ACUTE NEUROLOGY
Acute neurological
infections
Varun Sethi
Nicholas WS Davies
Abstract
Neuroinfection syndromes cause significant mortality and morbidity.
Clinical syndromes include meningitis, encephalitis, mass lesions
(abscesses), myelitis, radiculitis, neuritis, myositis and neuromus-
cular junction dysfunction. Symptoms can develop rapidly (acute)
or over weeks (subacute) or longer (chronic). Viruses, bacteria,
fungi or protozoa can be causal. Timely diagnosis and initiation of
treatment can reduce morbidity and mortality. This article briefly out-
lines the common acute neuroinfection syndromes. As some patho-
gens are more likely to be encountered in specific geographical
areas, information regarding travel to, and immigration from,
endemic areas must be carefully sought. Furthermore, different pop-
ulations have varied susceptibility to infection because of specific
defects in the host defence as a result of co-morbidities or treatment;
assessment of potential immunosuppression is mandatory in all
those presenting with neuroinfections. For more detailed discussion,
UK-specific guidelines are referenced.
Keywords Brain abscess; encephalitis; human immunodeficiency
virus (HIV); meningitis; meningoencephalitis; tuberculosis
Definition and incidence
Meningitis is an inflammation of the meninges, which can
involve the underlying cortex and spinal cord.1 Bacterial men-
ingitis is seen with an annual incidence of 2e6 per 100,000,
peaking in adolescence and at extremes of age. Viral meningitis
has an incidence of 10e15 per 100,000 per annum. Encephalitis
is an inflammation of the brain parenchyma; the estimated
incidence in England is 2.7e8.6 per annum. Meningo-encephalitis
describes meningitis with alteration in mental status, or en-
cephalitis with concomitant meningeal involvement. A brain
abscess is a focal collection of pus within the brain parenchyma,
and has an incidence of 0.3e0.9 per 100,000. Acute neuromus-
cular weakness can result from involvement of the anterior horn
cells, nerve root, peripheral nerve, neuromuscular junction or
muscle.
Varun Sethi MD PhD is a Locum Consultant in Neurology at the
Department of Neurosciences, Charing Cross Hospital, Imperial
College Healthcare NHS Trust, London, UK. Competing interests:
none declared.
Nicholas WS Davies PhD FRCP is a Consultant Neurologist at the
Department of Neurology, Chelsea and Westminster Hospital and
Department of Neurosciences, Charing Cross Hospital, Imperial
College Healthcare NHS Trust, London, UK. Competing interests:
none declared.
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Key points
C The presentation of acute neurological infections varies
depending on the causative agent, anatomical involvement
and host factors such as age, immune status and co-
morbidities; any recent travel history and patients vaccination
record should also be given due consideration
C Early diagnosis and treatment can help limit morbidity and
mortality
C Modern imaging and laboratory techniques aid diagnosis, but
a strong clinical suspicion of neuroinfection should warrant
initiation of treatment pending definitive results
C Post-infectious autoimmune neurological conditions can mimic
neuroinfections and, in the case of herpes simplex virus en-
cephalitis, be sequelae; these are beyond the scope of this
review
C All patients presenting with neuroinfections should be tested
for HIV; Syphilis is a re-emerging infection and must be sought
in individuals presenting with acute neurological
presentations
Acute meningitis
Acute meningitis presents with headache, neck stiffness, photo-
phobia, fever and altered mental status. Aetiological agents vary
based on host factors (Table 1). Hospital-acquired (nosocomial)
meningitis must be considered as a complication of neurosurgical
intervention. Complications of bacterial meningitis include sei-
zures from cerebritis, hydrocephalus, venous sinus thrombosis,
vasospasm, ischaemic stroke, brain abscess and subdural em-
pyema. Viral meningitis is usually benign and self-limiting, with
minimal sequelae.2
Lumbar puncture and cerebrospinal fluid (CSF) analysis
should be done as soon as clinically possible if there is no
contraindication (Table 2), and treatment for suspected bacterial
meningitis initiated. As per the UK joint specialist guidelines, all
immunocompetent adults with suspected meningitis or menin-
gococcal sepsis should be given intravenous ceftriaxone 2 g every
12 hours or cefotaxime 2 g every 6 hours. Patients aged 60
years and immunocompromised patients should additionally be
given intravenous ampicillin/amoxicillin 2 g every 4 hours. In
immunocompetent adults, dexamethasone (intravenously, 10 mg
every 6 hours) should be given before or up to 12 hours after
initiating antibiotics. If Streptococcus pneumoniae (pneumo-
coccus) is identified as a cause, corticosteroids should be
continued for 4 days. Vancomycin or rifampicin can be added in
patients with history of recent travel to a country with high risk
of pneumococcal resistance to first-line antibiotics; if there is
anaphylaxis to penicillin or cephalosporins, chloramphenicol can
be added.
After initial empirical treatment, choice of appropriate anti-
microbial is guided by Gram stain and polymerase chain reaction
(PCR) results. Fungal meningitis presents as subacute/chronic
1 Ó 2023 Published by Elsevier Ltd.
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Infections associated with specific host defence defects5

Drug/infection Effect on immune system Associated pathogens

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Treatment related
Corticosteroids Inhibition of phagocytes and T-cell function Bacterial, herpes virus, Candida species infections
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Cytotoxic drugs, i.e. methotrexate, Bone marrow suppression Gram-positive and Gram-negative bacteria, Candida species, invasive mould infections
DMP, 5-fluorouracil
Purine analogues, e.g. cladribine Neutropenia, lymphopenia, hypogammaglobulinaemia Encapsulated organisms, Gram-positive and Gram-negative organisms, herpes viruses
(HSV, VZV, CMV), mycobacteria, Candida species, Aspergillus species, Cryptococcus
Azathioprine Inhibition of B and T cell proliferation, decreased antibody Bacterial infections, VZV, CMV, PML, worsening of hepatitis B and C
production, myelosuppression
Ciclosporin, tacrolimus Inhibited production of interleukin-2 and cytokines by CD4 CMV, EBV, PTLD, PML, hepatitis C activation
cells
Mycophenolate Inhibition of B and T cell proliferation, decreased antibody Herpes viruses, hepatitis B and C activation, Candida species, cryptococcus, Aspergillus
production species
Phenytoin Immunoglobulin A deficiency, hypogammaglobulinaemia Bacteria including encapsulated organisms, respiratory viruses, enteroviruses, Giardia
Monoclonal antibodies
C Rituximab B cell depletion Hepatitis B reactivation, PML, possibly increased or severe complications of

ACUTE NEUROLOGY
mycobacterial disease
C Alemtuzumab Rapid but protracted peripheral lymphopenia (B and T cells) Infections caused by HSV, VZV and mycetes, Listeria monocytogenes
C Infliximab TNF inhibitors Reactivation of latent TB; hepatitis B, VZV, CMV infection
2

Related to co-morbidities and co-infections

HIV
C Acute HIV infection Self-limiting aseptic meningitis; rarely an acute encephalitis caused by HIV1/2
C Seroconversion Aseptic meningo-encephalitis, acute disseminated encephalomyelitis, transverse myelitis
or involvement of the peripheral nervous system with polymyositis, brachial neuritis or
cauda equina syndrome
C Early symptomatic phase VZV and peripheral neuropathy presenting during the early symptomatic phase
C With progressive CD4 decline AIDS-defining conditions including HAD, opportunistic infections (CMV, Toxoplasma,
Mycobacterium, Cryptococcus), PML, cerebral lymphoma, HIV cachexia
Diabetes mellitus Defects in humoral and cellular innate immunity Rhino-orbital-cerebral mucormycosis, non-tropical pyomyositis, pyogenic spinal
infections, Listeria meningitis, blastomycosis; infection with West Nile virus, VZV
Specific groups
Neonates Bacterial meningitis is often caused by group B Streptococcus, Listeria monocytogenes,
Escherichia coli (<3 months old) and pneumococcus, meningococcus, Haemophilus
Ó 2023 Published by Elsevier Ltd.

influenza type B (>3 months old)

Elderly individuals Streptococcus pneumoniae, Neisseria meningitidis, Listeria monocytogenes, aerobic
Gram-negative organisms
Pregnant women Bacterial meningitis caused by Listeria monocytogenes

DMP, 1,4-dimethyl pyridine; HAD, HIV-associated dementia; PTLD, post-transplant lymphoproliferative disease; TNF, tumour necrosis factor. For other abbreviations, see text.

Table 1
 ACUTE NEUROLOGY

meningitis but should be considered in the differential diagnosis,

Clear to turbid
especially in immunocompromised individuals.

Neutrophils
Increased

Negative
Elevated

Elevated
elevated
Aseptic

Acute encephalitis

Mildly

Low
Infectious encephalitis typically presents with acute onset of
fever, altered mental status and focal or generalized seizures.
Sporadic viral encephalitis in immunocompetent individuals is

Special tests, e.g. cryptococcal antigen

commonly caused by herpes simplex virus (HSV) type 1

Normal to mild increase, 0.2e0.5

(Figure 1), varicella-zoster virus (VZV) or enteroviruses. Sea-
sonal arthropod-borne encephalitis caused by flaviviruses such
as Japanese encephalitis virus, tick-borne encephalitis virus and

positive for Cryptococcus

West Nile virus depends on the geographical distribution of their
PCR (sensitivity, specificity for HSV >95% if Gram stain negative
vector. Other causes in immunocompromised individuals include
Culture positive
Listeria monocytogenes and cytomegalovirus (CMV).
Low to normal
High/very high

Lymphocytes

Imaging and CSF analysis are the mainstay of diagnosis. In

Clear/cloudy

viral encephalitis the CSF usually shows a lymphocytosis; an

0e1000
Normal
Fungal

initial polymorphonuclear response may be seen in the early

stages. Early (within 48 hours) neuroimaging and CSF exami-
nation may reveal normal findings and negative viral tests.
Repeat testing can be required. Readers are directed to other
sources for detailed guidance.
Normal to mild elevation, 0.5e1.0

In recent years there has been an increasing concern for

arthropod-borne encephalitides. Ticks, mites and mosquitoes act
as vectors leading to infections such as Japanese encephalitis,
Zika virus disease, tick-borne encephalitis, West Nile fever and
checked on day 2e10)

scrub typhus. Changing global ecological patterns are responsible

Normal to mild less
Normal to elevated

for these re-emerging infections and highlight the importance of

an up-to-date travel and vaccination history.
Lymphocytes
‘Gin’ clear

5e1000
Normal

Cerebral and epidural abscess

Viral

A subacute presentation of headache, fever, nausea and vomiting

High to very high, 1.0e1.5

with associated seizures or focal neurological signs should alert

Culture positive 50e80%
Low to very low (<30%)

clinicians to a possible space-occupying lesion (e.g. cerebral

ZiehleNeelsen stain

abscess). Biopsy or abscess drainage for microbiological studies

Elevated but <500

is not always possible. Appropriate imaging findings, clinical

Cloudy/yellow

in up to 80%
Lymphocytes
Tuberculosis

context and blood cultures help to refine the aetiological diag-

Increased

nosis. Risk factors include spread from local infection sites

Elevated
CSF findings in various central nervous system infections

positive

(sinusitis, otitis media), which often causes solitary abscesses,

and haematogenous spread from distant sites in patients with
endocarditis, etc (often multiple abscesses, at the greyewhite
Culture positive <80%
Blood culture positive

junction or vascular border zones). Complications of neurosur-

Gram stain positive

gical intervention, traumatic injury and other co-morbidities (see

Table 1) also predispose.
Turbid, cloudy

Low (<40%)
100e50,000

Lymphocytes Neutrophils

Common causes of pyogenic abscesses include Streptococcus

<60% PCR
Increased
Bacterial

Elevated

species, Haemophilus species, anaerobic organisms and Staphy-

<90%

lococcus aureus. In cases of penetrating trauma or neurosurgical

>1

complications, infection is caused by Staphylococcus species,

Streptococcus species, Enterobacteriaceae, Pseudomonas aerugi-
10e20 cm

50e66%

nosa and anaerobic organisms. An appropriate dose and duration

Normal

<0.45
Clear

of antimicrobial therapy (based on presumed aetiology or cul-

0e5
Nil

Nil

ture) must be given, in addition to eradication of the infection

source and anti-seizure medication if indicated. Surgical inter-
CSF/plasma glucose
White blood cells

vention can be required to drain abscesses associated with a

White blood cell
Red blood cells

Protein (g/litre)

mass effect or oedema. Corticosteroids can be used preopera-

CSF analysis

(cells/mm3)

tively to manage vasogenic oedema but prolonged use is

Pressure

avoided.
Others
Colour

types

Table 2

The triad of fever, back pain and neurological deficits should

highlight the possibility of a spinal epidural abscess (Figure 2),

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 ACUTE NEUROLOGY

Figure 1 Scans from a 67-year-old man with HSV encephalitis admitted after a seizure with a prodrome of a sore throat and memory impairment.
Magnetic resonance imaging on D3 shows an asymmetrical cortical and subcortical signal abnormality in the left more than right anteromedial
temporal lobe, amygdala, hippocampus and insula (chevrons) (a). Patchy restricted diffusion is noted as bright on diffusion-weighted imaging (b;
solid arrows), with hypointensity on apparent diffusion coefficient imaging (c; solid arrows) and lack of enhancement (d; open arrow).

increasingly seen in the context of spinal procedures, and intra-
venous drug use e a prolonged course of appropriate antibiotics
with surgical drainage is required. Co-infection with blood-borne
viruses such as HIV can further complicate the presentation and
result in very rapid progression of the infectious process.
Acute neuromuscular weakness
Rapid onset of weakness progressing within days can be caused
by acute infection although is better recognized as a post-
infectious condition in GuillaineBarre syndrome. The clinical
syndrome depends on the site of involvement and can involve
the bulbar and respiratory muscles. Although the preceding
infection noted in GuillaineBarre syndrome is Campylobacter
jejuni (up to 50% cases), other infectious agents associated
include CMV, EpsteineBarr Virus (EBV), influenza A, Myco-
plasma pneumoniae, Haemophilus influenza, HIV at serocon-
version, and hepatitis E, Zika, Japanese encephalitis,
chikungunya and severe acute respiratory syndrome coronavirus
2 viruses.
Other infectious causes of peripheral neuropathy/poly-
radiculopathy include infection with Corynebacterium diphther-
iae, Borrelia burgdorferi (Lyme disease) and Mycobacterium
leprae. Bilateral cranial nerve abnormalities with descending
weakness are seen in botulism. Clostridium tetani skin infection
can cause tetanus.
Inflammation of the spinal cord limited to the anterior horn
cells can present with a flaccid paresis syndrome caused classi-
cally by poliomyelitis viruses, but also by flaviviruses. HSV and
VZV can cause transverse myelitis. Infectious myositis can be
seen with dengue haemorrhagic fever and enterovirus infections.
Tuberculosis (TB) neuroinfection
Central nervous system (CNS) infection with Mycobacterium
tuberculosis can cause tubercular meningitis (TBM), tuber-
culoma, tubercular abscess, and spinal involvement with a pre-
dilection for involving the bones with TB spondylitis. TBM can
present similarly to bacterial/viral meningitis but typically is
more subacute. Because of the predilection for the basilar

Figure 2 Epidural abscess caused by methicillin-sensitive Staphylococcus aureus in a 28-year-old woman who presented with a week of shoulder
pain, progressing to weakness of the arms and legs. She needed catheterization on presentation. Magnetic resonance imaging of the cervico-
thoracic spine shows an extensive anterior and posterior epidural collection with subdural extension throughout the imaged spine on T2-weighted
(T2w) images (a; arrow), with T1 post-contrast enhancement (b; arrows).

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 ACUTE NEUROLOGY
meninges and cisterns, VIth, VIIth and IInd cranial nerve
involvement is often seen, as is the most common complication
of TBM e stroke.
The diagnosis and treatment of CNS TB should follow the
British Infection Association guidelines protocol. The recom-
mended treatment regimen for CNS TB caused by fully sensitive
M. tuberculosis is usually isoniazid, rifampicin, pyrazinamide
and ethambutol for 2 months, followed by rifampicin and
isoniazid alone for a further 10 months. All immunocompetent
patients with TBM should be given adjunctive corticosteroids
(dexamethasone 0.4 mg/kg per day reducing over 6e8 weeks).
Hydrocephalus, tuberculous cerebral abscess and vertebral TB
with paraparesis are indications for neurosurgical referral.
In patients with HIV infection, the British HIV Association
(bhiva.org) recommends the same antitubercular regimen. The
timing of the start of antiretroviral treatment involves balancing
risks of drug interactions (hiv-druginteractions.org), immune
reconstitution disease and opportunistic infections. For patients
with CD4 counts >100 cells/microlitre, initiation of antiretroviral
treatment may be delayed. Adjunctive corticosteroids are advised
for those with TBM and treated HIV infection.
HIV
In acute primary HIV infection (seroconversion), self-limiting
aseptic meningitis and rarely meningoencephalitis can occur. In
the period of chronic latent infection, recurrent VZV infection
(shingles) may be seen. HIV patients with CD4 counts <200
cells/microlitre are profoundly immunocompromised and are at
increased risk of HIV neuropathy and AIDS-defining illnesses
such as HIV-associated dementia; there is also greater risk of
opportunistic neuroinfections including space-occupying lesions
caused by Toxoplasmosis gondii, EBV-driven primary CNS lym-
phoma, progressive multifocal leukoencephalopathy (PML) and
Cryptococcus neoformans meningitis.
In the post-highly active antiretroviral therapy era, immune
reconstitution inflammatory syndrome must also be in the dif-
ferential diagnosis if clinical deterioration is noted after starting
treatment. This is a paradoxical worsening of clinical status
resulting from recovery of the immune response after therapy (or
removal of immunosuppression). This can be with (or without)
opportunistic infections, which if present can be noted simulta-
neously or after a delay.3
Syphilis
In the current era of pre-exposure prophylaxis for HIV behaviour
has changed and rates of Treponema pallidum infection are
increasing. Although tertiary syphilis with presentations such as
tabes dorsalis and generalized paresis of the insane are now
extremely rare, other forms of neurosyphilis are seen. Pre-
sentations are protean, so in addition to HIV, syphilis serology
should routinely be tested in any person presenting with a sus-
pected acute neurological infection.4
Neurological involvement can occur across all stages of
syphilis, including primary, secondary, early latent (early) and
late latent and tertiary (late) syphilis. Presentations include
meningitis, meningovascular syphilis presenting as stroke,
ocular syphilis (papillitis, optic neuritis, uveitis) and otic syph-
ilis. Gummatous syphilis can present as space-occupying lesions
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in the brain parenchyma causing seizures, focal neurological
deficits, increased intracranial pressure and progressive paresis.
Diagnostic tests depend on the disease stage. Direct detection
methods such as dark-field microscopy, fluorescent antibody
staining, immunohistochemistry and PCR can be used for in-
dividuals presenting with a primary chancre. Serodiagnostic tests
have become the mainstay of diagnosing syphilis, including in
asymptomatic patients:
 Non-treponemal tests (NTTs) measure immunoglobulin
(Ig) G and IgM in response to the lipidal material released
from dying cells. Commonly used NTTs include the rapid
plasma reagin (RPR) and Venereal Disease Research Labo-
ratory (VDRL) tests. These do not become positive until
about 15 days after infection, and are helpful in diagnosing
active syphilis. When interpreting these results it is impor-
tant to know if the patient has previously been diagnosed
with syphilis and if treatment for this was completed.
 Treponemal tests include the treponemal enzyme immu-
noassay (EIA) or treponemal chemiluminescent assay,
fluorescent treponemal antibody absorbed test, micro-
haemagglutination assay for antibodies to T. pallidum, T.
pallidum passive particle agglutination (TPPA) and T.
pallidum haemagglutination (TPHA) assays, and T. pal-
lidum immunoblot. These tests detect antibodies to T.
pallidum proteins and can be positive 6e14 days after a
primary ulcer appears; they thus help in diagnosing early
syphilis missed by NTTs. However, these tests remain
positive through life.
 T. pallidum-specific IgM antibody tests are the anti-
treponemal IgM EIA and immunoblot.
The British Association of Sexual Health guidelines on syphilis
suggest that an EIA/chemiluminescent assay, preferably detect-
ing both IgM and IgG, is the screening test of choice. A positive
screening test should be confirmed with a different treponemal
test using a second specimen. For monitoring the response to
treatment, a quantitative RPR or VDRL test should be used. It
must be remembered that serological tests can be falsely positive
in autoimmune disease, in older age or after intravenous drug
use, or falsely negative in the first 3 weeks after a chancre de-
velops, and in secondary or latent syphilis because of the pro-
zone phenomenon, especially in HIV-positive individuals. IgM is
negative in late syphilis.
A limitation of all syphilis serological tests is their inability to
distinguish between infection with T. pallidum subspecies pal-
lidum and the T. pallidum subspecies that cause (non-venereal)
yaws, pinta or bejel. Positive screening tests must be confirmed
with a different treponema test. A quantitative RPR/VDRL test is
recommended for ascertaining the response to treatment.
CSF must be examined in patients presenting with neuro-
syphilis to look for pleocytosis and undertake a CSF RPR. The
interpretation and cut-offs of these results are also influenced by
HIV status. Lumbar puncture should be done in all individuals
with syphilis who have: (1) neurological signs, (2) ocular
involvement, or (3) a CD4 count <350 cells/mm3, and (4) in HIV-
positive patients who are antiretroviral naive with an RPR >1:32.
Neurosyphilis is suggested by a positive CSF test (VDRL, RPR,
TPHA, TPPA, PCR) or CSF pleocytosis >20 cells/mm3 if the pa-
tient is antiretroviral naive, or >10 cells if the person is on an-
tiretroviral treatment.
5 Ó 2023 Published by Elsevier Ltd.
 ACUTE NEUROLOGY
Neurosyphilis treatment regimens include: (1) procaine
penicillin 2.4 MU intramuscularly plus probenecid 500 mg orally
four times daily for 10e14 days; (2) benzylpenicillin 10.8e14.4 g
daily given as 1.8e2.4 g intravenously every 4 hours for 10
e14 days; (3) doxycycline 200 mg orally twice daily for 28 days;
(4) amoxicillin 2 g orally three times daily plus probenecid
500 mg orally four times daily for 28 days; and (5) ceftriaxone 2 g
intramuscularly or intravenously once daily for 10e14 days.
After treatment the RPR and sometimes the CSF analysis should
be repeated to ensure complete treatment of infection.4
Patient groups warranting special attention
Children, pregnant women and elderly people
Changes in immune response and physiology makes these sub-
groups more vulnerable to infection and rapid deterioration. VZV
reactivation, for instance, is commonly seen in elderly pop-
ulations. It is also important to remain cognisant of decreasing
immunity to infections (e.g. tetanus, diphtheria) in elderly people
after the protection from initial immunization in their youth has
waned away. Co-morbidities such as diabetes mellitus, malig-
nancy or prolonged corticosteroid usage can also facilitate the
dissemination of infections via haematogenous spread from
varied sources, such as a urinary tract infection, skin infection,
dental abscess, pneumonia, etc.
Pharmacologically induced immunosuppression
Medications such as corticosteroids, steroid-sparing agents and
newer monoclonal antibody therapies can influence the host’s
response to infection. For example, rituximab, an anti-CD20
molecule that is now used to treat many antibody-mediated
neurological disorders, causes depletion of B cells and immu-
noglobulin concentrations; it can lead to reactivation of latent
hepatitis B and even JC virus disease (leading to PML). By sup-
pressing both T- and B-cell-mediated immunity, the use of
alemtuzumab has been associated with Listeria infection, which
commonly presents as a rhomboencephalitis.
Low-income societies
Lack of complete vaccination schedules with missed or delayed
boosters, together with limited access to diagnostic tests
(computed tomography, magnetic resonance imaging, serolog-
ical tests, etc) as well as appropriate therapy leads to differences
in the epidemiology of infection in this subgroup. A good history
and understanding of local epidemiology is important to limit
mortality and morbidity caused by neurological emergencies.
Returning travellers
When relevant, a detailed travel history including dates of travel
in the context of considered incubation periods, together with
information regarding immunization records, must be consid-
ered. Botulism, tetanus, Brucella, Borrelia, etc are known to
present with lower motor syndromes; Japanese B encephalitis,
viral haemorrhagic fevers such as Dengue and other viruses
including Zika and hepatitis E must be considered.
Influenza, Dengue fever, etc have a short (<10 day) incuba-
tion period. The incubation period of malaria, hepatitis (A, B, C,
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E), schistosomiasis, TB and brucellosis can be long (>21 days),
and an intermediate incubation period is seen in Q fever, viral
haemorrhagic fevers, malaria and African trypanosomiasis (10
e21 days).
Non- and partially immunized hosts
A large number of diseases are now vaccine preventable,
including hepatitis B, polio, diphtheria and tetanus. However, in
individuals who have not been vaccinated, are partially vacci-
nated, have missed boosters or have conditions where require-
ment for the booster is accelerated (immunosuppression,
immunomodulatory treatment), these aetiologies must be
considered with relevant presentations.
The migration of populations can also influence the local
epidemiology of disease; for example, as noted in parts of Lon-
don, individuals moving from a region in which TB is not
endemic to one where it is may not have been vaccinated as
children with the BCG (Bacillus CalmetteeGuerin) as this may
not be part of the local guidelines. A
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dence of encephalitis in England. Emerg Infect Dis 2013; 19:
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Kneen R, Michael BD, Menson E, et al. Encephalitis Guidelines
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