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LETTER TO THE EDITOR |
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Year : 2013 | Volume
: 6
| Issue : 4 | Page : 486-487 |
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Plasmodium vivax-induced Adult Respiratory Distress Syndrome
Arvind A Bamanikar, Swati Dhobale, Kiran Shinde
Department of Medicine, Padmashree Dr.D.Y.Patil Medical College, Hospital & Research Center (Dr.D.Y.Patil Vidyapeeth), Pimpri, Pune, India
Date of Web Publication | 17-Sep-2013 |
Correspondence Address: Arvind A Bamanikar Department of Medicine, Padmshree Dr. D.Y. Patil Medical College, Hospital & Research Center (Dr.D.Y.Patil Vidyapeeth), Sant Tukram Nagar, Pimpri, Pune - 411 018 India
Source of Support: None, Conflict of Interest: None | Check |
DOI: 10.4103/0975-2870.118301
How to cite this article: Bamanikar AA, Dhobale S, Shinde K. Plasmodium vivax-induced Adult Respiratory Distress Syndrome. Med J DY Patil Univ 2013;6:486-7 |
Sir,
In last few years severe manifestations of vivax malaria have been reported from India and many other countries. We came across a case of vivax malaria with Adult Respiratory Distress Syndrome (ARDS),which occurred before starting anti-malarial treatment in a young patient having low parasitemia. An original article [1] reiterates that severe manifestations of vivax malaria in India are becoming common now. Most of the reports on ARDS in malaria are noticed after starting anti-malarial treatment. Our case, presented with ARDS before starting the antimalarial drugs, which may be pointing toward an additional unexplained mechanism responsible for ARDS. Hence, it would be worth putting more efforts in research on the pathogenesis in vivax induced ARDS.
We are reporting a case of a 32-year female patient was admitted with fever and dyspnea of 2 days duration. On admission, her temperature was 38°C, pulse 108/min, respiratory rate 34/min and blood pressure 90/70 mm of Hg. She was conscious and well oriented. On examination purpuric skin rash was present on legs. On auscultation of lungs bilateral basal crackles were heard; Liver was enlarged 4 cm below sub costal margin. There was no splenomegaly. Neurological examination was normal. There were no signs of acute congestive cardiac failure. Oxygen saturation was 75% on room air.
On hematological examination her hemoglobin level was 10.2 g/dl, total leukocyte count 10,000/mm 3 , platelets 30,000/mm 3 . Reticuloyte count was 1.5%. Peripheral film examination showed Plasmodium vivax (0.2%). Rapid antigen test as well as peripheral blood film examination was negative for Falciparum infection. Arterial blood gas analysis showed hypoxemia and PaO2/FiO2 ratio was 120. Biochemical tests revealed blood urea 80 mg/dl serum creatinine 1.9 mg/dl, total bilirubin 4.3 mg/dl, direct 2.8 mg/dl, alanine amino transferase (ALT) 67 IU/L, aspartate transaminase (AST) 47 IU/L, alkaline phosphatase (ALP) 87 IU/L Urine and blood cultures were negative. X-ray chest showed bilateral non-homogenous
opacities [Figure 1].
Serology for dengue and leptospirosis were negative. Electrocardiogram and 2D echocardiograph were normal. Patient was managed in intensive care unit and treated with artesunte and amoxicillin clavulanic acid combination. The fluid and electrolyte balance was monitored on intravenous fluids. Acid base balance and oxygen saturation was monitored by arterial blood gas analysis.
The renal parameters returned to normal after 2 days. However, hypoxemia was getting worse in spite of continuous oxygen supply (6 l/min) by nasal route. Hence, patient was put on non-invasive ventilation. In view of marginal improvement in hypoxemia, patient was intubated and ventilated, which was effective in bringing the oxygen saturation to normal. Patient was able to breathe normally, and oxygen saturation on room air was normal. After extubation, patient was observed in general ward before discharge from hospital.
Patient was reassessed in 4-week time and was completely asymptomatic.
An estimate of approximately 2.85 billion people living under risk of this infection with the burden of more than half of all malaria cases in Asia is due to P. vivax. [2] ARDS is rarely seen with P. vivax.
There have been at least 22 case reports (1997-2009) of non-cardiogenic pulmonary oedema/acute lung injury/ARDS in vivax malaria almost all of which have excluded concurrent infection with Plasmodium falciparum. Almost all of these cases developed after the commencement of antimalarial chemotherapy, raising the possibility of a pulmonary inflammatory response to parasite killing.
Cytoadherence and erythrocyte sequestration, which are crucial in the pathophysiology of severe P. falciparum malaria and long believed not to occur in P. vivax infections, may also have an important role, either directly or as a means of localizing the inflammatory response to parasites adhering in the lungs, brain placenta or spleen. The recent proof of such phenomena in P. vivax infections in vitro [3] - albeit with a lower magnitude but with similar intensity than P. falciparum - anticipated by clinical observations has opened new avenues to explore how this parasite causes disease.
Only three reports are available of histopathological examination of fatal pulmonary complications allegedly caused by vivax malaria. Those cases were reported in the early 1900s, and the diagnoses lacked PCR polymerase chain reaction confirmation of P. vivax and exclusion of P. falciparum, [4] but this study stands out different as authors have documented malaria confirmed by PCR with post-mortem histopathological findings of ARDS due to P. vivax in this article.
Future research at the bench will have to focus on furthering our understanding of the inflammatory response caused by P. vivax and identifying the specific cytokines involved in response to this infection. Overcoming current barriers for P. vivax research also requires the long-awaited development of a continuous in vitro culture [5] which will be paramount to our understanding of this disease.
Whilst it is found across a larger swathe of the globe and potentially affects a larger number of people receive a tiny fraction of the research attention and financing around 3%. This neglect, coupled with the inherently more complex nature of vivax biology, means important knowledge gaps remain that limit our current ability to control the disease effectively.
References | | |
1. | Nadkar MY, Huchche AM, Singh R, Pazare AR. Clinical profile of Severe Plasmodium vivax malaria in a Tertiary Care centre in Mumbai. J Assoc Physicians India 2012;60:11-3 |
2. | Kochar DK, Saxena V, Singh N, Kochar SK, Kumar SV, Das A. Plasmodium vivax malaria. Emerg Infect Dis 2005;11:132-4. [PUBMED] |
3. | Carvalho BO, Lopes SC, Nogueira PA, Orlandi PP, Bargieri DY, Blanco YC, et al. On the cytoadhesion of Plasmodium vivax-infected erythrocytes. J Infect Dis 2010;202:638-47 |
4. | Valecha N, Pinto RG, Turner GD, Kumar A, Rodrigues S, Dubhashi NG, et al. Histopathology of fatal respiratory distress caused by Plasmodium vivax malaria. Am J Trop Med Hyg 2009;81:758-6 |
5. | Mueller I, Galinski MR, Baird JK, Carlton JM, Kochar DK, Alonso PL, et al. Key gaps in the knowledge of Plasmodium vivax, a neglected human malaria parasite. Lancet Infect Dis 2009;9:555-66 |
[Figure 1]
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