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Meningococcemia Treatment & Management

  • Author: Mahmud H Javid, MBBS; Chief Editor: John L Brusch, MD, FACP  more...
 
Updated: Oct 14, 2015
 

Approach Considerations

Because mortality may be reduced with early antibiotic therapy, patients with a meningococcal rash should receive parenteral antibiotics by means of an intravenous (IV) or intramuscular (IM) route as soon as the diagnosis is suspected. In the United Kingdom, prehospital treatment with benzylpenicillin is recommended.[64]

Intramuscular antibiotic injections may be less effective in a patient with shock and poor tissue perfusion.

Other than antimicrobial treatment, supportive measures in meningococcal disease may be needed to correct circulatory collapse. Any adrenal insufficiency requires corticosteroid replacement.

Medical care for meningococcal infections should also address community management and the emergency management of meningococcal septicemia and meningitis.[7] This may include treating shock and increased ICP, as well as the use of new and experimental therapies.[2]

Chemoprophylaxis for meningococcal infection should be administered to intimate household, daycare center, and nursery school contacts of sporadic cases. Vaccinate household and other intimate contacts.

Although increasingly well recognized and managed in children, meningococcal disease often is poorly managed in adults in medical settings. Fluid resuscitation may not be sufficiently aggressive, early intubation often is not considered, and the rapidity of disease progression in an adult often is not understood.

For information regarding the recognition and management of meningococcal disease in family practice, see the chart below. Additional resources are available at Meningitis.org.

Chart for family practice recognition and manageme Chart for family practice recognition and management of meningococcal disease (courtesy of Meningitis.org).

Treatment of complications

Any complications of meningococcal disease must also be treated. One of the most common complications that occurs during the course of treatment is arthritis, which has been found in about 10% of patients with meningococcal disease. This complication usually occurs within the first few days of treatment and manifests as effusion of a large joint, often the knee. Joint effusions usually resolve without a change in therapy; occasionally, repeated arthrocentesis is needed to control symptoms.

Other possible complications include ischemic conditions caused by the coagulation abnormality and neurologic complications of meningitis. The patient must be observed for any neurologic sequelae; the frequency of neurologic abnormalities seems to be related to the severity of the acute disease. Some neurologic sequelae can develop in the absence of meningitis.

Inpatient care

Hospitalization is required for severely ill patients with fever, headache, and petechiae. Promptly begin antibiotic treatment. Respiratory precautions generally include placement of the patient in a private room with proper air handling and the use of a respiratory mask by any person entering the patient's room. Discontinue respiratory isolation precautions after 24 hours of antibiotics.

Monitor blood pressure, urine output, and cardiac function, as well as platelets, fibrin, and fibrin degradation products.

Supportive care may be needed, including maintenance of fluid and electrolyte balance and vasoactive drugs in shock (eg, dopamine).

Suspect fulminant meningococcemia in patient with hypotension and severe coagulation abnormalities. In such cases, monitoring in an intensive care setting is required.

Diet and activity

Patients with meningitis or fulminant meningococcemia are at risk of vomiting and should be prevented from taking anything by mouth prior to substantial clinical improvement with antimicrobial therapy.

The level of patient activity is determined by the severity of the presentation. Bed rest is recommended for patients suspected of having meningococcal disease. In most severe cases, patients are bed bound.

Transfer

Once the patient is stabilized, attempt to transfer him or her to a tertiary care center because meningococcal sepsis frequently produces multisystem organ dysfunction. Transfer to a PICU is necessary in approximately 20% of pediatric cases of meningococcal infection.

Guidelines

Several clinical guideline summaries related to meningococcal disease are available, as follows:

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Emergency Management of Meningococcal Infection

Although many meningococcal infections rapidly improve when treated with antibiotics, meningococcal disease may quickly progress in some cases; the time lag from the appearance of the first symptoms to death may be only a few hours.

Because the mortality rate in meningococcal disease is 10%, all patients with fever and petechiae warrant urgent initial assessment and treatment and subsequent careful and repeated assessment. The initial assessment should be conducted to identify major clinical problems.

The following findings may help in the identification of severely ill patients whose condition may deteriorate and who are likely to need intensive care:

  • Shock
  • Absence of meningitis
  • Rapidly extending rash
  • Low WBC count
  • Coagulopathy
  • Deteriorating level of consciousness

Shock and increased ICP, which are underlying processes in meningococcal disease that lead to death, may coexist. However, increased ICP is more common in patients with only meningitis.

For information about the emergency management of meningococcal disease in children and adults, see the flow charts below.

Flow chart shows guidelines for the emergency mana Flow chart shows guidelines for the emergency management of meningococcal disease in children. These guidelines may be reprinted for use in clinical areas and are available at Meningitis.org.
Flow chart shows guidelines for the emergency mana Flow chart shows guidelines for the emergency management of meningococcal disease in adult patients. These guidelines may be reprinted for use in clinical areas and are available from Meningitis.org.

Managing shock

After basic life support and antibiotics are administered, the next priority is treating shock. Basic life support should include the administration of oxygen at a rate of 10-15L/min by means of a facial mask.

Any patient with cool extremities, prolonged capillary refill time, and tachycardia should be considered to have shock.

The initial therapy for shock is volume replacement at a rate of 20mL/kg. In the United Kingdom, the use of 4.5% human albumin solution is generally recommended, although some US and UK centers use normal saline. A satisfactory response to volume replacement is a reduction in heart rate and improved peripheral perfusion. The first bolus of fluid may be repeated to achieve this response.

The patient's condition may stabilize with only volume replacement, but the patient requires close monitoring and reassessment to detect further signs of shock or pulmonary edema (due to capillary leak syndrome). The goal of circulatory support is to maintain tissue perfusion and oxygenation.[25]

Patients who do not respond to initial volume replacement require further volume replacement and may need inotropic support, such as the use of dopamine or dobutamine (10-20 mcg/kg/min), which may be administered via a peripheral vein until central venous access is established. Patients with persistent hypotension may need an infusion of adrenaline (0.1-5 mcg/kg/min), which must be administered via central venous access.

Endotracheal intubation and ventilation are recommended in patients who still have signs of shock after they have received volume replacement of more than 40mL/kg. Even patients who are apparently awake and alert have a high risk of pulmonary edema.

Some patients require fluid replacement with as much as twice their circulating blood volume in the first hours after presentation, but additional volume should be administered only after positive pressure ventilation is established.

Biochemical correction of acidosis, hypoglycemia, hypokalemia, hypocalcemia, and hypomagnesemia is usually required. Correct coagulopathy and anemia with the use of fresh frozen plasma and blood, as appropriate.

Managing raised intracranial pressure

Suspect increased ICP if the patient has a decreased level of consciousness; focal neurological signs; unequal, dilated or poorly reacting pupils; abnormal posturing or seizures; or relative hypertension or bradycardia or if the patient is agitated or combative. Because papilledema is a late sign, its absence should not reassure the treating team, because raised ICP can still be present.

After initiating basic life support measures and administering antibiotics, the therapeutic goal is to maintain oxygen and nutrient delivery to the brain. For this reason, shock must be corrected in individuals with both shock and increased ICP to maintain cerebral perfusion pressure. After correcting shock with volume replacement and inotropic support as necessary, cautiously manage the fluid balance to avoid further increasing the ICP.

Consider the use of mannitol (0.25 g/kg IV over 10 min), followed by furosemide (1 mg/kg IV), when increased ICP is suspected. These drugs can help to control the ICP during elective intubation.

Immediately institute measures to stabilize the ICP. These may include intubation and ventilation in order to control PaCO2 between 4-4.5 kPa, sedation and muscle relaxation, and elevation of the patient's head by 30°.

In addition, find and correct biochemical abnormalities and treat seizures, if present, using standard resuscitation guidelines; do not attempt lumbar puncture.

Treatment of patients with limited shock and no increased ICP

Reassess patients with limited shock and no increased ICP, as well as patients who respond rapidly to minimal volume replacement, for signs of deterioration during the first 48 hours following admission.

The use of corticosteroids in meningitis may be considered. Several studies revealed that adjunctive dexamethasone reduces sensorineural hearing loss (but not mortality or other neurologic sequelae) in children and infants with H influenzae type B meningitis. Few adverse effects occur with dexamethasone administration. No reports of delayed CSF sterilization or treatment failure are known. A meta-analysis of findings from randomized, controlled trials suggested that such treatment has a benefit in preventing sequelae in meningococcal meningitis and pneumococcal meningitis in childhood.

Although data are poor for meningococcal meningitis, the pathophysiologic events are likely to be similar to those of other forms of bacterial meningitis. In some animal models, anti-inflammatory therapy was beneficial. No evidence of the benefits of steroid use in patients with septic shock is known, and steroid use is necessary only with meningitis.

If hypoadrenalism is suspected because of resistance to large doses of inotropic drugs, administer adrenal replacement doses of hydrocortisone.

Steroids have not yet been proven helpful in septicemia. A phase 2, multicenter pilot study is underway in the United Kingdom to examine the safety and endocrine/inflammation/coagulation profiles seen in low-dose replacement corticosteroid therapy for sepsis in children and to inform a large, multicenter trial. Replacement corticosteroids should not currently be used routinely in pediatric sepsis (and are now controversial in adult sepsis).[65, 66]

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Pharmacologic Therapy

The most important measure in treating meningococcemia is early detection and rapid administration of antibiotics. Penicillin G has been 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.[67, 68] . Because of failure effectiveness and easier administration schedule, the third-generation cephalosporins have become the preferred class of antibiotics.

These cephalosporins penetrate sufficiently into CSF from blood and are useful in the treatment of bacterial meningitis. They are known to have a potent action against meningococci, as do chloramphenicol, and rifampin. Meningococci have also been found to be susceptible to ciprofloxacin at low concentrations.

Meningococci are not inherently susceptible to vancomycin, polymyxin, or achievable serum levels of aminoglycoside antibiotics.

Intensive supportive care is required for patients with fulminant meningococcemia. Components of treatment include antibiotic therapy, ventilatory support, inotropic support, and IV 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.

Empiric therapy

Empiric antibiotic therapy ensures coverage of likely meningeal pathogens when no rash is present, when the etiology of meningitis is uncertain, and when an immediate microbiologic diagnosis is unavailable. This therapy can be modified in favor of appropriate specific therapy when the organism is grown or when its antibiotic sensitivities are known.

A third-generation cephalosporin is the appropriate antibiotic until culture results are available. Although meningococcal infection is the most common bacterial cause of a petechial or purpuric rash and meningitis, other organisms (including H influenzae type B and Streptococcus pneumoniae) can cause shock and a nonblanching rash.

Although H influenzae type B is now an uncommon cause of meningitis in developed countries with modern vaccination programs, antibiotic therapy should cover this organism. Most cases of bacterial meningitis are due to N meningitides, and most other cases are due to S pneumoniae. In the United States, most cases are due to S pneumoniae.

Empiric antibiotic therapy for meningitis based on age is as follows:

  • Neonates - Ampicillin and cefotaxime
  • Infants aged 1-3 months - Ampicillin and cefotaxime
  • Older infants, children, and adults - Cefotaxime or ceftriaxone

In 2007 the US Food and Drugs Administration (FDA) issued an alert that led to changes in the prescribing information for ceftriaxone. Dilution, mixing, or y-site infusion with calcium-containing IV solutions may increase the risk for precipitant to formin vivo. Initially, the FDA recommended that ceftriaxone no longer be administered within 48 hours of the completion of calcium-containing solutions, including parenteral nutrition, regardless of whether the drugs were administered by different infusion catheters.[69, 70]

In the United Kingdom, the Medicines and Healthcare Products Regulatory Agency (MRHA) issued a drug safety bulletin stating that ceftriaxone should not be given simultaneously with calcium-containing infusions.[71]

However, in April 2009, the FDA changed its advice; the agency no longer cautions against the use of ceftriaxone and calcium-containing solutions, except in neonates younger than 28 days.[72]  

Dexamethasone is indicated in the treatment of known or suspected pneumococcal meningitis in adults and children with H influenzae type B meningitis. It is of no benefit in meningococcal meningitis. If started empirically, it should be discontinued as soon as N meningitides is retrieved.[73]

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Surgical Treatment of Ischemic Complications

Patients who survive the initial acute phase of fulminant meningococcemia are at increased risk for serious complications as a result of poor tissue perfusion.[74]

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, débridement 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.[75] Avoid early limb amputation, because significant tissue recovery may occur as the disease progresses.

Poor tissue perfusion may also lead to dental complications that require extensive extraction of severely affected teeth.[76]

Anecdotally, fasciotomy may preserve limb and digit function in severe meningococcal septicemia when impending peripheral gangrene and increased compartment pressures are present. Measure compartment pressures and assess peripheral pulses with Doppler ultrasonography when patients have impaired limb perfusion or severe edema.

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Monitoring and Follow-Up

Pericarditis can occur while patients are recuperating from meningococcemia. Consider pericarditis in patients with fever and shortness of breath upon minimal exertion during the recovery period.

Late skeletal deformities are rare, but epiphyseal avascular necrosis and epiphyseal-metaphyseal defects have been described. These usually occur in the lower extremities and result in angular deformity and inequality of leg length.

Observe patients for any late neurologic sequelae. Abnormal findings on electroencephalography or cerebral computed tomography (CT) scanning, as well as epileptogenic activity, sensorineural hearing loss, impaired vestibular function, and neuropsychological impairment, have been found in up to 30% of survivors 1 year after an episode of meningococcal disease. The frequency of serious neurologic sequelae in individuals who survive an episode is 3%.

Follow-up care at least 6 weeks after meningococcal infection should include the following:

  • Ongoing management of specific complications such as amputations, skin grafting, or renal failure
  • Full physical examination
  • Assessment of plasma complement levels - Eg, total hemolytic complement, C3, and C4, with or without properdin
  • Serologic confirmation of the diagnosis if no diagnosis was made at the time of presentation
  • Audiologic function testing
  • Basic assessment of psychological status after intensive care, if relevant
  • Possible vaccination of contacts if an outbreak of group A, C, Y, or W-135 disease occurs
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Vaccination

Meningococci are gram-negative diplococci. Pathogenic strains are enveloped in a polysaccharide capsule, which facilitates invasion and which is an obvious target for candidate vaccines. The serogroup of the organism is assigned from the reaction of sera to the polysaccharide capsule.[77, 78, 79]

Purified polysaccharide vaccines against encapsulated bacteria (which, in addition to meningococci, include Haemophilus and pneumococci) are poorly immunogenic in young children. In contrast, the conjugate vaccine for group C meningococci in which the serogroup C meningococcal polysaccharide is conjugated to the protein CRM197 appears to provide immunogenic protection to young children. It was administered to all children during 1999-2000 in the United Kingdom.

In January 2001, the short-term effectiveness of this vaccine in England was reported to be 97% for teenagers and 92% for toddlers. These early results confirmed the superiority of this vaccine to plain C polysaccharide vaccines.

The UK immunization schedule has since changed to include a meningococcal booster at 12 months (combined with H influenzae type b [Hib] booster) because studies showed that the efficacy of the vaccine declined at 1 year to around 80%.

In 2013, the CDC’s Advisory Committee on Immunization Practices (ACIP) published a compilation and summary of all of its recommendations regarding the prevention and control of meningococcal disease in the United States.[4] The ACIP recommended that routine vaccination be provided to adolescents aged 11 through 18 years (with a single dose of vaccine administered at age 11 or 12 years and a booster dose given at age 16 years for persons who received the first dose before age 16 years).

In addition, the ACIP recommended that persons aged 2 months or older who are at increased risk for meningococcal disease also be vaccinated, including the following:

  • Persons aged ≥2 months with certain medical conditions such as anatomic or functional asplenia or complement component deficiency (dosing schedule and interval for booster dose varies by age at time of previous vaccination)
  • Special populations such as unvaccinated or incompletely vaccinated first-year college students living in residence halls, military recruits, or microbiologists with occupational exposure (indication for booster dose 5 years after prior dose if at continued risk)
  • Persons aged ≥9 months who travel to or reside in countries in which meningococcal disease is hyperendemic or epidemic, particularly if contact with the local population will be prolonged

Types of vaccines

Four meningococcal vaccines are available in the United States: 1 quadrivalent polysaccharide vaccine (MPSV4), 2 quadrivalent conjugate vaccines (MenACWY), and 1 bivalent conjugate vaccine (meningococcal groups C and Y and Hib tetanus toxoid conjugate vaccine [Hib-MenCY-TT]). Age range and dosing information for these are as follows[4] :

  • MPSV4 (Menomune, Sanofi Pasteur)- Approved by the FDA for use as a single dose in persons 2 years of age and older
  • MenACWY-D (Menactra, Sanofi Pasteur) – Approved as a single dose for persons 2-55 years old and as a 2-dose series in children 9-23 months old
  • MenACWY-CRM (Menveo, Novartis Vaccines) – Approved as a single dose for persons 2-55 years old
  • Hib-MenCY-TT (MenHibrix; GlaxoSmithKline Biologicals) – Approved by the FDA as a 4-dose series for children aged 6 weeks through 18 months
  • Trumenba is a serogroup B meningococcal vaccine that was FDA approved in October 2014.
  • Bexsero is a serogroup B meningococcal vaccine that was approved by the FDA in January 2015 for use in patients aged 10-25 years. [80, 81]

The Hib-MenCY-TT vaccine, licensed in June 2012, was the first meningococcal vaccine approved for use in young infants. It is indicated only for infants at high risk for meningococcal disease.[82, 83] The CDC decided not to recommend its routine use in all infants, because the current frequency of meningococcal disease is low and because the vaccine does not contain serotype B, which is responsible for more than half of meningococcal disease cases in children aged 0-59 months.

In October 2013, the ACIP voted to expand the recommendations for the MenACWY-CRM vaccine to include use in infants and young toddlers who are at increased risk for meningococcal disease.[84] The expanded recommendations include the following:

  • Children aged 2 through 23 months with complement deficiencies or asplenia
  • Those living in areas experiencing outbreaks
  • Those traveling to or living in areas with high rates of meningococcal disease, including sub-Saharan Africa and Mecca

The recommended administration schedule for MenACWY-CRM vaccine is at ages 2, 4, 6, and 12 months, with booster doses 3 years after the primary vaccination series and every 5 years thereafter for children who remain at increased risk.

Administration of quadrivalent meningococcal conjugate vaccine (serogroup A, C, W, and Y [MCV 4]) was recommended to protect the high-risk adolescent population. A recent study demonstrated that the meningococcal carriage problems were reduced from 7% prior to vaccine availability in 2005 to 3.2%-4% afterward. Nongroupable (nonpathogenic) strains comprised 88% of the meningococci isolated from the nasopharynx of tested adolescents. Such a reduction may explain, at least partially, the dramatic reduction of severe meningococcal disease.[85]

Serogroup B vaccines

Vaccines against group B serotypes are difficult to make. Because the polysaccharide capsule of the group B meningococcus is chemically and antigenically identical to human brain and fetal antigens, it is poorly immunogenic in humans, and its use may induce autoimmunity.

Other bacterial components, such as bacterial outer membrane proteins, are being investigated for use in vaccines. Vaccines have been prepared by using simple complexes of these proteins. These include vaccines involving outer membrane vesicles, containing outer membrane proteins in spheres of the bacterial lipid membrane.

Although some serogroup B vaccine trials demonstrate an overall efficacy of more than 50%, protection for the most vulnerable age group has not been demonstrated. In those individuals with a detectable immune response, serum bactericidal activity after vaccination seems to be limited to the strain in the vaccine.

Safety considerations

The safety of meningococcal polysaccharide vaccine in pregnant women has not been evaluated, and it should be avoided unless the risk of infection is high. The vaccine is also not routinely indicated for health care workers in the United States.

The risk of Guillain-Barré Syndrome (GBS) seems to be slightly increased among recipients of the MCV4 vaccine.[86] The CDC estimated the rate to be 0.2 per 100,000 person-months in individuals aged 11-19 years who received the vaccine. The background rate was estimated at 0.11 per 100,000 person-months in this population group.

The CDC recommends that persons with a history of GBS not receive MCV4, although persons with a history of GBS at especially high risk for meningococcal disease (eg, microbiologists routinely exposed to isolates of N meningitidis) might consider vaccination.

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Prevention of Secondary Cases

Antimicrobial chemoprophylaxis of close contacts is the primary means of preventing secondary cases of sporadic meningococcal disease. Person-to-person transmission can be interrupted by administration of an antimicrobial that eradicates the asymptomatic nasopharyngeal carrier state. Sulfonamides, rifampin, minocycline, ciprofloxacin, and ceftriaxone are the drugs that have been shown to eradicate meningococci from the nasopharynx.

Because the rate of disease in secondary contacts is highest immediately after the onset of the disease in the patient, chemoprophylaxis should be administered as soon as possible, preferably within 24 hours. If chemoprophylaxis is delayed by more than 14 days, it is probably of limited value, although it is still recommended until 4 weeks after the patient's presentation.

Infection risks

Meningococcal infection is probably introduced into families by asymptomatic adults and then spread through 1 or more household contacts to infect younger family members. Household contacts are defined as individuals who live in the same house with a person who has a meningococcal disease. An operational definition commonly used by public health authorities includes persons eating and sleeping under the same roof as the index case.

The attack rate of meningococcal disease among household contacts has been estimated to be several hundred times greater than that in the general population. The secondary attack rate is inversely proportional to age and is estimated to be approximately 10% in household contacts aged 1-4 years.

The risk of acquiring meningococcal disease may also be increased in other closed populations, such as those of daycare facilities and nursery schools.

Health care workers who are exposed to aerosol secretions from patients with meningococcal disease are 25 times more likely to contract the disease than is the general population.

The likelihood of acquiring infection is increased 100-1000 times in intimate contacts of individuals with meningococcemia.

Chemoprophylaxis

The American Academy of Pediatrics recommends antimicrobial chemoprophylaxis for contacts of persons with invasive meningococcal disease, including household members, individuals at daycare centers and nursery schools, and persons directly exposed to the patient's oral secretions (eg, kissing, sharing of food or beverages) within the 7 days preceding the onset of the illness in the index case.

The decision to administer chemoprophylaxis to other populations should be reached only after consultation with public health authorities, who have a better understanding of the patterns of disease that currently exist in the community.

Consider antimicrobial chemoprophylaxis in hospital personnel who have had direct exposure to the oral secretions of a patient with meningococcal disease from such activities as mouth-to-mouth resuscitation, endotracheal intubation, or endotracheal tube management.

To further decrease the risk of infection in the clinical setting, staff caring for patients with known or suspected meningococcal infections should wear masks, in addition to taking standard precautions.

Patients with meningococcal disease who are hospitalized should be placed on respiratory precautions for the first 24 hours of effective antimicrobial therapy. When this is done, the risk for hospital personnel with casual or indirect contact is believed to be negligible. Antimicrobial chemoprophylaxis is not recommended in hospital personnel who have only casual or indirect contact with a patient with meningococcal disease.

For travelers, antimicrobial chemoprophylaxis should be considered for any passenger who had direct contact with respiratory secretions from an index patient or for anyone seated directly next to an index patient on a prolonged flight (ie, one that lasts ≥8h).

Prophylactic drugs

Rifampin is commonly used for meningococcal prophylaxis of household contacts in the United States, where one third of the prevalent strains are sulfadiazine resistant. A 2-day course of rifampin is recommended. The rapid emergence of rifampin-resistant meningococci precludes the use of this drug in large populations. Chemoprophylaxis of sulfadiazine-resistant meningococci with rifampin should be accompanied by close observation of household contacts for signs of disease.

A single dose of ciprofloxacin has been found to provide an effective alternative to rifampin for the eradication of meningococcal carriage in adults. Ciprofloxacin is not recommended in persons younger than 18 years because it has caused cartilage damage in immature experimental animals.

A single IM injection of ceftriaxone has been found to eradicate meningococcal carriage. The chemoprophylactic dose of ceftriaxone is 250 mg IM in adults and 125 mg IM in children. Ceftriaxone is preferred in children who refuse oral medication and may be used in pregnancy.

Meningococcal isolates that are susceptible to sulfadiazine can be eradicated with a 2-day course of sulfadiazine. The high incidence of adverse effects has limited acceptance of minocycline as a means of eradicating the carrier state.

Meningococcal disease can be prevented by vaccination with group-specific meningococcal capsular polysaccharides.[87] Purified polysaccharides of groups A, C, Y, and W-135 meningococci have been used to stimulate group-specific humoral bactericidal antibodies.

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Consultations

Consultations in meningococcal disease include the following:

  • Surgeon - In cases involving gangrene of the extremities
  • Hematologist - May be needed to manage coagulopathy
  • Cardiologist - May be needed upon evidence of heart failure or pericarditis
  • Infectious disease specialist - To assist in management and to provide guidance in antimicrobial therapy
  • Preventive medicine specialist - To evaluate the community risk associated with an index case and to initiate reporting to local and regional health authorities if indicated
  • Orthopedist and/or vascular surgeon

Make sure that the local department of health is notified of suspected and/or proven cases of meningococcal infection to assist in the evaluation of close contacts and in prophylaxis.

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Contributor Information and Disclosures
Author

Mahmud H Javid, MBBS Consultant in Infectious Diseases, Shifa International Hospital, Pakistan

Mahmud H Javid, MBBS is a member of the following medical societies: Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Shadab Hussain Ahmed, MD, AAHIVS, FACP, FIDSA Professor of Clinical Medicine, The School of Medicine at Stony Brook University Medical Center; Adjunct Clinical Associate Professor, Department of Medicine, New York College of Osteopathic Medicine of New York Institute of Technology; Attending Physician, Department of Medicine, Division of Infectious Diseases, Director of HIV Prevention Services, Administrative HIV Designee, Nassau University Medical Center

Shadab Hussain Ahmed, MD, AAHIVS, FACP, FIDSA is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

John L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Katrina Cathie, BM (Hons), MRCPCH,  Fellow in Paediatric Clinical Research, Southampton NIHR Respiratory Biomedical Research Unit, University Hospital Southampton NHS Foundation Trust, UKKatrina Cathie, BM(Hons), MRCPCH is a member of the following medical societies: Royal College of Paediatrics and Child Health

Disclosure: Nothing to disclose.

Joanna L Chan, MD Mohs Fellow, California Skin Institute

Joanna L Chan, MD is a member of the following medical societies: American Academy of Dermatology and American Society for Dermatologic Surgery

Disclosure: Nothing to disclose.

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, 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, Pediatric Infectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Saul N Faust, MA, MBBS, PhD, MRCPCH Senior Lecturer in Pediatric Immunology and Infectious Diseases, University of Southampton; Director, Wellcome Trust Clinical Research Facility, Southampton University Hospitals NHS Trust, UK

Saul N Faust, MA, MBBS, PhD, MRCPCH is a member of the following medical societies: British Paediatric Allergy, Immunology and Infectious Group, European Society for Paediatric Infectious Diseases, International Society for Infectious Diseases, and Royal College of Paediatrics and Child Health

Disclosure: Xoma Consulting fee Consulting; GSK Honoraria Consulting; Wyeth travel and registration fee to conference investigator in study being presented at meeting; Sanofi Pasteur Consulting fee Consulting; Pfizer Consulting fee Consulting

Aaron Glatt, MD Professor of Clinical Medicine, New York Medical College; President and CEO, Former Chief Medical Officer, Departments of Medicine and Infectious Diseases, St Joseph Hospital (formerly New Island Hospital)

Aaron Glatt, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Infectious Diseases Society of America, International AIDS Society, and SocietyforHealthcareEpidemiology of America

Disclosure: Nothing to disclose.

Thomas A Hoffman, MD Professor, Department of Internal Medicine, Division of Infectious Diseases, Jackson Memorial Hospital, University of Miami

Thomas A Hoffman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

David Jaimovich, MD Chief Medical Officer, Joint Commission International and Joint Commission Resources

David Jaimovich, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Michael Levin, PhD, FRCP, FRCPCH Head, Professor, Imperial College School of Medicine at St Mary's Hospital, Department of Pediatrics, London, England

Disclosure: Nothing to disclose.

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.

Joseph Richard Masci, MD Professor of Medicine, Professor of Preventive Medicine, Mount Sinai School of Medicine; Director of Medicine, Elmhurst Hospital Center

Joseph Richard Masci, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Association of Professors of Medicine, and Royal Society of Medicine

Disclosure: Nothing to disclose.

Mary D Nettleman, MD, MS, MACP Professor and Chair, Department of Medicine, Michigan State University College of Human Medicine

Mary D Nettleman, MD, MS, MACP is a member of the following medical societies: American College of Physicians, Association of Professors of Medicine, Central Society for Clinical Research, Infectious Diseases Society of America, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Gregory J Raugi, MD, PhD Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; 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.

Nanette Silverberg, MD Assistant Clinical Professor, Department of Dermatology, Columbia University College of Physicians and Surgeons; Director of Pediatric Dermatology, Department of Dermatology, St Luke's Roosevelt Hospital Center, Maimonides Medical Center and Beth Israel Medical Center

Nanette Silverberg 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.

Darvin Scott Smith, MD, MSc, DTM&H Adjunct Assistant Professor, Department of Microbiology and Immunology, Stanford University School of Medicine; Chief of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, Kaiser Redwood City Hospital

Darvin Scott Smith, MD, MSc, DTM&H is a member of the following medical societies: American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International Society of Travel Medicine

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Elizabeth L Tanzi, MD Co-Director, Laser Surgery, Washington Institute of Dermatologic Laser Surgery; Assistant Professor, Department of Dermatology, Johns Hopkins University School of Medicine

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.

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

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.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Dorsum of the hand showing petechiae. Courtesy of Professor Chien Liu.
Petechiae on the palm. Courtesy of Professor Chien Liu.
Petechiae on lower extremities. Courtesy of Professor Chien Liu.
Conjunctival petechiae. Courtesy of Professor Chien Liu.
Gram-negative intracellular diplococci. Courtesy Professor Chien Liu.
Scattered petechiae in a patient with acute meningococcemia.
Purpura in a young adult with fulminant meningococcemia.
The legs of a 22-year-old woman in septic shock with a rapidly evolving purpuric rash. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
A 9-month-old baby in septic shock with purpuric Neisseria meningitis skin lesions. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
The leg of a 9-month-old infant in septic shock with a rapidly evolving purpuric rash. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
Neisseria meningitis purpuric lesions on the ear and cheek of a 9-month-old infant who is in septic shock. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
Lesions caused by Neisseria meningitis bacteremia on the palm of the hand of a 9-month-old infant. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
Areas with frequent epidemics of meningococcal disease. This is known as the Meningitis Belt of Africa; visitors to these locales may benefit from meningitis vaccine. Image courtesy of CDC.
Child with severe meningococcal disease and purpura fulminans.
Flow chart shows guidelines for the emergency management of meningococcal disease in children. These guidelines may be reprinted for use in clinical areas and are available at Meningitis.org.
Flow chart shows guidelines for the emergency management of meningococcal disease in adult patients. These guidelines may be reprinted for use in clinical areas and are available from Meningitis.org.
Chart for family practice recognition and management of meningococcal disease (courtesy of Meningitis.org).
 
 
 
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