Medicine chapters
Cerebral toxoplasmosis and brain abscess
Cerebral toxoplasmosis is a reactivated parasitic infection causing multiple ring-enhancing brain lesions in people with advanced HIV; a pyogenic brain abscess is a focal bacterial infection spreading from the ear, sinuses, teeth, blood or trauma.
- Toxoplasma gondii is caught from cat faeces (oocysts), undercooked meat (tissue cysts) or across the placenta; in advanced HIV (CD4 under 100) it reactivates as multiple ring-enhancing lesions, typically in the basal ganglia.
- Toxoplasmosis is treated with pyrimethamine + sulfadiazine + folinic acid; improvement within 2–3 weeks confirms the diagnosis, while a single lesion suggests lymphoma.
- A brain abscess comes from the ear, sinuses, teeth, the blood (lung, heart, cyanotic heart disease) or trauma; it shows a ring-enhancing lesion with restricted diffusion; LP is contraindicated; treat by aspiration and weeks of IV antibiotics.
On this page
Overview
Both conditions present as a space-occupying lesion with infection: headache, fever (not always), focal signs, seizures and raised intracranial pressure, with ring-enhancing lesions on contrast imaging.
- Cerebral toxoplasmosis is the commonest cause of focal brain lesions in advanced HIV.
- Pyogenic brain abscess follows spread of bacteria from a nearby or distant focus.
Other ring-enhancing lesions to consider: tuberculoma (common in Pakistan), neurocysticercosis, glioblastoma, metastases and primary CNS lymphoma.
Part 1: Cerebral toxoplasmosis
The parasite and its life cycle
- Toxoplasma gondii is an obligate intracellular protozoan.
- Definitive host: the cat (sexual cycle in the cat gut). Cats shed oocysts in faeces, which mature in soil.
- Intermediate hosts: humans, sheep, pigs, cattle, rodents and birds, which carry tissue cysts in muscle and brain for life.
Mode of transmission
| Route | How |
|---|---|
| Oocysts in cat faeces | Contaminated soil, unwashed vegetables, cleaning litter trays, gardening |
| Tissue cysts in meat | Undercooked or raw meat (lamb, pork, beef) |
| Transplacental | Primary infection in pregnancy → congenital toxoplasmosis |
| Rare | Organ transplant, blood transfusion, laboratory accident |
It is not spread person to person by ordinary contact.
Clinical pictures
- Immunocompetent: most infections are silent. Some get a glandular-fever-like illness with cervical lymphadenopathy, fever and malaise; rarely hepatitis, myocarditis or chorioretinitis.
- Congenital: chorioretinitis, hydrocephalus, diffuse intracranial calcification, microcephaly, seizures, learning disability. Transmission is commoner late in pregnancy but damage is worse when infection is early.
- Immunocompromised (HIV, transplant): reactivation of latent cysts, usually when the CD4 count is below about 100 cells/mm³, causing cerebral toxoplasmosis (encephalitis and multiple abscesses); also chorioretinitis and pneumonitis.
Cerebral toxoplasmosis in HIV: clinical features
Subacute over days to weeks: headache, fever, confusion, focal signs (hemiparesis, aphasia, ataxia; present in over half), seizures, drowsiness. Movement disorders (hemichorea) point to basal ganglia lesions.
Diagnosis
- Imaging: contrast CT or MRI shows multiple ring-enhancing lesions with surrounding oedema, typically at the basal ganglia and grey-white (corticomedullary) junction. MRI is more sensitive: an apparently single lesion on CT is often one of several on MRI.
- Serology: Toxoplasma IgG is positive in most (it reflects past infection that has reactivated); a negative IgG makes toxoplasmosis unlikely. IgM is usually absent in reactivation. (The Sabin-Feldman dye test is the classic IgG test; rising IgM shows acute infection.)
- Therapeutic test: start treatment; clinical and radiological improvement within about 2–3 weeks is effectively diagnostic.
- Brain biopsy if there is no response, a solitary lesion, or negative serology.
- LP is usually avoided because of mass effect; CSF Toxoplasma PCR is specific but insensitive.
| Feature | Cerebral toxoplasmosis | Primary CNS lymphoma |
|---|---|---|
| Number | Multiple | Often single |
| Site | Basal ganglia, grey-white junction | Periventricular, corpus callosum |
| Toxoplasma IgG | Positive | Positive or negative |
| CSF | - | EBV DNA (PCR) |
| Thallium SPECT / PET | Cold (low uptake) | Hot (high uptake) |
| Response to anti-Toxoplasma drugs | Improves in 2–3 weeks | No improvement |
In HIV, multiple ring-enhancing lesions = toxoplasmosis (treat empirically); a solitary lesion or no response after 2 weeks = think primary CNS lymphoma (biopsy).
Avoid giving steroids before a biopsy unless mass effect is dangerous: they shrink lymphoma and confuse the picture.
In HIV the lesions come from reactivation, so IgM is usually negative. A positive IgG with typical multiple lesions is enough to start treatment; waiting for IgM is wrong.
Management
- First line: pyrimethamine (a 200 mg loading dose followed by 50 mg each day) + sulfadiazine + folinic acid, for at least 6 weeks.
- Folinic acid (not folic acid) protects the marrow from pyrimethamine, a dihydrofolate reductase inhibitor, without blocking its effect on the parasite.
- Sulphonamide allergy: pyrimethamine + clindamycin, or atovaquone; high-dose co-trimoxazole is also used.
- Dexamethasone for significant oedema or mass effect, tapered quickly.
- Anticonvulsants if seizures occur.
- Antiretroviral therapy (ART): start once the patient is stable, about 2 weeks into treatment, to limit immune reconstitution inflammatory syndrome (IRIS).
- Secondary prophylaxis (maintenance): lower-dose pyrimethamine + sulfadiazine (or co-trimoxazole) until the CD4 count recovers on ART.
Prevention
- Primary prophylaxis with co-trimoxazole for HIV patients with CD4 below about 100 who are Toxoplasma IgG positive (the same drug also prevents Pneumocystis pneumonia).
- Avoid undercooked meat, wash vegetables, wear gloves for gardening and litter trays (especially in pregnancy and HIV).
Toxoplasmosis in pregnancy (brief)
- Spiramycin reduces placental transmission when the fetus is not yet infected.
- Pyrimethamine + sulfadiazine + folinic acid if fetal infection is confirmed (amniotic fluid PCR), after the first trimester.
- Infected infants are treated from birth.
Congenital toxoplasmosis triad: Chorioretinitis, Hydrocephalus, Intracranial calcification = "CHI" (diffuse calcification; CMV tends to be periventricular).
Part 2: Brain (cerebral) abscess
Aetiology: sources and organisms
| Source | Usual site of abscess | Usual organisms |
|---|---|---|
| Middle ear / mastoid (chronic otitis media) | Temporal lobe, cerebellum | Streptococci, anaerobes, Gram-negatives (Proteus, Pseudomonas) |
| Frontal / ethmoid sinusitis, dental infection | Frontal lobe | Streptococcus anginosus (milleri) group, anaerobes (Bacteroides) |
| Haematogenous spread: lung abscess, bronchiectasis, empyema, infective endocarditis, abdominal or pelvic sepsis | Multiple, at grey-white junction, middle cerebral artery territory | Mixed; Staph aureus in endocarditis |
| Cyanotic congenital heart disease (right-to-left shunt, e.g. tetralogy of Fallot), pulmonary AV malformations | Often multiple | Streptococci, anaerobes |
| Penetrating head injury, neurosurgery | At the wound | Staphylococcus aureus, Gram-negatives |
| Immunosuppression (HIV, transplant, steroids) | Often multiple | Toxoplasma, Nocardia, fungi (Aspergillus, Candida, Cryptococcus), TB, Listeria |
| No source found | - | In a significant minority |
Streptococcus anginosus (milleri) group and anaerobes are the commonest organisms; infections are often mixed.
A child with cyanotic congenital heart disease (e.g. tetralogy of Fallot) who develops headache, fever and focal signs has a brain abscess until proven otherwise; blood bypasses the lung's filtering through the shunt.
Pathology and stages
Early cerebritis (days, poorly defined inflamed brain) → late cerebritis → capsule formation (a collagen capsule, thinner on the ventricular side, so abscesses tend to rupture into the ventricle, causing ventriculitis with a poor outlook).
Clinical manifestations
It behaves like an expanding mass, often over days to two weeks:
- Headache (the commonest symptom), often worsening.
- Fever (common but often absent; a normal temperature does not exclude an abscess).
- Focal deficits: hemiparesis, aphasia, visual field defect (temporal lobe); ataxia, nystagmus (cerebellum); personality change (frontal lobe).
- Seizures.
- Raised intracranial pressure: vomiting, drowsiness, papilloedema.
- Signs of the source: discharging ear, sinus tenderness, dental sepsis, clubbing and cyanosis, murmur.
Blood tests: leucocytosis, raised ESR and CRP are usual but not invariable; blood cultures.
Radiological findings
- Contrast CT or MRI: a ring-enhancing lesion with a smooth, thin, regular wall and a low-density centre, surrounded by marked vasogenic oedema; mass effect; multiple lesions with haematogenous spread; possible gas.
- Diffusion-weighted MRI: restricted diffusion (bright on DWI, dark on ADC) in the pus. This is the key feature separating an abscess from a necrotic tumour or metastasis, which usually do not restrict.
- In early cerebritis, a poorly defined low-density area with patchy enhancement.
- Look for the source: CT of sinuses and mastoids, chest X-ray, echocardiography.
Ring-enhancing lesions "MAGIC DR": Metastasis, Abscess, Glioblastoma, Infarct (subacute), Contusion, Demyelination, Resolving haematoma (plus toxoplasmosis, tuberculoma, cysticercosis, lymphoma).
Management
- Urgent imaging; involve neurosurgery early.
- Do not perform a lumbar puncture: it risks coning and rarely gives the organism.
- Stereotactic (burr-hole) aspiration of the pus for Gram stain and culture, which also decompresses the lesion; excision for large, multiloculated, superficial, fungal or post-traumatic abscesses, or failure to improve.
- Empirical IV antibiotics with good brain penetration, e.g. ceftriaxone or cefotaxime + metronidazole; add vancomycin (or flucloxacillin) after trauma or surgery or when Staph aureus is likely. Adjust to culture.
- Continue IV antibiotics for several weeks, guided by repeat imaging, then often oral treatment.
- Dexamethasone only for dangerous oedema or mass effect (it may reduce antibiotic penetration and capsule formation).
- Anticonvulsants for seizures.
- Treat the source: mastoidectomy, sinus drainage, dental extraction, endocarditis treatment.
- Small abscesses, multiple abscesses or early cerebritis may be treated with antibiotics alone, with close imaging.
Prognosis
Mortality remains about 25% despite treatment; worse with coma, rupture into the ventricles and delayed diagnosis. Epilepsy is common in survivors; focal deficits may persist.
Related intracranial infections
- Subdural empyema: pus in the subdural space, usually from sinus or ear infection; rapidly progressive fever, headache, seizures and hemiparesis; needs urgent surgical drainage.
- Intracranial epidural abscess: thin layer of pus outside the dura, often from ear or sinus infection; slower, with cranial nerve palsies.
- Tuberculoma: the commonest intracranial mass where TB is common (South Asia); treat with anti-TB drugs (± steroids).
- Neurocysticercosis: pork tapeworm (Taenia solium) cysts with a scolex ("dot in a cyst") and calcification; a major cause of seizures in Pakistan; albendazole with steroids and anticonvulsants.
Expect: how humans catch Toxoplasma (cat faeces, undercooked meat, placenta; cat is the definitive host); multiple ring-enhancing basal ganglia lesions in HIV with CD4 below 100; treatment (pyrimethamine + sulfadiazine + folinic acid) and why folinic acid is added; diagnosis by response to empirical treatment and lymphoma as the differential; co-trimoxazole prophylaxis; congenital toxoplasmosis triad; brain abscess sources (ear → temporal lobe and cerebellum, sinus or teeth → frontal lobe, tetralogy of Fallot, endocarditis), organisms (S. anginosus, anaerobes, Staph after trauma), ring enhancement with restricted diffusion, LP contraindicated, aspiration plus ceftriaxone and metronidazole.
Quick revision
- Toxoplasma: cat is the definitive host; humans infected from oocysts, undercooked meat and transplacentally.
- HIV with CD4 under 100: multiple ring-enhancing lesions (basal ganglia, grey-white junction) = toxoplasmosis.
- Treat with pyrimethamine + sulfadiazine + folinic acid for at least 6 weeks; clindamycin or atovaquone if sulpha-allergic; response in 2–3 weeks confirms.
- Solitary lesion, periventricular, EBV in CSF, hot on thallium SPECT = primary CNS lymphoma.
- Prophylaxis: co-trimoxazole when CD4 under 100 and IgG positive; secondary prophylaxis until immune recovery.
- Brain abscess: ear (temporal, cerebellum), sinus/teeth (frontal), blood (multiple), cyanotic heart disease, trauma (Staph).
- Imaging: thin smooth ring enhancement, oedema, restricted diffusion on DWI.
- No LP; aspirate; ceftriaxone + metronidazole for weeks; treat the source; mortality about 25%, epilepsy common.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
How do people catch toxoplasmosis?
By swallowing oocysts from cat faeces in soil, on vegetables or in litter trays, by eating undercooked meat containing tissue cysts, or, for the fetus, across the placenta.
Why is folinic acid given with pyrimethamine?
Pyrimethamine blocks folate metabolism and can suppress the bone marrow; folinic acid bypasses the blocked step in human cells but is not used by the parasite, so it protects the patient without reducing the drug's effect.
What distinguishes a brain abscess from a tumour on MRI?
An abscess usually has a thin, smooth enhancing rim and shows restricted diffusion of the pus on diffusion-weighted images, whereas necrotic tumours have thicker irregular walls and usually do not restrict.
Why is lumbar puncture contraindicated in brain abscess?
The abscess acts as a mass that raises intracranial pressure, and removing CSF from below can cause the brain to herniate (coning); CSF rarely identifies the organism anyway.