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TPDN 1988, Vol. 48, No.32 Page 3
A closely related amoeba, Acanthamoeba spp, can also cause PAM. PAM caused by Acanthamoeba
spp, while potentially as fulminating, tends to follow a more chronic course. Recently, the
literature has described many cases of Acanthamoeba keratitis, an eye infection caused by this
ubiquitous amoeba. These cases are most often associated with the use of extended-wear contact
lenses and cleaning solutions which become contaminated with the amoeba.
Prepared by: Walter C. Bosworth, PhD, Director of Health, and Harold I. Nachimson, MD, Irving Health Officer, Irving Department of
Health.
REFERENCE:
1. Martinez AJ. Free-living amebas: natural history, prevention, diagnosis, pathology, and treatment of disease. Boca Raton, FL: CRC
Press, Inc, 1985.
2. Rivera F, et al. Pathogenic and free-living protozoa cultured from the nasopharyngeal and oral regions of dental patients. Environ
Res 1986; 39 (2): 364-71.
3. Rivera F, et al. A survey of pathogenic and free-living amoebae inhabiting swimming pool water in Mexico City. Environ Res
1983; 32 (1): 205-11.
4. Anderson K, Jamieson A. Primary amoebic meningoencephalitis. Lancet; April 22, 1972: 902-3.
CHILDHOOD CHLOROQUINE POISONINGS -- WISCONSIN AND WASHINGTON*
Each year the approximately 1 million Americans who travel to malarious areas may be advised to
take chloroquine weekly for prophylaxis. In addition, chloroquine is prescribed as therapy for
certain connective tissue disorders. Consequently, there are many opportunities for children
to be poisoned through chloroquine ingestion. To alert medical practitioners and the public to
this danger, the following cases of chloroquine poisoning recently reported to CDC are
presented.
Case 1. On August 6, 1987, a previously healthy 20-month-old girl was found unresponsive next
to an opened empty bottle of chloroquine phosphate. The chloroquine remained from a supply
dispensed to the child's grandfather for malaria prophylaxis. The amount of chloroquine base
the child swallowed was estimated at 800 mg.
Shortly after the emergency medical technicians arrived, the child suffered cardiac arrest.
Normal sinus rhythm was restored en route to the emergency room, but persistent hypotension
necessitated intravenous dopamine. The child began to have generalized seizures 1 hour after
ingestion; these were controlled with intravenous diazepam, phenytoin, and phenobarbital.
Charcoal hemoperfusion performed 7 hours after ingestion did not improve her condition. Serum
chloroquine concentrations before and after the procedure were 0.8 and 0.3 iug/mL, respectively
(2.5 and 0.94 u mol/L). Over the next week her neurologic condition gradually improved, and
mechanical ventilation was discontinued after the eighth day of hospitalization. Subsequent
cranial computerized tomography scans and electroencephalography revealed atrophy and decreased
voltage consistent with postanoxic encephalopathy. Rehabilitative efforts continue; currently,
she is able to make some purposeful movements but still requires feeding by gastrostomy.
Case 2. On January 20, 1988, a 17-month-old boy ingested 2.4g of chloroquine base. His
parents had recently returned from a tour of duty in Cameroon during which they had been taking
chloroquine for malaria prophylaxis; the chloroquine had been dispensed in Cameroon in an
envelope. The child was immediately taken to an emergency room, but 30 minutes after
ingestion, ventricular tachycardia, hypotension, apnea, and seizures developed. After two
hours of resuscitation, his condition was stabilized on intravenous epinephrine and diazepam.
*Reprinted from: CDC. MMWR 1988; 37(28): 437-9.