Meningitis is an inflammatory condition of the brain and the spinal cord typically induced by a bacterial, viral, or fungal infection. Some types of meningitis can be prevented with vaccines. Depending on the cause, meningitis can be self-limiting or life-threatening, requiring immediate antibiotic treatment.
Epidemiology
The yearly incidence of bacterial meningitis in the United States is nearly 1.38 cases per 100,000 individuals, with an estimated mortality rate of 14.3%. Meningitis is highly prevalent in Sub-Saharan Africa, also known as the meningitis belt, which stretches to Senegal from Ethiopia.
Non-polio enteroviruses such as echovirus and group B coxsackievirus are the most prevalent viral agents causing meningitis. Herpesviruses, Mumps, Parechovirus, Varicella-zoster virus, Epstein Barr virus, influenza, measles, and arboviruses are commonly found in Jamestown Canyon, La Crosse West Nile, and Powassan.
Fungal meningitis is commonly associated with immune-compromised individuals and chronic corticosteroid therapy. Mycobacterium tuberculosis also affects immunosuppressed individuals. Escherichia coli is a significant pathogen responsible for meningitis in the early years of life.
Anatomy
Pathophysiology
Meningitis is primarily transmitted through two routes of infection:
Contiguous direct spread
Organisms invade the cerebrospinal fluid through surrounding anatomical structures ( sinusitis, otitis media), foreign objects (trauma, traffic accidents, medical devices), or surgical procedures.
Hematogenous seeding
Following the mucosal invasion, bacteria enter the bloodstream via colonizing the nasopharynx. When bacteria enter the subarachnoid space, they penetrate the blood-brain barrier, triggering an inflammatory and immune-mediated response.
Viral invasion of the central nervous system can occur either through hematogenous seeding or retrograde transmission along neuronal pathways.
Etiology
Meningitis is transmitted from viruses, bacteria, fungi, and, less frequently, parasites. Meningeal inflammation is referred to as meningitis. The arachnoid mater, dura mater, and pia mater are three membranes that cover the skull’s vertebral canal, which shelters the brain and spinal cord.
Both viral and non-infectious factors, such as autoimmune diseases, malignancy, and medication responses, can also result in meningitis.
Risk factors include:
Under vaccination
Immunocompromised state
Chronic medical conditions
Bacterial endocarditis
Alcohol abuse
Malignancy
Sickle cell anemia
Splenectomy
Genetics
Prognostic Factors
Prognosis varies based on the etiologic organism patient’s age and immunological condition. The annual fatality rate for bacterial meningitis in the United States in 2010 was 14.3%.
The mortality rate associated with different pathogens varies, such as Neisseria meningitidis meningitis is 10.1%, Listeria monocytogenes is 18.1%, Group B Streptococcus is 11.1%, and Streptococcus pneumoniae is 17.9%.
1 g IM or IV every 12hrs for mild conditions
1-2 g IM or IV every 8hrs moderate to severe infections
2 g IV every 6-8hrs high dosing for infections
2 g IV every 4hrs for life-threatening infections
12 g is the maximum dose required per day
200 mg IV given initially, followed by 100 mg IV every 12hrs
maximum dose given per day is 400 mg
Meningococcal Meningitis Prophylaxis:
100 mg given orally every 12hrs for about five days
1-2 g IV or IM was given once a day or in equally divided doses 2x a day
maximum duration of therapy is 4-14 days
prolonged treatment recommends for complicated infections
At least ten days for Infections due to S. pyogenes
The usual dose for the treatment of meningitis is 1 to 3 g via Intravenous or Intramuscular administration two or four times a day for up to 10-14 days. The duration of the treatment depends on the severity and the nature of the infections
If the infection is severe, the dose can be increased up to 12 g per day
Dose Adjustments
Renal Dose Adjustment In case of renal insufficiency, the usual dose of ceftizoxime depends on the CrCl. If the CrCl is below 5 mL/min, then 0.25-0.5 g a day or 0.5-1 g via IV or IM in 2 days after undergoing dialysis. Loading dose is standard in renal insufficiency, which is 0.5-1 g. 0.25 -1g twice a day if CrCl falls between 5 and 49 mL/min and 0.5 – 1.5 g thrice a day if CrCl is between 50 and 79 mL/min
0-1 week: 50 mg per kg IV every 12hrs
1-4 weeks: 50 mg per kg IV every 8hrs
Age: 1 month-12 years
for weight: <50 kg
50-180 mg per kg IM or IV has given per day divided into 4 to 6 equal doses
for weight: >50 kg
1 g IM or IV given every 12hrs for mild conditions
1-2 g IM or IV every 8hrs moderate to severe infections
2 g IV every 6-8hrs high dosing for infections
2 g IV every 4hrs for life-threatening infections
12 g is the maximum dose required per day
Age: >12 years:
1 g IM or IV given every 12hrs for mild conditions
1-2 g IM or IV every 8hrs moderate to severe infections
2 g IV every 6-8hrs high dosing for infections
2 g IV every 4hrs for life-threatening infections
12 g is the maximum dose required per day
Higher doses are given to treat more severe or serious infections
In the neonates, 100 mg/kg each day in two divided doses
1–4-week-olds, 150 mg/kg each day in three divided doses
For more than 1 month to 12-year-olds, 180-300 mg/kg each day in four to six divided doses
100 mg/kg Intravenous injections as a loading dose
Dose Adjustments
Renal Impairment
Haemodialysis: 15 mg/kg intravenously at the end of each dialysis
CrCl above 30 mL/min: 15 mg/kg every 1-2 times a day
CrCl below 10 mL/min: 15 mg/kg every 36 to 48 hours
CrCl 10 to 30 mL/min: 15 mg/kg every 24 to 36 hours
IDSA Recommends for neonates 0-7 days a dose of 75 mg per kg per day IV given and divided in every 8-12hrs
IDSA Recommends for neonates 8-28 days a dose of 100-150 mg per kg per day IV divided every 6-8hrs
IDSA Recommends for infants and children a dose of 200 mg per kg per day given IV divided in every 6hrs
The total dose per day recommended is 12g
Meningitis is an inflammatory condition of the brain and the spinal cord typically induced by a bacterial, viral, or fungal infection. Some types of meningitis can be prevented with vaccines. Depending on the cause, meningitis can be self-limiting or life-threatening, requiring immediate antibiotic treatment.
The yearly incidence of bacterial meningitis in the United States is nearly 1.38 cases per 100,000 individuals, with an estimated mortality rate of 14.3%. Meningitis is highly prevalent in Sub-Saharan Africa, also known as the meningitis belt, which stretches to Senegal from Ethiopia.
Non-polio enteroviruses such as echovirus and group B coxsackievirus are the most prevalent viral agents causing meningitis. Herpesviruses, Mumps, Parechovirus, Varicella-zoster virus, Epstein Barr virus, influenza, measles, and arboviruses are commonly found in Jamestown Canyon, La Crosse West Nile, and Powassan.
Fungal meningitis is commonly associated with immune-compromised individuals and chronic corticosteroid therapy. Mycobacterium tuberculosis also affects immunosuppressed individuals. Escherichia coli is a significant pathogen responsible for meningitis in the early years of life.
Meningitis is primarily transmitted through two routes of infection:
Contiguous direct spread
Organisms invade the cerebrospinal fluid through surrounding anatomical structures ( sinusitis, otitis media), foreign objects (trauma, traffic accidents, medical devices), or surgical procedures.
Hematogenous seeding
Following the mucosal invasion, bacteria enter the bloodstream via colonizing the nasopharynx. When bacteria enter the subarachnoid space, they penetrate the blood-brain barrier, triggering an inflammatory and immune-mediated response.
Viral invasion of the central nervous system can occur either through hematogenous seeding or retrograde transmission along neuronal pathways.
Meningitis is transmitted from viruses, bacteria, fungi, and, less frequently, parasites. Meningeal inflammation is referred to as meningitis. The arachnoid mater, dura mater, and pia mater are three membranes that cover the skull’s vertebral canal, which shelters the brain and spinal cord.
Both viral and non-infectious factors, such as autoimmune diseases, malignancy, and medication responses, can also result in meningitis.
Risk factors include:
Under vaccination
Immunocompromised state
Chronic medical conditions
Bacterial endocarditis
Alcohol abuse
Malignancy
Sickle cell anemia
Splenectomy
Prognosis varies based on the etiologic organism patient’s age and immunological condition. The annual fatality rate for bacterial meningitis in the United States in 2010 was 14.3%.
The mortality rate associated with different pathogens varies, such as Neisseria meningitidis meningitis is 10.1%, Listeria monocytogenes is 18.1%, Group B Streptococcus is 11.1%, and Streptococcus pneumoniae is 17.9%.
https://www.ncbi.nlm.nih.gov/books/NBK459360/
medtigo
Meningitis
Updated :
February 14, 2024
Meningitis is an inflammatory condition of the brain and the spinal cord typically induced by a bacterial, viral, or fungal infection. Some types of meningitis can be prevented with vaccines. Depending on the cause, meningitis can be self-limiting or life-threatening, requiring immediate antibiotic treatment.
The yearly incidence of bacterial meningitis in the United States is nearly 1.38 cases per 100,000 individuals, with an estimated mortality rate of 14.3%. Meningitis is highly prevalent in Sub-Saharan Africa, also known as the meningitis belt, which stretches to Senegal from Ethiopia.
Non-polio enteroviruses such as echovirus and group B coxsackievirus are the most prevalent viral agents causing meningitis. Herpesviruses, Mumps, Parechovirus, Varicella-zoster virus, Epstein Barr virus, influenza, measles, and arboviruses are commonly found in Jamestown Canyon, La Crosse West Nile, and Powassan.
Fungal meningitis is commonly associated with immune-compromised individuals and chronic corticosteroid therapy. Mycobacterium tuberculosis also affects immunosuppressed individuals. Escherichia coli is a significant pathogen responsible for meningitis in the early years of life.
Meningitis is primarily transmitted through two routes of infection:
Contiguous direct spread
Organisms invade the cerebrospinal fluid through surrounding anatomical structures ( sinusitis, otitis media), foreign objects (trauma, traffic accidents, medical devices), or surgical procedures.
Hematogenous seeding
Following the mucosal invasion, bacteria enter the bloodstream via colonizing the nasopharynx. When bacteria enter the subarachnoid space, they penetrate the blood-brain barrier, triggering an inflammatory and immune-mediated response.
Viral invasion of the central nervous system can occur either through hematogenous seeding or retrograde transmission along neuronal pathways.
Meningitis is transmitted from viruses, bacteria, fungi, and, less frequently, parasites. Meningeal inflammation is referred to as meningitis. The arachnoid mater, dura mater, and pia mater are three membranes that cover the skull’s vertebral canal, which shelters the brain and spinal cord.
Both viral and non-infectious factors, such as autoimmune diseases, malignancy, and medication responses, can also result in meningitis.
Risk factors include:
Under vaccination
Immunocompromised state
Chronic medical conditions
Bacterial endocarditis
Alcohol abuse
Malignancy
Sickle cell anemia
Splenectomy
Prognosis varies based on the etiologic organism patient’s age and immunological condition. The annual fatality rate for bacterial meningitis in the United States in 2010 was 14.3%.
The mortality rate associated with different pathogens varies, such as Neisseria meningitidis meningitis is 10.1%, Listeria monocytogenes is 18.1%, Group B Streptococcus is 11.1%, and Streptococcus pneumoniae is 17.9%.
https://www.ncbi.nlm.nih.gov/books/NBK459360/
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