The Pathogenesis of Primary and Secondary Infection with Fasciola hepatica in Mice

1978 ◽  
Vol 15 (6) ◽  
pp. 763-769 ◽  
Author(s):  
R. A. Masake ◽  
R. B. Wescott ◽  
G. R. Spencer ◽  
B. Z. Lang
Keyword(s):  
Connective Tissue ◽  
Inflammatory Response ◽  
Host Response ◽  
Bile Ducts ◽  
Fasciola Hepatica ◽  
Secondary Infection ◽  
Chronic Phase ◽  
Inflammatory Cells ◽  
Duct System ◽  
Secondary Infections

Primary and secondary infections of F. hepatica in mice were compared to determine how prior exposure to the parasite affected host response. Mice with primary parenchymal Fasciola infections initially had hemorrhagic tunnels filled with inflammatory cells and connective tissue. These lesions were progressive and became most severe 30 days after exposure as the parasites entered the bile ducts. At this time there was much hyperplasia and thickening of all layers of the duct system near the parasites and occasionally severe periportal fibrosis. By 2 months after exposure regeneration of the damaged liver cells was complete although hyperplasia persisted in bile ducts containing flukes. In mice with secondary infections (mice exposed 40 to 50 days after first infection), the inflammatory response was faster and shorter. Most lesions were resolved by 30 days after the second exposure. There was little difference in histology of primary and secondary infections during the chronic phase of the disease.

scholarly journals Fascioliasis: una causa infrecuente de obstrucción de vía biliar. Reporte de un caso

2021 ◽  
Vol 51 (3) ◽  
Author(s):  
Amada Belén Geldres Molina ◽  
Juan Luis Romero García ◽  
Laura Isabel García Honores ◽  
Christian Eduardo Alcántara Figueroa
Keyword(s):  
Obstructive Jaundice ◽  
Biliary Tract ◽  
Bile Ducts ◽  
Fasciola Hepatica ◽  
Chronic Phase ◽  
Anthelmintic Treatment ◽  
Parasitic Disease ◽  
Endoscopic Retrograde ◽  
Adult Form ◽  
The Ideal

Hepatic fascioliasis is a parasitic disease caused by the fluke Fasciola hepatica. In the chronic phase of the disease, the adult form of the parasite adopts the bile ducts as the ideal environment to develop, causing them to dilate and simulating an obstructive jaundice process. The case of a 48-year-old woman is presented, who was admitted for jaundice, choluria and eight loss. After the corresponding complementary studies had been carried out, an endoscopic retrograde cholangiography (ERCP) was performed and an adult Fasciola hepatica parasite was extracted from the biliary tract. Subsequently, anthelmintic treatment with triclabendazole was started, resulting in a favorable evolution and resolution of the condition.

Hyperplasia of the bile duct in fascioliasis and its relation to the problem of nutrition in the liver-fluke, Fasciola hepatica L.

Parasitology ◽  
1963 ◽  
Vol 53 (1-2) ◽  
pp. 123-133 ◽  
Author(s):  
Ben Dawes
Keyword(s):  
Bile Duct ◽  
Connective Tissue ◽  
Bile Ducts ◽  
Inflammatory Process ◽  
Liver Fluke ◽  
Fasciola Hepatica ◽  
Fibrous Tissue ◽  
Feeding Habit ◽  
Glandular Tissue ◽  
Dense Fibrous Tissue

Histological investigations of the bile ducts of various hosts of F. hepatica during the early stages of infection, when the flukes are burrowing in the liver and have not yet reached the bile ducts, indicate that subtle changes are brought about, probably by chemical agencies and as a result of the inflammatory process, in the bile ducts of the hosts. The transitory appearance of minute cytoplasmic blebs at the free margins of the epithelial cells seems to inaugurate an intense hyperplasia of the epithelium with tubular ingrowths and adenomatous development of glandular tissue, and an associated fibrosis which produces a thick underlying layer of dense fibrous tissue. At the time of entry of the flukes into the biliary system the hyperplastic epithelium is intact, but soon the spines and suckers of the flukes abrade the superficial cells until this part of the duct is completely denuded. It is suggested that as a result of the inflammatory reaction, the fluke has been provided with a ‘pasture’ of hyperplastic epithelium and connective tissue on which it may continue to browse for considerable periods without necessarily affecting the host adversely. Tissue debris is found in the contents of the bile duct and similar homogenized materials occur in the caecal contents of the fluke. Previous researches have shown that the fluke will feed on various tissues, and it is suggested that this tissue-feeding habit persists during its life in the bile duct. These results agree with the findings of Müller (1923) but are at variance with the results obtained by other investigators, as is shown in discussion. The hyperplasia of the bile duct is not characteristic of fascioliasis, occurring also in clonorchiasis, opisthorchiasis and dicrocoeliasis, and in these and possibly other instances it is probably intimately connected with the nutrition of the flukes concerned.

scholarly journals The Pathology of Natural Fasciola hepatica Infection in Cattle

1969 ◽  
Vol 6 (3) ◽  
pp. 244-256 ◽  
Author(s):  
Timo Rahko
Keyword(s):  
Mast Cells ◽  
Bile Ducts ◽  
Fasciola Hepatica ◽  
Inflammatory Cells ◽  
Coagulative Necrosis ◽  
Chronic Infections ◽  
Hepatic Parenchyma ◽  
Hepatica Infection ◽  
Hepatic Cells

The pathology of bovinc livers during the parenchymal and chronic phases of natural Fasciola hepatica infections is described. Immature infections occurred from September to the middle of January. Significant changes of the hepatic parenchyma caused by immature flukes occurred in association with large migrational tracks. The changes included frequent thrombosis and haemorrhages, extensive disintegration and coagulative necrosis of hepatic cells, and abundant infiltrates of inflammatory cells. In chronic infections the proliferation and destruction of the mucosa of main bile ducts were pronounced. Normal mast cells were lacking in the portal areas surrounding fresh migrational tracks. In chronically infected livers mast cells occurred in great numbers.

scholarly journals IL6 inhibition in critically ill COVID-19 patients is associated with increased secondary infections

2020 ◽  
Author(s):  
Lucas M Kimmig ◽  
David Wu ◽  
Matthew Gold ◽  
Natasha N Pettit ◽  
David Pitrak ◽  
...  
Keyword(s):  
Critically Ill ◽  
Host Response ◽  
Diffuse Alveolar Damage ◽  
Secondary Infection ◽  
Evidence Based Treatment ◽  
Secondary Infections ◽  
Experimental Therapies ◽  
Physician Awareness ◽  
Post Mortem Findings ◽  
Anti Inflammatory

Background: Anti-inflammatory therapies such as IL-6 inhibition have been proposed for COVID-19 in a vacuum of evidence-based treatment. However, abrogating the inflammatory response in infectious diseases may impair a desired host response and predispose to secondary infections. Methods: We retrospectively reviewed the medical record of critically ill COVID-19 patients during an 8-week span and compared the prevalence of secondary infection and outcomes in patients who did and did not receive tocilizumab. Additionally, we included representative histopathologic post-mortem findings from several COVID-19 cases that underwent autopsy at our institution. Results: 111 patients were identified, of which 54 had received tocilizumab while 57 had not. Receiving tocilizumab was associated with a higher risk of secondary bacterial (48.1% vs. 28.1%, p=0.029 and fungal (5.6% vs. 0%, p=0.112) infections. Consistent with higher number of infections, patients who received tocilizumab had higher mortality (35.2% vs. 19.3%, p=0.020). Seven cases underwent autopsy. In 3 cases who received tocilizumab, there was evidence of pneumonia on pathology. Of the 4 cases that had not been given tocilizumab, 2 showed evidence of aspiration pneumonia and 2 exhibited diffuse alveolar damage. Conclusions: Experimental therapies are currently being applied to COVID-19 outside of clinical trials. Anti-inflammatory therapies such as anti-IL-6 therapy have the potential to impair viral clearance, predispose to secondary infection, and cause harm. We seek to raise physician awareness of these issues and highlight the need to better understand the immune response in COVID-19.

scholarly journals AB0713 PERIODONTAL DISEASES AND ITS ASSOCIATION WITH ANKYLOSING SPONDYLITIS/SPA: A SYSTEMATIC REVIEW

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1652.1-1652
Author(s):  
A. Pandey ◽  
V. Ravindran ◽  
M. Pandey ◽  
R. Rajak ◽  
V. Pandey
Keyword(s):  
Systematic Review ◽  
Ankylosing Spondylitis ◽  
Connective Tissue ◽  
Inflammatory Response ◽  
Periodontal Disease ◽  
Close Association ◽  
Case Control ◽  
Clinical Attachment Loss ◽  
Tnf Α ◽  
Host Inflammatory Response

Background:A close association between periodontal disease and Ankylosing spondylitis (AS) has long been specualted. Both diseases are characterized by dysregulation of the host inflammatory response, leading to further destruction of soft and hard connective tissue with there being evidence of increased levels of TNF-α and various interleukins in both patients of AS and periodontitis.Objectives:The aim of this systematic review was to appraise the available literature exploring the relationship between AS and periodontal disease.Methods:We searched Medline & Embase databases (from their inception till October 2019) using appropriate combinations of following search items with limits ‘(English, Human)’; Ankylosing spondylitis, spondyloarthritis, spondyloarthropathies, spondyloarthritides, spinal disease, musculoskeletal disease, Rheumatic disease AND periodontitis, periodontal disease, periodontoses, parodontoses, chronic periodontitis, gum disease, gingivitis, oral health, dental health, plaque index, bleeding on probing, probing pocket depth, clinical attachment loss. This search was supplemented by the manual search of bibliographies of articles selected and conferences proceedings of EULAR. Only be reviews, observational study of cross-sectional, cohort or case control type on adult patients with AS were selected. Data was extracted from a predesigned proforma. A close association between periodontal disease and Ankylosing spondylitis (AS) has long been specualted. Both diseases are characterized by dysregulation of the host inflammatory response, leading to further destruction of soft and hard connective tissue with there being evidence of increased levels of TNF-α and various interleukins in both patients of AS and periodontitis.Results:A total number of 984 articles were identified and 12 were selcted for detailed appraisal (Figure 1, PRISMA flow chart). They were all case control studies. The prevalence of periodontitis ranged from 38% to 88% in patients with AS whereas in the control group from 26% to 71 % in controls. Out of 12 studies, two showed significant changes in Plaque Index (PI), two studies showed altered Pocket Probing Depth (PPD), three showed significant increased in Clinical Attachment Loss (CAL) and increased Bleeding On Probing (BOP) was seen in 2 studies. In 7 studies, periodontitis was seen in a significant number of patients with AS (P<0.05). All studies reported that the prevalence of periodontal disease in AS patients was higher as compared to non-AS patients.Conclusion:Our systematic review found an association between AS and periodontal disease. Patients with AS show higher prevalence of periodontitis and a poor oral hygiene as compared to healthy controls. At practice level, this systematic review underscores the need for a collaboration between dentists and rheumatologist.Disclosure of Interests:None declared

scholarly journals Urokinase Attenuates Pulmonary Thromboembolism in an Animal Model by Inhibition of Inflammatory Response

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ying Shi ◽  
Zhirong Zhang ◽  
Danli Cai ◽  
Jing Kuang ◽  
Shuifang Jin ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Animal Model ◽  
Inflammatory Response ◽  
Inflammatory Cell ◽  
Pulmonary Thromboembolism ◽  
Thrombus Formation ◽  
Inflammatory Cells ◽  
Hemodynamic Instability ◽  
Synergistic Action ◽  
Determining Factor

Inflammatory response is an important determining factor for the mortality of patients with pulmonary thromboembolism. Inflammatory mediators can promote thrombus formation and increase hemodynamic instability. Urokinase is a commonly used drug for the treatment of PTE. The effect of urokinase on inflammatory reaction in PTE is still unclear. Our study was aimed at evaluating the effects of the intervention of urokinase and urokinase combined with aspirin in PTE rats. Results revealed that a large amount of infiltrated inflammatory cells surrounding the bronchus, vessels, and pulmonary mesenchyme, and even pulmonary abscess were observed in the PTE rats. CX3CL1/CX3CR1 coexpression, CX3CL1/NF-κB coexpression, and TXA2 were significantly higher. After treatment with urokinase, pulmonary embolism was partially dissolved and inflammatory cell infiltration was significantly reduced. The expression of TNNI3, BNP, D2D, PASP, PADP, PAMP, and TXA2, as well as CX3CL1/CX3CR1 coexpression and CX3CL1/NF-κB coexpression were significantly lowered. Aspirin showed no synergistic action. Therefore, these findings suggested the occurrence of inflammation during the process of PTE in rats. Urokinase treatment reduced the inflammatory response.

Use of Vicryl (Polyglactin 910) Mesh to Limit Epidural Scar Formation after Laminectomy

Neurosurgery ◽  
1990 ◽  
Vol 26 (4) ◽  
pp. 649-654 ◽  
Author(s):  
Charles E. Nussbaum ◽  
Joseph V. McDonald ◽  
Raymond B. Baggs
Keyword(s):  
Inflammatory Response ◽  
Subcutaneous Fat ◽  
Inflammatory Cells ◽  
Scar Formation ◽  
Good Survival ◽  
Polyglactin 910 ◽  
Chronic Inflammatory Response ◽  
Fat Grafts ◽  
Free Grafts ◽  
Vicryl Mesh

Abstract A variety of substances have been used at laminectomy sites to prevent postoperative epidural scarring. Free grafts of autologous subcutaneous fat are commonly used both clinically and experimentally. The free fat grafts usually survive, but decrease in size by about 50%. Postoperatively, subcutaneous seroma has been observed with the use of fat grafts, as well as recurrent symptoms of neural compression by the graft that required additional operations. When compared to the use of free fat grafts after laminectomy in dogs, Vicryl mesh produced slightly more scarring, but consistently less than that observed in control animals. The Vicryl mesh was resorbed by a minimal chronic inflammatory response over about 45 days. Seven of 11 fat-grafted zones showed signs of necrosis, at times with a greater collection of inflammatory cells than that associated with the Vicryl mesh. Of the 4 fat-grafted zones that showed good survival. 2 had gross evidence of neural compression. No surgical zone treated with Vicryl mesh exhibited evidence of neural compression. In view of these results, the use of Vicryl mesh at laminectomy sites may be a safer method of limiting postoperative epidural scar formation.

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