Dual Time Point Imaging (DTPI) technique is a specialised protocol adopted in 18F-Fluorodeoxyglucose (FDG) Positron Emission Tomography (PET) imaging. This technique is claimed to be useful in differentiating malignant and infective lesions. The authors adopted this technique in a patient diagnosed with tuberculous spondylodiscitis and psoas abscess which demonstrated higher Maximum Standardized Uptake Value (SUVmax) during initial scans as compared with those obtained on delayed scans. The SUVmax changes between the two time points are believed to be a valuable finding for chronic granulomatous infective lesions such as tuberculosis.

Interleukin-27 (IL-27) has a pleiotropic role either as a pro-inflammatory or anti-inflammatory cytokine in inflammatory related diseases. The role and involvement of IL-27 during malaria was investigated and the effects of modulating its release on the production of major inflammatory cytokines and the histopathological consequences in major affected organs during the infection were evaluated. Results showed that IL-27 concentration was significantly elevated throughout the infection but no positive correlation with the parasitaemia development observed. Augmentation of IL-27 significantly elevated the release of anti-inflammatory cytokine, IL-10 whereas antagonising and neutralising IL-27 produced the opposite. A significant elevation of pro-inflammatory cytokines (IFN-γ and IL-6) was also observed, both during augmentation and inhibition of IL-27. Thus, it is suggested that IL-27 exerts an anti-inflammatory activity in the Th1 type response by signalling the production of IL-10 during malaria. Histopathological examination showed sequestration of PRBC in the microvasculature of major organs in malarial mice. Other significant histopathological changes include hyperplasia and hypertrophy of the Kupffer cells in the liver, hyaline membrane formation in lung tissue, enlargement of the white and red pulp followed by the disappearance of germinal centre of the spleen, and tubular vacuolation of the kidney tissues. In conclusion, it is suggested that IL-27 may possibly acts as an anti-inflammatory cytokine during the infection. Modulation of its release produced a positive impact on inflammatory cytokine production during the infection, suggesting its potential in malaria immunotherapy, in which the host may benefit from its inhibition.

Group B streptococcus (GBS) is a common cause of infection in newborns and in early infants. However, GBS infection in an infant older than three months is infrequently reported in the literature. We reported a case of an apparently well six-month-old infant who died of sudden death due to GBS pneumonia, diagnosed at autopsy. The six-month-old, apparently well male infant was brought in dead to the Emergency Department. He underwent medicolegal autopsy four hours after death, as part of an overall sudden unexpected death in infancy investigation (SUDI). Apart from whitish froth oozing out of both nostrils, he appeared to be well-nourished infant without any deformity, syndromic features or obvious suspicious marks of injury externally. Internal examination showed generalized hyperinflated with patchy consolidation of upper and middle lobes of bilateral lung. Multiple matted mesenteric lymphadenopathy were also detected. Blood and lung tissue specimens collected under aseptic technique yielded growth of GBS. Post-mortem histology from consolidated lungs confirmed pneumonic features while mesenteric lymph nodes showed reactive changes inkeeping with underlying infective process. Death was attributed to GBS pneumonia. This case highlights the importance of a detailed autopsy in sudden unexpected death in infancy (SUDI) and the crucial role of post-mortem microbiological study in such cases. Relevant autopsy protocols that need to be employed during microbiological sampling are briefly discussed.

Background: The cytokine cascade in the immunopathogenesis of malaria infection had been widely studied. However, their specific association with survival and severe infection remained obscure.Methods: Thestudy investigated the cytokine profiles and histopathological features of malaria in the severe infection and survival models by using male ICR mice and male Sprague Dawley rats respectively.Results: The severe model, the infected ICR mice, exhibited a high parasitemia with 100% mortality after peak parasitemia at day 5 post-infection. The survival model, the infected Sprague Dawley rats, showed mild parasitemia with full recovery by day 14 of infection. Both severe and survival models showed similar histopathological severity during peak parasitemia. The severe model produced highly elevated levels of pro-inflammatory cytokines, TNF-α and IL-1α, and low levels of the anti-inflammatory cytokine, IL-4; while the survival model showed low levels of TNF-α and IL-1α with high levels of IL-4.Conclusion: There were differences in the pathogenesis of the severe and survival models of malaria infection. These could be a basis for immunotherapy of malaria in the future

Malaria infection still remains as one of the most prominent parasitic diseases afflicting mankind in tropical and subtropical regions. The severity of malaria infection has often been associated to exuberant host immune inflammatory responses that could possibly lead to severe immunopathological conditions and subsequent death of host tissues. Activin A is a protein belonging to the transforming growth factor-beta (TGF-β) family that regulates multiple physiological processes and pathological-associated diseases. The biological roles of activin A have been associated with manipulation of inflammation-related processes and modulation of host immune responses. This implies that activin A protein could play a role in malaria pathogenesis since malaria infection has been closely linked to severe immune responses leading to death, However, the actual in vivo role of activin A in malaria infection remains elusive. Hence, this study was undertaken to investigate the involvement of activin A in malaria infection as well as to assess the modulating effects of activin A on the cytokine releases (TNF-α, IFN-γ and IL-10) and histopathological changes in major affected organs (kidney, liver, lung, brain and spleen) in malarial mice infected with Plasmodium berghei ANKA. Our results showed that the concentrations of plasma activin A were significantly increased in malarial mice throughout the study periods. Also. the systemic activin A level was positively correlated with malaria parasitemia. This indicates that activin A could play a role in malaria pathogenesis and malaria parasitemia development. Plasma TNF-α, IFN-γ and IL-10 cytokine levels were significantly increased in malarial mice at day-5 post infection, suggesting that these cytokines attributed to severe malaria pathogenesis. Histopathological features such as sequestration of parasitized red blood cells (pRBCs) and hemozoin formation were amongst the most common pathological conditions observed in tissues of major affected organs (kidney, liver, lung, brain and spleen) in malarial mice. Neutralization of activin A production via recombinant mouse activin RIIA Fc chimera (rmActivin RIIA Fc chimera) had significantly reduced the parasitemia levels in malarial mice. The release of TNF-α cytokine was significantly reduced as well as the sequestration of parasitized pRBCs and hemozoin formation in major affected organs in malarial mice were also alleviated following inhibition of activin A production. Overall, this preliminary study suggests that activin A could play an immune modulation role in malaria pathogenesis through modulation of TNF-α release that benefits host from severe pathological destructions provoked by intensified inflammatory responses. Further studies are warranted to elucidate the precise mechanism of immune modulation mediated by activin A and its associated immune-modulation mediators in regulating the inflammatory responses elicited during the course of malaria infection.

Post-mortem microbiology (PMM) is an important tool in identifying possible causes of sudden unexpected death, as an infectious cause is highly suspected. However, contamination is a major problem in microbiology, and this has increased the difficulty determining the true pathogen that contributes to death in post-mortem cases. Skin commensals are common contaminants in blood cultures. This study was conducted to investigate the skin flora on early deceased bodies and observe the bacteria detected at different post-mortem intervals (PMIs). As blood is usually drawn from the neck and femoral sites for PMM examination, the two body sites were chosen as the sampling sites. Skin swab samples from the neck and femoral (n=80) of each early deceased body were collected by sterile cotton swabs. DNA was extracted from the swabs and then subjected to high-throughput 16S rRNA sequencing by using the Illumina MiSeq platform. Staphylococcus was found to be the most dominant genus in both neck and femoral sites. LEfSe results showed that Cutibacterium is significantly different at the neck site while Corynebacterium is more abundant at femoral site. There are significant differences at genus level between PMI<5H and PMI>5H at both neck and femoral sites. The findings of the present study may act as a reference for microbiologists and forensic pathologists when mixed growth or contamination occurs in post-mortem blood cultures.