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International Journal of Experimental... Aug 1990Young adult mice infected with MCMV were shown to develop inflammatory lesions in the peripancreatic and salivary gland adipose tissues. MCMV replication was detected by...
Young adult mice infected with MCMV were shown to develop inflammatory lesions in the peripancreatic and salivary gland adipose tissues. MCMV replication was detected by immunoperoxidase staining and electron microscopy in adipocytes, fibroblasts, endothelial cells and pericytes in brown and white adipose tissues. More infected cells were detected in C3H mice than in BALB/c, BALB.B, BALB.K or C57BL/6 mice. Peripancreatic steatitis consisted of a monocytic infiltrate surrounding focal necrosis of adipocytes, the severity of which was influenced by the route of inoculation, virus dose, and genetic susceptibility to disseminated MCMV-disease. C57BL/6 mice showed the greatest susceptibility with severe coalescing focal inflammation around areas of coagulative necrosis. Salivary gland adipose tissues exhibited lymphocytic steatitis, which was reduced in Nu/Nu mice.
Topics: Adipose Tissue; Animals; Cytomegalovirus Infections; Mice; Mice, Inbred Strains; Microscopy, Electron; Pancreas; Pancreatitis; Salivary Glands; Steatitis
PubMed: 2169300
DOI: No ID Found -
Surgery Apr 2000Infectious complications in severe pancreatitis are the main factors determining clinical course and outcome. The taurocholate model for acute necrotizing pancreatitis...
BACKGROUND
Infectious complications in severe pancreatitis are the main factors determining clinical course and outcome. The taurocholate model for acute necrotizing pancreatitis was evaluated for frequency and time course of pancreatic and extrapancreatic bacterial infection.
METHODS
Sixty-five male Wistar rats were divided into 5 groups of 13 animals each. Specimens for bacteriologic examination were taken, and pancreatitis was induced by intraductal infusion of 3% taurocholate under sterile conditions. Animals were killed 8, 16, 24, or 32 hours thereafter, and bacteriologic examination was performed. A control group of animals with intraductal infusion of 0.9% saline solution were killed after 32 hours.
RESULTS
There was no significant pancreatic infection in the control group and in the 8-hour group (1 of 13 rats). Sixteen and 24 hours after induction of pancreatitis, infection and inflammation of the pancreas were found in 77% (10 of 13 rats), and after 32 hours pancreatic infection occurred in 69% (9 of 13 rats). Extrapancreatic bacterial infection after 16 hours occurred in the liver (62%), spleen (62%), and mesenteric lymph nodes (46%). Bacteria infecting the pancreas reflected the bacterial spectrum of the large bowel and terminal ileum before induction of pancreatitis (Escherichia coli [77%], Proteus [43%], Enterococcus [37%], and Staphylococcus [23%]).
CONCLUSIONS
Pancreatic infection is an early and frequent finding in the taurocholate model of acute necrotizing pancreatitis. Infection occurs between 8 and 16 hours after induction of pancreatitis. The source of infecting bacteria seems to be the large bowel or the terminal ileum. We present a useful model of severe pancreatitis in which to study bacterial translocation, the further route of spread, and therapeutic approaches.
Topics: Acute Disease; Animals; Bacterial Infections; Enterococcus; Escherichia coli; Escherichia coli Infections; Hemorrhage; Leukocytes; Male; Necrosis; Pancreas; Pancreatic Diseases; Pancreatitis; Proteus mirabilis; Rats; Rats, Wistar; Staphylococcal Infections; Staphylococcus; Streptococcus agalactiae; Taurocholic Acid
PubMed: 10776434
DOI: 10.1067/msy.2000.104116 -
Veterinary Parasitology Jun 2016Although Eurytrema coelomaticum is considered a parasite with low pathogenicity, it may be associated with mortality and loss of productive performance in animals due to...
Although Eurytrema coelomaticum is considered a parasite with low pathogenicity, it may be associated with mortality and loss of productive performance in animals due to chronic pancreatitis. The aim of this study was to evaluate the occurrence of oxidative stress caused by E. coelomaticum in naturally infected cattle, correlating the biochemical findings with the parasite load and histopathological changes. For this study, blood and pancreas samples from 51 cattle were collected, and levels of the thiobarbituric acid reactive substances (TBARS), advanced oxidation protein products (AOPP) and ferric reducing ability of plasma (FRAP) were measured in the serum and pancreas, and superoxide dismutase (SOD) activity was measured in total blood. Parasite burden was determined opening the pancreatic ducts, and then fragments of pancreas were collected and fixed in 10% buffered formalin and routinely processed for histopathology. From the 51 collected pancreas, 33 (63.5%) were parasitized. The average parasite burden per pancreas was 532 (12-2,578). TBARS and FRAP showed higher levels in serum and pancreas of infected animals (p<0.05), with a positive correlation between the histopathological changes and the number of parasites. SOD level in blood was 42% higher in parasitized group compared with control group (p<0.05), as well as AOPP in serum. Based on these results, we concluded that in natural infection by E. coelomaticum in cattle, oxidative stress occurs, characterized by the occurrence of protein oxidation, lipid peroxidation and activation of antioxidant system.
Topics: Animals; Base Sequence; Cattle; Cattle Diseases; DNA, Helminth; Oxidative Stress; Pancreas; Pancreatic Diseases; Trematoda; Trematode Infections
PubMed: 27198785
DOI: 10.1016/j.vetpar.2016.04.034 -
World Journal of Surgery Mar 2002This study focuses on the relevance of Candida infection (albicans and non-albicans) in patients with necrotizing pancreatitis. Altogether, 92 patients with infected...
This study focuses on the relevance of Candida infection (albicans and non-albicans) in patients with necrotizing pancreatitis. Altogether, 92 patients with infected pancreatic necrosis were reviewed for Candida infection. All patients underwent surgical necrosectomy for infected pancreatic necrosis. Data from patients with Candida growth in intraoperative smears were compared to those obtained from patients without Candida infection. There were 22 patients (24%) with Candida infection. Patients with or without Candida infection were comparable regarding age, gender, etiology, and severity scores at admission. Candida patients suffered a higher mortality (64% vs.19%, p = 0.0001) and experienced more systemic complications (3.2 +/- 1.6 vs. 2.1 +/- 1.4; p= 0.004) than patients without Candida. Preoperative antibiotics were given significantly longer prior to Candida infection (19.0 +/- 13.2 vs. 6.4 +/- 10.3 days; p < 0.0001). With regard to the concomitant spectrum of bacteria, solitary gram-negative infection was rare in Candida patients (5% vs. 43%, p =0.0006). The presence of Candida in patients with infected pancreatic necrosis is associated with increased mortality. Our data provide evidence that application of antibiotics contributes to the development of Candida infection and to changes in the bacterial spectrum of infected necrosis with an increase in the incidence of gram-positive infection.
Topics: Adult; Aged; Antifungal Agents; Candida; Candidiasis; Female; Humans; Male; Middle Aged; Outcome Assessment, Health Care; Pancreas; Pancreatitis, Acute Necrotizing; Retrospective Studies; Risk Factors
PubMed: 11865377
DOI: 10.1007/s00268-001-0146-9 -
Human Pathology May 2004Infection with parainfluenza virus typically produces a mild, self-limited upper respiratory infection. However, parainfluenza infections have become increasingly...
Infection with parainfluenza virus typically produces a mild, self-limited upper respiratory infection. However, parainfluenza infections have become increasingly recognized as a source of severe morbidity and mortality in immunocompromised patients. In this retrospective study we identified 6 patients with congenital immunodeficiency and positive respiratory cultures for parainfluenza virus who died and underwent complete autopsy. Tissues obtained at autopsy were studied using hematoxylin and eosin-stained sections, immunoperoxidase staining for parainfluenza virus, and in selected cases, electron microscopy. All 6 patients exhibited typical cytopathic effects of parainfluenza virus, including giant cell formation, in lung and/or bronchial tissues. Parainfluenza virus infection was also documented by giant cell formation and immunohistochemistry in the pancreas (in 3 of 6 patients) and the kidney or bladder (in 2 of 4 patients). Anti-parainfluenza antibody also specifically reacted with cells in the gastrointestinal tract (in 2 of 4), spleen (in 4 of 6), thymus and/or lymph nodes (in 4 of 4), and small blood vessels in various organs (in 4 of 6). Pancreatic, bladder, colon, and thymic epithelial cell lines were susceptible to experimental infections with clinical isolates of parainfluenza virus type 3 in vitro. Parainfluenza virus infection was serious in patients with congenital immunodeficiencies, contributing directly to death in 5 of the 6 patients studied. Because this virus is capable of infecting tissues in the gastrointestinal and urinary systems as well as in the respiratory tract, body secretions and fluids from each of these locations should be considered potentially infectious.
Topics: Cell Line; Epithelium; Humans; Immunocompromised Host; Immunohistochemistry; Immunologic Deficiency Syndromes; Infant; Kidney; Lung; Male; Microscopy, Electron; Pancreas; Paramyxoviridae Infections; Retrospective Studies; Urinary Bladder
PubMed: 15138935
DOI: 10.1016/j.humpath.2003.11.012 -
Viruses Jan 2017Human enteroviruses (HEV), especially coxsackievirus serotype B (CVB) and echovirus (E), have been associated with diseases of both the exocrine and endocrine pancreas,...
Human enteroviruses (HEV), especially coxsackievirus serotype B (CVB) and echovirus (E), have been associated with diseases of both the exocrine and endocrine pancreas, but so far evidence on HEV infection in human pancreas has been reported only in islets and ductal cells. This study aimed to investigate the capability of echovirus strains to infect human exocrine and endocrine pancreatic cells. Infection of explanted human islets and exocrine cells with seven field strains of E6 caused cytopathic effect, virus titer increase and production of HEV protein VP1 in both cell types. Virus particles were found in islets and acinar cells infected with E6. No cytopathic effect or infectious progeny production was observed in exocrine cells exposed to the beta cell-tropic strains of E16 and E30. Endocrine cells responded to E6, E16 and E30 by upregulating the transcription of interferon-induced with helicase C domain 1 (IF1H1), 2'-5'-oligoadenylate synthetase 1 (OAS1), interferon-β (IFN-β), chemokine (C-X-C motif) ligand 10 (CXCL10) and chemokine (C-C motif) ligand 5 (CCL5). Echovirus 6, but not E16 or E30, led to increased transcription of these genes in exocrine cells. These data demonstrate for the first time that human exocrine cells represent a target for E6 infection and suggest that certain HEV serotypes can replicate in human pancreatic exocrine cells, while the pancreatic endocrine cells are permissive to a wider range of HEV.
Topics: Cytopathogenic Effect, Viral; Echovirus 6, Human; Gene Expression Profiling; Humans; Immunity, Innate; Immunologic Factors; Islets of Langerhans; Organ Culture Techniques; Pancreas, Exocrine; Viral Load; Viral Structural Proteins
PubMed: 28146100
DOI: 10.3390/v9020025 -
Alcohol (Fayetteville, N.Y.) Jul 2004Alcohol abuse is often associated with acute pancreatitis. The pathogenesis of alcoholic pancreatitis remains poorly understood, in part because of the lack of a... (Comparative Study)
Comparative Study
Alcohol abuse is often associated with acute pancreatitis. The pathogenesis of alcoholic pancreatitis remains poorly understood, in part because of the lack of a suitable animal model to study the mechanism or mechanisms of this disease. It has been proposed that ethanol predisposes or sensitizes the pancreas to the effects of co-factors, and the combination of the effects of ethanol on the pancreas and the actions of these co-factors results in alcoholic pancreatitis. A number of viruses are known to infect the pancreas, and we have suggested that one co-factor that could be involved in the development of alcoholic pancreatitis is a viral infection. One of the most-studied groups of viruses that infect the pancreas and cause pancreatitis in human beings is the coxsackieviruses. We have shown that short-term (5-14 days) and subchronic (>28 days) administration of ethanol to mice increases the severity of coxsackie B3-induced pancreas damage. We hypothesize that consumption of ethanol would result in an impairment of pancreas regeneration after injury, similar to the effect of ethanol on liver regeneration. With the use of the murine model of coxsackie B3-mediated alcoholic pancreatitis we have obtained preliminary data to support the hypothesis. Specifically, consumption of ethanol by mice is associated with changes in the replication of acinar cells and their organization into acini after viral-mediated injury. We believe that this model will be a valuable tool to study the biochemical and molecular mechanisms involved in alcoholic pancreatitis.
Topics: Alcoholism; Animals; Coxsackievirus Infections; Enterovirus B, Human; Ethanol; Female; Mice; Mice, Inbred C57BL; Pancreas; Pancreatitis, Alcoholic; Regeneration
PubMed: 15596086
DOI: 10.1016/j.alcohol.2004.07.001 -
World Journal of Gastroenterology Oct 2005To examine the effect of acute infection caused by herpesvirus (pseudorabies virus, PRV) on pancreatic ductal secretion.
AIM
To examine the effect of acute infection caused by herpesvirus (pseudorabies virus, PRV) on pancreatic ductal secretion.
METHODS
The virulent Ba-DupGreen (BDG) and non-virulent Ka-RREp0lacgfp (KEG) genetically modified strains of PRV were used in this study and both of them contain the gene for green fluorescent protein (GFP). Small intra/interlobular ducts were infected with BDG virus (10(7) PFU/mL for 6 h) or with KEG virus (10(10) PFU/mL for 6 h), while non-infected ducts were incubated only with the culture media. The ducts were then cultured for a further 18 h. The rate of HCO(3)(-) secretion (base efflux -J(B-)) was determined from the buffering capacity of the cells and the initial rate of intracellular acidification (1) after sudden blockage of basolateral base loaders with dihydro-4,4-diisothiocyanatostilbene-2,2-disulfonic acid (500 micromol/L) and amiloride (200 micromol/L), and (2) after alkali loading the ducts by exposure to NH(4)Cl. All the experiments were performed in HCO(3)(-)-buffered Ringer solution at 37 degrees (n = 5 ducts for each experimental condition). Viral structural proteins were visualized by immunohistochemistry. Virally-encoded GFP and immunofluorescence signals were recorded by a confocal laser scanning microscope.
RESULTS
The BDG virus infected the majority of accessible cells of the duct as judged by the appearance of GFP and viral antigens in the ductal cells. KEG virus caused a similarly high efficiency of infection. After blockage of basolateral base loaders, BDG infection significantly elevated -J(B-) 24 h after the infection, compared to the non-infected group. However, KEG infection did not modify -J(B-). After alkali loading the ducts, -J(B-) was significantly elevated in the BDG group compared to the control group 24 h after the infection. As we found with the inhibitor stop method, no change was observed in the group KEG compared to the non-infected group.
CONCLUSION
Incubation with the BDG or KEG strains of PRV results in an effective infection of ductal epithelial cells. The BDG strain of PRV, which is able to initiate a lytic viral cycle, stimulates HCO(3)(-) secretion in guinea pig pancreatic duct by about four- to fivefold, 24 h after the infection. However, the KEG strain of PRV, which can infect, but fails to replicate, has no effect on HCO(3)(-) secretion. We suggest that this response of pancreatic ducts to virulent PRV infection may represent a defense mechanism against invasive pathogens to avoid pancreatic injury.
Topics: Animals; Bicarbonates; Green Fluorescent Proteins; Guinea Pigs; Herpesvirus 1, Suid; In Vitro Techniques; Pancreatic Ducts; Pseudorabies
PubMed: 16273613
DOI: 10.3748/wjg.v11.i38.5997 -
BMJ Case Reports May 2021We describe the case of a 31-year-old man who presented with a 3-day history of right iliac fossa pain with associated nausea and vomiting. He denied any previous...
We describe the case of a 31-year-old man who presented with a 3-day history of right iliac fossa pain with associated nausea and vomiting. He denied any previous incidents of abdominal pain and had no relevant medical history or family history to note. Given the typical history, examination findings of localised peritonism and infection risk, he was taken to theatre for laparoscopic appendicectomy without diagnostic imaging. Intraoperatively, we noted gut malrotation and an inflammatory jejunal mass which was resected after converting to a mini-laparotomy. The inflammatory mass was reported to be an ectopic pancreatic tissue from histology. Given that this patient had tested positive for SARS-CoV-2 on admission, we propose a possible case of SARS-CoV-2 infection triggering inflammation of the ectopic pancreatic tissue.
Topics: Adult; COVID-19; Humans; Ilium; Intestinal Volvulus; Male; Pancreas; SARS-CoV-2
PubMed: 33972302
DOI: 10.1136/bcr-2021-241926 -
The Journal of Infectious Diseases Mar 1980Coxsackieviruses B1-B4 were inoculated intraperitoneally into 48-hr-old, 14-day-old, and three- to five-month-old Swiss-Webster mice. Immediate death occurred only among...
Coxsackieviruses B1-B4 were inoculated intraperitoneally into 48-hr-old, 14-day-old, and three- to five-month-old Swiss-Webster mice. Immediate death occurred only among mice less than 48 hr old, which died from fulminant encephalitis. Older mice usually survived. Myocarditis ensued in mice less than 48 hr old that were infected with coxsackieviruses B1 and B4. Several of the surviving mice developed left ventricular aneurysms, which resulted from transmural necrotizing myocarditis. In this group (coxsackieviruses B1 and B4), pathologic changes in the heart were synchronous with maximal cardiac titers of virus. Fourteen-day-old mice infected with coxsackieviruses B2 and B3 developed nontransmural necrotizing myocarditis in which maximal pathologic changes followed peak cardiac titers of virus by several days, whereas three- to five-month-old mice infected with coxsackieviruses B1, B2, B3, or B4 showed maximal susceptibility to destructive lesions in the exocrine glandular pancreas. Therefore, specific susceptibilities to infection with coxsackieviruses group B vary with age of the mouse, virus type (and strain), and organ.
Topics: Aging; Animals; Coxsackievirus Infections; Disease Models, Animal; Enterovirus; Female; Heart; Male; Meningoencephalitis; Mice; Myocarditis; Myocardium; Pancreas
PubMed: 6245156
DOI: 10.1093/infdis/141.3.394