Updated: Nov 17, 2009
Moraxella catarrhalis is a gram-negative, aerobic, oxidase-positive diplococcus that was first described in 1896. The organism has also been known as Micrococcus catarrhalis, Neisseria catarrhalis, and Branhamella catarrhalis. For most of the 20th century, M catarrhalis was considered a saprophyte of the upper respiratory tract associated with no significant pathogenic consequences.
Although the commensal status of M catarrhalis in the nasopharynx is still accepted, the organism is a common cause of otitis media and sinusitis and an occasional cause of laryngitis. M catarrhalis causes bronchitis and pneumonia in children and adults with underlying chronic lung disease and is occasionally a cause of bacteremia and meningitis, especially in immunocompromised persons. Bacteremia can be complicated by local infections such as osteomyelitis or septic arthritis. M catarrhalis is also associated with nosocomial infections.
Different studies have shown that M catarrhalis colonizes the upper respiratory tract in 28%-100% of humans in the first year of life. In adults, the colonization rate is 1%-10.4%. Colonization appears to be an ongoing process with an elimination-colonization turnover of various strains. Transmission is believed to be due to direct contact with contaminated secretions by droplets.
The endotoxin of M catarrhalis, a lipopolysaccharide similar to those found in the Neisseria species, may play a role in the disease process. Some strains of M catarrhalis have pili or fimbriae, which may aid adherence to the respiratory epithelium. Some strains produce a protein that confers resistance to complement by interference with formation of the membrane attack complex. M catarrhalis also expresses specific proteins for iron uptake that act as receptors for transferrin and lactoferrin.
Humoral responses against M catarrhalis appear to be age-dependent, with the titer of immunoglobulin G (IgG) gradually increasing in children. Antibody responses to outer-membrane proteins have been obtained, predominantly in the IgG3 subclass.
M catarrhalis is the third most common cause of otitis media and sinusitis in children (after Streptococcus pneumoniae and Haemophilus influenzae). M catarrhalis is estimated to be responsible for 3-4 million cases of otitis media annually, with an associated health care cost (direct and indirect) of $2 billion each year.
The most significant infections caused by M catarrhalis are upper respiratory tract infections, including otitis media and sinusitis in children and lower respiratory tract infections in adults. Infections with M catarrhalis in adults are more common if underlying conditions are present, especially in elderly persons. In a study of 42 cases of pneumonia with M catarrhalis isolated as single agent in sputum cultures, the mortality rate attributable to the underlying problems within 3 months of pneumonia was 45%.
In one study involving adult patients, the male-to-female ratio was 1.6:1.
M catarrhalis infections may occur at any age. Although colonization is more common in children, only a small percentage of positive cultures findings have clinical significance in the pediatric population. In one study, 9% of cultures positive for M catarrhalis in children younger than 5 years and 33% of isolates from children aged 6-10 years were found to be clinically significant. However, all cultures positive for M catarrhalis had clinical importance in adults.
Physical findings in M catarrhalis infections are similar to findings of infections with other organisms in the same location.
Bronchitis
Pneumonia, Community-Acquired
Sinusitis, Acute
Sinusitis, Chronic
Otitis media
Otitis media with effusion
Bacteremia
Endocarditis
Acute bronchitis
Chronic bronchitis
Other primary infections of other etiology
Medical care of M catarrhalis infection depends on the infection site, age of the patient, underlying condition(s), and severity of the disease.
Approximately 95% of M catarrhalis strains isolated in the United States produce beta-lactamase. Antibiotics such as penicillin, amoxicillin, and ampicillin are only effective against strains that do not produce beta-lactamase.
Topical ciprofloxacin/dexamethasone treatment for acute otitis media with otorrhea via tympanostomy tubes was found to have similar efficacy to that of topical ofloxacin in M catarrhalis infections.17
Treatment with oral azithromycin 500 mg once daily for 3 days was found comparable with a 10-day regimen of oral clarithromycin 500 mg twice daily in the treatment of acute exacerbation of chronic bronchitis.18
Telithromycin, a ketolide derivative of erythromycin A, demonstrated good in vitro activity against M catarrhalis in acute exacerbation of chronic bronchitis.19 However, severe liver disease associated with telithromycin use has been reported.20
The below antimicrobial drugs may be used in M catarrhalis infections, depending on the need for use of oral or parenteral medication, patient's age, underlying condition, sensitivity of the organism, and desired spectrum of coverage.
Therapy should cover likely pathogens in the context of this clinical setting. Nearly all M catarrhalis strains produce beta-lactamase.
Amoxicillin-clavulanate, second- and third-generation oral cephalosporins, and trimethoprim-sulfamethoxazole (TMP-SMX) are the most recommended agents. Alternatively, azithromycin, clarithromycin, or dirithromycin can be used. More than 90% of M catarrhalis strains have been shown to resist amoxicillin, and these rates vary by region.21 All other agents listed below are also effective.
Recommended dosing schedule of erythromycin may result in GI upset, causing one to prescribe an alternative macrolide or change to tid dosing. Covers most potential etiologic agents, including Mycoplasma species.
Although 10 d seems to be a standard course of treatment, treating until the patient has been afebrile for 3-5 d seems a more rational approach. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.
Has the added advantage of being a good anti-inflammatory agent by inhibiting migration of polymorphonuclear leukocytes.
500 mg (base, estolate, stearate) PO q6h or 400 mg (ethylsuccinate) PO q6h
20-50 mg/kg/d PO divided q6h
Inhibits CYP450 1A2, 3A3/4 isoenzymes; coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis; decreases metabolism of repaglinide, thus increasing serum levels and effects
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI side effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
Second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods. Determine proper dosage and route based on condition of patient, severity of infection, and susceptibility of causative organism.
500 mg PO q8h
20-40 mg/kg/d PO divided q8-12h; not to exceed 2 g/d
Alcoholic beverages consumed <72 h after taking cefaclor may produce disulfiramlike reactions; may increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics and aminoglycosides (eg, loop diuretics) may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Reduce dosage by half if CrCl is 10-30 mL/min and by three fourths if <10 mL/min (high doses may cause CNS toxicity); bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy; adjust dose in severe renal insufficiency; superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
Binds to 1 or more of the penicillin-binding proteins, which in turn inhibits cell wall synthesis and results in bactericidal activity.
500 mg PO qd
<12 years: 7.5-15 mg/kg/d PO divided q12h for 10 d
>12 years: Administer as in adults
Probenecid increases effect of cefprozil; coadministration with furosemide and aminoglycosides increases nephrotoxic effects of cefprozil
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
Second-generation cephalosporin maintains gram-positive activity that first-generation cephalosporins have; adds activity against Proteus mirabilis, H influenzae, Escherichia coli, Klebsiella pneumoniae, and M catarrhalis. Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose.
500 mg PO q12h
Children: 250 mg PO bid for 20 d
Adolescents: Administer as in adults
Disulfiramlike reactions may occur when alcohol is consumed within 72 h after taking cefuroxime; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patients receiving potent diuretics such as loop diuretics; coadministration with aminoglycosides increases nephrotoxic potential
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
Administer half dose if CrCl is 10-30 mL/min and quarter dose if <10 mL/min; fungal and microorganism overgrowth may occur with prolonged therapy
Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity of TMP-SMX includes common urinary tract pathogens, except Pseudomonas aeruginosa.
160 mg TMP/800 mg SMX PO q12h
<2 months: Do not administer
>2 months: 15-20 mg/kg/d PO tid/qid for 14 d, based on TMP
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 due to folate deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, persons with chronic alcoholism, elderly persons, those receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in G-6-PD deficiency; 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); give fluids to prevent crystalluria and stone formation
For septicemia and treatment of gynecologic infections caused by susceptible organisms. Arrests bacterial cell wall synthesis, which in turn inhibits bacterial growth. Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.
Moderate-to-severe infections: 2 g IV q6h
Infants and children: 50-180 mg/kg/d IV/IM divided q4-6h
>12 years: Administer as in adults
Probenecid may increase cefotaxime levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal impairment; has been associated with severe colitis
Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins.
Moderate-to-severe infections: 1-2 g IV q12-24h; not to exceed 4 g/d
Neonates >7 days: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d
Infants and children: 50-75 mg/kg/d IV/IM divided q12h; not to exceed 2 g/d
Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
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; caution with breastfeeding; caution with allergy to penicillin
Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins. Presence of piperazine side chain makes it structurally different from other cephalosporins and enhances antipseudomonal activity. Gram-negative spectrum includes M catarrhalis. Dosage depends on severity of infection and susceptibility of organism.
2 g IV q12h
Children and infants: 100-150 mg/kg/d IV/IM divided bid/tid; not to exceed 12 g/d
Adolescents: Administer as in adults
Nephrotoxicity may increase with aminoglycosides, furosemide, and ethacrynic acid; probenecid may increase cefoperazone levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May increase protime
Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins. Gram-negative spectrum includes M catarrhalis. Dosage depends on severity of infection and susceptibility of organism.
2 g IV q8h; not to exceed 6 g/d
Children and infants: 30-50 mg/kg IV q8h; not to exceed 6 g/d
Adolescents: Administer as in adults
Nephrotoxicity may increase with aminoglycosides, furosemide, and ethacrynic acid; probenecid may increase ceftazidime levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins. Gram-negative spectrum includes M catarrhalis. Dosage depends on severity of infection and susceptibility of organism.
2 g IV q8h; not to exceed 12 g/d
Children and infants >6 months: 50 mg/kg IV/IM q6-8h; not to exceed 12 g/d
Adolescents: Administer as in adults
Nephrotoxicity may increase with aminoglycosides, furosemide, and ethacrynic acid; probenecid may increase ceftizoxime levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal insufficiency; superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
Fluoroquinolone with activity against most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis, and consequently, growth.
500 mg PO q12h
<18 years: Not recommended
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4h 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
May cause seizures; avoid in renal insufficiency and in patients with CNS disorders
For pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.
500 mg PO qd
<18 years: Not recommended
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; levofloxacin reduces therapeutic effects of phenytoin; probenecid may increase levofloxacin 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, periodically evaluate organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may develop with prolonged or repeated antibiotic therapy
Treats mild-to-moderate microbial infections
500 mg PO on day 1; followed by 250 mg PO qd on days 2-5
<6 months: Not established
>6 months: 10 mg/kg PO once on day 1; not to exceed 500 mg/d, followed by 5 mg/kg PO qd on days 2-5; not to exceed 250 mg/d
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 enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals; caution in hospitalized, geriatric, or debilitated patients
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
500 mg PO q12h
15 mg/kg PO divided bid
Toxicity increases with coadministration of fluconazole and pimozide; clarithromycin effects decrease and adverse GI effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, HMG CoA-reductase inhibitors; 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
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
Not available in the United States. Inhibits RNA-dependent protein synthesis by binding to 50S ribosomal subunit. Antimicrobial spectrum includes M catarrhalis. Dosage depends on severity of infection and susceptibility of organism. Dosage depends on severity of infection and susceptibility of organism. In children, age, weight, and severity of infection determine proper dosage.
500 mg PO qd; administer with meal
Not established
May increase serum digoxin levels; may increase risk of ergot toxicity with ergotamine or dihydroergotamine
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
Associated with GI distress, pseudomembrane colitis, dizziness, headache, insomnia, pruritus
Pappas DE, Hendley JO, Hayden FG, et al. Symptom profile of common colds in school-aged children. Pediatr Infect Dis J. Jan 2008;27(1):8-11. [Medline].
Gehanno P, Panajotopoulos A, Barry B, et al. Microbiology of otitis media in the Paris, France, area from 1987 to 1997. Pediatr Infect Dis J. Jun 2001;20(6):570-3. [Medline].
Li WC, Chiu NC, Hsu CH, et al. Pathogens in the middle ear effusion of children with persistent otitis media: implications of drug resistance and complications. J Microbiol Immunol Infect. Sep 2001;34(3):190-4. [Medline].
Wald ER. Microbiology of acute and chronic sinusitis in children and adults. Am J Med Sci. Jul 1998;316(1):13-20. [Medline].
Hunter MH, King DE. COPD: management of acute exacerbations and chronic stable disease. Am Fam Physician. Aug 15 2001;64(4):603-12. [Medline].
Lieberman D, Lieberman D, Ben-Yaakov M, et al. Infectious etiologies in acute exacerbation of COPD. Diagn Microbiol Infect Dis. Jul 2001;40(3):95-102. [Medline].
Sethi S, Murphy TF. Bacterial infection in chronic obstructive pulmonary disease in 2000: a state-of-the-art review. Clin Microbiol Rev. Apr 2001;14(2):336-63. [Medline]. [Full Text].
Soler N, Torres A, Ewig S, et al. Bronchial microbial patterns in severe exacerbations of chronic obstructive pulmonary disease (COPD) requiring mechanical ventilation. Am J Respir Crit Care Med. May 1998;157(5 Pt 1):1498-505. [Medline].
Aronovitz G. Treatment of upper and lower respiratory tract infections: clinical trials with cefprozil. Pediatr Infect Dis J. Aug 1998;17(8 Suppl):S83-8. [Medline].
Manfredi R, Nanetti A, Valentini R, et al. Moraxella catarrhalis pneumonia during HIV disease. J Chemother. Oct 2000;12(5):406-11. [Medline].
Thórsson B, Haraldsdóttir V, Kristjánsson M. Moraxella catarrhalis bacteraemia. A report on 3 cases and a review of the literature. Scand J Infect Dis. 1998;30(2):105-9. [Medline].
Neumayer U, Schmidt HK, Mellwig KP, et al. Moraxella catarrhalis endocarditis: report of a case and literature review. J Heart Valve Dis. Jan 1999;8(1):114-7. [Medline].
Stefanou J, Agelopoulou AV, Sipsas NV, et al. Moraxella catarrhalis endocarditis: case report and review of the literature. Scand J Infect Dis. 2000;32(2):217-8. [Medline].
Tritton D, Watts T, Sieratzki JS. Peri-orbital cellulitis and sepsis by Branhamella catarrhalis. Eur J Pediatr. Jul 1998;157(7):611-2. [Medline].
Abdolrasouli A, Amin A, Baharsefat M, et al. Moraxella catarrhalis associated with acute urethritis imitating gonorrhoea acquired by oral-genital contact. Int J STD AIDS. Aug 2007;18(8):579-80. [Medline].
Uehara Y, Yagoshi M, Tanimichi Y, Yamada H, Shimoguchi K, Yamamoto S, et al. Impact of reporting gram stain results from blood culture bottles on the selection of antimicrobial agents. Am J Clin Pathol. Jul 2009;132(1):18-25. [Medline]. [Full Text].
Roland PS, Kreisler LS, Reese B, et al. Topical ciprofloxacin/dexamethasone otic suspension is superior to ofloxacin otic solution in the treatment of children with acute otitis media with otorrhea through tympanostomy tubes. Pediatrics. Jan 2004;113(1 Pt 1):e40-6. [Medline]. [Full Text].
Swanson RN, Lainez-Ventosilla A, De Salvo MC, et al. Once-daily azithromycin for 3 days compared with clarithromycin for 10 days for acute exacerbation of chronic bronchitis: a multicenter, double-blind, randomized study. Treat Respir Med. 2005;4(1):31-9. [Medline].
Sethi S, Anzueto A, Farrell DJ. Antibiotic activity of telithromycin and comparators against bacterial pathogens isolated from 3,043 patients with acute exacerbation of chronic bronchitis. Ann Clin Microbiol Antimicrob. Mar 8 2005;4:5. [Medline].
Dore DD, DiBello JR, Lapane KL. Telithromycin use and spontaneous reports of hepatotoxicity. Drug Saf. 2007;30(8):697-703. [Medline].
Hwang PH. A 51-year-old woman with acute onset of facial pressure, rhinorrhea, and tooth pain: review of acute rhinosinusitis. JAMA. May 6 2009;301(17):1798-807. [Medline].
McMichael JC. Progress toward the development of a vaccine to prevent Moraxella (Branhamella) catarrhalis infections. Microbes Infect. Apr 2000;2(5):561-8. [Medline].
McMichael JC. Vaccines for Moraxella catarrhalis. Vaccine. Dec 8 2000;19 Suppl 1:S101-7. [Medline].
O'Brien MA, Prosser LA, Paradise JL, Ray GT, Kulldorff M, Kurs-Lasky M, et al. New vaccines against otitis media: projected benefits and cost-effectiveness. Pediatrics. Jun 2009;123(6):1452-63. [Medline].
Abuhammour WM, Abdel-Haq NM, Asmar BI, et al. Moraxella catarrhalis bacteremia: a 10-year experience. South Med J. Nov 1999;92(11):1071-4. [Medline].
Bitnun A, Allen UD. Medical therapy of otitis media: use, abuse, efficacy, and morbidity. J Otolaryngol. 1998;27 Suppl 2:26-36. [Medline].
Bootsma HJ, van Dijk H, Vauterin P, et al. Genesis of BRO beta-lactamase-producing Moraxella catarrhalis: evidence for transformation-mediated horizontal transfer. Mol Microbiol. Apr 2000;36(1):93-104. [Medline].
Christensen JJ. Moraxella (Branhamella) catarrhalis: clinical, microbiological and immunological features in lower respiratory tract infections. APMIS Suppl. 1999;88:1-36. [Medline].
de Lalla F. Cefixime in the treatment of upper respiratory tract infections and otitis media. Chemotherapy. Sep 1998;44 Suppl 1:19-23. [Medline].
Enright MC, McKenzie H. Moraxella (Branhamella) catarrhalis--clinical and molecular aspects of a rediscovered pathogen. J Med Microbiol. May 1997;46(5):360-71. [Medline].
Gunnarsson RK, Holm SE, Söderström M. The prevalence of potential pathogenic bacteria in nasopharyngeal samples from healthy children and adults. Scand J Prim Health Care. Mar 1998;16(1):13-7. [Medline].
Johnson DM, Biedenbach DJ, Beach ML, et al. Antimicrobial activity and in vitro susceptibility test development for cefditoren against Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus species. Diagn Microbiol Infect Dis. Jun 2000;37(2):99-105. [Medline].
Karalus R, Campagnari A. Moraxella catarrhalis: a review of an important human mucosal pathogen. Microbes Infect. Apr 2000;2(5):547-59. [Medline].
McGregor K, Chang BJ, Mee BJ, et al. Moraxella catarrhalis: clinical significance, antimicrobial susceptibility and BRO beta-lactamases. Eur J Clin Microbiol Infect Dis. Apr 1998;17(4):219-34. [Medline].
Mikucka A, Janicka G, Krawiecka D, et al. Antibiotic-sensitivity of Moraxella catarrhalis isolated from clinical materials in 1997-1998. Med Sci Monit. Mar-Apr 2000;6(2):300-4. [Medline].
Miravitlles M, Espinosa C, Fernandez-Laso E, et al. Relationship between bacterial flora in sputum and functional impairment in patients with acute exacerbations of COPD. Study Group of Bacterial Infection in COPD. Chest. Jul 1999;116(1):40-6. [Medline].
Murphy TF. Lung infections. 2. Branhamella catarrhalis: epidemiological and clinical aspects of a human respiratory tract pathogen. Thorax. Feb 1998;53(2):124-8. [Medline].
Cunha BA. Pneumonia Essentials. 2nd Ed. Royal Oak, MI: Physicians Press; 2008.
Principi N. Oral cephalosporins in the treatment of acute otitis media. Clin Microbiol Infect. 2000;6 Suppl 3:61-3. [Medline].
Pérez JL, Pulido A, Pantozzi F, et al. Butyrate esterase (4-methylumbelliferyl butyrate) spot test, a simple method for immediate identification of Moraxella (Branhamella) catarrhalis [corrected]. J Clin Microbiol. Oct 1990;28(10):2347-8. [Medline].
Traub WH, Leonhard B. Susceptibility of Moraxella catarrhalis to 21 antimicrobial drugs: validity of current NCCLS criteria for the interpretation of agar disk diffusion antibiograms. Chemotherapy. May-Jun 1997;43(3):159-67. [Medline].
Varon E, Levy C, De La Rocque F, et al. Impact of antimicrobial therapy on nasopharyngeal carriage of Streptococcus pneumoniae, Haemophilus influenzae, and Branhamella catarrhalis in children with respiratory tract infections. Clin Infect Dis. Aug 2000;31(2):477-81. [Medline].
Walker ES, Neal CL, Laffan E, et al. Long-term trends in susceptibility of Moraxella catarrhalis: a population analysis. J Antimicrob Chemother. Feb 2000;45(2):175-82. [Medline].
Wise R, Andrews JM. A comparison of the activity of ciprofloxacin and levofloxacin with other agents against respiratory tract pathogens. J Chemother. Aug 1998;10(4):276-9. [Medline].
Moraxella catarrhalis, Neisseria catarrhalis, N catarrhalis, Micrococcus catarrhalis, M catarrhalis, Branhamella catarrhalis, B catarrhalis, upper respiratory tract infections, lower respiratory tract infections, otitis media, sinusitis, chronic obstructive pulmonary disease, COPD, pneumonia, Moraxella catarrhalis infection, M catarrhalis infection, M catarrhalis endocarditis, M catarrhalis pneumonia, M catarrhalis otitis media, M catarrhalis sinusitis, M catarrhalis bacteremia, Moraxella catarrhalis endocarditis , Moraxella catarrhalis pneumonia , Moraxella catarrhalis otitis media , Moraxella catarrhalis sinusitis , Moraxella catarrhalis bacteremia
Michael Constantinescu, MD, Staff Pathologist, Christus St Frances Cabrini Hospital
Michael Constantinescu, MD is a member of the following medical societies: American Society for Clinical Pathology, College of American Pathologists, and United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.
Joseph A Bocchini, Jr, MD, Medical Director of Children's Hospital, Director of Clinical Virology Laboratory, Chairman, Professor, Chief of Infectious Disease Section, Department of Pediatrics, Louisiana State University at Shreveport
Joseph A Bocchini, Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.
Ronald Silberman, PhD, Director of Clinical Microbiology Laboratory, Louisiana State University Hospital; Professor, Department of Pathology, Louisiana State University Medical Center at Shreveport
Ronald Silberman, PhD is a member of the following medical societies: American Society for Microbiology
Disclosure: Nothing to disclose.
James D Cotelingam, MBBS, MD, Head of Hematopathology, Director of Clinical Laboratories, Professor, Department of Pathology, Louisiana State University at Shreveport
James D Cotelingam, MBBS, MD is a member of the following medical societies: American College of Physician Executives, American Society for Clinical Pathology, Association of Military Surgeons of the US, College of American Pathologists, and New York Academy of Sciences
Disclosure: Nothing to disclose.
Maria D Mileno, MD, Assistant Professor, Department of Internal Medicine, Division of Infectious Diseases, Brown University
Maria D Mileno, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine, and Sigma Xi
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings
Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
© 1994-
by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)