MICROM 442 Midterm II
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286 terms
Terms | Definitions |
|---|---|
 H. influenzae is a primary pathogen for? | pediatric, 6 to 18 months of age |
| Feature of H flu that makes it virulent? | type b capsule (PRP) |
| Main source of vaccine? | protein linked PRP conjugate |
| Type B H. flu causes which diseases? | meningitis at 2 years or younger, epiglottitis and pneumonia 2-5 years |
| capsule helps against immune system how? | antiphagocytic |
| failed vaccine was conjugated with? | carbohydrate |
| non-typable H. flu causes? | otitis media |
| route of spread for meningitis? | respiratory tract -> bacteremia -> CNS |
| epiglottitis symptoms? | rapid progression within 24 hours sore throat fever barking cough |
| otitis media and sinusitis source of infection | displacement from normal microbiota |
| cellulitis and sinusitis source of infection | respiratory tract infection |
| requirements of h. flu diagonsis | requires x factor (hematin) requires v factor (NAD) growth on CA |
| difference between h. influenzae and h. parainfluenzae? | h. para does not require X, biology similar to non-encapsulated h. influenzae |
| shape of haemophilus? | gram negative coccobacilli |
| common diseases for h. ducreyii? | venereal disease in developing world enhances HIV transmission |
| symptoms of h. d? | chancroid with satellite lesions |
| diagnosis of h. d | gram stain, culture on chocolate and vancoymcin (33 degrees, 5% CO2) rule out syphilis with dark field stop serology |
| Bordatella pertussis site of infection | ciliated respiratory epithelium that lines the airways |
| how does B. pertussis spread? | aerosolized droplets |
| BP uses what for attachment | FHA and pili |
| toxins of BP? | TCT (tracheal cytotoxin) PG-fragment that destroys ciliated cells via NO and IL-1 PT: AB toxin, ADP-ribosylates G-protein, increased cAMP creates lymphocytosis ACT: catalyzes ATP to cAMP, acts as hemolysin |
| what controls BP toxins? | Bvg, two component regulatory system |
| Clinical manifestations of BP? | whooping cough/pertussis |
| whooping cough characteristics | 95% attack rate for unimmunized asymptomatic carriage cause of persistent cough |
| BP vaccine part of which vaccine? | DTaP |
| complications from BP infection? | pneumonia dehydration malnourishment brain damage |
| BP symptoms caused by what other Bordatella? | B. parapertussis |
| diagnosis of BP? | lymphocytosis culture on selective media DFA PCR |
| growth characteristic of Bordatella? | fastidious |
| Other Bordetella? | bronchiseptica: kennel cough, sepsis hinzii: HIV patient blood, ascending cholangitis holmesii: cultured from blood of patients with significant medical problems |
| Mycoplasma pneumonia characteristics | smallest free-living bacteria pleomorphic filaments no cell wall sterol cell membrane strict aerobe no alternative sigma factors "austere genome" terminal organelle |
| MP causes | respiratory tract infections: tracheobronchitis, pneumonia, "walking pneumoniae" |
| MP causes disease in which age group? | children and adolescents |
| MP attachment via? | adhesin protein P1 |
| MP diagnosis? | PCR |
| how does LP facilitate phagocytosis? | porin molecule binds C3 |
| Type IV secretion used for? | altered phagosome, delays phagolysosomal fusion, resembles autophagy |
| LP life in macrophage? | nutrient acquisition from macrophage until bacteria starves, kills mac and moves on |
| clinical manifestation of LP | Legionaires disease: headache, myalgia, rising fever, dry cough, necrotizing pneumoniae, |
| different serogroups of LP | epidemic (group 1) nosocomial (group 6) |
| other clinical manifestations of LP? | Pontiac fever |
| other Legionella? | micdadei |
| LP diagonsis? | DFA, carbol fuchisin culture with BCYE pH<7.0 |
| General characteristics of Neisseria? | GNDC require enrich medium and CO2 oxidase positive differentiate via sugar utilization |
| host range of Neisseria | obligate human pathogens |
| structure/antigengs of GC | gram negative cell wall Por/Opa LOS pili |
| Pili host receptors | CD46 of male urogenital epithelial cells CR3 of female cervical epithelium |
| Variation of pili | phase variation sequence variation antigenic variations |
| Antigenic variation of pili | 6 different immunodominant variability regions pilS (silent genes) pilE (active gene) pilin variation via recombination transformation or intrachromosomal 10e6 different variants of pilin |
| Outer membrane proteins of GC? | Por (OMP I) and Opa (OMP II) |
| Por characteristics | 50-60% of total protein most abundant structural surface protein trimers for aqueous channels for porin function involved with attachment and invasion of host (binds to CR3) |
| Por antigenic variations | one antigenic type, with some variation 1A = disseminated, 1B = genital infections |
| Opa characteristics | ~12 genes (3-4 in MC) 0-3 genes may be expressed functions in close attachment to host cells |
| What determines colony morphology of GC? | Opa |
| What does Opa bind to? | cell surface proteoglycans extracellular matrix proteins |
| Variation in opa | phase and antigenic may relate to microenvironment |
| Cervical isolates of Opa are? | positive for Opa |
| Elsewhere in GU Opa is | negative |
| Phase variation of OPA | separate promoters constitutively transcribed translationlly controlled |
| Phase variation of OPA is controlled by? | CTCTT repeats that change frame even number of repeats = in frame? |
| Antigenic variation of Opa | 12 opa genes recombination inf hypervariable region |
| Lipooligosaccharide (LOS) general characteristics | similar to LPS of enterics, but lacks repeating subunits maybe sialyated in vivo |
| LOS aid in pathogenicity | production of inflammatory mediators attachment to some host cells serum resistant if sialyated |
| male vs. female pathogenesis | acute in males asymptomatic in females |
| cases of pathogenesis in males | pili attachment to GU tract (CD46) cannot internalize Opa leads to closer adhesion to host cells leading to internalization |
| GC pathogenesis in males: invasion | enter and multiply within epithelial cells, which reach the mucosa triggers inflammatory response leads to hematogenous |
| GC pathogenesis in females | Pili and Por bind to CR3 of cervical epithelium iC3b deposits on LOS, binds to CR3 internalization does not trigger inflammatory response |
| Natural immunity to GC caused by? | colonization with commensal Neisseria and others killing by NHS and complement |
| Immune response to GC | IgM and IgG and IgA against Por and Los Opsonic antibodies against pili and Opa GC phagocytosed by neutrophils (fate?) |
| Evasion of immune response by GC | antigenic/phase variation sialyation of LOS IgA protease |
| Clinical manifestation | Urethritis Cervicitis Salpingitis Dissemination |
| Asympytomatic percentage of carriers of GC | 40% males 80% females |
| GC Urethritis in males | 1-14 day incubation Dysuria/urethral discharge edema and erythema spontaneous resolution without therapy |
| complications of urethritis | epididymitis prostatis |
| GC GU infections in females | dysuria discharge instramenstrual bleeding inflammation of fallopian tube |
| Disseminated gonorrhea | leads to lesions arithritis dermatitis 0.5-3% untreated patients |
| Dx GC | culture via TM media Gram stain for intracellular GNDC PCR |
| Treatment of GC | cephalosporins, quinolones rise of penicillin resistance |
| MC general characteristics | same as GC (has capsule) genetic islands that separate it out |
| major antigens of MC | CPS, LOS, pili, OMPs |
| What determines serological groups of MC? | Capsule (ABCWY cause most serious disease) |
| Target of vaccines | CPS |
| Pathogenesis of MC | attachment via pili to oropharynx extracellular pathogen disseminated from pharynx via blood stream, cross blood brain barrier at choroid plexus (vasculated portion of BBB) |
| Evasion of immune response | IgA protease for intracellular survival and IgA inactivation |
| Immunity via? | presence of bactericidal antibodies against Por Opc and LOS opsonic antibodies during carriage of N. lactamica and other cross-reactive species |
| Susceptibility via? | Lack of active complement LOS induces TNF and IL = shock, hemorrhages, meningitis |
| Manifestations of MC if entered blood | meningitis (30-40%) meningococcemia (10-30%) first 2 combined (30-40) fulminant meningoccemia (10-20%) (DEAD IN A DAY!) |
| causes of fulminant meningococcemia | lack of complement, opsonization, bacteridicidal antibodies |
| Clinical manifestations | asymptomatic carriage (usually transient) meningitis (can occur without signs of sepsis) meningococcemia fulminent MC (inflammatory response to LOS) |
| MC Dx | CSF gram stain DX latex agglutination (CPS) PCR |
| Treatment of MC | Pen G with (children + steroid theapy) cephaosporins |
| lysis of MC good or bad? | bad, leads to inflammation |
| Review the differential characteristics between pathogenic spirochetes | ... |
| Spriochetes include | Treponema, Leptospira, Borrelia |
| cell wall structure of spirochetes | ... |
| what is the working definition of an anaerobe? | fails to grow on the surface of a solid medium in air containing 5-10% CO2 |
| How is oxygen toxic to anaerobes? | Can be converted to H2O2 Lack catalase and SOD Reduced activity for some enzymes |
| How is one predisposed to anaerobe pathogenesis? | surgery (bowel) vascular disease impaired host defense prolonged antibiotic therapy chronic disease mixed wound infection |
| Virulence factors associated with anaerobes | antibiotic resistance (Bacteroides) Exotoxins/Exoenzymes (neurotoxins from C. tet and C. bot) Degradative enzymes (lecithinase from C. perf) |
| Diagnostic associations of anaerobes | Putrid color Transport filled with CO2 or N2 Gram stain (spore formers) Fastidious Anaerobic culturing |
| Treatment of anaerobes | Drainage/debridement of necrotic tissue Combination of Abx |
| How to prevent anaerobe infection | avoid reduction of redox potential prevent movement of normal flora to non-desired places prophylactic antibiotics after certain surgeries/procedures |
| Sporeforming anaerobes that cause disease | Clostridum: tetani, botulinum, perfringens, septicum, novyi, histolyticum, difficile |
| Which Clostridia cause myonecrosis? | perfringens, septicum, novyi, histolyticum |
| Clostridum general characteristics | anaerobic, gram positive spore forming, strict anaerobes |
| Natural reservoir for clos? | soil, GI tract of humans and other animals |
| Etiology of Clostridial wound infections | mixed infection following surgery or trauma |
| Common pathogens with Clostridial wound infections | perfrigens (A), septicum, novyi, histolyticum |
| How can a wound infection manifest? | superficial wound contamination anaerobic cellulitis/crepitus(gas) gas gangrene |
| Main source of pathogenesis of clostridial wound infections? | toxins alpha toxin (phospholipase or lecithinase C) theta toxin (perfringolysin) pore forming others |
| Host defenses present? | None. |
| Dx of Clostridial wound infections | gas in tissues (could be other bacteria) typical lesions |
| Lab cultures to verify Clostridial Dx? | many, plump gram positive bacilli anaerobic growth double zone of hemolysis lecithinase activity nagler reaction |
| Treatment/Prevention of Clostridial WI? | debridement/cleansing penicillin hyperbaric O2/antitoxin (controversial) |
| Main cause of anaerobic food poisoning? | Clostridium perfringens |
| Source of C. perf? | Meat products |
| How many cells required for C. perf infection? | 10E6 - 10E7 cells/gm |
| Virulence factors associated with C. perf? | spore germination produce enterotoxin when in small intestine during sporulation |
| Effect of C. perf enterotoxin? | pores in enterocytes |
| Dx of C. perf | 7-22 hours post ingestion diarrhea, cramps, ab pain verify via spores |
| Treatment of C. perf? | supportive therapy, has low mortality rate |
| Source of C. bot spores? | soil, silt, vegetation |
| Types of foods incriminated in C. bot poisoning? | home canned foods preserved fish prepared meats uncooked |
| Symptoms of botulism | 12-96 hour incubation period flaccid paralysis |
| Action of botulinum toxin | absorbed in intestine transported to neuromuscular junctions via blood stream block neurotransmitter secretion paralysis leading to respiratory failure and death |
| host defenses against BT | immunity per type does not induce protective immunity |
| Dx of BT | vomitting, constipation paralysis of motor nerves |
| Lab Dx of BT | Isolation Demonstration of toxin CSF to rule out others |
| Treatment/Control of BT | suspicion will initiate therapy eliminate unabsorbed toxin: lavage/enemas eliminate source neutralize unbound supportive care (respiratory) antitoxin therapy antibiotics for wound and infantile |
| Movement of tetanus toxin | Move along nerve fibers |
| High risk population for tetanus? | Elderly, 50% mortality for older than 60 years |
| Action of tetanus toxin? | Blocks secretion of inhibitory neurotransmitters |
| Clinical Dx of tet? | clinical manifestations cramping and twitching of muscles around wound early diagnosis is critical |
| Lab Dx of tet? | isolation of organism spores = presumptive demonstration of toxin |
| Immunity against tetanus | antitoxin toxoid immunization recovery does not grant immunity |
| Treatment of tetatnus | antibiotics airway maintenance GABA agonists tetanus immune globulin |
| Structure of tetanus and botulinum toxins | 150 kDa that is released via cell autolysis Three domains: Hc (neurospecific binding), Hn (membrane translocation), L (catalytic activity) |
| Processing of TT and BT | proteolysis cleaves L chain off, reduction reduces sulfur bridge, release light unit that is transported to neuron |
| Catalytic effects of TT and BT | Cleaves membrane protein that prevents fusion with cell membrane |
| Site of TT | VAMP |
| Site of BT | GBDF = VAMP C = Syntaxin AE = SNAP25 |
| Pseudomembraenous colitis is associated with? | Clostridium difficile |
| Two principal toxins | exotoxins TcdA and TcdB (45% homology at AA) |
| Domains of TcdAB? | receptor binding membrane translocation glucosyl transferase activity |
| Catalytic activity of TcdAB? | inactivate Rho proteins via glucose transfer |
| Pathology of C. dif | colon severe abdominal pain: watery diarrhea, mucus, blood pseudomembrane 27-44% mortality rate |
| Dx of C. dif | pseudomembrane isolate from stool, test for toxin assay for toxin |
| Host defense to C. dif | unknown, toxin is decent Ag |
| Treatment of C. dif | Vancomycin and metronidazole |
| epidemiology of C. dif | healthcare associated virulent strain isolated with mutation in regulatory gene, (16 to 24x more AB toxin) resistant to fluoroquinolones |
| Nonsporeforming anaerobic disease agents | Bacteroides Prevotella Fusobacterium |
| General characteristics of NSF anaerobes | 1/3 of anaerobic clinical isolates normal flora on mucosal surfaces extracellular parasites |
| most common organism in GI tract? | Bacteroides fragilis |
| What is a common between the NSF anaerobes? | Generally oxygen tolerant |
| Where is B. frag found? | GI, vagina, cervix |
| Where does B. frag cause disease? | lower half of body |
| Is B. frag bile resistant? | yes |
| What diseases does B. frag cause? | intra-abdominal abscesses skin and soft tissue infections mild diarrhea |
| What virulence factors does B. frag have? | CPS exoenzymes: SOD, peroxidase, ECMases endotoxin pili penR |
| Dx of BF | abscesses gram stain and culture |
| Tx of BF | antibiotics drainage of abscess |
| General characteristics of Prevotella melaninogenica | part of oral microbiota also found on external genitalia black pigment on blood agar |
| Dx of PM | periodontal disease aspiration pneumonia lung abscesses chronic sinusitis otitis |
| Virulence factors of PM | capsule extracellular enzymes: phospholipase A |
| Dx of PM | Gram stain and culture |
| Tx of PM | antibiotics (penicillin, metronidazole) |
| Characteristics of Fusobacterium necrophorum and nucleatum | thin rods with pointed ends normal microbiota of oral cavity infect upper half of body necrophorum has lipase and leukocidal toxin |
| Characteristics of Actinomyces israelii | gram-positive anaerobic rod branching, filamentous, no spores slow growing |
| CM of AI | cervicofacial infections via poor hygiene and disruption of mucosal barrier or aspiration actinomycosis |
| Dx of AI | sulfur granule like colony on pus culture biochemical tests |
| Tx of I | high doses of penicillin with long term therapy |
| What defines a biofilm infection? | associated with some sort of surface bacteria live in matrix encased groups or colonies infection is confined to a particular location infection is resistant in vivo despite antibiotic sensitive |
| What are common themes for most bacterial pathogens? | Adhere to host Evade host immune system Establish colonization and reproduce |
| What are the common themes in Salmonella and Yersinia pathogenesis? | Gram negative facultative anaerobic rodes Cause systemic and GI diseases Utilize T3SS encoded on pathogenicity islands Adhere to M-cells of peyer's patches |
| Host range of Salmonella? | wide range of vertebrate hosts |
| What type of pathogen is salmonella? | facultative intracellular pathogen that can resides in mononuclear phagocytes |
| What are the mechanisms of salmonella host adaptation? | Many, but poorly understood |
| Cell shape for Salmonella | Gram-negative rod with peritrichous flagellae |
| Does Salmonella ferment lactose? | No |
| What other indication of Salmonella? | H2S formation |
| What types of media used to select/isolate Salmonella? | SS, Hektoen, XLT, Mac |
| Serology of Salmonella? | O antigen from LPS, H antigen from flagella, Vi-antigen: polysaccharide capsule |
| Clinical manifestations of non typhoid Salmonella | fever, ab cramps, diarrhea (sometimes bloody), localized sepsis, global sepsis |
| How is non-typhoid Salmonella spread? | ingestion of contaminated food, water, or contact with infected animals |
| What causes salmenoellosis? | 50% either Typhimurium or Enteritidis, Newport next prevalent |
| Clinical manifestations of Typhoidal Salmonella? | fever, headache, constipation, malaise, chills, myalgia, confusions, delirium, intestinal perforation, death |
| Where can etiologal agent of typhoid be isolated from? | blood stream, marrow, stool, urine |
| What causes typhoid? | Salmonella enterica serogroup Typhi |
| Clincal features of Typhi | 10-14 day incubation found in stool 2nd week on carriers |
| Where can Typhi reside? | gallbladder |
| Which SPI encodes Vi antigen | SPI7 |
| Vaccines exist? | Yes, Ty21, live attenuated |
| Main differences between Typhi and Typhimurium? | Typhi is host adapted Typhi causes systemic infection with little diarrhea Typhi has a vaccine Typhi can evoke carrier state |
| Route of infection for Salmonella | oral ingestion (smaller dose required if food is buffered) travel to distal ileum where uptake is mediated by M-cells and CD18+ Invade M-cells and CD18 via SPI-1 Ruffling up epithelial cells facilitates uptake Encounter phagocytic cells in lamina propria, survival mediated by SPI-2 |
| What does SPI-1 secrete? | SipA and SipC that mediate actin rearrangement, inducing uptake, not required for systemic invasion |
| What does SPI-2 do? | prevent assembly of NADPH oxidase on SCVs, allowing systemic infection |
| SPI-3 does? | magnesium transport required for macrophage growth |
| Spi 4 is for? | survival in macrophages |
| SPI-5 encodes what? | Pips, required for enterititis and possible neutrophil attraction |
| SPI-7 encodes? | Vi antigen plasmid can be lost in vitro, found in all clinical isolates |
| Yersinia virulence factors? | Invasin Yops Yersinabactin |
| What does invasin do? | facilitate uptake by host cells |
| What does YopE do? | depolymerizes actin |
| What does YopO do? | phosphorylates host proteins-disrupts cell signalling |
| What does YopT do? | depolymerizes actin |
| What does YopH do? | dephosphorylates signal transuction proteins |
| What does YopP do? | inhibits macrophage apoptosis prevents TNFa release |
| What does yersinia infection mimic? | apendicitis |
| Which enterics are part of normal flora? | E. coli Klebsiella Enterobacter Proteus Serratia |
| What enterics are not part of normal flora? | Salmonella Shigella Yersinia Pathogenic E. coli |
| What types of ideas do pathogenic enterics cause? | endotoxic shock UTIs diarrhea |
| What does E. coli cause? | UTI, gastroenteritis, septicemia (from UTI/GE), neonatal meningitis |
| Source of E. coli infection? | Patients own flora |
| What are the 6 pathogenic categories of pathogenic E. coli? | Enterotoxigenic Enteropathogenic Enteroinvasive Enterohemmorhagic Enteraggregative Diffuse aggregative |
| What does ETEC cause? | traveler's diarrhea |
| What are ETEC's main virulence factors? | LT and ST LT1 similar to CTX LT2 no known role STa STb |
| How to treat ETEC? | hydration |
| Large/Small dose required for ETEC? | Large |
| What does EPEC case? | severe watery diarrhea, nausea, vomiting, dehydration |
| Dx EPEC? | DNA probe for virulence genes |
| Tx EPEC? | hydration |
| Which EC are most prevalent in developing world? | ETEC and EPEC |
| Virulence factors of EHEC? | Stx-1 and Stx2 similar to Shiga toxin |
| Where are Stx12 encoded? | Bacteriophage |
| What does production of phage? | antibiotics |
| What does Stx1 do? | block protein synth -> cell death |
| What does Stx2 do? | develoment of hemolytic uremic syndrome |
| What does EHEC do? | cause lesions on mucosal surface |
| Common source of EHEC in the US | Cattle, 99% positive! |
| What does EIEC cause? | water diarrhea that progresses to bloody |
| Main theme of infection for EIEC | invade epithelial cell multiple within epithelial cell spread to adjacent cell |
| What does EIEC look like? | Shigella (main difference is LPS) |
| EAEC causes? | watery diarrhea |
| Which EC infect small bowel? | ETEC, EPEC, EAEC |
| Which EC infect large bowel? | EIEC |
| What is the main reservoir for Shigella? | human GI tract |
| What are the four groups of Shigella? | Group A: dysenteriae Group B: flexneri Group C: boydii Group D: sonnei |
| What differentiates the four groups of Shigella? | O-antigen of LPS |
| What does Shigella cause? | HUS reactive arthritis ulcers abscesses |
| Epidemiology of Shigella? | low inoculum required humans only reservoir most cases in children person to person spread |
| Pathogenesis of Shigella | acid tolerant virulence plasmid |
| What is the Shiga toxin used for? | HUS, fround in dysteriae |
| What protein is responsible for Shigella actin based motility? | IscA |
| Look at the handout for | Shigella infection route |
| route for microbes | colonize -> multiply -> transmission |
| colonize -> multiply for human = | infection |
| multiply -> transmission for human = | disease |
| transient assumes | indigenous |
| carrier assumes | pathogen |
| where does microbiota on a sterile baby come from? | birth canal, skin, respiration, environment |
| skin microbiota? | staph epi, propioni, diph |
| conjunctiva microbiota? | staph epi, corynebact |
| mouth microbiota? | s. mutans, neisseria, moraxella |
| stomach microbiota? | sterile! |
| colon microbiota? | anaerobes: bacteroides, fuso, clostri facultative: enterics, yeast, bifido |
| nares microbiota? | same as skin + staph aureus |
| nasopharynx microbiota | similar to mouth plus s. pneumo, mc, h. flu |
| larynx ears, sinus | sterile! |
| uriniary tract | sterile if healthy! |
| vaginal microbiota | childbearing: lactobac, O2- GNRS, GPC, Gard, Myco, urea nonchildbearing: mixed, from skin, colon, perineum |
| benefits of indigenous microbiota | prime, exclude, nutrition |
| other sterile places? | blood, bottom of lung, kidney |
| key mouse study showed? | + microbiota = more BW, ate less, stored more - microbiota = skinny, ate more, stored less |
| can a dead pathogen causes infectious disease? | no |
| ML | MC/GC |
| Tinsdale | c. diph |
| fletcher | leptospira |
| charcoal | legionella |
| TCBS | vibrio |
| sources of antibiotics? | 1. naturally-occuring 2. semi-synthetic 3. synthetic |
| define therapeutic index (TI) | a measure of the relative difference between the effective dose and the toxic dose TI = toxic dose/therapeutic dose |
| MBC ~ MIC, cidal or static? | bactericidal |
| MBC >>> MIC, cidal or static? | bacteriostatic |
| when would a physician recommend bactericidal therapy? | immunocompromised hosts sites of infection |
| how to assay antimicrobial activity? | in vitro: kirby-bauer (qualitative) disc diffusion, broth dilution, agar dilution, e-test (quantitative) |
| clinical pharmacology aspects of antibiotics | absorption protein binding tissue distribution |
| two classes of antimicrobial activity | time-dependent killing concentration-dependent killing |
| things to consider when combining antibiotics | 1. broadened spectrum 2. reduce likelihood of resistance 3. efficacy |
| three classes of antibiotic combos | synergistic antagonistic additive |
| major mechanisms of resistance | drug modification alteration of drug site decrease access to target site |
| major classes of antimicrobial agents | 1. inhibit cell wall synthesis 2. inhibit protein synthesis 3. inhibit nucleic acid synthesis 4. antimetabolites 5. misc |
| what antibiotics inhibit cell wall synthesis? | beta lactams, glycopeptides |
| what antibiotics inhibit protein synthesis? | aminoglycosides tetracyclines macrolides lincosamides streptogramins oxazolidinones chloramphenicol |
| which antibiotics inhibit nucleic acid synthesis? | quinolones rifampin |
| which antibiotics are antimetabolites? | trimethoprim sulfamethoxazole |
| miscellaneous antibiotics? | metronidazole nitrofurantoin lipopeptides |
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