Updated: Jun 17, 2009
Bronchitis is one of the top conditions for which patients seek medical care. Bronchitis is characterized by inflammation of the bronchial tubes (or bronchi), which are the air passages that extend from the trachea into the small airways and alveoli. Triggers may be infectious agents, such as viruses or bacteria, or noninfectious agents, such as smoking or inhalation of chemical pollutants or dust.
Acute bronchitis is manifested by cough and, occasionally, sputum production that last for no more than 3 weeks. Although bronchitis should not be treated with antimicrobials, it is frequently difficult to refrain from prescribing them. Accurate testing and decision-making protocols regarding who might benefit from antimicrobial therapy would be useful but are not currently available.
Chronic bronchitis is defined clinically as cough with sputum expectoration for at least 3 months during a period of 2 consecutive years. Chronic bronchitis is associated with hypertrophy of the mucus-producing glands found in the mucosa of large cartilaginous airways. As the disease advances, progressive airflow limitation occurs, usually in association with pathologic changes of emphysema. This condition is called chronic obstructive pulmonary disease (COPD). When a stable patient experiences sudden clinical deterioration with increased sputum volume, sputum purulence, and/or worsening of shortness of breath, this is referred to as an acute exacerbation of chronic bronchitis as long as conditions other than acute tracheobronchitis are ruled out.
Generally, bronchitis is a diagnosis made by exclusion of other conditions such as sinusitis, pharyngitis, tonsillitis, and pneumonia.
Respiratory viruses are the most common causes of acute bronchitis. The most common viruses include influenza A and B, parainfluenza, respiratory syncytial virus, and coronavirus, although an etiologic agent is identified only in a minority of cases.1
During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently, the air passages become clogged by debris and irritation increases. In response, copious secretion of mucus develops, which causes the characteristic cough of bronchitis. For instance, with mycoplasmal pneumonia, bronchial irritation results from the attachment of the organism (Mycoplasma pneumoniae) to the respiratory mucosa, with eventual sloughing of affected cells. Acute bronchitis usually lasts approximately 10 days. If the inflammation extends downward to the ends of the bronchial tree, into the small bronchi (bronchioles), and then into the air sacs, bronchopneumonia results.
Chronic bronchitis is a condition associated with excessive tracheobronchial mucus production sufficient to cause cough with expectoration for at least 3 months for more than 2 consecutive years. The alveolar epithelium is both the target and the initiator of inflammation in chronic bronchitis.
A predominance of neutrophils and the peribronchial distribution of fibrotic changes result from the action of interleukin 8, colony-stimulating factors, and other chemotactic and proinflammatory cytokines. Airway epithelial cells release these inflammatory mediators in response to toxic, infectious, and inflammatory stimuli, in addition to decreased release of regulatory products such as ACE or neutral endopeptidase.
Chronic bronchitis can be categorized as simple chronic bronchitis, chronic mucopurulent bronchitis, or chronic bronchitis with obstruction. Mucoid sputum production characterizes simple chronic bronchitis. Persistent or recurrent purulent sputum production in the absence of localized suppurative disease, such as bronchiectasis, characterizes chronic mucopurulent bronchitis. Chronic bronchitis with obstruction must be distinguished from chronic infective asthma. The differentiation is based mainly on the history of the clinical illness. Patients who have chronic bronchitis with obstruction present with a long history of productive cough and a late onset of wheezing, whereas patients who have asthma with chronic obstruction have a long history of wheezing with a late onset of productive cough.
Chronic bronchitis may result from a series of attacks of acute bronchitis, or it may evolve gradually because of heavy smoking or inhalation of air contaminated with other pollutants in the environment. When so-called smoker's cough is continual rather than occasional, the mucus-producing layer of the bronchial lining has probably thickened, narrowing the airways to the point where breathing becomes increasingly difficult. With immobilization of the cilia that sweep the air clean of foreign irritants, the bronchial passages become more vulnerable to further infection and the spread of tissue damage.
In one study, acute bronchitis affected 44 of 1000 adults annually, and 82% of episodes occurred in fall or winter.2 By way of comparison, 91 million cases of influenza, 66 million cases of the common cold, and 31 million cases of other acute upper respiratory tract infections occurred during that same year.
According to estimates from national interviews taken by the National Center for Health Statistics in 2006, approximately 9.5 million people, or 4% of the population, were diagnosed with chronic bronchitis. These statistics may underestimate the prevalence of COPD by as much as 50% because many patients underreport their symptoms and their conditions remain undiagnosed. However, an overdiagnosis of chronic bronchitis by patients and clinicians has also been suggested. The term bronchitis is often used as a common descriptor for a nonspecific and self-limited cough, thereby falsely increasing its incidence even though the patient does not meet the criteria for diagnosis.
Acute bronchitis is common throughout the world and is one of the top 5 reasons for seeking medical care in countries that collect such data.
Bronchitis is almost always self-limited in individuals who are otherwise healthy, although it may result in absenteeism from work and school. Severe cases occasionally produce deterioration in patients with significant underlying cardiopulmonary disease or other comorbidities.
No difference in racial distribution is reported; however, bronchitis occurs more frequently in populations with a low socioeconomic status and in people who live in urban and highly industrialized areas.
Bronchitis affects males more than females.
Although found in all age groups, acute bronchitis is most frequently diagnosed in children younger than 5 years, whereas chronic bronchitis is more prevalent in people older than 50 years. In the United States, up to two thirds of men and one fourth of women have emphysema at death.
Obtain a complete history, including information on exposure to toxic substances and smoking. Patients with chronic bronchitis are often overweight and cyanotic. Initially, cough is present in the winter months. Over the years, the cough progresses from hibernal to perennial, and mucopurulent relapses increase in frequency, the duration and severity of which increase to the point of exertional dyspnea.
Symptoms of acute bronchitis include the following:
The physical examination findings in acute bronchitis can vary from normal-to-pharyngeal erythema, localized lymphadenopathy, and rhinorrhea to coarse rhonchi and wheezes that change in location and intensity after a deep and productive cough. Diffuse wheezes, high-pitched continuous sounds, and the use of accessory muscles can be observed in severe cases. Occasionally, diffuse diminution of air intake or inspiratory stridor occurs; these findings indicate obstruction of a major bronchi or the trachea, which requires sequentially vigorous coughing, suctioning, and, possibly, intubation or even tracheostomy.
Acute bronchitis is usually caused by infections, such as those caused by Mycoplasma species, Chlamydia pneumoniae, Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae, and by viruses, such as influenza, parainfluenza, adenovirus, rhinovirus, and respiratory syncytial virus. Exposure to irritants, such as pollution, chemicals, and tobacco smoke, may also cause acute bronchial irritation.
| Alpha1-Antitrypsin Deficiency | Gastroesophageal Reflux Disease |
| Asthma | Influenza |
| Bronchiectasis | Pharyngitis, Bacterial |
| Bronchiolitis | Pharyngitis, Viral |
| Chronic Bronchitis | Pneumonia |
| Chronic Obstructive Pulmonary Disease | Sinusitis, Acute |
| Cough | Sinusitis, Chronic |
| Expectoration | Streptococcus Group A Infections |
Goblet cell hyperplasia, mucosal and submucosal inflammatory cells, edema, peribronchial fibrosis, intraluminal mucous plugs, and increased smooth muscle are characteristic findings in small airways in chronic obstructive lung disease.
Therapy is generally aimed toward alleviation of symptoms.
Primary care providers can usually treat acute bronchitis unless severe complications occur or the patient has underlying pulmonary disease or immunodeficiency.
The value of a diet of fruits and vegetables is debatable, and the value of antioxidants is not proven.
Bed rest is recommended.
Therapy for acute bronchitis is generally aimed toward alleviation of symptoms and includes the use of analgesics, antipyretics, antitussives, and expectorants.
Several studies have shown conflicting results on the use of zinc as an adjunct treatment against influenza A. Most studies demonstrated favorable results; however, participants complained of a bad taste and significant nausea. On June 16, 2009, the US Food and Drug Administration (FDA) issued a public health advisory and notified consumers and health care providers to discontinue use of intranasal zinc products. The intranasal zinc products (Zicam Nasal Gel/Nasal Swab products by Matrixx Initiatives) are herbal cold remedies that claim to reduce the duration and severity of cold symptoms and are sold without a prescription. The FDA received more than 130 reports of anosmia (inability to detect odors) associated with intranasal zinc. Many of the reports described the loss of smell with the first dose.13
Studies have focused on healthy individuals (patients with asthma excluded) or patients with COPD. Antimicrobials appear to offer a small benefit when treating patients with COPD, and trimethoprim-sulfamethoxazole (TMP-SMZ) remains a good and inexpensive choice. Amoxicillin and doxycycline are also good alternatives. Therefore, extending antimicrobial use to patients with asthma and others with limited cardiopulmonary reserve may be reasonable.
Inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins. Addition of clavulanate inhibits beta-lactamase–producing bacteria.
Good alternative antibiotic for patients allergic to or intolerant of the macrolide class. Usually well tolerated and provides good coverage of most infectious agents. Not effective against Mycoplasma and Legionella species. Half-life of oral dosage is 1-1.3 h. Has good tissue penetration but does not enter cerebrospinal fluid.
For children >3 mo, base dosing protocol on amoxicillin content. Because of different amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs >40 kg.
500 mg PO q8h for 7-10 d; not to exceed 2 g/d
<3 months: 125 mg/5 mL PO susp based on amoxicillin; 30 mg/kg/d divided bid for 7-10 d
>3 months: 45 mg/kg/d PO q12h for 7-10 d if using 200 mg/5 mL or 400 mg/5 mL susp; 40 mg/kg/d PO q8h for 7-10 d if using 125 mg/5 mL or 250 mg/5 mL susp
>40 kg: Administer as in adults
Coadministration with warfarin or heparin increases risk of bleeding; may act synergistically against selected microorganisms when coadministered with aminoglycosides; coadministration with allopurinol may increase incidence of amoxicillin rash; may decrease efficacy of oral contraceptives when administered concomitantly
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatic impairment may occur with prolonged treatment in elderly persons; diarrhea may occur; adjust dose in renal impairment; cross-allergy may occur with other beta-lactams and cephalosporins
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Indicated for staphylococcal, streptococcal, chlamydial, and mycoplasmal infections.
250-500 mg PO qid or 333 mg PO tid
30-50 mg/kg/d PO divided qid
Toxicity increases with coadministration of fluconazole and pimozide; effects decrease and adverse GI effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG-CoA reductase inhibitors; cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents; serum digoxin concentrations may increase (antibiotic reduces gut flora that metabolize digoxin in >10% of patients)
Documented hypersensitivity; hepatic impairment; coadministration of pimozide or cisapride
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; erythromycin estolate formulation may cause cholestatic jaundice; adverse GI effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur; coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; administer half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be a sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies
Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected.
Concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues.
Treats mild-to-moderate microbial infections.
Day 1: 500 mg PO
Days 2-5: 250 mg PO qd or 500 mg PO qd for 3 d
12 mg/kg PO qd; not to exceed 500 mg/dose
May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Documented hypersensitivity; hepatic impairment; do not administer with pimozide
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzyme levels and cholestatic jaundice; caution in impaired hepatic function, prolonged QT intervals, or pneumonia; caution in patients who are hospitalized, geriatric, or debilitated
May be an option outside the United States. Treats gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and, possibly, 50S ribosomal subunit(s). Less effective than erythromycin.
250-500 mg PO qid
<8 years: Not recommended
>8 years: 25-50 mg/kg/d (10-20 mg/lb) PO qid
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants
Documented hypersensitivity, severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Semisynthetic cephalosporin administered as prodrug. Hydrolyzed by esterases during absorption and distributed in circulating blood as active cefditoren. Bactericidal activity results from inhibition of cell wall synthesis via affinity for penicillin-binding proteins. No dose adjustment necessary for mild renal impairment (CrCl 50-80 mL/min/1.73 m2) or mild-to-moderate hepatic impairment. Indicated for acute exacerbation of chronic bronchitis caused by susceptible strains of S pyogenes. The 400-mg dose is indicated for AECB caused by susceptible strains of H influenzae, Haemophilus parainfluenzae, S pneumoniae (penicillin-susceptible strains only), or M catarrhalis.
200 mg PO with meals bid for 10 d
Moderate renal impairment (CrCl 30-49 mL/min/1.73 m2): No more than 200 mg PO bid
Severe renal impairment (CrCl <30 mL/min/1.73 m2): 200 mg PO qd
<12 years: Not established
>12 years: Administer as in adults
Absorption reduced with H2 receptor antagonists, and antacids of magnesium and aluminum hydroxides may reduce absorption; probenecid may increase plasma concentrations of cefditoren
Documented hypersensitivity to drug, penicillin, related compounds, or milk protein sodium caseinate; carnitine deficiency or inborn errors of metabolism that may result in clinically significant carnitine deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May cause diarrhea, nausea, and vaginal moniliasis (yeast infection); pseudomembranous colitis may occur; clinical manifestations of carnitine deficiency may occur with prolonged use; prolonged use may result in emergence and overgrowth of resistant organisms; caution in breastfeeding
Inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid, resulting in inhibition of bacterial growth. Antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa. As with tetracycline, it has in vitro activity against B pertussis. Not useful in mycoplasmal infections.
160 mg TMP/800 mg SMZ PO q12h for 10-14 d
<2 months: Do not administer
>2 months: 15-20 mg/kg/d, based on TMP, PO tid/qid for 14 d
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly patients; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity, megaloblastic anemia from folate deficiency, late pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid in infants because of the possibility of kernicterus; discontinue at first appearance of rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, patients with chronic alcoholism, elderly patients, patients receiving anticonvulsant therapy, patients with malabsorption syndrome); hemolysis may occur in individuals who are G-6-PD deficient; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation
Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria
250-500 mg PO q8h; not to exceed 3 g/d
20-50 mg/kg/d PO divided q8h
Reduces efficacy of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; may enhance risk of candidiasis
Has a bacteriocidal property by inhibiting the DNA gyrase and, consequently, cell growth.
250-500 mg PO bid for 7-14 d
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Semisynthetic macrolide antibiotic that reversibly binds to P site of 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl t-RNA from ribosomes, causing bacterial growth inhibition.
250-500 mg PO bid for 7-14 d
7.5 mg/kg PO bid for 7-14 d
Toxicity increases with coadministration of fluconazole and pimozide; effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, carbamazepine, ergot alkaloids, triazolam, and HMG-CoA reductase inhibitors
Plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increases in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents; decreases metabolism of repaglinide, thus increasing serum levels and effects
Documented hypersensitivity; coadministration of pimozide
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; give half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies
Broad-spectrum, synthetically derived bacteriostatic antibiotic in tetracycline class. Almost completely absorbed, concentrates in bile, and is excreted in urine and feces as biologically active metabolite in high concentrations.
Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. May block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
100 mg PO bid on d 1, then 100 mg PO qd for 7-10 d
<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO in 1-2 divided doses; not to exceed 200 mg/d
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Sparse data attest to the efficacy of expectorants outside the test tube.
Treats minor cough resulting from bronchial and throat irritation.
10 mL PO q4h; not to exceed 40 mL/24h
<2 years: Not recommended
2-6 years: 2.5 mL PO q4h
6-12 years: 5 mL PO q4h
>12 years: Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Not to be used to treat productive cough or persistent chronic cough resulting from emphysema
The prototype antitussive, codeine, has been used successfully in some chronic cough and induced-cough models, but scant clinical data for upper respiratory tract infections.
5-10 mL PO q4-8h; not to exceed 60 mL/d
1-1.5 mg/kg of codeine/d PO divided qid
Increases toxicity of CNS depressants
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Not to be administered for productive cough or persistent chronic cough from emphysema; caution in renal impairment
Studies (although limited) have shown an advantage to using bronchodilators and possible superiority to antibiotics for relieving bronchitis symptoms.
Relaxes bronchial smooth muscle by action on beta2 receptors with little effect on cardiac muscle contractility.
2-4 mg/dose PO divided tid/qid; not to exceed 32 mg/d
MDI: 2 puffs q4-6h; not to exceed 12 inhalations/d
0.1-2 mg/kg PO tid
Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, TCAs, and sympathomimetic agents
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders
Influenza vaccinations offer greater protection for the appropriate populations because they offer coverage for influenza A and B. However, amantadine and rimantadine can be useful during epidemics of influenza A. Zanamivir (Relenza) and oseltamivir (Tamiflu) are the newest agents and are effective for both influenza A and B.
Oseltamivir resistance emerged in the United States during the 2008-2009 influenza season. The CDC has revised interim recommendations for antiviral treatment and prophylaxis of influenza. Preliminary data from a limited number of states indicate a high prevalence of influenza A (H1N1) virus strains resistant to oseltamivir. Because of this, zanamivir is recommended as the initial choice for antiviral prophylaxis or treatment when influenza A infection is proven or exposure is suspected. A second-line alternative is a combination of oseltamivir plus rimantadine rather than oseltamivir alone. Local influenza surveillance data and laboratory testing can assist physicians regarding the antiviral agent choice.
Influenza A viruses, including the 2 subtypes H1N1 and H3N2, and influenza B viruses currently circulate worldwide, but the prevalence of each can vary among communities and within a single community over the course of an influenza season. In the United States, 4 prescription antiviral medications (ie, oseltamivir, zanamivir, amantadine, rimantadine) are approved for treatment and chemoprophylaxis of influenza.
Since January 2006, the neuraminidase inhibitors (oseltamivir, zanamivir) have been the only recommended influenza antiviral drugs because of widespread resistance to the adamantanes (amantadine, rimantadine) among influenza A (H3N2) virus strains. The neuraminidase inhibitors have activity against influenza A and B viruses, while the adamantanes have activity against only influenza A viruses. In 2007-2008, a significant increase in the prevalence of oseltamivir resistance was reported among influenza A (H1N1) viruses worldwide. During the 2007-2008 influenza season, 10.9% of H1N1 viruses tested in the United States were resistant to oseltamivir. The 2008-2009 influenza vaccine is expected to be effective against oseltamivir-resistant influenza A virus.14
Complete recommendations are available from in a CDC Health Advisory.
Inhibitor of neuraminidase, which is a glycoprotein on the surface of the influenza virus that destroys the infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, release of viruses from infected cells and viral spread are decreased. Effective against both influenza A and B. To be inhaled through Diskhaler oral inhalation device. Circular foil disks containing 5-mg blisters of drug are inserted into supplied inhalation device.
Treatment: 10 mg (2 inhalations, 5 mg/inhalation) inhaled PO q12h for 5 d; initiate within 2 d of symptom onset
Prophylaxis: 10 mg (2 inhalations, 5 mg/inhalation) inhaled PO qd for 10 d; initiate within 36 h of exposure
Treatment
<7 years: Not established
>7 years: Administer as in adults
Prophylaxis
<5 years: Not established
>5 years: Administer as in adults
None reported
Documented hypersensitivity, obstructive airway disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Monitor respiratory status; may cause bronchospasm; caution in breastfeeding
Inhibits viral replication of influenza A virus H1N1, H2N2, and H3N2. Prevents viral penetration into host by inhibiting uncoating of influenza A. Because of resistance, not recommended by the CDC as of the 2005-2006 influenza season. Laboratory testing by CDC on the predominant strain of influenza (H3N2) currently circulating in the United States shows that it is resistant to these drugs.
200 mg PO qd or 100 mg PO bid
<10 years: 5 mg/kg PO qd, up to 150 mg/d
>10 years: Administer as in adults
Acetaminophen and aspirin reduce levels when taken concurrently; cimetidine increases plasma levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hepatic impairment
Inhibits neuraminidase, which is a glycoprotein on the surface of influenza virus that destroys an infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, decreases release of viruses from infected cells and thus viral spread. Effective to treat influenza A or B. Start within 40 h of symptom onset. Available as cap and oral susp.
Acute illness: 75 mg PO bid for 5 d
Prophylaxis: 75 mg PO qd for 10 d
Acute illness
<1 year: Not indicated
>1 year:
<15 kg: 30 mg PO bid for 5 d
>15-23 kg: 45 mg PO bid for 5 d
>23-40 kg: 60 mg PO bid for 5 d
>40 kg: Administer as in adults
Prophylaxis
<1 year: Not established
>1 year:
<15 kg: 30 mg PO qd for 10 d
>15-23 kg: 45 mg PO qd for 10 d
24-40 kg: 60 mg PO qd for 10 d
>40 kg: Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal impairment, chronic cardiac or respiratory disease, and breastfeeding; do not use in children <1 y (preclinical trials have demonstrated death in young animals, possibly related to immature blood-brain barriers); postmarketing reports (mostly from Japan) of self-injury and delirium in patients with influenza (reports primarily among children), unknown if oseltamivir directly contributes to this behavior (monitor for abnormal behavior throughout treatment period)
Often helpful in relieving the associated lethargy, malaise, and fever associated with illness.
Usually DOC for treatment of mild to moderate pain if no contraindications exist.
400-800 mg PO q4-6h
10 mg/kg PO q6-8h
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of MTX toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
DOC for treatment of pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.
325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 doses (2.6 g) in 24 h
Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity, G-6-PD deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in people with chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; present in many OTC products and combined use with these products may result in cumulative doses exceeding recommended maximum dose
Knutson D, Braun C. Diagnosis and management of acute bronchitis. Am Fam Physician. May 15 2002;65(10):2039-44. [Medline].
Macfarlane J, Holmes W, Gard P, et al. Prospective study of the incidence, aetiology and outcome of adult lower respiratory tract illness in the community. Thorax. Feb 2001;56(2):109-14. [Medline].
[Best Evidence] Poole PJ, Black PN. Mucolytic agents for chronic bronchitis or chronic obstructive pulmonary disease. Cochrane Database Syst Rev. Jul 19 2006;3:CD001287. [Medline].
[Guideline] Braman SS. Chronic cough due to acute bronchitis: ACCP evidence-based clinical practice guidelines. Chest. Jan 2006;129(1 Suppl):95S-103S. [Medline].
[Guideline] Braman SS. Chronic cough due to chronic bronchitis: ACCP evidence-based clinical practice guidelines. Chest. Jan 2006;129(1 Suppl):104S-115S. [Medline].
American Academy of Pediatrics. Committee on Drugs. Use of codeine- and dextromethorphan-containing cough remedies in children. American Academy of Pediatrics. Committee on Drugs. Pediatrics. Jun 1997;99(6):918-20. [Medline].
[Best Evidence] Smucny J, Becker L, Glazier R. Beta2-agonists for acute bronchitis. Cochrane Database Syst Rev. Oct 18 2006;CD001726. [Medline].
Aagaard E, Gonzales R. Management of acute bronchitis in healthy adults. Infect Dis Clin North Am. Dec 2004;18(4):919-37; x. [Medline].
Gonzales R, Steiner JF, Lum A, Barrett PH Jr. Decreasing antibiotic use in ambulatory practice: impact of a multidimensional intervention on the treatment of uncomplicated acute bronchitis in adults. JAMA. Apr 28 1999;281(16):1512-9. [Medline].
Siempos II, Dimopoulos G, Korbila IP, Manta K, Falagas ME. Macrolides, quinolones and amoxicillin/clavulanate for chronic bronchitis: a meta-analysis. Eur Respir J. Jun 2007;29(6):1127-37. [Medline].
Korbila IP, Manta KG, Siempos II, Dimopoulos G, Falagas ME. Penicillins vs trimethoprim-based regimens for acute bacterial exacerbations of chronic bronchitis: meta-analysis of randomized controlled trials. Can Fam Physician. Jan 2009;55(1):60-7. [Medline].
[Best Evidence] El Moussaoui R, Roede BM, Speelman P, Bresser P, Prins JM, Bossuyt PM. Short-course antibiotic treatment in acute exacerbations of chronic bronchitis and COPD: a meta-analysis of double-blind studies. Thorax. May 2008;63(5):415-22. [Medline].
United States Food and Drug Administration. Zicam cold remedy nasal products (Cold Remedy Nasal Gel, Cold Remedy Nasal Swabs, and Cold Remedy Saws, Kids Size). MedWatch Public Health Advisory. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm166996.htm. Accessed June 16, 2009.
Update: influenza activity--United States, September 28-November 29, 2008. MMWR Morb Mortal Wkly Rep. Dec 12 2008;57(49):1329-32. [Medline].
Nichol KL, Wuorenma J, von Sternberg T. Benefits of influenza vaccination for low-, intermediate-, and high-risk senior citizens. Arch Intern Med. Sep 14 1998;158(16):1769-76. [Medline].
[Guideline] Fiore AE, Shay DK, Broder K, et al. Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP), 2008. MMWR Recomm Rep. Aug 8 2008;57:1-60. [Medline].
Clay KD, Hanson JS, Pope SD, Rissmiller RW, Purdum PP 3rd, Banks PM. Brief communication: severe hepatotoxicity of telithromycin: three case reports and literature review. Ann Intern Med. Mar 21 2006;144(6):415-20. [Medline].
Blinkhorn RJ. Upper respiratory tract infection. In: Textbook of Pulmonary Medicine. 5th ed. Boston, Mass: Little Brown & Company; 1993:405-07.
Gonzales R, Sande MA. Uncomplicated acute bronchitis. Ann Intern Med. Dec 19 2000;133(12):981-91. [Medline].
Gwaltigy, Jack MJ. Acute bronchitis. In: Douglas & Barnett's Principles of Practice of Infectious Disease. 4th ed. New York, NY: Churchill Livingstone; 1995:606-08.
Harris RH, MacKenzie TD, Leeman-Castillo B, et al. Optimizing antibiotic prescribing for acute respiratory tract infections in an urban urgent care clinic. J Gen Intern Med. May 2003;18(5):326-34. [Medline].
Huchon GJ, Gialdroni-Grassi G, Leophonte P, Manresa F, Schaberg T, Woodhead M. Initial antibiotic therapy for lower respiratory tract infection in the community: a European survey. Eur Respir J. Aug 1996;9(8):1590-5. [Medline].
Palmer DA, Bauchner H. Parents' and physicians' views on antibiotics. Pediatrics. Jun 1997;99(6):E6. [Medline].
Siegel D, Sande MA. Patterns of antibiotic use in a busy metropolitan emergency room: analysis of efficacy and cost-appropriateness. West J Med. May 1983;138(5):737-41. [Medline].
Smucny J, Fahey T, Becker L, Glazier R, McIsaac W. Antibiotics for acute bronchitis. Cochrane Database Syst Rev. 2000;CD000245. [Medline].
Wark P. Bronchitis (acute). Clin Evid. Jun 2004;1923-32. [Medline].
bronchitis, acute bronchitis, chronic bronchitis, upper respiratory tract infection, URTI, flu, influenza, chronic obstructive pulmonary disease, COPD, excessive tracheobronchial mucus production, simple chronic bronchitis, chronic mucopurulent bronchitis, chronic bronchitis with obstruction, flu, bronchopneumonia, bronchiectasis, inflammation of bronchial tubes, Mycoplasma pneumoniae, M pneumoniae, Chlamydia pneumoniae, C pneumoniae, Streptococcus pneumoniae, S pneumoniae, Moraxella catarrhalis, M catarrhalis, Haemophilus influenzae, H influenzae, mycoplasmal pneumonia, pharyngeal erythema, localized lymphadenopathy, right ventricular hypertrophy, cystic fibrosis, parainfluenza, adenovirus, rhinovirus, respiratory syncytial virus, cigarette smoking, air pollution
Jazeela Fayyaz, DO, Senior Fellow, Department of Pulmonology, Lenox Hill Hospital
Jazeela Fayyaz, DO is a member of the following medical societies: American College of Physicians and American Thoracic Society
Disclosure: Nothing to disclose.
Ali Hmidi, MD, Staff Physician, Department of Internal Medicine, Brooklyn Hospital Center, Cornell University
Disclosure: Nothing to disclose.
Jeffrey Nascimento, DO, MS, Fellow, Department of Pulmonary Medicine, Lenox Hill Hospital
Jeffrey Nascimento, DO, MS is a member of the following medical societies: American College of Chest Physicians, American Medical Association, American Osteopathic Association, American Thoracic Society, New York County Medical Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Roger B Olade, MD, MPH, Medical Director, Providence Health Group
Roger B Olade, MD, MPH is a member of the following medical societies: American College of Occupational and Environmental Medicine and American College of Physicians
Disclosure: Nothing to disclose.
Klaus-Dieter Lessnau, MD, FCCP, Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital
Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Artificial Internal Organs, American Thoracic Society, Physicians for Social Responsibility, and Society of Critical Care Medicine
Disclosure: sepracor Ownership interest None
Helen M Hollingsworth, MD, Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center
Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, and Massachusetts Medical Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.
Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.
Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.