What are the risk factors for bacterial meningitis. How is bacterial meningitis diagnosed and treated. What are the potential complications of untreated bacterial meningitis. How can bacterial meningitis be prevented.

Understanding Bacterial Meningitis: An Overview

Bacterial meningitis is a severe infection of the meninges, the protective membranes covering the brain and spinal cord. This life-threatening condition requires immediate medical attention and prompt treatment. As we delve into the intricacies of bacterial meningitis, we’ll explore its causes, symptoms, diagnosis, and treatment options.

Common Causes and Risk Factors of Bacterial Meningitis

Bacterial meningitis can be caused by various bacteria, with the most common culprits varying by age group. The primary causative agents include:

• Streptococcus pneumoniae (pneumococcus)
• Neisseria meningitidis (meningococcus)
• Group B Streptococcus
• Haemophilus influenzae type b (Hib)
• Listeria monocytogenes

Several risk factors can increase an individual’s susceptibility to bacterial meningitis. These include:

• Age (infants and older adults are at higher risk)
• Living in close quarters (e.g., college dormitories, military barracks)
• Compromised immune system
• Recent head trauma or neurosurgery
• Cochlear implants
• Certain medical conditions (e.g., sickle cell disease, diabetes)

Recognizing the Symptoms of Bacterial Meningitis

Early detection of bacterial meningitis is crucial for successful treatment. The symptoms can develop rapidly, often within hours or days. Common signs and symptoms include:

• Sudden high fever
• Severe headache
• Stiff neck
• Nausea and vomiting
• Confusion or altered mental state
• Sensitivity to light (photophobia)
• Seizures
• Skin rash (in some cases of meningococcal meningitis)

Is bacterial meningitis more common in certain age groups. While bacterial meningitis can affect individuals of all ages, it is more prevalent in infants, young children, and older adults. The epidemiology has shifted in recent years due to widespread vaccination programs, with the median age of patients increasing from 30.3 years in 1998-1999 to 41.9 years in 2006-2007.

Diagnostic Approaches for Bacterial Meningitis

Diagnosing bacterial meningitis involves a combination of clinical evaluation and laboratory tests. The key diagnostic procedures include:

1. Physical examination: Checking for signs of meningeal irritation (e.g., Kernig’s sign, Brudzinski’s sign)
2. Lumbar puncture: Analysis of cerebrospinal fluid (CSF) for cell count, glucose levels, and protein content
3. Blood cultures: To identify the causative bacteria
4. Imaging studies: CT or MRI scans to detect complications or rule out other conditions
5. Polymerase chain reaction (PCR) testing: To rapidly identify bacterial DNA in CSF

How quickly should bacterial meningitis be diagnosed and treated. Bacterial meningitis is a medical emergency that requires immediate diagnosis and treatment. Ideally, antibiotic therapy should be initiated within one hour of the patient’s arrival at the hospital, even before the diagnosis is confirmed.

Treatment Strategies for Bacterial Meningitis

The treatment of bacterial meningitis primarily involves antimicrobial therapy, supportive care, and management of complications. The key components of treatment include:

• Empiric antibiotic therapy: Started immediately, often before the specific causative agent is identified
• Targeted antibiotic therapy: Based on culture results and antibiotic sensitivity testing
• Corticosteroids: To reduce inflammation and potentially decrease complications
• Fluid management: To maintain adequate hydration and electrolyte balance
• Seizure control: Anticonvulsants may be necessary in some cases
• Intracranial pressure management: In cases of severe brain swelling

What is the typical duration of antibiotic treatment for bacterial meningitis. The duration of antibiotic therapy varies depending on the causative organism and the patient’s response to treatment. Generally, treatment lasts 7 to 14 days, but it may be extended in certain cases, such as those involving Listeria monocytogenes.

Potential Complications and Long-term Effects

Bacterial meningitis can lead to severe complications if not treated promptly. These may include:

• Hearing loss
• Cognitive impairment
• Seizure disorders
• Hydrocephalus
• Brain damage
• Septic shock
• Death

Can the complications of bacterial meningitis be reversed. Some complications of bacterial meningitis may be reversible with prompt treatment, while others may result in permanent damage. The severity and reversibility of complications depend on factors such as the causative organism, the patient’s age and overall health, and the timeliness of treatment initiation.

Prevention Strategies and Vaccination

Preventing bacterial meningitis involves a combination of vaccination and public health measures. Key preventive strategies include:

• Routine childhood vaccinations against Hib, pneumococcus, and meningococcus
• Meningococcal vaccination for adolescents and high-risk adults
• Pneumococcal vaccination for older adults and individuals with certain medical conditions
• Chemoprophylaxis for close contacts of individuals with meningococcal meningitis
• Maintaining good hygiene practices, such as frequent handwashing
• Avoiding close contact with individuals who have meningitis

How effective are vaccines in preventing bacterial meningitis. Vaccines have significantly reduced the incidence of bacterial meningitis caused by certain pathogens. For example, the introduction of the Hib vaccine has nearly eliminated Hib meningitis in countries with high vaccination rates. Similarly, pneumococcal and meningococcal vaccines have led to substantial reductions in cases caused by these bacteria.

The Impact of Vaccination on Meningitis Epidemiology

The widespread implementation of vaccination programs has dramatically altered the landscape of bacterial meningitis. Some notable changes include:

• A shift in the median age of affected individuals
• Reduction in overall incidence rates
• Changes in the predominant causative organisms
• Decreased mortality rates in vaccinated populations

Has the introduction of vaccines eliminated the risk of bacterial meningitis entirely. While vaccines have significantly reduced the incidence of bacterial meningitis, they have not eliminated the risk entirely. Some strains of bacteria are not covered by current vaccines, and vaccine efficacy can vary. Additionally, individuals with compromised immune systems may still be at risk despite vaccination.

The Role of Public Health Measures in Meningitis Control

Public health initiatives play a crucial role in controlling the spread of bacterial meningitis. These measures include:

1. Surveillance systems to monitor disease trends and outbreaks
2. Rapid response protocols for suspected cases
3. Education programs to raise awareness about symptoms and prevention
4. Vaccination campaigns targeting high-risk populations
5. Contact tracing and prophylaxis for close contacts of infected individuals

How do public health agencies respond to meningitis outbreaks. In the event of a meningitis outbreak, public health agencies typically implement a multifaceted response. This may include initiating mass vaccination campaigns, distributing prophylactic antibiotics to close contacts, conducting extensive contact tracing, and issuing public health alerts to healthcare providers and the general public.

The Importance of Global Cooperation in Meningitis Prevention

Bacterial meningitis remains a global health concern, particularly in regions with limited access to vaccines and healthcare. International cooperation is essential for:

• Sharing surveillance data and research findings
• Coordinating vaccine development and distribution efforts
• Implementing global vaccination strategies
• Providing support to resource-limited countries
• Collaborating on public health initiatives and outbreak responses

What initiatives are in place to address bacterial meningitis on a global scale. Several global initiatives aim to combat bacterial meningitis worldwide. These include the World Health Organization’s Global Roadmap to Defeat Meningitis by 2030, the Meningitis Research Foundation’s global advocacy efforts, and various international partnerships focused on vaccine development and distribution in low- and middle-income countries.

Emerging Research and Future Directions in Meningitis Treatment

Ongoing research in the field of bacterial meningitis focuses on several key areas:

• Development of more effective and broadly protective vaccines
• Exploration of novel antibiotic therapies to combat antibiotic-resistant strains
• Investigation of adjunctive therapies to reduce inflammation and neurological complications
• Improvement of rapid diagnostic techniques for faster and more accurate identification of causative organisms
• Study of long-term outcomes and rehabilitation strategies for meningitis survivors

What are some promising areas of research in bacterial meningitis treatment. Emerging areas of research include the development of universal vaccines that provide protection against multiple strains of meningitis-causing bacteria, the use of immunomodulatory therapies to mitigate the inflammatory response, and the exploration of personalized treatment approaches based on genetic factors and individual immune responses.

The Potential of Immunotherapy in Meningitis Treatment

Immunotherapy is an exciting area of research in the treatment of bacterial meningitis. Potential applications include:

• Monoclonal antibodies targeting specific bacterial antigens
• Immune system modulators to enhance the body’s natural defenses
• Cytokine therapies to regulate the inflammatory response
• Stem cell-based approaches for neurological repair and regeneration

Could immunotherapy revolutionize the treatment of bacterial meningitis. While still in the early stages of research, immunotherapy holds promise for improving outcomes in bacterial meningitis. By targeting specific aspects of the immune response and bacterial pathogenesis, these approaches could potentially enhance the effectiveness of antibiotic therapy and reduce the risk of long-term complications.

The Importance of Interprofessional Collaboration in Meningitis Care

Effective management of bacterial meningitis requires a coordinated effort from various healthcare professionals. Key team members may include:

• Emergency medicine physicians
• Infectious disease specialists
• Neurologists
• Critical care specialists
• Microbiologists
• Pharmacists
• Nurses
• Rehabilitation specialists

How does interprofessional collaboration improve outcomes in bacterial meningitis cases. Interprofessional collaboration ensures comprehensive patient care, from rapid diagnosis and initiation of treatment to management of complications and long-term follow-up. This team-based approach can lead to improved outcomes, reduced mortality rates, and better quality of life for survivors of bacterial meningitis.

The Role of Telemedicine in Meningitis Management

Telemedicine is increasingly being utilized in the management of bacterial meningitis, particularly in remote or underserved areas. Benefits of telemedicine in this context include:

• Rapid consultation with specialists
• Remote monitoring of patients during treatment
• Improved access to expert guidance for local healthcare providers
• Enhanced coordination of care across different healthcare facilities
• Facilitation of follow-up care and rehabilitation services

Can telemedicine improve access to specialized care for bacterial meningitis patients in remote areas. Telemedicine has the potential to significantly improve access to specialized care for patients with bacterial meningitis in remote or underserved areas. By enabling real-time consultation with experts and facilitating the transfer of medical information, telemedicine can help ensure that patients receive timely and appropriate treatment, regardless of their geographic location.

Bacterial Meningitis – StatPearls – NCBI Bookshelf

Continuing Education Activity

Bacterial meningitis is an infection of the meninges that results in inflammation. It is a serious and life-threatening condition that requires prompt diagnosis and treatment. This activity reviews the evaluation and treatment of bacterial meningitis and highlights the role of the interprofessional team in caring for patients with this condition.

Objectives:

• Identify the risk factors associated with development of bacterial meningitis in children and adults.

• Describe common history and physical findings in a patient with bacterial meningitis.

• Review the treatment and management options available for bacterial meningitis.

• Outline interprofessional team strategies for improving care coordination and communication to advance the treatment of bacterial meningitis, minimize complications, and improve outcomes.

Access free multiple choice questions on this topic.

Introduction

Bacterial meningitis is a bacterial infection of the meninges, which is the protective covering for the brain and spinal cord resulting in inflammation. It is a serious and life-threatening condition that requires prompt diagnosis and treatment.[1][2][3]

Etiology

Bacterial meningitis is caused by a bacterial infection of the meninges, resulting in inflammation. The infection is either community-acquired or nosocomial. Community-acquired bacterial meningitis is the result of the invasion of the bacteria into the meninges from bacteremia or direct extension from local infection. The most common bacterial culprit varies by age. Group B Streptococcus is common in infants less than 2 months of age while Streptococcus pneumoniae is the most common in all other age groups, with the exception of 11 – 17 year old, where Neisseria meningitidis is still the most common cause.  

Listeria monocytogenes and gram-negative bacteria such as Escherichia coli, Klebsiella, Enterobacter, Pseudomonas aeruginosa are other less common causes.  Hemophilus influenzae is still occasionally encountered in nonvaccinated individuals. Nosocomial infections are caused by S. pneumonia, Staphylococcus aureus, Staphylococcus albus, and gram-negative bacilli. As per Thigpen etal. out of the 1670 cases reported in the U.S. during 2003–2007, S. pneumoniae was the predominant infective species (58.0%), followed by GBS (18.1%), N. meningitidis (13.9%), H. influenzae (6.7%), and L. monocytogenes (3.4%).[4] Infectious meningitis may also be caused by viruses, fungi, and protozoa. Meningitis may also be non-infectious in etiology and can be caused by cancer, medications, or inflammatory conditions.[5][6]

Epidemiology

Bacterial meningitis was previously more common in pediatric patients. However, as vaccines are developed and utilized, the prevalence of acute bacterial meningitis has decreased and the epidemiology of causative microorganisms has changed. Vaccinations have increased the median age of patients infected. In 2006 there were 72,000 meningitis-related hospitalizations in the United States. The majority of these cases were due to viral infection (54.6%). Bacterial infections accounted for 21.8% of cases, and 7.3% were due to fungi and parasite infections, while 17.2% were due to an unspecified cause. There was an 8% in-hospital mortality rate for patients with bacterial meningitis, and it rose substantially for patients older than 45. [7][8][9] The annual incidence of meningitis in the United States decreased from 2.00 cases per 100,000 population in 1998–1999 to 1.38 cases per 100,000 population in 2006–2007 while the median age of patients increased from 30.3 years in 1998–1999 to 41.9 years in 2006–2007.[4] As per CDC data, rates of meningococcal disease have been declining in the United States since the late 1990s. In 2017, there were about 350 total cases of meningococcal disease reported (incidence rate of 0.11 cases per 100,000 persons).

Several possible risk factors for bacterial meningitis have been identified. Patients with an abnormal communication between the nasopharynx and subarachnoid space are thought to be at increased risk. This abnormal communication can be due to a congenital abnormality or a result of trauma. Patients who have undergone neurosurgery, sustained skull fractures, or have cochlear implants are also at increased risk. Other at-risk patient populations are the immunosuppressed and people that live in close personal contact with others in places like college dorms or military barracks.

Pathophysiology

Bacteria require access to the meninges to cause meningitis. There are several mechanisms for entry. Bacteremia, or bacteria in the blood, can result in bacteria crossing the blood-brain barrier. This can only be accomplished by certain bacteria, most notably N. meningitidis and S. pneumoniae. Direct extension of otitis media or sinusitis to the central nervous system (CNS) may also occur. Dural defects, either congenital or acquired, allow bacteria to enter the CNS. Nosocomial bacterial meningitis is the result of the manipulation of the meninges during neurosurgical procedures. Invasion of bacteria into the subarachnoid space results in inflammation of the meninges.

Although several factors may be involved, lipopolysaccharide in the walls of gram-negative organisms and techoic acid in the walls of gram-positive microorganisms activate brain microglia, leading to a cascade of inflammatory changes that causes cortical microvascular permeability with diffuse cerebral edema, resulting in increased intracranial pressure. This causes the patient to experience headaches and fevers. Blood-brain barrier breakdown occurs secondary to the infection and inflammatory response. Altered mental status, seizures, and focal neurologic deficits occur due to decreased perfusion and increased intracranial pressure. 

History and Physical

Fever, neck stiffness, and altered mental status are the classic triad of symptoms for meningitis; however, all three are only present in 41% of cases of bacterial meningitis. The triad is most commonly seen in elderly patients. Seventy percent of patients will present with at least one of these symptoms. Common early symptoms of the disease include fever, headache, and confusion which can progress to obtundation, focal neuro deficits, and seizures. History should include questioning about any recent neurosurgical procedures, immunization status, and living arrangements. A physical exam may reveal nuchal rigidity or positive Kernig’s or Brudzinski’s signs. However, the absence of these does not reliably rule out the disease. Brudzinski’s sign occurs when passive flexion of the neck causes involuntary flexion of the knee. Kernig’s sign is resistance or pain with knee extension when the patient is supine, and their hip is flexed to 90 degrees. These signs are thought to be secondary to meningeal irritation. The fundoscopic exam may reveal papilledema due to increased intracranial pressure. A rapidly spreading petechial rash, known as purpura fulminans, would suggest a Meningococcal infection.

Evaluation

Patients presumed to have bacterial meningitis should receive a lumbar puncture to obtain a cerebrospinal fluid (CSF) sample. The CSF should be sent for Gram stain, culture, complete cell count (CBC), and glucose and protein levels. Bacterial meningitis typically results in low glucose and high protein levels in the cerebrospinal fluid. As CSF glucose levels are dependent on circulating serum glucose levels, the CSF to serum glucose ratio is considered more reliable parameter for the diagnosis of acute bacterial meningitis than absolute CSF glucose levels. A neutrophil predominance on cell count would be expected. 

The diagnosis would be confirmed with bacteria identified on gram stain or culture. A non-contrast CT scan of the head should be performed before lumbar puncture if the patient has a risk of herniation. Risk factors include papilledema on the exam, new onset seizures, focal neurologic deficits, or is immunocompromised. Consider delaying the lumbar puncture if the patient has unstable vital signs, coagulation abnormalities, or has had a recent seizure. Treat with antibiotics empirically if testing is going to be delayed. Blood cultures should be obtained as 53% of patients have concurrent bacteremia. Elevated C-reactive protein or procalcitonin levels would suggest a bacterial rather than viral etiology.[10][11][12]

Treatment / Management

Timely administration of antibiotics is essential. Delays in the administration of 3 to 6 hours are associated with increased mortality. The identified bacteria determine antibiotic selection. Empiric treatment with ceftriaxone and vancomycin should strongly be considered if the diagnosis is going to be delayed. Patients who are immunocompromised or older than 50 should also receive ampicillin. Patients with bacterial meningitis due to head trauma or post-neurosurgical procedure need to be covered for methicillin resistant Staphylococcus aureus and aerobic gram-negative organisms. They should receive vancomycin and ceftazidime or cefepime. Acyclovir can also be administered for HSV coverage. Antibiotics can then be narrowed once the culture and sensitivities have resulted. Dexamethasone may increase survival if given at the time of antibiotic administration for S. pneumoniae infections. It has not been shown to improve outcomes for meningitis caused by other bacteria. Patients suspected of having meningococcal meningitis should be placed in droplet precautions until they have received 24 hours of antibiotics. Close contacts should also be treated prophylactically. Ciprofloxacin, rifampin, or ceftriaxone may be used. Close contacts are defined as people within 3 feet of the patient for more than 8 hours during the seven days before and 24 hours after receiving antibiotics. People exposed to the patient’s oral secretions during this time should also be treated.[13][14][15]

Differential Diagnosis

• Brain Abscess

• Brain Neoplasms

• Encephalitis

• Leptospirosis

• Noninfectious meningitis, including medication-induced meningeal inflammation

• Pediatrics, Meningitis and Encephalitis

• Stroke

• Subdural empyema

Prognosis

The mortality for bacterial meningitis varies from 10-15%.  Survival depends on early recognition of acute bacterial meningitis, followed by administration of appropriate antibiotic therapy. Delay in treatment can result in increased intracranial pressure causing decreased cerebral perfusion and may rapidly lead to loss of consciousness and death.

Complications

It is estimated that 25% of people with meningococcal disease, will have complications. Complications are not uncommon in other causes of bacterial meningitis. Severity can vary from person to person, and they can be temporary or permanent. Delayed therapy can result in vascular inflammation with cerebral infarction. Other long-term complications include 

• seizures

• problems with memory and concentration

• problems with movement, balance and co-ordination 

• learning difficulties 

• speech problems

• vision loss

• hearing loss

Pearls and Other Issues

Vaccines are available to help prevent bacterial meningitis. Children can get a meningitis vaccine around ages 11 to 12, followed by a booster vaccine at age 16. Bacterial meningitis is more common in infants under 1 year of age and young people ages 16 to 21. College students living in dorms or other close quarters are at increased risk. In addition, adults with underlying immunocompromise state such as status post splenectomy, are at higher risk.

Enhancing Healthcare Team Outcomes

Bacterial meningitis is a serious CNS infection with high morbidity and mortality. To improve patient outcomes, it is best managed by an interprofessional team that includes an infectious disease expert, emergency department physician, laboratory professional, internist, nurse practitioner, and a pediatrician. The key is to start prompt treatment without delay. One should not wait for cultures if suspicion is high of meningitis. The infectious disease specialist should consult with a board-certified infectious disease pharmacist so optimal antimicrobial therapy based on the latest antibiogram data can be initiate empirically, enhancing the chance for successful treatment. These patients need inpatient treatment until all symptoms have disappeared, therefore the nursing staff will be responsible for administration as well as monitoring for therapeutic effectiveness and adverse drug events, reporting any concerns to the team. The outlook for patients with delayed diagnosis or treatment is poor. More important, delays also lead to litigation. [16][17]

Review Questions

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• Comment on this article.

References

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Ramgopal S, Walker LW, Vitale MA, Nowalk AJ. Factors associated with serious bacterial infections in infants ≤60 days with hypothermia in the emergency department. Am J Emerg Med. 2019 Jun;37(6):1139-1143. [PubMed: 31006603]

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Lien CY, Lee JJ, Tsai WC, Chen SY, Huang CR, Chien CC, Lu CH, Chang WN. The clinical characteristics of spontaneous Gram-negative bacterial meningitis in adults: A hospital-based study. J Clin Neurosci. 2019 Jun;64:101-105. [PubMed: 31005474]

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Fuentes-Antrás J, Ramírez-Torres M, Osorio-Martínez E, Lorente M, Lorenzo-Almorós A, Lorenzo O, Górgolas M. Acute Community-Acquired Bacterial Meningitis: Update on Clinical Presentation and Prognostic factors. New Microbiol. 2019 Apr;41(4):81-87. [PubMed: 30994177]

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Thigpen MC, Whitney CG, Messonnier NE, Zell ER, Lynfield R, Hadler JL, Harrison LH, Farley MM, Reingold A, Bennett NM, Craig AS, Schaffner W, Thomas A, Lewis MM, Scallan E, Schuchat A., Emerging Infections Programs Network. Bacterial meningitis in the United States, 1998-2007. N Engl J Med. 2011 May 26;364(21):2016-25. [PubMed: 21612470]

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Chacon-Cruz E, Roberts C, Rivas-Landeros RM, Lopatynsky-Reyes EZ, Almada-Salazar LA, Alvelais-Palacios JA. Pediatric meningitis due to Neisseria meningitidis, Streptococcus pneumoniae and Group B Streptococcus in Tijuana, Mexico: active/prospective surveillance, 2005-2018. Ther Adv Infect Dis. 2019 Jan-Dec;6:2049936119832274. [PMC free article: PMC6413420] [PubMed: 30886712]

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Linder KA, Malani PN. Meningococcal Meningitis. JAMA. 2019 Mar 12;321(10):1014. [PubMed: 30860561]

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Dubot-Pérès A, Mayxay M, Phetsouvanh R, Lee SJ, Rattanavong S, Vongsouvath M, Davong V, Chansamouth V, Phommasone K, Moore C, Dittrich S, Lattana O, Sirisouk J, Phoumin P, Panyanivong P, Sengduangphachanh A, Sibounheuang B, Chanthongthip A, Simmalavong M, Sengdatka D, Seubsanith A, Keoluangkot V, Phimmasone P, Sisout K, Detleuxay K, Luangxay K, Phouangsouvanh I, Craig SB, Tulsiani SM, Burns MA, Dance DAB, Blacksell SD, de Lamballerie X, Newton PN. Management of Central Nervous System Infections, Vientiane, Laos, 2003-2011. Emerg Infect Dis. 2019 May;25(5):898-910. [PMC free article: PMC6478220] [PubMed: 31002063]

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Mohan A, Munusamy C, Tan YC, Muthuvelu S, Hashim R, Chien SL, Wong MK, Khairuddin NA, Podin Y, Lau PS, Ng DC, Ooi MH. Invasive Salmonella infections among children in Bintulu, Sarawak, Malaysian Borneo: a 6-year retrospective review. BMC Infect Dis. 2019 Apr 18;19(1):330. [PMC free article: PMC6471830] [PubMed: 30999894]

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El-Naggar W, Afifi J, McMillan D, Toye J, Ting J, Yoon EW, Shah PS., Canadian Neonatal Network Investigators‖ Epidemiology of Meningitis in Canadian Neonatal Intensive Care Units. Pediatr Infect Dis J. 2019 May;38(5):476-480. [PubMed: 30986789]

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Haydar SM, Hallit SR, Hallit RR, Salameh PR, Faddoul LJ, Chahine BA, Malaeb DN. Adherence to international guidelines for the treatment of meningitis infections in Lebanon. Saudi Med J. 2019 Mar;40(3):260-265. [PMC free article: PMC6468200] [PubMed: 30834421]

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Simone L, Lyttle MD, Roland D, Stephens D, Schuh S., Pediatric Emergency Research Canada (PERC) and the Pediatric Emergency Research United Kingdom and Ireland (PERUKI) networks. Canadian and UK/Ireland practice patterns in lumbar puncture performance in febrile neonates with bronchiolitis. Emerg Med J. 2019 Mar;36(3):148-153. [PubMed: 30728189]

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Le Turnier P, Navas D, Garot D, Guimard T, Bernard L, Tattevin P, Vandamme YM, Hoff J, Chiffoleau A, Dary M, Leclair-Visonneau L, Grégoire M, Pere M, Boutoille D, Sébille V, Dailly E, Asseray N., High-Dose Ceftriaxone CNS Infections Study Group. Tolerability of high-dose ceftriaxone in CNS infections: a prospective multicentre cohort study. J Antimicrob Chemother. 2019 Apr 01;74(4):1078-1085. [PubMed: 30698733]

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Ferraro M, Morucci L, Coppeta L, De Carolis G, Pietroiusti A, Franco E, Magrini A. Managing the risk of bacterial meningitis among healthcare workers. Occup Med (Lond). 2019 Apr 13;69(2):113-117. [PubMed: 30496490]

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Young N, Thomas M. Meningitis in adults: diagnosis and management. Intern Med J. 2018 Nov;48(11):1294-1307. [PubMed: 30387309]

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Poi BN, Pasupulety Venkata NK, Auckland CR, Paul SP. Neonatal meningitis and maternal sepsis caused by Streptococcus oralis. J Neonatal Perinatal Med. 2018;11(3):331-334. [PubMed: 30040747]

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Biondi EA, Lee B, Ralston SL, Winikor JM, Lynn JF, Dixon A, McCulloh R. Prevalence of Bacteremia and Bacterial Meningitis in Febrile Neonates and Infants in the Second Month of Life: A Systematic Review and Meta-analysis. JAMA Netw Open. 2019 Mar 01;2(3):e190874. [PMC free article: PMC6583289] [PubMed: 30901044]

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Xu M, Hu L, Huang H, Wang L, Tan J, Zhang Y, Chen C, Zhang X, Huang L. Etiology and Clinical Features of Full-Term Neonatal Bacterial Meningitis: A Multicenter Retrospective Cohort Study. Front Pediatr. 2019;7:31. [PMC free article: PMC6381005] [PubMed: 30815433]

Disclosure: Tyler Runde declares no relevant financial relationships with ineligible companies.

Disclosure: Fatima Anjum declares no relevant financial relationships with ineligible companies.

Disclosure: John Hafner declares no relevant financial relationships with ineligible companies.

Bacterial Meningitis – StatPearls – NCBI Bookshelf

Continuing Education Activity

Bacterial meningitis is an infection of the meninges that results in inflammation. It is a serious and life-threatening condition that requires prompt diagnosis and treatment. This activity reviews the evaluation and treatment of bacterial meningitis and highlights the role of the interprofessional team in caring for patients with this condition.

Objectives:

• Identify the risk factors associated with development of bacterial meningitis in children and adults.

• Describe common history and physical findings in a patient with bacterial meningitis.

• Review the treatment and management options available for bacterial meningitis.

• Outline interprofessional team strategies for improving care coordination and communication to advance the treatment of bacterial meningitis, minimize complications, and improve outcomes.

Access free multiple choice questions on this topic.

Introduction

Bacterial meningitis is a bacterial infection of the meninges, which is the protective covering for the brain and spinal cord resulting in inflammation. It is a serious and life-threatening condition that requires prompt diagnosis and treatment.[1][2][3]

Etiology

Bacterial meningitis is caused by a bacterial infection of the meninges, resulting in inflammation. The infection is either community-acquired or nosocomial. Community-acquired bacterial meningitis is the result of the invasion of the bacteria into the meninges from bacteremia or direct extension from local infection. The most common bacterial culprit varies by age. Group B Streptococcus is common in infants less than 2 months of age while Streptococcus pneumoniae is the most common in all other age groups, with the exception of 11 – 17 year old, where Neisseria meningitidis is still the most common cause.   

Listeria monocytogenes and gram-negative bacteria such as Escherichia coli, Klebsiella, Enterobacter, Pseudomonas aeruginosa are other less common causes. Hemophilus influenzae is still occasionally encountered in nonvaccinated individuals. Nosocomial infections are caused by S. pneumonia, Staphylococcus aureus, Staphylococcus albus, and gram-negative bacilli. As per Thigpen etal. out of the 1670 cases reported in the U.S. during 2003–2007, S. pneumoniae was the predominant infective species (58.0%), followed by GBS (18.1%), N. meningitidis (13.9%), H. influenzae (6.7%), and L. monocytogenes (3.4%).[4] Infectious meningitis may also be caused by viruses, fungi, and protozoa. Meningitis may also be non-infectious in etiology and can be caused by cancer, medications, or inflammatory conditions.[5][6]

Epidemiology

Bacterial meningitis was previously more common in pediatric patients.  However, as vaccines are developed and utilized, the prevalence of acute bacterial meningitis has decreased and the epidemiology of causative microorganisms has changed. Vaccinations have increased the median age of patients infected. In 2006 there were 72,000 meningitis-related hospitalizations in the United States. The majority of these cases were due to viral infection (54.6%). Bacterial infections accounted for 21.8% of cases, and 7.3% were due to fungi and parasite infections, while 17.2% were due to an unspecified cause. There was an 8% in-hospital mortality rate for patients with bacterial meningitis, and it rose substantially for patients older than 45. [7][8][9] The annual incidence of meningitis in the United States decreased from 2.00 cases per 100,000 population in 1998–1999 to 1.38 cases per 100,000 population in 2006–2007 while the median age of patients increased from 30.3 years in 1998–1999 to 41.9 years in 2006–2007.[4] As per CDC data, rates of meningococcal disease have been declining in the United States since the late 1990s. In 2017, there were about 350 total cases of meningococcal disease reported (incidence rate of 0.11 cases per 100,000 persons).

Several possible risk factors for bacterial meningitis have been identified. Patients with an abnormal communication between the nasopharynx and subarachnoid space are thought to be at increased risk. This abnormal communication can be due to a congenital abnormality or a result of trauma. Patients who have undergone neurosurgery, sustained skull fractures, or have cochlear implants are also at increased risk. Other at-risk patient populations are the immunosuppressed and people that live in close personal contact with others in places like college dorms or military barracks.

Pathophysiology

Bacteria require access to the meninges to cause meningitis. There are several mechanisms for entry. Bacteremia, or bacteria in the blood, can result in bacteria crossing the blood-brain barrier. This can only be accomplished by certain bacteria, most notably N. meningitidis and S. pneumoniae. Direct extension of otitis media or sinusitis to the central nervous system (CNS) may also occur. Dural defects, either congenital or acquired, allow bacteria to enter the CNS. Nosocomial bacterial meningitis is the result of the manipulation of the meninges during neurosurgical procedures. Invasion of bacteria into the subarachnoid space results in inflammation of the meninges.

Although several factors may be involved, lipopolysaccharide in the walls of gram-negative organisms and techoic acid in the walls of gram-positive microorganisms activate brain microglia, leading to a cascade of inflammatory changes that causes cortical microvascular permeability with diffuse cerebral edema, resulting in increased intracranial pressure. This causes the patient to experience headaches and fevers. Blood-brain barrier breakdown occurs secondary to the infection and inflammatory response. Altered mental status, seizures, and focal neurologic deficits occur due to decreased perfusion and increased intracranial pressure.  

History and Physical

Fever, neck stiffness, and altered mental status are the classic triad of symptoms for meningitis; however, all three are only present in 41% of cases of bacterial meningitis. The triad is most commonly seen in elderly patients. Seventy percent of patients will present with at least one of these symptoms. Common early symptoms of the disease include fever, headache, and confusion which can progress to obtundation, focal neuro deficits, and seizures. History should include questioning about any recent neurosurgical procedures, immunization status, and living arrangements. A physical exam may reveal nuchal rigidity or positive Kernig’s or Brudzinski’s signs. However, the absence of these does not reliably rule out the disease. Brudzinski’s sign occurs when passive flexion of the neck causes involuntary flexion of the knee. Kernig’s sign is resistance or pain with knee extension when the patient is supine, and their hip is flexed to 90 degrees. These signs are thought to be secondary to meningeal irritation. The fundoscopic exam may reveal papilledema due to increased intracranial pressure. A rapidly spreading petechial rash, known as purpura fulminans, would suggest a Meningococcal infection.

Evaluation

Patients presumed to have bacterial meningitis should receive a lumbar puncture to obtain a cerebrospinal fluid (CSF) sample. The CSF should be sent for Gram stain, culture, complete cell count (CBC), and glucose and protein levels. Bacterial meningitis typically results in low glucose and high protein levels in the cerebrospinal fluid. As CSF glucose levels are dependent on circulating serum glucose levels, the CSF to serum glucose ratio is considered more reliable parameter for the diagnosis of acute bacterial meningitis than absolute CSF glucose levels. A neutrophil predominance on cell count would be expected. 

The diagnosis would be confirmed with bacteria identified on gram stain or culture. A non-contrast CT scan of the head should be performed before lumbar puncture if the patient has a risk of herniation.  Risk factors include papilledema on the exam, new onset seizures, focal neurologic deficits, or is immunocompromised. Consider delaying the lumbar puncture if the patient has unstable vital signs, coagulation abnormalities, or has had a recent seizure. Treat with antibiotics empirically if testing is going to be delayed. Blood cultures should be obtained as 53% of patients have concurrent bacteremia. Elevated C-reactive protein or procalcitonin levels would suggest a bacterial rather than viral etiology.[10][11][12]

Treatment / Management

Timely administration of antibiotics is essential. Delays in the administration of 3 to 6 hours are associated with increased mortality. The identified bacteria determine antibiotic selection. Empiric treatment with ceftriaxone and vancomycin should strongly be considered if the diagnosis is going to be delayed. Patients who are immunocompromised or older than 50 should also receive ampicillin. Patients with bacterial meningitis due to head trauma or post-neurosurgical procedure need to be covered for methicillin resistant Staphylococcus aureus and aerobic gram-negative organisms. They should receive vancomycin and ceftazidime or cefepime. Acyclovir can also be administered for HSV coverage. Antibiotics can then be narrowed once the culture and sensitivities have resulted. Dexamethasone may increase survival if given at the time of antibiotic administration for S. pneumoniae infections. It has not been shown to improve outcomes for meningitis caused by other bacteria. Patients suspected of having meningococcal meningitis should be placed in droplet precautions until they have received 24 hours of antibiotics. Close contacts should also be treated prophylactically. Ciprofloxacin, rifampin, or ceftriaxone may be used. Close contacts are defined as people within 3 feet of the patient for more than 8 hours during the seven days before and 24 hours after receiving antibiotics. People exposed to the patient’s oral secretions during this time should also be treated.[13][14][15]

Differential Diagnosis

• Brain Abscess

• Brain Neoplasms

• Encephalitis

• Leptospirosis

• Noninfectious meningitis, including medication-induced meningeal inflammation

• Pediatrics, Meningitis and Encephalitis

• Stroke

• Subdural empyema

Prognosis

The mortality for bacterial meningitis varies from 10-15%.  Survival depends on early recognition of acute bacterial meningitis, followed by administration of appropriate antibiotic therapy. Delay in treatment can result in increased intracranial pressure causing decreased cerebral perfusion and may rapidly lead to loss of consciousness and death.

Complications

It is estimated that 25% of people with meningococcal disease, will have complications. Complications are not uncommon in other causes of bacterial meningitis. Severity can vary from person to person, and they can be temporary or permanent. Delayed therapy can result in vascular inflammation with cerebral infarction. Other long-term complications include 

• seizures

• problems with memory and concentration

• problems with movement, balance and co-ordination 

• learning difficulties 

• speech problems

• vision loss

• hearing loss

Pearls and Other Issues

Vaccines are available to help prevent bacterial meningitis. Children can get a meningitis vaccine around ages 11 to 12, followed by a booster vaccine at age 16. Bacterial meningitis is more common in infants under 1 year of age and young people ages 16 to 21. College students living in dorms or other close quarters are at increased risk. In addition, adults with underlying immunocompromise state such as status post splenectomy, are at higher risk.

Enhancing Healthcare Team Outcomes

Bacterial meningitis is a serious CNS infection with high morbidity and mortality. To improve patient outcomes, it is best managed by an interprofessional team that includes an infectious disease expert, emergency department physician, laboratory professional, internist, nurse practitioner, and a pediatrician. The key is to start prompt treatment without delay. One should not wait for cultures if suspicion is high of meningitis. The infectious disease specialist should consult with a board-certified infectious disease pharmacist so optimal antimicrobial therapy based on the latest antibiogram data can be initiate empirically, enhancing the chance for successful treatment. These patients need inpatient treatment until all symptoms have disappeared, therefore the nursing staff will be responsible for administration as well as monitoring for therapeutic effectiveness and adverse drug events, reporting any concerns to the team. The outlook for patients with delayed diagnosis or treatment is poor. More important, delays also lead to litigation. [16][17]

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References

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Lien CY, Lee JJ, Tsai WC, Chen SY, Huang CR, Chien CC, Lu CH, Chang WN. The clinical characteristics of spontaneous Gram-negative bacterial meningitis in adults: A hospital-based study. J Clin Neurosci. 2019 Jun;64:101-105. [PubMed: 31005474]

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Fuentes-Antrás J, Ramírez-Torres M, Osorio-Martínez E, Lorente M, Lorenzo-Almorós A, Lorenzo O, Górgolas M. Acute Community-Acquired Bacterial Meningitis: Update on Clinical Presentation and Prognostic factors. New Microbiol. 2019 Apr;41(4):81-87. [PubMed: 30994177]

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Thigpen MC, Whitney CG, Messonnier NE, Zell ER, Lynfield R, Hadler JL, Harrison LH, Farley MM, Reingold A, Bennett NM, Craig AS, Schaffner W, Thomas A, Lewis MM, Scallan E, Schuchat A., Emerging Infections Programs Network. Bacterial meningitis in the United States, 1998-2007. N Engl J Med. 2011 May 26;364(21):2016-25. [PubMed: 21612470]

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Chacon-Cruz E, Roberts C, Rivas-Landeros RM, Lopatynsky-Reyes EZ, Almada-Salazar LA, Alvelais-Palacios JA. Pediatric meningitis due to Neisseria meningitidis, Streptococcus pneumoniae and Group B Streptococcus in Tijuana, Mexico: active/prospective surveillance, 2005-2018. Ther Adv Infect Dis. 2019 Jan-Dec;6:2049936119832274. [PMC free article: PMC6413420] [PubMed: 30886712]

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Linder KA, Malani PN. Meningococcal Meningitis. JAMA. 2019 Mar 12;321(10):1014. [PubMed: 30860561]

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Dubot-Pérès A, Mayxay M, Phetsouvanh R, Lee SJ, Rattanavong S, Vongsouvath M, Davong V, Chansamouth V, Phommasone K, Moore C, Dittrich S, Lattana O, Sirisouk J, Phoumin P, Panyanivong P, Sengduangphachanh A, Sibounheuang B, Chanthongthip A, Simmalavong M, Sengdatka D, Seubsanith A, Keoluangkot V, Phimmasone P, Sisout K, Detleuxay K, Luangxay K, Phouangsouvanh I, Craig SB, Tulsiani SM, Burns MA, Dance DAB, Blacksell SD, de Lamballerie X, Newton PN. Management of Central Nervous System Infections, Vientiane, Laos, 2003-2011. Emerg Infect Dis. 2019 May;25(5):898-910. [PMC free article: PMC6478220] [PubMed: 31002063]

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Mohan A, Munusamy C, Tan YC, Muthuvelu S, Hashim R, Chien SL, Wong MK, Khairuddin NA, Podin Y, Lau PS, Ng DC, Ooi MH. Invasive Salmonella infections among children in Bintulu, Sarawak, Malaysian Borneo: a 6-year retrospective review. BMC Infect Dis. 2019 Apr 18;19(1):330. [PMC free article: PMC6471830] [PubMed: 30999894]

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El-Naggar W, Afifi J, McMillan D, Toye J, Ting J, Yoon EW, Shah PS., Canadian Neonatal Network Investigators‖ Epidemiology of Meningitis in Canadian Neonatal Intensive Care Units. Pediatr Infect Dis J. 2019 May;38(5):476-480. [PubMed: 30986789]

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Haydar SM, Hallit SR, Hallit RR, Salameh PR, Faddoul LJ, Chahine BA, Malaeb DN. Adherence to international guidelines for the treatment of meningitis infections in Lebanon. Saudi Med J. 2019 Mar;40(3):260-265. [PMC free article: PMC6468200] [PubMed: 30834421]

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Simone L, Lyttle MD, Roland D, Stephens D, Schuh S., Pediatric Emergency Research Canada (PERC) and the Pediatric Emergency Research United Kingdom and Ireland (PERUKI) networks. Canadian and UK/Ireland practice patterns in lumbar puncture performance in febrile neonates with bronchiolitis. Emerg Med J. 2019 Mar;36(3):148-153. [PubMed: 30728189]

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Le Turnier P, Navas D, Garot D, Guimard T, Bernard L, Tattevin P, Vandamme YM, Hoff J, Chiffoleau A, Dary M, Leclair-Visonneau L, Grégoire M, Pere M, Boutoille D, Sébille V, Dailly E, Asseray N., High-Dose Ceftriaxone CNS Infections Study Group. Tolerability of high-dose ceftriaxone in CNS infections: a prospective multicentre cohort study. J Antimicrob Chemother. 2019 Apr 01;74(4):1078-1085. [PubMed: 30698733]

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Ferraro M, Morucci L, Coppeta L, De Carolis G, Pietroiusti A, Franco E, Magrini A. Managing the risk of bacterial meningitis among healthcare workers. Occup Med (Lond). 2019 Apr 13;69(2):113-117. [PubMed: 30496490]

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Biondi EA, Lee B, Ralston SL, Winikor JM, Lynn JF, Dixon A, McCulloh R. Prevalence of Bacteremia and Bacterial Meningitis in Febrile Neonates and Infants in the Second Month of Life: A Systematic Review and Meta-analysis. JAMA Netw Open. 2019 Mar 01;2(3):e190874. [PMC free article: PMC6583289] [PubMed: 30901044]

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Xu M, Hu L, Huang H, Wang L, Tan J, Zhang Y, Chen C, Zhang X, Huang L. Etiology and Clinical Features of Full-Term Neonatal Bacterial Meningitis: A Multicenter Retrospective Cohort Study. Front Pediatr. 2019;7:31. [PMC free article: PMC6381005] [PubMed: 30815433]

Disclosure: Tyler Runde declares no relevant financial relationships with ineligible companies.

Disclosure: Fatima Anjum declares no relevant financial relationships with ineligible companies.

Disclosure: John Hafner declares no relevant financial relationships with ineligible companies.

Serous meningitis. What is Serous Meningitis?

IMPORTANT
The information in this section should not be used for self-diagnosis or self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.

Serous meningitis is an inflammation of the pia mater of a serous nature, the cause of which can be viruses (most often), bacteria, fungi, systemic diseases, tumors, cerebral cysts. In most cases, the disease is acute with febrile condition, headache, meningeal symptom complex, sometimes with damage to the cranial nerves. Diagnosis is based on epidemiological data, the results of a neurological examination, data from the analysis of cerebrospinal fluid, bacteriological and virological studies, EEG, MRI of the brain. Therapy includes etiotropic treatment, dehydration, detoxification, antibiotic therapy, antipyretic, anticonvulsant, neurometabolic drugs.

• Causes of serous meningitis
• Symptoms of serous meningitis
• Clinic of individual forms of serous meningitis
  • Acute lymphocytic choriomeningitis
  • Tuberculous meningitis
  • AIDS fungal meningitis
  • Serous meningitis in mumps
• Diagnosis of serous meningitis
• Treatment of serous meningitis
  • Prognosis and prevention of serous meningitis
• Prices for treatment

General

Serous meningitis is an acute inflammatory process in the pia mater of the brain, which has a serous character. It can be caused by viruses, fungi and bacteria. In some cases, serous meningitis may be non-infectious aseptic in nature. A feature of serous inflammation is the production of a transparent serous exudate by the cerebral membranes, containing a small amount of leukocytes. Unlike purulent meningitis, serous meningitis is not accompanied by necrosis of cellular elements and the formation of pus, so it has a milder course and a favorable prognosis. Serous meningitis occurs mainly in children between the ages of 3 and 6 years. In adults, the serous form of inflammation of the cerebral membranes is extremely rare, mainly in young people 20-30 years of age.

Serous meningitis

Causes of serous meningitis

In 80% of cases, the serous form of meningitis is caused by a viral infection. The causative agents can be enteroviruses, Epstein-Barr virus, herpes virus, cytomegalovirus, paramyxovirus (the causative agent of mumps), adenoviruses, influenza, polio and measles viruses. In rare cases, serous meningitis develops against the background of a bacterial infection, for example, with syphilis and tuberculosis. Even more rarely, it has a fungal etiology. Serous meningitis of an infectious nature occurs when infected from a patient or carrier, if the defenses of the immune system could not cope with the pathogen that entered the body.

Infection is possible by airborne droplets, contact and waterways. In the first case, the infectious agent is transmitted through the air, where it enters with breathing, coughing, sneezing of the patient. The contact path is realized through touching the skin of the sick person or objects infected with pathogens that have fallen on them from the mucous membranes, skin or wounds of the patient. The water route of transmission is characteristic of enteroviruses, therefore, outbreaks of enteroviral meningitis occur mainly in the summer during the swimming season.

Non-infectious aseptic serous meningitis can occur with tumors of the cerebral membranes and intracerebral tumors, with brain cysts, systemic diseases (SLE, periarteritis nodosa). In the practice of infectious disease specialists and specialists in the field of neurology, viral lymphocytic choriomeningitis (Armstrong meningitis) is also encountered, in which domestic mice and rats are the source of infection. The virus enters the human body through the consumption of water and foods contaminated with the urine, feces and nasal mucus of infected rodents.

Symptoms of serous meningitis

Serous meningitis of viral etiology usually has an incubation period ranging from 3 to 18 days. Characterized by an acute manifestation of the disease with a rise in body temperature to 40 ° C, intense cephalalgia (headache), intoxication symptom complex. The latter is manifested by weakness, general weakness, myalgia and arthralgia. A two-wave temperature curve can be observed with a decline on the 3rd-4th day and a repeated rise after a few days. Cephalgia has a constant exhausting character; aggravated by head movements, bright light, sharp sounds and noise; not stopped by analgesics. Anorexia, nausea, repeated vomiting are noted. A characteristic symptom is general and skin hyperesthesia – painful perception of stimuli (sounds, light, touch). It is better for patients to be in a quiet and darkened room.

Serous meningitis is often accompanied by manifestations of acute respiratory viral infections: rhinitis, cough, sore throat, etc. Symptoms of cranial nerve damage may occur: diplopia, strabismus, difficulty swallowing, drooping of the upper eyelid. Typical is the patient’s posture – lying on his side with limbs pressed to the body and his head thrown back (the so-called “position of a pointing dog”). There is tension (rigidity) of the posterior neck muscles, which does not allow the patient to tilt his head forward so that his chin reaches his chest. There may be slight deafening of the patient, drowsiness. When ascertaining more severe disorders of consciousness (sopor or coma), one should think about the presence of another disease.

Meningitis in children occurs against the background of a capricious and whiny state. Often there is a convulsive syndrome. In infants, bulging fontanelles are observed. Raising a small child in an upright position and holding it by the armpits, parents note that he bends his legs and tries to pull them to the tummy (Lesage symptom, or “hanging” symptom).

Clinic of individual forms of serous meningitis

Acute lymphocytic choriomeningitis

The incubation period takes 6-13 days. Not only the soft cerebral membranes are affected, but also the choroid plexuses of the cerebral ventricles. The manifestation of lymphocytic choriomeningitis may be preceded by a prodrome in which the patient feels increased fatigue and some weakness; possible sore throat (pharyngitis) and runny nose. Then the body temperature rises to febrile values. In this case, the symptoms of meningitis may occur immediately, or there may be a flu-like form of the onset of the disease, in which the manifestations of meningitis appear with the beginning of the second wave of temperature rise. Otherwise, lymphocytic choriomeningitis has the same clinic as other forms of serous meningitis.

Tuberculous meningitis

Serous meningitis of tuberculous etiology occurs against the background of already existing tuberculosis of the lungs, kidneys, larynx, genitals or other localizations. The course of tuberculous meningitis is subacute. The prodromal period can last up to 3 weeks, manifested by fatigue, sweating, moderate cephalalgia, subfebrile condition, decreased appetite. Meningeal symptoms appear gradually. Possible decreased vision, slight ptosis, strabismus. If anti-tuberculosis therapy is not carried out, focal symptoms develop over time: aphasia, paresis, etc. In patients who have previously been treated with anti-tuberculosis drugs, meningitis may have a chronic course.

AIDS fungal meningitis

Serous meningitis of fungal etiology in patients with AIDS occurs with a minimum of clinical manifestations. Gradual development is characteristic, sometimes within 2-3 weeks. The temperature may remain subfebrile. Cephalgia does not have such an intense character. Liquor-hypertensive syndrome (intracranial hypertension) is observed only in 40% of patients. Possible lethargy and drowsiness. Rigidity of the muscles of the occipital group, as well as other meningeal symptoms may be absent.

Serous meningitis in mumps

Paramyxovirus meningitis is 3 times more common in males. Usually the symptoms of meningitis appear 1-3 weeks after the onset of mumps. Sometimes they are observed simultaneously, and in 10% of cases precede the clinic of mumps. Typically acute course with high fever, intense cephalalgia, vomiting, pronounced meningeal syndrome. In young children, drowsiness and weakness are often noted. There may be signs of FMN damage, ataxia, paresis, abdominalgia (abdominal pain), convulsive seizures. The penetration of paramyxovirus into the internal organs is accompanied by the development of pancreatitis, orchitis, adnexitis.

Diagnosis of serous meningitis

According to the characteristic clinical picture and the presence of a meningeal symptom complex (typical posture, stiffness of the posterior muscles, positive Kerneg’s symptoms, lower and upper Brudzinsky’s symptoms, in infants – Lesage’s symptom), not only a neurologist, but also a local therapist or pediatrician can suggest the presence of meningitis. A thorough study of the history of the disease (identifying contacts with sick individuals, determining the duration of the incubation period, the nature of the onset of the disease, etc. ) and conducting additional examination methods are necessary to establish the type and etiology of meningitis.

Serous meningitis is accompanied by typical inflammatory changes in the clinical blood test, but usually the rise in ESR and leukocytosis are less pronounced than with purulent meningitis. To isolate the pathogen, bacterial culture of swabs from the pharynx and nose, virological studies using PCR, RIF, and ELISA are performed. In patients with immunodeficiency, immunological studies aimed at verifying the pathogen are not very informative, since they can give false results.

Serous meningitis can be confirmed by examining the cerebrospinal fluid. Serous inflammation of the pia mater is characterized by slightly opalescent or clear cerebrospinal fluid with a slightly elevated protein content. Tuberculous and fungal meningitis are accompanied by a decrease in glucose levels. The cerebrospinal fluid flows out under increased pressure. In the first few days, neutrophilic leukocytosis may be noted, which resembles a picture of bacterial meningitis. Then lymphocytes begin to predominate in the cerebrospinal fluid, which is more typical for viral meningitis. Therefore, lumbar puncture must be repeated and compared with CSF study data at different periods of the disease.

With tuberculous and syphilitic etiology of meningitis, pathogens can be detected by microscopy of cerebrospinal fluid after special staining of smears. If serous meningitis has a viral origin, then the pathogen is not detected. If necessary, the following examinations can be additionally prescribed: electroencephalography, MRI of the brain, Echo-EG, tuberculin tests, RPR test, ophthalmologist’s consultation, ophthalmoscopy. Differential diagnosis is carried out with purulent meningitis of pneumococcal, meningococcal and other etiologies, with tick-borne encephalitis, arachnoiditis, subarachnoid hemorrhage.

Treatment of serous meningitis

A patient with suspected serous meningitis requires hospitalization and inpatient treatment. First of all, etiotropic therapy is needed. In case of viral genesis of meningitis, antiviral treatment is carried out with interferon preparations, in case of herpetic infection – with acyclovir. Immunoglobulin is administered in parallel to patients with reduced immunity. Since the exact determination of the etiology of meningitis takes time, antibiotic therapy with broad-spectrum drugs (ceftazidime, ceftriaxone) is carried out. With confirmed tuberculous meningitis, anti-tuberculosis treatment is prescribed (ftivazid, rifampicin, isoniazid, etc.).

For the purpose of detoxification, infusion therapy is carried out, to combat the liquor-hypertension syndrome – dehydration (the introduction of diuretics: furosemide, acetazolamide). With febrile condition, antipyretics (ibuprofen, paracetamol) are prescribed, with convulsive syndrome – detomidine, diazepam, valproic acid. At the same time, neuroprotective and neurotropic therapy is carried out – nootropics (gamma-aminobutyric acid, piracetam, glycine), B vitamins, pig brain hydrolyzate, etc. are prescribed.

Prognosis and prevention of serous meningitis

In the vast majority of cases, with correct and timely therapy, serous meningitis has a favorable outcome. Usually the temperature begins to subside already on the 3rd-4th day, a repeated wave of febrile condition is rarely observed. On average, serous meningitis lasts about 10 days, with a maximum of 2 weeks. As a rule, it passes without leaving behind any consequences. In some cases, after suffering meningitis, liquor-hypertension syndrome, frequent cephalalgia, asthenia, emotional instability, memory impairment, and difficulty concentrating may persist. However, these residual effects disappear within a few weeks or months. Tuberculous meningitis has a serious prognosis; without the use of anti-tuberculosis pharmaceuticals, it leads to death on the 23-25th day of illness. With a late start of anti-tuberculosis treatment, the prognosis is serious – relapses and complications are possible.

The best prevention of meningitis of any etiology is a strong immune system, i.e. a healthy diet, an active lifestyle, hardening, etc. Preventive measures should also include timely treatment of acute infections, isolation of patients, vaccination against tuberculosis, drinking only purified or boiled water, thorough washing of fruits and vegetables, personal hygiene.

You can share your medical history, what helped you in the treatment of serous meningitis.

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1. treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.

   Purulent meningitis – causes, symptoms, diagnosis and treatment

   Purulent meningitis is an inflammatory process that occurs in the pia mater of the brain when pyogenic microorganisms (pneumococci, meningococci, streptococci, etc. ) penetrate it. Purulent meningitis is characterized by high body temperature, intense headache, nausea, vomiting, disorders of the cranial nerves, early onset of meningeal symptoms, hyperesthesia, impaired consciousness, and psychomotor agitation. It is possible to diagnose purulent meningitis on the basis of a typical clinical picture and data from the analysis of cerebrospinal fluid. Purulent meningitis is an indication for mandatory antibiotic therapy. Decongestants, glucocorticosteroids, tranquilizers, anticonvulsants and other symptomatic therapy are used.

   General information

   Purulent meningitis is an inflammation of the meninges (meningitis) that has a bacterial etiology. Purulent meningitis occurs with a frequency of 3.3 cases per 100,000 population. All age categories are susceptible to the disease, but most often purulent meningitis develops in children under 5 years of age. It is noted that purulent meningitis often occurs against the background of a weakened state of the immune system. An increase in the incidence is observed in the winter-spring period. Since the beginning of the 90s of the last century, there has been a significant decrease in the incidence of purulent meningitis, a decrease in the number of deaths and cases of severe complications.

   Purulent meningitis

   Causes of purulent meningitis

   Purulent meningitis can be caused not only by meningococcal infection, but also by pneumococci, Haemophilus influenzae and other bacteria. Almost half of the cases of purulent meningitis are due to Haemophilus influenzae. In 20% of cases, the cause of purulent meningitis is meningococcus, in 13% of cases – pneumococcus. In newborns, purulent meningitis often results from streptococcal infection, salmonellosis, or E. coli infection.

   Depending on the mechanism of penetration of the pathogen into the membranes of the brain in neurology, primary and secondary purulent meningitis are distinguished. Primary purulent meningitis develops with hematogenous spread of the pathogen from the nasal cavity or pharynx, where it enters from the external environment. Infection occurs from sick persons and carriers by airborne droplets and contact. Direct infection of the meninges is possible with a skull fracture and open craniocerebral injury, open injuries of the mastoid process and paranasal sinuses, insufficiently careful observance of asepsis rules during neurosurgical interventions.

   Secondary purulent meningitis occurs against the background of a primary septic focus in the body, the infection from which penetrates into the membranes of the brain. Contact spread of pyogenic microorganisms can be observed with a brain abscess, osteomyelitis of the bones of the skull, septic sinus thrombosis. Hematogenous and lymphogenous spread of the pathogen is possible from an infectious focus of any localization, but most often occurs with long-term infections of the ENT organs (acute otitis media, chronic purulent otitis media, sinusitis).

   The penetration of pathogens of purulent meningitis through the blood-brain barrier is facilitated by a weakened state of the body’s immune system, which can be caused by frequent acute respiratory viral infections, hypovitaminosis, stress, physical overload, a sharp change in climate.

   Classification of purulent meningitis

   Depending on the severity of clinical manifestations, purulent meningitis is classified into mild, moderate and severe forms. Severe forms of the disease are observed mainly against the background of a sharp decrease in immunity and in patients with a removed spleen.

   According to the characteristics of the course, fulminant, abortive, acute and recurrent purulent meningitis are distinguished. The most common acute purulent meningitis with typical cerebral and meningeal symptoms. The fulminant course of purulent meningitis from the first hours of the disease is characterized by a rapid increase in cerebral edema, leading to impaired consciousness and vital functions. The abortive variant is distinguished by an erased clinical picture, in which the symptoms of intoxication come to the fore. Recurrent purulent meningitis can occur with insufficient or belated treatment of the acute form of the disease, as well as in the presence of a chronic focus of purulent infection in the body.

   Symptoms of purulent meningitis

   The incubation period of primary purulent meningitis lasts on average from 2 to 5 days. Typically acute onset with a sharp rise in body temperature to 39-40°C, severe chills, intense and growing headache, nausea and repeated vomiting. Psychomotor agitation, delirium, impaired consciousness may be observed. In 40% of cases, purulent meningitis occurs with a convulsive syndrome. Shell symptoms specific for meningitis (symptom of Kernig, Brudzinsky, Guillain, neck stiffness) are expressed from the first hours of the disease and intensify on the 2nd-3rd day. Severe hyperesthesia and a decrease in abdominal reflexes against the background of a general increase in deep reflexes are typical. Perhaps the appearance of a diffuse hemorrhagic rash.

   Focal symptoms accompanying purulent meningitis most often consist in dysfunction of various cranial nerves. The most commonly observed damage to the oculomotor nerves, leading to double vision, the development of strabismus, drooping of the upper eyelid and the appearance of a difference in the size of the pupils (anisocoria). Less common is neuritis of the facial nerve, damage to the trigeminal nerve, dysfunction of the optic nerve (loss of visual fields, decreased visual acuity) and vestibulocochlear nerve (progressive hearing loss). More severe focal symptoms indicate the spread of inflammatory changes to the substance of the brain or the development of vascular disorders such as ischemic stroke caused by vasculitis, reflex spasm, or thrombosis of cerebral vessels.

   When the inflammatory process passes to the substance of the brain, one speaks of the development of meningoencephalitis. At the same time, purulent meningitis proceeds with the addition of focal symptoms characteristic of encephalitis in the form of paresis and paralysis, speech disorders, changes in sensitivity, the appearance of pathological reflexes, and increased muscle tone. Hyperkinesis, hallucinatory syndrome, sleep disturbances, vestibular ataxia, behavioral and memory disorders are possible. The spread of the purulent process to the ventricles of the brain with the development of ventriculitis is manifested by spastic attacks of the type of hormetonia, flexion contractures of the arms and extensor legs.

   Complications of purulent meningitis

   An early and severe complication that may be accompanied by purulent meningitis is cerebral edema, leading to compression of the brain stem with vital centers located in it. Acute cerebral edema, as a rule, occurs on the 2-3rd day of the disease, with a fulminant form – in the first hours. Clinically, it is manifested by motor restlessness, impaired consciousness, respiratory distress and disorders of the cardiovascular system (tachycardia and arterial hypertension, in the terminal stage giving way to bradycardia and arterial hypotension).

   Other complications of purulent meningitis may include: septic shock, adrenal insufficiency, subdural empyema, pneumonia, infective endocarditis, pyelonephritis, cystitis, septic panophthalmitis, etc. real symptoms and focal neurological symptoms in the form of damage to the cranial nerves, as a rule, allow the neurologist to assume that the patient has purulent meningitis. It is more difficult to diagnose in cases where purulent meningitis has an abortive course or occurs a second time against the background of symptoms of an existing septic focus of another localization. To confirm purulent meningitis, it is necessary to perform a lumbar puncture, during which an increased pressure of the cerebrospinal fluid, its turbidity or opalescent color is detected. Subsequent examination of the cerebrospinal fluid determines an increased content of protein and cellular elements (mainly due to neutrophils). Identification of the pathogen is carried out during microscopy of smears of cerebrospinal fluid and when it is sown on nutrient media.

   For diagnostic purposes, a blood test and detachable elements of the skin rash are also performed. With the assumption of the secondary nature of purulent meningitis, additional examinations are carried out aimed at finding the primary infectious focus: consultation of an otolaryngologist, pulmonologist, therapist; radiography of the paranasal sinuses, otoscopy, radiography of the lungs.

   It is necessary to differentiate purulent meningitis from viral meningitis, subarachnoid hemorrhage, meningism phenomena in other infectious diseases (typhus, leptospirosis, severe forms of influenza, etc.).

   Treatment of purulent meningitis

   All patients with purulent meningitis should be treated in a hospital setting. Such patients should immediately undergo a lumbar puncture and bacterioscopic examination of the cerebrospinal fluid. Immediately after the establishment of the etiology of meningitis, the patient is prescribed antibiotic therapy. In most cases, it is a combination of ampicillin with cephalosporin drugs (ceftriaxone, cefotaxime, ceftazidime). With purulent meningitis of unknown etiology, initial therapy consists of intramuscular administration of aminoglycosides (kanamycin, gentamicin) or their combination with ampicillin. Severe purulent meningitis may require intravenous or intrathecal antibiotics.

   In order to reduce hydrocephalus and cerebral edema in purulent meningitis, dehydration therapy (furosemide, mannitol) is prescribed. Pathogenetic treatment of purulent meningitis also includes the use of glucocorticosteroid drugs (dexamethasone, prednisone), the doses of which depend on the severity of the disease. Along with this, the necessary symptomatic therapy is performed. In case of sleep disorders, tranquilizers are prescribed; for the relief of psychomotor agitation and convulsions – lytic mixtures (chlorpromazine, diphenhydramine, trimeperidine), diazepam, valproic acid; with hypovolemia and the development of infectious-toxic shock, infusion therapy is performed.

   In the recovery period after the acute phase of purulent meningitis, it is recommended to take nootropic and neuroprotective drugs, vitamin therapy and restorative treatment. Treatment of patients with secondary purulent meningitis should include the elimination of the primary septic focus, including by surgical intervention (sanitation for otitis media, frontotomy, ethmoidotomy, sphenotomy, removal of an intracerebral abscess, etc. ).

   Prognosis of purulent meningitis

   According to some reports, purulent meningitis is fatal in 14% of cases. However, with timely started and correctly carried out treatment, purulent meningitis has a generally favorable prognosis. After suffering meningitis, asthenia, liquor-dynamic disorders, sensorineural hearing loss, and some mild focal symptoms can be observed. Severe consequences of purulent meningitis (hydrocephalus, amaurosis, deafness, dementia, epilepsy) are rare nowadays.

   Prevention of purulent meningitis

   Vaccination is by far the most effective way to prevent purulent meningitis. Vaccinations are carried out against the main pathogens of purulent meningitis: Haemophilus influenzae, meningo- and pneumococci. In Russia, these vaccines are not considered mandatory and are administered according to indications or at the request of patients.

   Vaccination against Haemophilus influenzae is mainly given to children aged 3 months to 5 years and people suffering from immunodeficiency states as a result of HIV infection, immunosuppressive therapy for cancer, removal of the thymus or spleen, etc.