CNS Infections "Bugs and Brains" Dr Tahseen Siddiqui-CME 2025"

Tahseen J. Siddiqui, M.D
Infectious Disease Consultant
Medical Director, Infection Control & Prevention
Humboldt Park Health
Sept’2025
Central Nervous System (CNS) Infections
Types, Causes, Diagnosis, Management & Emerging Challenges

By the end of this session, participants will be able to:
Classify major types of CNS infections
Recognize clinical features, caveats and complications
Interpret key diagnostic tests
Initiate evidence-based treatment
Identify management strategies
Review recent advances and guidelines

1) In CNS infections, rapid diagnosis and prompt treatment are critical
In reducing the risk of mortality and long-term disability
TRUE FALSE
2) Classic clinical triad (fever, headache, and nuchal rigidity)
is almost always present at the onset
TRUE FALSE
3) Strep Pneumo and N.meningitides account for 80% of all adult cases of
community-acquired meningitis
TRUE FALSE
4) Following penetrating trauma and neurosurgical procedures/VPS, Coag neg
staph epi and Staph aureus are usually represent contamination of specimen
TRUE FALSE

 CNS Infections, involve the brain and spinal cord
 Potentially life-threatening and may cause high morbidity
including severe neurological damage and death if not
diagnosed and treated promptly.

• By Pathogen:
• Bacterial
• Streptococcus pneumoniae, Neisseria meningitidis, Listeria
monocytogenes
• Tuberculous meningitis presents with a subacute onset
• Primarily involves the basal meninges
• CSF analysis shows elevated protein, decreased glucose, and
lymphocytic pleocytosis
• Typically requires prolonged RIPE therapy combined with steroids
• Viral
• Herpes Simplex Virus (most prevalent in developed countries)
• Enteroviruses, West Nile Virus
• Fungal
• Cryptococcus neoformans, Candida species
• Parasitic
• Toxoplasma gondii, Naegleria fowleri
• Prion Diseases (rare)
• Classified by Anatomical Location:
• Meningitis – affecting the meninges,
typically bacterial in origin
• Encephalitis – involving the brain
parenchyma, primarily viral causes
• Myelitis – targeting the spinal cord
• Abscess – a localized brain infection:
• * Frequently polymicrobial
• * Can result from contiguous spread
(e.g., sinusitis, otitis) or
hematogenous dissemination (e.g.,
endocarditis)

 Streptococcus pneumoniae (58%)
 Group B Streptococci (18%)
 Neisseria meningitis (13.9%)
 Listeria monocytogenes (3.4%) (malignancy)
 Haemophilus influenzae (6.7%)
 M. tuberculosis, Travel Hx, HIV- Immunosuppressants,
alcoholics
 T. pallidum, B. burgdorferi,
 Leptospira (through exposure to animal/rodent's
fluids or infected water)
 Brucella (through exposure to cattle or
unpasteurized milk) rare in USA
 Nocardia asteroides (found in the soil; can cause
infection in immunocompromised
 **Strep Pneumo and N.meningitides account for
80% of all adult cases

 In Children/young adults (2-29y)
 N. meningitides (60%) Strep pneumo (27%), GBS (5%), H.
Influenzae (5%), Listeria (2%)
 In Adults (30-59y)
 Strep pneumo (61%), N. Meningitidis (18%), H. Influenzae
(12%), Listeria (2%)
 In adults >60y
 Strep pneumo (61%), N. meningitidis (18%), H.influ (12%) and
Listeria (12%), GBS (3%)

 Penetrating trauma and neurosurgical procedures/VPS
 Coag neg staph epi and Staph aureus (most common)
 Gram neg enterobacteria (E.coli, Enterobacter, Citrobacter, A. baum)
 Pseudomonas spp.
 Cutibacterium acnes ( shunts) present within 4 weeks post op
 Tx with empiric iv vanco and cefepime or merupenem
(aztreonam or cipro if PCN allergy) 10-14 days with source
control
 Basilar skull Fracture (S. pneumoniae, H. influenzae & group A
beta hemolytic streptococci (Vanco/rocephin)

Neisseria meningitidis meningitis
Slide 1. Streptococcus pneumoniae meningitis
Most common cause of meningitis in adults
>20 years of age
• Risk factors include • coexisting acute or
chronic pneumococcal sinusitis or otitis media
or pneumonia • alcoholism, diabetes •
splenectomy, hypogammaglobulinemia,
complement deficiency, and • head trauma with
basilar skull fracture and CSF rhinorrhea
Second most common cause of acute
bacterial meningitis
Up to 60% of cases in children and young
adults between the ages of 2 and 20
Petechial or purpuric skin lesions can provide
an important clue

Haemophilus influenzae meningitis
The CSF reveals a high concentration
of neutrophils containing gram-
negative coccobacilli, primarily found
inside the cytoplasm of the white blood
cells.
Listeria monocytogenes Meningitis
This CSF shows a small number of
neutrophils along with two slender gram-
positive bacilli. While Gram stains of
cerebrospinal fluid are positive in
approximately 80% of bacterial meningitis
cases overall, organisms are identified in
only about 40% of Listeria meningitis
cases. Furthermore, even when bacteria are
present, their numbers may be minimal and
difficult to observe.

S aureus and coagulase-
negative staphylococci
 Following invasive
neurosurgical procedures,
particularly shunting
procedures for hydrocephalus
L. monocytogenes
 Important cause of meningitis
in neonates (<1 month of age),
pregnant women, individuals
>60 years, and
immunocompromised
individuals

 Classic clinical triad (fever, headache, and nuchal rigidity)
 Altered mental status- occurs in >75%
 Nausea, vomiting, and photophobia
 Seizures - initial presentation or during the illness
 Raised ICP • Headache, vomiting, blurring of vision, ataxia • Decreased level
of consciousness • Papilledema • Dilated poorly reactive pupils • Sixth nerve
palsy • Decerebrate posturing • Cushing reflex (bradycardia, hypertension,
and irregular respirations) • Cerebral herniation
 Kernig's and Brudzinski’s signs
 Extracranial infection (eg, sinusitis, otitis media, mastoiditis, pneumonia) may
be noted.
 Arthritis is seen with N meningitidis,
 Rash. Petechiae and cutaneous hemorrhages are seen classically with N
meningitidis; (can occur with other bacterial and viral infections)
 Endotoxic shock with vascular collapse is characteristic of severe N
meningitidis infection.

 Blood cultures • Fundus examination • CT, MRI • CSF examination via
Lumbar puncture
 Lumbar Puncture (if no signs of raised ICP) Fundus examination • CT,
MRI
 Opening pressure-correlates with increased risk of morbidity and
mortality in bacterial and fungal meningitis
 Take tube #1 to chemistry lab for glucose and protein.
 Take tube #2 to hematology lab for cell count with differential.
 Take tube #3 to microbiology and immunology lab for Gram stain,
bacterial culture, acid-fast bacillus (AFB) stain and tuberculosis (TB)
cultures, India ink stain and fungal cultures, CIE, VDRL, and
cryptococcal antigen, if indicated.
 Hold tube #4 for repeat cell count with differential, if needed
 Serology/PCR for viruses

 Blood cultures (prior to antibiotics)
 CBC with differential
 Serum electrolytes and liver profile (dehydration or SIADH, to
assess organ functioning and adjust antibiotic dosing)
 Serum glucose as baseline for determining normal CSF glucose;
 Coagulation profile and (require platelets or FFP prior to LP.)
 CSF GS/CX (Cult- pos 60-90%) but 10-20% if prior abx
 Serum/CSF- VDRL/cryptococcal antigen/WNV serolgy
 CSF PCR viral (Enterovirus/HSV)
 CSF Latex agglutination or counter immunoelectrophoresis (CIE)
on CSF for specific bacterial antigens (partially treated meningitis)
Early detection (~24-48h)

Opening Pressure.
AIDS patients with crypto meningitis have increased risk of blindness, death unless
open pressure maintained at <30 cm
Pyogenic meningitis- strong predictors ( WBC>2000/PMN 1200/GLU <34/ Prot >220)
CSF Lactate – better then WBC in diff b/w bacterial vs viral etio (viral <2 mmol/L)

•Prior antibiotics may cause gram-positive organisms to appear gram negative and decrease
culture yield on average 20%.
•In Bacterial Meningitis : Lymphocytosis with normal CSF chemistries seen in 15-25%,
especially when cell counts <1000 or if partially treated.
•In Viral meningitis: PMN pleocytosis may be indistinguishable from early bacterial
meningitis- Up to 48 hours,
After 8-12 hours, reexamine the CSF. If initial granulocytosis changes to mononuclear
predominance, CSF glucose remains normal, and patient continues to look well, the infection is
most likely nonbacterial.
•Nontraumatic RBCs in 80% of HSV, although 10% have normal CSF results
•~90% of patients with VP shunts have CSF WBC count >100 cells/mm3 are infected; CSF
glucose usually normal, and organisms are less pathogenic (Staph epi, Propionibacterium acnes,
and diphtheroids) and S aureus, coliforms
lowest levels of CSF glucose are seen in TB, primary amebic meningoencephalitis,
neurocysticercosis
•An aseptic profile - bacterial (eg, Mycoplasma, Listeria, Leptospira species, Borrelia burgdorferi
[Lyme], spirochetes), partially treated bacterial , HSV and arboviruses
•TB meningitis and parasites resemble the fungal profile more closely.

 Obtain blood cultures and initiate treatment before imaging
studies and LP in patients with suspected bacterial meningitis
 Head CT scan (contrast) or MRI (gadolinium)
 In patients with evidence of head trauma, immunosuppression,
altered mental status, or focal findings.
 Presence of papilledema and inability to fully assess fundi or
neurologic status are indications for CT scan prior to LP.
 .
 Results may be normal or demonstrate small ventricles,
effacement of sulci, and contrast enhancement over
convexities.
 Late findings include venous infarction and communicating
hydrocephalus.
 Rule out brain abscess, sinus or mastoid infection, skull
fracture, and congenital anomalies.
 Chest radiography- 50% of patients with pneumococcal
meningitis also have evidence of pneumonia
Non Contrast CT- mild ventriculomegaly
and sulcal effacement.
contrast-enhanced, axial T1-
weighted magnetic resonance
image shows leptomeningeal
enhancement

AGE CAUSATIVE ORGANISM TREATMENT
<1 MONTH GBS, E.COLI/GNRs, listeria Ampicillin + cefotaxime or
Amp plus gentamicin
1-3 months Pneumococci, meningococci, H influenzae Vancomycin IV + ceftriaxone
or cefotaxime
3 months-
adulthood
Pneumococci, meningococci, H influ. Vancomycin IV +ceftriaxone
or cefotaxime
>50
yrs/alcoholis
m/ chronic
illness
Pneumococci, aerobic gram – bacilli, listeria,
meningococci
Ampicillin + vancomycin+
cefotaxime or ceftriaxone
+/- Rifampin

 Adult doses: ceftriaxone (2 g IV q12h) vancomycin (loading
20-25mg/kg then 15-20 mg/kg IV q 8-12h Ampicillin 50-100
mg/kg IV q6h
 Suspected/confirm HSV – Acyclovir 10 mh/kg q8h x 21 days
 Chloramphenicol (PCN allergic) 50-100 mg/kg/d PO/IV
divided q6h
 Dexamethasone- 10 mg q 6h about 15-20 prior to or
simultaneously with 1st
dose of abx for suspected
pneumococcal/Hemophilus meningitis, TB meningitis, raised
ICP
 PCN/cephalosporin allergy- Chloramphenicol plus vanco +/-
Rifampin
 (Alt- aztreonam/cefepime/levo-cipro)

• Meningococal meningitis/ H. flu needs droplet/contact isolation and PEP
• close contact with a patient suspected of N. meningitidis infection for at least 4 hours
during the week prior to symptom onset (such as household members, healthcare,
daycare attendees, or cellmates), or those exposed to the patient’s nasopharyngeal
secretions (e.g., through kissing, mouth-to-mouth resuscitation, intubation, or
nasotracheal suctioning) are considered at risk.
• Ciprofloxacin -single oral dose of 500 mg (>16y) or
• Ceftriaxone 250 mg IM x1 adults ( child <16y 125 mg IMx1
• Rifampin (adults or >12y) 600 mg orally twice daily, typically for a total of four
doses, children under 1 month receive 5 mg/kg every 12 hours, children over 1
month receive 10 mg/kg every 12 hours;
• Meningococcal vaccination is advised primarily during confirmed outbreaks or
for travelers visiting regions experiencing epidemics/asplenia
• H.Influenza (Hib) in infants

 CSF lympho-pleocytosis and normal CSF glucose, negative
bacteria on Gram stain), is the most common CNS infection
 Most common microorganisms are enteroviruses (primarily
cause infection in the summer and early fall, account for up to
80% of all cases), human herpesvirus-2 (HHV-2), lymphocytic
choriomeningitis virus (LCM), HIV, and other viruses.
 Aseptic meningitis can also follow infection with Borrelia
burgdorferi, the causative agent of Lyme disease, and
neurosyphilis etc plus drug-induced (NSAIDs, metronidazole,
IVIG), autoimmune dis, cancer etc

• Caused by Treponema pallidum during the primary or secondary stages
of infection.
• Affects both immunocompetent and immunocompromised individuals,
particularly those with HIV/AIDS.
• Develops within months after inoculation but is often asymptomatic.
• Fever is frequently absent; however, symptoms such as headache and
confusion may be present.
• Typical cerebrospinal fluid (CSF) analysis reveals an aseptic profile
with lymphocytosis, elevated protein levels, normal glucose, and
positive serologic tests for syphilis, including CSF VDRL and FTA-Abs.
• Treatment involves aggressive administration of Penicillin G at 24
million units per day intravenously for 14 days.
• For patients allergic to penicillin, desensitization protocols are
recommended.
• Initiation of penicillin G may trigger the release of endotoxins, causing a
skin rash and an inflammatory response known as the Jarisch-
Herxheimer reaction.

• Caused by Borrelia burgdorferi during the second stage of
infection
• Results from exposure to an ixodid tick
• Symptoms appear after the characteristic Lyme disease rash
has subsided
• Peripheral and cranial neuropathies are observed in
approximately 71% of affected individuals
• Cerebrospinal fluid (CSF) analysis reveals an aseptic pattern
with lymphocytosis, elevated protein, normal glucose levels,
and positive serologic tests for B. burgdorferi
• Recommended treatment consists of ceftriaxone 2 g/day IV or
penicillin G 20 million units/day IV for 10 to 14 days
• Doxycycline 100 mg/day IV serves as an alternative for
patients with allergies to penicillins or cephalosporins
• Clinical symptoms generally show gradual improvement over a
span of weeks to months

 Enteroviruses
(Poliovirus/Echovirus/
Coxsackievirus A/B)
 Paramyxovirus
(Mumps/Measles virus)
 Herpesvirus (HSV-1 and HSV
2/Varicella-zoster
virus/EBV/CMV/HHV*-6 HHV-7
 West Nile Virus
 HIV
 Rabies virus
 LCM virus (Lymphocytic
choriomeningitis)
Morbilliform
rash with
pharyngitis
and
adenopathy
may suggest a
viral etiology
(eg, Epstein-
Barr virus
[EBV],
cytomegalovir
us [CMV],
adenovirus,
HIV).
HIV encephalitis
HIV encephalitis.
Plain CT scan. Bilateral and
symmetric diffuse
hypodensity in the
periventricular white matter
without any mass effect

 HIV-associated meningitis develops within days to weeks after
acute HIV infection.
 It appears as a mononucleosis-like illness and is rarely
associated with encephalitis. Tx with HAART
 Varicella zoster virus (VZV), or HHV-3, and CMV are causes of
meningitis in immunocompromised hosts, especially patients
with AIDS and transplant recipients.

 Mostly HSV-1
 HSV-2 Less freq/ may precede by genital herpes 5-7 days but not often- Recurrent
pattern
 Mortality 70% without Tx
 Symptoms include headache and fever for up to 5 days, followed by personality and
behavioral changes
 Early onset seizures/ localizing signs (temporal lobe), partial paralysis, hallucinations,
and altered levels of consciousness
 CSF- Aseptic profile
 CSF-HSV PCR (Gold standard) (sen 98%/Spec 94%)- if neg/high index of susp- rept LP
in 3-7 days
 CSF viral cult- insensitive
 MRI- early Nl- later tempral lobe necrosis (edema/shift- poor prog)
 Tx with acyclovir 10 mh/kg iv q 8h x 10-14 days (Can change to oral valacyclovir 1g q
8h if improvement- limited data)
 Rapid initiation of acyclovir therapy is crucial to reduce mortality and morbidity risks
 Steroids only reduce cerebral edema in patients with severe HSE.

MRI of the brain is the preferred imaging
study. Abnormalities are found in 90% of
patients with HSE; MRI may be normal early
in the course of illness.
Findings of localized temporal abnormalities
are highly suggestive of HSE, but
confirmation of the diagnosis depends on the
identification of HSV by means of PCR or
brain biopsy.
Head CT may show changes in the temporal
and/or frontal lobe, but CT is less sensitive
than MRI.
Approximately one third of patients with HSE
have normal CT findings on presentation.
Electroencephalography
Electroencephalography (EEG) shows focal
abnormalities, such as spike and slow- or
periodic sharp-wave patterns over the
involved temporal lobes.
EEG is 84% sensitive to abnormal patterns in
HSE but lacks specificity (32%)
Axial gadolinium-enhanced T1-
weighted image reveals
enhancement of the right anterior
temporal lobe and parahippocampal
gyrus. At the right anterior temporal
tip is a hypointense, crescentic
region surrounded by enhancement
consistent with a small epidural
abscess.

 Immunosuppressed (Transplant/AIDS-CD4 <50))
 Cytomegaloviral (CMV) infection usually presents
as an encephalo-ventriculitis with possible
meningeal involvement.
 Tx with Ganciclovir 5,g/kg iv qd
 Valganciclovir 900 mg po qd
Proton density-weighted (SE, 2700/30) axial
and coronal images disclose hyperintensity
surrounding the frontal horns and trigones of
the lateral ventricles and also involving the
splenium of the corpus callosum (arrows).

Arboviruses are the most common causes of episodic
encephalitis with
The 2 most common arboviruses
1) St Louis encephalitis, found throughout the United States but
principally in urban areas around the Mississippi River
(1) Geographically misnamed California virus (in particular,
the strain that causes LaCross encephalitis [LAC]), which
affects children in rural areas in states of the northern
Midwest and East.
Among the other arboviruses causing encephalitis, the
deadliest and, fortunately, most uncommon, Eastern equine
encephalitis (EEE), is encountered in New England and
surrounding areas; the milder Western equine encephalitis
(WEE) is most common in rural communities west of the
Mississippi River.

 May be asymptomatic
 West Nile fever [WNF], febrile illnesses (non-localized,
self-limited illnesses with headache, myalgias,
arthralgias, skin rash or lymphadenopathy
 Meningitis: fever, headache, stiff neck, and pleocytosis
in CSF
 Myelitis: fever and acute bulbar or limb paresis or
flaccid paralysis
 Encephalitis: fever, headache, and AMS-confusion to
coma
 cranial and peripheral neuritis or other neuropathies,
including Guillain-Barré syndrome.
WNV: between the months of July and September.
incubation period ranges from three to 14 days.

Laboratory criteria for diagnosis
Four-fold or greater change in virus-specific serum antibody
titer, OR Isolation of virus, viral antigen or genomic sequences
in tissue, blood, CSF, or other body fluid, OR
Virus-specific immunoglobulin M (IgM) antibodies
demonstrated in CSF by antibody capture enzyme immunoassay
(EIA)
No specific treatment is available.
In severe cases treatment consists of supportive care

Rodent-borne (common house mouse) viral (Arenaviridae-LCMV ) meningoencephalitis.
Infections from pet rodents(mice, hamsters, or guinea pig) fresh urine, droppings, saliva, or nesting
materials.
Vertical transmission (Pregnancy)-congenital hydrocephalus, chorioretinitis, and mental retardation.
Transmission -directly introduced into broken skin, the nose, the eyes, or the mouth, or presumably,
via the bite of an infected rodent, organ transplantation
Onset of symptoms usually occurs 8-13 days after exposure
 A characteristic biphasic febrile illness then follows.
 The initial phase, which may last as long as a week, fever, malaise, lack of appetite, muscle aches,
headache, nausea, and vomiting. Other symptoms that appear less frequently include sore throat,
cough, joint pain, chest pain, testicular pain, and parotid (salivary gland) pain.
 Following a few days of recovery, the second phase -symptoms of meningitis (for example, fever,
headache, and a stiff neck) or characteristics of encephalitis (for example, drowsiness, confusion,
sensory disturbances, and/or motor abnormalities, such as paralysis).
 LCMV has also been known to cause acute hydrocephalus, which often requires surgical shunting
to relieve increased intracranial pressure.
 Rarely, myelitisand myocarditis
 Diag : Serology/ Viral Cultures/ PCR CSF
 Supportive tx
 Exposure to rodents suggests infection with lymphocytic choriomeningitis (LCM) virus
and Leptospira infection.

 Patients with rabies could present atypically with aseptic
meningitis, and rabies should be suspected in a patient with a
history of animal bite (eg, skunk, raccoon, dog, fox, bat).
 Hallucinations, seizures, personality changes, aphasia, ataxia,
CN deficits,
 CSF-Similar to viral meningitis Opening pressure
↑↑
 1. Wash with soap and water after the exposure
 2. Rabies immunoglobulin (RIG)
 3. Rabies vaccination
 Given at day 0, 3, 7, 14, and 28

• Caused by the JC virus
• Primarily affects immunocompromised
individuals, especially those with AIDS
• Diagnosis:
• MRI reveals periventricular white matter lesions
• Cerebrospinal fluid (CSF) is usually normal PCR testing
for JC virus DNA is utilized
• Treatment:
• No effective therapies currently available
• Both cytarabine and cidofovir have demonstrated no
significant benefit
•Slow virus
infections
•Also implicated
in the measles-
related
subacute
sclerosing
panencephaliti
s (SSPE)

• The most common fungal cause of chronic meningitis is
Cryptococcus neoformans, an encapsulated yeast,
primarily affecting patients with HIV/AIDS.
• Other causative fungi include Coccidioides immitis,
Histoplasma capsulatum, Blastomyces dermatitidis,
Aspergillus fumigatus, Candida albicans, and Sporothrix
schenckii.
• Immunocompromised patients are particularly
susceptible, and clinical presentation varies
depending on the specific fungal pathogen.

Cryptococcal meningitis is the most common opportunistic
infection of the CNS, affecting 5-7% of patients with
AIDS.
Typically manifests with headache, fever, and lethargy, with
additional symptoms such as visual disturbances, cranial
nerve palsies, ataxia, seizures, and cognitive changes.
Diagnosis involves cerebrospinal fluid (CSF) lymphocytic
pleocytosis, Positive Crypto ag/ fungal cultures, and markedly
increased opening pressure during lumbar puncture.
C. neoformans can be identified via India ink staining or
cryptococcal antigen detection, although these may be
negative in capsule-deficient strains.
Treatment consists of Amphotericin B deoxycholate (0.7–1
mg/kg/day) combined with flucytosine (100 mg/kg/day) for 2
weeks, followed by oral fluconazole 400 mg daily for at least
10 weeks. Long-term fluconazole maintenance therapy
(typically 400 mg daily) is recommended for secondary
prophylaxis.

Chronic meningitis include:
Taenia solium (pork tapeworm-Neurocycticercosis, the most
common parasitic infection of the CNS )
Toxoplasma gondii,
Angiostrongylus cantonensis (Rat lungworm),
Acanthamoeba species.
Echinococcus granulosus (Hydated Disease)

NEUROCYSTICERCOSIS
• Caused by the larvae (cysticerci) of the pork tapeworm,Taenia solium
(pork tapeworm)
• The most common parasitic infection of the CNS
• Predominantly found in Latin America, Asia, Africa, and certain regions
of Europe
• May involve subcutaneous tissue, muscle, or the central nervous system
(approximately 50% present with meningitis)
• Can be asymptomatic or chronic meningitis include, though symptoms
such as intense headache, seizures, visual disturbances, and ischemic
cerebrovascular events may occur
• Cerebrospinal fluid (CSF) analysis typically shows elevated protein levels,
normal glucose, and eosinophilia
• Treatment: albendazole 400 mg orally twice daily for 15 days, followed
by 400 mg once daily for another 15 days, along with prednisone 60 mg
orally daily for 3 days

TOXOPLASMA
TOXOPLASMA
ENCEPHALITIS
ENCEPHALITIS
 T. gondii (protozoan parasite)
 Primary/Acute infx-- Ingestion of infective oocysts via consuming
raw/undercooked food contaminated with cat feces or by contaminated
environmental samples (such as fecal-contaminated soil or changing the
litter box of a pet cat) .
 Re-Activation
 Trans placentally from mother to fetus
 Blood transfusion or organ transplantation .
 Diag: Serology Anti-Toxoplasma immunoglobulin detection
 (IgM) antibody response in newly acquired toxoplasmosis or
Toxoplasma encephalitis
 Rising serum (IgG) titers
 Toxoplasma gondii by PCR may facilitate the diagnosis and follow-up of
toxoplasmosis in patients with AIDS (sensitivity of 83.3% and specificity
of 95.7%.)
 CT scan or MRI
 Single or multiple hypodense/r ing-enhancing or hypointense lesions in
white matter and basal ganglia with mass effects may be observed.
 Tx-Most healthy people recover from toxoplasmosis without treatment.
 Persons who are ill can be treated with a combination of drugs such as
pyrimethamine and sulfadiazine, plus folinic acid.
tissue cyst and tachyzoites in the
brain parenchyma
Ring-enhanced lesions in
the right basal ganglia and
the left frontal lobe with a
large mass effect and
peripheral oedema.
ring-enhanced parieto-occipital
lesion with a large mass effect
and peripheral oedema.

• This rare, free-living amoeba is commonly found in warm freshwater
environments such as lakes, rivers, hot springs, and poorly chlorinated
swimming pools.
• It is predominantly present in southern tier states
• The organism enters the body through the nasal passages and migrates to the
brain via the olfactory nerve.
• It causes Primary Amebic Meningoencephalitis (PAM), a rapidly progressing and
severe brain infection.
• Symptoms typically develop within 1 to 12 days after exposure and include
headache, fever, and nausea, which may advance to stiff neck, seizures,
hallucinations, and coma.
• The infection carries a fatality rate exceeding 97%, with only a small number of
survivors documented globally.
• Preventive strategies involve avoiding warm freshwater activities during hot
weather, using nose clips or avoiding submersion of the head, and ensuring
swimming pools are adequately chlorinated.
• Diagnosis through cerebrospinal fluid (CSF) wet mount examination.
• Treatment options include Amphotericin B, Miltefosine, dexa

• Plasmodium falciparum
• Risk factors include living in or traveling to malaria-endemic areas and
being a child under the age of 10.
• The primary diagnostic criteria are: (1) an unresponsive coma lasting over
six hours without localized response to pain following a generalized seizure;
(2) detection of asexual forms of P. falciparum in the bloodstream; and (3)
exclusion of alternative causes of encephalopathy, such as viral or bacterial
infections.
• The histopathological characteristic of this encephalopathy is the
accumulation of parasitized red blood cells (PRBCs) within cerebral
capillaries and venules.
• Treatment consists of intravenous quinine and exchange transfusion when
peripheral parasitemia exceeds 10% of circulating erythrocytes.
• Mortality rates vary from 25% to 50%. Without intervention, cerebral
malaria is fatal within 24 to 72 hours.

 Hydrocephalus
 Seizures
 Hearing loss
 Cognitive deficits
 Stroke (especially in TBM)
 Subdural Empyema & Epidural Abscess

 The most common organisms are streptocooci,
staphylococci and anaerobes
 May develop from:
 Spread from a cranial infection
 Sinusitis
 Dental infection- anaerobes, frontal lobe
 Otitis media, (temporal lobe and cerebellum-
Strep, pseudomonas, haemophilus)
 Head trauma
 Neurosurgery
 Hematogenous spread- MCA

 Symptoms
 Headache, fever, focal/general neuro deficits
 Mass effect, Cerebral edema
 Frontal lobe-hemiparesis
 Temporal lobe-dysphasia
 Cerebellum-ataxia
 Diagnosis
 MRI, CT
 Gram stain and culture by needle aspiration
 NO LP!
 Emergency surgical evacuation of empyema
 3rd generation cephalosporin, vancomycin & metronidazole
(Parenteral)
 Fluid gram stain and culture
 Treatment-Parenteral antibiotics-6-8wks
 Rocephin and Metronidazole
 Trauma-Use cefepime or ceftazidime for pseudomonas and
vancomycin for staphylococci
 Neurosurgical Drainage

 Drug-Induced: (i.e.NSAIDs, bactrim, azathioprine,allupurinol)
 Carcinomatous: metastatic ca/lymphoma)
 Neurosarcoidosis- acute or chronic meningitis, meningeal mass lesions ,
meningitis is usually is caused by opportunistic organisms, (cryptococc)
 CNS vasculitis-SLE/WG/Behcet’s- Chronic meningitis treated with high-
dose corticosteroids and cyclophosphamide

 Molecular diagnostics (e.g., multiplex PCR panels)
 MRI spectroscopy for abscess vs tumor
 New antivirals and antifungal
 smNGS (metagenomic next-generation sequencing)

 Rapid diagnosis and treatment are critical
 High risk of mortality and long-term disability
 CSF analysis is key
 Tailored therapy based on age, immune status, and setting
 Follow current IDSA/CDC guidelines
 Exposure to rodents suggests infection with lymphocytic
choriomeningitis (LCM) virus and Leptospira infection.

CNS Infections "Bugs and Brains" Dr Tahseen Siddiqui-CME 2025"

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