Generally, both fenitrothion and malathion are rapidly metabolized, and their elimination half-lives in blood are 0.8–4.5 h and 3–6 h, respectively [18, 19]. In addition, 10 µg/mL concentration of fenitrothion or malathion decreased by > 25% or 100%, respectively, after 24 h at room temperature [20]. Therefore, in forensic autopsy cases of fenitrothion or malathion poisoning, the detected blood concentrations of these compounds may be lower than the ingested antemortem blood concentrations because a certain period has passed since death. Several previously reported fenitrothion or malathion fatal poisoning cases based on cadaveric blood or serum collected from the femoral vein, or the cardiac chambers [21–25] were not presented (Table 3). Therefore, it was difficult to determine the fatal cardiac blood concentrations of fenitrothion or malathion. However, the cardiac blood fenitrothion concentrations in our case was ranged of 2.63–2.98 µg/mL. In view of the time elapsed since his death, we thought that these values were within the range of fenitrothion intoxication concentrations. Conversely, the cardiac blood malathion concentrations were relatively low compared with the findings in other fatal malathion poisoning cases (Table 3). In our case, the outside temperature of the area in which he was found was 24.5°C; thus, malathion might have decomposed after his death.
In humans, butyrylcholinesterase (BuChE), also known as serum ChE, is produced is secreted into serum [10, 26]. Acute poisoning of fenitrothion or malathion in humans is often fatal and life-threatening, and the serum ChE activities were remarkably reduced to a few % of the normal values [18, 21]. Cadaveric ChE levels based on blood samples collected within 24 h after death were slightly decreased [27]. However, in fatal OP poisoning cases, serum ChE levels were decreased considerably below the normal range [7–9]. In our case, the serum ChE level was 200 IU/L, which was not reduced compared with that in previous reported cases of OPs acute poisoning. Serum ChE levels in males gradually decrease with age, ranging 200–450 IU/L in 70-year-olds [28]. Considering the age of the studied subject, this finding appeared to reflect age-related declines in serum ChE activity rather than OP-related decreases.
In Japan, the causative microorganisms of pneumonia in the elderly are more diverse than those in the young [14, 29]. As a parameter indicating the severity of pneumonia, lung weight on autopsy has been considered useful [30]. In the present case, the left lung weight on autopsy was 730 g, which was more obviously weighted than that of non-pneumonia. To identify the causative pathogens in fatal autopsy cases of pneumonia, histopathological examination using lung tissue can identify specific pathogens and corroborate the microbiological diagnosis [31]. In autopsy cases of patients who died of pneumonia, the inferior lobes of the left and right lungs were the most common sites of pneumonia [32]. As microscopic findings in the patients with pneumococcal pneumonia, intra-alveolar fibrinous exudates with neutrophils and mononuclear cells and marked capillary congestion have been observed [15]. We observed white turbid inferior lobes in both lungs during the autopsy. Also, the remarkable inflammatory cell infiltration, distended capillaries, and congestion with prominent neutrophilic infiltration and erythrocytes were found within the alveolar space of both lung lobes. Because the presence of desquamated bronchiole mucosal epithelial cells in the lungs on histopathology was observed (Fig. 1B), it was believed to reflect the oral ingestion of fenitrothion and malathion, and these compounds were aspirated intratracheally. In OP poisoning, the impairment of the diaphragm and thoracic skeletal muscles cause respiratory paralysis, and high ACh concentrations in the central nervous system cause respiratory depression [2]. Therefore, in our case, it may be rapidly exacerbated respiratory decline following the oral ingestion of fenitrothion and malathion.
S. pneumoniae is the most common causative microorganism of community-acquired pneumonia (CAP) in the elderly [13, 15, 29, 30]. The diagnosis of pneumonia caused by S. pneumoniae is traditionally obtained through culture-based investigations; however, S. pneumoniae is difficult to isolate, and bacteremic pneumococcal pneumonia comprises only one-fourth of all cases of CAP [32]. For these reasons, an S. pneumoniae urinary antigen detection kit is recommended for identifying the causative agent in patients with CAP [32, 33]. The IMMUNOCATCH™ S. pneumoniae pneumococcal urinary antigen test is a useful tool for the qualitative detection of S. pneumoniae capsular antigen [32]. We confirmed a positive reaction for S. pneumoniae with this kit using urine collected at autopsy and identified S. pneumoniae as the causative agent of bacterial pneumonia.
In conclusion, we determined that the direct cause of death in the present case was severe bacterial pneumonia caused by S. pneumoniae infection, and the oral ingestion of both fenitrothion and malathion was further and rapidly exacerbated respiratory function, hastening death. This unusual case provides that organophosphorus pesticide intoxication was not necessarily the direct cause of death.