Patterns and diagnostic criteria of necrotizing fasciitis

Although the condition is not common, if the diagnosis of necrotizing fasciitis was established late, many life-threatening complications might develop as sepsis and septic shock, which might lead to multiorgan damage. In the present literature review, we aim to discuss the classification and clinical patterns of necrotizing fasciitis, in addition to the diagnostic criteria and modalities that were reported among studies in the literature to evaluate such cases. Two main types of necrotizing fascitis were reported in the literature, including the poly and monomicrobial types, however, the diagnostic criteria for each are usually similar. Establishing an early diagnosis is essential to achieve better management and reduce the potential development of complications and death. The clinical patterns are the cornerstone for establishing the diagnosis, however, laboratory investigations might also be used as valid approaches to confirm the diagnosis. Many laboratory models have been proposed to establish the diagnosis of necrotizing fasciitis with variable sensitivities and specificities, and the laboratory risk indicator for necrotizing fasciitis (LRINEC) remains the commonest most efficacious modality. A tissue biopsy can also be used within the clinical settings for indicating the infection, however, it should not hinder the intended surgical interventions. Studies also show that magnetic resonance imaging can adequately detect liquefactive necrosis and is reported with a higher sensitivity than computed tomography. Although the condition is not very common, it might lead to severe consequences, and therefore, early extensive treatment and interventional approaches are encouraged.

Pathogenesis of Equid Alphaherpesvirus 1 Infection in the Central Nervous System of Mice

Equid alphaherpesvirus 1 (EHV-1) causes myeloencephalopathy in horses and occasionally in non-equid species. Although mouse models have been developed to understand EHV-1 pathogenesis, few EHV-1 strains have been identified as highly neurovirulent to mice. The aim of this study was to evaluate the pathogenesis of 2 neurovirulent EHV-1 strains in mice, and to characterize the inflammatory cells and expression of chemokines and the apoptosis marker caspase-3 in the brain of infected mice. C57BL/6J mice were inoculated intranasally with EHV-1 strains A4/72 or A9/92 and evaluated on 1, 2, and 3 days post inoculation (DPI). EHV-1-infected mice showed severe neurological signs at 3 DPI. Ultrastructural analysis revealed numerous viral nucleocapsids and fewer enveloped virions within degenerated and necrotic neurons and in the surrounding neuropil. Histologically, at 3 DPI, there was severe diffuse neuronal degeneration and liquefactive necrosis, prominent microgliosis, and perivascular cuffing composed of CD3+ cells (T cells) and Iba-1+ cells (macrophages), mainly in the olfactory bulb and ventral portions of the brain. In these areas, moderate numbers of neuroglial cells expressed CCL5 and CCL2 chemokines. Numerous neurons, including those in less affected areas, were immunolabeled for cleaved caspase-3. In conclusion, neurovirulent EHV-1 strains induced a fulminant necrotizing lymphohistiocytic meningoencephalitis in mice, with microgliosis and expression of chemokines and caspase-3. This model will be useful for understanding the mechanisms underlying the extensive neuropathology induced by these viral infections.

Macroscopic and Microscopic Identification in Native Chicken (Gallus domesticus) Organ with Helminthiasis

The native chickens collected from the Blimbing Malang Market were found with a state of lethargy and diarrhea. Native chickens were dissected to find out pathological abnormalities that occurred in the chicken's body by carrying out physical examinations and histopathological examinations. Based on the results of observations and examinations carried out both macroscopically and microscopically after necropsy chickens, the organs of chickens that have pathological abnormalities are the duodenum, jejunum and pulmo. The duodenum and jejunum had nematode infestations which showed villi erosion, hemorrhage, liquefactive necrosis, and inflammatory cell infiltration. Pulmo had hemorrhagic parabronchii, atelectasis of blood capillaries, cloudy swelling, and congestion of blood vessels. The visible abnormality of the small intestine organ damage leads to chicken disease to nematode worm infestation.

Salivary Metabolomics Fingerprint of Chronic Apical Abscess with Sinus Tract: A Pilot Study

Chronic apical abscess (CAA) is a lesion of apical periodontitis mostly characterized by areas of liquefactive necrosis with disintegrating polymorphonuclear neutrophils surrounded by macrophages. Its presence leads to local bacterial infection, systemic inflammatory response, pain, and swelling. The use of a novel approach for the study of CAA, such as metabolomics, seems to be important since it has proved to be a powerful tool for biomarkers discovery which could give novel molecular insight on CAA. So, the aim of this study was to verify the possibility to identify the metabolic fingerprint of CAA through the analysis of saliva samples. Nineteen patients were selected for this study: eleven patients affected by CAA with a sinus tract constituted the study group whereas eight patients without clinical and radiographic signs of CAA formed the healthy control group. Saliva samples were collected from each subject and immediately frozen at −80°C. Metabolomic profiles were obtained using a gas chromatography/mass spectrometry instrument. Subsequently, in order to compare the two groups, a multivariate statistical model was built that resulted to be statistically significant. The class of metabolites characterizing the CAA patients was closely related to the bacterial catabolism, tissue necrosis, and presence of a sinus tract. These preliminary results, for the first time, indicate that saliva samples analyzed by means of GC/MS metabolomics may be useful for identifying the presence of CAA, leading to new insights into this disease.

Ischemic myelopathy caused by fibrocartilaginous embolism in a horse

ABSTRACT: This report described clinical, epidemiological, and pathological aspects of ischemic myelopathy caused by fibrocartilaginous embolism (FCE) in a 10-year-old, mixed breed gelding. Clinically, the horse presented acute hind limbs paralysis, with a clinical course of approximately 24 hours. At necropsy, no gross lesions were observed. Cross-sections of the spinal cord revealed focally extensive areas of malacia from the T10 to L4 segments. Focally extensive areas of liquefactive necrosis involving the gray matter and adjacent white matter were observed on histologic sections. The lumen of multiple blood vessels in the periphery of the necrotic areas was occluded by fibrocartilaginous emboli that strongly stained with alcian blue. Clinical signs, gross necropsy, and histological findings observed in this case were identical to those described in the literature for ischemic myelopathy caused by FCE in the horse and other species.

Liquefaction of the brain following stroke shares a similar molecular and morphological profile with atherosclerosis and mediates secondary neurodegeneration in an osteopontin dependent mechanism

Here we used mouse models of heart and brain ischemia to compare the inflammatory response to ischemia in the heart, a protein rich organ, to the inflammatory response to ischemia in the brain, a lipid rich organ. We report that ischemia-induced inflammation resolves between 1 and 4 weeks in the heart compared to between 8 and 24 weeks in the brain. Importantly, we discovered that a second burst of inflammation occurs in the brain between 4 and 8 weeks following ischemia, which coincided with the appearance of cholesterol crystals within the infarct. This second wave shares a similar cellular and molecular profile with atherosclerosis and is characterized by high levels of osteopontin (OPN) and matrix metalloproteinases (MMPs). In order to test the role of OPN in areas of liquefactive necrosis, OPN-/- mice were subjected to brain ischemia. We found that at 7 weeks following stroke, the expression of pro-inflammatory proteins and MMPs was profoundly reduced in the infarct of the OPN-/- mice, although the number of cholesterol crystals was increased. OPN-/- mice exhibited faster recovery of motor function and a higher number of neuronal nuclei (NeuN) positive cells in the peri-infarct area at 7 weeks following stroke. Based on these findings we propose that the brain liquefies after stroke because phagocytic cells in the infarct are unable to efficiently clear cholesterol rich myelin debris, and that this leads to the perpetuation of an OPN-dependent inflammatory response characterized by high levels of degradative enzymes.Significance StatementThe inflammatory response to ischemia in the brain is different to the response to ischemic injury in other organs. In the brain, and for unknown reasons, dead tissue liquefies in response to ischemia by the process of liquefactive necrosis. However, the data we present here demonstrate that there is overlap between the pathophysiology of liquefactive necrosis and atherosclerosis. Specifically, we show that chronic stroke infarcts contain foamy macrophages, cholesterol crystals, high levels of OPN and MMPs, and a similar cytokine profile to atherosclerosis. Therefore, because cholesterol is a central component of myelin, liquefactive necrosis in response to stroke may be caused by an inflammatory response to cholesterol-rich myelin debris that is driven in large part by OPN and MMPs.