Malaria lan J. Dunn and Philip E.S. Palmer
ALARIA HAS become a major plague throughout the world. The World Health Organization (WHO) estimates that more than 40% of the worlds' population, 2,000 million people, are at risk. Perhaps half of these, 1,000 million, have the disease, and there is no doubt that more than 2 million die every year. Malaria kills 1 million people every year in Africa alone. It does not respect age, and children are at particular risk; according to WHO, two children die of malaria every minute. Because of modern travel, malaria is not confined to the tropics and numerous cases will be seen in North America and Europe.l-4 There are four frequent varieties, all caused by the genus Plasmodium. They are P. falciparum, P vivax, P. malariae, and P. ovale. Of these four, P. falciparum and P. vivax are the most common, and mixed infection can occur. Transmission is by the anopheline mosquitoe or, occasionally, by blood transfusion, or more rarely organ transplantation. Repeated infection can produce some immunity, and the hemoglobinopathies, particularly sickle cell anemia and [3-thalassemia, offer some protection. The clinical presentation is very broad, far wider than the classical combination of severe recurrent chills and fevers. Malaria may present as nausea and vomiting, headache, coma and various neurological signs, hemoglobinuria or renal failure, and acute dyspnea. Malaria should probably be suspected in any patient of any age returning from the tropics, or living there, in whom there is a feverish illness that does not respond to treatment in the expected way. The laboratory diagnosis is made by recognition of the parasite within red cells, but in the tropics it may be more important to treat the patient first and confirm the diagnosis later. Malaria is not a benign illness. There are two complications of importance to the radiologist, mainly because they can so easily be mistaken for something other than malaria. It is important to recognize when imaging can be helpful, and also when it has little to contribute. Pulmonary complications develop in as many as 10% of patients with malaria; there may be insignificant respiratory complaints or there may be
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pneumonia or patchy bronchopneumonia. Radiographically, a generalized increase in interstitial markings has also been reported. 5,6Far more important is the severe pulmonary edema that may develop at any time, even when the patient is apparently responding satisfactorily to antimalarial treatment, v,8 There are no specific characteristics to suggest malaria; it is more often mistaken for fluid overload, or early cardiac failure (Fig 1). It is an ominous development that may not respond even to early treatment. Cerebral malaria is an important aspect of the infection, which also may be fatal unless treated vigorously. Computed tomography scanning has not shown any early abnormalities that significantly help to make the diagnosis in the early stages. Focal and asymmetrical cerebral edema have been reported, which do not always correlate with the clinical neurological findings. 9-11 It has been suggested that the brain damage may be the result of intracranial hypertension, and magnetic resonance imaging has demonstrated acute hemorrhage and infarction 5 days after onset: the T1- and T2-weighted images are compatible with hemorrhage and infarct, which improve after treatment. In a few patients, focal lesions have been demonstrated, which coincide with the neurological signs; however, such findings a r e u n u s u a l . 12,13 For most patients with cerebral malaria, immediate scanning is not going to alter treatment. Scanning may be far more important if recovery is incomplete and there are residual neurological changes. Similarly, in infants and young children with cerebral malaria, sonography is unlikely to show any specific findings that will affect treatment. Many other imaging results will add to clinical
From the Department of Radiology, University of British Columbia, Vancouver, British Columbia, Canada; and the Deparment of Radiology, University of California, Davis, Davis, CA. Address reprint requests to Ian J. Dunn, MD, PhD, FRCP(C), Brooke Radiology Associates, 150-5791 No. 3 Rd, Richmond, British Columbia, Canada V6X 2C9. Copyright © 1998 by W.B. Saunders Company 0037-198X/97/3301-000858.00/0
Seminars in Roentgenology, Vol XXXIII, No 1 (January), 1998: pp 79-80
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Fig 1. Severe pulmonary edema that developed in a patient during treatment for P. falciparum malaria is shown. This is not the response to fluid overload, it is very difficult to treat, and is often fatal. 15 (Reprinted with permission. TM)
suspicions that the illness might be malaria, but these contribute little to patient m a n a g e m e n t . For example, the spleen will be enlarged, but i m a g i n g is only important if injury is suspected, because
rupture of the spleen m a y occur with m i n i m a l trauma. Splenic infarction and subsequent infection can also occur. The liver m a y enlarge or remain normal. Portal hypertension m a y develop. Sonography in chronic malaria will show that the kidneys are small and contracted, but during acute renal failure, the kidneys m a y be enlarged. ~4,15 In tropical countries, clinicians are well aware of the possibility of malaria and treat the patients accordingly. In nontropical countries, where malaria is u n c o m m o n , radiologists have to be aware that the clinicians m a y not have considered that possibility. The recognition of p u l m o n a r y edema as a result of the infection and not of treatment, and the k n o w l e d g e that cerebral s c a n n i n g will contribute very little in the early stages of cerebral malaria but may be helpful when the clinical response is less than satisfactory, is information which m a y make all the difference to the patients w h e n they are seriously ill.
REFERENCES
1. WHO: Expert Conunittee on Malaria, 18th Report. Tech Rep Ser WHO, Geneva, 1986, p 735 2. WHO: Malaria: The call for action. World Health Forum 14:203-204, I993 3. Malaria tests India's public health system. BMJ 309: t1831184, 1994 (editorial) 4. Hendrickse RG, Hasan AH, Olumide LO, et al: Malaria in early childhood: An investigation of 500 seriously ill children in whom a "clinical" diagnosis of malaria was made on admission to the children's emergency room at the University College Hospital, Ibadan (Nigeria). Ann Trop Med Parasitol 65:1-20, 1971 5. Hsieh Shu Chen, Wang Chia-Juei, Chu'chih P'ing, et al: Certain unusual manifestations of Tertian Malaria. Chin Med J 84:307-312, 1965 6. Rauber K, Enkerlin HL, Riemann H, et al: Pulmonale manifestation bei Malaria. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 146:507-510, 1987 7. Fein IA, Rackow EL, Shapiro L: Acute pulmonary edema
inplasmodiumfalciparummalaria.AmRevRespirDisl18:425429, 1978
8. Godard JE, Hanson RA: Interstitial pulmonary edema in acute malaria. Radiology 101:523-524, 1971 9. Cayea P, Rubin E, Teixidor HS: Atypical pulmonary malaria. Am J Radiol 137:51-55, 1981 10. Newton CRJC, Peshu N, Kendall B, et al: Brain swelling and ischaemia in Kenyans with cerebral malaria. Arch Dis Child 70:281-287, 1994 11. Looareesuwan S, Warrell DA, White NJ, et at: Do patients with cerebral malaria have cerebral oedema? A cornpurer tomography study. Lancet 1:434-437, 1983 12, Millan JM, Millan JMS, Munoz M, et al: CNS complicadons in acute malaria: MR findings. Am J Neuroradiol 14:493494, 1993 I3. Thomas SD: Clinical and histological correlation of cerebral malaria. Trop Geogr Med 23:232-238, 1971 14. Gilles HM: Quartan malaria and childhood nephrosis. Medical Surveys and Clinical Trials (ed 3). New York, Oxford University Press, 1975 15. Palmer PES, Reeder MM: Malaria, in The Imaging of Tropical Diseases, With Epidemological, Pathological, and Clinical Correlation (ed 2). Heidelberg, Springer-Verlag(in press)