case study of a child with meningitis

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Acute Bacterial Meningitis Case Study

Bacterial meningitis is a life-threatening infection of the linings or meninges of the brain and spinal cord. Survivors may experience hearing loss or deafness, brain damage, seizures, and/or the retention of fluid on the brain. Symptoms may be mistaken for the flu. Find out what happens to a 14-year-old when bacteria invade his central nervous system.

Module 4: Meningitits

A 14-year old male complained to his parents of feeling quite ill with...

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Case-based learning: meningitis

Causes, diagnosis and initial management options for adults and children with meningitis.

JL / The Pharmaceutical Journal

Meningitis is the second leading infection-related cause of death in children in the world, second only to pneumonia [1] . It is responsible for more deaths than malaria, AIDS, measles and tetanus combined [1] . The disease is more prevalent in children under the age of four years and in teenagers. In England, there has been a decline in confirmed cases of invasive meningococcal disease over the past two decades, from 2,595 cases in 1999/2000 to 755 cases in 2017/2018, which is a small increase from the 748 cases reported in 2016 and 2017 [2] .

Pharmacists have a vital role in raising awareness of the signs and symptoms of meningitis, while also maximising the benefit of the national immunisation programme to reduce the incidence of the disease. This article will cover initial management options, with a focus on children and neonates.

Meningitis — inflammation of the membranes covering the brain and spinal cord (meninges) — can be caused by viruses, bacteria or fungi.

Meningococcal disease encompasses meningococcal septicaemia (25% of cases), meningococcal meningitis (15% of cases) or a combination of the two (60% of cases) [3] . Up to 95% of meningitis in the UK is aseptic, where there is no growth on cerebrospinal fluid (CSF) culture, usually with a viral aetiology (e.g. enteroviruses) [3] .

Bacterial meningitis is most commonly caused by Neisseria meningitidis (also known as meningococcus), although the main pathogens alter with age. As such, N. meningitidis , Streptococcus pneumoniae (also known as pneumococcus) and Haemophilus influenzae type b are the leading causes of meningitis in children older than three months; however, Streptococcus agalactiae , Escherichia coli , S. pneumoniae and Listeria monocytogenes are more common in children younger than three months [3] .

The bacteria that cause meningitis are very common — they are present in the nasopharynx in around one in ten people who may not ever show any symptoms of disease. The reasons why some people develop meningitis while others do not are not yet fully understood. However, it is thought that genetic variations in the genes for Factor H and Factor H-related proteins may have a role to play [4] . These proteins regulate a part of the body’s immune system called the complement system, which recognises and kills invading bacteria.

Risk factors

In general, young children are at the highest risk of bacterial meningitis and septicaemia, but other age groups, including older people, can also be vulnerable to specific types. One study found that meningococcal meningitis was less frequent in older patients, whereas pneumococcal, listerial and meningitis of unknown origin were more frequent [3], [5] . People with low immunity, for example, those with HIV or those having chemotherapy treatment for cancer, may also be at an increased risk.

Individual countries show seasonal patterns of bacterial meningitis. For instance, increased cases have been observed between the months of December and March in the United States, France and the UK [6] . There is also evidence that mass gatherings and exposure to cigarette and wood smoke can make people more susceptible to certain causes of meningitis and septicaemia, potentially from interference with mucosal immunity [7] .

Depending on the cause, cases of meningitis may be isolated. However, those who have been in close contact with someone with bacterial meningitis may be at increased risk of disease.

Pathophysiology

Infection occurs through transmission of contaminated respiratory droplets or saliva. Pili on the bacterial surface are thought to disrupt endothelial cell junctions in the blood–brain barrier, allowing the pathogens to penetrate it [8] . Once they have entered the subarachnoid space (the area of the brain between the arachnoid membrane and the pia mater), the pathogens replicate rapidly. This causes the production of several inflammatory mediators, including lymphocytes and inflammatory cytokines, as well as local immunoglobulin production by plasma cells. This enhances the influx of leukocytes into the CSF, which releases toxic substances that contribute to the production of cyctotoxic oedema and increased intracranial pressure. It is this process that can contribute to neurological damage and even death [9] , [10] .

Signs, symptoms and immediate management

Symptoms typically occur within 3–7 days after transmission [3] . Early, non-­specific symptoms of meningitis include:

• Irritability;
• Ill appearance;
• Refusing food/drink;
• Other aches and respiratory symptoms;
• Vomiting/nausea;

Healthcare professionals should be aware that classic signs of meningitis that include neck stiffness, bulging fontanelle and high-pitched cry are often absent in infants with bacterial meningitis [3] , [11] . Less common early symptoms include shivering, diarrhoea, abdominal pain and distention, coryza and other ear, nose and throat symptoms [3] .

General features of meningitis include a non­-blanching rash that can appear anywhere on the body, altered mental state, shock, unconsciousness and toxic or moribund state. If a patient presents with these symptoms, the glass test (also known as the ‘Tumbler test’; see Figure 1) may be used to aid diagnosis, where the side of a clear glass should be firmly pressed against the rash; if it does not fade under pressure, the patient may have septicaemia and needs urgent medical attention (see Figure 2) [3] , [12] . However, it should be noted that the National Institute for Health and Care Excellence’s Clinical Knowledge Summary states that the glass test should not be used solely for diagnosing bacterial meningitis and meningococcal septicaemia [13] .

Figure 1: Glass or ‘tumbler’ test

Source: Alamy Stock Photo / Mediscan

A rash that does not fade under pressure is a sign of meningococcal septicaemeia. However, this test should not be used solely in diagnosis.

The classic rash associated with meningitis usually looks like small, red pin pricks that spreads quickly over the body and turns into red or purple blotches. However, a rash is not always present with meningitis and may be less visible in darker skin tones. It is, therefore, important to also check the soles of the feet, palms of the hands and eyelids in the patient with suspected meningitis [3] .

Furthermore, if the patient is a child or young person, it is important for healthcare professionals to consider other non-specific features of their presentation, such as the level of parental or carer concern (particularly compared with previous illness in the child or young person or their family), how quickly the illness is progressing, and clinical judgement of the overall severity of the illness [3] .

Figure 2: Immediate management of suspected meningitis in children and neonates

Source: National Institute for Health and Care Excellence [3]

CRP: C-reactive protein; CSF: cerebrospinal fluid; CT: computerised tomography; EDTA: ethylenedianinetetraacetic acid; FBC: full blood count; GCS: Glasgow coma scale; HSV: herpes simplex virus; ICP: intracranial pressure; IV: intravenous; LFT’s: liver function tests; LP: lumbar puncture; Mg: magnesium test; PCR: polymerase chain reaction; TB: tuberculosis; U+E’s: urea and electrolytes; WBC: white blood cell.

Prevention and vaccination

As meningitis can be caused by several different pathogens, there are several vaccinations available that can offer some protection against the disease (see Table) [10] .

Case studies

Several case studies show how assessment and treatment of meningitis varies by patient. All patients, events and incidents in these case studies are fictitious and should only be used as examples in the clinical setting.

Case study 1: a toddler with mild meningitis

Eva is a three-year-old girl who is on holiday with her grandparents. Eva is unusually tired and is complaining that her legs are aching. This morning, Eva’s grandparents noticed a very small purple rash on her leg, and so they have to come to the pharmacy for advice. Eva has no fever or any other symptoms, but her grandmother has a cold sore.

Assessment and diagnosis

The rash does not fade under pressure when a glass is pressed against it.

Petechiae and purpura are significantly more common with invasive meningococcal infection than with pneumococcal meningitis, which rarely presents with a rash [13] . However, although the glass test is widely promoted in patient information leaflets, the National Institute for Health and Care Excellence (NICE) has found no evidence on its use. The test is not promoted in the NICE guidelines. Consequently, the glass test should not be used as the only test for diagnosing the condition [12] . Public Health England is also informed that Eva may have meningitis, and 999 is called.

Treatment options

On arrival at hospital, Eva is showing signs of shock — she is tachycardic with increased drowsiness and cold peripheries. After having initial tests, she is treated for shock with a fluid bolus of 20mL/kg sodium chloride 0.9% over 10 minutes. A lumbar puncture is contraindicated in shock and, therefore, Eva is empirically started on intravenous (IV) ceftriaxone and steroids. She is also started on IV aciclovir, owing to her history of contact with the herpes simplex virus.

Advice and recommendations

Eva is treated with antibiotics for ten days and her grandparents are both prescribed rifampicin as chemoprophylaxis. Antibiotic prophylaxis should be given as soon as possible (ideally within 24 hours) after the diagnosis of the index case [12] .

Case study 2: a baby with meningitis

Katherine is a mother of two young children who comes into the pharmacy and asks for advice. She has a young baby, Jacob, who is six weeks old and Esmé who is four years old. Jacob has a blocked nose and fever. Katherine explains that Esmé had gastroenteritis with cold symptoms and fever last week, but no rash. Katherine is worried about Jacob and asks for advice.

Katherine brings her children into the consultation room for further assessment. Jacob has been more unsettled than usual and does not want to feed as much as normal. Upon examination, Jacob has a rash on his stomach and back, which his mother says was not present this morning. His rash looks like red blotches and does not fade with the glass test. Owing to his age, Jacob is too young to have received any vaccinations.

It is important to remain calm and inform Katherine that you think Jacob may have meningitis, as he has the characteristic rash, as well as other known symptoms. Jacob needs to be taken to hospital for emergency assessment and an ambulance is called.

On arrival at the hospital, Jacob has blood tests taken and a lumbar puncture. He is started on intravenous (IV) cefotaxime with amoxicillin (if he was three months or older, IV ceftriaxone would be administered) with full-volume maintenance fluids and enteral feeds as tolerated [3] . Corticosteroids must not be used in children aged younger than three months with suspected or confirmed bacterial meningitis.

Jacob has hourly observations initially for heart rate, blood pressure, respiratory rate, oxygen saturation, fluid balance and Glasgow Coma Scale (GCS). The GCS is a neurological scale used to describe the level of consciousness in a person following a traumatic brain injury — the lower the number, the more severe the brain injury. Public Health England is also informed that Jacob may have meningitis.

In children younger than three months, ceftriaxone may be used as an alternative to cefotaxime (with or without ampicillin or amoxicillin); however, it should not be used in premature babies or in babies with jaundice, hypoalbuminaemia or acidosis, as it may exacerbate hyperbilirubinaemia [3] .

The microbiology consultant calls the ward to confirm that Jacob has Group B streptococcal meningitis. As per the National Institute for Health and Care Excellence’s guidelines, Jacob will need treating with IV cefotaxime for at least 14 days [3] .

Before discharge, Katherine is given the contact details of several patient support organisations, including meningitis charities that can offer support and written information to signpost her to further help. Jacob has an audiology appointment booked in two weeks and will be seen by a paediatrician after this. At this appointment, the following morbidities will be considered:

• Hearing loss;
• Orthopaedic complications;
• Skin complications (including scarring from necrosis);
• Psychosocial problems;
• Neurological and developmental problems;
• Kidney failure.

Outcome of the advice

Jacob makes a full recovery from his meningitis with no lasting effects. 

Case study 3: an adult with suspected meningitis

Jane is a paediatric haematology nurse who comes into the pharmacy asking to buy paracetamol. She says she has a terrible headache and upset stomach. She seems confused and disorientated; talking to her further highlights that something is not right.

Jane explains that she has not felt well since last night and has spent most of the day in bed, as she feels like she has no energy. However, some of what Jane also says does not make sense, and she is finding it hard to follow the conversation. She has no fever or rash.

Vomiting, severe headache and confusion are all symptoms of meningitis. Using a symptoms checker, such as the one by the Meningitis Research Foundation , to help with decision making.

Upon further questioning, it is clear that Jane must go to a hospital immediately and an ambulance is called. Jane presented with confusion and disorientation, which might indicate a stroke; however, bacterial meningitis can cause stroke.

When the paramedics arrive at the pharmacy, they find Jane has a Glasgow Coma Scale of 4/15. Once Jane arrives in hospital, they follow the stroke pathway, but she is now also febrile. Jane has a lumbar puncture and the results show she has bacterial meningitis. She also has a CT scan that shows an infarct on her right temporal lobe. Jane is treated in hospital with antibiotics and steroids, and eventually discharged to go home after three weeks.

Jane was working in the paediatric intensive care unit the week preceding the symptoms. She was looking after a child with Haemophilus influenzae type b (Hib). The patient was in a neutral pressure side room with a positive pressure lobby — this is an infection control measure to prevent the spread of microbial contaminants outside the patient’s side room. The lobby had been used to store an apheresis machine; however, the door between the side room and lobby had been left open, inadvertently leading to the exposure of Hib.

Although Jane has now fully recovered, she has to wear glasses owing to damage to her optical nerve. She also has tinnitus and occasionally suffers from severe headaches.

Recovering from meningitis/complications

Some of the most common complications associated with meningitis are [10] :

• Hearing loss, which may be partial or total — people who have had meningitis will usually have a hearing test after a few weeks to check for any problems;
• Recurrent seizures;
• Problems with memory and concentration;
• Problems with coordination, movement and balance;
• Learning difficulties and behavioural problems;
• Vision loss, which may be partial or total;
• Loss of limbs — amputation is sometimes necessary to stop the infection spreading through the body and remove damaged tissue;
• Bone and joint problems, such as arthritis;
• Kidney problems.

Overall, it is estimated that up to one in every ten cases of bacterial meningitis is fatal.

Useful resources

• Meningitis Research Foundation
• Meningitis Now
• National Institute for Health and Care Excellence clinical guideline [CG102]

[1] UNICEF, WHO, World Bank Group & United Nations. Levels and Trends in Child Mortality Report. 2017. Available at: https://www.unicef.org/publications/index_101071.html (accessed June 2019)

[2] Public Health England. Invasive meningococcal disease in England: annual laboratory confirmed reports for epidemiological year 2017 to 2018. 2018. Available at: https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/751821/hpr3818_IMD.pdf (accessed June 2019)

[3] National Institute for Health and Care Excellence. Meningitis (bacterial) and meningococcal septicaemia in under 16s: recognition, diagnosis and management. Clinical guideline [CG102]. 2015. Available at: https://www.nice.org.uk/guidance/cg102 (accessed June 2019)

[4] Davila S, Wright VJ, Khor CC et al . Genome-wide association study identifies variants in the CFH region associated with host susceptibility to meningococcal disease. Nat Genet 2010;42(9):772–776. doi: 10.1038/ng.640

[5] Domingo P, Pomar V, de Benito N & Coll P. The spectrum of acute bacterial meningitis in elderly patients.  BMC Infect Dis 2013;13:108. doi: 10.1186/1471-2334-13-108

[6] Paireau J, Chen A, Broutin H et al . Seasonal dynamics of bacterial meningitis: a time-series analysis. Lancet Glob Health 2016;4(6):e370–e377. doi: 10.1016/S2214-109X(16)30064-X

[7] Cooper LV, Robson A, Trotter CL et al . Risk factors for acquisition of mening ococcal carriage in the African meningitis belt. Trop Med Int Health 2019;24(4):392–400. doi: 10.1111/tmi.13203

[8] Kolappan S, Coureuil M, Yu X et al . Structure of the Neisseria meningitidis type IV pilus.  Nat Commun 2016;7:13015. doi: 10.1038/ncomms13015

[9] Tunkel AR & Scheld WM. Pathogenesis and pathophysiology of bacterial meningitis. Clin Microbiol Rev 1993;6(2):118–136. doi: 10.1128/CMR.6.2.118

[10] Sáez-Llorens X & McCracken GH Jr. Bacterial meningitis in children. Lancet 2003;361(9375):2139–2148. doi: 10.1016/S0140-6736(03)13693-8

[11] NHS Choices. Meningitis. 2019. Available at: https://www.nhs.uk/conditions/meningitis (accessed June 2019)

[12] Baines P, Reilly N & Gill A. Paediatric meningitis: clinical features and diagnosis. Clin Pharm 2009;1:307–310. URI: 10971150

[13] The National Institute for Health and Care Excellence. Clinical Knowledge Summaries: meningitis — bacterial meningitis and meningococcal disease. 2019. Available at: https://cks.nice.org.uk/meningitis-bacterial-meningitis-and-meningococcal-disease (accessed June 2019)

[14] NHS Choices. Pneumococcal vaccination. 2019. https://www.nhs.uk/conditions/vaccinations/pneumococcal-vaccination (accessed June 2019)

[15] Cooper LV, Robson A, Trotter C et al. Risk factors for acquisition of meningococcal carriage in the African meningitis belt. Trop Med Int Health 2019;24(4):392–400. doi: 10.1111/tmi.13203

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Patient information : See related handout on meningitis , written by the authors of this article.

Author disclosure: No relevant financial affiliations.

The etiologies of meningitis range in severity from benign and self-limited to life-threatening with potentially severe morbidity. Bacterial meningitis is a medical emergency that requires prompt recognition and treatment. Mortality remains high despite the introduction of vaccinations for common pathogens that have reduced the incidence of meningitis worldwide. Aseptic meningitis is the most common form of meningitis with an annual incidence of 7.6 per 100,000 adults. Most cases of aseptic meningitis are viral and require supportive care. Viral meningitis is generally self-limited with a good prognosis. Examination maneuvers such as Kernig sign or Brudzinski sign may not be useful to differentiate bacterial from aseptic meningitis because of variable sensitivity and specificity. Because clinical findings are also unreliable, the diagnosis relies on the examination of cerebrospinal fluid obtained from lumbar puncture. Delayed initiation of antibiotics can worsen mortality. Treatment should be started promptly in cases where transfer, imaging, or lumbar puncture may slow a definitive diagnosis. Empiric antibiotics should be directed toward the most likely pathogens and should be adjusted by patient age and risk factors. Dexamethasone should be administered to children and adults with suspected bacterial meningitis before or at the time of initiation of antibiotics. Vaccination against the most common pathogens that cause bacterial meningitis is recommended. Chemoprophylaxis of close contacts is helpful in preventing additional infections.

Patients with meningitis present a particular challenge for physicians. Etiologies range in severity from benign and self-limited to life-threatening with potentially severe morbidity. To further complicate the diagnostic process, physical examination and testing are limited in sensitivity and specificity. Advanc`es in vaccination have reduced the incidence of bacterial meningitis; however, it remains a significant disease with high rates of morbidity and mortality, making its timely diagnosis and treatment an important concern. 1

WHAT IS NEW ON THIS TOPIC: BACTERIAL MENINGITIS

In 2015, the Advisory Committee on Immunization Practices gave meningococcal serogroup B vaccines a category B recommendation (individual clinical decision making) for healthy patients 16 to 23 years of age (preferred age 16 to 18 years).

Meningitis is an inflammatory process involving the meninges. The differential diagnosis is broad ( Table 1 ) . Aseptic meningitis is the most common form. The annual incidence is unknown because of underreporting, but European studies have shown 70 cases per 100,000 children younger than one year, 5.2 cases per 100,000 children one to 14 years of age, and 7.6 per 100,000 adults. 2 , 3 Aseptic is differentiated from bacterial meningitis if there is meningeal inflammation without signs of bacterial growth in cultures. These cases are often viral, and enterovirus is the most common pathogen in immunocompetent individuals. 2 , 4 The most common etiology in U.S. adults hospitalized for meningitis is enterovirus (50.9%), followed by unknown etiology (18.7%), bacterial (13.9%), herpes simplex virus (HSV; 8.3%), noninfectious (3.5%), fungal (2.7%), arboviruses (1.1%), and other viruses (0.8%). 5 Enterovirus and mosquito-borne viruses, such as St. Louis encephalitis and West Nile virus, often present in the summer and early fall. 4 , 6 HSV and varicella zoster virus can cause meningitis and encephalitis. 2

Causative bacteria in community-acquired bacterial meningitis vary depending on age, vaccination status, and recent trauma or instrumentation 7 , 8 ( Table 2 9 ) . Vaccination has nearly eliminated the risk of Haemophilus influenzae and substantially reduced the rates of Neisseria meningitidis and Streptococcus pneumoniae as causes of meningitis in the developed world. 10 Between 1998 and 2007, the overall annual incidence of bacterial meningitis in the United States decreased from 1 to 0.69 per 100,000 persons. 1 This decrease has been most dramatic in children two months to 10 years of age, shifting the burden of disease to an older population. 1 Annual incidence is still highest in neonates at 40 per 100,000, and has remained largely unchanged. 1 Older patients are at highest risk of S. pneumoniae meningitis, whereas children and young adults have a higher risk of N. meningitidis meningitis. 1 , 11 Patients older than 60 years and patients who are immunocompromised are at higher risk of Listeria monocytogenes meningitis, although rates remain low. 11

Presentation

Presentation can be similar for aseptic and bacterial meningitis, but patients with bacterial meningitis are generally more ill-appearing. Fever, headache, neck stiffness, and altered mental status are classic symptoms of meningitis, and a combination of two of these occurs in 95% of adults presenting with bacterial meningitis. 12 However, less than one-half of patients present with all of these symptoms. 12 , 13

Presentation varies with age. Older patients are less likely to have headache and neck stiffness, and more likely to have altered mental status and focal neurologic deficits 11 , 13 ( Table 3 11 – 13 ) . Presentation also varies in young children, with vague symptoms such as irritability, lethargy, or poor feeding. 14 Arboviruses such as West Nile virus typically cause encephalitis but can present without altered mental status or focal neurologic findings. 6 Similarly, HSV can cause a spectrum of disease from meningitis to life-threatening encephalitis. HSV meningitis can present with or without cutaneous lesions and should be considered as an etiology in persons presenting with altered mental status, focal neurologic deficits, or seizure. 15

The time from symptom onset to presentation for medical care tends to be shorter in bacterial meningitis, with 47% of patients presenting after less than 24 hours of symptoms. 16 Patients with viral meningitis have a median presentation of two days after symptom onset. 17

Examination findings that may indicate meningeal irritation include a positive Kernig sign, positive Brudzinski sign, neck stiffness, and jolt accentuation of headache (i.e., worsening of headache by horizontal rotation of the head two to three times per second). Physical examination findings have shown wide variability in their sensitivity and specificity, and are not reliable to rule out bacterial meningitis. 18 – 20 Examples of Kernig and Brudzinski tests are available at https://www.youtube.com/watch?v=Evx48zcKFDA and https://www.youtube.com/watch?v=rN-R7-hh5x4 .

Because of the poor performance of clinical signs to rule out meningitis, all patients who present with symptoms concerning for meningitis should undergo prompt lumbar puncture (LP) and evaluation of cerebrospinal fluid (CSF) for definitive diagnosis. Because of the risk of increased intracranial pressure with brain inflammation, the Infectious Diseases Society of America recommends performing computed tomography of the head before LP in specific high-risk patients to reduce the possibility of cerebral herniation during the procedure ( Table 4 ) . 7 , 21 , 22 However, recent retrospective data have shown that removing the restriction on LP in patients with altered mental status reduced mortality from 11.7% to 6.9%, suggesting it may be safe to proceed with LP in these patients. 22

The CSF findings typical of aseptic meningitis are a relatively low and predominantly lymphocytic pleocytosis, normal glucose level, and a normal to slightly elevated protein level ( Table 5 9 ) . Bacterial meningitis classically has a very high and predominantly neutrophilic pleocytosis, low glucose level, and high protein level. This is not the case for all patients and can vary in older patients and those with partially treated bacterial meningitis, immunosuppression, or meningitis caused by L. monocytogenes . 11 It is important to use age-adjusted values for white blood cell counts when interpreting CSF results in neonates and young infants. 23 In up to 57% of children with aseptic meningitis, neutrophils predominate the CSF; therefore, cell type alone cannot be used to differentiate between aseptic and bacterial meningitis in children between 30 days and 18 years of age. 24

CSF results can be variable, and decisions about treatment with antibiotics while awaiting culture results can be challenging. There are a number of clinical decision tools that have been developed for use in children to help differentiate between aseptic and bacterial meningitis in the setting of pleocytosis. The Bacterial Meningitis Score has a sensitivity of 99% to 100% and a specificity of 52% to 62%, and appears to be the most specific tool available currently, although it is not widely used. 25 – 27 The score can be calculated online at http://reference.medscape.com/calculator/bacterial-meningitis-score-child .

Serum procalcitonin, serum C-reactive protein, and CSF lactate levels can be useful in distinguishing between aseptic and bacterial meningitis. 28 – 33 C-reactive protein has a high negative predictive value but a much lower positive predictive value. 28 Procalcitonin is sensitive (96%) and specific (89% to 98%) for bacterial causes of meningitis. 29 , 30 CSF lactate also has a high sensitivity (93% to 97%) and specificity (92% to 96%). 31 – 33 CSF latex agglutination testing for common bacterial pathogens is rapid and, if positive, can be useful in patients with negative Gram stain if LP was performed after antibiotics were administered. This test cannot be used to rule out bacterial meningitis. 7

Because CSF enterovirus polymerase chain reaction testing is more rapid than bacterial cultures, a positive test result can prompt discontinuation of antibiotic treatment, thus reducing antibiotic exposure and cost in patients admitted for suspected meningitis. 34 Similarly, polymerase chain reaction testing can be used to detect West Nile virus when seasonally appropriate in areas of higher incidence. HSV and varicella zoster viral polymerase chain reaction testing should be used in the setting of meningoencephalitis.

INITIAL MANAGEMENT

Prompt recognition of a potential case of meningitis is essential so that empiric treatment may begin as soon as possible. The initial management strategy is outlined in Figure 1 . 7 , 9 Stabilization of the patient's cardiopulmonary status takes priority. Intravenous fluids may be beneficial within the first 48 hours, but further study is needed to determine the appropriate intravenous fluid management. 35 A meta-analysis of studies with variable quality in children showed that fluids may decrease spasticity, seizures, and chronic severe neurologic sequelae. 35 The next urgent requirement is initiating empiric antibiotics as soon as possible after blood cultures are drawn and the LP is performed. Antibiotics should not be delayed if there is any lag time in performing the LP (e.g., transfer to clinical site that can perform the test, need for head computed tomography before LP). 7 , 8 Droplet isolation precautions should be instituted for the first 24 hours of treatment. 23

ANTIMICROBIALS

Before CSF results are available, patients with suspected bacterial meningitis should be treated with antibiotics as quickly as possible. 8 , 22 , 36 , 37 Acyclovir should be added if there is concern for HSV meningitis or encephalitis. Door-to-antibiotic time lapse of more than six hours has an adjusted odds ratio for mortality of 8.4. 37 If CSF results are more consistent with aseptic meningitis, antibiotics can be discontinued, depending on the severity of the presentation and overall clinical picture. Selection of the appropriate empiric antibiotic regimen is primarily based on age ( Table 2 9 ) . Specific pathogens are more prevalent in certain age groups, but empiric coverage should cover most possible culprits. Viral meningitis (non-HSV) management is focused on supportive care.

Treatment of tuberculous, cryptococcal, or other fungal meningitides is beyond the scope of this article, but should be considered if risk factors are present (e.g., travel to endemic areas, immunocompromised state, human immunodeficiency virus infection). These patients, as well as those coinfected with human immunodeficiency virus, should be managed in consultation with an infectious disease subspecialist when available.

Length of treatment varies based on the pathogen identified ( Table 6 7 ) . Intravenous antibiotics should be used to complete the full treatment course, but outpatient management can be considered in persons who are clinically improving after at least six days of therapy with reliable outpatient arrangements (i.e., intravenous access, home health care, reliable follow-up, and a safe home environment). 7

CORTICOSTEROIDS

Corticosteroids are traditionally used as adjunctive treatment in meningitis to reduce the inflammatory response. The evidence for corticosteroids is heterogeneous and limited to specific bacterial pathogens, 38 – 44 but the organism is not usually known at the time of the initial presentation. A 2015 Cochrane review found a nonsignificant reduction in overall mortality (relative risk [RR] = 0.90), as well as a significant reduction in severe hearing loss (RR = 0.51), any hearing loss (RR = 0.58), and short-term neurologic sequelae (RR = 0.64) with the use of dexamethasone in high-income countries. 41 The number needed to treat to decrease mortality in the S. pneumoniae subgroup was 18 and the number needed to treat to prevent hearing loss was 21. 38 , 41 There was a small increase in recurrent fever in patients given corticosteroids (number needed to harm = 16) with no worse outcome. 38 , 41

The best evidence supports the use of dexamethasone 10 to 20 minutes before or concomitantly with antibiotic administration in the following groups: infants and children with H. influenzae type B, adults with S. pneumoniae , or patients with Mycobacterium tuberculosis without concomitant human immunodeficiency virus infection. 7 , 8 , 42 , 45 Some evidence also shows a benefit with corticosteroids in children older than six weeks with pneumococcal meningitis. 45

Because the etiology is not known at presentation, dexamethasone should be given before or at the time of initial antibiotics while awaiting the final culture results in all patients older than six weeks with suspected bacterial meningitis. Dexamethasone can be discontinued after four days or earlier if the pathogen is not H. influenzae or S. pneumoniae , or if CSF findings are more consistent with aseptic meningitis. 46

REPEAT TESTING

Repeat LP is generally not needed but should be considered to evaluate CSF parameters in persons who are not clinically improving after 48 hours of appropriate treatment. Repeating the LP can identify resistant pathogens, confirm the diagnosis if initial results were negative, and determine the length of treatment for neonates with a gram-negative bacterial pathogen until CSF sterilization is documented. 7 , 47

Prognosis varies by age and etiology of meningitis. In a large analysis of patients from 1998 to 2007, the overall mortality rate in those with bacterial meningitis was 14.8%. 1 Worse outcomes occurred in those with low Glasgow Coma Scale scores, systemic compromise (e.g., low CSF white blood cell count, tachycardia, positive blood cultures, abnormal neurologic examination, fever), alcoholism, and pneumococcal infection. 11 – 13 , 16 Mortality is generally higher in pneumococcal meningitis (30%) than other types, especially penicillin-resistant strains. 12 , 48 , 49 Viral meningitis outside the neonatal period has lower mortality and complication rates, but large studies or reviews are lacking. One large cohort study found a 4.5% mortality rate and a 30.9% rate of complications, such as developmental delay, seizure disorder, or hearing loss, for childhood encephalitis and meningitis combined. 50 Tuberculous meningitis also has a higher mortality rate (19.3%) with a higher risk of neurologic disease in survivors (53.9%). 51 A recent prospective cohort study also found that males had a higher risk of unfavorable outcomes (odds ratio = 1.34) and death (odds ratio = 1.47). 52

Complications from bacterial meningitis also vary by age ( Table 7 1 , 11 , 12 , 46 , 53 – 56 ) . Neurologic sequelae such as hearing loss occur in approximately 6% to 31% of children and can resolve within 48 hours, but may be permanent in 2% to 7% of children. 53 – 56 An audiology assessment should be considered in children before discharge. 8 Follow-up should assess for hearing loss (including referral for cochlear implants, if present), psychosocial problems, neurologic disease, or developmental delay. 57 Testing for complement deficiency should be considered if there is more than one episode of meningitis, one episode plus another serious infection, meningococcal disease other than serogroup B, or meningitis with a strong family history of the disease. 57

VACCINATION

Vaccines that have decreased the incidence of meningitis include H. influenzae type B, S. pneumoniae , and N. meningitidis . 58 – 60 Administration of one of the meningococcal vaccines that covers serogroups A, C, W, and Y (MPSV4 [Menomune], Hib-MenCY [Menhibrix], MenACWY-D [Menactra], or MenACWY-CRM [Menveo]) is recommended for patients 11 to 12 years of age, with a booster at 16 years of age. However, the initial dose should be given earlier in the setting of a high-risk condition, such as functional asplenia or complement deficiencies, travel to endemic areas, or a community outbreak. 60 There are also two available vaccines for meningococcal type B strains (MenB-4C [Bexsero] and MenB-FHbp [Trumenba]) to be used in patients with complement disease or functional asplenia, or in healthy individuals at risk during a serogroup B outbreak as determined by the Centers for Disease Control and Prevention. 60

The Advisory Committee on Immunization Practices recently added a category B recommendation (individual clinical decision making) for consideration of vaccination with serogroup B vaccines in healthy patients 16 to 23 years of age (preferred age of 16 to 18 years). 60 , 61 The serogroup B vaccines are not interchangeable, so care should be taken to ensure completion of the series with the same brand that was used for the initial dose.

CHEMOPROPHYLAXIS

Treatment with chemoprophylactic antibiotics should be given to close contacts 7 , 62 , 63 ( Table 8 9 , 14 , 64 – 68 ) . Appropriate antibiotics should be given to identified contacts within 24 hours of the patient's diagnosis and should not be given if contact occurred more than 14 days before the patient's onset of symptoms. 63 Options for chemoprophylaxis are rifampin, ceftriaxone, and ciprofloxacin, although rifampin has been associated with resistant isolates. 62 , 63

This article updates a previous article on this topic by Bamberger . 9

Data Sources: The terms meningitis, bacterial meningitis, and Neisseria meningitidis were searched in PubMed, Essential Evidence Plus, and the Cochrane database. In addition, the Infectious Diseases Society of America, the National Institute for Health and Care Excellence, and the American Academy of Pediatrics guidelines were reviewed. Search dates: October 1, 2016, and March 13, 2017.

The authors thank Thomas Lamarre, MD, for his input and expertise.

Thigpen MC, Whitney CG, Messonnier NE, et al.; Emerging Infections Program Network. Bacterial meningitis in the United States, 1998–2007. N Engl J Med. 2011;364(21):2016-2025.

Kupila L, Vuorinen T, Vainionpää R, Hukkanen V, Marttila RJ, Kotilainen P. Etiology of aseptic meningitis and encephalitis in an adult population. Neurology. 2006;66(1):75-80.

Martin NG, Iro MA, Sadarangani M, Goldacre R, Pollard AJ, Goldacre MJ. Hospital admissions for viral meningitis in children in England over five decades: a population-based observational study. Lancet Infect Dis. 2016;16(11):1279-1287.

Lee BE, Davies HD. Aseptic meningitis. Curr Opin Infect Dis. 2007;20(3):272-277.

Hasbun R, Rosenthal N, Balada-Llasat JM, et al. Epidemiology of meningitis and encephalitis in the United States from 2011–2014 [published online ahead of print April 17, 2017]. Clin Infect Dis . https://academic.oup.com/cid/article-abstract/doi/10.1093/cid/cix319/3737650/Epidemiology-of-Meningitis-and-Encephalitis-in-the?redirectedFrom=fulltext [login required]. Accessed April 30, 2017.

Petersen LR, Brault AC, Nasci RS. West Nile virus: review of the literature. JAMA. 2013;310(3):308-315.

Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis. 2004;39(9):1267-1284.

National Institute for Health and Care Excellence. Meningitis (bacterial) and meningococcal septicaemia in children and young people. Quality standard (QS19); June 2012. https://www.nice.org.uk/guidance/qs19 . Accessed October 1, 2016.

Bamberger DM. Diagnosis, initial management, and prevention of meningitis. Am Fam Physician. 2010;82(12):1491-1498.

McIntyre PB, O'Brien KL, Greenwood B, van de Beek D. Effect of vaccines on bacterial meningitis worldwide. Lancet. 2012;380(9854):1703-1711.

Weisfelt M, van de Beek D, Spanjaard L, Reitsma JB, de Gans J. Community-acquired bacterial meningitis in older people. J Am Geriatr Soc. 2006;54(10):1500-1507.

van de Beek D, de Gans J, Spanjaard L, Weisfelt M, Reitsma JB, Vermeulen M. Clinical features and prognostic factors in adults with bacterial meningitis [published correction appears in N Engl J Med . 2005;352(9): 950]. N Engl J Med. 2004;351(18):1849-1859.

Wang AY, Machicado JD, Khoury NT, Wootton SH, Salazar L, Hasbun R. Community-acquired meningitis in older adults: clinical features, etiology, and prognostic factors. J Am Geriatr Soc. 2014;62(11):2064-2070.

Sáez-Llorens X, McCracken GH. Bacterial meningitis in children. Lancet. 2003;361(9375):2139-2148.

Bijlsma MW, Brouwer MC, Kasanmoentalib ES, et al. Community-acquired bacterial meningitis in adults in the Netherlands, 2006–14:a prospective cohort study. Lancet Infect Dis. 2016;16(3):339-347.

Ihekwaba UK, Kudesia G, McKendrick MW. Clinical features of viral meningitis in adults: significant differences in cerebrospinal fluid findings among herpes simplex virus, varicella zoster virus, and enterovirus infections. Clin Infect Dis. 2008;47(6):783-789.

Steiner I, Benninger F. Update on herpes virus infections of the nervous system. Curr Neurol Neurosci Rep. 2013;13(12):414.

Waghdhare S, Kalantri A, Joshi R, Kalantri S. Accuracy of physical signs for detecting meningitis: a hospital-based diagnostic accuracy study. Clin Neurol Neurosurg. 2010;112(9):752-757.

Curtis S, Stobart K, Vandermeer B, Simel DL, Klassen T. Clinical features suggestive of meningitis in children: a systematic review of prospective data. Pediatrics. 2010;126(5):952-960.

Nakao JH, Jafri FN, Shah K, Newman DH. Jolt accentuation of headache and other clinical signs: poor predictors of meningitis in adults. Am J Emerg Med. 2014;32(1):24-28.

Joffe AR. Lumbar puncture and brain herniation in acute bacterial meningitis: a review. J Intensive Care Med. 2007;22(4):194-207.

Glimåker M, Johansson B, Grindborg Ö, Bottai M, Lindquist L, Sjölin J. Adult bacterial meningitis: earlier treatment and improved outcome following guideline revision promoting prompt lumbar puncture. Clin Infect Dis. 2015;60(8):1162-1169.

Siegel JD, Rhinehart E, Jackson M, Chiarello L; Healthcare Infection Control Practices Advisory Committee. 2007 guideline for isolation precautions: preventing transmission of infectious agents in healthcare settings. https://www.cdc.gov/hicpac/pdf/isolation/Isolation2007.pdf . Accessed October 1, 2016.

Negrini B, Kelleher KJ, Wald ER. Cerebrospinal fluid findings in aseptic versus bacterial meningitis. Pediatrics. 2000;105(2):316-319.

Nigrovic LE, Kuppermann N, Macias CG, et al.; Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. Clinical prediction rule for identifying children with cerebrospinal fluid pleocytosis at very low risk of bacterial meningitis. JAMA. 2007;297(1):52-60.

Nigrovic LE, Malley R, Kuppermann N. Meta-analysis of bacterial meningitis score validation studies. Arch Dis Child. 2012;97(9):799-805.

Dubos F, Korczowski B, Aygun DA, et al. Distinguishing between bacterial and aseptic meningitis in children: European comparison of two clinical decision rules [published correction appears in Arch Dis Child . 2011;96(4):407]. Arch Dis Child. 2010;95(12):963-967.

Gerdes LU, Jørgensen PE, Nexø E, Wang P. C-reactive protein and bacterial meningitis: a meta-analysis. Scand J Clin Lab Invest. 1998;58(5):383-393.

Henry BM, Roy J, Ramakrishnan PK, Vikse J, Tomaszewski KA, Walocha JA. Procalcitonin as a serum biomarker for differentiation of bacterial meningitis from viral meningitis in children: evidence from a meta-analysis. Clin Pediatr (Phila). 2016;55(8):749-764.

Vikse J, Henry BM, Roy J, Ramakrishnan PK, Tomaszewski KA, Walocha JA. The role of serum procalcitonin in the diagnosis of bacterial meningitis in adults: a systematic review and meta-analysis. Int J Infect Dis. 2015;38:68-76.

Huy NT, Thao NT, Diep DT, Kikuchi M, Zamora J, Hirayama K. Cerebrospinal fluid lactate concentration to distinguish bacterial from aseptic meningitis: a systemic review and meta-analysis. Crit Care. 2010;14(6):R240.

Sakushima K, Hayashino Y, Kawaguchi T, Jackson JL, Fukuhara S. Diagnostic accuracy of cerebrospinal fluid lactate for differentiating bacterial meningitis from aseptic meningitis: a meta-analysis. J Infect. 2011;62(4):255-262.

Viallon A, Desseigne N, Marjollet O, et al. Meningitis in adult patients with a negative direct cerebrospinal fluid examination: value of cytochemical markers for differential diagnosis. Crit Care. 2011;15(3):R136.

Archimbaud C, Chambon M, Bailly JL, et al. Impact of rapid enterovirus molecular diagnosis on the management of infants, children, and adults with aseptic meningitis. J Med Virol. 2009;81(1):42-48.

Maconochie IK, Bhaumik S. Fluid therapy for acute bacterial meningitis. Cochrane Database Syst Rev. 2016(11):CD004786.

Sudarsanam TD, Rupali P, Tharyan P, Abraham OC, Thomas K. Pre-admission antibiotics for suspected cases of meningococcal disease. Cochrane Database Syst Rev. 2013(8):CD005437.

Proulx N, Fréchette D, Toye B, Chan J, Kravcik S. Delays in the administration of antibiotics are associated with mortality from adult acute bacterial meningitis. QJM. 2005;98(4):291-298.

van de Beek D, Farrar JJ, de Gans J, et al. Adjunctive dexamethasone in bacterial meningitis: a meta-analysis of individual patient data. Lancet Neurol. 2010;9(3):254-263.

Mongelluzzo J, Mohamad Z, Ten Have TR, Shah SS. Corticosteroids and mortality in children with bacterial meningitis. JAMA. 2008;299(17):2048-2055.

Thwaites GE, Nguyen DB, Nguyen HD, et al. Dexamethasone for the treatment of tuberculous meningitis in adolescents and adults. N Engl J Med. 2004;351(17):1741-1751.

Brouwer MC, McIntyre P, Prasad K, van de Beek D. Corticosteroids for acute bacterial meningitis. Cochrane Database Syst Rev. 2015(9):CD004405.

Prasad K, Singh MB, Ryan H. Corticosteroids for managing tuberculous meningitis. Cochrane Database Syst Rev. 2016(4):CD002244.

Beardsley J, Wolbers M, Kibengo FM, et al.; CryptoDex Investigators. Adjunctive dexamethasone in HIV-associated cryptococcal meningitis. N Engl J Med. 2016;374(6):542-554.

Fritz D, Brouwer MC, van de Beek D. Dexamethasone and long-term survival in bacterial meningitis. Neurology. 2012;79(22):2177-2179.

Kimberlin DW, Long SS, Brady MT, Jackson MA, eds. Red Book: 2015 Report of the Committee on Infectious Diseases . 30th ed. Elk Grove Village, Ill.: American Academy of Pediatrics; 2015:370,631.

van de Beek D, de Gans J, Tunkel AR, Wijdicks EF. Community-acquired bacterial meningitis in adults. N Engl J Med. 2006;354(1):44-53.

Costerus JM, Brouwer MC, van der Ende A, van de Beek D. Repeat lumbar puncture in adults with bçacterial meningitis. Clin Microbiol Infect. 2016;22(5):428-433.

Schuchat A, Robinson K, Wenger JD, et al. Bacterial meningitis in the United States in 1995. Active Surveillance Team. N Engl J Med. 1997;337(14):970-976.

Edmond K, Clark A, Korczak VS, Sanderson C, Griffiths UK, Rudan I. Global and regional risk of disabling sequelae from bacterial meningitis: a systematic review and meta-analysis. Lancet Infect Dis. 2010;10(5):317-328.

Rantakallio P, Leskinen M, von Wendt L. Incidence and prognosis of central nervous system infections in a birth cohort of 12,000 children. Scand J Infect Dis. 1986;18(4):287-294.

Chiang SS, Khan FA, Milstein MB, et al. Treatment outcomes of childhood tuberculous meningitis: a systematic review and meta-analysis. Lancet Infect Dis. 2014;14(10):947-957.

Dias SP, Brouwer MC, Bijlsma MW, van der Ende A, van de Beek D. Sex-based differences in adults with community-acquired bacterial meningitis: a prospective cohort study. Clin Microbiol Infect. 2017;23(2):121.e9-121.e15.

Richardson MP, Reid A, Tarlow MJ, Rudd PT. Hearing loss during bacterial meningitis [published correction appears in Arch Dis Child . 1997;76(4):386]. Arch Dis Child. 1997;76(2):134-138.

Baraff LJ, Lee SI, Schriger DL. Outcomes of bacterial meningitis in children: a meta-analysis. Pediatr Infect Dis J. 1993;12(5):389-394.

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Worsøe L, Cayé-Thomasen P, Brandt CT, Thomsen J, østergaard C. Factors associated with the occurrence of hearing loss after pneumococcal meningitis. Clin Infect Dis. 2010;51(8):917-924.

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Patel M, Lee CK. Polysaccharide vaccines for preventing serogroup A meningococcal meningitis. Cochrane Database Syst Rev. 2005(1):CD001093.

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Bacterial meningitis in children

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• Emre Basatemur , consultant in paediatric emergency medicine
• The Royal London Hospital, London, UK
• Correspondence to E Basatemur emre.basatemur{at}nhs.net

BMJ Best Practice takes healthcare professionals quickly and accurately to the latest clinical information, whenever and wherever they need it

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What you need to know

Classic signs of meningitis (neck stiffness, bulging fontanelle, high pitched cry) are often absent in infants with bacterial meningitis

Around half of young infants diagnosed with bacterial meningitis are afebrile on presentation

Escalate early. Consult a senior doctor in emergency medicine or paediatrics if you suspect bacterial meningitis

Bacterial meningitis is a life threatening inflammation of the meninges, which most commonly affects children under 2 (especially those under 3 months). It is a notifiable disease in the UK.

This article, based on BMJ Best Practice, covers assessment of and initial management of suspected bacterial meningitis acquired by children in the community; the condition may also be associated with invasive procedures or head trauma, but meningitis associated with healthcare, and infants with meningitis in neonatal units, are beyond the scope of the article.

Epidemiology

A 2018 study reported the overall incidence of bacterial meningitis in western countries as 0.7 to 0.9 per 100 000 people per year. Incidence has decreased by 3% to 4% since the 1990s. 1 In the UK, 2594 cases of meningitis (due to any cause) were reported in children from 2004 to 2011. The overall incidence in African countries is 10-40 per 100 000 people per year. 1 The incidence of culture-proven bacterial meningitis in newborns is estimated at 0.3 per 1000 live births in developed countries. 2

Widespread immunisation programmes in the UK and other developed countries, particularly the use of Haemophilus influenzae type b (Hib) …

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• Second Opinion

Meningitis in Children

What is meningitis in children?

Meningitis is a swelling (inflammation) of the thin membranes that cover the brain and the spinal cord. These membranes are called the meninges.

What causes meningitis in a child?

Meningitis is most often caused by a bacterial or viral infection that moves into the cerebral spinal fluid (CSF). CSF is the fluid that protects and cushions the brain and spinal cord. A fungus or parasite may also cause meningitis. This is more common only in children with a weak immune system.

Meningitis caused by a virus is more common and usually less severe. Bacterial meningitis is usually more severe and may lead to long-term complications or death.

Viruses that can cause meningitis include polioviruses, the mumps virus (paramyxovirus), the flu virus, and West Nile virus.

Bacteria that can cause meningitis include group B streptococcus, E. coli, Haemophilus influenzae type b (Hib), and a strep bacteria that causes pneumonia. Syphilis, tuberculosis, and Lyme disease bacteria can also cause meningitis. The bacteria, viruses, and fungi that cause meningitis usually grow in a person’s respiratory tract. A child may have no symptoms at all, but may carry the organism in his or her nose and throat. They may be spread by:

Close contact with someone carrying the infection

Touching infected objects, such as doorknobs, hard surfaces, or toys, and then touching nose, mouth, or eyes

Droplets from a sneeze, close conversation, or kissing

An infection usually starts in the respiratory tract. In a child, it may first cause a cold, sinus infection, or ear infection. It can then go into the bloodstream and reach the brain and spinal cord.

Which children are at risk for meningitis?

A child is more at risk for meningitis if he or she has an infection caused by a number of viruses, bacteria, or fungi. Children with a weakened immune system are at great risk.

What are the symptoms of meningitis in a child?

The symptoms of meningitis vary depending on what causes the infection. The symptoms may start several days after your child has had a cold and runny nose, or diarrhea and vomiting. Symptoms can occur a bit differently in each child. Symptoms may appear suddenly. Or they may develop over several days.                                                                                                                                         

In babies, symptoms may include:

Irritability

Sleeping more than usual

Poor feeding

Crying that can’t be soothed

High-pitched cry

Arching back

Bulging soft spots on the head (fontanelles)

Changed temperament

Purple-red splotchy rash

In children age 1 or older, symptoms may include:

Refusing to eat

Reduced level of consciousness

Eyes sensitive to light (photophobia)

Nausea and vomiting

Neck stiffness

A purple-red splotchy rash

The symptoms of meningitis can be like other health conditions. Make sure your child sees his or her healthcare provider for a diagnosis.

How is meningitis diagnosed in a child?

The healthcare provider will ask about your child’s symptoms and health history. He or she may also ask about your family’s health history. He or she will give your child a physical exam. Your child may also have tests, such as:

Lumbar puncture (spinal tap).  This is the only test that diagnoses meningitis. A needle is placed into the lower back, into the spinal canal. This is the area around the spinal cord. The pressure in the spinal canal and brain is measured. A small amount of cerebral spinal fluid (CSF) is removed and sent for testing to see if there is an infection or other problems.

Blood tests. These can help diagnose infections that cause meningitis. 

CT scan or MRI.  These are tests that show images of the brain. A CT scan is sometimes done to look for other conditions that may cause similar symptoms as meningitis. An MRI may show inflammatory changes in the meninges. These tests give more information. But meningitis can’t be diagnosed using these tests alone.

Nasal, throat, or rectal swabs. These tests help diagnose viral infections that cause meningitis.

How is meningitis treated in a child?

Treatment will depend on your child’s symptoms, age, and general health. It will also depend on how severe the condition is.                                         

Treatment varies by type of meningitis. The treatments by type include:

Bacterial meningitis.  Treatment is started as quickly as possible. The healthcare provider will give your child IV (intravenous) antibiotics, which kill bacteria. Your child will also get a corticosteroid medicine. The steroid works by decreasing the swelling (inflammation) and reducing pressure that can build up in the brain. Steroids also reduce the risk for hearing loss and brain damage. 

Viral meningitis.  Most children get better on their own without treatment. In some cases, treatment may be done to help ease symptoms. There are no medicines to treat the viruses that cause viral meningitis. The only exception is herpes simplex virus, which is treated with IV antiviral medicine. Babies and children with a weakened immune system may need to stay in the hospital.

Fungal meningitis.  Your child may get IV antifungal medicine.

Tuberculous (TB) meningitis.  Your child will be treated with a course of medicines over 1 year. Treatment is done with several medicines for the first few months. This is followed by other medicines for the remaining time.

While your child is recovering from meningitis, he or she may also need:

Increased fluid intake by mouth or IV fluids in the hospital

Medicines to reduce fever and headache. Don’t give aspirin or medicine that contains aspirin to a child younger than age 19 unless directed by your child’s provider. Taking aspirin can put your child at risk for Reye syndrome. This is a rare but very serious disorder. It most often affects the brain and the liver.

Supplemental oxygen or breathing machine (respirator) if your child has trouble breathing

Talk with your child’s healthcare providers about the risks, benefits, and possible side effects of all treatments.

What are the possible complications of meningitis in a child?

Bacterial meningitis is usually more severe and may lead to long-term complications. Some children may have long-term problems with seizures, brain damage, hearing loss, and disability. Bacterial meningitis can also cause death.

How can I help prevent meningitis in my child?

Several vaccines are available to prevent some of the bacterial infections that can cause meningitis. These include:

H. influenzae type b vaccine (Hib). This is given as a 3- or 4-part series during your child's routine vaccines starting at 2 months old.

PCV13 pneumococcal vaccine. The American Academy of Pediatrics recommends this vaccine for all healthy children younger than age 2. PCV13 can be given along with other childhood vaccines. It is recommended at ages 2 months, 4 months, 6 months, and 12 to 15 months. One dose is also advised for older children who did not get the 4-dose series, and for those at high risk for pneumococcal disease.

PPSV23 pneumococcal vaccine . This vaccine is also recommended for older children at high risk for pneumococcal disease.

Meningococcal vaccine. This vaccine is part of the routine vaccine schedule. It is given to children ages 11 to 12, with a booster given at age 16. It is given to teens entering high school if they were not vaccinated at age 11 or 12. A booster is also given at age 16 to 18, or up to 5 years later. Babies and young children at increased risk may also have this vaccine. Ask your child's healthcare provider about the number of doses and when they should be given.

Vaccines that protect against viruses such as measles, mumps, chickenpox, and the flu can prevent viral meningitis.                                                    

Talk with your child’s healthcare provider if you have questions about the vaccines. 

You and your child can do other things to prevent the spread of infections. Proper handwashing and staying away from people who are sick can help prevent meningitis.

When should I call my child’s healthcare provider?

Call the healthcare provider if your child has:

Not received vaccines

Contact with someone who has meningitis

Symptoms that don’t get better, or get worse

New symptoms

Key points about meningitis in children

Meningitis is an inflammation of the thin membranes that cover the brain and the spinal cord.

It is most often caused by a bacterial or viral infection that moves into the cerebral spinal fluid. A fungus or parasite may also cause meningitis.

A lumbar puncture (spinal tap) is the only test that diagnoses meningitis. A needle is placed into the lower back, into the spinal canal.

Several vaccines are available to prevent some of the bacterial and viral infections that can cause meningitis.

Tips to help you get the most from a visit to your child’s healthcare provider:

Know the reason for the visit and what you want to happen.

Before your visit, write down questions you want answered.

At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you for your child.

Know why a new medicine or treatment is prescribed and how it will help your child. Also know what the side effects are.

Ask if your child’s condition can be treated in other ways.

Know why a test or procedure is recommended and what the results could mean.

Know what to expect if your child does not take the medicine or have the test or procedure.

If your child has a follow-up appointment, write down the date, time, and purpose for that visit.

Know how you can contact your child’s provider after office hours. This is important if your child becomes ill and you have questions or need advice.

Related Links

• Brain and Behavior Center
• Neonatal Neurology
• Neonatal Neurology Services
• Conjunctivitis in Children
• Brain Abscess in Children
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9:  Bacterial Meningitis

Jonathan C. Cho

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Patient presentation.

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Chief Complaint

“I have severe headaches and fevers.”

History of Present Illness

DJ is a 54-year-old Caucasian female who presents to the emergency department with worsening headache, neck pain, and back pain of 2 days duration. She also complains of low-grade fevers and chills that developed over the past 24 hours. Her son, who is present during her exam, states that she seems more lethargic and has difficulty maintaining her balance. In addition, she reports 3 to 4 episodes of nausea and vomiting.

Past Medical History

CHF, COPD, HTN, epilepsy, stroke, hypothyroidism, anxiety

Surgical History

Hysterectomy, cholecystectomy

Family History

Father had HTN and passed away from a stroke 4 years ago; mother has type II DM and epilepsy; brother has HTN

Social History

Divorced but lives with her two sons who are currently attending college. Smokes ½ ppd × 27 years and drinks alcohol occasionally.

Home Medications

Advair 250 mcg/50 mcg 1 puff BID

Albuterol metered-dose-inhaler 2 puffs q4h PRN shortness of breath

Alprazolam 0.5 mg PO daily

Aspirin 81 mg PO daily

Atorvastatin 20 mg PO daily

Carvedilol 6.25 mg PO BID

Citalopram 20 mg PO daily

Divalproex sodium 500 mg PO BID

Furosemide 20 mg PO daily

Levothyroxine 88 mcg PO daily

Levetiracetam 500 mg PO BID

Lisinopril 20 mg PO daily

Physical Examination

Vital signs.

Temp 101.2°F, P 72, RR 23 breaths per minute, BP 162/87 mm Hg, pO 2 91%, Ht 5′3″, Wt 56.4 kg

Lethargic, female with dizziness and in mild to moderate distress.

Normocephalic, atraumatic, PERRLA, EOMI, pale or dry mucous membranes and conjunctiva, poor dentition

Diminished breath sounds and crackles bilaterally.

Cardiovascular

NSR, no m/r/g

Soft, non-distended, non-tender, bowel sounds hyperactive

Genitourinary

Normal female genitalia, no complaints of dysuria or hematuria

Lethargic, oriented to place and person, (–) Brudzinski’s sign, (+) Kernig’s sign

Extremities

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Article Contents

Case 2 diagnosis: chronic meningococcal meningitis, clinical pearls.

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Case 2: A nine-year-old girl with prolonged fever and headache

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Tahara Bhate, Tobias R Kollmann, Keyvan Hadad, Case 2: A nine-year-old girl with prolonged fever and headache, Paediatrics & Child Health , Volume 19, Issue 4, April 2014, Pages 177–178, https://doi.org/10.1093/pch/19.4.177a

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A previously healthy nine year-old girl presented to the authors' institution (BC Children's Hospital, Vancouver, British Columbia) with a four-week history of fevers, vomiting, headache and abdominal pain. She was first seen in a community hospital following a 24 h history of fever followed by headache, emesis and a generalized erythematous, macular rash. Petechiae were not noted. A diagnosis of viral gastroenteritis was made. The rash subsided quickly but the remainder of her symptoms persisted.

Ten days later, she presented again to the same hospital with daily fevers, daily episodes of emesis and debilitating headaches. Her investigations included a normal complete blood cell count, and her urine culture was positive for Escherichia coli . She was discharged on cephalexin for five days; however, her symptoms failed to resolve.

She was subsequently referred and admitted to the authors' tertiary care centre. Review of her history revealed daily fevers accompanied by severe nausea and emesis, along with severe headaches without photophobia. There was no history of recent travel or ill contacts. She denied night sweats, neck stiffness or joint pain. Her records indicated a 5 kg weight loss over four weeks.

Physical examination revealed a stable patient with normal vital signs. General examination was unremarkable and no neck stiffness or neurological deficit was detected.

Laboratory investigations on admission showed leukocytosis (white blood cell count 11.2×10 9 /L) and thrombocytosis (platelet count 423×10 9 /L [normal range 150×10 9 /L to 400×10 9 /L]). Erythrocyte sedimentation rate was elevated (76 mm/h). Urine and blood cultures were negative.

Abdominal ultrasound revealed a large echogenic right kidney, suggesting possible pyelonephritis. A computed tomography scan of the head and a chest radiograph were normal.

A further investigation was performed to reveal the diagnosis.

Given the ultrasound results, a provisional diagnosis of partially treated urinary tract infection was made. To complete the diagnostic workup, a lumbar puncture was performed at 12 h of admission and before initiation of antibiotic therapy.

The cerebrospinal fluid (CSF) was cloudy, with an opening pressure of 38 cmH 2 O. Analysis of the CSF revealed a glucose level of <1.1 mmol/L, a protein level of 2.33 mg/L, white blood cell count of 1740×10 6 /L and red blood cell count of 2×10 6 /L. Polymerase chain reaction performed on the CSF was positive for Neisseria meningitidis serogroup B. The patient was started on intravenous cefotaxime and became afebrile within 12 h of therapy. To facilitate comprehensive evaluation of exposure and possible chemoprophylaxis of close contacts, the case was reported to the BC Centre for Disease Control (Vancouver, British Columbia). All symptoms resolved within 24 h to 48 h. She was discharged after completion of a seven-day course of intravenous cefotaxime. Of note, the patient was subsequently shown to have no complement deficiency, nor was she asplenic. At discharge, she was found to have moderately severe left-sided sensorineural hearing loss; this remained unchanged six weeks later.

Infection with Neisseria meningitidis remains an important cause of morbidity and mortality. Prompt recognition of symptoms and initiation of therapy are essential to prevent possibly serious morbidity and mortality. The infection may be limited to blood or to the meninges, or may involve a combination of both.

The most common findings of an acute meningeal infection are neck stiffness, fever and altered mental status. Here, however, we present a case of chronic meningococcal meningitis. Chronic and/or recurrent infections with N meningitidis are exceedingly rare, and are mostly confined to patients with deficiencies of terminal complement components (C5 to C9), C3 or properdin, or with anatomical or functional asplenia. Chronic meningococcemia presents as a triad of spiking fever, vasculitic rash and large-joint arthralgia. The diagnosis is challenging because bacterial cultures are frequently negative, at least in the initial stages of the illness. Meningeal involvement in chronic meningococcemia can occur as a late complication.

Our patient was both young and fully immunocompetent, in contrast to reports of this condition in the elderly (1) and in a patient with a complement deficiency (2–5). Additionally, our patient had no clinically detectable neurological findings; this differed from previous case reports (1,2,6) and increased the diagnostic challenge. Our case did, however, resemble other published reports on chronic meningitis due to N meningitidis in that the blood cultures were negative and the response to appropriate antibiotic treatment was rapid. The outcomes of published cases appear to be highly variable, ranging from none to mild gait ataxia or sensorineural hearing loss, as demonstrated in our patient.

Chronic meningococcal meningitis can exist in the absence of acute or chronic meningococcemia.

Patients with chronic meningococcal meningitis may not always demonstrate classic meningeal signs or neurological deficits. A lumbar puncture is, thus, essential for the diagnosis.

Chronic meningococcal meningitis should be considered in the differential diagnosis of fever or headache associated with emesis.

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2-Year-Old with Tuberculous Meningitis

A case study.

Geary, Siobhan; Agnew, Michelle

Questions or comments about this article may be directed to: Siobhan Geary, MS RN CNS CNRN, by phone at 916/733-6025 or by e-mail at [email protected] . She is a pediatric ICU clinical nurse specialist at Sutter Medical Center, Sacramento, CA.

Michelle Agnew, BSN RN, is a neuroscience nurse educator at Sutter Medical Center.

Tuberculous meningitis (TBM) may occur with tuberculosis infection, and young children are more prone to this disease. The clinical manifestations, time course, and treatment of TBM are unlike those of other types of meningitis, and the disease presents unique challenges for nurses caring for these patients. This case study highlights the typical presentation, course, and management of TBM in a pediatric patient and provides an overview of this devastating disease. Specific nursing issues related to the care of these children are outlined.

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2-year-old with tuberculous meningitis: a case study

Affiliation.

• 1 Sutter Medical Center, Sacramento, CA, USA. [email protected]
• PMID: 15115363
• DOI: 10.1097/01376517-200404000-00006

Tuberculous meningitis (TBM) may occur with tuberculosis infection, and young children are more prone to this disease. The clinical manifestations, time course, and treatment of TBM are unlike those of other types of meningitis, and the disease presents unique challenges for nurses caring for these patients. This case study highlights the typical presentation, course, and management of TBM in a pediatric patient and provides an overview of this devastating disease. Specific nursing issues related to the care of these children are outlined.

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• Presentation and outcome of tuberculous meningitis among children: experiences from a tertiary children's hospital. Nabukeera-Barungi N, Wilmshurst J, Rudzani M, Nuttall J. Nabukeera-Barungi N, et al. Afr Health Sci. 2014 Mar;14(1):143-9. doi: 10.4314/ahs.v14i1.22. Afr Health Sci. 2014. PMID: 26060471 Free PMC article.
• Unilateral meningeal thickening: a rare presentation of tuberculous meningitis. Praharaj SS, Sharma MC, Prasad K, Misra NK, Mahapatra AK. Praharaj SS, et al. Clin Neurol Neurosurg. 1997 Feb;99(1):60-2. doi: 10.1016/s0303-8467(96)00589-6. Clin Neurol Neurosurg. 1997. PMID: 9107471
• Triphasic waves in a patient with tuberculous meningitis. Konno S, Sugimoto H, Nemoto H, Kitazono H, Murata M, Toda T, Nakazora H, Nomoto N, Wakata N, Kurihara T, Fujioka T. Konno S, et al. J Neurol Sci. 2010 Apr 15;291(1-2):114-7. doi: 10.1016/j.jns.2009.12.027. Epub 2010 Feb 8. J Neurol Sci. 2010. PMID: 20116807
• A Child with Tuberculous Meningitis Complicated by Cortical Venous and Cerebral Sino-Venous Thrombosis. Dhawan SR, Chatterjee D, Radotra BD, Vaidya PC, Vyas S, Sankhyan N, Singhi PD. Dhawan SR, et al. Indian J Pediatr. 2019 Apr;86(4):371-378. doi: 10.1007/s12098-018-2830-x. Epub 2019 Jan 9. Indian J Pediatr. 2019. PMID: 30623313 Review.
• Standardized Methods for Enhanced Quality and Comparability of Tuberculous Meningitis Studies. Marais BJ, Heemskerk AD, Marais SS, van Crevel R, Rohlwink U, Caws M, Meintjes G, Misra UK, Mai NTH, Ruslami R, Seddon JA, Solomons R, van Toorn R, Figaji A, McIlleron H, Aarnoutse R, Schoeman JF, Wilkinson RJ, Thwaites GE; Tuberculous Meningitis International Research Consortium. Marais BJ, et al. Clin Infect Dis. 2017 Feb 15;64(4):501-509. doi: 10.1093/cid/ciw757. Clin Infect Dis. 2017. PMID: 28172588 Free PMC article. Review.

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• DOI: 10.1016/j.jpedcp.2024.200123
• Corpus ID: 272077220

Status Epilepticus with Fever in a Toddler with Pyogenic Meningitis due to Complicated Acute Sphenoid Sinusitis

• Jay Pershad , Lexi Crawford , +3 authors Craig Shapiro
• Published in The Journal of Pediatrics… 1 August 2024
• The Journal of Pediatrics: Clinical Practice

28 References

Continuous direct intraarterial treatment of meningitis-induced vasospasm in a pediatric patient: illustrative case, a 20-year study of intracranial pyogenic complications of sinusitis in children, parainfectious cerebral vasculopathy complicating bacterial meningitis: acute-short lived vasospasm followed by delayed-long lasting vasculitis, treatment of hyponatremia in children with acute bacterial meningitis, pediatric paranasal sinuses—development, growth, pathology, & functional endoscopic sinus surgery, accuracy of the axillary temperature screening compared to core rectal temperature in infants, acute isolated sphenoid sinusitis in children: a case series and systematic review of the literature., suppurative intracranial complications of pediatric sinusitis: a single-center experience., treatment and outcome of childhood cerebral sinovenous thrombosis., clinical features of complex febrile seizure caused by primary human herpesvirus 6b infection., related papers.

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Vaccine Safety: Fever and Vaccines

Fevers are one of the most common side effects of vaccination. Often, fevers are associated with illness, and, therefore, it is understandable that parents have concerns when their child develops a fever after vaccination. However, fevers are a normal part of immune responses. So, a fever after vaccination offers evidence that the child’s immune system is responding to the vaccine, and as a result, building immunity against the virus or bacteria that the vaccine targets.

What is a fever?

A fever is a body temperature that is higher than normal. Most people have a normal body temperature around 98.6ᴼF (37ᴼC). But, baseline body temperatures vary between people, and they also vary throughout the day within individuals. 

Because fevers are associated with illness, many people think of them as a bad thing. But, fevers, even high fevers, are a normal and important part of the immune response. First, by turning up the temperature in the body, fevers make the body a less welcoming host for germs, thereby limiting their ability to reproduce in the body. Second, higher temperatures also serve to activate some of the signaling chemicals that guide immune responses.

Why do vaccines cause fevers?

Vaccines prepare the immune system to protect against viruses or bacteria that could make people sick. The way this happens is that they introduce components of the germs that are known to activate the immune response. However, vaccines will not cause a significant enough immune response that the person suffers untoward events, such as can occur during natural infections. With this said, in some cases the immune response is strong enough to cause detectable symptoms, like a mild fever.

Knowing that vaccines can cause a fever, sometimes parents wonder if a lack of fever means the vaccine is not working. However, not everyone who responds to a vaccine will develop a fever.

How high do fevers get after vaccination?

Sometimes a rapid rise in a child’s temperature, not the actual height of the temperature, will cause a fever-induced (febrile) seizure. While febrile seizures are scary, they do not result in permanent or long-lasting effects. One study suggested that less than 7% of febrile seizures in children younger than 6 years of age were caused by vaccinations. The researchers also found that febrile seizures following receipt of vaccines were not different from those caused by infections when it came to duration, likelihood of another seizure in the same 24-hour period, need for ICU admission, length of hospital stay, or requirement for anti-seizure medications. Any questions or concerns about fevers should be discussed with a healthcare provider, and an episode of a febrile seizure should be reported to the healthcare provider, so that it can be added to the child’s medical record.

When should I expect a fever to appear after vaccination?

Most fevers occur within a week of vaccination; however, because vaccines cause immunity in different ways, depending on how they are made, there is some variation regarding exactly when fevers following vaccination are most likely to occur. Additionally, because some vaccines require more than one dose to be effective, fevers may be more likely after later doses. The timing and frequency of fevers after many common vaccines are listed below.

Vaccines against individual pathogens

• Pfizer-BioNTech mRNA vaccine, 1-2 days after vaccination, lasting 1 day in 10-20 of 100 vaccine recipients when given as a booster dose. Fever occurs less frequently in an unvaccinated vaccine recipient.
• Moderna mRNA vaccine (adults), 1-2 days after vaccination, lasting 1 day in 10 of 100 adult vaccine recipients when given as a booster dose. Fever occurs less frequently in an unvaccinated vaccine recipient.
• Moderna mRNA vaccine (children), 1-2 days after vaccination, lasting 1 day in 20-30 of 100 children when given as a booster dose. Fever occurs less frequently in an unvaccinated vaccine recipient.
• Novavax COVID-19 vaccine, 1-3 days after vaccination, lasting 1-2 days in 1-17 of 100 vaccine recipients. Fever occurs less frequently in older age groups.

Haemophilus influenzae type b (Hib)

• ActHIB, 2 days after vaccination in about 2 of 100 vaccine recipients
• Hiberix, 4 days after vaccination in 14-19 of 100 vaccine recipients; fevers occur more frequently after the second and third doses
• PedvaxHIB, 6 to 48 hours after vaccination in 1-18 of 100 vaccine recipients

Hepatitis B

• Heplisav-B, 0 to 7 days after vaccination in 1-2 of 100 vaccine recipients
• Engerix B, 1 to 17 days after vaccination in 2 of 100 vaccine recipients
• Recombivax, in 1-10 of 100 vaccine recipients

Hepatitis A

• Havrix, 0 to 4 days after vaccination in 3 of 100 vaccine recipients
• Vaqta, 1 to 5 days after vaccination in 10 of 100 vaccine recipients

Human papillomavirus

• Gardasil 9, 0 to 5 days after vaccination in 6-7 of 100 vaccine recipients

Meningitis ACWY

• Menactra, 0 to 7 days after vaccination in 5-12 of 100 vaccine recipients; fevers occur more frequently in those younger than 2 years of age
• Menveo, 0 to 7 days after vaccination in 3-9 of 100 vaccine recipients; fevers occur more frequently after the third and fourth doses
• Menquadfi, 0 to 7 days after vaccination in 1-2 of 100 vaccine recipients

Meningitis B

• Trumenba, 0 to 7 days after vaccination in 2-6 of 100 vaccine recipients; fevers occur more frequently after the first dose
• Bexsero, 0 to 7 days after vaccination in 1-4 of 100 vaccine recipients; fevers occur more frequently after the second dose

Pneumococcal

• Prevnar 13 (conjugate version), 0 to 7 days after vaccination in 24-35 of 100 infant vaccine recipients; fewer than 10 of 100 older children who receive this vaccine will experience fever
• Pneumovax 23 (polysaccharide version), 1-2 of 100 vaccine recipients will experience fever
• RotaTeq, 0 to 7 days after vaccination in 17-20 of 100 vaccine recipients
• Rotarix, 0 to 7 days after vaccination in 25-28 of 100 vaccine recipients

Varicella (chickenpox)

• Varivax, 0 to 42 days after vaccination in 10 of 100 vaccine recipients; most fevers occur 14 to 27 days after vaccination

Shingles (zoster)

• Shingrix, 0 to 7 days after vaccination in 28 of 100 vaccine recipients 50 to 59 years of age; in 24 of 100 vaccine recipients 60 to 69 years of age; in 14 of 100 vaccine recipients 70 years of age and older

Vaccines against multiple pathogens

Measles, mumps, and rubella.

• MMR II, 0 to 14 days after vaccination in 2 of 100 vaccine recipients
• Daptacel, 0 to 3 days after vaccination in 11-20 of 100 vaccine recipients
• Infanrix, 0 to 4 days after vaccination in 8-12 of 100 vaccine recipients; fevers occur more frequently after the second dose

DTaP combined with other components (combination vaccines)

• Plus polio - Quadracel, 0 to 7 days after vaccination in 6 of 100 vaccine recipients
• Plus polio – Kinrix, 0 to 4 days after vaccination in 1 of 100 vaccine recipients
• Plus polio and Hib - Pentacel, 0 to 3 days after vaccination in 6-16 of 100 vaccine recipients
• Plus polio and hepatitis B - Pediarix, 0 to 4 days after vaccination in 28-39 of 100 vaccine recipients
• Plus polio, Hib, and hepatitis B – Vaxelis™, 0 to 5 days after vaccination in 19 to 29 of 100 vaccine recipients (Prevnar 13 and RotaTeq were also administered at the same visit)
• Boostrix, 0 to 15 days after vaccination in 19 of 100 vaccine recipients
• Adacel, 0 to 15 days after vaccination in 1-5 of 100 vaccine recipients; fevers occur more frequently in children than adults

Hepatitis A and hepatitis B

• Twinrix, 0 to 4 days after vaccination in 2-4 of 100 vaccine recipients

Measles, mumps, rubella, and varicella (chickenpox)

• ProQuad, 0 to 5 days after vaccination in 8-20 of 100 vaccine recipients; fevers occur most frequently after the first dose

What about medications for fever?

Should i give my child medication prior to a vaccine visit to prevent fever after vaccination.

No. Giving medication prior to a vaccine visit is not recommended because they may decrease the child’s immune response to the vaccine. Studies of patients who got fever-reducing medication prior to vaccination had lower antibody responses compared with patients that did not receive medicine, suggesting that their immune response to the vaccine was lower as a result of reducing the fever.

Should I give my child medication to treat a fever after vaccination or during illness?

In most cases a child does not need to be medicated for a fever unless they are extremely uncomfortable. The most important thing to do when a child has a fever is to make sure they stay hydrated by drinking plenty of fluids. If you are not sure whether the child should get medicine to address fever or other symptoms, talk to your child’s healthcare provider. 

Infectious Diseases & Fevers

Additional resources.

• Treating a Fever: What to Consider (video)
• Parts of the Immune System (webpage)

Reviewed by Lori Handy, MD, MSCE on January 04, 2024

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Parents urged to vaccinate children ahead of potential surge in measles cases

Parents are urged to ensure children are fully vaccinated against 'easily preventable' measles, whooping cough and meningitis.

Health officials have issued a warning over a potential surge in measles cases ahead of the beginning of the new school year.

Parents are being urged to ensure their children are fully vaccinated against “easily preventable” diseases such as measles, whooping cough, meningitis, diphtheria and polio as part of a six-week campaign by the UK Health Security Agency (UKHSA), the Department of Health and Social Care (DHSC) and NHS England.

It comes amid concerns that uptake of the MMR (measles, mumps, and rubella) vaccine is still too low in some areas of England.

There was a surge of measles cases in England in 2023 following an outbreak of the disease in Birmingham. UKHSA data shows there have been 2,278 lab-confirmed measles cases in England from the start of 2024 up to 5 August.

In the four weeks to 5 August, there were 153 cases, most of which were in London which sparked an MMR catch-up campaign.

According to the UKHSA, in the past 12 months the NHS has administered 180,000 additional MMR doses, with more than 51,000 of these given to children aged five or under.

More than 13 per cent of previously unvaccinated children younger than five had their first dose of the jab during the period, while uptake of the second dose among black, Caribbean or African children aged between three and five was up by 4.9 per cent.

Dr Vanessa Saliba, consultant epidemiologist at the UKHSA, said: “As a mum and doctor it is especially tragic to see kids suffering when these diseases are so easily preventable.

Two MMR jabs offer the best and safest protection against measles but if unvaccinated children are at risk of serious illness or life-long complications. No parent wants this for their child.

Measles – the symptoms to watch out for Measles usually starts with cold-like symptoms, followed by a rash a few days later. Some people may also get small spots in their mouth. The first symptoms of measles include: a high temperature a runny or blocked nose sneezing a cough red, sore, watery eyes Spots in the mouth Small white spots may appear inside the cheeks and on the back of the lips a few days later. These spots usually last a few days. A rash usually appears a few days after the cold-like symptoms. The rash starts on the face and behind the ears before spreading to the rest of the body. The spots of the measles rash are sometimes raised and join together to form blotchy patches. They’re not usually itchy. The rash looks brown or red on white skin. It may be harder to see on brown and black skin. It’s very unlikely to be measles if you’ve had both doses of the MMR vaccine or you’ve had measles before.

“It is encouraging that parents whose children have missed vaccines are now coming forward, but we are a long way from ensuring all are protected and safe. And importantly vaccination is also about not spreading the disease to others who may be more vulnerable.

“Measles is highly infectious and is still circulating in many areas across the country. It only takes one case to get into a school or nursery where many children are unprotected for numbers to suddenly surge.”

As measles cases rise - should we also worry about mumps and rubella?

Davina Barrett, from Walsall, said it was “awful” when her then three-month-old son Ezra contracted the illness.

“We were so shocked at how bad Ezra got quite quickly,” she said. “The rash spread rapidly and covered his entire body. Seeing him struggling to breathe and being hooked up to oxygen was awful. I had no idea measles could make babies so ill.

“Parents need to know that they are not just protecting their own child, but that the MMR vaccine could save the life of a baby like Ezra who is too young to have his own protection. Measles can be nasty but it’s entirely preventable.”

Steve Russell, national director for vaccinations and screening at NHS England, said: “The NHS is clear that measles can be really dangerous and so it is critical that children get vaccinated.

“So far, NHS efforts have led to thousands more young people getting protected, with over 13 per cent of previously unvaccinated children under the age of five getting protected, but we know there is more to do. We are encouraging parents to come forward if their children are not fully protected and have been invited by their GP.”

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• Volume 78, Issue 10
• Implications of child poverty reduction targets for public health and health inequalities in England: a modelling study between 2024 and 2033
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• http://orcid.org/0000-0001-8649-6913 Ronan McCabe 1 ,
• http://orcid.org/0000-0001-7286-8106 Roxana Pollack 1 ,
• Philip Broadbent 1 ,
• http://orcid.org/0000-0002-3060-939X Rachel M Thomson 1 ,
• http://orcid.org/0000-0002-2863-4983 Erik Igelström 1 ,
• http://orcid.org/0000-0003-0085-5263 Anna Pearce 1 ,
• http://orcid.org/0000-0002-1294-6851 Clare Bambra 2 ,
• http://orcid.org/0000-0003-3480-6566 Davara Lee Bennett 3 ,
• http://orcid.org/0000-0003-3533-3238 Alexiou Alexandros 3 ,
• http://orcid.org/0000-0002-4573-4628 Konstantinos Daras 3 ,
• http://orcid.org/0000-0002-5828-7724 David Taylor-Robinson 3 ,
• http://orcid.org/0000-0002-4208-9475 Benjamin Barr 3 ,
• http://orcid.org/0000-0001-6593-9092 Srinivasa Vittal Katikireddi 1
• 1 MRC/CSO Social & Public Health Sciences Unit , University of Glasgow , Glasgow , UK
• 2 Population Health Sciences Institute , Newcastle University Institute for Health and Society , Newcastle upon Tyne , UK
• 3 Public Health, Policy & Systems , University of Liverpool , Liverpool , UK
• Correspondence to Dr Ronan McCabe, MRC/CSO Social & Public Health Sciences Unit, University of Glasgow, Glasgow G12 8TB, UK; ronan.mccabe{at}glasgow.ac.uk

Background We investigated the potential impacts of child poverty (CP) reduction scenarios on population health and health inequalities in England between 2024 and 2033.

Methods We combined aggregate local authority-level data with published and newly created estimates on the association between CP and the rate per 100 000 of infant mortality, children (aged <16) looked after, child (aged <16) hospitalisations for nutritional anaemia and child (aged <16) all-cause emergency hospital admissions. We modelled relative, absolute (per 100 000) and total (per total population) annual changes for these outcomes under three CP reduction scenarios between 2024 and 2033— low-ambition (15% reduction), medium-ambition (25% reduction) and high-ambition (35% reduction)—compared with a baseline CP scenario (15% increase). Annual changes were aggregated between 2024 and 2033 at national, regional and deprivation (IMD tertiles) levels to investigate inequalities.

Results All CP reduction scenarios would result in substantial improvements to child health. Meeting the high-ambition reduction would decrease total cases of infant mortality (293; 95% CI 118 to 461), children looked after (4696; 95% CI 1987 to 7593), nutritional anaemia (458, 95% CI 336 to 574) and emergency admissions (32 650; 95% CI 4022 to 61 126) between 2024 and 2033. Northern regions (eg, North East) exhibited the greatest relative and absolute benefit. The most deprived tertile would experience the largest relative, absolute and total benefit; under high-ambition reduction, total infant mortality cases were predicted to fall by 126 (95% CI 51 to 199) in the most deprived tertile compared with 71 (95% CI 29 to 112) in the least between 2024 and 2033.

Conclusions Achieving reductions in CP could substantially improve child health and reduce health inequalities in England.

• INEQUALITIES
• CHILD HEALTH

Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information. Alternatively, the data is also available through the place-based longitudinal data resource: https://pldr.org/ .

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See:  https://creativecommons.org/licenses/by/4.0/ .

https://doi.org/10.1136/jech-2024-222313

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WHAT IS ALREADY KNOWN ON THIS TOPIC

Child poverty is a key determinant of population health and health inequalities.

WHAT THIS STUDY ADDS

Child poverty is responsive to policy. We are the first to explore the health impact of meeting hypothetical future child poverty targets in England between 2024 and 2033. We show that reducing child poverty across this period would substantially improve child health and reduce health inequalities.

HOW THIS STUDY MIGHT AFFECT RESEARCH, PRACTICE OR POLICY

We demonstrate the importance of renewed policy efforts to reduce child poverty.

Child poverty is a key determinant of population health and health inequalities. 1 Experiencing child poverty is associated with worse outcomes across a wide range of early years health indicators, with evidence suggesting that these associations are often causal. 2–4 Child poverty also likely reinforces the clustering and accumulation of adverse exposures. 5 Government policy exerts a major influence over rates of child poverty. For example, higher levels of social spending were associated with lower levels of child poverty across European countries in the aftermath of the 2008 financial crisis, whereas countries such as the UK that have enacted high levels of austerity following the crisis—including retrenchment of social spending and local government budgets—have exhibited worse trends in child health outcomes. 6–9

In the UK, progress had been made in reducing child poverty with the ‘New Labour’ Government (1997–2010) introducing several policies under the aim of being “(…) the first generation to end child poverty (in the UK)”. 10 These included targeted measures to supplement income such as the Child Tax Credit and increases in Child Benefit, alongside other measures to improve early years services such as Sure Start programmes. 10 11 Consequently, relative child poverty (before housing costs, BHC) declined from 27% to 20% across this period (a 25.9% reduction) 12 ; corresponding declines in infant mortality rates were observed, particularly in the most deprived areas. 13 However, following the 2008 financial crash and the subsequent enactment of austerity measures by consecutive Conservative-led Governments since 2010, child poverty levels began rising from 17% in 2014 to 23% (BHC) in 2020. 12 This period coincided with a rise in infant mortality. 9 Child poverty is responsive to policy; levels fell to 19% in 2021 following a brief uplift in social spending which was withdrawn by the end of that same year, with levels rising back to 22% in 2023. 12 14 The UK also exhibits wide geographical variation in child poverty levels and its devolved governments have (although limited) powers to influence levels; for example, in 2021, the Scottish Government introduced the weekly Scottish Child Payment for low-income parents/carers, although the impact of this policy on child poverty has not been evaluated yet. 15 16 The societal effects of the COVID-19 pandemic and the ongoing ‘cost of living’ crisis have heightened concerns about the level of child poverty in the UK and its current and future impact on child health. 17–21 While some broad measures have been taken by the UK Government in response to this situation, there has been a lack of policy explicitly addressing rising child poverty—such as removing the ‘two-child limit’ and ‘benefit cap’ on financial support. 22 Similarly, the UK Government’s initiative to ‘level up’ regional inequalities makes no reference to child poverty, despite the wide regional variations in child poverty rates. 16 23 As such, it is important to understand how levels of child poverty could change under different hypothetical policy scenarios and the likely consequences these scenarios would have for child health.

We therefore aimed to investigate the potential impact of meeting different child poverty reduction scenarios on child health outcomes and inequalities in England over the next decade. We selected four child health outcomes which are associated with poverty and deprivation in childhood and for which there were local authority-level data available in England: (1) infant mortality; (2) children (<16 years old) entering local authority care; (3) child (<16 years old) hospital admissions for nutritional anaemia; and (4) child (<16 years old) all-cause emergency hospital admissions. 9 13 24–27 While children entering care is not a direct measure of health, it is associated with a range of short-term and long-term adverse health consequences. 24

Study setting and design

We created a dynamic policy simulation model using aggregated local authority-level data from England. This model allows for the exploration of ex-ante policy impacts under different scenarios between 2024 and 2033, drawing on existing data and published evidence of the relationship between child poverty and health outcomes. 28

This ecological study used data for 145 English upper-tier local authorities (UTLAs). We excluded four UTLAs due to either small population size or irreconcilable boundary changes over the study period (City of London, Isles of Scilly, Bournemouth, Christchurch, and Poole and Dorset) 24 and two further UTLAs due to a lack of published outcome data (Buckinghamshire and Northamptonshire). Exposure data on relative child poverty were acquired from the children in low-income families (CiLIF) statistics, compiled by the Department of Work and Pensions and His Majesty’s Revenue and Customs. 29 Outcome data for infant mortality were derived from the Office for National Statistics (ONS). 30 Data for looked-after children were obtained from the UK Government’s Department of Education, 31 and local authority-level data on the number of hospitalisations for nutritional anaemia and all-cause emergency admissions were derived from NHS Hospital Episode Statistics data and supplied by the University of Liverpool’s Place-Based Longitudinal Data Resource (PLDR). 32 Data on local authority-level income deprivation were derived from the 2019 Index of Multiple Deprivation (IMD), using the local authority average rank. 33

We used the prevalence of relative child poverty BHC, captured in the CiLIF statistics, as our study exposure. This was defined as the proportion of children <16 years old living in families with an income of <60% of the contemporary national median income BHC. We used the 2020 CiLIF estimate to project annual values forward until the study end date in 2033 for each UTLA (see ‘modelled scenarios’ below); while estimates have subsequently been published until 2023, these are at present provisional.

We examined four outcome measures at UTLA level: infant mortality, defined as the total number of deaths under the age of one per 100 000 live births per year; children looked after, defined as the total number of children (<16 years old) entering local authority care (whose care had been with local authorities for >24 hours period) per 100 000 of the <16 population per year; total child (<16 years old) hospitalisations for nutritional anaemia per 100 000 of the <16 population per year; and total child (<16 years old) all-cause emergency admissions per 100 000 of the <16 population per year. The final available values (numerator and denominator) for each outcome—2021 for infant mortality and children looked after, and 2019 for nutritional anaemias and emergency admissions—were held constant until start of the intervention period in 2024 (see online supplemental data ).

Supplemental material

Data analysis, effect estimates.

We calculated additional cases attributable to changes in child poverty for each scenario using separate effect estimates for each outcome. For infant mortality and looked-after children, we used published estimates. For the former, we used an estimate from a time trends analysis of local authority-level data in England between 2000 and 2017, where a one-point change in the prevalence of child poverty was associated with a change in infant mortality of 5.8 (95% CI 2.4 to 8.9) deaths per 100 000 live births. 9 For the latter, we used an estimate from a longitudinal ecological analysis of local authority-level data in England between 2015 and 2020, where a one-point change in the prevalence of child poverty was associated with a change in children looked after of 5.2 (95% CI 2.2 to 8.3) children per 100 000 children <16 years old. 24

For nutritional anaemia and emergency admissions, we did not find relevant estimates in the published literature. Instead, we derived estimates for each outcome from new analysis of annual local authority-level data from the PLDR 32 between 2015 and 2019. Estimates were derived using linear within-between regression analysis, in line with similar studies. 24 This approach uses the strengths of both fixed and random effects models, integrating information on differences between and across areas. We found that a one-point change in the prevalence of child poverty was associated with 0.53 (95% CI 0.39 to 0.67) and 37.7 (95% CI 3.8 to 72.1) additional cases per 100 000 children <16 years old for nutritional anaemia and emergency admissions, respectively.

Modelled policy scenarios

We modelled a baseline child poverty scenario as a logarithmic annual increase (ie, curvilinear with a falling rate of change over time) from the 2020 prevalence of child poverty for each UTLA, resulting in a total cumulative increase of 15% from 2020 to 2033. This formed the baseline scenario to which the effects of other scenarios were compared (see below); that is, we were interested in modelling the potential effects of successful action to reduce child poverty versus unsuccessful or no action. Using the 2023 baseline prevalence of child poverty, we then modelled three scenarios at UTLA level over a 10-year period from 2024 until 2033 (see table 1 ): (1) low ambition reduction, a cumulative exponential decrease (ie, increasing rate of change over time) in child poverty of 15% on 2023 levels between 2027 and 2033 (3-year delay); (2) medium ambition reduction, a cumulative exponential decrease of 25% on 2023 levels between 2026 and 2033 (2-year delay); and (3) high ambition reduction, a cumulative exponential decrease of 35% on 2023 levels between 2025 and 2033 (1-year delay). We understood these scenarios to be realistic in light of the 26% fall in prevalence previously observed in the UK between 1997 and 2010 under previous governments. 34 All scenarios were created using MS Excel (see online supplemental data ).

• View inline

Descriptive statistics for baseline exposure and outcomes, derived from modelled projections

Modelling approach

We calculated the annual number of attributable (avoided or added) cases at UTLA level for each outcome under each scenario: the annual relative change in child poverty (%) multiplied by the effect size per number exposed in that same year. We used a Monte Carlo approach to randomly sample (1000 iterations) from the distribution of the effect size of child poverty for each health outcome based on its mean and SE, taking the median of the sample to determine the point estimate of attributable cases, and the 2.5th and 97.5th percentiles for the upper and lower CIs. For each scenario compared with baseline, we report the change in cases for each outcome as the (1) total change per individuals exposed, (2) absolute change, as the risk difference (RD) per 100 000 exposed, and (3) relative change, as risk ratio (RR) at local authority level, regional level, national level and by IMD tertiles across the whole intervention period (2024–2033). Both RR and RD account for differences in population size and are thus suitable for comparison, but only compare extreme categories of the distribution. To quantify effects on inequalities in outcomes taking account for the whole distribution of deprivation, we estimated absolute and relative changes, respectively, as the difference in slope index of inequality (SII) and ratio of relative index of inequality (RII) under each scenario compared with baseline (see online supplemental appendix 1 for details). 35 The SII can be interpreted as the difference in the rate of outcomes between the hypothetically most and least deprived local authorities, whereas the RII can be interpreted as the ratio between those local authorities.

Across the 145 UTLAs included in analysis, the population-weighted mean prevalence of child poverty in 2023 projected under the baseline scenario was 20.7% ( table 1 ). At regional level, the prevalence of child poverty was typically higher in northern regions compared with southern, with the North East having the highest median prevalence at 27.6% (IQR=4.2) and the South East and South West both had the lowest at 15.4% (IQR=8.5–6.7, respectively) in 2023. Across IMD tertiles, the median prevalence was 27.8% (IQR=10.1) in the most deprived tertile and 13.9% (IQR=4.6) in the least deprived tertile. Cases per 100 000 in 2023 are given for each outcome in table 2 , with emergency admission being the most frequent and hospitalisations for nutritional anaemia being the least. For each outcome, cases tended to be highest in regions with high child poverty. Outcome trends (cases per 100 000 exposed) at national level over the period for which official data were available (2015–2019) are presented in online supplemental appendix 2 figure A : admissions fluctuated across this period although were rising 2017–2019, hospitalisations for nutritional anaemia continued rising, and infant mortality and children looked after both fell from 2017 onwards.

Modelled relative and absolute changes (95% CI) under three child poverty reduction scenarios between 2024 and 2033, relative to a baseline scenario of increasing child poverty

Modelled changes

Increasingly ambitious scenarios corresponded to greater relative and absolute beneficial effects, with effect sizes in the high-ambition policy target around twice that of the low-ambition target across all outcome measures at all levels of aggregation ( tables 2 and 3 , online supplemental appendix 2 tables A,B ).

Modelled relative and absolute changes by Index of Multiple Deprivation (IMD) tertile and change in Slope Index of Inequality (SII) under three child poverty reduction scenarios between 2024 and 2033, relative to a baseline scenario of increasing child poverty

Between 2024 and 2033 across England, compared with baseline, we anticipate a reduction in: infant mortality of 1.6% (293 avoided cases, 95% CI 118 to 461) under the high-ambition scenario versus 0.9% (155 avoided cases, 95% CI 62 to 244) under the low-ambition scenario; children looked after of 2% (4696 avoided cases, 95% CI 1987 to 7593) versus 1% (2483 avoided cases, 95% CI 1051 to 4015); hospitalisations for nutritional anaemia of 4.1% (458 avoided cases, 95% CI 336 to 574) versus 2.2% (242 avoided cases, 95% CI 177 to 304); and emergency admissions of 0.4% (32 650 avoided cases, 95% CI 4022 to 34 126) versus 0.2% (17 266 avoided cases, 95% CI 2127 to 32 324) ( table 2 and online supplemental appendix 2 table A ).

At regional level, estimated absolute reductions were typically higher in the north and west of England (eg, North East, West Midlands and Yorkshire and The Humber) compared with the south (see table 2 ); this pattern is highlighted in figures 1 and 2 for cases of emergency admissions avoided per 100 000 compared with baseline under the high-ambition scenario. Between 2024 and 2033, for all child poverty reduction scenarios, we anticipate cases avoided (compared with baseline) per 100 000 would be largest in the North East for all outcomes and smallest in the South East ( table 2 ). Under the high-ambition scenario, estimated total avoided cases in the North East would be 18 (95% CI 7 to 28) for infant mortality, 298 (95% CI 126 to 482) for children looked after, 29 (95% CI 21 to 36) for nutritional anaemias, and 2070 (95% CI 255 to 3876) for emergency admissions ( online supplemental appendix 2 table A ). Regional patterns of relative change were less uniform ( table 2 ), while total cases avoided were typically highest in regions with greater population size (eg, London) ( online supplemental appendix 2 table A ). At local authority level across reduction scenarios, absolute changes per 100 000 were highest in Middlesborough, Oldham, Bradford and Birmingham for all outcome measures (see online supplemental data ); this is visually displayed for emergency admissions in figures 1 and 2 .

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Absolute changes in avoided cases of emergency admissions (per 100 000) for the high ambition scenario (compared to baseline) at local authority level. Grey areas represent excluded local authorities.

Absolute changes in avoided cases of emergency admissions (per 100 000) for the high ambition scenario (compared to baseline) at region level.

Considering deprivation level, anticipated reductions on the difference scale (per 100 000) compared with baseline were highest in the most deprived tertile of UTLAs for all outcome measures (see table 3 ). Under the high-ambition scenario, this equated to a total avoided cases of 126 (95% CI 51 to 199) in the most deprived versus 71 (95% CI 29 to 112) in the least for infant mortality, 1907 (95% CI 807 to 3083) versus 1199 (95% CI 507 to 1939) for children looked after, 189 (95% CI 137 to 234) versus 117 (95% CI 86 to 146) for nutritional anaemias and 13 302 (95% CI 1639 to 24 903) versus 8 322 (95% CI 1025 to 15 581) for emergency admissions ( online supplemental appendix 2 table B ); total avoided cases under each scenario for each outcome measure are shown in figure 3 . Changes on the ratio scale followed a broadly similar pattern ( table 3 ). Greater reductions in child poverty were associated with greater reductions in absolute (SII difference) and relative (RII ratio) inequalities ( table 3 and online supplemental appendix 2 table C , respectively).

Estimated total avoided cases of four health outcomes under low, medium and high poverty reduction scenarios by Index of Multiple Deprivation (IMD tertile), 2024-2033.

Reducing child poverty will likely improve a range of child health outcomes and reduce health inequalities if similar or larger declines to those observed between 1997 and 2010 were achieved. We estimated relative, absolute and total changes in infant mortality, children looked after, nutritional anaemias and all-cause emergency admissions using local authority-level data in England under three different child poverty reduction scenarios between 2024 and 2033 compared with a baseline scenario of increasing child poverty. Achieving an ambitious but realistic reduction of 35% on 2023 levels would be expected to result in avoiding a total of 293 infant deaths, 4696 children entering care, 458 childhood admissions with nutritional anaemias and 32 650 childhood emergency admissions. These reductions would likely translate into significant savings for, and relieve pressure on, local authorities (in relation to children looked after) and health services. Benefits are likely to be greatest in the most disadvantaged areas, helping efforts to ‘level up’. Other health impacts that we have not been able to quantify are also likely.

We used administrative data from trusted sources and outcome estimates from previous empirical studies where available. Our modelling approach was simple and transparent, relying on a limited set of assumptions and a realistic baseline scenario (eg, we predicted mean relative child poverty BHC at 20.7%, whereas the provisional CiLif estimate for 2023 gives 20.1%). 29 However, there are limitations to this work. We focused here on a limited set of outcomes which capture different dimensions of child health and for which there were data readily available. However, future work could extend this analysis to look at other common child health outcomes such as obesity and mental health which are both associated with child poverty. 36 37 Relatedly, we used emergency admissions as a health outcome but acknowledge that they can be affected by health service access (changes in admission practice, transport, etc). Nonetheless, our analyses to parameterise the model excluded the COVID-19 pandemic when changes in practice were most likely to be problematic. We adopted the exposure of relative child poverty rate BHC. However, findings may have differed with alternative measures of child poverty such as absolute rates and rates after housing costs. Additionally, our analyses are predicated on the associations between child poverty and health outcomes accurately reflecting causal effects. While our analyses of changes within local authorities account for time-invariant confounding, risks of residual confounding remain. It is also possible that the effect estimates we observed for each outcome could differ as a consequence of the differing time periods for which data were available. Shorter time periods may lead to underestimated effect sizes within panel data analyses. 38 This might imply our estimates of the impacts on emergency admissions and nutritional anaemia are underestimated. Relatedly, it is possible that the relationship between child poverty and outcomes does not exhibit the linear dose–response relationship that we have assumed here. A few local authorities were excluded due to small numbers, with possible consequences for overall estimates. Finally, our analyses are based on aggregate (ecological) data which could be subject to the ecological fallacy; although, while individual-level data analyses are of interest, these may be subject to the atomistic fallacy (ie, addressing child poverty could have positive impacts for communities beyond the individual). 39 Aggregate data meant that we were also unable to account for variation within and between local authorities in the mechanisms influencing child poverty—for example, the depth of child poverty might differ and the health effects of addressing severe child poverty might differ from addressing less severe poverty. Furthermore, different policies to reduce child poverty (such as minimum wages, tax credits, welfare benefits) might have quite heterogenous effects that we do not distinguish. We would anticipate the impacts of the above factors to result in our estimates being conservative.

To our knowledge, this study is the first to explore the potential impacts of future child poverty reductions on a range of child health outcomes in England. It builds on previous empirical work that has highlighted the consequences of child poverty on outcomes such as infant mortality and children looked after in England. 9 13 24 For example, this research found that reductions in child poverty in the UK between 1997 and 2010 led to a reduction in infant mortality, while subsequent increases in child poverty led to increases in infant mortality. 9 13 Tying into factors influencing child poverty, previous studies have also found associations between increased local authority spending in England and reductions in hospital admissions for nutritional anaemia, although this association lacked precision among those <14 years old (rate ratio=0.97, 95% CI 0.90 to 1.05). 40 Similarly, a study using local authority data by the Nuffield Trust showed that, in 2015/2016, the number of emergency admissions was higher with increasing deprivation among those <14 years old. 26

We highlight that if policy-makers were to set and achieve child poverty targets for England—for example, through suggested measures such as removing the two-child limit and benefit cap 22 —this would likely improve child health, particularly among the most socioeconomically disadvantaged and ‘level up’ regional inequalities.

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Acknowledgments.

For the purpose of open access, the author(s) have applied a Creative Commons Attribution (CC BY) licence to any Author Accepted Manuscript version arising from this submission.

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Supplementary materials

Supplementary data.

This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.

• Data supplement 1
• Data supplement 2
• Data supplement 3

X @roxana_pollack, @Rachel_Thomson, @igelstorm, @ProfBambra, @benj_barr2, @vkatikireddi

BB and SVK contributed equally.

RM and RP contributed equally.

Contributors RM serves as guarantor for this study. SVK and BB conceptualised the study. RM, RP, DLB, AA and KD were involved in data curation. RP, EI, RMT and PB contributed to analysis code. RM finalised analysis code, conducted formal analyses and visualised findings. RM, RP, AP and SVK wrote the original draft. All authors were involved in the review and editing of the original draft.

Funding RM, RP, EI, RMT, AP and SVK declare funding from the Medical Research Council (MC_UU_00022/2) and the Scottish Government’s Chief Scientists Office (SPHSU17). CB declares funding from the Wellcome Trust (221266/Z/20/Z). AP declares funding from the Wellcome Trust (205412/Z/16/Z). SVK acknowledges funding from the European Research Council (949582). This work also received support from Population Health Improvement UK (PHI-UK), a national research network that seeks to transform health and reduce inequalities through change at the population level. UK Research and Innovation (UKRI) funding for the PHI-UK Policy Modelling for Health theme(s) is gratefully acknowledged [grant reference MR/Y030656/1].

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Competing interests None declared.

Provenance and peer review Not commissioned; externally peer reviewed.

Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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• J Undergrad Neurosci Educ
• v.18(2); Spring 2020

Meningitis in College Students: Using a Case Study to Expose Introductory Neuroscience Students to Primary Scientific Literature and Applications of Neuroscience

This case study was based on a popular press news article about Krystle Beauchamp Gridley’s experience with meningitis while in college ( Miller, 2019 ). Students in an introductory neuroscience course read the popular press news article as well as an empirical article that identified risk factors for contracting meningococcal disease in college ( Bruce et al., 2001 ). Students used information from the empirical article to identify Krystle’s risk factors for meningitis. Then, students evaluated their University’s policy on students receiving the meningococcal vaccine based on what they had learned. This case supports two important goals of neuroscience education, 1) exposing students to primary scientific literature early in their undergraduate education and 2) developing an understanding of the broader implications of scientific research for society. Students enjoyed learning about meningitis using the case-study method, reading the primary scientific article, and considering how scientific research can be applied to policy decisions. Further, the case was instrumental in supporting the content and process learning objectives.

BACKGROUND AND CONTEXT

Case studies play an important role in the advancement of science. For example, Scoville and Milner (1957) initially identified the critical role of the hippocampus in their seminal report of patient H.M.’s memory deficits following the resection of the medial temporal lobe. Case studies are also impactful pedagogical tools in the classroom. Case studies personalize course content and foster elaborative encoding, which promotes long-term retention. As noted by Meil (2007) , students may forget the functions of the hippocampus and frontal cortex but be able to remember the names and stories of H.M. and Phineas Gage. Classroom case studies can either be based on published case reports in peer-reviewed journals, such as the Journal of Clinical Neuroscience , or involve the application of course content to a story or scenario.

The current case study was based on a college student’s experience with meningitis that was presented in a popular press news article ( Miller, 2019 ). Students in an introductory neuroscience course learned about the individual’s experience and then identified risk factors for meningitis present in the case after reading an empirical article on risk factors for contracting meningitis in college ( Bruce et al., 2001 ). Exposure to reading and evaluating primary scientific literature during undergraduate education supports scientific literacy and success in graduate school ( Kozeracki et al., 2006 ). However, many faculty do not incorporate primary scientific literature into introductory courses due to the focus on content versus process-based learning objectives ( Coil et al., 2010 ). This lack of exposure subsequently results in students being intimidated by primary scientific literature once they reach upper-level courses ( Smith, 2001 ). As such, there has been a call to begin developing scientific process skills, including reading and interpreting primary literature, early in students’ undergraduate education ( Coil et al., 2010 ).

The last part of the case required students to apply what they had learned about meningococcal disease. Students evaluated their University’s policy on students receiving the meningococcal vaccine. The goal of this component of the case was to expose students to the broader impacts of scientific research for society and policy-based decisions. In addition to understanding the scientific process and quantitative reasoning, the Vision and Change in Undergraduate Biology Education: A Call to Action report by the American Association for the Advancement of Science includes understanding how science intersects society as a core competency of biological sciences, including neuroscience ( Brewer & Smith, 2011 ).

The current case study on meningitis makes multiple contributions to neuroscience education. Whereas most neuroscience case studies have been implemented in upper-level undergraduate courses (e.g., Cook-Snyder, 2017 ; Sawyer & Frenzel, 2018 ; Mitrano, 2019 ; Ogilvie, 2019 ; Watson, 2019 ; cf. Roesch & Frenzel, 2016 ), the current case was implemented in an introductory neuroscience course. Further, students evaluated the case in relation to an empirical report on risk factors for contracting meningococcal disease in college, supporting their knowledge of how an individual case can fit within the context of broader scientific investigation. Lastly, students applied what they learned to evaluate their University’s policy, demonstrating the practical implications of scientific research for society. Student materials and implementation notes are available from the corresponding author or from [email protected] .

LEARNING OBJECTIVES

Content objectives.

At the end of the case, students will be able to:

• Identify the layers of the meninges on the brain and spinal cord.
• Provide symptoms of meningitis.
• Describe tests that can be performed in order to diagnose an individual with meningitis.
• Identify risk and protective factors for meningitis in college students.
• Understand the effectiveness of the meningococcal vaccines for different strains of the bacteria that cause meningitis.
• Apply their knowledge to evaluate their University’s policy on students receiving the meningococcal vaccine.

Process Objectives

• Read and interpret primary scientific literature.
• Begin learning how statistics can be used to evaluate scientific hypotheses.
• Identify real-world implications of neuroscience research.

COURSE OVERVIEW

This case on meningitis was implemented in an introductory neuroscience course that included 30 students. Prerequisites for the course included either introductory psychology or introductory biology. Students completing the course ranged from first-semester freshman to seniors. Students primarily intended to major in Neuroscience (53%), Psychology (23%), and Biology (17%). The case was presented the third week of the semester as we began covering the structure of the nervous system, including cerebrospinal fluid, the meninges, neural development, and gross anatomy. The case was the students’ first exposure to primary scientific literature in the course.

The case was designed to reinforce knowledge of the meninges, expose students to primary scientific literature, and require students to apply knowledge learned in class to a real-world situation. As such, the case included a news article describing the experiences of a college student that contracted meningitis, an empirical article evaluating risk factors for contracting meningitis, and an evaluation of the University’s policy on students receiving the meningococcal vaccine. This case would be appropriate for neuroscience, psychology, or biology courses that include a unit on neuroanatomy. Alternatively, this case could also be used to educate students about the immunological mechanisms of vaccinations or to facilitate a discussion about ethics associated with vaccination.

CLASSROOM IMPLEMENTATION

This case implementation in the classroom involved a modified think-pair-share approach. Students independently completed guided readings prior to class. Then, students discussed responses in small groups during the class meeting prior to the larger class discussion. Before the class period during which the discussion of the case took place, students:

• Read a short textbook passage about the meninges (i.e., dura mater, arachnoid mater, pia mater). The passage identified characteristics of each layer of the meninges as well as their location in relation to the brain and spinal cord.
• Read and answered four questions about a popular press news article about Krystle Beauchamp Gridley’s experience with meningitis ( Miller, 2019 ). Specifically, students were asked to list signs and symptoms of meningitis experienced by Krystle, identify how doctors diagnosed Krystle with meningitis, whether there was anything Krystle could have done to avoid contracting meningitis, and the long-term effects of meningitis experienced by Krystle.
• Read and answered questions about an empirical article from the Journal of the American Medical Association titled, “Risk factors for meningococcal disease in college students” ( Bruce et al., 2001 ). Students were asked to consider how details of Krystle’s case aligned with risk factors identified in the article and assess whether her meningitis could have been avoided if she had received the meningococcal vaccine.

During the 50-minute class meeting, students learned about anatomical directions and the layers of the meninges for the first 25–30 minutes of class. The remainder of the class period was spent on the case study in which there were three pair-and-share opportunities. Students discussed their responses in groups of 3–4 students and then we had a group discussion. During the first pair-and-share, students discussed Krystle’s experience with meningitis. Second, they considered Krystle’s case in relation to risk factors identified in the empirical article after a brief discussion of statistics. I explained that scientists typically use a threshold of.05 for determining whether an effect is statistically significant. Then, together as a class, we identified which risk factors in Tables 2 and 3 from the JAMA article were significant predictors of meningococcal disease and which were not. Based on that discussion, students identified Krystle’s risk factors and spent the most time discussing the fact that Krystle did not receive the meningococcal vaccine. We discussed that the meningococcal vaccine most college students receive protects against some, but not all, of the serogroups that commonly cause meningococcal disease. Additionally, the specific serogroup that caused Krystle’s meningitis was not identified in the news article, so we were unable to definitively state whether the meningococcal vaccine would have protected Krystle from contracting meningitis. Lastly, the students were provided with and asked to evaluate the University’s policy on students receiving the meningococcal vaccine (which can be found on most Universities’ websites).

CASE ASSESSMENT

The questions students answered when completing the case study were not evaluated because I intended for students to perceive the activity as a learning opportunity versus an assessment. The University’s Institutional Review Board approved the case assessment, and students consented to having their data from the exam and evaluation of the case study contribute to the present report. Learning objectives for the case study were included on the list of exam objectives, which students received a week before the exam. Four questions on the first exam (8 points) related to the meninges or meningococcal disease. Two questions were multiple-choice with four response options, and two questions were short answer. The multiple-choice questions required students to 1) provide the order of the layers of the meninges in relation to the brain and 2) identify which medical procedure was most likely used to test for meningitis. Twenty-six of 29 students (89.66%) correctly identified the order of the layers of meninges relative to the brain as well as the procedure used to diagnose meningitis (one student’s performance on the multiple-choice questions is missing because the scantron was not evaluated with the rest of the class). The first short-answer question required students to identify two symptoms of meningitis. Twenty-nine of 30 students (96.6%) received full credit on this question. One student correctly identified only one symptom of meningitis. The second question required students to identify one precaution that can be taken to reduce the probability of contracting meningitis; 100% of students correctly identified that vaccination can protect individuals from contracting meningitis.

After the conclusion of the case study, students completed an anonymous evaluation of the meningitis case. Students responded to eight statements regarding the case using a 5-point Likert-scale (1 = Strongly Disagree, 5 = Strongly Agree; See Table 1 ). Students overall responded favorably to the case study. Another goal of the case study was for students to consider how scientific knowledge can be applied to real-world situations. Students agreed that it is important to consider the broader impacts of scientific knowledge ( M = 4.48 ±.63), and ratings were lower for students indicating that they had previously thought about the way scientific knowledge can affect policies ( M = 3.53 ± 1.14). Most students did not respond to the open-ended question at the end of the questionnaire that asked for other feedback about the case study. However, one student commented, “case studies are a great way for undergraduate student to learn, in a memorable way, about different ailments.”

Presents the mean (± SD) for items on the evaluation questionnaire.

The meningitis case was the first case presented in the semester and the student’s first exposure to primary scientific literature. Self-reported data indicated that the majority of the students enjoyed learning about meningitis using the case-study method, reading the primary scientific article, and considering how scientific research can be applied to policy decisions. Students performed well on the examination questions, and the case provided students with low-stakes exposure to primary scientific literature before they completed four graded empirical article evaluations. As such, the case was effective in promoting the identified content and process objectives.

There are many ways this case can be adapted in the future. Students could independently investigate the meninges or which meningococcal serogroups are targeted by the quadrivalent meningococcal vaccination. The case study could also be adapted for courses in immunology or epidemiology. For example, the case study could be focused on the meningococcal serogroups or involve students comparing data from the JAMA article to recent reports by the CDC (2019 ; ( https://www.cdc.gov/meningococcal/surveillance/index.html ). Further, how the case study is applied could be modified. Rather than evaluate their University’s policy on students receiving the meningococcal vaccine, students could create their own policy, which would challenge them to think at a higher level of Bloom’s taxonomy. Students could also consider the costs versus benefits of the vaccinations given the rarity of meningococcal disease. For example, a relatively recent article in The New York Times discussed concerns related to the cost of the vaccinations in relation to the rarity of meningococcal disease ( Luthra, 2017 ).

Acknowledgements

This case study was supported by the Neuroscience Case Network (NeuroCaseNet; NSF-RCN-UBE Grant #1624104). The author would also like to thank Darlene Mitrano, Ph.D., for providing feedback on the case study and editing the manuscript.

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Polio and Israel’s attrition genocide in Gaza

The re-emergence of polio in Gaza is yet another sign of Israel’s genocidal strategies at work.

In August, the Palestinian Health Ministry announced Gaza’s first proven case of polio infection in 25 years. The virus had infected a 10-month-old baby in Deir el-Balah, leaving him paralysed. While only one case has been confirmed so far, this does not mean it is the only one or that the spread of the virus is limited.

While polio can cause paralysis and even death, many of those who are infected with the virus do not show any symptoms. That is why testing and medical evaluation are needed to properly determine the scale of the breakout. But that is nearly impossible in Gaza, given Israel’s wholesale destruction of its healthcare sector.

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We do know that the type 2 poliovirus (cVDPV) was identified in six sewage samples, collected from two different sites in Khan Younis and Deir el-Balah in July. After these findings were made public, World Health Organization Director-General Tedros Ghebreyesus warned that it is “just a matter of time before [the virus] reaches the thousands of children who have been left unprotected”.

Israel rejected calls by the United Nations for a ceasefire and agreed to localised “humanitarian pauses” for just a few days. In parallel, it intensified its bombing of Gaza and mass expulsions of civilians. Between 19 and 24 August, the Israeli army issued the highest number of evacuation orders in one week since October 7, leading the UN to temporarily halt humanitarian operations.

Nevertheless, a vaccination campaign was officially launched on Sunday. The rollout started in the central Gaza Strip – Deir el-Balah governorate – and in the coming days is supposed to be extended to Khan Younis in the southern Strip and then the northern governorates, where Israel has been severely limiting aid and mobility.

It is unclear if the UN will reach its target of vaccinating 640,000 children given the difficult conditions of operation, the dramatic number of displaced people, the Israeli restriction on fuel supplies needed to run generators and fridges to store the vaccines and Israel’s refusal to fully stop fighting.

For the vaccine to be effective, two doses need to be administered at least one month apart. There is still no guarantee that conditions will be in place for the second stage of the vaccination drive.

Unfortunately, a polio outbreak is not the only health emergency Palestinians in Gaza are facing. Other dangerous infectious diseases, including hepatitis and meningitis, are also spreading across the Strip. More than 995,000 cases of acute respiratory infections and 577,000 cases of acute watery diarrhoea have also been registered in Gaza since October.

In addition, hundreds of thousands of chronically ill people are not getting the adequate care they need, which leads to many preventable deaths that are not recorded in the official Gaza death toll.

All of this is a reflection of Israel’s attrition genocide: that is, the destruction of the conditions of survival of Palestinians as a group through techniques of killing less visible than the horrific livestreamed violence we have been witnessing for the last 11 months.

To borrow from Jewish-Polish lawyer Raphael Lemkin, who introduced the notion of genocide in 1944, the “endangering of health” and the creation of conditions of life “inimical to health” constitute one of the main techniques of genocide.

Over the past 11 months, Israel has all but obliterated Gaza’s health system. Recent data published by the WHO Global Health Cluster speak for itself: in the first 300 days of the war, 32 out of 36 hospitals were damaged, 20 (out of 36) hospitals and 70 primary healthcare centres (out of 119) are not functioning. Some 492 attacks on healthcare were reported, which resulted in the death of 747 people.

The Israeli army has also systematically destroyed the water and sewage system in Gaza. According to an Oxfam report published in July, people in Gaza are left with only 4.74 litres of water per person per day for all uses, including drinking, cooking, and washing.

This means a 94 percent reduction in the amount of water available before October, and a level significantly below the internationally accepted minimum standard of 15 litres of water per person per day for basic survival in emergencies.

Simultaneously, Israel has destroyed 70 percent of all sewage pumps and 100 percent of wastewater treatment plants since October. The destruction and obstruction of Gaza’s water and sanitation infrastructures have had catastrophic effects on public health, certainly causing a significant number of indirect deaths.

Prominent public health reports have projected terrifying scenarios when it comes to deaths caused by the spread of infectious diseases in Gaza. According to a London School of Hygiene and Johns Hopkins University study , thousands of Palestinians may have died in the last six months due to infectious diseases.

Israel’s narrative to justify these deaths is that they are the result of a tragic humanitarian crisis provoked by Palestinians. But they were not unintended, as more honest statements of Israeli officials have revealed.

In November 2023, former head of Israel’s National Security Council Giora Eiland and current adviser to Defence Minister Yoav Gallant wrote on Yedioth Aharonoth that “the international community warns us of a humanitarian disaster in Gaza and of severe epidemics. We must not shy away from this, as difficult as that may be”, adding that “after all, severe epidemics in the south of the Gaza Strip will bring victory closer and reduce casualties among army soldiers”.

Netanyahu’s finance minister, Bezalel Smotrich, tweeted that he agreed with “every word” written by Eiland in his column. In other words, infectious diseases are among the genocide-by-attrition tools considered by the Israeli leadership.

This is not a completely new story. Israel has already subjected Palestinians to systematic policies of slow death and disablement, with the highest peaks during the two Intifadas. But since October 7, these policies have reached an unprecedented level and they meet two key standards of the Genocide Convention.

First, by obliterating the healthcare sector and obstructing the distribution of healthcare supplies and services, Israel is ensuring that Palestinians in Gaza face serious bodily and mental harm.

Second, by destroying almost entirely the water and sewage system and creating a debilitating environment, the Israeli military has inflicted on Gaza Palestinians conditions of life calculated to bring about its physical destruction in whole or in part.

This is how Israel pursues attrition genocide in Gaza.

The views expressed in this article are the author’s own and do not necessarily reflect Al Jazeera’s editorial stance.