With a mortality rate ranging between 20%-60%, bacterial meningitis in the neonatal period remains one of the deadliest illnesses affecting children. In the first month of life, treated cases can have a mortality rate ranging up to 40%, and ranging to 10% after the neonatal period. Several factors contribute to neonatal vulnerability of this disease. The most significant factor is the immaturity of infants’ immune systems, particularly preterm infants.
Due to the fact that infants are not given their first set of vaccines until 2 months of age, the danger of bacteremia, which could lead to bacterial meningitis, is significant. These populations are at the greatest risk: preterm newborns, males, infants in daycare and the poor.
Offspring of women with a history of STIs, or of those are infected with group B streptococcus are at a higher risk for neonatal meningitis. Another pathogen identified in the neonatal population, Listeria, may be transmitted to babies from mothers who have consumed specific foods. The most common bacteria causing neonatal meningitis is Group B streptococcus.
Epidemiology
Due to their immature cellular and humoral immune systems, neonates are predisposed to sepsis and meningitis. Ten to twenty percent of sick infants younger than three months are diagnosed with a severe bacterial illness. In wealthy nations, the incidence of neonatal meningitis is believed to be 0.3 per 1000 births, however this number is likely an underestimated.
Only 30% to 50% of children in the newborn intensive care unit who are examined for sepsis have a lumbar puncture, and it occurs 75% of the time after the introduction of broad-spectrum antibiotics. Consequently, the outcomes of the culture may be impacted. The death rate is between 10 and 15 percent, and morbidity is significant.
Up to fifty percent of infants who survive the disease experience chronic neurological sequelae, such as seizures, cognitive deficits, motor issues, and visual and auditory impairment. In underdeveloped nations, the frequency is greater, ranging from 0.8-6.1 per 1000 births, with a death rate as high as 58%.
It’s likely that cases are underreported in these countries, so the prevalence is likely higher. Multiple sources indicate that the mortality rate of this condition has decreased dramatically during the past four decades. Despite numerous breakthroughs in medicine and neonatology, mortality rates have not changed.
Anatomy
Pathophysiology
The most typical mechanism by which this disease occurs is through a primary bloodstream infection with CNS involvement. Early-onset and late-onset infections appear differently, with early-onset infections originating predominantly from the mother.
Numerous pathogens are exposed to the newborn during the birthing process. These can be transmitted via the vaginal canal to amniotic membranes that have ruptured, or through touch with the newborn’s skin during passage from the birth canal. O like Listeria monocytogenes can be transferred through the placenta.
Late-onset infections are predominantly nosocomial in origin. Inadequate hand hygiene among sick and uninfected newborns is a significant risk factor for this condition. Ventilators, catheters, feeding tubes and endotracheal tubes can also carry infection.
The introduction of the virus through the blood-brain barrier is considerably simpler in neonates. From the late gestation period until the postnatal phase, the barrier is still developing, resulting in heightened susceptibility to infection. Since the newborn’s brain is still developing after birth, the cerebral arteries are more vulnerable, resulting in more severe sickness symptoms.
The newborn’s immune system, especially the phagocytic response, is severely undeveloped. Complement and antimicrobial proteins and peptides are lacking in the newborn immune system, although the phagocytic response is only temporarily reduced, reaching adult levels by day three of life.
Etiology
Due to their immature immune systems, newborns are particularly susceptible to this disease. Various pathogens cause this illness depending on the location of infection, gestational age, and the child’s age. The distribution of organisms in newborn sepsis and meningitis are comparable. The disease has either an early or a late onset.
Early onset happens within the initial 72 hours of a child’s life. In premature newborns, late-onset is most prevalent, and a different spectrum of infections is observed in this population. By administering intrapartum antibiotics to treat Group B streptococcus infection, the prevalence of early-onset meningitis has drastically reduced.
GBS remains the leading cause of both neonatal sepsis and meningitis, accounting for almost 40 percent of all early-onset infections. The next most prevalent infection in this group is E. coli, which has emerged as the leading cause of early-onset meningitis and sepsis among newborns with a birth weight below 1.5kgs.
In the group with late onset, the incidence is proportional to birth weight and gestational age. Staphylococcus aureus and coagulase-negative staphylococci are the most prevalent pathogens, followed by Klebsiella and E.coli. Listeria is another bacterium implicated in early-onset meningitis, and antibiotic coverage should also take this into account.
Late-onset disease should include additional species in the nosocomial environment, including methicillin-resistant Staphylococcus aureus and pseudomonas aeruginosa in neonatal intensive care units. Viral infections, such as HSV and enterovirus, should also be considered during treatment.
Genetics
Prognostic Factors
Although mortality rates for neonatal meningitis have significantly decreased through the years, the disease is still responsible for high morbidity rates.
It causes significant neurological issues such as seizures, behavioral issues, auditory and visual impairments, profound mental retardation and learning disabilities.
A study conducted in Tunisia, indicated that 21.9% of children in the reviewed study suffered from profound neurological complications.
Some factors which are known to cause a worse prognosis include:
Lower neonatal weight
High levels of CSF proteins
Respiratory problems
Pleocytosis of lesser than 500 cells per ml
Shock
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK532264/
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With a mortality rate ranging between 20%-60%, bacterial meningitis in the neonatal period remains one of the deadliest illnesses affecting children. In the first month of life, treated cases can have a mortality rate ranging up to 40%, and ranging to 10% after the neonatal period. Several factors contribute to neonatal vulnerability of this disease. The most significant factor is the immaturity of infants’ immune systems, particularly preterm infants.
Due to the fact that infants are not given their first set of vaccines until 2 months of age, the danger of bacteremia, which could lead to bacterial meningitis, is significant. These populations are at the greatest risk: preterm newborns, males, infants in daycare and the poor.
Offspring of women with a history of STIs, or of those are infected with group B streptococcus are at a higher risk for neonatal meningitis. Another pathogen identified in the neonatal population, Listeria, may be transmitted to babies from mothers who have consumed specific foods. The most common bacteria causing neonatal meningitis is Group B streptococcus.
Due to their immature cellular and humoral immune systems, neonates are predisposed to sepsis and meningitis. Ten to twenty percent of sick infants younger than three months are diagnosed with a severe bacterial illness. In wealthy nations, the incidence of neonatal meningitis is believed to be 0.3 per 1000 births, however this number is likely an underestimated.
Only 30% to 50% of children in the newborn intensive care unit who are examined for sepsis have a lumbar puncture, and it occurs 75% of the time after the introduction of broad-spectrum antibiotics. Consequently, the outcomes of the culture may be impacted. The death rate is between 10 and 15 percent, and morbidity is significant.
Up to fifty percent of infants who survive the disease experience chronic neurological sequelae, such as seizures, cognitive deficits, motor issues, and visual and auditory impairment. In underdeveloped nations, the frequency is greater, ranging from 0.8-6.1 per 1000 births, with a death rate as high as 58%.
It’s likely that cases are underreported in these countries, so the prevalence is likely higher. Multiple sources indicate that the mortality rate of this condition has decreased dramatically during the past four decades. Despite numerous breakthroughs in medicine and neonatology, mortality rates have not changed.
The most typical mechanism by which this disease occurs is through a primary bloodstream infection with CNS involvement. Early-onset and late-onset infections appear differently, with early-onset infections originating predominantly from the mother.
Numerous pathogens are exposed to the newborn during the birthing process. These can be transmitted via the vaginal canal to amniotic membranes that have ruptured, or through touch with the newborn’s skin during passage from the birth canal. O like Listeria monocytogenes can be transferred through the placenta.
Late-onset infections are predominantly nosocomial in origin. Inadequate hand hygiene among sick and uninfected newborns is a significant risk factor for this condition. Ventilators, catheters, feeding tubes and endotracheal tubes can also carry infection.
The introduction of the virus through the blood-brain barrier is considerably simpler in neonates. From the late gestation period until the postnatal phase, the barrier is still developing, resulting in heightened susceptibility to infection. Since the newborn’s brain is still developing after birth, the cerebral arteries are more vulnerable, resulting in more severe sickness symptoms.
The newborn’s immune system, especially the phagocytic response, is severely undeveloped. Complement and antimicrobial proteins and peptides are lacking in the newborn immune system, although the phagocytic response is only temporarily reduced, reaching adult levels by day three of life.
Due to their immature immune systems, newborns are particularly susceptible to this disease. Various pathogens cause this illness depending on the location of infection, gestational age, and the child’s age. The distribution of organisms in newborn sepsis and meningitis are comparable. The disease has either an early or a late onset.
Early onset happens within the initial 72 hours of a child’s life. In premature newborns, late-onset is most prevalent, and a different spectrum of infections is observed in this population. By administering intrapartum antibiotics to treat Group B streptococcus infection, the prevalence of early-onset meningitis has drastically reduced.
GBS remains the leading cause of both neonatal sepsis and meningitis, accounting for almost 40 percent of all early-onset infections. The next most prevalent infection in this group is E. coli, which has emerged as the leading cause of early-onset meningitis and sepsis among newborns with a birth weight below 1.5kgs.
In the group with late onset, the incidence is proportional to birth weight and gestational age. Staphylococcus aureus and coagulase-negative staphylococci are the most prevalent pathogens, followed by Klebsiella and E.coli. Listeria is another bacterium implicated in early-onset meningitis, and antibiotic coverage should also take this into account.
Late-onset disease should include additional species in the nosocomial environment, including methicillin-resistant Staphylococcus aureus and pseudomonas aeruginosa in neonatal intensive care units. Viral infections, such as HSV and enterovirus, should also be considered during treatment.
Although mortality rates for neonatal meningitis have significantly decreased through the years, the disease is still responsible for high morbidity rates.
It causes significant neurological issues such as seizures, behavioral issues, auditory and visual impairments, profound mental retardation and learning disabilities.
A study conducted in Tunisia, indicated that 21.9% of children in the reviewed study suffered from profound neurological complications.
Some factors which are known to cause a worse prognosis include:
Lower neonatal weight
High levels of CSF proteins
Respiratory problems
Pleocytosis of lesser than 500 cells per ml
Shock
https://www.ncbi.nlm.nih.gov/books/NBK532264/
medtigo
Neonatal Meningitis
Updated :
July 21, 2022
With a mortality rate ranging between 20%-60%, bacterial meningitis in the neonatal period remains one of the deadliest illnesses affecting children. In the first month of life, treated cases can have a mortality rate ranging up to 40%, and ranging to 10% after the neonatal period. Several factors contribute to neonatal vulnerability of this disease. The most significant factor is the immaturity of infants’ immune systems, particularly preterm infants.
Due to the fact that infants are not given their first set of vaccines until 2 months of age, the danger of bacteremia, which could lead to bacterial meningitis, is significant. These populations are at the greatest risk: preterm newborns, males, infants in daycare and the poor.
Offspring of women with a history of STIs, or of those are infected with group B streptococcus are at a higher risk for neonatal meningitis. Another pathogen identified in the neonatal population, Listeria, may be transmitted to babies from mothers who have consumed specific foods. The most common bacteria causing neonatal meningitis is Group B streptococcus.
Due to their immature cellular and humoral immune systems, neonates are predisposed to sepsis and meningitis. Ten to twenty percent of sick infants younger than three months are diagnosed with a severe bacterial illness. In wealthy nations, the incidence of neonatal meningitis is believed to be 0.3 per 1000 births, however this number is likely an underestimated.
Only 30% to 50% of children in the newborn intensive care unit who are examined for sepsis have a lumbar puncture, and it occurs 75% of the time after the introduction of broad-spectrum antibiotics. Consequently, the outcomes of the culture may be impacted. The death rate is between 10 and 15 percent, and morbidity is significant.
Up to fifty percent of infants who survive the disease experience chronic neurological sequelae, such as seizures, cognitive deficits, motor issues, and visual and auditory impairment. In underdeveloped nations, the frequency is greater, ranging from 0.8-6.1 per 1000 births, with a death rate as high as 58%.
It’s likely that cases are underreported in these countries, so the prevalence is likely higher. Multiple sources indicate that the mortality rate of this condition has decreased dramatically during the past four decades. Despite numerous breakthroughs in medicine and neonatology, mortality rates have not changed.
The most typical mechanism by which this disease occurs is through a primary bloodstream infection with CNS involvement. Early-onset and late-onset infections appear differently, with early-onset infections originating predominantly from the mother.
Numerous pathogens are exposed to the newborn during the birthing process. These can be transmitted via the vaginal canal to amniotic membranes that have ruptured, or through touch with the newborn’s skin during passage from the birth canal. O like Listeria monocytogenes can be transferred through the placenta.
Late-onset infections are predominantly nosocomial in origin. Inadequate hand hygiene among sick and uninfected newborns is a significant risk factor for this condition. Ventilators, catheters, feeding tubes and endotracheal tubes can also carry infection.
The introduction of the virus through the blood-brain barrier is considerably simpler in neonates. From the late gestation period until the postnatal phase, the barrier is still developing, resulting in heightened susceptibility to infection. Since the newborn’s brain is still developing after birth, the cerebral arteries are more vulnerable, resulting in more severe sickness symptoms.
The newborn’s immune system, especially the phagocytic response, is severely undeveloped. Complement and antimicrobial proteins and peptides are lacking in the newborn immune system, although the phagocytic response is only temporarily reduced, reaching adult levels by day three of life.
Due to their immature immune systems, newborns are particularly susceptible to this disease. Various pathogens cause this illness depending on the location of infection, gestational age, and the child’s age. The distribution of organisms in newborn sepsis and meningitis are comparable. The disease has either an early or a late onset.
Early onset happens within the initial 72 hours of a child’s life. In premature newborns, late-onset is most prevalent, and a different spectrum of infections is observed in this population. By administering intrapartum antibiotics to treat Group B streptococcus infection, the prevalence of early-onset meningitis has drastically reduced.
GBS remains the leading cause of both neonatal sepsis and meningitis, accounting for almost 40 percent of all early-onset infections. The next most prevalent infection in this group is E. coli, which has emerged as the leading cause of early-onset meningitis and sepsis among newborns with a birth weight below 1.5kgs.
In the group with late onset, the incidence is proportional to birth weight and gestational age. Staphylococcus aureus and coagulase-negative staphylococci are the most prevalent pathogens, followed by Klebsiella and E.coli. Listeria is another bacterium implicated in early-onset meningitis, and antibiotic coverage should also take this into account.
Late-onset disease should include additional species in the nosocomial environment, including methicillin-resistant Staphylococcus aureus and pseudomonas aeruginosa in neonatal intensive care units. Viral infections, such as HSV and enterovirus, should also be considered during treatment.
Although mortality rates for neonatal meningitis have significantly decreased through the years, the disease is still responsible for high morbidity rates.
It causes significant neurological issues such as seizures, behavioral issues, auditory and visual impairments, profound mental retardation and learning disabilities.
A study conducted in Tunisia, indicated that 21.9% of children in the reviewed study suffered from profound neurological complications.
Some factors which are known to cause a worse prognosis include:
Lower neonatal weight
High levels of CSF proteins
Respiratory problems
Pleocytosis of lesser than 500 cells per ml
Shock
https://www.ncbi.nlm.nih.gov/books/NBK532264/
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