Dear Label_Name,

Greetings! I hope you are well.

I am writing on behalf of an international publishing house, Science and Education Publishing, USA (http://www.sciepub.com).

Science and Education Publishing (SciEP) is a multidisciplinary open access publisher of Journals covering the fields of Science, Technology and Medicine. All SciEP publications are subject to high-quality peer review, editorial and production processes and are freely available online.

Welcome to the April, 2013 edition of SciEP newsletter, providing monthly summaries of articles on science & education related topics of interest to scientist and professionals. The mission of our journals is to provide an open access forum for publishing new findings on issues pertinent to scientific and academic field. We also invite you to submit original research papers, review articles, short reports, or case studies are considered for publication in our Multidisciplinary Journals.

American Journal of Public Health Research
DOI: 10.12691/ajphr-1-1-3

The Implementation of a Tele-Homecare System with Service Oriented Architecture and HL7 Message Transmission Standard
Ching-Sung Wang

American Journal of Medical and Biological Research
DOI: 10.12691/ajmbr-1-1-2

The Influence of Ethanol on Pyruvate Kinases Activity in Vivo, in Vitro, in Silico
Lelevich Sergey Vladimirovich, Khrustalev Vladislav Victorovich, Barkovsky Eugene Victorovich, Shedogubova Tatyana Aleksandrovna

American Journal of Medical Sciences and Medicine
DOI: 10.12691/ajmsm-1-1-1

Clinical and Histological Features in Wegener Granulomatosis
Li Cavoli Gioacchino, Passantino Rita, Bono Luisa, Tortorici Calogera, Ferrantelli Angelo, Giammarresi Carlo, Rotolo Ugo

American Journal of Infectious Diseases and Microbiology
DOI: 10.12691/ajidm-1-1-2

The Curse of Lymphatic Filariasis: Would the Continual Use of Diethylcarbamazine Eliminate this Scourge in Papua New Guinea?
Anne Lanham, Lillian Mwanri

We have released issues of some journals on February 2013.
American Journal of Public Health Research
American Journal of Medical Sciences and Medicine
American Journal of Medical and Biological Research
American Journal of Pharmacological Sciences
American Journal of Clinical Medicine Research
American Journal of Nursing Research
American Journal of Cancer Prevention
American Journal of Medicine Studies
American Journal of Infectious Diseases and Microbiology
American Journal of Cardiovascular Disease Research
American Journal of Biomedical Research
American Journal of Mechanical Engineering
American Journal of Microbiological Research
Journal of Preventive Medicine
American Journal of Food and Nutrition
American Journal of Hypertension Research
American Journal of Sports Science and Medicine
Journal of Cancer Research and Treatment
American Journal of Zoological Research
Journal of Biomedical Engineering and Technology
American Journal of Microbiological Research
Biomedical Science and Engineering

We are pleased to announce that submissions are now being accepted for peer review for all the journals across all our subject areas in SciEP.

Please submit your manuscript via our online submission system:
http://www.sciepub.com/author/signin

To unsubscribe from our mailing list, please click on the following link: unsubscribe

I am looking forward to hearing from you.

Kind regards,

David Rain
Email:join@sciepub.com
Science and Education Publishing (http://www.sciepub.com)

Think outside the Box for Diagnosing Malaria as a Cause of Sickle Cell Crisis in an Urban Hospital - Case Report

Hasan. M, Iriarte. B, Patel. S, Madison. G MD*

Internal Medicine, Mercy Philadelphia Hospital, Philadelphia, PA

Abstract: Plasmodium falciparum (PF) causes the most deadly form of malaria. This is a case of a 43 year old male with sickle cell disease who presented to a community hospital in Philadelphia and was admitted for sickle cell crisis secondary to Plasmodium falciparum malaria. His last visit to malaria endemic area (Nigeria) was 13 months prior, when he contracted malaria and was treated successfully by the local health center. Sickle cell disease is known to have a protective effect against malaria. This case illustrates the importance of high index of suspicion that clinician must have when encountering patients with prior histories of malaria or traveling to remote, endemic areas, even in patients with sickle cell disease and those who are outside of the one year window period of exposure.

Keywords: Plasmodium falciparum, sickle cell disease, sickle cell trait

Citation: Hasan. M, Iriarte. B, Patel. S, Madison. G MD, Think outside the Box for Diagnosing Malaria as a Cause of Sickle Cell Crisis in an Urban Hospital - Case Report. American Journal of Medical Case Reports, 6 (2). 39-40. January 2018. doi:10.12691/ajmcr-6-2-8

1. Case Report

A 43-year-old male with a past medical history of sickle cell anemia and appendectomy, originally from Nigeria, who recently moved to Philadelphia from Georgia 2 months ago, presented to the emergency room in a community hospital in Philadelphia with complaints of dizziness, shortness of breath, jaundice, severe chest pain and back pain for 1-2 days duration, and was admitted for sickle cell crisis. His only home medication was folic acid. Initial physical examination showed RR 16 per min, HR 76/min, Temp 98.1°F, oxygen saturation of 100% on room air. The physical examination showed significant scleral icterus, enlarged liver, and blisters below the right nostril. The patient’s labs were significant for anemia with a hemoglobin of 5.2 g/dl, hematocrit of 15%, MCV of 92 fL, reticulocytosis with absolute reticulocyte 0.21 thou /µL (50-100X10⁹L), percent reticulocyte count of 8.6%, and increased bilirubin (total bilirubin 5.2 mg/dL and direct bilirubin of 1.4 mg/dL). Hemoglobin electrophoresis and peripheral smears were sent on admission. He was started on IV fluids and IV pain medication. He developed fevers up to 103.8°F within 24 hours of admission. Chest x-ray showed no active pulmonary disease, blood and urine cultures were negative. CT abdomen without contrast showed evidence of remote left renal infarct, enlarged liver, atrophic calcified spleen, and biconcave lumbar vertebral endplates all consistent with the patient’s history of sickle cell anemia. On the second hospital day, his sickle cell crisis was resolving however he still remained febrile. He was then started on oral Valtrex for oral herpes and oral doxycycline empirically. Persistent fevers raised concern for underlying undiagnosed infection. Further history revealed that 13 months ago, during his last trip to Nigeria, the patient had developed malaria and was treated with an antimalarial regimen. The specific regimen is unknown with which he had made full recovery.

His malaria rapid antigen test was found to be positive, peripheral blood smear showed ring-form trophozites of p. falciparum (A) along sickled erythrocytes (B). The parasitemia level was 1.73% (0.0001-0.0004% higher is required for a positive level). He was treated with atovaquone/proguanil 4 tablets daily for 3 days. With treatment, he showed prompt clinical improvement, and his fevers resolved.

Figure 1. Thin peripheral blood smear showed ring-form trophozites of p. falciparum (A) along sickled erythrocytes (B)

2. Discussion

Plasmodium falciparum (PF) causes the deadliest form of malaria and is accountable for more 50% of all malaria cases worldwide. [1,2] The incubation period is 7-15 days but recrudescence is possible within a year after an untreated or incompletely treated infection. [2] A recrudescence is thought to originate from circulating Plasmodium blood stages which do not cause fever before a certain level of a microscopically detectable parasitemia is reached. [3] It is not possible to estimate how common recrudescence infection with P. falciparium might be, but with more than 50% malaria caused by P. falciparium worldwide even if only a small proportion of untreated or partially treated infection becomes indolent, this represents a large potential reservoir of sustained transmission.

Although the exact mechanism for recrudescence is unclear in our patient, possibilities include incomplete treatment of his first episode of malaria, drug resistance, inappropriate regimen or re-infection prior to leaving the endemic regimen 13 months prior. It is notable that exposure risks have increased with the expansion of air travel [4] and even rare cases where malaria was acquired from contact with packages sent from an endemic region have been reported [5].

Another important aspect of this case resides in the fact that the patient has sickle cell disease (Hb SS) which is known to have protective effects against infection with P. falciparum compared to sickle cell trait (Hb AS), but is associated with higher mortality and morbidity [6]. In a study investigating patients with sickle cell disease in West Kenya, blood slides of 728 cases of malarial parasites were studied, and parasite was found in only 0.5% in sickle cell disease (HbSS), compared to 35.5% in HbAA, and 5.8% in sickle cell trait (HbAS). Malaria prevalence per genotypic group were 44.1% in HbAAs, 36.2% in HbASs, and 20% in HbSSs [7].

Innate and acquired mechanisms have been postulated as protective in patients with sickle cell trait and sickle cell disease, however they are not fully understood. [8,9] One of them is increased cell sickling, which has been proven in studies using cultured parasitized sickle trait red cells, revealing that increased sickling promotes a faster removal of these cells. [10] Another mechanism is the impaired growth of the parasite caused by various factors such as deoxygenation, disregulated microRNA insertion, loss of potassium, increase activity of the calcium-potassium dependent channel and enhanced phagocytosis [11,12,13,14].

This case illustrates the importance of a high index of suspicion that a clinician must have, to consider P. falciparum malaria as a cause of sickle cell crisis in a patient in the urban setting with a history of treated malaria more than a year prior in a malaria endemic region.

References

[1]  
Rich, S. M.; Leendertz, F. H.; Xu, G.; Lebreton, M.; Djoko, C. F.; Aminake, M. N.; Takang, E. E.; Diffo, J. L. D.; Pike, B. L.; Rosenthal, B. M.; Formenty, P.; Boesch, C.; Ayala, F. J.; Wolfe, N. D. (2009). “The origin of malignant malaria”. Proceedings of the National Academy of Sciences. 106 (35): 14902-14907. PMC 2720412.

[2]   | Roberts, Larry S.; Janovy, John (2005). Foundations of Parasitology (7th ed.). McGraw-Hill Education (ISE Editions). ISBN 0-07-111271-5.
[3]   | Richter J, Franken G, Holtfreter MC, Walter S, Labisch A, Mehlhorn H. Clinical implications of a gradual dormancy concept in malaria. Parasitol Res. 2016 Jun; 115(6): 2139-48.
[4]   | Huang Z1, Tatem AJ. Global malaria connectivity through air travel. Malar J. 2013 Aug 2; 12: 269.
[5]   | Al Hammadi A1, Mitchell M1, Abraham GM2, Wang JP1. Recrudescence of Plasmodium falciparum in a Primigravida After Nearly 3 Years of Latency. Am J Trop Med Hyg. 2017 Mar; 96(3): 642-644.
[6]   | Comparative study of clinical presentation and hematological indicesin hospitalized sickle cell patients with severe Plasmodium falciparum malaria. Purohit, PR, Mohanty PK, Das P, Panigrahi, J, Das K, Journal of Infection and Public Health. 2017, 805.
[7]   | Aluoch, J. R. (1997), Higher resistance to Plasmodium falciparum infection in patients with homozygous sickle cell disease in western Kenya. Tropical Medicine & International Health, 2: 568-571.
[8]   | Gong L, Maiteki-Sebuguzi C, Rosenthal PJ, et al. Evidence for both innate and acquired mechanisms of protection from Plasmodium falciparum in children with sickle cell trait. Blood 2012; 119: 3808.
[9]   | Bunn HF. The triumph of good over evil: protection by the sickle gene against malaria. Blood 2013; 121: 20.
[10]   | Luzzatto L, Nwachuku-Jarrett ES, Reddy S. Increased sickling of parasitised erythrocytes as mechanism of resistance against malaria in the sickle-cell trait. Lancet 1970; 1: 319.
[11]   | Olson JA, Nagel RL. Synchronized cultures of P falciparum in abnormal red cells: the mechanism of the inhibition of growth in HbCC cells. Blood 1986; 67: 997.
[12]   | LaMonte G, Philip N, Reardon J, et al. Translocation of sickle cell erythrocyte microRNAs into Plasmodium falciparum inhibits parasite translation and contributes to malaria resistance. Cell Host Microbe 2012; 12:187.
[13]   | Friedman MJ. Ultrastructural damage to the malaria parasite in the sickled cell. J Protozool 1979; 26: 195.
[14]   | Friedman MJ, Roth EF, Nagel RL, Trager W. Plasmodium falciparum: physiological interactions with the human sickle cell. Exp Parasitol 1979; 47: 73.