Vibrio vulnificus is a halophilic Gram-negative bacillus found worldwide in warm coastal waters. The pathogen has the ability to cause primary sepsis in certain high-risk populations, including patients with chronic liver disease, immunodeficiency, iron storage disorders, end-stage renal disease, and diabetes mellitus. Most reported cases of primary sepsis in the USA are associated with the ingestion of raw or undercooked oysters harvested from the Gulf Coast. The mortality rate for patients with severe sepsis is high, exceeding 50% in most reported series. Other clinical presentations include wound infection and gastroenteritis. Mild to moderate wound infection and gastroenteritis may occur in patients without obvious risk factors. Severe wound infection is often characterized by necrotizing skin and soft-tissue infection, including fasciitis and gangrene. V. vulnificus possesses several virulence factors, including the ability to evade destruction by stomach acid, capsular polysaccharide, lipopolysaccharide, cytotoxins, pili, and flagellum. The preferred antimicrobial therapy is doxycycline in combination with ceftazidime and surgery for necrotizing soft-tissue infection.

Background:Endotoxin is a lipopolysaccharide (LPS) constituent of the outer membrane of most gram negative bacteria. Ubiquitous in the environment, it has been implicated as a cause or con-tributing factor in several disparate disorders from sepsis to heatstroke and Type II diabetes mellitus. Starting at birth, the innate immune system develops cellular defense mechanisms against environmen-tal microbes that are in part modulated through a series of receptors known as toll-like receptors. Endo-toxin, often referred to as LPS, binds to toll-like receptor 4 (TLR4)/ myeloid differentiation protein 2 (MD2) complexes on various tissues including cells of the innate immune system, smooth muscle and endothelial cells of blood vessels including coronary arteries, and adipose tissue. Entry of LPS into the systemic circulation ultimately leads to intracellular transcription of several inflammatory mediators. The subsequent inflammation has been implicated in the development and progression atherosclerosis and subsequent coronary artery disease and heart failure.Objective:The potential roles of endotoxin and TLR4 are reviewed regarding their role in the pathogen-esis of atherosclerotic heart disease.Conclusion:Atherosclerosis is initiated by inflammation in arterial endothelial and subendothelial cells, and inflammatory processes are implicated in its progression to clinical heart disease. Endotoxin and TLR4 play a central role in the inflammatory process, and represent potential targets for therapeutic intervention. Therapy with HMG-CoA inhibitors may reduce the expression of TLR4 on monocytes. Other therapeutic interventions targeting TLR4 expression or function may prove beneficial in athero-sclerotic disease prevention and treatment.

Heatstroke is life-threatening condition characterized by hyperthermia and central nervous system disturbances. It can also be classified as a form of systemic inflammatory response syndrome with multiple organ dysfunction and in many ways resembles sepsis. Like sepsis, most patients with heatstroke demonstrate a hyperdynamic hemodynamic response. In contrast to sepsis, rhabdomyolysis may complicate management and initial fluid resuscitation is not well defined. We present an illustrative case report and review of literature.

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Traditionally, the management of patients with pulmonary embolism has been accomplished with anticoagulant treatment with parenteral heparins and oral vitamin K antagonists. Although the administration of heparins and oral vitamin K antagonists still plays a role in pulmonary embolism management, the use of these therapies are limited due to other options now available. This is due to their toxicity profile, clearance limitations, and many interactions with other medications and nutrients. The emergence of direct oral anticoagulation therapies has led to more options now being available to manage pulmonary embolism in inpatient and outpatient settings conveniently. These oral therapeutic options have opened up opportunities for safe and effective pulmonary embolism management, as more evidence and research is now available about reversal agents and monitoring parameters. The evolution of the pharmacological management of pulmonary embolism has provided us with better understanding regarding the selection of anticoagulants. There is also a better understanding and employment of anticoagulants in pulmonary embolism in special populations, such as patients with liver failure, renal failure, malignancy, and COVID-19.

Methicillin-resistant Staphylococcus aureus (MRSA) has become the dominant strain of Staphylococcus aureus in many communities of the United States. As a result, many clinicians are now empirically covering for this pathogen in the treatment of various skin and soft-tissue infections. Should this practice apply to cellulitis? In order to answer this question, we defined cellulitis and reviewed the pathogenesis, microbiology, and current studies of inpatient and outpatient antimicrobial therapy. The current evidence suggests empirical MRSA coverage for community-acquired cellulitis may not be necessary in non-purulent (non-suppurative) forms of this infection. Most cases are non-purulent and not amenable to culture although antibody studies indicate streptococci are the most common etiologic agents. Current studies of antimicrobial therapy tend to agree with this finding. Empirical beta-lactam therapy directed primarily at streptococci appears sufficient for non-purulent cellulitis regardless of the prevalence of MRSA in the community.