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Mucormycosis is a rare, emerging angioinvasive infection caused by ubiquitous filamentous fungi. In recent decades, an increase in cutaneous or post-traumatic mucormycosis has been reported. We describe two cases of post-traumatic wound infections with Mucor circinelloides, a mucor species only rarely reported as a cause of post-traumatic mucormycosis. Often considered lethal, management required a combination of medical and surgical therapies to achieve a favorable outcome in both cases.

Cardiogenic shock during a pheochromocytoma crisis is a life-threatening disorder. This case report illustrates a 49-year-old male with profound cardiogenic shock, extreme hemodynamic instability (systolic blood pressure ranging from 45 up to 290 mmHg in a cyclic pattern), and progressive multiple organ failure in the presence of a unilateral adrenal mass. Emergency adrenalectomy led to rapid hemodynamic stabilization. Histological investigation confirmed the diagnosis of pheochromocytoma. This case indicates that emergency adrenalectomy, although usually not considered first choice, is a valid option in cardiogenic shock and extremely fluctuating hemodynamics due to a pheochromcytoma-induced catecholamine storm.

Invasive infection with Lancefield group C streptococci in humans is extremely rare, with the vast majority of clinical isolates belonging to Streptococcus dysgalactiae subsp. equisimilis. We report a case of meningoencephalitis in a 69-year-old man caused by Streptococcus equi subsp. equi, a microbe that causes strangles in Equus caballus (i.e., the horse). This is only the fourth infection with this subtype of the central nervous system (CNS) reported in humans. The invasiveness of these bacteria, known to be capable of releasing strongly immunogenic exotoxins, is illustrated by white matter lesions that are present in the acute phase. This patient initially recovered well after treatment with antibiotics and glucocorticoids. However, the patient was readmitted 5 months later with multiple intraparenchymatous cerebral haemorrhages. Cerebral angiography confirmed the presence of a suspected superficial dural arteriovenous fistula (DAVF), which is seldom reported after CNS infection. The invasiveness of these bacteria was illustrated by white matter lesions present in the acute phase and the occurrence of a de novo dural arteriovenous fistula in the follow-up period.

We present a case of a 3-year-old boy with neurodegeneration. Family history reveals Rendu-Osler-Weber disease. Magnetic resonance imaging (MRI) of the spinal cord and spinal angiography showed a spinal arteriovenous fistula with venous aneurysm, causing compression of the lumbar spinal cord. Embolisation of the fistula was executed, resulting in clinical improvement. A week after discharge he was readmitted with neurologic regression. A second MRI scan revealed an intraspinal epidural haematoma and increase in size of the aneurysm with several new arterial feeders leading to it. Coiling of the aneurysm and fistulas was performed. Postoperative, the spinal oedema increased despite corticoids, causing more extensive paraplegia of the lower limbs and a deterioration of his mental state. A laminectomy was performed and the aneurysm was surgically removed. Subsequently, the boy recovered gradually. A new MRI scan after two months showed less oedema and a split, partly affected spinal chord. This case shows the importance of excluding possible arteriovenous malformations in a child presenting with progressive neurodegeneration. In particular when there is a family history for Rendu-Osler-Weber disease, scans should be performed instantly to rule out this possibility. The case also highlights the possibility of good recovery of paraplegia in paediatric Rendu-Osler-Weber patients.

L-Arginine is converted to the highly reactive and unstable nitric oxide (NO) and L-citrulline by an enzyme named nitric oxide synthase (NOS). NO decomposes into other nitrogen oxides such as nitrite (NO2−) and nitrate (NO3−), and in the presence of superoxide anion to the potent oxidizing agent peroxynitrite (ONOO−). Activated rodent macrophages are capable of expressing an inducible form of this enzyme (iNOS) in response to appropriate stimuli, i.e., lipopolysaccharide (LPS) and interferon-γ (IFNγ). Other cytokines can modulate the induction of NO biosynthesis in macrophages. NO is a major effector molecule of the anti-microbial and cytotoxic activity of rodent macrophages against certain micro-organisms and tumour cells, respectively. The NO synthesizing pathway has been demonstrated in human monocytes and other cells, but its role in host defence seems to be accessory. A delicate functional balance between microbial stimuli, host-derived cytokines and hormones in the microenvironment regulates iNOS expression. This review will focus mainly on the known and proposed mechanisms of the regulation of iNOS induction, and on agents that can modulate NO release once the active enzyme has been expressed in the macrophage.

Activated cholesterol-laden macrophages in atherosclerotic lesions are believed to influence the progression of this disease. The induction of nitric oxide synthase (iNOS) activity was investigated in control and cholesterol-laden J774 macrophages, obtained by pre-incubation with oxidized or acetylated low density lipoproteins (oxLDL, acLDL). Loading with oxLDL caused a small induction of NOS activity in unstimulated cells, as indicated by nitrite and citrulline accumulation in the supernatant. However, it suppressed the iNOS activity resulting from stimulation of the cells with lipopolysaccharide with or without interferon-γ. AcLDL had no inhibitory effect, indicating that cholesterol accumulation as such was not responsible. Since the induction of NOS in macrophages is inhibited by glucocorticoids, the possibility that a glucocorticoid-like factor, formed during oxidation of LDL, may cause the inhibition, was investigated. However, addition of the glucocorticoid receptor antagonist mifepristone did not prevent the oxLDL-dependent NOS inhibition, indicating that the glucocorticoid receptor is not involved in the suppressive effect of oxLDL.