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      Drugs & Diseases > Infectious Diseases

      Haemophilus Influenzae Infections Medication

      Updated: Aug 30, 2023
      • Author: Joseph Adrian L Buensalido, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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      Medication

      Medication Summary

      Initially, patients with invasive and serious H influenzae infections are best treated with an intravenous third-generation cephalosporin until antibiotic sensitivities become available. It is important to monitor the resistance rates (in the hospital or the region) of H influenzae to the different antibiotics to guide empiric antimicrobial choices while awaiting susceptibility results.

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      Antibiotics

      Class Summary

      Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting. Penicillins are useful in management of mucosal infections caused by nonencapsulated H influenzae. However, up to 25-50% of isolates produce beta-lactamase so are resistant to this class of drugs. Third-generation cephalosporins are highly effective in H influenzae infections. Meropenem or ampicillin and chloramphenicol are alternative regimens.

      Azithromycin (Zithromax)

      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.

      Plasma concentrations are very low, but tissue concentrations are much higher, giving it value in treating intracellular organisms. Has a long tissue half-life.

      Cefotaxime (Claforan)

      Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.

      Ceftriaxone (Rocephin)

      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 one or more penicillin-binding proteins. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse because of the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested. Highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose excreted unchanged in urine, and remainder secreted in bile and, ultimately, in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding has been reported to decrease from 95% bound at plasma concentrations < 25 mcg/mL to 85% bound at 300 mcg/mL.

      Cefuroxime (Ceftin, Zinacef)

      This second-generation cephalosporin maintains gram-positive activity of first-generation cephalosporins; adds activity against Proteus mirabilis, H influenzae, Escherichia coli, Klebsiella pneumoniae, and Moraxella catarrhalis. Binds to penicillin-binding proteins and inhibits final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. It is not recommended for treatment of Hib meningitis but may be used for other Hib infections. Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration.

      Ampicillin (Marcillin, Omnipen, Polycillin, Principen)

      Broad-spectrum penicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take PO medication.

      Amoxicillin (Trimox, Amoxil, Trimox)

      Derivative of ampicillin and has similar antibacterial spectrum, namely certain gram-positive and gram-negative organisms. Superior bioavailability and stability to gastric acid and has broader spectrum of activity than penicillin. Somewhat less active than that of penicillin against pneumococcus. Penicillin-resistant strains also resistant to amoxicillin, but higher doses may be effective. More effective against gram-negative organisms (eg, Neisseria meningitidis, H influenzae) than penicillin. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

      Amoxicillin and clavulanic acid (Augmentin)

      Amoxicillin 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 or intolerant to the macrolide class. Is usually well tolerated and provides good coverage to most infectious agents. Not effective against Mycoplasma and Legionella species. The half-life of oral dosage form is 1-1.3 h. Has good tissue penetration but does not enter CSF. For children >3 months, 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. The bid dosing schedule reduces incidence of diarrhea.

      Chloramphenicol (Chloromycetin)

      May be used in patients who are allergic to penicillins and cephalosporins. Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Active in vitro against a wide variety of bacteria, including gram-positive, gram-negative, aerobic, and anaerobic organisms. Well-absorbed from GI tract and metabolized in the liver, where it is inactivated by conjugation with glucuronic acid and then excreted by the kidneys. Oral form is not available in the United States.

      Erythromycin and sulfisoxazole (Eryzole, Pediazole)

      Erythromycin is a macrolide antibiotic with a large spectrum of activity. Erythromycin binds to the 50S ribosomal subunit of the bacteria, which inhibits protein synthesis. Sulfisoxazole expands erythromycin's coverage to include gram-negative bacteria. Sulfisoxazole inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid. Good choice for PO therapy for otitis media. May be used in patients who are allergic to penicillins and cephalosporins.

      Meropenem (Merrem IV)

      Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria. Has slightly increased activity against gram-negative species and slightly decreased activity against staphylococci and streptococci compared with imipenem. In contrast to imipenem, indicated for treatment of bacterial meningitis, including pediatric meningitis.

      Rifampin (Rifadin)

      Used for chemoprophylaxis in Hib infections.

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      Glucocorticoids

      Class Summary

      These agents are used as adjunctive therapy in H influenza meningitis for the anti-inflammatory effects and prevention of sensorineural deafness. Administer before or with antibiotics, not after. Utility of steroids has been demonstrated primarily in nonimmunized children, and its usefulness in adults or vaccinated children is not known.

      Dexamethasone (Decadron, Baldex)

      Has many pharmacologic benefits but significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, and inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6, IL-2, and IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down granulocyte aggregates and improves pulmonary microcirculation.

      Adverse effects are hyperglycemia, hypertension, weight loss, GI bleeding or perforation synthesis, cerebral palsy, adrenal suppression, and death. Most of the adverse effects of corticosteroids are dose-dependent or duration-dependent.

      Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining property of hydrocortisone.

      Patients can be switched from an IV to PO regimen in a 1:1 ratio.

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