Abdullah Abu Sayeed

Background: Gastrointestinal (GI) parasitic infections are a common health concern in captive snakes, potentially affecting their well‐being. This study aimed to determine the prevalence and associated risk factors of helminth and protozoan infections in venomous and non‐venomous snakes. Methods: A total of 174 faecal samples were collected from venomous and non‐venomous captive snakes housed at the Venom Research Centre of Chattogram, Bangladesh, between September 2024 and January 2025. Venomous snakes were housed individually in climate‐controlled terrariums and received biannual deworming; faecal samples were collected six months post‐treatment. In contrast, non‐venomous snakes were not dewormed and were kept either individually in climate‐controlled terrariums or group‐housed in unregulated terrariums. All collected faecal samples underwent routine coproscopy to identify the eggs and oocysts of helminths and protozoan parasites. Results: Results demonstrated that the overall prevalence of GI parasitic infections was 39.1% (95% CI: 31.8–46.8). Helminths were significantly more prevalent (100%) than protozoa (8.8%). Non‐venomous snakes exhibited a higher prevalence of parasitic infections (70.8%) than venomous snakes (34%). Multiple infections were more common in non‐venomous snakes (76.5%) than in venomous snakes (47.1%). Nematodes were the most frequently detected helminths (91.2%), while Cestodes were found only in venomous snakes. Among venomous snakes, Ophiophagus hannah had the highest infection rate (66.7%), while among non‐venomous species, Python molurus and Ptyas mucosa showed the highest prevalence (80%). Risk factor analysis revealed that juveniles had significantly higher odds of infection (aOR = 2.55, p = 0.005), while snakes housed in controlled terrariums had lower infection risks (aOR = 0.143, p = 0.001). Conclusion: This study provides the first record of GI parasitic infections in venomous and non‐venomous captive snakes in Bangladesh, highlighting the need for regular monitoring and appropriate therapeutic measures to mitigate their impact.

Background: We investigated the accuracy of predicting preload responsiveness by means of a passive leg raising test (PLR) using the perfusion index (PI) in critically ill patients showing signs of hypoperfusion in a resource-limited setting. Methods: We carried out a prospective observational single center study in patients admitted for sepsis or severe malaria with signs of hypoperfusion in Chattogram, Bangladesh. A PLR was performed at baseline, and at 6, 24, 48, and 72 h. Preload responsiveness assessed through PI was compared to preload responsiveness assessed through cardiac index (CI change ≥5%), as reference test. The primary endpoint was the accuracy of preload responsiveness prediction of PLR using PI at baseline; secondary endpoints were the accuracies at 6, 24, 48, and 72 h. Receiver operating characteristic (ROC) curves were constructed. Results: The study included 34 patients admitted for sepsis with signs of hypoperfusion and 10 patients admitted for severe malaria. Of 168 PLR tests performed, 143 had reliable PI measurements (85%). The best identified PI change cutoff to discriminate responders from non–responders was 9.7%. The accuracy of PLR using PI in discriminating a preload responsive patient at baseline was good (area under the ROC 0.87 95% CI 0.75–0.99). The test showed high sensitivity and negative predictive value, with comparably lower specificity and positive predictive value. Compared to baseline, the AUROC of PLR using PI was lower at 6, 24, 48, and 72 h. Restricting the analysis to sepsis patients did not change the findings. Conclusions: In patients with sepsis or severe malaria and signs of hypoperfusion, changes in PI after a PLR test detected preload responsiveness. The diagnostic accuracy was better when PI changes were measured at baseline.

Fever is a common cause of hospital admission in Bangladesh but causative agents, other than malaria, are not routinely investigated. Enteric fever is thought to be common. Adults and children admitted to Chittagong Medical College Hospital with a temperature of ≥38.0 °C were investigated using a blood smear for malaria, a blood culture, real-time PCR to detect Salmonella Typhi, S. Paratyphi A and other pathogens in blood and CSF and an NS1 antigen dengue ELISA. We enrolled 300 febrile patients with a negative malaria smear between January and June 2012: 156 children (aged ≤15 years) and 144 adults with a median (interquartile range) age of 13 (5–31) years and median (IQR) illness duration before admission of five (2–8) days. Clinical enteric fever was diagnosed in 52 patients (17.3 %), lower respiratory tract infection in 48 (16.0 %), non-specific febrile illness in 48 (16.0 %), a CNS infection in 37 patients (12.3 %), urinary sepsis in 23 patients (7.7 %), an upper respiratory tract infection in 21 patients (7.0 %), and diarrhea or dysentery in 21 patients (7.0 %). Malaria was still suspected in seven patients despite a negative microscopy test. S. Typhi was detected in blood by culture or PCR in 34 (11.3 %) of patients. Of note Rickettsia typhi and Orientia tsutsugamushi were detected by PCR in two and one patient respectively. Twenty-nine (9 %) patients died during their hospital admission (15/160 (9.4 %) of children and 14/144 (9.7 %) adults). Two of 52 (3.8 %) patients with enteric fever, 5/48 (10.4 %) patients with lower respiratory tract infections, and 12/37 (32.4 %) patients with CNS infection died. Enteric fever was confirmed in 11.3 % of patients admitted to this hospital in Bangladesh with non-malaria fever. Lower respiratory tract and CNS infections were also common. CNS infections in this location merit more detailed study due to the high mortality.

In visceral leishmaniasis (VL), retinal changes have previously been noted but not described in detail and their clinical and pathological significance are unknown. A prospective observational study was undertaken in Mymensingh, Bangladesh aiming to describe in detail visible changes in the retina in unselected patients with VL. Patients underwent assessment of visual function, indirect and direct ophthalmoscopy and portable retinal photography. The photographs were assessed by masked observers including assessment for vessel tortuosity using a semi-automated system. 30 patients with VL were enrolled, of whom 6 (20%) had abnormalities. These included 5 with focal retinal whitening, 2 with cotton wool spots, 2 with haemorrhages, as well as increased vessel tortuosity. Visual function was preserved. These changes suggest a previously unrecognized retinal vasculopathy. An inflammatory aetiology is plausible such as a subclinical retinal vasculitis, possibly with altered local microvascular autoregulation, and warrants further investigation.

Existing evidence suggests that there is often limited understanding among participants in clinical trials about the informed consent process, resulting in their providing consent without really understanding the purpose of the study, specific procedures, and their rights. The objective of the study was to determine the subjects’ understanding of research, perceptions of voluntariness and motivations for participation in a malaria clinical trial.

Magnetic resonance imaging (MRI) allows detailed study of structural and functional changes in the brain in patients with cerebral malaria. In a prospective observational study in adult Bangladeshi patients with severe falciparum malaria, MRI findings in the brain were correlated with clinical and laboratory parameters, retinal photography and optic nerve sheath diameter (ONSD) ultrasound (a marker of intracranial pressure). Of 43 enrolled patients, 31 (72%) had coma and 12 (28%) died. MRI abnormalities were present in 79% overall with mostly mild changes in a wide range of anatomical sites. There were no differences in MRI findings between patients with cerebral and non-cerebral or fatal and non-fatal disease. Subtle diffuse cerebral swelling was common (n = 22/43), but mostly without vasogenic oedema or raised intracranial pressure (ONSD). Also seen were focal extracellular oedema (n = 11/43), cytotoxic oedema (n = 8/23) and mildly raised brain lactate on magnetic resonance spectroscopy (n = 5/14). Abnormalities were much less prominent than previously described in Malawian children. Retinal whitening was present in 36/43 (84%) patients and was more common and severe in patients with coma. Cerebral swelling is mild and not specific to coma or death in adult severe falciparum malaria. This differs markedly from African children. Retinal whitening, reflecting heterogeneous obstruction of the central nervous system microcirculation by sequestered parasites resulting in small patches of ischemia, is associated with coma and this process is likely important in the pathogenesis.

Epidemiological data on malaria in Bangladesh are sparse, particularly on severe and fatal malaria. This hampers the allocation of healthcare provision in this resource-poor setting. Over 85% of the estimated 150,000-250,000 annual malaria cases in Bangladesh occur in Chittagong Division with 80% in the Chittagong Hill Tracts (CHT). Chittagong Medical College Hospital (CMCH) is the major tertiary referral hospital for severe malaria in Chittagong Division.

Severe organophosphate compound (OPC) poisoning is an important clinical problem in many countries of the world. Unfortunately, little clinical research has been performed and little evidence exists with which to determine the best therapy. A study was therefore undertaken to determine the optimal dosing regimen for atropine in the treatment of OPC poisoning. An open-label randomized clinical trial was conducted in Chittagong Medical College Hospital, Chittagong, Bangladesh, on 156 hospitalized individuals with OPC poisoning from June to September 2006. The aim was to compare the efficacy and safety of conventional bolus doses with individualized incremental doses of atropine for atropinization followed by continuous atropine infusion for management of OPC poisoning. Inclusion criteria were patients with a clear history of OPC poisoning with clear clinical signs of toxicity, i.e. features of cholinergic crisis. The patients were observed for at least 96 h. Immediate outcome and complications were recorded. Out of 156 patients, 81 patients received conventional bolus dose atropine (group A) and 75 patients received rapidly incremental doses of atropine followed by infusion (group B). The mortality in group ‘A’ was 22.5% (18/80) and in group ‘B’ 8% (6/75) (p < 0.05). The mean duration of atropinization in group ‘A’ was 151.74 min compared to 23.90 min for group ‘B’ (p < 0.001). More patients in group A experienced atropine toxicity than in group ‘B’ (28.4% versus 12.0%, p < 0.05); intermediate syndrome was more common in group ‘A’ than in group ‘B’ (13.6% versus 4%, p < 0.05), and respiratory support was required more often for patients in group ‘A’ than in group ‘B’ (24.7% versus 8%, p < 0.05). Rapid incremental dose atropinization followed by atropine infusion reduces mortality and morbidity from OPC poisoning and shortens the length of hospital stay and recovery. Incremental atropine and infusion should become the treatment of choice for OPC poisoning. Given the paucity of existing evidence, further clinical studies should be performed to determine the optimal dosing regimen of atropine that most rapidly and safely achieves atropinization in these patients.