Authors: Marina N. Boushra, MD (EM Resident Physician, Vidant Medical Center) and Cassandra Bradby, MD (EM Attending Physician, Vidant Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)
A 75-year-old man with a history of diabetes, hypertension, and dementia presents to the emergency department with a complaint of altered mental status. His nursing home caretaker endorses a dry cough for one week that has recently become productive and fevers with a Tmax of 38.9 ºC. She notes that he is not “acting like himself,” and elaborates that he is sleeping more, talking less, and has had multiple episodes of urinary incontinence, which is unusual for him. His vitals on arrival are T 38.5º C, HR 110, RR 30, BP 100/70. His exam is notable for somnolence, increased work of breathing with accessory muscle use, coarse rales at the base of the right lung, tachycardia, and dry mucus membranes.
Bacterial infections are a common diagnosis in the emergency department, and emergency physicians are often tasked with providing antibiotics for outpatient management or beginning antibiotics prior to admission. Antibiotic treatment is not without side effects, and treatment started in the emergency department is frequently empiric. Therefore, an understanding of the most likely causative organisms as well as local patterns of susceptibility and resistance is paramount to adequate treatment, appropriate antibiotic selection, and responsible antibiotic stewardship. Important historical details to elicit include allergies, recent antibiotic use, prior antibiotic failure, dialysis use, use of immunosuppressants or history of immunocompromise, culture results of prior infections, and contact with healthcare facilities, including recent hospitalization, living in a care facility, or recent invasive procedures such as ureteral catheterizations or intubation. These details offer vital information regarding possible bacterial resistance or the presence of opportunistic infection. Because multiple empiric regimens exist for infectious disease in the emergency department, contacting the hospital pharmacy about the local antibiogram may help tailor the empiric regimen to local microbial susceptibilities. Please keep this in mind with the recommendations discussed in each table. The following is a discussion of the most common or most emergent ED-diagnosed bacterial infections, their most likely causative organisms, and current recommendations for empiric treatment.
Pneumonia is infection of the pleural parenchyma and can be broadly divided into community-acquired (CAP) and hospital-acquired pneumonia (HAP). A third category of pneumonia, healthcare-associated pneumonia, is discussed in more detail later in this paper. The majority of pneumonia is community-acquired but historical details such as recent hospitalization, intubation, or ventilator dependence should raise concern for HAP and multi-drug resistant organisms (MDROs). Travel history may be important for more rare causes of pneumonia. In patients with known or suspected HIV or AIDS, pneumocystis pneumonia should be strongly considered.
Community-Acquired Pneumonia (CAP)
CAP can be caused by a variety of pathogens, with the most common bacterial cause being Streptococcus pneumonia1–3. Other common organisms include respiratory viruses, Haemophilus influenza, and Mycoplasma pneumoniae1–3. In patients requiring ICU admission, S. pneumoniae is still common, but there is increased prevalence of Legionella pneumophila, Staphylococcus aureus, gram-negative bacilli, and influenza4. It is important to remember these differences in etiology and to cover adequately for these serious organisms in patients requiring ICU admission. Patients with risk factors for aspiration pneumonia should receive additional anaerobic coverage. Treatment for CAP has become increasingly more complicated due to rising resistance to antibiotics. Risk factors for drug resistance include age >65, alcoholism, medical comorbidities, immunosuppressive illness or medication use, and use of beta-lactam, macrolide, or fluoroquinolone antibiotics in the last 3-6 months5,6.
Treatment should be initiated as soon as a diagnosis of CAP is made to prevent decompensation. CAP can often be treated on an outpatient basis. Studies have shown that physicians often use inconsistent criteria when making the decision to admit patients for the treatment of CAP and overestimate short-term patient mortality, leading to an increased rate of unnecessary hospitalizations7. The 2007 guidelines for the Infectious Disease Society of America (IDSA) and the American Thoracic Society (ATS) recommend using the CURB-65 score or Pneumonia Severity Index (PSI), both well validated prediction rules and decision aids, to aid in the risk stratification of patients and making the decision to admit for inpatient treatment7–9. Interestingly, a recent article investigating oral vs. intravenous fluoroquinolones for non-critically ill patients with CAP showed no difference in mortality, ICU transfers, or need for vasopressors or intubation10. Studies have shown shorter time to treatment and shorter hospital stays for patients started on oral rather than intravenous antibiotics11. As such, it is important to consider oral therapy in non-critically ill patients with CAP who are being admitted for treatment but are able to tolerate oral medication.
Studies have shown similar efficacy in CAP for fluoroquinolones and macrolides plus a penicillin or cephalosporin12. Importantly, there is a high rate of macrolide resistance in S. pneumoniae in the United States; as such, macrolides should not be used as empiric monotherapy in areas where resistance to macrolides is >25%5,13–15. Recommended regimens are outlined in the Table 1 below. The IDSA is expected to publish new guidelines for the treatment of CAP that better reflect current trends in resistance in the summer of 2017.
Hospital-Acquired (nosocomial) Pneumonia (HAP)
Pneumonia patients with recent hospitalizations present a challenge in antibiotic selection. While the pneumonia may be caused by an MDRO picked up in the healthcare environment, it is also possible that the patient has a simple community-acquired organism. The multi-drug resistant (MDR) score assesses a particular patient’s risk for infection with an MDRO16,17. Patients with a high MDR score should be presumed to have a pneumonia due to a resistant organism and treated accordingly with broad-spectrum coverage as outlined in Table 1 below. Patients with low MDR scores can be treated with the more narrow-spectrum coverage used for CAP, with the possibility of widening the spectrum in the event of treatment failure. The Shorr score is a similar scoring tool to assess the risk of infection by an MDR and tailor empiric coverage appropriately18. Antibiotic treatment for presumed HAP should cover for Staphylococcus aureus and Pseudomonas aeruginosa19. Local antimicrobial prevalence and susceptibility, especially within the hospital, is helpful to determining a regimen, but can often be deferred to the judgement of the admitting team. Empiric regimens as recommended in the 2016 IDSA/ATS guidelines for empiric management of HAP are outlined in Table 1 below.
Healthcare-Associated Pneumonia (HCAP)
Healthcare-associated pneumonia (HCAP) refers to pneumonia that may have been acquired in healthcare facilities such as nursing homes and dialysis centers. It was formerly grouped with HAP due to presumed increased susceptibility to MDROs. Several studies, however, have shown no increased susceptibility to MDROs in patient with HCAP, and it is conspicuously missing from the IDSA/ATS guidelines on the management of HAP19–24. As such, in the absences of other historical susceptibilities to MDROs such as comorbidities or severe illness, patients with HCAP may be treated as CAP19–24.
Table 1: Empiric Treatment of Pneumonia based on type, setting, and patient-specific factors8,19
|CAP||Outpatient||No recent antibiotics, co-morbidities, high-rate of resistance||-Doxycycline 100mg bid for five days
-Azithromycin 500mg on day 1 followed by 250mg for four days.*
-Clarithromycin 500mg bid for seven days*
|Recent antibiotics, co-morbidities, high-rate of resistance||-Levofloxacin 750mg daily for five days
-Moxifloxacin 400mg daily for five days
-Gemifloxacin 320mg daily for five days
-Combination therapy with a beta-lactam (amoxicillin 1g tid, amoxicillin-clavulanate 2g bid, cefpodoxime 200mg bid, or cefuroxime 500mg bid) PLUS either a macrolide (azithromycin 500mg on day 1, followed by 250mg for four days, or clarithromycin 500mg bid for five days) or doxycycline 100mg bid for five days.
|Inpatient||Mild-Moderate disease, managed on general floor||-Levofloxacin 750mg IV or po
-Moxifloxacin 400mg IV or po
-Combination therapy with a beta-lactam (cefotaxime 1-2g, ampicillin-sulbactam 1.5-3g, ceftriaxone 1-2g) PLUS a macrolide (azithromycin 500mg IV, or clarithromycin 500mg orally)
|Severe disease requiring ICU admission||-Combination therapy with a beta-lactam (cefotaxime 1-2g, ampicillin-sulbactam 1.5-3g, ceftriaxone 1-2g) PLUS a respiratory fluoroquinolone (levofloxacin 750mg IV, or moxifloxacin 400mg IV) OR azithromycin 500mg IV.
-If penicillin allergic, a respiratory fluoroquinolone PLUS aztreonam 1g
-If MRSA suspected, add vancomycin 15-20mg/kg IV
|HAP||Inpatient||Combination therapy is warranted, with one from each of the following 3 categories:
1) Piperacillin-tazobactam 4.5 g IV, Cefepime 2 g IV, Ceftazidime 2g IV, Imipenem/cilastatin 500mg IV
2) Azithromycin 500mg IV, Ciprofloxacin 400mg IV, Levofloxacin 750mg IV, or Gentamicin 5-7mg/kg IV
3) Vancomycin 15-20mg/kg IV, Linezolid 600mg IV
*Macrolide antibiotics should not be used as empiric monotherapy in areas of known S. pneumoniae resistance >25% to macrolides. If such resistance exists, pair with a beta-lactam as shown in the table above.
Urinary Tract Infection
Urinary tract infections can involve the lower urinary tract (cystitis) or the upper tract (pyelonephritis). Urinary tract infections are very common in women, with sexually active women being at higher risk. Risk factors for urinary tract infections include recent sexual intercourse, prior urinary tract infections, and recent spermicide use25. When present in men, urinary tract infections are typically associated with underlying anatomical anomalies, recent catheterization, or other risk factors. While not all urinary tract infections in males are necessarily complicated, a search for these risk factors should be conducted when a male is diagnosed with a urinary tract infection.
Urinary tract infections in women begin by bacterial colonization of the vagina by fecal bacteria, which may ascend via the urethra to infect the bladder and kidneys. Uncomplicated cystitis and pyelonephritis in women is typically caused by Escherichia coli, though Proteus mirabilis, Klebsiella pneumoniae, and Streptococcus saprophyticus are occasionally found26,27. Empiric treatment for uncomplicated urinary tract infections is best tailored to the regional E. coli sensitivities and is outlined in Table 328. Of note, this table may be modified based on local resistance patterns. Sterile pyuria should raise concern for a possible sexually-transmitted infection (STI) and patients who fail to improve despite appropriate antibiotic treatment should be tested for STI.
Complicated Urinary Tract Infection
A complicated urinary tract infection is one which is associated with a condition that increases the risk for therapeutic failure, as outlined in Table 2. The microbial spectrum of complicated UTI is more broad, including not only the typical organisms associated with uncomplicated UTI but also more varied and resistant pseudomonal, staphylococcal, and Serratia species as well as fungi29,30. Complicated lower urinary tract infections may be managed as an outpatient, but indications for hospitalization include inability to tolerate oral therapy or suspected/ documented infection with a resistant organism such as extended-spectrum beta-lactamase producing organisms (ESBLs). Complicated pyelonephritis is the progression of infection resulting in emphysematous pyelonephritis, corticomedullary or perinephric abscess, or papillary necrosis. Complicated pyelonephritis is an indication for admission and intravenous antibiotic treatment.
Table 2: Conditions that increase the risk of treatment failure in UTI (complicated UTI)
|Anatomic abnormality of the urinary tract|
|Symptoms >7 days prior to presentation|
|Presence of an indwelling foreign body (ureteral catheter, nephrostomy tube, ureteral stent)|
UTI and Asymptomatic Bacteriuria in the Pregnant Patient
Urinary tract infection and colonization in pregnant patients are worth special mention. While asymptomatic bacteriuria in a non-pregnant female does not warrant treatment, studies have shown a high rate of progression to symptomatic cystitis and pyelonephritis in pregnant patients31. As such, current recommendations suggest that any bacteriuria in a pregnant patient should be treated with antibiotics32. Additionally, although urinary tract infection in a pregnant woman is, by definition, complicated, fluoroquinolones, the first-line treatment for complicated cystitis, are a pregnancy class C medication and should be avoided33. Mild urinary tract infections in pregnant females are treated similarly to uncomplicated UTIs, as shown in Table 3 below. Follow-up cultures for resolution are important in this patient population34.
Table 3: Empiric treatment of uncomplicated and complicated urinary tract infections28,31,35.
|Urinary Tract Infection||Recommended regimen|
|Uncomplicated cystitis||-Nitrofurantoin 100mg bid for five days*
-Trimethoprim-sulfamethoxazole 160/800mg bid for three days
-Cephalexin 500mg BID for 3-7 days
-Fosfomycin 3g in a single dose*
-Ciprofloxacin 250mg bid or Levofloxacin 250mg once per day for three days**
-Ciprofloxacin 500mg bid or 1000mg daily for five to ten days
-Levofloxacin 750mg daily for five to ten days
-Levofloxacin 500mg IV
-Ceftriaxone 1g IV
-Ertapenem 1g IV
-Gentamicin 3-5mg/kg IV +/- ampicillin 1-2g every 4-6 hours***
-Tobramycin 3-5mg/kg IV +/- ampicillin 1-2g every 4-6 hours***
-Ciprofloxacin 500mg po bid for seven days or 1000mg daily for seven days
-Levofloxacin 750mg po daily for five to seven days
-Levofloxacin 500mg IV
-Ceftriaxone 1g IV
-Ertapenem 1g IV
-Gentamicin 3-5mg/kg IV
-Tobramycin 3-5mg/kg IV
|Complicated Pyelonephritis –||Inpatient, mild-moderate disease:
-Ceftriaxone 1g IV
-Ciprofloxacin 400mg IV
-Levofloxacin 750 mg IV
-Aztreonam 1g IV
Inpatient, severe disease:
-Cefepime 2g IV
-Ampicillin 1g IV four times per day plus Gentamicin 5mg/kg IV daily
-Piperacillin-tazobactam 3.375g IV
-Meropenem 500mg IV
-Imipenem 500mg IV
-Doripenem 500mg IV
|Asymptomatic bacteriuria and acute cystitis in the pregnant patient||-Nitrofurantoin 100mg po bid for five to seven days (in second or third trimester)*
-Trimethoprim-sulfamethoxazole 160/800 mg po bid for three days****
-Fosfomycin 3g po in a single dose*
-Amoxicillin-clavulanate 500mg po tid for three to seven days
-Cephalexin 500mg po bid for three to seven days
-Cefpodoxime 100mg po bid for three to seven days
*Fosfomycin and nitrofurantoin should be avoided if there is concern for early pyelonephritis.
**Fluoroquinolones, if possible, should be reserved for other important uses to avoid resistance against this class of antibiotics.
***Adding ampicillin provides Enterococcus coverage
****Should be avoided in first trimester and at term
Cellulitis and Soft-Tissue Infection
Cellulitis and Erysipelas
Cellulitis and erysipelas are bacterial skin infections that differ in that erysipelas involves the upper dermis and superficial lymphatics while cellulitis involves the deeper dermis and subcutaneous fat tissue. Both manifest with localized skin erythema, edema, warmth, and pain. Because of the more superficial nature of erysipelas, these lesions are typically more raised and better demarcated than cellulitis. Erysipelas also presents more acutely and with more systemic symptoms such as fevers and chills. The most common pathogens in cellulitis are beta-hemolytic streptococci and S. aureus, including methicillin-resistant S. aureus (MRSA)36–38. Beta-hemolytic streptococci are the most common cause of erysipelas36,39.
Lesions consistent with cellulitis should be examined closely for the presence of a drainable abscess. History is particularly important in the patient with possible cellulitis as cellulitis associated with human or animal bites or with water exposure needs different coverage than uncomplicated cellulitis. The presence of an indwelling device near the region of cellulitis is also important, as it is an indication of device infection.
The treatment of uncomplicated cellulitis is based on whether or not there is associated purulence. Current guidelines group erysipelas with non-purulent cellulitis in terms of treatment, as the lesions are often difficult to distinguish from each other and are caused by a similar spectrum of organisms. Patients with purulent cellulitis should receive empiric coverage for MRSA pending culture results40. Patients with non-purulent cellulitis or erysipelas should receive empiric coverage for beta-hemolytic streptococcus and MSSA, although patients with systemic symptoms, recurrent infection, or prior infection with MRSA should receive additional MRSA coverage36. Cellulitis can typically be managed as an outpatient; patients with signs of systemic toxicity, rapid progression, indwelling devices, or failure of outpatient management should be admitted for parenteral antibiotics. In addition to antibiotics, elevation of the affected area is an important aspect of treatment as it helps promotes drainage of edema and inflammatory substances, speeding symptomatic improvement36.
Table 4: Empiric treatment of cellulitis and erysipelas36
|Uncomplicated nonpurulent cellulitis without MRSA risk factors or erysipelas||Outpatient||-Dicloxacillin 500mg po qid for 5-10 days
-Cephalexin 500mg po qid for 5-10 days
-Clindamycin 450mg po tid for 5-10 days
|Inpatient||-Cefazolin 1-2g IV tid
-Ceftriaxone 1g IV every 24 hours
-Oxacillin or nafcillin IV every 4 hours
-Clindamycin 600-900mg IV tid
|Uncomplicated purulent cellulitis or nonpurulent cellulitis with MRSA risk factors
|Outpatient||-Clindamycin 300-450mg po 3-4 times per day for 5-7 days
-Trimethoprim/sulfamethoxazole 1-2 DS tablets po bid for 5-7 days
-Doxycycline 100mg bid for 5-7 days
|Inpatient||-Vancomycin 15-20mg/kg/dose IV bid
-Clindamycin 600mg IV tid
-Linezolid 600mg IV two times per day
-Daptomycin 4mg/kg/dose IV once daily
Skin abscesses are most commonly due to S. aureus (MRSA or MSSA), although polymicrobial infection with flora from the skin or adjacent mucosal tissues is also common36,40–42. Risk factors for MRSA infection include recent hospitalization or antibiotic use, contact with healthcare environments, institutionalization, HIV infection, intravenous drug use, and diabetes. Source control, in the form of warm compresses to promote drainage or incision and drainage, is important. The role of antibiotics following source control is debated. Studies have shown a slightly increased cure rate with the use of antibiotics following incision and drainage of uncomplicated abscesses, but also a higher rate of diarrhea and adverse effects43,44. Antibiotics should be started for large (>2cm) or multiple abscesses, extensive surrounding cellulitis, systemic symptoms, immunocompromise or co-morbidities, the presence of an indwelling device, or in cases where incision and drainage alone fails to achieve adequate clinical response36. Hospitalization and parenteral antibiotics should be considered for patients with extensive skin involvement or signs of systemic toxicity.
Table 5: Empiric antibiotic treatment of abscesses following source control36
|Outpatient||If suspicion for MRSA:
-Clindamycin 300-450mg po 3-4 times per day for 5-7 days
-Trimethoprim/sulfamethoxazole 1-2 DS tablets po bid for 5-7 days
-Doxycycline 100mg po bid for 5-7 days
If no suspicion for MRSA:
-Dicloxacillin 500mg po bid for 5-7 days
-Cephalexin 500mg po bid for 5-7 days
|Inpatient||-Vancomycin 15-20mg/kg/dose IV bid
-Clindamycin 600mg IV tid
-Linezolid 600mg IV two times per day
-Daptomycin 4mg/kg/dose IV once daily
Sexually-Transmitted and Vulvovaginal Infections
Sexually transmitted infections (STI) are a diagnosis of immense public health importance. While the results of lab testing are often not available in the emergency department, physicians should have a low threshold for the initiation of treatment in patients with presentations consistent with STI. Treatment for common STIs is outlined in Table 6 below45. Counseling patients about safe sex practices and urging them to inform their partners is paramount to infection control.
Pelvic Inflammatory Disease
Pelvic inflammatory disease (PID) is infection of the upper genital tract (uterus, endometrium, fallopian tubes, ovaries) in women. PID may extend to involve adjacent structures, causing periappendicitis, pelvic peritonitis, and perihepatitis (Fitz-Hugh-Curtis syndrome). The majority of PID is caused by ascending sexually-transmitted infections (STI), with Neisseria gonorrhea and Chlamydia trachomatis being the most commonly implicated pathogens in PID45. The diagnosis of PID is often a presumptive one based on presentation. Due to the risk for tubal scarring leading to infertility or risk of ectopic pregnancy, even minimal symptoms without an alternative diagnosis warrant the start of antibiotic therapy to reduce the risk of serious complications due to delay of therapy. Mild to moderate disease can be treated as an outpatient. Indications for hospitalization and intravenous antibiotics include pregnancy, clinically severe disease, complicated PID (pelvic abscess), and intolerance to, noncompliance with, or failure of oral antibiotics. Empiric coverage for inpatient and outpatient management of pelvic inflammatory disease are outlined in Table 646,47.
Table 6: Recommended treatment regimens for select genitourinary infections45–47
|Chlamydia||-Azithromycin (1g po in one dose)
-Doxycycline (100mg bid for 7 day)
|Gonorrhea*||-Ceftriaxone (250mg IM or IV in one dose) plus azithromycin (1g po in one dose) or doxycycline (100mg bid for 7 days)|
|Trichomonas||-Metronidazole (2g po in a single dose or 500mg bid for seven days)
-Tinidazole (2g po in a single dose)
|Bacterial Vaginosis||-Metronidazole (500mg po bid for seven days)
-Metronidazole vaginal gel 0.75% (5g intravaginally for five days)
-Clindamycin vaginal gel 2% (5g intravaginally for seven days)
|Candida Vulvovaginitis||–Fluconazole (150mg po in one dose)|
|Outpatient management||-Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)
-Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)
|Inpatient management||-Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)
-Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)
*Patients with gonorrhea should also be treated for chlamydia due to high rates of concomitant infection.
While meningitis is not as common an emergency department diagnosis as the bacterial infections discussed above, patients with meningitis are often quite ill, and knowledge of appropriate antibiotic coverage can speed time to therapy. The most common causes of community-acquired meningitis in adults in developed countries are Streptococcus pneumoniae, Neisseria meningitidis, and, in older adults, Listeria monocytogenes48,49. Empiric treatment should be initiated as soon as meningitis is suspected. Empiric regimens should include ceftriaxone (2g every 12 hours) or cefotaxime (2g every 4-6 hours) for coverage of N. meningitidis and S. pneumoniae as well as vancomycin due to increasing rates of S. pneumoniae resistance to third-generation cephalosporins50,51. In patients >50 years of age or with immunocompromise, ampicillin (2g every 4 hours) should be added to provide coverage for L. monocytogenes49.
Adverse Effects of Antibiotic Use
A discussion of antibiotic use in the emergency department would be remiss without mention of the adverse effects of antibiotics commonly used in the ED. While the use of certain antibiotics may be unavoidable due to patient allergies or susceptibility patters, knowledge of the adverse effects of antibiotics may help guide therapeutic choices and inform or temper patient expectations.
Clostridium difficile infection should always be a consideration when starting antibiotics. Clindamycin is the most common culprit in antibiotic-associated C. difficile infection, but cephalosporins, penicillins, and fluoroquinolones are also common causes52–56. Aminoglycosides, tetracyclines, metronidazole, and vancomycin are rarely associated with C. difficile infection, though any antibiotic use increases the risk for C. difficile infection57. Other important adverse effects include QT prolongation with arrhythmia associated with macrolide and fluoroquinolone use and the risk of peripheral neuropathy and (the uncommon, but oft-cited) tendon rupture with fluoroquinolone use. Common or serious side effects of antibiotics used in the emergency department are summarized in Table 7 below.
Table 7: Common and serious adverse effects of commonly used antibiotics
|Antibiotic||Common Adverse Effects||Serious Adverse Effects||Comments|
|Beta-lactams||C. diff infection, diarrhea||Hypersensitivity reactions||High risk of C. diff, especially with broader coverage and with ampicillin|
|Macrolides||Diarrhea, nausea, vomiting, abdominal pain||QT prolongation (especially with erythromycin)|
|Clindamycin||C. diff infection, diarrhea||Serious hypersensitivity reactions||Most common cause of C. diff|
|Fluoroquinolones||Anorexia, nausea, vomiting, abdominal pain||Tendon rupture, peripheral neuropathy, QT prolongation||High C. diff risk|
|Tetracyclines||Nausea, diarrhea, photosensitivity||Inhibition of bone growth and tooth discoloration (a concern in children)||Low C. diff risk|
|Vancomycin||Abdominal pain, nausea||Nephrotoxicity, ototoxicity, Red man syndrome, hypotension||Red man syndrome can be prevented with pretreatment with antihistamines|
|Aminoglycosides||Nephrotoxicity, ototoxicity||Need frequent monitoring of drug levels|
|Metronidazole||Headache, dizziness, metallic taste||Disulfiram-like reaction||Low C. diff risk|
Table 8: Common and serious bacterial infections and recommended empiric treatment
|Infection||Important organisms to cover||Recommended Regimens|
|Community-acquired pneumonia||S. pneumoniae||CAP outpatient: doxycycline, macrolide +/- penicillin or cephalosporin
CAP inpatient, mild: respiratory fluoroquinolone, macrolide + penicillin or cephalosporin
|S. pneumoniae, L. pneumophila, S. aureus||CAP inpatient, severe: penicillin or cephalosporin+ fluoroquinolone OR azithromycin|
|Hospital-acquired pneumonia||S. pneumoniae, MRSA, P. aeruginosa||HAP inpatient: anti-pseudomonal penicillin or cephalosporin, or fluoroquinolone, or carbapenem + vancomycin/linezolid|
|Uncomplicated cystitis||E. coli||Nitrofurantoin or fosfomycin or TMP/SMX or ciprofloxacin
|Complicated cystitis or uncomplicated pyelonephritis||E. coli, Pseudomonas sp., Staphylococcus sp.||Outpatient: Fluoroquinolone
Inpatient: Fluoroquinolone or aminoglycoside or third-generation cephalosporin or carbapenem
|Complicated pyelonephritis||E. coli, Pseudomonas sp., Staphylococcus sp.||Inpatient, mild-moderate: third-generation cephalosporin or monobactam
Inpatient, severe: anti-pseudomonal penicillin or cephalosporin, carbapenem
|Asymptomatic bacteriuria or simple cystitis in the pregnant patient||E. coli||Nitrofurantoin or TMP/SMX or fosfomycin, or penicillin or cephalosporin with gram-negative coverage|
|Nonpurulent cellulitis or abscess without MRSA risk factors, erysipelas||Beta-hemolytic streptococcal species, MSSA||Outpatient and inpatient: staphylococcal penicillin or cephalosporin|
|Purulent cellulitis, nonpurulent cellulitis or abscess with MRSA risk factors||Beta-hemolytic streptococcal species, MSSA, MRSA||Outpatient: Clindamycin or TMP/SMX or doxycycline
Inpatient: Vancomycin or clindamycin
|Chlamydia||C. trachomatis||Azithromycin or doxycycline|
|Gonorrhea||N. gonorrhea AND C. trachomatis||Ceftriaxone plus azithromycin or doxycycline|
|Trichomonas||Trichomonas vaginalis||Metronidazole or tinidazole|
|Bacterial vaginosis||Polymicrobial, anaerobic gram-negative rods||Metronidazole oral or intravaginal gel or clindamycin|
|Candida Vulvovaginitis||C. albicans, C. glabrata||Fluconazole|
|Pelvic Inflammatory Disease||N. gonorrhea, C. trachomatis||Inpatient and outpatient: third generation cephalosporin plus doxycycline|
|Bacterial meningitis||S. pneumoniae, N. meningitidis, L. monocytogenes (if >50 years or immunocompromised)||Vancomycin plus third generation cephalosporin +/- ampicillin if age >50 or immunocompromised|
References / Further Reading
- Johansson, N., Kalin, M., Tiveljung-Lindell, A., Giske, C. G. & Hedlund, J. Etiology of community-acquired pneumonia: increased microbiological yield with new diagnostic methods. Clin. Infect. Dis. 50, 202–9 (2010).
- Jain, S. et al. Community-Acquired Pneumonia Requiring Hospitalization among U.S. Adults. N. Engl. J. Med. 373, 415–27 (2015).
- Gadsby, N. J. et al. Comprehensive Molecular Testing for Respiratory Pathogens in Community-Acquired Pneumonia. Clin. Infect. Dis. 62, 817–23 (2016).
- Cillóniz, C. et al. Microbial aetiology of community-acquired pneumonia and its relation to severity. Thorax 66, 340–6 (2011).
- Vanderkooi, O. G. et al. Predicting antimicrobial resistance in invasive pneumococcal infections. Clin. Infect. Dis. 40, 1288–97 (2005).
- Ramsdell, J., Narsavage, G. L. & Fink, J. B. Management of Community-Acquired Pneumonia in the Home: An American College of Chest Physicians Clinical Position Statement. Chest 127, 1752–1763 (2005).
- Fine, M. J. et al. The hospital admission decision for patients with community-acquired pneumonia. Results from the pneumonia Patient Outcomes Research Team cohort study. Arch. Intern. Med. 157, 36–44 (1997).
- Mandell, L. A. et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin. Infect. Dis. 44 Suppl 2, S27-72 (2007).
- Lim, W. S. et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax 58, 377–82 (2003).
- Belforti, R. K. et al. Association Between Initial Route of Fluoroquinolone Administration and Outcomes in Patients Hospitalized for Community-acquired Pneumonia. Clin. Infect. Dis. 63, 1–9 (2016).
- Cyriac, J. M. & James, E. Switch over from intravenous to oral therapy: A concise overview. J. Pharmacol. Pharmacother. 5, 83–7 (2014).
- Ruhe, J. & Mildvan, D. Does Empirical Therapy with a Fluoroquinolone or the Combination of a β-Lactam Plus a Macrolide Result in Better Outcomes for Patients Admitted to the General Ward? Infect. Dis. Clin. North Am. 27, 115–132 (2013).
- Low, D. E. What Is the Relevance of Antimicrobial Resistance on the Outcome of Community-Acquired Pneumonia Caused by Streptococcus pneumoniae? (Should Macrolide Monotherapy Be Used for Mild Pneumonia?). Infect. Dis. Clin. North Am. 27, 87–97 (2013).
- Daneman, N., McGeer, A., Green, K., Low, D. E. & Toronto Invasive Bacterial Diseases Network. Macrolide resistance in bacteremic pneumococcal disease: implications for patient management. Clin. Infect. Dis. 43, 432–8 (2006).
- Jones, R. N., Sader, H. S., Moet, G. J. & Farrell, D. J. Declining antimicrobial susceptibility of Streptococcus pneumoniae in the United States: report from the SENTRY Antimicrobial Surveillance Program (1998-2009). Diagn. Microbiol. Infect. Dis. 68, 334–6 (2010).
- Park, S. C. et al. Validation of a scoring tool to predict drug-resistant pathogens in hospitalised pneumonia patients. Int. J. Tuberc. Lung Dis. 17, 704–709 (2013).
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