TRANSACTIONS OF THEROYALSOCIETY OF TROPICAL MEDICINEAND HYGIENE(1992)86, 137
-Report Urinary frequency malaria
in falciparum
DeH. J. de Silval*, S. Herathl and N. R. de Siba partments of ‘Medicine and 2Parasitology, Faculty of Medicine, University of Peradeniya, Peradeniya, Kandy, Sri Lanka
We report a case of Plasmodium falciparum malaria presenting with urinary frequency. A 70 year old woman living in an areahvnoendemic for falciparum malaria was admzted to our hospital with low backacheand urinary frequency of one week’s duration. Two weeksbefore admission the patient had developed mild fever without chills or rigors, which lasted 2 d. Shehad not sought any treatment for the fever., and had been afebrile since that time. Frequency of mlcturition had gradually increased over the week to more than 30 times per day on admission to hospital. Small volumes of urine were passed at a time, and the patient complained of a constant feeling of incomplete bladder emptying. There was no increased thirst, dysuria, haematuria or abdominal pain. The low backachewas constant, but mild. There was no discharge or bleeding from the vagina, and the bowels were regular. The patient denied any previous episodes of malaria and was not receiving any medication, including malaria prophylaxis. There was no history of renal, genitourinary or psychiatric illness. On examination the natient was afebrile and well hvdrated. The spleen was enlarged and palpable 2 cm below the left costal margin, and was firm and non-tender. There was no hepatomegalyand the urinary bladder was not distended. There was no local tendernessover the back, and the cardiovascular, respiratory and nervous systems were clinically normal. Rectal and vaginal examinationswere alsonormal. A thin blood film was positive for asexualstagesof P. falciparum (parasite densiiy 0.3%). The followinginvestigations were within normal limits: haemoglobin concentration (12.8 gidl), white cell count (8.2~ 109/litre), ervthrocvte sedimentation rate (12 mm in first hour), fasting blood glucose (4.6 mmolilitre), blood urea (3.2 mmolilitre), serum sodium (128 mmolilitre) potassium (3.7 mmolilitre) and calcium (2.3 mmolilitre), serum albumin (40 gilitre), urine albumin, sugar, deposit and specific gravity (1.020), and abdominal X-ray. Urine culture wasnegative. The patient was treated with a course of chloroquine (total dose 1.8 g), and within 2 d she becameasymptomatic. On discharge from hospital 3 d later the freauencv of micturition was 4/d. At follow-uu 2 weeksand again at 2 months following dischargefrom hospital she remained asymptomatic, receiving no medication, and blood films were negative for malarial parasiteson both occasions. Malaria can present with clinical featureswhich do not conform to the classicalpattern, especiallyin patients living in endemic areas.This may be due to developmentof a degree of immunity, use of prophylactic anti-malarial drugs, the indiscriminate use (abuse) of anti-malarial drugs; or the presenceof chloroquine resistance(BRUCECHWATT, 1985).The results of a field study conductedin an areaendemic for malaria in Sri Lanka (EDIRISINGHE et al., 1987) showed that classicalfeaturesof malaria were seenin only a minority of patients, and that evenpatients seeking treatment for what was apparently their first attack of malaria presentedwith a variety,of unusual symptoms and signs. Skeletal muscle necrosis(DE SILVA et al., -1~
~~
,
*Author for correspondence.
137
1988) and raised plasma creatine kinase and myoglobin levels suggestingmuscle damage (MILLER et al., 1989) have beenreported in falciparum malaria. This has led to suggestionsthat muscle may be an important site of parasite sequestration (WHO, 1990). In the absenceof another probable causeto explain the patient’s symptoms, and with the dramatic symptomatic responseto chloroquine, it is reasonableto assumea causalrelationship between the P. falciparum infection and the urinary symptoms in our patient, an associationwhich has not been previously reported. The urinary frequency may have been due to sequestrationof the parasite in the detrusor muscle of the urinary bladder leading to ‘bladder irritability’. References Bruce-Chwatt, L. J. (1985). Essential Malariology. London: William Heinemann Medical Books. De Silva. H. 1.. Goonetilleke. A. K. E.. Senaratne. N.. Ramesh, N.: Jayawickrema, ‘U. S., Jayasmghe, K. S.‘A. & Amarasekera, L. R. (1988). Skeletal muscle necrosis in severe falciparum malaria. ‘British Medical Journal, 296, 1039. Edirisinahe. I. S.. Balasuriva, S. & Kumarasiri, P. V. R. (1987). Changing patterns of clinical malaria: a field study. Ceylon MedicalJournal, 32,35-42. Miller, K. D., White, N., Lott, L. A., Roberts, J. M. & Greenwood, B. M. (1989). Biochemical evidence of muscle injury in African children with severe malaria. Journal of Infectious Diseases.159. 139-142. WHO (1990). Severe and complicated malaria, 2nd edition. Transactionsof the Royal SocieQ of Tropical Medicine and Hygiene, 84, supplement 2.
Received 12 August 1991; acceptedfor publication 25 September 1991 Addendum
Since submitting this report, we have encountered another patient with a similar condition. A 23 year old man, also from an area endemic for malaria, presentedwith mild fever (without chills or rigors), mild~backache and urinary frequency (20-30 per-day). He had oreviouslv had several (>lO) attacks of malaria. but had never had urinary frequency’during any of them: Phvsical examination, including rectal examination, was normal apart from a barely palpable spleen. A blood film was oositive for asexualstagesof both P. falciaarum and P. z&ax. All other invest&ions, including a&urineculture, were normal. He too responded dramatically to chloroquine (1.8 g), and 4 d after commencement of treatment was asymptomatic with the urinary frequency falling to 5 per day. He was discharged from hospital on a 14 d courseof primaquine.
-Report Urinary frequency malaria
in falciparum
DeH. J. de Silval*, S. Herathl and N. R. de Siba partments of ‘Medicine and 2Parasitology, Faculty of Medicine, University of Peradeniya, Peradeniya, Kandy, Sri Lanka
We report a case of Plasmodium falciparum malaria presenting with urinary frequency. A 70 year old woman living in an areahvnoendemic for falciparum malaria was admzted to our hospital with low backacheand urinary frequency of one week’s duration. Two weeksbefore admission the patient had developed mild fever without chills or rigors, which lasted 2 d. Shehad not sought any treatment for the fever., and had been afebrile since that time. Frequency of mlcturition had gradually increased over the week to more than 30 times per day on admission to hospital. Small volumes of urine were passed at a time, and the patient complained of a constant feeling of incomplete bladder emptying. There was no increased thirst, dysuria, haematuria or abdominal pain. The low backachewas constant, but mild. There was no discharge or bleeding from the vagina, and the bowels were regular. The patient denied any previous episodes of malaria and was not receiving any medication, including malaria prophylaxis. There was no history of renal, genitourinary or psychiatric illness. On examination the natient was afebrile and well hvdrated. The spleen was enlarged and palpable 2 cm below the left costal margin, and was firm and non-tender. There was no hepatomegalyand the urinary bladder was not distended. There was no local tendernessover the back, and the cardiovascular, respiratory and nervous systems were clinically normal. Rectal and vaginal examinationswere alsonormal. A thin blood film was positive for asexualstagesof P. falciparum (parasite densiiy 0.3%). The followinginvestigations were within normal limits: haemoglobin concentration (12.8 gidl), white cell count (8.2~ 109/litre), ervthrocvte sedimentation rate (12 mm in first hour), fasting blood glucose (4.6 mmolilitre), blood urea (3.2 mmolilitre), serum sodium (128 mmolilitre) potassium (3.7 mmolilitre) and calcium (2.3 mmolilitre), serum albumin (40 gilitre), urine albumin, sugar, deposit and specific gravity (1.020), and abdominal X-ray. Urine culture wasnegative. The patient was treated with a course of chloroquine (total dose 1.8 g), and within 2 d she becameasymptomatic. On discharge from hospital 3 d later the freauencv of micturition was 4/d. At follow-uu 2 weeksand again at 2 months following dischargefrom hospital she remained asymptomatic, receiving no medication, and blood films were negative for malarial parasiteson both occasions. Malaria can present with clinical featureswhich do not conform to the classicalpattern, especiallyin patients living in endemic areas.This may be due to developmentof a degree of immunity, use of prophylactic anti-malarial drugs, the indiscriminate use (abuse) of anti-malarial drugs; or the presenceof chloroquine resistance(BRUCECHWATT, 1985).The results of a field study conductedin an areaendemic for malaria in Sri Lanka (EDIRISINGHE et al., 1987) showed that classicalfeaturesof malaria were seenin only a minority of patients, and that evenpatients seeking treatment for what was apparently their first attack of malaria presentedwith a variety,of unusual symptoms and signs. Skeletal muscle necrosis(DE SILVA et al., -1~
~~
,
*Author for correspondence.
137
1988) and raised plasma creatine kinase and myoglobin levels suggestingmuscle damage (MILLER et al., 1989) have beenreported in falciparum malaria. This has led to suggestionsthat muscle may be an important site of parasite sequestration (WHO, 1990). In the absenceof another probable causeto explain the patient’s symptoms, and with the dramatic symptomatic responseto chloroquine, it is reasonableto assumea causalrelationship between the P. falciparum infection and the urinary symptoms in our patient, an associationwhich has not been previously reported. The urinary frequency may have been due to sequestrationof the parasite in the detrusor muscle of the urinary bladder leading to ‘bladder irritability’. References Bruce-Chwatt, L. J. (1985). Essential Malariology. London: William Heinemann Medical Books. De Silva. H. 1.. Goonetilleke. A. K. E.. Senaratne. N.. Ramesh, N.: Jayawickrema, ‘U. S., Jayasmghe, K. S.‘A. & Amarasekera, L. R. (1988). Skeletal muscle necrosis in severe falciparum malaria. ‘British Medical Journal, 296, 1039. Edirisinahe. I. S.. Balasuriva, S. & Kumarasiri, P. V. R. (1987). Changing patterns of clinical malaria: a field study. Ceylon MedicalJournal, 32,35-42. Miller, K. D., White, N., Lott, L. A., Roberts, J. M. & Greenwood, B. M. (1989). Biochemical evidence of muscle injury in African children with severe malaria. Journal of Infectious Diseases.159. 139-142. WHO (1990). Severe and complicated malaria, 2nd edition. Transactionsof the Royal SocieQ of Tropical Medicine and Hygiene, 84, supplement 2.
Received 12 August 1991; acceptedfor publication 25 September 1991 Addendum
Since submitting this report, we have encountered another patient with a similar condition. A 23 year old man, also from an area endemic for malaria, presentedwith mild fever (without chills or rigors), mild~backache and urinary frequency (20-30 per-day). He had oreviouslv had several (>lO) attacks of malaria. but had never had urinary frequency’during any of them: Phvsical examination, including rectal examination, was normal apart from a barely palpable spleen. A blood film was oositive for asexualstagesof both P. falciaarum and P. z&ax. All other invest&ions, including a&urineculture, were normal. He too responded dramatically to chloroquine (1.8 g), and 4 d after commencement of treatment was asymptomatic with the urinary frequency falling to 5 per day. He was discharged from hospital on a 14 d courseof primaquine.
