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How benign is benign tertian malaria?

Introduction

Malaria is a well-known cause of morbidity and mortality in India. Among the four species of Plasmodium, Plasmodium falciparum and P. vivax are commonly found in our country and only few cases of P. malariae have been reported from Orissa and Karnataka (1). Benign tertian malaria is an acute febrile illness caused by P. vivax in which the paroxysm of fever comes every third-day (48 h). It usually has a benign course. Classically, severe malaria is caused by P. falciparum. Literature, however, shows isolated reports of severe P. vivax malaria associated with thrombocytopenia, cerebral malaria, disseminated intravascular coagulation, acute respiratory distress syndrome (ARDS), hepatic dysfunction and renal involvement (2-14). This is a retrospective study to determine the incidence of various complications of P. vivax malaria based on review of case records.

Material & Methods

The case records of all the patients of P. vivax malaria cases admitted to St. Stephen's Hospital, Delhi from September 2005-August 2006 were studied. Complete blood count and peripheral blood findings, liver and kidney function tests were reviewed. The results of rapid diagnostic test for malaria (OptiMAL test, Diamed AG, Switzerland) were correlated with the peripheral blood smear findings in the patients in whom it was requested. Additional abnormal results like a positive direct Coomb's test were noted. All abnormal laboratory results were clinically correlated.

Results

The peak incidence of malaria was seen in the month of September 2005 followed by August 2006 (Fig. 1). There were a total of 265 cases of malaria, 221 were due to P. vivax, 41 caused by P. falciparum, two cases of mixed infection and in one case the species could not be identified as the blood smear showed only malarial pigment. Among the patients with P. vivax malaria, 161 were males and 60 were females with age ranging from two months to 75 years (median age 32 years). Thirty-seven patients were in the paediatric age group in the age ranging from two months to 12 years (median age 3 years). Thrombocytopenia was present in 213 (96.3%) patients and of which 13(6%) patients had a count <2 0 x [10.sup.3]/[micro]l. Sixty (27.1%) patients showed hepatic dysfunction based on raised liver enzymes. SGOT ranged from 43-1901 U/l and SGPT ranged from 44-848 U/l. Seven patients had liver enzymes three times the normal level. Nine (4%) patients had serum bilirubin >3 mg/dl with normal liver enzymes. Seventeen (7%) patients had serum creatinine above 1.2 mg/dl. One patient went into acute renal failure with serum creatinine of 10.64 mg/dl and her peripheral blood smear showed red cell fragments and microspherocytes (Fig. 2a). Two children had positive direct Coomb's test with the smear showing agglutination of red blood cells around the parasitized RBC (Fig. 2b). Three maternal deaths occurred due to ARDS, diagnosis based on blood gas analysis, chest radiograph and normal central venous pressure. The peripheral blood smear showed heavy parasitaemia with >5% RBCs parasitized and WBC agglutinates. Phagocytosed parasites were seen in the neutrophils (Figs. 2c and d). Rapid diagnostic test for malaria based on specific Plasmodium LDH antigen (OptiMAL test) was done on 21 of these patients. Sixteen patients were positive for P. vivax and five were positive for P. falciparum. There was no discrepancy in the diagnosis between peripheral blood smear examination and the rapid diagnostic test.

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[FIGURE 2 OMITTED]

Discussion

Malaria is a common infection in most parts of the world. Benign tertian malaria generally has an uncomplicated course but sporadically, all complications usually associated with P. falciparum malaria have also been reported in vivax malaria (2-14). Profound thrombocytopenia is a well recognized complication of falciparum malaria but there have been conflicting reports regarding thrombocytopenia in vivax malaria (3,5,6). In our study, thrombocytopenia was a common finding in the patients with vivax malaria. Direct lytic effect, immunological reactions, splenic sequestration and oxidative stress are some of the suggested mechanisms for thrombocytopenia (15-17). Although 96.3% of our patients had low platelets, none of them had bleeding complications and hence did not require platelet transfusion. There is a paucity of reports of hepatic dysfunction in benign tertian malaria (7). Malarial hepatitis has been well-described in falciparum malaria (8,9). In our study group 4% of patients had only indirect bilirubinemia suggesting haemolysis and 27.1% patients had raised liver enzymes indicative of "malarial hepatitis" due to direct hepatic injury by the parasite. All patients with P. vivax malaria were screened for G6PD enzyme deficiency before starting primaquine therapy and showed normal activity of the enzyme. This rules out a possibility of oxidant haemolysis in these patients as cause of indirect bilirubinemia. Renal manifestations of malaria have a wide spectrum. Though renal involvement is more common in falciparum malaria, there have been reports of acute renal failure, electrolyte abnormality, abnormal urinary sediment, and increased urinary protein excretion in vivax malaria (10,11). Seven percent of patients had raised serum creatinine and one patient went into acute renal failure in our study. This patient had received quinine hydrochloride and the peripheral blood smear showed red cell fragments and microspherocytes. Quinine associated haemolytic uremic syndrome is known to occur (18). Two children had positive direct Coomb's test with the smear showing agglutination of red cells around the parasitized RBC ruling out a false positive test as previously reported in literature (19). Respiratory complication in P. vivax malaria seem to be underdiagnosed. Acute non-cardiogenic pulmonary oedema, ARDS, acute pulmonary injury and interstitial pneumonia are some of the reported complications (14). Small airway obstruction, gas exchange alteration, increased phagocytic activity and accumulation of pulmonary monocytes are the suggested mechanisms (13). In our study group, three maternal deaths occurred due to ARDS. The diagnosis was based on blood gas analysis, chest radiograph and normal central venous pressure. The patients had heavy parasitaemia with WBC agglutinates which showed phagocytosed parasites. It is postulated that these WBC agglutinates produce the ARDS. None of the patients presented with cerebral malaria.

This paper highlights that thrombocytopenia, hepatic dysfunction, renal involvement and ARDS do complicate benign tertian malaria. Close monitoring of such patients for respiratory complications should be done since ARDS appears to be associated with a fatal outcome and aggressive exchange transfusions to decrease the parasitic load and WBC agglutinates may be beneficial and life-saving.

References

(1.) Lal S, Sonal GS, Phukar PK. Status of malaria in India. J Indian Acad Clin Med 2000; 5: 19-23.

(2.) Islam N, Qamruddin K. Unusual complications in benign tertian malaria. Trop Geogr Med 1995; 47: 141-3.

(3.) Makkar RP, Monga SM, Gupta AK. Plasmodium vivax malaria presenting with severe thrombocytopenia. Braz J Infect Dis 2002; 47: 24-6.

(4.) Kochar DK, Saxena V, Singh N, Kumar SV, Das A. Plasmodium vivax malaria. Emerg Infect Dis 2005. Available from: http://www.cdc.gov/ncidod/EID/vol11no01/040519.htm

(5.) Rodriguez MAJ, Sanchez E, Varges M, Piccolo C, Colina R, Arria M, et al. Occurence of thrombocytopenia in Plasmodium vivax malaria. Clin Infect Dis 2005; 4: 130-1.

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(10.) Prakash J, Singh AK, Kumar NS, Saxena RK. Acute renal failure in Plasmodium vivax malaria. JAPI 2003; 51: 265-7.

(11.) Maheswari A, Singh AK, Sinha DK, Tripathi K, Prakash J. Spectrum of renal diseases in malaria. JAMA 2004; 102(3): 143-8.

(12.) Beg MA, Khan R, Baig SM, Gulzar Z, Hussain R, Smego RA. Cerebral involvement in benign tertian malaria. Am J Trop MedHyg 2002; 67(3): 230-2.

(13.) Anstey NM, Jacups SP, Cain T, Pearson T, Zieseng PJ, Fisher DA. Pulmonary manifestations of uncomplicated falciparum and vivax malaria: cough, small airway obstruction, impaired gas exchange and increased phagocytic activity. J Infect Dis 2002; 185: 1326-34.

(14.) Lomar AV, Vidal JE, Lomar FP, Barbas CV, Mato GJ, Boulos M. Acute respiratory distress syndrome due to vivax malaria : case report and literature review. Braz J Infect Dis 2005; 9(5): 425-30.

(15.) Fajarda LF, Tallent C. Malarial parasites within human platelets. JAMA 1974; 229: 1205.

(16.) Yamaguchi S, Kubota T, Yamaguchi T, Okamoto K, Izumi T, Takeda M. Severe thrombocytopenia suggesting immunological mechanisms in two cases of vivax malaria. Am JHematol 1997; 56(3): 183-6.

(17.) Erel O, Vural H, Aksoy N, Aslan G, Ulukenligil M. Oxi dative stress of platelets and thrombocytopenia with vivax malaria. Clin Biochem 2001; 34(4): 341-4.

(18.) Aster RH. Quinine sensitivity : a new cause of hemolytic uremic syndrome. Ann Intern Med 1993; 119(3): 243-4.

(19.) Ghosh K, Javeri KN, Mohanty D, Parmar BD. False positive serological test in acute malaria. British JBiomed Sci 2001; 58(1): 20-3.

Corresponding author: Dr Archna Sharma, Department of Haematology, St. Stephen's Hospital, Tis Hazari, Delhi-110 054, India.

E-mail: drarchna_sharma@rediffmail.com

Received: 27 January 2009

Accepted in revised form: 7 April 2009

Archna Sharma & Uma Khanduri

Department of Haematology, St. Stephen S Hospital, Delhi, India
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Article Details
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Author:Sharma, Archna; Khanduri, Uma
Publication:Journal of Vector Borne Diseases
Article Type:Report
Geographic Code:9INDI
Date:Jun 1, 2009
Words:1563
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