Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
128 Cards in this Set
- Front
- Back
|
Acute exacerbations of Chronic Bronchitis are the result of___________ or ________. What is the prevalence of each
|
* viruses or * bacteria
* Viruses (35%) * Bacterial (50%) * Atypicals (5-20%) |
|
|
What are the most common bacterial pathogens in acute exacerbations of Chronic Bronchitis?
|
* Haemophilus influenzae (likes COPD lungs) 24-26%
* Haemophilus parainfluenzae 10-20% * Streptococcus pneumoniae 15-30% * Moraxella catarrhalis 5-15% * Gram-negative bacilli (high incidence) 5-40% - (Klebsiella pneumoniae, Enterobacter aerogenes, Serratia marcescens, P. aeruginosa) * Staphylococcus aureus 0-2% |
|
|
Which atypicals are most likley involved in acute exacerbations of Chronic Bronchitis?
|
* Chlamydia pneumoniae
* Mycoplasma pneumoniae |
|
|
Antibiotic Therapy for Acute Bronchitis Without Underlying Chronic Bronchitis
|
* Antibiotics are not appropriate for uncomplicated acute bronchitis without underlying lung disease.
* These cases are typically viral in nature and usually resolve with time. * When patients with a history of COPD are excluded: - Antibiotics = placebo - Azithromycin = vitamin C (However, antibiotics are significantly more effective than placebo in patients with acute bacterial exacerbation of chronic bronchitis) |
|
|
Treatment goals of chronic bronchitis
|
* Reduce signs/symptoms of exacerbations
- Reduce quanitiy sputum - Return the quality of the sputum back to baseline * Reduce number of (future) exacerbations - Bacterial suppression can help delay future exacerbations |
|
|
Nonpharmacologic therapy
in the treatment of Chronic Bronchitis |
* Rest (reduce O2 consumption and demand)
* Reduce or quit smoking * Maintain hydration * Humidifier or vaporizer (mobilize sputum) * Chest physiotherapy (loosening things) |
|
|
Pharmacologic Therapy in the treatmetn of Chronic Bronchitis
|
* Mucolytics of questionable benefit (H2O best)
* Bronchodilators may be beneficial (improve oxygenation and open airways) (but not theophylline 12-24 hrs to see any benefit at all – not direct MOA) * Antibiotics may provide more rapid resolution of signs/symptoms and improvement in pulmonary function - Clinical benefits have not been consistently proven - Antibiotics are controversial but commonly used |
|
|
When should antibiotics not be used in Bronchitis patients?
|
Those with acute uncomplicated infections
(i.e. not those with exacerbations of chronic disease) |
|
|
What are the cardinal s/sxn of Acute Bacterial Exacerbations of Chronic Bronchitis (ABECB)?
|
1. Worsening of dyspnea (Changes/worsening of pulmonary function)
2. Increase in sputum purulence 3. Increase in sputum volume When patients having these three symptoms were treated with a broad-spectrum antibiotic, these patients had a higher cure rate, fewer therapeutic failures, and a more rapid rate of lung recovery than if treated with placebo. |
|
|
What does pureulent green sputum indicate?
|
94% sensitive and 77% specific for high bacterial load in sputum
Indicates baceterial infection |
|
|
Efficacy of Antibiotic Therapy in Patients With ABECB
|
* Meta-analysis of randomized trials published from 1955 through 1994
* Suggested a small but significant improvement due to antibiotic therapy in patients with exacerbations * Improvement may be clinically significant, especially in patients with low baseline flow rates * Bottom line: improvement in pulmonary fxn * The pts w/ worst baseline pulmonary fxn had the best benefit from antibiotic treatment |
|
|
Goals for Antibiotic Therapy in the treatment of ABECB
|
* Rapidly relieve the clinical symptoms
* “Eradicate” the infection (never totally eradicate) Dramatically reduce population * Increase the interval between exacerbations - Decrease the number of exacerbations per year - Decrease frequency of PCP visits and hospitalizations - Decrease use of antibiotics - Lower total costs for treatment |
|
|
Uncomplicated AECB (Class II)
|
CLASSIFICATION
* FEV1 >35%–50% predicted (COPD but better fxn) * <4 AECB/yr * No comorbidities * Low PCN resistance ETIOLOGY * Viral infection usually precedes a bacterial infection * H. influenzae * S. pneumoniae * M. catarrhalis * C. pneumoniae ANTIBIOTIC THERAPY * Macrolide * Doxycycline * 2nd-/3rd-generation Cephalosporin * Amox/clav (Fluoroquinolone 3rd-4th line so reserve for more ill patients) |
|
|
Complicated AECB
(Class III) |
CLASSIFICATION
* FEV1 >35%–50% predicted * Older * > or = 4 AECB/yr * Comorbidities (congestive heart failure, diabetes, chronic renal or hepatic disease) * Increased PCN resistance (d/t frequent antibiotic use) ETIOLOGY * H. influenzae * S. pneumoniae * M. catarrhalis * Gram-negative bacilli * (P. aeruginosa) ANTIBIOTIC THERAPY * Fluoroquinolone – drug of choice - the fluoroquinolones, and more specifically levo and cipro, are most effective against gram-negatives and P. aeruginosa. * 2nd/3rd-generation Cephalosporin * Amox/clav |
|
|
Chronic bronchial sepsis (Class IV)
|
CLASSIFICATION
* Recurrent antibiotics and/or steroids * Bronchiectasis ETIOLOGY * In addition to the usual respiratory pathogens, gram-negative organisms such as Enterobacteriacea and Pseudomonas should be considered ANTIBIOTIC THERAPY * Empiric therapy is anti-psuedomonal * Based on sputum culture |
|
|
AECB: Host Factors Associated With Poor Treatment Outcome
|
Treatment failure or relapse in up to 20-30% of patients:
- Inadequate antibiotic - Frequency of exacerbation - Severity of lung disease - History of pneumonia/sinusitis - History of cardiopulmonary disease - Need for home oxygen - Use of steroids |
|
|
Usual duration of Pharmacologic Therapy of Chronic Bronchitis
|
* Usual duration of therapy = 7-10 days but depends on patient response
* Prophylaxis infrequently recommended for patients with >4-6 exacerbations/year - Amoxicillin - Doxycycline - TMP-SMX - Unusual |
|
|
Prevention of AECB
|
* Appropriate management of underlying diseases is most effective method of preventing AECB
* Vaccinations recommended for appropriate candidates - Polyvalent pneumococcal - Conjugated Haemophilus influenzae type b - Influenza |
|
|
T.R. is a 64 y.o. female with a 60 pack-year smoking history and mild-moderate COPD (chronic bronchitis). She presents to her primary care physician’s office with complaints of increased sputum production x 2 days. She also feels more fatigued than usual. She has a slight fever and is producing thin, clear sputum in slightly greater quantities than usual. The benefits of antibiotic therapy in T.R. at the present time would be:
a. Decreased chance of worsening pulmonary function. b. Rapid resolution of signs & symptoms. c. Decreased exacerbation of chronic bronchitis in the future. d. None. |
NONE
|
|
|
B.B. is a 48 y.o. male with COPD and a 40 pack-year smoking history. He has approximately 2-3 exacerbations per year and his last recorded FEV1 was 55%. His last exacerbation was 2 months ago; he was treated with oral cefuroxime at that time. He now presents with fever, worsening oxygenation, and increased production of purulent sputum. The most appropriate treatment for this exacerbation of chronic bronchitis would be:
A. Moxifloxacin B. Amoxicillin/clavulanate C. Doxycycline D. Cefpodoxime proxetil |
Doxycycline
* Best reason not to use a beta-lactam in this pt is because of recent treatment with cefuroxime |
|
|
F.C. is a 59 y.o. female with history of COPD, CHF, CAD, HTN, and type II DM. She has 5-6 exacerbations/year and her last recorded FEV1 was 46%. She presents to her PCP with signs/symptoms consistent with an exacerbation. The most appropriate treatment for F.C. would be:
A. Ciprofloxacin d/t CA nature of infection B. Azithromycin C. Levofloxacin D. Amoxicillin |
Levofloxacin
|
|
|
V.Y. is a 59 y.o. male with history of steroid-dependent COPD, CHF, CAD, HTN, and type II DM. He has 5-6 exacerbations/year and his last recorded FEV1 was 46%. He now presents to his PCP with complaints of increased sputum production x 2 days. He feels more fatigued than usual, has a slight fever, and is producing quantities of thick greenish sputum in slightly greater quantities than usual. The most appropriate treatment for V.Y. would be:
A. Amoxicillin/clavulanate B. Doxycycline C. Azithromycin D. No antibiotic |
Amoxicillin/clavulanate– class III patient
|
|
|
What is the Peritoneal cavity?
|
- Extends from bottom of diaphragm to floor of pelvis
- Contains stomach, small bowel, large bowel, liver, -gallbladder, and spleen - Fallopian tubes enter this space in females - Intact mucous membranes control the invasiveness of the indigenous bacteria of gut |
|
|
What is the Retro-peritoneal cavity?
|
Duodenum, pancreas, kidneys, adrenal glands, great vessels, most mesenteric vascular structures
|
|
|
What host factors are protective against IAI
|
- Peristalsis: interferes with bacterial adherence
- Stomach acid: kills ingested bacteria - Intact mucosa: deters adherence of virulent bacteria - Norma flora: prevents virulent bacterial colonization, overgrowth and translocation - Immune barriers: mucosal immune cells, mesenteric lymph nodes, Kupfer cells of liver |
|
|
Normal Flora of the Mouth
|
Oral aerobes
Streptococci |
|
|
Normal Flora of the stomach
|
<100 bacteria/mL
Primarily oral flora Streptococci Lactobacillus |
|
|
Normal flora of the Duodenu, and Jejunum
|
lactobacilli
streptococci Enteribacteriaseae: -E. coli - Klebsiella -Enterobacter |
|
|
Normal flora of the Illeum
|
Enteribacteriaseae:
-E. coli - Klebsiella -Enterobacter Bacteroides spp. |
|
|
Normal flora of the appendix
|
Just kidding LOL sorry getting punchy
|
|
|
Normal flora of the large intestine
|
lactobacilli
streptococci incl. S. faecalis Enteribacteriaseae: -E. coli - Klebsiella -Enterobacter Bacteroides spp: - B. fragilis - B. theteioteomicron - B. vugatus Pseudomonas aerugenosa Candida albicans |
|
|
Impairment of Host Factors as a Cause for IAI
|
- Decreased peristalsis (e.g., neoplasms causing obstruction)
- Reduced stomach acid (e.g., H2-antagonists, proton pump inhibitors, antacids) - Mucosal damage (e.g., bowel disease, tumors, surgery, trauma) - Altered flora (e.g., antibiotics, tumors, bowel disease) - Altered immunity |
|
|
Define Intra-abdominal Infection
|
- Infection within the peritoneum or retro-peritoneal space
- Localized infection * contained within visceral structures * e.g. cholecystitis * Abscess = purulent collection of fluid separated from surrounding tissue by a wall comprised of inflammatory cells and adjacent organs. Become a barier to antibiotic tx - Generalized infection * Peritonitis = acute inflammation of the peritoneal lining due to microorganisms, chemicals, irradiations, or foreign body injury |
|
|
Three Classifications of Intra-abdominal Infection
|
- Primary Peritonitis = spontaneous bacterial peritonitis (SBP)
* Primary peritonitis occurs without an evident source. * Occurs in patients with ascites - Cirrhosis - Chronic actice and acute viral hepatitis - Congestive Heart Failure - Metastatic malignant disease - Systemic lupus erythmatosus - Lymphedema - Secondary Peritonitis - Tertiary Peritonitis |
|
|
Primary Peritonitis: Epidemiology
|
- Children = occurs with post-necrotic cirrhosis from viral hepatitis, or nephrotic syndrome
- Adults = usually occurs in patients with: * alcoholic cirrhosis and ascites * nephrotic syndrome * congestive heart failure * metastatic malignant disease * systemic lupus erythematosus (Acsites – fluid, blood flow, oxygen, electrolytes, glucose, etc all very yummy for bacteria Any bacteria gets in = infection) |
|
|
Primary Peritonitis in Cirrhosis
|
- Occurs in 10-30% of patients with liver cirrhosis
- Incidence rises to >40% with ascitic fluid protein content <1 gm/dL (b/c correlates to poor liver fxn) - Risk factors * Previous SBP episode (predisposition) * Low ascitic fluid protein (marker of severe liver disease) * Gastrointestinal bleeding (Marker of severe disease) * Severity of liver disease - Prognosis * 40-70% of patients will have SBP recurrences * One year survival 30-50% (poor prognostic factor) |
|
|
1° Peritonitis: Pathogenesis
|
- Hematogenous spread
* Portosystemic shunting in cirrhosis decreases removal of bacteria by hepatic reticuloendothelial system (loss of filtering mechs - Lymphatic disruption * Bacteria contaminate hepatic lymph nodes and pass into ascitic fluid - Impairment of bactericidal activity by alteration of peritoneal defenses * Proportional to severity of liver disease |
|
|
What are the three pillars of management for complicated intra-abdominal infections?
|
1. Removal or control of the source of contamination (Source control to stop leakage into peritoneal cavity)
2. Physiological support (Feeding, fluids, ventilation, other supportive care.) 3. Antimicrobial therapy |
|
|
Goals of Antimicrobial Therapy for Intra-abdominal Infections
|
1. Eradicate infecting pathogens
2. Reduce risk of recurrent infections 3. Shorten clinical manifestations of infection The above goals should be achieved while minimizing risks of adverse events and maximizing cost-effectiveness of therapy |
|
|
What is the effect of appropriate antibiotic therapy on outcome measures for intra-abdominal infections?
|
Wound infection: little to no difference
Abcess: incidences are MUCH lower if patient is started on appropriate therapy. There is also a significant reduction in incidence if patient is switched to appropriate therapy. Re-operation: Risk is HIGH with inappropriate therapy and lower with change to appropriate therapy and MUCH lower with appropriate therapy from the start. Death: Risk is highest with inappropriate therapy and MUCH lower with appropriate therapy from the start and with change to appropriate therapy |
|
|
Discuss antibiotic therapy regimens useful in the treatment of IAIs.
|
* Clindamycin has been reported to inhibit more than 95% of the anaerobes.
- It is active against only certain gram-positive cocci (eg, Staphylococcus aureus and Streptococcus pyogenes) but not enterococci, and has virtually no activity against Enterobacteriaceae. * Metronidazole is active against strict anaerobes. - Its in vitro activity is poor against aerobes, microaerophiles, and anaerobes that may become somewhat aerotolerant on subculture. - Since gram-negative bacilli and microaerophilic gram-positive cocci are frequent copathogens in polymicrobial anaerobic infection, metronidazole should be used in combination with another agent. * Bacteroides fragilis and other Bacteroides species are usually resistant to first-, second-, and third-generation cephalosporins, although cefoxitin is distinctly more active than any of the other second generations against Bacteroides species. - First- and second-generation cephalosporins are active against most strains of Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae, and the third generations demonstrate improved activity against the Enterobacteriaceae. * Penicillin G and ampicillin have excellent activity against all anaerobes, with the exception of Bacteroides species. - The combination of ticarcillin or piperacillin with the ß-lactamase inhibitors clavulanic acid or tazobactam, respectively, confer activity against ß-lactamase–producing strains of Bacteroides fragilis, Escherichia coli, and Klebsiella pneumoniae. - Because of this combined spectrum of activity, monotherapy is possible for polymicrobial anaerobic intra-abdominal infections. * Aminoglycosides have excellent coverage against Enterobacteriaceae and Pseudomonas aeruginosa. - Other than that, they do not have much advantage over penicillins or cephalosporins. - An aminoglycoside is often included with a ß-lactam antibiotic for empiric treatment of critically ill patients in whom a resistant pathogen, like Pseudomonas aeruginosa, is suspected. * The fluoroquinolones are active against almost all aerobic gram-negative bacilli. * Ciprofloxacin is most potent against Pseudomonas aeruginosa. |
|
|
What is the guideline prefered antibiotic regimen for IAI?
|
* No prefered regimen.
* The single most important criterion that guides the selection of an initial empiric antimicrobial regimen is the activity of the agent against the common pathogens that cause intra-abdominal infections. The recommended therapies are active against the typical aerobic and anaerobic pathogens observed in patients with community-acquired infections. * Antimicrobial agents differ with regard to their coverage of Enterococcus and the extent of their gram-negative coverage. * Routine coverage of enterococci is not necessary in most patients with community-acquired intra-abdominal infections and should not be a primary consideration in the choice of antimicrobial agents. * Regarding activity against gram-negative organisms, some antimicrobials, such as second-generation cephalosporins or ampicillin/sulbactam, provide less coverage of such organisms as Enterobacter and Pseudomonas than broader-spectrum agents in their classes do. |
|
|
Single agents for use in IAI.
|
* Ampicillin/sulbactam
* Cefotetan * Cefoxitin * Ertapenem * Imipenem/cilastin * Meropenem * Piperacillin/tazobactam * Ticacillin/clavulanic acid * Doripenem * Tigecycline * Moxifloxacin |
|
|
Combination regimens for use in IAI.
|
* Aminoglycoside + anti-anaerobe agent
- amikacin, gentamicin, netilmicin, or trobramycin - PLUS clindamycin or metronidazole * Aztreonam + clindamycin * Cefuroxime + metronidazole * Ciprofloxacin + metronidazole * Levofloxacin + metronidazole * 3rd/4th gen cephalosporin + anti-anaerobe agent - cefepime, cefotaxime, ceftazadime, ceftizoxime, ceftriaxone - PLUS clindamycin or metronidazole |
|
|
Regimens Currently Recommended for Initial Empiric Treatment of Complicated IAIs
|
* Single Agents for use in Mild-to-moderate severity: perforated or abscessed appendicitis and other infections
- Cefoxitin, ertapenem, moxifloxacin, tigecycline, or ticarcillin-clavulante * Single agents for use in High risk or severity: severe physiologic disturbance, advanced age, or immunocompromised state - Imipenem/cilastatin, meropenem, doripenem, or piperacillin/tazobactam * Combination Regimens for use in Mild-to-moderate severity CA-IAI - Metronidazole + cefazolin, cefuroxime, ceftriaxone, cefotaxime, ciprofloxacin, or levofloxacin * Combination Regimens for use in High risk or severity CA-IAI - Metronidazole + cefepime, ceftazidime, ciprofloxacin, or levofloxacin |
|
|
What organisms are seen in health-care associated complicated intra-abdominal infections at institution?
|
* <20% resistant P. aeruginosa, ESBL-producing Enterobacteriaceae, Acinetobacter, or other MDR GNB
* ESBL-producing Enterobacteriaceae * P. aeruginosa >20% resistant to ceftazidime * MRSA |
|
|
What agents are recommended for use against health-care associated complicated intra-abdominal infections at an institution that sees <20% resistant P. aeruginosa, ESBL-producing Enterobacteriaceae, Acinetobacter, or other MDR GNB?
|
* Carbapenem (imipenem, meropenem, doripenem
* Piperacillin-tazobactam * Ceftazidime or cefepime, + metronidazole |
|
|
What agents are recommended for use against health-care associated complicated intra-abdominal infections at an institution that sees ESBL-producing Enterobacteriaceae?
|
* Carbapenem (imipenem, meropenem, doripenem
* Piperacillin-tazobactam * Aminoglycoside |
|
|
What agents are recommended for use against health-care associated complicated intra-abdominal infections at an institution that sees P. aeruginosa >20% resistant to ceftazidime?
|
* Carbapenem (imipenem, meropenem, doripenem
* Piperacillin-tazobactam * Aminoglycoside |
|
|
What agents are recommended for use against health-care associated complicated intra-abdominal infections where MRSA is likely?
|
Vancomycin
|
|
|
What bug should always be covered in hospital acquired IAI?
|
* Remember – anti-psuedomonal regimens for hospital aquired
* Then choose regimen based on resistance profile w/in your hospital |
|
|
What agents are recommended for Initial Empiric Treatment of community-acquired acute cholecystitis of mild-to-moderate severity?
|
Cefazolin, cefuroxime, or ceftriaxone
|
|
|
What agents are recommended for Initial Empiric Treatment of community-acquired cholecystitis of severe physiologic disturbance, advanced age, or immunocompromised state?
|
Imipenem/cilastatin, meropenem, doripenem, piperacillin/tazobactam, ciprofloxacin, levofloxacin, or cefepime, + metronidazole
|
|
|
What agents are recommended for Initial Empiric Treatment of Health-care associated biliary infection of any severity?
|
Imipenem/cilastatin, meropenem, doripenem, piperacillin/tazobactam, ciprofloxacin, levofloxacin, or cefepime, + metronidazole, + vancomycin
Remember - CA – gram- no need to cover anaerobes HA – add anaerobes back in esp anti-pseudomonal activity |
|
|
Treatment of secondary peritonitis
|
* Utilize culture and sensitivity information
* Duration of therapy is variable: 4-7 days or longer depending on adequacy of source control, patient response * If patient does not improve within 4 days, consider - Undrained focus of infection or other source control issue - Resistance - Superinfection |
|
|
J.J. is a 63-year-old man with colon cancer. One day after surgical resection of his colon he develops N/V, anorexia, fever to 103F, shaking chills and abdominal pain. Exam reveals rebound tenderness, a rigid abdomen, and WBC count of 13,000 cells/mm3. Which of the following antibiotic regimens is LEAST appropriate for treatment of J.J.’s secondary peritonitis?
A. Ciprofloxacin + metronidazole B. Ceftazidome + metronidazole C. Cefepime alone D. Meropenem alone E. Tigecycline alone |
Cefepime alone
This patient has classic signs and symptoms of an intra-abdominal infection; he should be treated as a secondary peritonitis due to his history of colon cancer and recent abdominal surgery. Appropriate antibiotics must cover both Gram-negative aerobes and anaerobes. The only drug option here that does NOT cover both of those categories of pathogens is cefepime; it has good Gram-negative aerobic coverage but minimal/no anaerobic coverage for peritonitis infections. Cefepime would therefore be the least appropriate choice; any of the others would provide the required spectrum of activity. The MOST appropriate choice, according to the new IDSA guidelines, would probably be meropenem. Because the onset of the infection was after a surgical procedure, many clinicians would argue that this should be considered a hospital-acquired infection and the guidelines would specify carbapenem monotherapy as being appropriate in this patient (assuming low resistance rates in the hospital). However, the other options would still be considered appropriate by many. |
|
|
J.J. is a 63-year-old man with colon cancer. One day after surgical resection of his colon he develops N/V, anorexia, fever to 103F, shaking chills and abdominal pain. Exam reveals rebound tenderness, a rigid abdomen, and WBC count of 13,000 cells/mm3.
Which of the following regimens would be MOST appropriate for J.J. if he was known to have a severe allergy to penicillins? A. Levofloxacin alone. B. Aztreonam alone. C. Gentamicin + vancomycin. D. Cefuroxime + metronidazole. E. Aztreonam + penicillin. F. Metronidazole + tobramycin. |
Metronidazole + tobramycin.
Automatically take out choices #4 and #5 because of the penicillin allergy; since there are other appropriate treatment options available there is no reason to mess with either a penicillin or a cephalosporin with potential cross-hypersensitivity. Levofloxacin and aztreonam have good Gram-negative aerobic activity but no useful anaerobic activity. Gent + vanco also lacks the anaerobic coverage and would not be a good regimen. The most appropriate choice is therefore #6, metronidazole + tobramycin. |
|
|
J.J. is a 63-year-old man with colon cancer. One day after surgical resection of his colon he develops N/V, anorexia, fever to 103F, shaking chills and abdominal pain. Exam reveals rebound tenderness, a rigid abdomen, and WBC count of 13,000 cells/mm3.
Which of the following statements regarding the treatment of J.J.’s peritonitis is TRUE? A. J.J. should be treated with parenteral antibiotics for 14-21 days. B. J.J. could potentially be switched to oral antibiotics if responding well to parenteral drugs. C. J.J. should be treated with no more than 5-7 days of antibiotics. D. Complications related to J.J.’s infection would be very unusual and would not be expected. |
J.J. could potentially be switched to oral antibiotics if responding well to parenteral drugs.
The usual duration of therapy will be in the 7-10 day range, but this is variable depending on patient response. Parenteral antibiotics for 14-21 days is a little long to start with, and there’s no rule that J.J. has to get parenteral antibiotics for the entire treatment duration. He might require more than 5-7 days, especially if he is slow to respond (he’s an older patient with a serious underlying disease and a bad infection). Complications in a case such as this, with this type of patient, would be not at all uncommon and you’d almost expect it. So choice #2 would be the most appropriate; you can start him on parenteral antibiotics and switching to PO drugs after exhibiting a good response is certainly an option. |
|
|
Pathogenesis of Intra-abdominal Abscess
|
* Contamination of abdomen followed by localization of infection
* Location depends (at least partially) on site of primary process * May take days to weeks to evolve * Abscess environment typically acidic, less aerobic, high bacterial burden - Microbes = anaerobes, facultative bacteria |
|
|
Etiology of Intra-abdominal Abscess
|
* Previous secondary peritonitis (appendicitis, pancreatitis, diverticulitis, genitourinary tract lesions)
* Surgery * Trauma |
|
|
Clinical presentation of Intra-abdominal Abscess
|
* Often non-specific complaints
* Abdominal pain may be either localized or quite vague * Low grade fever * May result in peritonitis, sepsis if abscess ruptures |
|
|
Diagnosis of Intra-abdominal Abscess
|
* Exploratory laparotomy
* Ultrasound or CT scan (most accurate) * Should be considered in any post-operative patient who develops fever several days to weeks after surgery |
|
|
Bacteriology of Intra-abdominal Abscess
|
* Similar to that seen in secondary peritonitis
* Anaerobes more numerous than aerobic bacilli |
|
|
Treatment of Intra-abdominal Abscess
|
* Surgery
* Percutaneous drainage * Antibiotics similar to those for 2 peritonitis - Penetration issues - Low pH in abscess adversely effects activity of clindamycin, aminoglycosides - Inoculum effect may decrease activity of-lactams - -lactamase production among many pathogens may be an issue * General supportive care |
|
|
C.C. is a 53 y.o. male with a history of alcoholic liver disease (ALD) complicated by one episode of upper GI bleeding, refractory ascites, and encephalopathy. He presents with vague abdominal pain, low-grade fever, and mental status changes. He is suspected to have SBP. The most appropriate initial action would be:
A. Start empiric antibiotics. B. Perform a pericentesis. C. Perform a lumbar puncture. D. None of the above |
Perform a pericentesis.
As always, cultures should be obtained before starting antibiotic therapy. Although it’s reasonably predictable what organisms are potentially causing this infection, it would still be nice to know the specific pathogen and antibiotic susceptibilities. Pericentesis, or tap of the ascitic fluid, should therefore be performed and samples sent for culture and susceptibility before initiating antibiotics. |
|
|
C.C. is a 53 y.o. male with a history of alcoholic liver disease (ALD) complicated by one episode of upper GI bleeding, refractory ascites, and encephalopathy. He presents with vague abdominal pain, low-grade fever, and mental status changes. He is suspected to have SBP. A pericentesis is performed and shows ascitic fluid with a WBC count of 450 cells/mm3 and both protein and LDH are slightly elevated. The most appropriate action would now be to:
A. Begin antibiotics for treatment of SBP. B. Hold off on antibiotics and repeat the pericentesis; the results are inconclusive. C. Hold off on antibiotics and treat C.C. for encephalopathy. D. Hold off on antibiotics and observe C.C. for several days. |
Begin antibiotics for treatment of SBP
The elevated white blood cell count, and slightly elevated protein and LDH, are all consistent with SBP. This finding, along with the clinical signs and symptoms which are also consistent with SBP, makes a pretty convincing picture for the presence of infection and the need to treat. It would therefore be most appropriate to immediately begin antibiotic treatment for SBP. The results are not inconclusive (particularly along with the clinical findings) and antibiotics should not be withheld on these grounds. Either treating the encephalopathy first or observing for several days would unnecessarily increase the risk of complications and mortality, which is already considerable. So, the most appropriate action at this time would be to initiate antibiotic therapy. |
|
|
C.C. is a 53 y.o. male with a history of alcoholic liver disease (ALD) complicated by one episode of upper GI bleeding, refractory ascites, and encephalopathy. He presents with vague abdominal pain, low-grade fever, and mental status changes. He is suspected to have SBP. A pericentesis is performed and shows ascitic fluid with a WBC count of 450 cells/mm3 and both protein and LDH are slightly elevated.
C.C. is to be treated for SBP. Which of the following antibiotic regimens would you choose? Assume that C.C. has no known drug allergies. A. Piperacillin/tazobactam B. Moxifloxacin C. Ceftazidime D. Levofloxacin E. Doxycycline F. Ceftriaxone G. Azithromycin |
Ceftazidime OR Doxycycline
The most common organisms causing SBP are enteric Gram-negative aerobic bacilli and aerobic streptococci. Third-generation cephalosporins and certain fluoroquinolones are recommended as empiric therapy and would be appropriate in this case, so either levofloxacin or ceftriaxone would be suitable choices. Piperacillin/tazobactam would not be appropriate because neither antipseudomonal nor anaerobic activity are required; it’s too broad spectrum. Ceftazidime would also be inappropriate because of the antipseudomonal activity. Moxifloxacin would be not be the most desirable choice because of its anaerobic activity, which is not required in this case. Doxycycline and azithromycin are not particularly great against the enteric Gram-negatives and would not be great choices here. |
|
|
C.C. is a 53 y.o. male with a history of alcoholic liver disease (ALD) complicated by one episode of upper GI bleeding, refractory ascites, and encephalopathy. He presents with vague abdominal pain, low-grade fever, and mental status changes. He is suspected to have SBP. A pericentesis is performed and shows ascitic fluid with a WBC count of 450 cells/mm3 and both protein and LDH are slightly elevated.
After treatment of his SBP is completed, should C.C. receive antibiotic prophylaxis against repeat episodes? A. Yes; he is at high risk for recurrence due to refractory ascites. B. No; he is likely to have recurrent episodes of infection but antibiotics would be of questionable value in C.C. C. Yes; every patient with ALD should receive prophylactic antibiotics. D. No; he is not at high risk of recurrent infection. |
Yes; he is at high risk for recurrence due to refractory ascites.
Not every patient with alcoholic liver disease would be appropriate for SBP prophylaxis since not every patient has advanced disease with refractory ascites, so choice #3 would not be correct. This patient is at very high risk of recurrent infection because of his refractory ascites and because he has now already had an episode of SBP. Antibiotic prophylaxis would potentially be of greatest benefit in exactly this type of patient, so prophylaxis should be strongly considered for this patient. |
|
|
Types of CNS Infections
|
* Meningitis
* Encephalitis * Meningoencephalitis * Brain abscess * Subdural empyema * Epidural abscess * Prosthetic device (e.g. shunt infection) |
|
|
Pathogens involved in CNS Infections
|
* Bacteria
* Viruses * Fungi * Parasites |
|
|
Cerebrospinal Fluid (CSF)
|
* Protective “shock absorber” for the brain and spinal cord
* Produced in the ventricles by the choroid plexus * Produced at a rate of ~ 500 ml/day - Total volume of 110-160 mL in adults - Total volume of 40-60 in infants * Removed by arachnoid villi and vertebral venus plexus * Complete CSF exchange every 3-4 hours |
|
|
Blood Brain Barrier
|
* Crucial in protecting the brain and maintaining homeostasis within the CNS
* Capillary endothelia of the brain * Packed tightly together producing a protective barrier * Separates blood from the interstitial fluid of the brain |
|
|
Meninges Anatomy
|
* Dura mater – lies beneath and adherent to the skull
* Pia Mater – lies over the brain tissue * Arachnoid – middle layer between the dura mater and pia mater * Subarachnoid space – between the pia mater and arachnoid |
|
|
Define meningitis
|
inflammation of the membranes covering the brain and spinal cord
|
|
|
Define Septic meningitis
|
infection due to bacterial invasion from hematogenous spread
|
|
|
Define Aseptic meningitis
|
inflammation of the meninges due to causes other than bacteria
|
|
|
Define Acute vs. Chronic
meningitis |
Hours to days vs. > 4 weeks
|
|
|
Define Encephalitis
|
Inflammation of the brain
|
|
|
What are the methods of developing bacterial memingitis?
|
* Hematogenous – most common
- Spread from the blood * Contiguous - Translocation from parameningeal focus (e.g. sinusitis, otitis media) * Inoculation - Direct entry (e.g. head trauma, neurosurgery) |
|
|
Discuss Hematogenous Spread
|
* Nasopharyngeal colonization
- N. meningitidis - H. influenzae - strep pneumoniae * Systemic invasion causing bacteremia * Bacteria becomes encapsulated protecting it from host defenses |
|
|
How are the meninges invaded by bacteria?
|
* Bacteria in the blood replicate to sufficient numbers to invade BBB
* Mechanism of entry - Unknown – possibly adherence to cerebral capillaries or epithelium of choroids plexus |
|
|
How do bacteria survive in the subarachnoid space?
|
CSF host defenses are poor allowing bacterial proliferation
|
|
|
Subarachnoid Inflammation
|
* Mediated by contents within bacterial cell wall
- Lipopolysaccharide, endotoxin, teichoic acid * Production of inflammatory cytokines - IL-1, IL-6, prostaglandins, TNF, etc. * Inflammation causes increased permeability of BBB |
|
|
Manifestations of Menigitis
|
* Influx of albumin
- Brain edema - Increased intracranial pressure - Altered cerebral blood flow * Neuronal injury, cerebral ischemia, and irreversible brain damage - Loss of cerebrovascular autoregulation |
|
|
Risk Factors for developing meningitis
|
* Respiratory tract infections
* Otitis media * Cochlear implants * Head trauma * Alcoholism * Cigarette smoking or exposure * High-dose steroids * Splenectomy * Sickle cell disease * Immunoglobulin deficiency * Immunosuppression |
|
|
Presentation and Diagnosis of meningitis
|
* Headache, stiff neck (>90%)
* Fever (>90%) * Altered mental status (>80%) * Kernig’s sign (>50%) - Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees. * Brudzinski’s sign (>50%) - Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed. * Vomiting (35%) * Seizures (30%) * Focal deficits (10-20%) |
|
|
Diagnosis of meningitis
|
* Culture and sensitivities of urine, blood, sputum
* CBC - increased WBC > 10,000 cells/uL - increased Neutrophils with bandemia * CT scan for hydrocephalus or abscesses * Lumbar puncture for CSF examination - increased opening pressures > 180 mm H20 |
|
|
Manifestations of Menigitis
|
* Influx of albumin
- Brain edema - Increased intracranial pressure - Altered cerebral blood flow * Neuronal injury, cerebral ischemia, and irreversible brain damage - Loss of cerebrovascular autoregulation |
|
|
Risk Factors for developing meningitis
|
* Respiratory tract infections
* Otitis media * Cochlear implants * Head trauma * Alcoholism * Cigarette smoking or exposure * High-dose steroids * Splenectomy * Sickle cell disease * Immunoglobulin deficiency * Immunosuppression |
|
|
Presentation and Diagnosis of meningitis
|
* Headache, stiff neck (>90%)
* Fever (>90%) * Altered mental status (>80%) * Kernig’s sign (>50%) - Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees. * Brudzinski’s sign (>50%) - Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed. * Vomiting (35%) * Seizures (30%) * Focal deficits (10-20%) |
|
|
Diagnosis of meningitis
|
* Culture and sensitivities of urine, blood, sputum
* CBC - increased WBC > 10,000 cells/uL - increased Neutrophils with bandemia * CT scan for hydrocephalus or abscesses * Lumbar puncture for CSF examination - increased opening pressures > 180 mm H20 |
|
|
CSF Lab Parameters
|
|
|
|
Manifestations of Menigitis
|
* Influx of albumin
- Brain edema - Increased intracranial pressure - Altered cerebral blood flow * Neuronal injury, cerebral ischemia, and irreversible brain damage - Loss of cerebrovascular autoregulation |
|
|
Risk Factors for developing meningitis
|
* Respiratory tract infections
* Otitis media * Cochlear implants * Head trauma * Alcoholism * Cigarette smoking or exposure * High-dose steroids * Splenectomy * Sickle cell disease * Immunoglobulin deficiency * Immunosuppression |
|
|
Presentation and Diagnosis of meningitis
|
* Headache, stiff neck (>90%)
* Fever (>90%) * Altered mental status (>80%) * Kernig’s sign (>50%) - Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees. * Brudzinski’s sign (>50%) - Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed. * Vomiting (35%) * Seizures (30%) * Focal deficits (10-20%) |
|
|
Diagnosis of meningitis
|
* Culture and sensitivities of urine, blood, sputum
* CBC - increased WBC > 10,000 cells/uL - increased Neutrophils with bandemia * CT scan for hydrocephalus or abscesses * Lumbar puncture for CSF examination - increased opening pressures > 180 mm H20 |
|
|
CSF Lab Parameters
|
|
|
|
Pathogens involved in meningitis
|
* Historically - 1980’s
- 45% H. influenzae - 18% S. pneumoniae - 14% N. meningitidis * After 1990 - H. influenzae vaccine - 47% S. pneumoniae - 25% N. meningitidis - 8% L. monocytogenes - 7% H. influenzae * After 2000 – Pneumococcal vaccine - Children < 2: 70% decline in pneumococcal meninigitis - Children < 5: 60% decline - Adult invasive S. pneumo infections decreased as well |
|
|
Haemophilus influenzae in meningitis
|
* Only accounts for 7% of cases
- Decreased due to vaccination programs - Vaccination starts at 2 months of age * Mortality ~ 6% * Close contact transmission |
|
|
Neisseria Meningitidis in meningitis
|
* Accounts for 25% of cases
* 60% of cases in 2-18 years of age * Mortality rate ~ 10% * Easily transmitted to close contacts * Unique Immune reaction - Fever, arthritis, pericarditis approximately 10-14 days after infection * Petechiae in 50% of patients |
|
|
Streptococcus Pneumoniae in meningitis
|
* Most common cause of meningitis in adults
* Mortality - Adults 20-30% - Children 4-17% * Coma and seizures common * 29-56% of patients have neurologic sequelae |
|
|
Listeria monocytogenes in meningitis
|
* ~ 8% of meningitis cases
* ~ 20% of cases in > 60 yo * Mortality ~ 15% * GI bug - Milk, cheese, poultry, beef * Neonates, alcoholics, immunosuppressed, and elderly |
|
|
Desired Antimicrobial Characteristics in meningitis
|
* Coverage of likely pathogens
* Bactericidal activity * Therapeutic levels achieved in the CSF * Antimicrobial activity may promote release of bacterial factors that promote inflammation |
|
|
Factors impacting antimicrobial penetration into the CNS
|
* Meningeal inflammation
- Increases antibiotic penetration * Molecular weight - Lower MW compounds pass through easier * Lipid solubility - Higher lipid solubility passes through easier * pH - Un-ionized compounds can diffuse the BBB * Protein binding - Only free drug can diffuse across the BBB |
|
|
Antimicrobial CSF Penetration:
Agents with Very Good penetration |
Chloramphenicol, metronidazole, TMP/SMX, rifampin and other TB drugs
(penetrate CSF well regardless of meningial inflammation) |
|
|
Antimicrobial CSF Penetration:
Agents with Good penetration |
PCNs, most 3rd and 4th generation cephalosporins, carbapenems, Fluoroquinolones, vancomycin, linezolid, acyclovir
(Adequate CSF penetration achieved when meninges are inflammed) |
|
|
Antimicrobial CSF Penetration:
Agents with Fair to Poor penetration |
Aminoglycosides, macrolides, cefazolin, amphotericin B, itraconazole
(inadequate penetration even with meningeal inflammation) |
|
|
Ways to Increase CSF Concentrations of antibiotics
|
* High dose therapy
- Examples: * Ceftriaxone 2g q12h * Vancomycin 30-40mg/kg/day * Ampicillin 2g IV q4h * Direct instillation of antibiotics into the CSF - Intrathecal or intraventricular administration * Block drug transport out of the CNS - Probenicid |
|
|
Empiric Antibiotic Selection for children ages 0-4 weeks old with bacterial meningitis
|
* Pathogens
- Strep agalactiae, Enterococcus, Listeria monocytogenes, E. coli, Klebsiella, Enterobacter * Treatment - Ampicillin + cefotaxime or gentamicin |
|
|
Empiric Antibiotic Selection for children ages 1 month to 4 years old with bacterial meningitis
|
* Pathogens
- H. influenzae - N. meningitidis - Strep pneumoniae * Treatment - Cefotaxime or ceftriaxone ± Vancomycin Cefotaxime is alternative to Ceftriaxone in all cases. However, neonates should only receive cefotaxime, not ceftriaxone (it may cause biliary sludging). Vancomycin should be given based upon local incidence of penicillin resistant S. pneumoniae. Give Vancomycin until minimum inhibitory concentrations (MICs) for cefotaxime or ceftriaxone are available |
|
|
Empiric Antibiotic Selection for ages 5 years to 29 years old with bacterial meningitis
|
* Pathogens
- H. influenzae - N. meningitidis - Strep pneumoniae * Treatment - Ceftriaxone ± Vancomycin Cefotaxime is alternative to Ceftriaxone in all cases. However, neonates should only receive cefotaxime, not ceftriaxone (may cause biliary sludging). Vancomycin should be given based upon local incidence of penicillin resistant S. pneumoniae. Give Vancomycin until minimum inhibitory concentrations (MICs) for cefotaxime or ceftriaxone are available |
|
|
Empiric Antibiotic Selection for ages 30-60 years old with bacterial meningitis
|
* Pathogens
- N. meningitidis _ Strep pneumoniae * Treatment - Ceftriaxone ± Vancomycin Cefotaxime is alternative to Ceftriaxone in all cases. However, neonates should only receive cefotaxime, not ceftriaxone (may cause biliary sludging). Vancomycin should be given based upon local incidence of penicillin resistant S. pneumoniae. Give Vancomycin until minimum inhibitory concentrations (MICs) for cefotaxime or ceftriaxone are available |
|
|
Empiric Antibiotic Selection for ages > 60 years of ageold with bacterial meningitis
|
* Pathogens
- Strep pneumoniae - Listeria monocytogenes - E. coli - Klebsiella - Enterobacter * Treatment - Ampicillin + Ceftriaxone or Aminoglycoside ± Vancomycin Aminoglycosides – gentamicin, tobramycin, or amikacin Cefotaxime is alternative to Ceftriaxone in all cases. However, neonates should only receive cefotaxime, not ceftriaxone (may cause biliary sludging). Vancomycin should be given based upon local incidence of penicillin resistant S. pneumoniae. Give Vancomycin until minimum inhibitory concentrations (MICs) for cefotaxime or ceftriaxone are available |
|
|
Empiric Antibiotic Selection for Immunocompromised patients with bacterial meningitis
|
* Pathogens
- Any including Viral and Fungal * Treatment - Vancomycin + ceftazidime or - cefepime +/- Rifampin +/- fluconazole +/- acyclovir |
|
|
Microbe Specific Therapy in meningitis
|
* Adjust and narrow antimicrobial therapy as indicated
* Set duration of therapy - Typically 7-14 days * H. Influenzae, Strep Pneumo, N. Meningitidis - 21 days if resistant gram negative or viral |
|
|
Adjunctive Therapy for meningitis
|
* Glucocorticoids
- Children 8 weeks to 12 years old + Dexamethasone 0.6 mg/kg/day IV divided q6h for 2-4 days + Reduces neurologic and audiologic sequelae of H. influenzae and Strep pneumoniae - Adults + Dexamethasone 10mg IV q6h x 4 days + Reduces mortality, neurologic, and audiologic sequelae of all cause meningitis *Majority of benefit seen with S. pneumoniae meningitis - Administer at or up to 15 minutes before initiation of antimicrobial therapy - Dexamethasone decreases mortality for Mycobacterium tuberculosis meningitis, but does not prevent disability |
|
|
What might be a downfall to steroid therapy in meningitis?
A. Immunosuppression B. Decreased antibiotic penetration into CSF C. Drug interactions D. Decreased antibiotic effectiveness E. GI bleed F. Increased blood glucose G. All of the above |
All of the above
|
|
|
Prevention Chemoprophylaxis of meningitis
|
* H. influenzae
- Child <4 years of age and unvaccinated - Child care facilities - Nursing home residents - Rifampin 20mg/kg/day up to 600mg po qd for 4 days - Minocycline is alternative in adults * Strep pneumoniae - Generally not recommended * N. Meningitidis - All close contacts (home and daycare) - Rifampin 10mg/kg q12h up to 600mg po q12h x 48 hours - Ciprofloxacin 500mg x 1 or ceftriaxone 125mg or 250mg IM x 1 are alternatives * Strep agalactiae - High risk deliveries - Ampicillin 1-2 grams q6hrs until delivery - Clindamycin or erythromycin for penicillin allergy |
|
|
Immunoprophylaxis for meningitis
|
Immunoprophylaxis
Vaccinations * H. influenzae - 4 doses for initial immunization * Strep pneumoniae - Infants - >65 years old - DM, CAD, COPD, chronic liver disease, asplenic, alcoholics, immunosuppressed * N. meningitidis - Not routine – 1 dose if adult, 2 doses if <10 yo Asplenic patients should receive vaccination against H.influenzae, strep pneumoniae, and N. meningitidis. |
|
|
Monitoring Parameters
|
* Similar to other infectious diseases
* Clinical signs and symptoms - Fever, AMS, Stiff neck - Improvement should occur within 24-48 hours * Laboratory tests - CBC with diff, chem-7, renal function * Antibiotic side effects |
|
|
Other CNS Infections
|
Mycobacterium Tuberculosis
Viral Fungal Parasite Drug induced Shunt Infections Brain Abscess |
|
|
Viral Encephalitis
|
* Enteroviruses (polio, coxsackie), mumps, herpes simplex, adenovirus, cytomegalovirus, lymphocytic choriomeningitis virus, Epstein-Barr, varicella, and HIV.
* Diagnosis - PCR * Presentation - Headache, mild fever, nuchal rigidity, malaise, drowsiness, nausea, vomiting, and photophobia * Herpes simplex virus - Acyclovir 10mg/kg IV q8h for 14-21 days - Alternative: Foscavir 40mg/kg q8h * Cytomegalovirus (CMV) - Ganciclovir 5mg/kg IV q12h x 14 days - Continue maintenance ganciclovir or valganciclovir QD |
|
|
What might be a downfall to steroid therapy in CNS infections
Immunosuppression Decreased antibiotic penetration into CSF Drug interactions Decreased antibiotic effectiveness GI bleed Increased blood glucose All of the above |
Increased blood glucose
All of the above |
|
|
what is the key point with adding steroids in the treatment on CNS infections
|
have to be given at pr up to 15 minutes prior Ab because want to prevent the inflammaiton caused by the breaking of the bacterial cell membranes, thus releasing endotoxins
there is no benefit if you give them after AB |
|
|
RM is a 3 week old WM brought to the ED by his parents after 24 hours of fussiness, emesis/spitting, and fever (100.6 F).
In the ED the patient experienced a seizure with arm, leg, and neck involvement. IV lorazepam was given and stopped the seizure. The patient was loaded with 20mg/kg phenobarbital Lumbar Puncture Results CSF Protein 156, glucose 20, WBC 15, RBCs 5 Gram stain results pending What is the appropriate empiric antimicrobial therapy? Vancomycin + Rifampin Ampicillin + Gentamicin Ceftriaxone + Vancomycin Cefepime + Ampicillin + Dexamethasone |
Ampicillin + Gentamicin
|
|
|
RM’s gram stain of the CSF comes back as gram negative diplococci and he is believed to have N. meningitidis.
You also notice RM’s two year old sister running around the NICU. Does RM’s sister need prophylaxis and if so what are the apropriate agents A. Ampicillin + Cefotaxime B. Rifampin x 48hrs C. Ciprofloxacin x 1 dose D. Minocycline x 48hrs |
yes
B. Rifampin x 48hrs |
|
|
RM’s gram stain of the CSF comes back as gram negative diplococci and he is believed to have N. meningitidis.
You also notice RM’s two year old sister running around the NICU. Cultures from the CSF confirm that RM has N. Meningitidis meningitis How would you change RMs current therapy? DC gentamicin and continue ampicillin for 8 weeks DC gentamicin and ampicillin. Start cefotaxime and treat for a total of 7 days. DC gentamicin and start Vancomycin for 14 days Continue current therapy for 10 days |
DC gentamicin and ampicillin. Start cefotaxime and treat for a total of 7 days.
|
|
|
BM is a 75 yo WM who comes into the ED with altered mental status, fever, increased WBCs and headache. CSF results show increased protein, 10,000 WBCs, glucose 20. Gram stain is pending.
His PMH is significant for a anaphylactic allergy to Penicillin. HOw would you treat Vancomycin + Ceftriaxone + Ampicillin Vancomycin + Aztreonam Vancomycin + Chloramphenicol + TMP/SMX Aztreonam + TMP/SMX |
Vancomycin + Chloramphenicol + TMP/SMX
|
