With this mid-twentieth century title paraphrasing an
interesting article by Petersdorf, Swarner and Garcia, I preface a question
that has been bugging me: Why is it that glucose drops in (bacterial) CNS
infections? While I’m not 100% sure of the answer, and the question keeps
coming back, I feel I can venture some possible explanations:
- Bacteria clog up the pipe that connects the blood with the brain. As
a result, glucose barely gets through. Drano to the rescue.
- It is a laboratory conspiration. They know how to fool you.
Furthermore, there will be a massive earthquake next Cinco de Mayo along Route
66, and we all will go straight to hell. Your inner voice is right. Just run
the case by your ID partner, he may protect you from them.
- Bacteria reach for the brain master switch, turn it on and swallow
the key — the “brain hyper-utilization” theory. It’s like
going on vacations in the summer and leaving the AC set at 60·. The
result: a glucose energetic crisis. If you believe this, you probably also
voted for Obama and oppose offshore drilling.
- Bacteria are insatiable and primitive. They only want to eat and
procreate. And they are millions and counting, so they will get what they want
— the “bacterial metabolism” theory. This has more distant roots
in your past. Your mom was giving you antibiotics even for a loose tooth.
- As bacteria run on sugar, white cells are deployed to the CNS to hide
it. The more the white cells, the faster glucose disappears. Because of old
resentments, WBCs will kill with a machete any bacterium with a sugar breath.
And I mean kill it — for real. Beheaded germs lose the proteins via their
severed jugular veins. The result is a mess, and there is no clear winner. The
prognosis is guarded. Either you’ve stolen your child’s PlayStation,
or you are in bad need for vacations to a remote island.
- Bacteria never liked glucose too much. They would do Splenda if they
could. White cells, in turn, are picky. They are the ones to blame.
But I truly believed that it was related to a
dysfunction in the blood-to-CSF glucose pump. For instance, some genetic
mutations of the GLUT1 gene can result in various problems, with CSF
hypoglycorrhachia being perhaps the worst. Those kids can benefit from
Cancerous cells in vitro have a rapid glycolytic rate
compared with normal cells. It would make sense that they would utilize more
glucose. However, in a patient with leptomeningeal carcinomatosis presenting
with low CSF glucose, IV infusion of the sugar did not increase his CSF levels,
suggesting an abnormal blood-to-CSF transport of glucose
Ital J Neurol Sci. 1988;9:83-88). But Petersdorf and pals, in
their detailed studies in which mongrel dogs were branded with 100 million
pneumococci intrathecally, demonstrated that bacteria per se did not reduce CSF
glucose, but that this occurred only in the presence of hungry leukocytes
(Petersdorf RG. Proc Soc Exp Biol Med. 1960;104:65-68).
It is curious that there is no wide consensus to define
low CSF glucose. Some will say less than 50 mg/dL, or 40 mg/dL, or less than
half of your serum glucose concentration. If you do a peripheral stick, do you
do it before or after? Before — you don’t want the lumbar tap to
result in an epinephric, stressed child. How long before? That gets less clear.
The lag time for equalization between the CSF space and blood compartment is
0.5 to 4 hours. So obtaining simultaneous peripheral glucose levels may be
misleading, but based on correlation studies in fasting individuals, there is
agreement in obtaining a level 30 minutes to 1 hour before the tap. And
regarding the well-known association with bacterial meningitis,
hypoglycorrhachia can also present in patients with metabolic disorders,
aseptic meningitis, meningeal carcinomatosis, subarachnoid hemorrhage and
Despite all this, and from the clinician point of view,
it makes more sense to me and to my neurosurgeon colleagues to imagine a
bacterium reclined against the posterior ventricular horn, indulging on glucose
and pooping proteins. That would explain so much.
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