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404 Zeehaida M.Pmd Tropical Biomedicine 29(3): 398–404 (2012) Case series of naturally acquired Plasmodium knowlesi infection in a tertiary teaching hospital Azira, N.M.S.1,3, Zairi, N.Z.1, Amry, A.R.2 and Zeehaida, M.1* 1Department of Medical Microbiology and Parasitology, Universiti Sains Malaysia, 16150, Kubang Kerian, Kelantan, Malaysia 2Department of Medicine, School of Medical Sciences, Universiti Sains Malaysia, 16150, Kubang Kerian, Kelantan, Malaysia 3Cluster of Pathology and Laboratory Medicine, Faculty of Medicine, Universiti Teknologi Mara, 40450 Shah Alam *Corresponding author email: [email protected] Received 1 January 2012; received in revised form 1 June 2012; accepted 2 June 2012 Abstract. Plasmodium knowlesi is a simian malaria parasite and is recently recognized as the fifth malaria parasite infecting humans. Manifestation of the infection may resemble other infection particularly dengue fever leading to inappropriate management and delay in treatment. We reported three cases of naturally acquired P. knowlesi in Hospital Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia. Clinical manifestations were quite similar in those cases. Microscopically, the diagnosis might be challenging. These cases were confirmed by polymerase chain reaction method which serves as a gold standard. INTRODUCTION and Palawan, Philipines (Luchavez et al., 2008). Numerous cases have been reported Plasmodium knowlesi is a simian malaria in travelers to these areas, which makes it parasite and is recently recognized as the fifth not only a local disease occurring in the malaria parasite infecting humans (White, Southeast Asian countries but it has been 2008). Human infections with P. knowlesi exported to other countries (Kantele et al., are more common than previously thought 2008; Bronner et al., 2009; Ennis et al., 2009; (Singh et al., 2004). In Malaysia, the first case Ong et al., 2009; Figtree et al., 2010). of naturally acquired P. knowlesi was Plasmodium knowlesi can cause severe reported by Chin et al. (1965) and in Sarawak malaria in 6.5% of human infection the infection was associated with severe (Daneshvar et al., 2009). In previous manifestation of multi organ failure (Cox- publications, death has been reported in Singh et al., 2008). Currently the disease is some cases with hyperparasitemia (Cox- not only confined to that particular area Singh et al., 2008; Daneshvar et al., 2009; but it is widely distributed in other places Singh & Daneshvar, 2010) and the overall case in Malaysia (Singh et al., 2004; Cox Singh fatality rate was 1.8% (Daneshvar et al., 2009). et al., 2008; Vythilingam et al., 2008; Singh In terms of diagnosis, it is difficult to & Daneshvar, 2010). There have been many ascertain diagnosis by blood film microscopy reported P. knowlesi cases from neighbouring as the parasite is often incorrectly identified. countries: Thailand (Jongwutiwes et al., Plasmodium knowlesi is commonly, 2004, Sermwittayawong et al., 2012), misidentified as Plasmodium malariae Vietnam (Van den Eede et al., 2009), since the late blood stages are morpho- Indonesian Borneo (Figtree et al., 2010) logically similar on microscopy, and Singapore (Ng et al., 2008; Ong et al., 2009) molecular methods of detection are 398 necessary for accurate diagnosis (Singh et pain, vomiting, jaundice or headache. On al., 2004; Cox-Singh et al., 2008; Wilairatana further questioning, there was a history of et al., 2010). Polymerase chain reaction jungle tracking one week prior to the onset of (PCR) remains the best method for accurate fever. Clinically, patient was pink, sweating diagnosis of P. knowlesi malaria (Cox-Singh and lethargic. He was febrile with on and off et al., 2008; Wilairatana et al., 2010). spiking temperature daily ranging from 38ºC In this case report we highlight the to 39.5ºC (Figure 1). Systemic review was atypical presentation of thrombocytopenia unremarkable. in P. knowlesi infection which mimicked On admission, his full blood count showed dengue fever. In our local setting where both normal haemoglobin (12.3 g/dL), haematocrit dengue and malaria are still endemic, P. level of 39.6% and total white cells (6.3 X103 knowlesi infection should be included as one uL ), but platelet count was low (97X109/L). of the differential diagnosis in any patients His platelet count had reduced to 45 X109/L presenting with thrombocytopenia. on the next day. Dengue serology revealed positive IgM Case Report 1 and negative IgG. Coagulation profiles were A 71-year-old Malay male, presented with normal except for partial thromboplastin time fever for 8 days prior to admission associated was prolonged. Liver function test revealed with chills, rigors, poor oral intake, body ache, borderline high alkaline phosphatase (121 joint pain and minimal cough. However, in IU/L) and normal transaminases. Total this patient, there was no history of retro- bilirubin (56umol/L) (direct bilirubin: orbital pain, bleeding tendencies, abdominal 27umol/L, indirect bilirubin: 29 umol/L) and Case 1 Case 2 Case 3 Figure 1. Temperature chart above showing fever spikes ranging from every 24h to 36h apart in three different cases 399 lactate dehydrogenase (997 IU/L) were (44.9 seconds). Full blood picture revealed raised. Blood urea and serum electrolytes P. malariae infection. However, blood film levels were normal. In view of positive IgM for malarial parasite showed presence of for dengue serology, he was initially treated Plasmodium falciparum with level of as dengue fever. However, fever persisted parasitaemia 40/ul blood. Owing to the and the clinical picture was atypical for discrepancy in these results, the blood dengue fever. Serial blood films for malaria sample was sent to a referral laboratory parasites (BFMP) were then ordered; they for confirmation of Plasmodium species showed atypical P. malariae but features by PCR which yielded P. knowlesi. Liver with level of parasitaemia of 10520/uL function tests revealed high alanine blood. Blood sample was sent to a referral transaminase (201 IU/L) and aspartate laboratory for confirmation of Plasmodium transaminase (94IU/L), borderline high species by PCR which yielded P. knowlesi. alkaline phosphatase (122 IU/L) and raised Other blood investigations such as Typhidot, total bilirubin (33umol/L). Blood potassium blood and urine cultures were negative. level was low (2.8mmol/L). Sodium, urea and Antimalarial drugs were prescribed creatinine were normal. Other micro- only on day 9 of admission. Patient was biological investigations such as Typhidot, treated with tablet chloroquine 600mg stat blood and urine cultures were negative. and 300mg after 6 hours then 300mg once Initially, in view of high haematocrit, he daily for 2 days, tablet fansidar 500/25mg was given fluid therapy. Excessive fluid (3 tablets) stat and tablet doxycycline 100mg therapy was given and unfortunately, he once daily for a week. Patient responded developed iatrogenic fluid overload with well to above treatment. No more spiking pleural effusion. He was treated with tablet temperature noted after 24 hours of treatment chloroquine 600mg stat, then 300mg once with oral chloroquine and was discharged daily, tablet Fansidar 3 tablets stat and well after BFMP were negative twice. tablet primaquine 40mg stat then once daily for two days. After two days of treatment, Case Report 2 he responded well and afebrile. He was A 36-year-old Malay male, presented with discharged well after negative BFMP twice. intermittent fever for three days prior to admission associated with sweating, chills, Case Report 3 rigors, retro-orbital pain, jaundice, rashes A previously healthy 47-year-old Malay male over both lower limbs. However, there was with no known medical illness claimed no bleeding tendencies, tea coloured urine, having intermittent fever for nearly two pale stool or abdominal pain. There was weeks duration associated with chills, history of visiting the jungle about 2 to 3 sweating, myalgia, joint pain and night weeks before the onset of fever. sweat. Four days prior to admission, he had Clinically, patient had jaundice, daily vomiting, loose stools three times per day and spiking temperature ranging from 38ºC to mild epigastric pain. There was no history of 40.6ºC (Figure 1), slightly tachycardia and bleeding tendencies, blackish stool or urinary presence of petechial rashes over both tract infection symptoms. There was history lower limb. His blood pressure was stable. of jungle tracking prior to onset of fever. On abdominal examination, there was On examination, he had on and off hepatomegaly about 2 fingers breath spiking temperature ranging from 39ºC to palpable and others systemic review was 38.8ºC (Figure 1), was alert and conscious, unremarkable. Full blood count taken on dehydrated, had tinged jaundice, was not admission showed thrombocytopenia tachypnoiec and had no petechial rash. Vital (platelet of 39 X109/L) and high haematocrit signs were stable. On abdominal examination, level of 44.6%. Other blood indices were his liver and spleen were enlarged. Other normal. Dengue serology was negative. systemic review was unremarkable. On Partial thromboplastin time was prolonged admission, his full blood count showed 400 mild to moderate anaemia with 10.5 g/dL Pertaining to case 1, patient was initially haemoglobin, low 2.5 x X103 /uL total white treated as dengue fever in view of positive cells count, markedly low platelet count of dengue IgM. Later, the dengue IgG was also 14 X 109/L and normal haematocrit level of positive in this patient. However, as he 33%. Despite of low platelet count, no bleeding presented with prolonged fever and the tendencies or bruises observed. haematocrit level was normal, these features Full blood picture showed normocytic did not really correlate with dengue fever. normochromic anaemia, left shifted cells and The most likely diagnosis was malaria thrombocytopenia most probably due to following a positive BFMP result. A positive underlying infection. Dengue serology and dengue IgM in this patient may suggest a typhidot were negative while blood culture double infection with P. knowlesi and dengue did not grow any organism. Coagulation virus.
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