at the neuromuscular junction, leading to flaccid paralysis.
No stimulation -> no action potentials -> floppy.
A bacterial endotoxin produces a response that includes complement activation. What physiological problems occur, and why?
Histamine release causing hypotension and edema from C3A and C5a release, as well as neutrophil chemotaxis.
GP anaerobic bacillus: what could it be?
Clostridium
Bugs that stain well on Giemsa stain
Chlamydia, Borrelia, Rickettsia, Trypanosomes, Plasmodium
Fever, rash, vomiting, desquamation, end-organ failure with elevated LFTs, elevated bilirubin, associated with prolonged tampon use
Tampon-related S.aureus toxic shock syndrome. REMOVE THE TAMPON - source control! Very treatable in those cases.
GP cocci, aerobic, catalase-positive, coagulase negative
S.epidermidis (sensitive to novobiocin), S.saprophyticus (not sensitive to novobiocin), other Staph species
A bacterial endotoxin leads to macrophage activation. What cytokines are released, and what signs/symptoms occur as a result?
IL-1 and IL-6 lead to fever. TNF-alpha leads to fever and hypotension. Nitric oxide leads to vasodilation, leading to hypotension.
Second most common cause of uncomplicated UTI
Staph saprophyticus
GP aerobic branching filaments, acid-fast
Nocardia
Non-bloody diarrhea and vomiting 2-6 hours after eating contaminated food
Most likely due to preformed toxin from S.aureus, a heat-stable enterotoxin
GP cocci in chains, alpha-hemolytic
Viridans strep (no capsule); S.pneumoniae (encapsulated)
Coral red fluorescence on Woods lamp in an area of the skin subject to maceration
Erythrasma - Cornyebacterium minutissimum
Lesions in young kids that are round erosions with scale
Bullous impetigo - treat with oral ABX
Patients with chronic granulomatous disease have recurrent infections with certain catalase+ organisms: which ones, and why?
Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E.coli, Staph, H. Pylori… This is because in CGD, patients’ disease is due to NADPH oxidase deficiency, and so they have a decreased neutrophil response to catalase-positive organisms.
Erythrasma treatment
Anti-inflammatory topical ABX or antifungals
Pathogen most commonly implicated in abscess formation
Staph aureus
Infection causing a raised erythematous plaque with sharply demarcated border, sometimes on the face, that occurs with fever, chills, and malaise
Erysipelas, caused by S.pyogenes. Treat with oral ABX.
GP cocci in chains, no hemolysis
S.bovis, enterococcus
Lesions with honey-colored crusting
Non-bullous impetigo, most commonly due to S.aureus
Define generalized transduction.
Lytic phage infects bacterium, and when the bacterium lyses, parts of its DNA are packaged in phage capsids, leading to transfer of those genes to another bacterium when it is infected by the phage.
Infections caused by dermatophytes
Tinea capitis (scalp), cruris (groin, spares the scrotum), pedis (feet), corporis (body)
Which generation of cephalosporins is best for treating methicillin-susceptible staph aureus?
1st gen (cefazolin, Cephalexin) or 2nd gen cefuroxime.
Tinea workup on KOH prep
Branching septate hyphae
Topical treatment for tinea infections
Clotrimazole or terbinafine
This bacterial toxin causes spastic paralysis and “lockjaw” - what is it, and how does it work?
Tetanospasmin, from Clostridium tetani. Protease that cleaves SNARE proteins. Prevents release of inhibitory neurotransmitters (GABA, glycine) from cells in spinal cord, leading to tetany.
No inhibition -> tons of action potentials -> tetany.
Rash in groin, under breasts, skin folds, involving scrotum, with satellite pustules and papules
Intertrigo - caused by Candida
Serpiginous burrows, very itchy, often in web spaces, wrist, penis, scrotum, breast
Scabies
First-line therapy for MRSA
Vancomycin
KOH prep of Malassezia furfur
Spaghetti and meatballs - hyphae and spores
First-line therapy for streptococci
Penicillins - Penicillin G (IV) or V (oral), aminopenicillins
Patient presents with pharyngitis and fever. A gram stain from a swab of the pharynx reveals gram-positive cocci in chains. The patient has, in the past, developed urticaria after taking amoxicillin. What is the best choice of treatment for this patient?
Allergic to penicillins, so this patient should be given a macrolide, which is second-line therapy for streptococci (this patient has an infection with S.pyogenes). Macrolides include erythromycin, azithromycin, clarithromycin.
A patient presents with symptoms of meningitis, and gram stain and culture of the patient’s CSF reveal penicillin-resistant strep pneumo. What is your first choice of drug for this patient?
Vancomycin - inhibits peptidoglycan synthesis.
Pathogen causing pityriasis versicolor (light or dark or salmon-colored plaques on skin, transmitted via direct contact - think young adults at the gym)
Malassezia furfur
First-line therapy for MSSA
Semi-synthetic penicillins: oxacillin, nafcillin, dicloxacillin
This cephalosporin can be used to treat MRSA.
Ceftaroline - 5th generation cephalosporin with broad gram positive and gram negative coverage, including MRSA. Does not cover pseudomonas.
Your hospital has discovered a few patients with a strain of MRSA that is also resistant to vancomycin. How would you treat it?
Linezolid or daptomycin
Why don’t Mycobacteria gram stain well?
Their cell wall has high lipid content
Is penicillin V/G bacteriocidal or bacteriostatic in GPRs, GPCs, GNCs, and spirochetes?
Bacteriocidal
List the classes of antibiotics that interfere with peptidoglycan crosslinking.
Penicillins - penicillinase sensitive (penicillin G and V, ampicillin, amoxicillin) and penicillinase resistant semi-synthetics (Oxacillin, nafcillin, dicloxacillin), as well as the anti-pseudomonas ones (piperacillin, ticarcillin)
Cephalosporins
Carbapenems (imipenem, meropenem, doripenem, ertapenem)
Monobactams (aztreonam)
What are first-line therapies for enterococcus, and what allows them to be bacteriocidal?
Penicillin + gentamicin, and then second line is ampicillin + gentamicin. The gentamicin is an aminoglycoside that makes this treatment bacteriocidal rather than bacteriostatic.
List the penicillins that will kill pseudomonas.
Piperacillin and ticarcillin, which are second-line therapy for pseudomonas
When treating an infection with piperacillin or ticarcillin, if you suspect the bug may produce a beta-lactamase, what should you do?
Add a beta-lactamase inhibitor (clavulanate, etc) because these drugs are susceptible to penicillinases.
What are the key beta lactamase inhibitors?
Clavulanate, tazobactam
Why are semi-synthetic penicillins able to work in bacteria that produce penicillinases?
They have a bulky R group that blocks access of the beta-lactamase to the beta-lactam ring.
Which antibacterials interfere with folic acid synthesis and reduction, therefore interfering with DNA methylation?
Sulfonamides (sulfamethoxazole, etc) - block DHFR. Trimethoprim blocks THFR.
What antibacterial interferes with mRNA synthesis by inhibiting DNA-dependent RNA polymerase?
Rifampin (RNA pol inhibitor, ramps up microsomal cytochrome p450, red-orange body fluids - non-hazardous side effect, rapid resistance if used alone)
What is the risk of monotherapy with rifampin in TB patients?
High risk of resistance if used alone
TB prophylaxis
Isoniazid
What is the standard set of four drugs used to treat TB?
Rifampin, isoniazid, pyrazinamide, ethambutol
What infections should be treated with metronidazole?
Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (including C.diff), H.pylori (with PPI+clindamycin)
What is the MOA of an antibacterial that is good for treating anaerobic infections below the diaphragm?
Metronidazole - forms toxic free radical metabolites that lead to DNA damage. It is bacteriocidal and anti-protozoal.
These bactericidal drugs require O2-dependent active transport to get into cells, where they irreversibly bind to the 30S subunit. They don’t have any activity alone against strep or enterococci, and need to be used in combo with a beta-lactam in those organisms in order to be able to penetrate the cell wall. What are they?
Aminoglycosides - gentamicin and tobramycin.
Can’t be used for anaerobes, abscesses, atypical bacteria.
What are the major side effects of aminoglycosides?
Reversible nephrotoxicity, irreversible oto toxicity due to loss of hair cells, risk of neuromuscular blockade, and teratogenic.
Give in once-daily doses to decrease toxicity, and monitor if treating for more than 5-7 days.
These drugs bind to the 30S subunit and prevent attachment of AA-tRNA. They are bacteriostatic. What are they?
Tetracyclines - tetracycline, doxycycline, minocycline.
How does resistance to tetracyclines develop?
Decreased uptake of the drug or increased efflux of the drug due to transport pumps encoded on plasmids.
Do tetracyclines have activity against pseudomonas or anaerobes?
No!
What organisms can be treated with tetracyclines?
Staph aureus, Strep pneumo, GPRs, atypical bacteria, zoonotics, malaria. Can treat intracellular pathogens!
Used for CAP, skin and soft tissue infection, Lyme disease, other tick-borne illnesses (think Erlichia and Anaplasma especially), STIs
This member of the lincosamide class of antibiotics reversibly binds to the 50s ribosomal subunit, blocking peptide translocation. It is good for treating anaerobic infection above the diaphragm.
Clindamycin
This drug is helpful for treating lung and oral abscesses, or for treating strep in combo with a beta-lactam, but it has a high risk of C.diff infection following its use.
Clindamycin
What is the MOA of linezolid and other oxazolidinones?
Inhibits protein synthesis by binding to the 50S ribosome, inhibiting formation of the initiation complex and 70S ribosome. It is bacteriostatic… But kills them slowly.
What is the clinical use of linezolid?
MRSA, VRE, other highly resistant gram positives.
Can linezolid be used for GNs?
No! Can’t be used for GNs, anaerobes, atypicals.
What are the major side effects of linezolid?
Bone marrow suppression, especially thrombocytopenia; peripheral neuropathy; serotonin syndrome
What are the major side effects of macrolides?
GI motility issues, QTc prolongation, hepatitis, reversible ototoxicity
What classes of drugs are used to treat atypical CAP?
Tetracyclines, macrolides, fluoroquinolones
What are some mechanisms by which bacteria can develop resistance to macrolides?
1) alter the target site by methylation of 23S (encoded by the erm gene)
2) enhanced efflux pumps (mef gene on a transposon)
3) mutate 50s binding site
4) drug inactivation by an enzyme
What is the MOA of macrolides?
Inhibits protein synthesis by binding to the 23S part of the 50S ribosomal subunit, interfering with tRNA attachment and peptide elongation.
Are macrolides bacteriocidal or bacteriostatic?
Bacteriostatic?
First-line therapy for pseudomonas
Cefepime, ceftazidime
This antibacterial drug only reaches adequate concentrations in urine. What is it?
Nitrofurantoin - used for treatment of UTIs. Inhibits protein synthesis, DNA synthesis, cell wall synthesis, etc. Good for GNRs, especially E.coli, with moderate activity against enterobacter. Does not work well against pseudomonas or anaerobes.
These drugs inhibit DNA topoisomerases, causing DNA supercoiling. They are bactericidal. What are they?
Fluoroquinolones - ciprofloxacin, levofloxacin, moxifloxacin
Which fluoroquinolone has the best activity against pseudomonas?
Ciprofloxacin. Levofloxacin has some at high dose. Moxifloxacin does not.
Which fluoroquinolone has poor/no activity against GP and anaerobes?
Ciprofloxacin
A mutation in DNA gyrase or topoisomerase IV will cause resistance to which class of antibacterial drugs?
Fluoroquinolones
What are the major adverse effects associated with fluoroquinolones?
C.diff, GI effects, tendinitis and tendon rupture, CNS symptoms, peripheral neuropathy, hepatitis. Only use these when there’s not really another good treatment option!
This class of antibiotics can turn urine and other bodily fluids orange.
Rifampin (of the rifamycin class). This is a harmless side effect.
What are the major side effects of rifamycin?
GI, hepatitis, P450 drug interactions, orange urine
What are the major side effects of metronidazole?
Bad taste, GI effects, peripheral neuropathy, vomiting if taken with alcohol.
What organisms is TMP-sulfa useless for?
Pseudomonas, anaerobes, atypicals
What is a consequence of long-term use of trimethoprim?
Folate deficiency
How do beta-lactams enter GP bacteria?
Diffuse directly across the peptidoglycan cell wall
How do beta-lactams enter GN bacteria?
Pass through porins in the cell wall
Clinical uses of natural penicillins
Streptococci, enterococci, meningococcus, syphilis, gas gangrene (used with clindamycin), periodontal infection
This is used as a treatment for HiB due to 30% prevalence of making beta-lactamases.
Amox+clavulanate
Which beta-lactam can cause neutropenia?
Oxacillin
Which generations of cephalosporins are good for streptococci?
All of them!
Clinical uses of cefazolin and Cephalexin:
GPC, plus Proteus, E.coli, Klebsiella.
Clinical uses of 2nd generation cephalosporins:
Add anaerobes! GPC, Proteus, E.coli, Klebsiella, but also Hflu, Enterobacter, Neisseria, Serratia
Clinical uses of 3rd gen cephalosporins:
Ceftriaxone for meningitis, gonorrhea, disseminated Lyme disease
Ceftazidime for pseudomonas
Clinical uses of 4th gen cephalosporin (cefepime)
Pseudomonas…. But also other GNs, GPs
Clinical uses of ceftaroline (5th gen cephalosporin)
Broad GP and GN coverage, including MRSA. Does not cover Pseudomonas.
Cefepime has good CNS penetration, but this leads to an adverse effect. What is it?
Altered mental status in the elderly
Which cephalosporins have good CNS penetration?
Ceftriaxone, ceftazidime, cefepime
What is a problematic side effect of ceftriaxone?
Biliary sludging
What are some adverse reactions associated with cephalosporins as a class?
Hypersensitivity reactions, cross-reactivity with penicillins, diarrhea, vitamin K deficiency
Which carbapenem does not have good pseudomonas coverage?
Ertapenem
What is the spectrum of use for carbapenems?
GP cocci, GNRs, anaerobes, including pseudomonas.
What bacteria are not covered by carbapenems?
MRSA, MRSE, E.faecium, VRE, C.diff, Burkholderia. Ertapenem does not cover pseudomonas or Acetinobacter
Side effects associated with carbapenems:
Rash, diarrhea, CNS toxicity lowering seizure threshold
This antibacterial is not very susceptible to beta-lactamases, binds to PBP3 and prevents peptidoglycan cross-linking, and does not have cross-allergenicity with penicillins. What is it?
Aztreonam (a monobactam)
Spectrum of activity of aztreonam
GNRs only. This will work for pseudomonas
This drug inhibits peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors, and is bacteriocidal against most bacteria, except C.diff (static).
Vancomycin
What side effects are associated with vancomycin?
Nephrotoxicity, ototoxicity, thrombophlebitis, Red man syndrome
A patient being treated for a MRSA infection inpatient is receiving his medications intravenously when he gets concerned because he is flushed and appears bright red. What drug is he most likely receiving, and how can this problem be fixed?
Vancomycin - slow the infusion rate!
This drug is a cyclic lipopeptide that inserts itself into the bacterial cell wall and essentially blows up the cell. What is it, and what kinds of infections can it not be used for?
Daptomycin - rapidly cidal. Can’t be used for lung infections because the drug is inhibited by pulmonary surfactant
What is a major side effect of daptomycin?
Myopathy, rhabdomyolysis
This rapidly cidal drug is used to treat MRSA skin infections, bacteremia, endocarditis, and VRE, but not pneumonia.
Daptomycin
This TB prophylactic agent can also cause drug-induced lupus.
Isoniazid
This drug is used for prevention of gonococcal conjunctivitis in newborns. What is its mechanism of action?
Erythromycin - binds to the 23S part of the 50S subunit and prevents translocation of ribosomes.
Prophylaxis in HIV patients for pneumocystis jirovecii
TMP-sulfa
This antifungal binds ergosterol and forms membrane pores in the fungi.
Amphotericin B
Side effects associated with Amphotericin B
EVERYTHING. Fever/chills, hypotension, nephrotoxicity, anemia, arrhythmias, IV phlebitis.
Topical drug that works like Amphotericin B
Nystatin
These antifungals inhibit ergosterol synthesis
Azoles - clotrimazole, fluconazole, intraconazole, etc
What kind of fungal infection is treated with terbinafine?
Dermatophyte infections (tinea)
How do echinocandins work?
Inhibit synthesis of beta-glucan
What drugs are used to treat Trypanosoma brucei?
Suramin and melarsoprol (suramin w/o CNS involvement)
What drug is used to treat Trypanosoma cruzi?
Nifurtimox
This drug is used for treatment of malaria but resistance to it builds up in P.falciparum.
Chloroquine
Treatment for P.falciparum
Atovaquone/proguanil
These drugs are used for influenza prophylaxis and treatment. What are they and how do they work?
Oseltamivir, zanamivir. Block release of virus by inhibiting influenza neuraminidase.
What are the limitations of adamantanes (amantadine, rimantadine)?
These drugs interfere with viral uncoating in influenza A, but don’t work for influenza B. They are not used to to adverse effects and the rapid emergence of resistance, as well as the fact that they are limited to influenza A only.
When should you initiate influenza treatment with neuraminidase inhibitors?
Ideally within 24hours, but ASAP
These drugs are used in treatment of HSV and VZV. What are they and how do they work?
Acyclovir, famcyclovir, valacyclovir. They are nucleoside analogues that inhibit viral DNA polymerization, blocking replication of the virus.
Why do acyclovir, famcyclovir, and valacyclovir not work in CMV infection?
CMV lacks the thymidine kinase that phosphorylates those drugs in HSV/VSV infection, so the drugs would be ineffective. Use ganciclovir/valganciclovir instead.
What are side effects of nucleoside analogues used in treatment of HSV/VSV?
Nephrotoxicity (from crystalline nephropathy - prevent with proper hydration), headache
This drug can be used to substantially reduce subclinical viral shedding in HSV infection.
Acyclovir
Side effects of ganciclovir/valganciclovir
Bone marrow suppression causing leukopenia and pancytopenia, renal toxicity, may impair fertility
What causes ganciclovir resistance, and what drugs should you use instead?
Mutations in UL97 prevent activation of ganciclovir by phosphorylation. In this case, treat with cidofovir or foscarnet.
What’s a serious side effect of cidofovir?
It’s very nephrotoxic
What are side effects of foscarnet?
Nephrotoxicity and electrolyte wasting
What are the 5 classes of drugs typically used in HIV HAART, and list a few examples of each
NRTIs - abacavir, tenofovir, zidovudine. These are nucleosides that competitively inhibit nucleotide binding to reverse transcriptase. NNRTIs - efavirenz. These bind to RT at a different site, inhibiting it. Protease inhibitors - navir. These prevent maturation of new viruses by inhibiting HIV-1 protease (pol gene) f. Integrate inhibitors - elite graver. Fusion inhibitors: enfuvirtide, maraviroc.
Typical components of cART regimen
3 drugs or more, typically 2 are NRTIs and often one is an integrase inhibitor. The use of multiple drugs is to prevent resistance.
This antiretroviral binds gp41, inhibiting viral entry.
Enfuvirtide
This antiretroviral prevents HIV entry through CCR5.
Maraviroc
Chronic watery diarrhea in HIV+ patient
Cryptosporidium
EBV presentation in HIV patients with CD4 count <500
Oral hairy leukoplakia
Pneumonia in HIV patient
Pneumocystis jirovecii- ground-glass opacities on CXR
Cavitation or infiltrates on CXR of AIDS patient, presenting with hemoptysis
Aspergillus infection
Meningitis with an encapsulated yeast that stains with India ink and has capsular antigen, in an HIV+ patient
Cryptococcus neoformans
Cotton-wool spots on fundus copy in an HIV+ patient
CMV retinitis - treat with valganciclovir or ganciclovir
Ring-enhancing CNS lesion that is solitary in an HIV patient
CNS B-cell lymphoma from EBV
Oval yeast cells within macrophages, and presentation of fever, weight loss, fatigue, cough, dyspnea, etc
Histoplasmosis
Multiple ring-enhancing lesions on brain MRI
Toxoplasma gondii causing brain abscesses
Reheated rice food poisoning, that starts quickly and ends quickly
B.cereus
Pneumonia in an alcoholic, currant jelly sputum
Klebsiella
Meningitis in a newborn
Group B strep, E.coli, listeria
Osteomyelitis with no pertinent history
Staph aureus
Vaginal infection with fishy odor, thin white discharge, clue cells, no inflammation, elevated pH
Bacterial vaginosis
Slapped cheek rash
Parvovirus B19 -ssDNA virus
