HIV & Opportunistic Infections
- HIV wrecks the immune system, so the brain stops fighting off bugs that healthy people shrug off — and a handful of them show up on imaging.
- The big three to know cold: toxoplasmosis (multiple ring-enhancing lesions that love the basal ganglia), primary CNS lymphoma (often a solitary periventricular enhancing mass that hugs the ependyma), and PML (non-enhancing white matter disease that doesn't push on anything).
- The classic battle on the scan is toxo vs. lymphoma — and the tools that break the tie are restricted diffusion, thallium SPECT/PET uptake, and a response (or not) to empiric toxo treatment.
- HIV itself can directly cause HIV encephalopathy: symmetric, non-enhancing white matter signal change with brain volume loss.
- Always anchor what you're seeing to the CD4 count — the lower it drops, the scarier the menu of possibilities gets.
Think of the immune system as the bouncer at a very exclusive club called Your Brain. Normally the bouncer is enormous, alert, and turns away every sketchy organism that wanders up. HIV slowly poisons the bouncer until he's dozing on a stool. Now the riff-raff strolls right in — parasites, fungi, weird reactivated viruses — and they each leave a different kind of mess on the floor. Our whole job on the scan is to read the mess and name the culprit.
The single most useful number in this entire topic isn't on the image at all: it's the CD4 count, a measure of how many functioning immune cells are left. High CD4, healthy bouncer, boring brain. Once CD4 drops low (think under 200, and especially under 100 cells/µL), the opportunists come out to play.
Toxoplasmosis: the ring-enhancing crowd
Cerebral toxoplasmosis is reactivation of a parasite a huge chunk of the population already carries silently. With the bouncer asleep, it wakes up and sets up little abscesses.
On contrast MRI it classically makes multiple ring-enhancing lesions with a lot of surrounding edema, and it has a real fondness for the basal ganglia and the gray–white junction. "Ring-enhancing" just means the contrast lights up the rim of the lesion while the dead center stays dark — like a glazed donut where only the glaze glows.
Because toxo is so common and so treatable, the real-world move is often to start empiric anti-toxoplasma therapy and rescan in a couple of weeks. Lesions that shrink were toxo. Lesions that don't budge make everyone start worrying about lymphoma.
Primary CNS lymphoma: the great impersonator
The classic exam showdown is toxoplasmosis versus primary CNS lymphoma, because both can make enhancing brain lesions in someone with AIDS — and the management could not be more different.
Lymphoma in the immunocompromised brain tends to be a periventricular mass that contacts the ependymal surface, and it more often shows up as a single lesion than a scattered crowd. The tie-breakers:
| Feature | Toxoplasmosis | Primary CNS lymphoma |
|---|---|---|
| Number | Usually multiple | More often solitary |
| Favorite spot | Basal ganglia, gray–white junction | Periventricular, contacts ependyma |
| Diffusion (DWI) | Less restricted (often facilitated) | Tends to restrict (densely packed cells) |
| Thallium SPECT / FDG-PET | Cold (low uptake) | Hot (avid uptake) |
| Response to anti-toxo trial | Shrinks | Stays put |
None of these signs is a perfect, all-or-nothing rule — toxo and lymphoma overlap and occasionally coexist. Treat the table as a stack of probabilities, not a coin-flip switch. When the picture stays muddy, the answer is tissue: biopsy.
PML: the lesion that respects no anatomy except white matter
Progressive multifocal leukoencephalopathy (PML) is the brain getting eaten by reactivated JC virus. It's the quiet weirdo of the group because it breaks two habits the others share.
First, it lives in white matter and skips over the cortex. Second — and this is the giveaway — it's typically non-enhancing and causes no mass effect. Most lesions swell and shove neighbors aside; PML just dissolves white matter in place without pushing on anything, often asymmetrically, frequently in the back of the brain. On MRI you see patchy T2/FLAIR-bright white matter with little to no enhancement and no mass effect.
"Non-enhancing, no mass effect, white-matter only" is the PML fingerprint. If a lesion is busy lighting up with contrast and squashing the ventricles, you should be thinking toxo or lymphoma — not PML.
HIV encephalopathy itself
HIV doesn't only open the door for other bugs — it directly injures the brain too. HIV encephalopathy shows up as symmetric, non-enhancing white matter signal change (bright on T2/FLAIR) accompanied by brain volume loss that looks too advanced for the patient's age.
A couple more guests at the party
When CD4 is truly in the basement, the menu widens. Cryptococcal infection can fill the perivascular spaces with gelatinous material (the so-called gelatinous pseudocysts, often in the basal ganglia) and cause meningitis. CMV can produce a periventricular ependymal enhancement pattern. Both of these overlap with the broader world of meningitis and ventriculitis, and the inflammatory mimics over in HSV and autoimmune encephalitis are worth keeping in the back pocket.
The one thing to walk away with
When you see brain lesions in HIV, don't just name a disease — read the grammar of the lesion and pair it with the CD4 count. Ring-enhancing and multiple in the basal ganglia? Start thinking toxo. Solitary, periventricular, restricting on diffusion and hot on PET? Lymphoma climbs the list. Non-enhancing white matter with no mass effect? PML. The scan rarely shouts the answer, but it almost always whispers it — if you let the pattern, not the panic, do the talking.