eMedicine Specialties > Dermatology > Bacterial Infections

Meningococcemia: Treatment & Medication

Author: Elizabeth L Tanzi, MD, Co-Director, Laser Surgery, Washington Institute of Dermatologic Laser Surgery
Coauthor(s): Nanette Silverberg, MD, Assistant Clinical Professor, Department of Dermatology, Columbia University School of Medicine; Director of Pediatric Dermatology, Department of Dermatology, St Luke's Roosevelt Hospital Center, Maimonides Medical Center and Beth Israel Medical Center
Contributor Information and Disclosures

Updated: Sep 11, 2009

Treatment

Medical Care

  • The most important measure in treating meningococcemia is early detection and rapid administration of antibiotics. Penicillin G is the antibiotic of choice for susceptible isolates. A third-generation cephalosporin (eg, cefotaxime, ceftriaxone) can be used initially in septic patients while the diagnosis is being confirmed or in countries such as the United Kingdom or Spain, where penicillin-resistant strains of N meningitidis have been isolated.6
  • Intensive supportive care is required for patients with fulminant meningococcemia. Components of treatment include antibiotic therapy, ventilatory support, inotropic support, and intravenous fluids. Central venous access facilitates the administration of massive amounts of volume expanders and inotropic medications needed for adequate tissue perfusion. If disseminated intravascular coagulation (DIC) is present, fresh frozen plasma may be indicated. Treatment is individualized depending on the severity of hemodynamic compromise of the patient.
  • Many experimental and alternate therapies have been tried with varying success.7 Currently under study are treatments to inhibit inflammatory mediators (eg, monoclonal antibodies to endotoxin, tumor necrosis factor, interleukin 1, interleukin 6, and interferon-gamma). Anecdotal reports show removal of inflammatory mediators by dialysis may offer some benefit. Fibrinolytic treatment using recombinant tissue plasminogen activator or the administration of highly purified protein C concentrate may prove to be helpful adjuncts to conventional therapy to improve tissue perfusion in the presence of DIC.8
  • Several clinical guideline summaries related to meningococcal disease are available, as follows:

Surgical Care

Patients who survive the initial acute phase of fulminant meningococcemia are at increased risk for serious complications as a result of poor tissue perfusion.12

  • Early in the course of tissue injury, conservative therapy is recommended until a distinct line of demarcation is apparent between viable and nonviable tissue.
  • Once the patient is stable, debridement of all necrotic tissue is essential and may necessitate extensive removal of skin, subcutaneous tissue, and muscle.
  • Large defects may be covered using microvascular free flaps or skin grafts.
  • The use of artificial skin can spare the patient immediate use of autograft sites, which frequently are limited.13
  • Avoid amputation whenever useful function of a limb can be salvaged.
  • Poor tissue perfusion may also lead to dental complications that require extensive extraction of severely affected teeth.14

Consultations

  • Infectious disease specialist - To assist in management and provide guidance in antimicrobial therapy
  • Preventive medicine specialist - To evaluate the community risk associated with an index case and initiate reporting to local and regional health authorities if indicated

Medication

The goals of pharmacotherapy are to eradicate the microorganism, to reduce morbidity, and to prevent complications.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.


Penicillin G (Pfizerpen)

Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Adult

300,000 U/kg/d up to 24 million U/d IV in divided doses q4h until 5-7 d after temperature has returned to normal

Pediatric

Administer as in adults

Probenecid can increase effects; coadministration of tetracyclines can decrease effects; may increase methotrexate toxicity; may decrease contraceptive efficacy; may interfere with immunological response to live typhoid vaccine; concurrent administration with aminoglycoside therapy may result in inactivation of aminoglycoside (amikacin appears to possess greatest stability in presence of penicillins; in treatment of severely ill patients requiring both penicillin and aminoglycoside therapy, amikacin is aminoglycoside of choice)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function, preexisting seizure disorder, or patients with electrolyte abnormalities (contains 1.7 mEq of potassium per million U)


Chloramphenicol (Chloromycetin)

Binds to 50-S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria. Use if patient is allergic to penicillin.

Adult

1 g IV q6h until 5-7 d after temperature has returned to normal

Pediatric

12.5-25 mg/kg IV q6h until 5-7 d after temperature has returned to normal; not to exceed 2-4 g/d

If administered concurrently with barbiturates, serum levels may decrease while barbiturate levels may increase, causing toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity (chloramphenicol levels may be increased or decreased); may antagonize effect of beta-lactam antibiotics; dosing adjustments of cyclosporine or tacrolimus may be required with concurrent penicillin administration; may interfere with immunological response to live typhoid vaccine

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

Precautions

Use only for indicated infections or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (eg, aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately every 2 d while in therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, anemia, or findings attributable to chloramphenicol; adjust dose in liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (gray syndrome); may result in false-positive reaction for urine glucose using copper reduction methods (Clinitest, Benedict solution, or Fehling solution)


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.
Use for penicillin-resistant strains.

Adult

2 g IV/IM q12h until 5-7 d after temperature has returned to normal

Pediatric

50-100 mg/kg/d IV/IM divided q12h until 5-7 d after temperature has returned to normal; not to exceed 2 g/d

Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Documented hypersensitivity; hyperbilirubinemic neonates (increased risk of bilirubin encephalopathy [kernicterus])

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

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; caution in breastfeeding; caution in history of gastrointestinal disease, particularly colitis; may interfere with immunological response to live typhoid vaccine


Rifampin (Rimactane, Rifadin)

Inhibits DNA-dependent bacterial but not mammalian RNA polymerase.
Use for chemoprophylaxis after contact. Regimen below does not treat active infection.

Adult

600 mg PO bid for 2 d

Pediatric

10 mg/kg PO bid for 2 d

Induces microsomal enzymes, which may decrease effects of acetaminophen, oral anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, oral contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; blood pressure may increase with coadministration of enalapril; coadministration with isoniazid may result in higher rate of hepatotoxicity than with either agent alone (discontinue one or both agents if alterations in LFTs occur)

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

Precautions

Obtain CBC counts and baseline clinical chemistry values prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs; if treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur


Cefotaxime (Claforan)

Arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth. Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.
Use for penicillin-resistant strains.

Adult

Bacterial septicemia (for life-threatening infections): 2 g IV q4h

Pediatric

Neonates, premature and normal gestational age: 0-1 week: 50 mg/kg IV q12h;
1-4 week: 50 mg/kg IV q8h
1 month to 12 years and <50 kg: 50-180 mg/kg/d IV divided into 4-6 doses depending on type and severity of infection; not to exceed 12 g/d
1 month to 12 years and >50 kg: 2 g IV q6-8h

Probenecid may increase levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

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; has been associated with severe colitis; caution in history of gastrointestinal disease, especially colitis; may result in falsely elevated theophylline serum levels as measured by HPLC (EMIT, TDx) theophylline assay methods do not appear to be subject to cefotaxime interference); may interfere with immunological response to live typhoid vaccine

More on Meningococcemia

Overview: Meningococcemia
Differential Diagnoses & Workup: Meningococcemia
Treatment & Medication: Meningococcemia
Follow-up: Meningococcemia
References

References

  1. Horino T, Kato T, Sato F, et al. Meningococcemia without meningitis in Japan. Intern Med. 2008;47(17):1543-7. [Medline].

  2. Razminia M, Salem Y, Elbzour M, Teves D, Deshmukh H, Khosla S. Importance of early diagnosis and therapy of acute meningococcal myocarditis: a case report with review of literature. Am J Ther. May-Jun 2005;12(3):269-71. [Medline].

  3. Jarva H, Ram S, Vogel U, Blom AM, Meri S. Binding of the complement inhibitor C4bp to serogroup B Neisseria meningitidis. J Immunol. May 15 2005;174(10):6299-307. [Medline].

  4. Nkosi J, Thakrar A, Kumar K, et al. Meningococcal serotype Y myopericarditis. Diagn Microbiol Infect Dis. Feb 2009;63(2):223-7. [Medline].

  5. Endler G, Marculescu R, Starkl P, et al. Polymorphisms in the interleukin-1 gene cluster in children and young adults with systemic meningococcemia. Clin Chem. Mar 2006;52(3):511-4. [Medline].

  6. Tuncer AM, Gur I, Ertem U, et al. Once daily ceftriaxone for meningococcemia and meningococcal meningitis. Pediatr Infect Dis J. Oct 1988;7(10):711-3. [Medline].

  7. Aiuto LT, Barone SR, Cohen PS, Boxer RA. Recombinant tissue plasminogen activator restores perfusion in meningococcal purpura fulminans. Crit Care Med. Jun 1997;25(6):1079-82. [Medline].

  8. Rivard GE, David M, Farrell C, Schwarz HP. Treatment of purpura fulminans in meningococcemia with protein C concentrate. J Pediatr. Apr 1995;126(4):646-52. [Medline].

  9. [Guideline] American Academy of Pediatrics Committee on Infectious Diseases. Prevention and control of meningococcal disease: recommendations for use of meningococcal vaccines in pediatric patients. Pediatrics. Aug 2005;116(2):496-505. [Medline].

  10. [Guideline] Centers for Disease Control and Prevention (CDC) Advisory Committee on Immunization Practices. Revised recommendations of the Advisory Committee on Immunization Practices to Vaccinate all Persons Aged 11-18 Years with Meningococcal Conjugate Vaccine. MMWR Morb Mortal Wkly Rep. Aug 10 2007;56(31):794-5. [Medline].

  11. [Guideline] Scottish Intercollegiate Guidelines Network (SIGN). Management of invasive meningococcal disease in children and young people. A national clinical guideline. National Guidelines Clearinghouse. May 2008.

  12. Herrera R, Hobar PC, Ginsburg CM. Surgical intervention for the complications of meningococcal-induced purpura fulminans. Pediatr Infect Dis J. Aug 1994;13(8):734-7. [Medline].

  13. Besner GE, Klamar JE. Integra Artificial Skin as a useful adjunct in the treatment of purpura fulminans. J Burn Care Rehabil. Jul-Aug 1998;19(4):324-9. [Medline].

  14. Faibis S, Widmer R, Sapir S, Peretz B, Shapira J. Meningococcal septicaemia and dental complications: a literature review and two case reports. Int J Paediatr Dent. May 2005;15(3):213-9. [Medline].

  15. Aaberge IS, Oster P, Helland OS, et al. Combined administration of meningococcal serogroup B outer membrane vesicle vaccine and conjugated serogroup C vaccine indicated for prevention of meningococcal disease is safe and immunogenic. Clin Diagn Lab Immunol. May 2005;12(5):599-605. [Medline].

  16. Zeidan A, Tariq S, Faltas B, Urban M, McGrody K. A case of primary meningococcal pericarditis caused by Neisseria meningitidis serotype Y with rapid evolution into cardiac tamponade. J Gen Intern Med. Sep 2008;23(9):1532-5. [Medline].

  17. Parmentier L, Garzoni C, Antille C, Kaiser L, Ninet B, Borradori L. Value of a novel Neisseria meningitidis--specific polymerase chain reaction assay in skin biopsy specimens as a diagnostic tool in chronic meningococcemia. Arch Dermatol. Jun 2008;144(6):770-3. [Medline].

  18. Centers for Disease Control and Prevention. Prevention and control of meningococcal disease. Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. Jun 30 2000;49:1-10. [Medline].

  19. Darmstadt GL. Acute infectious purpura fulminans: pathogenesis and medical management. Pediatr Dermatol. May-Jun 1998;15(3):169-83. [Medline].

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  21. Hazelzet JA. Diagnosing meningococcemia as a cause of sepsis. Pediatr Crit Care Med. May 2005;6(3 Suppl):S50-4. [Medline].

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  23. Ikeda C, Capozzi A. Management of skin loss in meningococcal infection. Ann Plast Surg. Oct 1987;19(4):375-7. [Medline].

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  25. Periappuram M, Taylor MR, Keane CT. Rapid detection of meningococci from petechiae in acute meningococcal infection. J Infect. Nov 1995;31(3):201-3. [Medline].

  26. Ploysangam T, Sheth AP. Chronic meningococcemia in childhood: case report and review of the literature. Pediatr Dermatol. Nov-Dec 1996;13(6):483-7. [Medline].

  27. Salzman MB, Rubin LG. Meningococcemia. Infect Dis Clin North Am. Dec 1996;10(4):709-25. [Medline].

  28. Schaller RT Jr, Schaller JF. Surgical management of life-threatening and disfiguring sequelae of fulminant meningococcemia. Am J Surg. May 1986;151(5):553-6. [Medline].

  29. van Deuren M, van Dijke BJ, Koopman RJ, et al. Rapid diagnosis of acute meningococcal infections by needle aspiration or biopsy of skin lesions. BMJ. May 8 1993;306(6887):1229-32. [Medline].

Further Reading

Keywords

meningococcemia, meningococcal sepsis, meningococcal disease, meningococcal infection, meningitis, bacteremia, meningococcemia, acute meningococcal septicemia, adrenal hemorrhage, Waterhouse-Friderichsen syndrome, meningococcal septicemia

Contributor Information and Disclosures

Author

Elizabeth L Tanzi, MD, Co-Director, Laser Surgery, Washington Institute of Dermatologic Laser Surgery
Elizabeth L Tanzi, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, and American Society for Laser Medicine and Surgery
Disclosure: Nothing to disclose.

Coauthor(s)

Nanette Silverberg, MD, Assistant Clinical Professor, Department of Dermatology, Columbia University School of Medicine; Director of Pediatric Dermatology, Department of Dermatology, St Luke's Roosevelt Hospital Center, Maimonides Medical Center and Beth Israel Medical Center
Nanette Silverberg, MD is a member of the following medical societies: American Academy of Dermatology, American Academy of Pediatrics, American Association of University Women, American Medical Association, American Medical Women's Association, Dermatology Foundation, International Society of Pediatric Dermatology, Phi Beta Kappa, Sigma Xi, Society for Pediatric Dermatology, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Medical Editor

Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle
Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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