Clostridial Myonecrosis: A Comprehensive Review of Toxin Pathophysiology and Management Strategies.

Clostridial myonecrosis, commonly known as gas gangrene (GG), is a rapidly progressing and potentially fatal bacterial infection that primarily affects muscle and soft tissue. In the United States, the incidence of GG is roughly 1000 cases per year, while, in developing countries, the incidence is higher. This condition is most often caused by Clostridium perfringens, a Gram-positive, spore-forming anaerobic bacterium widely distributed in the environment, although other Clostridium species have also been reported to cause GG. The CP genome contains over 200 transport-related genes, including ABC transporters, which facilitate the uptake of sugars, amino acids, nucleotides, and ions from the host environment. There are two main subtypes of GG: traumatic GG, resulting from injuries that introduce Clostridium spores into deep tissue, where anaerobic conditions allow for bacterial growth and toxin production, and spontaneous GG, which is rarer and often occurs in immunocompromised patients. Clostridium species produce various toxins (e.g., alpha, theta, beta) that induce specific downstream signaling changes in cellular pathways, causing apoptosis or severe, fatal immunological conditions. For example, the Clostridium perfringens alpha toxin (CPA) targets the host cell's plasma membrane, hydrolyzing sphingomyelin and phosphatidylcholine, which triggers necrosis and apoptosis. The clinical manifestations of clostridial myonecrosis vary. Some patients experience the sudden onset of severe pain, swelling, and muscle tenderness, with the infection progressing rapidly to widespread tissue necrosis, systemic toxicity, and, if untreated, death. Other patients present with discharge, pain, and features of cellulitis. The diagnosis of GG primarily involves clinical evaluation, imaging studies such as X-rays, computer tomography (CT) scans, and culture. The treatment of GG involves surgical exploration, broad-spectrum antibiotics, antitoxin, and hyperbaric oxygen therapy, which is considered an adjunctive treatment to inhibit anaerobic bacterial growth and enhance the antibiotic efficacy. Early recognition and prompt, comprehensive treatment are critical to improving the outcomes for patients affected by this severe and life-threatening condition.

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.

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.