Acute bacterial septic vasculopathy

Abstract

Nine of 32 patients were immunosuppressed. The foci of sepsis were variable; in 17 patients, the focus was not identified. Although Neisseria meningitidis was the most common causal agent, several microorganisms were identified. Cutaneous manifestations were an early event in 90.6% of patients. The most common skin signs were purpuric lesions and petechiae. Overall mortality was 28.1%; 65.5% of patients survived without sequelae. Skin biopsies showed thrombi in 100% of cases. Other common findings were inflammatory infiltrate, blood extravasation, and epidermal involvement. Bacteria within the vascular wall were seen in 21.9% of cases and fibrinoid necrosis in 25%. A comparison of ISPs with NISPs disclosed that meningococcemia was more common in the latter group, and the presence of pustules was more common in the former. Histopathology testing revealed that fibrinoid necrosis and bacterial invasion of the vessel wall were more common in ISPs than in NISPs. Conclusions Several microorganisms can cause septic vasculopathy. Clinical presentation is variable and does not depend on the microorganism or the pathogenic mechanism. Histopathologically, septic vasculopathy is a thrombo-occlusive vasculopathy with variable morphology. Cutaneous lesions are an early event and allow for rapid diagnosis.

Severe Septic Vasculitis Preceding Thoracic Empyema: Staphylococcus aureus Enterotoxin Deposition in Vessel Walls as a Possible Pathomechanism

“…Different microorganisms can cause septic vasculitis (1,8,9). In our case, MSSA was the causative agent.…”

“…Septic vasculitis in the skin manifests as purpuric papules, plaques, petechiae, vesicles, bullae and pustules, which generally appear in the early stage of systemic sepsis (1,8,9). The current case presented widespread cutaneous manifestations that preceded the diagnosis of thoracic empyema symptoms by 2 weeks.…”

“…Septic vasculitis or septic vasculopathy is defined as vascular changes occurring in patients with sepsis (1). Although the process whereby the cutaneous changes develop has yet to be fully clarified, several complex pathogenic mechanisms of septic vasculitis are assumed, such as disseminated intravascular coagulation, direct vessel wall invasion by the microorganism, immune-mediated vasculitis and septic embolism (2).…”

“…Although the process whereby the cutaneous changes develop has yet to be fully clarified, several complex pathogenic mechanisms of septic vasculitis are assumed, such as disseminated intravascular coagulation, direct vessel wall invasion by the microorganism, immune-mediated vasculitis and septic embolism (2). Although these have been observed histopathologically, there have been no investigations of whether the toxins directly affect skin vessels (1). We present here a case of septic vasculitis that preceded thoracic empyema, in which deposition of Staphylococcus aureus enterotoxin (SE) on the vessel walls was a factor in the severe cutaneous manifestations.…”

Neutrophilic Panniculitis: Algorithmic Approach to a Heterogeneous Group of Disorders

“…17 Septic thrombi containing microorganisms may be found in secondary infective panniculitis. 18 Epithelioid granulomas, with or without admixed neutrophils, are strongly indicative of infection when present in a background of neutrophilic panniculitis (Figure 3, D). 19 Lastly, demonstration of microorganisms on hematoxylin-eosin, tissue Gram, Grocott methenamine silver, or Fite stains, or positive microbial cultures would confirm the diagnosis.…”