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patients living in areas endemic with bancroftian filariasis.[8] Oral myiasis with active filariasis patients can be treated with a single annual dose of albendazole 400 mg along with diethylcarbamazine 6 mg/kg or ivermectin 200-400 µg/kg body weight.[9]

Poor oral hygiene, ulcerated lesions, severe halitosis, and alcoholism are the pathological factors associated with oral myiasis. Weak, senile, pediatric, or mentally handicapped patients who are unable to defend themselves and who often present with a lack of labial sealing are attacked by flies and consequently by the disease.[10] The prevention of human myiasis is important, and involves the control of fly population, general cleanliness of dwelling areas, and provision for basic sanitation and health education. In our case, the patient represented with healed Hansen’s disease and elephantiasis with infestation of oral myiasis, which, according to our knowledge is the first report.

REFERENCES

1. LaurenceSM.Dipterouslarvaeinfection.BrMedJ1909;9:88.2. Sankari LS, Ramakrishnan K. Oral myiasis caused by Chrysomya

bezziana.JOralMaxillofacPathol2010;14:16‑8.3. SheikhS,PallagattiS,SinglaI,KaluchaA,AggarwalA,KaurH.Oral

Myiasis:Areview.JClinExpDent2011;3:e465‑8.

4. Ramli R, RahmanAR.Oralmyiasis: Case report.Malays JMed Sci2002;9:47‑50.

5. Thami GP, Baurah MC, Sharmce SC, Behera NK. Nasal myiasis inleprosyleadingtounusualtissuedestruction.JDermatol1995;22:348‑50.

6. BaligaM,RamanathanA,UppalN.Oralfilariasis:Acasereport.BrJOralMaxillofacSurg2010;48:143‑4.

7. ShermanRA.Woundmyiasis inurban and suburbanUnitedStates.ArchInternMed2004;160:14.

8. SrinivasanR,PaniSP.Myiasisinhumanfilariallymphedema.SoutheastAsianJTropMedPublicHealth1992;23:807‑8.

9. Palumbo E. Filariasis: Diagnosis, treatment and prevention. ActaBiomed2008;79:106‑9.

10. GealhWC,FerreiraGM,FarahGJ,TeodoroU,CamariniET.TreatmentoforalmyiasiscausedbyCochliomyiahominivorax:Twocasestreatedwithivermectin.BrJOralMaxillofacSurg2009;47:23‑6.

Access this article onlineQuick Response Code:

Website: www.jnsbm.org

DOI: 10.4103/0976-9668.107322

How to cite this article: Candamourty R, Venkatachalam S, Yuvaraj V, Sujee C. Oral myiasis in an adult associated with filariasis and Hansen's disease. J Nat Sc Biol Med 2013;4:259-62.

Source of Support: Nil. Conflict of Interest: None declared.

Symmetrical peripheral gangrene with Plasmodium falciparum malaria

AbstractSymmetric peripheral gangrene is rare and relatively uncommon complication of malaria. We report a case of a 50-year-old male who survived Plasmodium falciparum infection with disseminated intravascular coagulation. Symmetric peripheral gangrene in our case, which ultimately required amputation of the toes, was most likely due to interaction between parasitic factors and host factors.

Key words: Gangrene, heavy parasitemia, Plasmodium falciparum, severe malaria

Amrita Gupta, Yogita Dwivedi, Avanish Kumar

Saxena, Komal Joshi

Department of Anaesthesia and Critical Care, SN Medical College, Agra, Uttar PradeshI, India

Address for correspondence: Dr. Amrita Gupta, Department Of Anaesthesia and Critical Care, SN Medical College, Agra, Uttar Pradesh, India. E-mail: amritagupta78@gmail.com

INTRODUCTION

Plasmodium falciparum is a protozoan parasite and one of the species of Plasmodium that cause malaria in humans. It

is transmitted by the bite of female Anopheles mosquito. It causes the most dangerous form of malaria, with highest mortality and morbidity due to a distinct property called as sequestration. Symmetric peripheral gangrene (SPG)

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is defined as symmetrical distal ischemic damage at two or more sites in the absence of large vessel obstruction.[1] This syndrome has been reported in several conditions such as bacterial infections, Disseminated Intravascular Coagulation (DIC), low cardiac output states, drugs like ergot, vasopressin, noradrenaline, and rarely associated with P. falciparum malaria. We report a unique case of SPG with falciparum malaria infection.

CASE REPORT

A 50-year-old uneducated male of low socioeconomic status was scheduled for amputation of toes. To start with, he had complaint of fever associated with chills and rigors for 3 weeks. He consulted a local practitioner who prescribed some tablets about which patient could not give the details. He noticed blackening of toes of both the feet, which was slow and progressive over 1 week. As he was not responding to the treatment, he was rushed to our medical college. There was no history of trauma, significant drug ingestion particularly ergot, alcohol consumption or smoking. On physical examination, he was febrile, dehydrated, and had pallor; there was no icterus, cyanosis, edema, or significant

lymphadenopathy. A pulse rate of 120/min, respiratory rate of 24/min, and blood pressure of 90/70 mmHg was recorded. All peripheral pulses were palpable. On systemic examination, mild hepatosplenomegaly was present and rest of the systemic examination was normal. On local examination, there was blackish discoloration of all toes, extending up to malleoli [Figures 1 and 2]. Intavenous line was secured. Ringer lactate was started and investigations were sent for. Reports were as follows [Table 1].

Peripheral blood smear showed ring forms of P. falciparum with occasional gametocytes. Three consecutive blood cultures for bacteria were negative. Color Doppler study of the lower limbs revealed normal flow in both the femorals and the popliteal, with slightly reduced flow in tibial and dorsalis pedis artery with hypoechogenic shadow in its lumen.

The patient was given i.v. quinine, loading dose of 20 mg/kg followed by a maintenance dose of 10 mg/kg thrice a day for 2 days. Then, the patient was shifted to oral quinine (dose 10 mg/kg) thrice a day and oral paracetamol 500 mg thrice a day for 5 days. Two units of packed cell transfusion were also given. Fever subsided within 5 days of treatment. His peripheral smear for malarial parasite became negative after 7 days of quinine course. Line of demarcation did not progress any further. For management of gangrene, amputation was planned. All repeated blood investigations were within normal limits except prothrombin time 16.5 s, fibrinogen level 2.9 g/L (normal value 1.5-4 g/L), and D-dimer 1.7. The surgery was done under total i.v. anesthesia.

DISCUSSION

The exact mechanism which may trigger intravascular coagulation in malaria infection is not known. But heavy parasitemia causing activation of the complement system,[2]

Table 1: Investigation reportsParameter Patient

valuesReference values

Hemoglobin 7 g/dL 11-13 g/dLTotal leukocyte count 17,900/mm3 4000-11,000/mm3

Platelets 146,000/mm3 140,000-450,000/mm3

Prothrombin time 16.5 11.5-15.5SGOT 283.9 7-21 IU/LSGPT 235.5 8-32 IU/LINR 1.0 <1.5D-dimer 1.8 0‑0.5mg/l FEU (fibrinogen

equivalent units)Random blood sugar 84 g/dL 70-125 mg/dL

Figure 1: Gangrenous feet Figure 2: Symmetrical peripheral gangrene

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triggering the coagulation pathway,[3] and alteration in lipid distribution across the parasitized erythrocytes activating the intrinsic coagulation pathway have been proposed.[4] Parasitized erythrocytes get sequestrated in the microcirculation by molecular interaction with endothelial receptors, chiefly intercellular adhesion molecule (ICAM-I),[5] Vascular adhesion molecule (VCAM-I), thrombospondin, and histidine-rich protein.[6]

The presence of tight packing of parasitized erythrocytes due to decreased deformability of red cells or adherence of infected red cell to microvascular endothelium will initiate a microcirculatory obstruction in malaria[7] (Mac phasen et al. 1985).

In spite of the ever widening etiological spectrum of SPG, recent literature points to 100% association with DIC, a with high mortality rate up to 35% and the rate of amputation ranging from 70% to 90%.[8,9] However, in our case, DIC, parasitic factors (like cytoadherence tissue sequestration, rosette formation), and host factors like dehydration are sufficient to produce occlusion of peripheral vessels which may have predisposed to SPG.

REFERENCES

1. Molos MA, Hall JC. Symmetrical peripheral gangrene andDisseminated Intravascular Coagulation. Arch Dermatol1985;121:1057‑61.

2. Clemens R, Pramoolsinsap C, Lorenz R, Pukrittayakamee S,BockHL,WhiteNJ.Activationofthecoagulationcascadeinseverefalciparum malaria through intrinsic pathway. Br J Haemotol1994;87:100‑5.

How to cite this article: Gupta A, Dwivedi Y, Saxena AK, Joshi K. Symmetrical peripheral gangrene with Plasmodium falciparum malaria. J Nat Sc Biol Med 2013;4:262-4.

Source of Support: Nil. Conflict of Interest: None declared.

Access this article onlineQuick Response Code:

Website: www.jnsbm.org

DOI: 10.4103/0976-9668.107323

3. Philips RE, Looaresuwan S, Warrell DA, Lee SH,Karbwang J, Warrell MJ, et al. The importance of anemiain cerebral and uncomplicated falciparum malaria: Role ofcomplications, dyserythropoesis and iron sequestration. Q J Med1986;58:305‑23.

4. MohantyD,MarwahaN,GhoshK,ChauhanAP,ShahS,SharmaS,et al.VascularocclusionanddisseminatedintravascularcoagulationinfalciparumMalaria.BrMedJ(ClinResEd)1985;290:115‑6.

5. RojanasthienS,SurakamolleartV,BoonpucknavigS.Haematologicalandcoagulationinmalaria.JMedAssocThai1992;75:190‑4.

6. WhiteNJ.Malaria.In:CookG,editor.Manson’sTrophicalDisease.Hospital for Tropical Disease. UK: University of London; 1996.p.1087‑164.

7. MacPherson GG, Warrell MJ, White NJ, Looareesuwan S,WarrellDA.Humancerebralmalaria.Aquantitiativeultrastructuralanalysis of parasitized erythrocyte sequestration. Am J Pathol1985;119:385‑401.

8. Ghosh SK, Bandyopadhyay D, Ghosh A. Symmetrical peripheralgangrene: A prospective study of 14 consecutive cases in atertiary‑carehospitalineasternIndia.JEurAcadDermatolVenereol2009;23:1‑5.

9. DavisMD,DyKM,NelsonS.Presentationandoutcomeofpurpurafulminans associated with peripheral gangrene in 12 patients atMayoClinic.JAmAcadDermatol2007;57:944‑56.

Oral presentation in dengue hemorrhagic fever: A rare entity

AbstractOne of the major health hazards which is prevalent and dangerous is the dengue fever which causes the death of many people. This may be associated with a variety of mucocutaneous manifestations which may be of help in early diagnosis. Many biochemical assays and hematological investigations may aid in the further diagnosis and treatment of the fatal disease. Oral lesions are rare to occur and if present, are often mistaken for platelet abnormality. This case report highlights the importance of oral lesions and it is the first of its kind to be reported as dengue hemorrhagic fever.

Key words: Dengue fever, Dengue hemorrhagic fever, Dengue virus

R. Mithra, Pavitra Baskaran, M. Sathyakumar1

Department of Oral Medicine and Radiology,1Department of Oral and Maxillofacial Pathology SRM Kattankulathur Dental College, Potheri, Kanchipuram District, Tamil Nadu, India

Address for correspondence: Dr. R. Mithra, Department of Oral Medicine and Radiology, SRM Kattankulathur Dental College, Potheri, Kanchipuram District, Tamil Nadu, India. E-mail: mithra_omed2009@yahoo.co.in