Paitoon Narongchai

Forensic entomology cases in Thailand: a review of cases from 2000 to 2006

This paper presents and discusses 30 cases of cadavers that had been transferred for forensic entomology investigations to the Department of Forensic Medicine, Faculty of Medicine, Chiang Mai University, northern Thailand, from 2000 to 2006. Variable death scenes were determined, including forested area and suburban and urban outdoor and indoor environments. The fly specimens found in the corpses obtained were the most commonly of the blow fly of family Calliphoridae, and consisted of Chrysomya megacephala (F.), Chrysomya rufifacies (Macquart) Chrysomya villeneuvi Patton, Chrysomya nigripes Aubertin, Chrysomya bezziana Villeneuve, Chrysomya chani Kurahashi, Lucilia cuprina (Wiedemann), Hemipyrellia ligurriens (Wiedemann), and two unknown species. Flies of the family Muscidae [Hydrotaea spinigera Stein, Synthesiomyia nudiseta (Wulp)], Piophilidae [Piophila casei (L.)], Phoridae [Megaselia scalaris (Loew)], Sarcophagidae [Parasarcophaga ruficornis (F.) and three unknown species], and Stratiomyiidae (Sargus sp.) were also collected from these human remains. Larvae and adults of the beetle, Dermestes maculatus DeGeer (Coleoptera: Dermestidae), were also found in some cases. Chrysomya megacephala and C. rufifacies were the most common species found in the ecologically varied death scene habitats associated with both urban and forested areas, while C. nigripes was commonly discovered in forested places. S. nudiseta was collected only from corpses found in an indoor death scene.

First Report of Human Myiasis Caused by Chrysomya megacephala and Chrysomya rufifacies (Diptera: Calliphoridae) in Thailand, and Its Implication in Forensic Entomology

Abstract We report a forensic entomology case associated with human myiasis in Chiang Mai Province, northern Thailand. The remains of a 53-yr-old-male were concurrently infested with third instars of the two blow fly species, Chrysomya megacephala (F.) and Chrysomya rufifacies (Macquart), near a severe tumor lesion presented on the lower right leg. The presence of third instars, ≈5 d old, on the day following postmortem indicated that myiasis occurred before death. This is the first report of both fly species acting as a myiasis-producing agent in Thailand. Unsynchronized data between the age of fly larvae due to myiasis premortem and verified age/condition of the corpse suggest a potential complication and error in the estimation of postmortem interval if other predisposition fly infestations are not considered.

Inhibitory effects of caffeic acid ester analogues on free radicals and human liver microsome CYP1A2 activities

Ethyl caffeate (EC), octyl caffeate(OC), benzyl caffeate(BC) and phenethyl caffeate(PC) were synthesized and evaluated for scavenging of superoxide anion, nitric oxide radical and 1,1-diphenyl-1-picrylhydrazyl radical (DPPH). Antioxidant activity was investigated with reducing power method. Pooled human liver microsome was used for investigating the effects on cytochrome P450 1A2 (CYP1A2) catalytic activities by using phenacetin as a substrate. Dixon and Cornish-Bowden plots were used for enzyme kinetic analysis. The EC, OC, BC and PC potentially inhibited superoxide anion, nitric oxide and DPPH radicals. IC(50) values of superoxide anion scavenging of EC, OC, BC and PC were 16.42, 79.83, 123.69 and 123.69 µg/ml, respectively. EC was more potent than OC and BC in terms of nitric oxide radical scavenger: IC(50) values of EC, OC and BC were 24.16, 37.34 and 52.64 µg/ml, respectively. In addition, the IC(50) values of EC, OC, BC and PC on DPPH radical scavenging were 70.00, 184.56, 285.34 and 866.54 µg/ ml, respectively. The IC(50) values of EC, OC, BC and PC on phenacetin O-deethylation were 124.98, 111.86, 156.68 and 31.05 µg/ml, respectively. Enzyme kinetics showed that the type of inhibition mechanism was mixed-type. The result of this study shows that caffeic acid ester analogues potentially scavenge free radicals and inhibit catalytic activity of CYP1A2. This may lead to important implications in the prevention of CYP1A2-mediated chemical carcinogenesis.

Deactivation Study of ñ-Amanitin Toxicity in Poisonous Amanita spp. Mushrooms by the Common Substances In Vitro

The purpose of this research was to find out the substance which deactivate α-Amanitin Toxicity The materials and methods used in the study include analysis with high performance liquid chromatography (HPLC) to: 1.Demonstrate the standard α-amanitin at concentrations of 25, 50 and 100 μg/ml 2.Determine the deactivation of α-amanitin with 1) 18% acetic acid 2), calcium hydroxide 40 mg/ml, 3) potassium permanganate 20 mg/ml, 4) sodium bicarbonate 20 mg/ml 3.Report the statistical analysis as the mean ± standard deviation (SD) and paired t-test. The result revealed that potassium permanganate could eliminate 100 percent of the α-amanitin at 25, 50 and 100 μg/ml. Calcium hydroxide, sodium bicarbonate and acetic acid had lower elimination rates at those concentrations: 68.43 ± 2.58 (-71.4, -67.2, -66.7%), 21.48 ± 10.23 (-29.4, -25.2, -9.9%) and 3.21 ± 0.02% (-3.2, -3.2, +1.1%), respectively. The conclusion of this study was suggested that potassium permanganate could be applied as an absorbent substance during gastric lavage in patients with mushroom poisoning. It also might be effective as a cleansing wash for uncooked mushrooms. Investigation of potassium permanganate’s ability to absorb α-amanitin in animal models and humans should be considered. .

Neurological Involvement and Hepatocellular Injury Caused by a Snake With Hematotoxin Envenomation

Venomous snakes with hematotoxin-Russells viper (Daboia spp), Malayan pit viper (Calloselasma rhodostoma), and green pit viper (Cryptelytrops albolabris and C macrops, previously named Trimeresurus spp) are commonly found in Thailand. Coagulation factor activation, thrombocytopenia, hyperfibrinolysis, and disseminated intravascular coagulation are the main mechanisms of hemorrhaging from these snake bites. The neurological involvement and hepatocellular injury after Russells viper bites were reported in Sri Lanka, but there is no report from Southeast Asia. This case was a 12-year-old hill tribe boy who had ptosis and exotropia of the left eye, respiratory distress, and prolonged venous clotting time, prothrombin time, and activated partial thromboplastin time; low fibrinogen and platelet count; and transaminitis after being bitten by a darkish-colored snake. He did not respond to antivenom for cobra, Malayan pit viper, or Russells viper. However, his neurological abnormalities, respiratory failure, and hepatocellular injury improved, and coagulopathy was finally corrected after receiving antivenom for green pit viper. The unidentified snake with hematotoxin was alleged for all manifestations in this patient.