Development of purpura fulminans by Candida glabrata and Mucormycosis infection post-surgery.

Purpura fulminans (PF) is a disorder with multifactorial causes that lead to acute localize skin microvasculature thrombosis. PF can be classified as one of the manifestations of disseminated vascular coagulation (DIC). Although, there are three types of PF including hereditary (autosomal dominant) due to mutations in single nucleotide polymorphisms (PROC and PROS1) and serpin family C member 1 (SERPINC1) genes. Idiopathic or acquired type of PF is complex and the pathophysiology is ambiguous, however, low levels of protein C and S were observed. The acute infectious form of PF occurs post-bacterial infection (e.g., Neisseria). The clinical presentation is limited to skin findings or systematic manifestation (shock, disseminated intravascular coagulation, or death). We are presenting two cases of PF sharing similar clinical manifestations developed within 12 h post-operatively with distinct micro-organisms infection. The first patient's wound culture grew fluffy mold, and the sequencing confirmed a Mucormycosis, Absidia corymbifera species, while the second patient was infected by cutaneous Candida glabrata which led to the development of PF. Our findings suggest that surgery can trigger local immunological responses in susceptible individuals such as concealed protein C and S deficiency or microorganism toxins that initiated the rapidly developing of PF in those patients.

JAPANESE ENCEPHALITIS VIRUS TRIGGERED OVERLAPPING MILLER FISHER SYNDROME WITH BICKERSTAFF ENCEPHALITIS IN A YOUNG FILIPINO CRUISE LINE WORKER.

Japanese encephalitis virus is an RNA flavivirus and one of the rare pathogens that can cause encephalitis. The main vector is the Culex tritaeniorhynchus mosquito. The virus is very close in pathophysiology and structure to the West Nile and St. Louis encephalitis viruses. It is endemic in Asia and Western Pacific areas, mostly during the summer; only a few cases have been reported outside those regions. We present the case of a young Filipino cruise line male worker with signs and symptoms of Japanese encephalitis concomitantly with Miller Fisher syndrome and Bickerstaff brainstem encephalitis. The patient developed obtundation, ataxia, areflexia, flaccid paralysis, and ophthalmoplegia, which were preceded by a few days of constitutional symptoms (fever, malaise, fatigue and anorexia). Physical examination showed various stages of erythema nodosum on the lower extremities. Analysis of cerebrospinal fluid was positive for anti-GQ1b, West Nile IgG and Japanese encephalitis IgM. Despite the neurological complications and bradyarrhythmia occurring during hospitalization, the patient recovered completely under our regimen. LEARNING POINTS: Insidious onset of bilateral paralysis preceded by fever is most likely encephalitis.Japanese encephalitis virus led to the development of variant forms of Guillain-Barré syndrome in our patient.Supportive care resulted in significant recovery despite the severity of the condition.

Prior viral infection determines the mode and severity of monkeypox virus.

OBJECTIVES: Monkeypox (MPox) is a zoonotic virus in the genus Orthopoxvirus. It is transmitted from animal to human, and between humans. The clinical presentations vary, starting with a prodrome phase to different skin findings and systemic complications. METHODS: We present two distinctive cases of MPox co-infected with other viruses (hepatitis C virus [HCV] and HIV) by clinical and histopathological analysis. RESULTS: Surprisingly, the MPox patient with a history of HCV developed different skin pathological characteristics (less severe inflammatory changes than the classic patient with HCV or MPox alone). In contrast, patients living with HIV presenting with MPox had severe inflammatory cutaneous changes and distortion of the skin architecture. CONCLUSION: Our findings strongly suggest that MPox infections likely occur in the presence of one or more previous other viral infections, and the prior infection with specific microbes determines the severity of MPox infection.

Transactivation Response DNA-Binding Protein of 43 (TDP-43) and Glial Cell Roles in Neurological Disorders.

The trans-activation response DNA-binding protein of 43kDa (TDP-43) is involved in the pathogenesis of multiple brain disorders. As scientists are unraveling TDP-43 function and its impact on various diseases, we have begun to subcategorize them into TDP-43 proteinopathies. Furthermore, glial cell dysfunction contributes to various disorders, and TDP-43 is involved with glial cells via multiple pathways (direct or indirect) that aggravate the pathophysiology of such disorders. We are only now discovering and understanding the vast and diverse roles TDP-43 plays on neuronal cells and its effects on gliosis and neurodegenerative pathologies. It has multiple roles: mRNA maturation and splicing, transporting and maintaining mRNA stability, a component of stress granules and ubiquitination of dysfunctional or misfolded proteins, transcription of microtubule "Futsch" protein, and a role in maintaining synapse integrity and possibly more as we continue to research and uncover the labyrinth of the neuronal network. TDP-43 could also have a detrimental impact on glial cell activation and pathophysiology in diseases where TDP-43 is associated with its pathogenesis. We will review the pathophysiology of various neurological disorders that are associated with the alteration of the TDP-43 levels along with glial cell activation. Further, multiple diseases have glial cell participation in the pathogenesis, and the role of TDP-43 has not yet been investigated. We, therefore, explore those disorders in the context of both TDP-43 and glial cells involvement. This step will enhance the understanding of neurodegeneration where further research could prompt curative modalities with the advancement of technology.

Improving the performance of mini-channel heat sink by using wavy channel and different types of nanofluids.

The combination of nano fluid and changing cross-section mini-channel heat sink effects have become a remarkable choice for the use of thermal devices such as miniature electronic devices to be effectively cooled. In this paper, the comparison of three dimensional straight and wavy channel configuration with using different types nano fluids are numerically investigated. The effects of wave amplitude and A particular type of volume fraction of (Copper Oxide CuO, Dimond Al2O3, Iron Oxide Fe3O4, Titanium Oxide TiO2 and Silver Ag-nano fluids are offered. Three amplitudes of waves (0.15 mm, 0.2 mm and 0.25 mm) and Reynold's number from 200 to 1000 and concentration volume varieties from 0 to 0.075 are used. The effect on thermal resistance, pressures drop, factor of friction of the mini channel is displayed. It is observed that the mini-channel sink's heat transfer efficiency is greatly enhanced compared to the straight channel in an event of adding distilled water as accoolant. The results indicate that nano fluid and wavy mini-channel can boost the heat sink's hydrothermal efficiency and Ag- water nano fluid in term of heat transfer, it outperforms other nanofluids an enhancement in the Nusselt number reached to 54% at concentration volume 0.075.

Pneumocystis jirovecii pneumonia and deep vein thrombosis in a patient with glioblastoma multiforme.

We present a case of disseminated Pneumocystis jirovecii pneumonia in a patient with a medical history of glioblastoma multiforme associated with acute deep-vein thrombosis. The patient presented to the emergency department with clinical features of pulmonary infection, and the chest images showed pneumonia. Antibiotics were initiated (azithromycin, cefepime, and vancomycin) and the patient was transferred to the ward for further management, where the condition of the patient continued to worsen over the second day. The patient developed bilateral lower extremity swelling and the doppler ultrasound revealed bilateral lower extremity acute deep vein thrombosis. Laboratory results showed pancytopenia and transaminitis. However, a repeated chest X-ray showed ground-glass changes and interstitial infiltrates, suggestive of atypical infection. We indeed identified D-glucan which hints to a disseminated form of Pneumocystis jirovecii pneumonia infection in this patient. We further confirmed the Pneumocystis jirovecii pneumonia by polymerase chain reaction test from the fluid obtained via bronchoalveolar lavage. We, therefore, initiated intravenous trimethoprim/ sulfamethoxazole treatment with an anticoagulant, and the patient's condition improved. Our findings strongly suggest a possible link between Pneumocystis jirovecii pneumonia infection and thrombogenesis, with impact in medical practice.