Myocarditis complicating Plasmodium vivax malaria is an extremely rare complication. We report this development in a young girl who was diagnosed to have P. vivax malaria on the basis of peripheral smear. While undergoing antimalarial treatment, she developed respiratory distress requiring invasive mechanical ventilation and inotropic support due to cardiogenic shock secondary to myocarditis. Cardiovascular complications are well recognized with Plasmodium falciparum malaria. Nevertheless, a high index of suspicion should be maintained for the same in Plasmodium vivax infection especially if symptoms of heart failure develop in a young patient

Almas, Aysha

Lalani, Saima

Nasir, Noreen

Samani, Zahra Aziz

English

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eCommons@AKUDepartment of Medicine Department of MedicineMay 2014Myocarditis complicating Plasmodium vivaxmalaria.Noreen NasirAga Khan University, noreen.nasir@aku.eduSaima LalaniAga Khan UniversityZahra Aziz SamaniAga Khan UniversityAysha Almasaysha.almas@aku.eduFollow this and additional works at: http://ecommons.aku.edu/pakistan_fhs_mc_med_medPart of the Infectious Disease Commons, and the Pulmonology CommonsRecommended CitationNasir, N., Lalani, S., Samani, Z. A., Almas, A. (2014). Myocarditis complicating Plasmodium vivax malaria.. JCPSP: Journal of theCollege of Physicians and Surgeons--Pakistan, 24, s96-s98.Available at: http://ecommons.aku.edu/pakistan_fhs_mc_med_med/202S96 Journal of the College of Physicians and Surgeons Pakistan 2014, Vol. 24 (Special Supplement 2): S96-S98INTRODUCTIONMalaria continues to be a major public health problem inthe tropical developing world. According to the WorldHealth Organization, in 2010, there were an estimated216 million cases of malaria in 106 endemic countriesand territories and an estimated 655,000 deathsbecause of the disease worldwide. It is endemicthroughout South and South-East Asia, South Americaand Africa. Furthermore, approximately half theworld's population is at risk of developing malariaparticularly those that reside in low to middle incomecountries.1Plasmodium (P.) vivax is the most widespread of the fourPlasmodium species (P. falciparum, P. vivax, P. malariaeand P. ovale) that infect human with up to 2·5 billionpeople at risk and an estimated 80 million to 300 millionclinical cases every year.2 It is manifested by suddenonset of fever with chills, headaches and vomiting butthe illness is self-limiting in most cases. Also known asbenign tertian malaria, it is not always benign bycourse.3 Serious life threatening complications havebeen reported from endemic regions. On the other hand,Plasmodium falciparum is well-known to be significantlyassociated with severe clinical course and complicationssuch as cerebral malaria, multiorgan failure, shock andfatal outcome.4Cardiac complications have rarely been reported inpatients affected by this type of infection. We report herea case of Plasmodium vivax malaria with an unusualcomplication of myocarditis and cardiogenic shock.CASE REPORTA 20 years old girl with no prior co-morbids presented toemergency room (ER) with complains of fever for 8days, lower abdominal pain and nausea and vomiting for2 days. The fever was high grade without chills, rigors,or cough associated with it. The abdominal pain wasdull, constant and non-radiating in character. Onexamination, she appeared toxic and dehydrated withcollapsed neck veins. Initial vital signs included a heartrate of 107 beats/minute, blood pressure of 82/59 mmHg and afebrile at that time. Systemic examinationrevealed generalized tenderness of the upper abdomenwith no apparent visceromegaly and positive gutsounds, with coarse crackles and decreased breathsounds at the right base of lung. Rest of the examinationwas unremarkable.The results of the initial investigations revealedhemoglobin level of 12.3 g/dl, hematocrit of 36, white cellcount of 10,200/ul and platelets of 25,000/cubicmillimeter. Her peripheral film showed trophozoites andgametocytes of Plasmodium vivax malaria. Her bloodurea nitrogen was 29 mg/dl, serum creatinine was 0.9mg/dl; serum concentration of sodium was 132 meq/l, ofpotassium was 3.3 meq/l, of chloride was 105 meq/l andof bicarbonate was 23.2 meq/l. Her coagulation profileshowed prothrombin time of 11 seconds, activatedpartial thrombin time of 30.4 seconds. Her blood culturesreported no growth whereas her immunohistochemistryfor Plasmodium vivax was positive. A chest radiographshowed infiltrates in the right lower zone. Hence, shewas diagnosed as a case of P. vivax malaria with rightlower lobe pneumonia and hypovolemic shock. She wastreated with Chloroquine phosphate, Levofloxacin 750mg intravenous (IV) daily and resuscitated withintravenous (IV) fluids and admitted in the main medicalward.In the ward, she became tachypneic with a respiratoryrate of 40 breaths per minute. Her oxygen saturationdropped to 90% on room air and on examination, sheCASE REPORTMyocarditis Complicating Plasmodium vivax MalariaNoreen Nasir1, Saima Lalani2, Zahra Aziz Samani2 and Aysha Almas1ABSTRACTMyocarditis complicating Plasmodium vivax malaria is an extremely rare complication. We report this development in ayoung girl who was diagnosed to have P. vivax malaria on the basis of peripheral smear. While undergoing antimalarialtreatment, she developed respiratory distress requiring invasive mechanical ventilation and inotropic support due tocardiogenic shock secondary to myocarditis. Cardiovascular complications are well recognized with Plasmodiumfalciparum malaria. Nevertheless, a high index of suspicion should be maintained for the same in Plasmodium vivaxinfection especially if symptoms of heart failure develop in a young patient.Key Words: Plasmodium vivax malaria.   Myocarditis.   Acute respiratory distress syndrome.1 Department of Medicine, The Aga Khan University, Karachi.2 Medical Student, The Aga Khan University, Karachi.Correspondence: Dr. Noreen Nasir, Instructor, Internal Medicine,The Aga Khan University and Hospital, Stadium Road,Karachi.E-mail: noreen.nasir@aku.eduReceived: April 13, 2012;   Accepted: November 18, 2013.was noted to have jugular venous distention andbilateral fine inspiratory crackles. Her electrocardiogramshowed sinus tachycardia with a heart rate of 140 beatsper minute. Arterial blood gas showed respiratoryalkalosis. At this point, it was thought that she haddeveloped complicated malaria with pneumonia withpossible acute respiratory distress syndrome (ARDS).Her medications were modified and she was switchedto Piperacillin/Tazobactam 4.5 g IV TID, Quininedihydrochloride 20 mg/kg IV stat followed by 10 mg/kgIV TID and she was transferred to the intensive care unit.Subsequently, she developed hypoxemic respiratoryfailure necessitating intubation and mechanicalventilation. She required high ventilator support and apositive end expiratory pressure (PEEP) of 25 cm H2O.Vasopressors were started for shock. Her centralvenous pressure (CVP) at this time was persistentlymore than 16 mmH2O, leading to a suspicion ofpulmonary edema due to a cardiac cause. A2-dimensional transthoracic echocardiogram wasperformed at this point which revealed an ejectionfraction of 30% with severe global hypokinesia. Cardiacchambers, however, were normal in size and mild tomoderate mitral regurgitation as shown in Figures 1and 2. The high CVP and low ejection fraction ruled outthe development of ARDS. Hence, this patient haddeveloped myocarditis secondary to P. vivax malaria.Her IV fluids were stopped and she was started oninotropes, dopamine, dobutamine and diuresed withfurosemide. Her repeat CXR confirmed parenchymalfluid in lungs and bilateral pleural effusions. Bloodpicture also revealed a platelet count of 55 and positivemalarial parasite on peripheral film with scanty gameto-cytes of Plasmodium vivax of 1-10/100 power field. Over the next 48 hours, the patient's ventilatoryrequirements gradually improved. Repeat completeblood count (CBC) showed negative malarial parasite onperipheral film. On 8th day a repeat echocardiogramrevealed normal left ventricular systolic function andejection fraction of 60%. The patient was extubated onthe 10th day of admission. Her CBC significantly hadimproved with platelets of 558,000, hemoglobin of 10.9g/dl and a negative peripheral smear for malarialparasite. Subsequently, the patient was shifted out ofICU to medical ward again and sent home.DISCUSSIONWe report a case of P. vivax malaria complicated bysecondary myocarditis. Plasmodium vivax infection canrarely cause various complications which includeARDS/ALI, acute kidney injury, severe anemia andthrombocytopenia, hemophagocytic syndrome, as wellas cerebral malaria.3,4 Although there are many casesreporting cardiac complications associated withPlasmodium falciparum infection, they have rarely beenreported to be caused by P. vivax infection.There are four case reports in literature aboutPlasmodium vivax infection complicated by myocarditis.Two of these have been described in children with onlyone case reported in an adult patient. The first case wasreported by Herrera et al. about an 8 years old boy whodied due to fatal myocarditis following Plasmodium vivaxmalaria.5 The second case was reported by Kim et al.which links P. vivax infection with myocarditis.6 Thepatient presented with fever and chills after travel to anendemic region in South Korea and was diagnosed withP. vivax malaria. Subsequently, she developed chestpain and non-specific ST-T wave changes in lead II, IIIand AVF on ECG and was found to have elevatedtroponin levels. Her ejection fraction was 61% withsuspicious hypokinetic motion on inferior cardiac walland normal global left ventricular systolic function. Shewas conservatively managed and her chest painresolved followed by cardiac markers which returned tobaseline over a few days. ECG in this patient showedsinus tachycardia and ST-T flattening in anterior leadsand she developed cardiogenic shock due to severemyocarditis. A 2-dimensional echocardiogram showedseverely reduced left ventricular systolic function, anejection fraction of 30% and global hypokinesia. Shesubsequently required assisted ventilation and invasivehemodynamic monitoring. Hence, this is the first case toreport development of cardiogenic shock secondary tomyocarditis in a patient with P. vivax malaria. In a thirdreported case, Plasmodium vivax malaria presentedwith an unexpected combination of cerebral malariacomplicated by myocarditis in a 12 years old child.7 Afourth case report from Northern India is about anadolescent girl who presented with fever, jaundice andright upper quadrant abdominal pain. Her clinical course,similar to our patient was complicated with thedevelopment of respiratory distress secondary topulmonary edema, culminating in mechanical venti-lation. An echocardiogram subsequently revealedgeneralized hypokinesia and an ejection fraction of40%.8Myocarditis complicating P. vivax malaria is extremelyrare. The exact incidence and pathophysiology of thisentity remains obscure. In Plasmodium falciparumassociated myocarditis, the mechanism of myocardialinjury is a result of a number of parasitic toxins releasedin the course of infection that activate the immuneMyocarditis complicating Plasmodium vivax malaria Figure 1: Echocardiogram. Figure 2: Echocardiogram.Journal of the College of Physicians and Surgeons Pakistan 2014, Vol. 24 (Special Supplement 2): S96-S98 S97Noreen Nasir, Saima Lalani, Zahra Aziz Samani and Aysha AlmasS98 Journal of the College of Physicians and Surgeons Pakistan 2014, Vol. 24 (Special Supplement 2): S96-S98response.9 Inflammatory cytokines like TNFα are knownto exert toxic effects on the heart causing myocardialinjury. Another mechanism of cardiac injury in malaria isocclusion of capillaries by parasites and parasitizedRBCs causing ischemic cardiomyopathy.10 Also severemetabolic acidosis and hypoglycemia can compromisemyocardial integrity and function with high concen-trations of circulating cardiac biomarkers.Acute myocarditis has a variable clinical course, rangingfrom asymptomatic disease to congestive heart failureand sudden death. Early recognition of this complicationis important as it may lead to cardiogenic shock whichcarries a high mortality. These patients require intensivecare with invasive hemodynamic monitoring and inotro-pic support. Despite global efforts aimed at eradicationand control of malaria, this disease remains one of themost important public health challenges of these time.REFERENCES1. World Health Organization. World malaria report. Geneva:WHO Press; 2011. 2. Guerra CA, Snow RW, Hay SL. Mapping the global extent ofmalaria in 2005. Trends Parasitol 2006; 22:353-8.3. Picot S. Is Plasmodium vivax still a paradigm for uncomplicatedmalaria? Med Mal Infect 2006; 36:406-13.4. Aggarwal A, Rath S, Shashiraj. Plasmodium vivax malariapresenting with severe thrombocytopenia. J Trop Pediatr 2005;51:120-2.5. Herrera JM. [Cardiac lesions in P. vivax malaria. Study of acase with coronary and myocardial damage]. Arch Inst CardiolMex 1960; 30:26-36. Spanish.6. Kim SA, Kim ES, Rhee MY, Choi SI, Huh HJ, Chae SL, et al.A case of myocarditis associated with Plasmodium vivaxmalaria. J Travel Med 2009; 16:138-40.7. Mustafa SA, Patra V, Ali SS. Plasmodium vivax myocarditis ina child. Int Multidiscipl Res J 2011; 204:45-6.8. Ahmad S, Dhar M, Bishnoi S, Shirazi N, Bhat NK. Acutemyocarditis in P. vivax malaria: an extremely rare complication.Trop Doct 2013; 43:35-6. 9. Kern P, Hemmer CJ, Van Damme J. Elevated tumour necrosisfactor alpha and interleukin-6 serum levels as markers forcomplicated Plasmodium falciparum malaria. Am J Med 1989;87:139.10. Costenaro P1, Benedetti P, Facchin C, Mengoli C, Pellizzer G.Fatal myocarditis in course of Plasmodium falciparuminfection: case report and review of cardiac complications inmalaria. Case Rep Med 2011. 

Myocarditis complicating Plasmodium vivax malaria.

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Myocarditis complicating Plasmodium vivax malaria.

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