Koopowitz, A. K.

Linton, D. M.

Pillans, P.

Potgieter, P. D.

University of Queensland eSpace

578 SAMJ VOL 76 18 NOV 1989
4. Brabin BJ. An analysis of malaria in pregnancy in Africa. Bull WHO 1983;
61: 1005-1016.
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WHO 1968; 38: 69-88.
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during pregnancy. Br Med] 1985; 290: 1466-1467.
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recommendations for South African travellers. S Afr Med] 1989; 75:
255-256.
8. Briggs GG, Freeman RK, Yaffe SJ. Drugs in Pregnancy and Lactation. 2nd
ed. Baltimore: Williams & Willins, 1986.
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Pharmaceutical Press, 1989.
10. Dukes MNG. MeyJer's Side Effects of Drugs: An Encyclopaedia of Adverse
Reactions and Interactions. 11 th ed. Amsterdam: E1sevier, 1988.
Quinine-resistant malaria
To the Editor: A 27-year-old New Zealander arrived in Cape
Town in mid-June 1989 from northern Zimbabwe, where she had
been on a working holiday. During the 9 months that she had
spent in Zimbabwe she had taken pyrimethamine plus dapsone
(Maloprim) as malaria prophylaxis. Two months before leaving
Zimbabwe she had developed symptoms that she attributed to
malaria and had treated herself with chloroquine. The dosage and
duration of this therapy is uncertain, but she experienced im-
provement. She was asymptomatic and had discontinued malaria
prophylaxis on arrival in Cape Town.
On 2 July the patient consulted a pharmacist after the onset of
another episode of what she considered to be malaria. She took 3
pyrimethamine plus chloroquine (Fansidar) tablets, but 3 days
later, when there had been no improvement, she presented to a
local general practitioner with a 5-day history of headache, fever,
rigors and malaise. She was found to be pyrexial with a tempera-
ture of 38,5°C, but there was no evidence of hepatomegaly or
splenomegaly. She had no neck stiffness or focal neurological
signs. A full blood count was unremarkable, but a blood slide
revealed scanty trophozoites of Plasmodium falciparum.
Therapy with quinine sulphate 650 mg 3 times a day for 10 days
as well as tetracycline 250 mg 4 times a day for 10 days was
commenced. Four days after starting to take the quinine the
patient was asymptomatic.
She remained well until 27 July, when she had a succession of
black-outs and was referred to a neurologist. At this stage she had
a vague headache as well as slight photophobia, mild confusion,
forgetfulness and inability to organise her thoughts. She was
referred to Groote Schuur Hospital, where she was found to be
jittery and tremulous with occasional myoclonic jerks. Fundoscopy
showed blurred upper disc margins and she was assessed as having
encephalopathy; a diagnosis of cerebral malaria was considered.
Lumbar puncture showed protein 0,6 g/l in the cerebrospinal
fluid, normal glucose, I + globulin, and I + red blood cells.
There were 25 Iymphocytes, but no organisms or polymorphs.
Ziehl-Neelsen sraining was negative. No encapsulated yeasts were
seen. Serological tests for Cryptococcus were negative~ as was the
CSF VDRL test. A computed tomography scan of the head was
normal. Biochemical investigations showed an elevated serum
lactate dehydrogenase value of 232 U/I (normal 60 - 200 U/I), a
serum aspartate aminotransferase value of 46 U/I (normal 0 - 40
U/I), a serum alanine transaminase value of 100 U/I (normal 0 - 53
U/I), and a y-glutamyltranspeptidase value of 99 U/I (normal
0- 50 U/l). The results of other tests were within normallitnits.
On 30 July the patient had a generalised seizure lasting 2
minutes, and thereafter developed status epilepticus. She required
intubation and mechanical ventilation with large doses of thio-
pentone sodium intravenously to control the seizures.
A thin malaria blood smear on 30 July revealed a few gameto-
cytes characteristic of P. falciparum. The thick preparations showed
occasional trophozoites.
A diagnosis of possible quinine-resistant malaria was made and
the patient was given mefloquin 750 mg orally followed by 2
further doses of mefloquin 500 mg in the next 24 hours. The
additional doses of mefloquin were given because there was some
concern that she might not have absorbed the initial dose. In
addition, as further antimalarial therapy co-trimoxazole 10 ml
twice a day was given intravenously for the next 10 days. Intra-
venous phenytoin 100 mg 6-hourly, as well as the thiopentone
sodium infusion, was used to prevent further seizures. Electro-
encephalograms were taken and blood smears examined daily. A
blood smear on 2 August revealed no further evidence of
P. falciparum, and four subsequent blood smears·remained negative
for parasites.
While on ventilation the patient was noted to have moderately
elevated blood pressure (diastolic 100 mmHg), which was controlled
on hydralazine 25 mg 6-hourly.
The intravenous thiopentone was discontinued after 5 days and
she was maintained on phenytoin 100 mg 6-hourly intravenously
and phenobarbitone 120 mg orally daily. She regained conscious-
ness on 9 August and was extubated 2 days later.
The patient'S history was considered to be reliable and she was
thought to have been compliant with her medication. It is therefore
our opinion that she had quinine-resistant malaria.
A. K. Koopowitz
D. M. Linton
P. D. Potgieter
P. Pillans
Departments of Medicine, Anaesthetics and Pharmacology
University of Cape Town and
Groote Schuur Hospital
Cape Town
M edical aid societies and rising costs
of medical care
To the Editor: Having read Mr Speedie's comment l on my
letter,2 I wish to try to put some facts in their true perspective.
In 1980 medical fees increased by 50%. This adjustment was
necessary because these fees had fallen behind; it was not done to
build up a reserve to siphon off in the years that were to follow.
And it was only done after the Minister of Health had told the
medical schemes to get their act together. So in anybody's language
the only sensible thing to do would be to use 1980 as the basis to
work from. But Mr Speedie does not. I think it can be said
without any fear of contradiction that this is juggling with figures.
With what motive? This time the reader can supply the answer.
Now a look at what is really happening (Table I) shows a
completely different picture from the one Mr Speedie tries to
present. And doctors are now again ± 50% behind! I agree with
Mr Speedie that it is farcical to suggest that their increases should
be less than the consumer price index (CPI) or actual cost
increases, but what boggles the mind is why he thinks the same
does not apply to doctors and hospitals. By the way, I never
suggested that subscriptions to medical schemes should not rise in
sympathy with increases in the cost of health care, as Mr Speedie
incorrectly states. This would be just as farcical as the situation is
for doctors at present, with the inadequate increases in their fees
by medical schemes.
Everybody knows that medical schemes are (unluckily) not
obliged by law to pay doctors and hospitals directly, but the law
TABLE I. COMPARISON OF CONSUMER 'PRICE INDEX, I
DOCTORS' FEES AND MEDICAL AID FEES*
Year CPI Doctors' fees Medical aid
1980 100 100 100
1981 115 109 100
1982 132 116 137
1983 149 133 147
1984 166 153 195
1985 193 153 244
1986 228 172 323
1987 265 172 345
1988 299 203 389
• Based on Green' and figures obtained from the Secretary of the Northern
Transvaal Branch of the Medical Association of South Africa (personal communi-
cation).


Quinine-resistant malaria

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