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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Summary. Infection frequently complicates the course of severe acute pancreatitis and might manifest as infected pancreatic necrosis, pancreatic abscess or an infected peripancreatic fluid collection. Pancreatic necrosis occurs in roughly 21% of all cases of pancreatitis. In patients with necrosis involving more than one-half of the pancreas, the incidence of subsequent infection is as high as 40%-70%. More than 50% of these infection yield a polymicrobial isolate with predominance of enteric bacteria but recently, the microbiologic pattern has shifted toward more resistant gram-negative bacilli, gram-positive cocci and yeast, a reflection of exposure to broad-spectrum antimicrobial agents. Given the morbidity associated with infection, many commentators have advocated prophylactic antimicrobial therapy in patients with necrosis to the point that this measure has been incorporated into routine practice. However, there is controversy over the risks and potential benefit. Currently, advise against the routine use of prophylactic systemic antibiotics and antifungals (side-effect selection of resistant microbes and fungi). However, there may be some patients who benefit from prophylaxis, and additional studies and investigations are ongoing. Antibiotics should not be given early in the disease course because most symptoms are due to the inflammatory response, not an infectious etiology. Antibiotics are indicated when CT scans indicate a pancreatic phlegmon, empirically in the case of severe pancreatitis associated with septic shock, or with documented fine - needle aspiration biopsy identification of bacteria. Under those circumstances, antibiotic coverage is warranted to prevent systemic gram-negative sepsis. Infected pancreatic necrosis should be treated with carbapenems because they can effectively penetrate pancreatic tissue. Other conditions, such as biliary pancreatitis associated with cholangitis, mandate antibiotic coverage.
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PMID:[Antibiotics for pancreatitis--still controversial?]. 2312 Aug 50

Coxsackievirus B1, a member of the Picornaviridae family is a non-enveloped single-stranded RNA virus associated with human diseases including myocarditis and pancreatitis. Infection of the intestinal mucosa, lined by polarized epithelial cells, requires interaction of coxsackievirus with apically located DAF (decay-accelerating factor) before transport to the basolaterally located CAR (coxsackie and adenovirus receptor), where entry is mediated by endocytosis. As with many other non-enveloped viruses, coxsackievirus has to induce lysis of host cells in order to perpetuate infection. However, recent evidence indicates that virus spread to secondary sites is not only achieved by a lytic mechanism and a non-lytic cell-cell strategy has been suggested for coxsackievirus B3. A physical interaction between infected and non-infected cells has been shown to be an efficient mechanism for retroviral transmission and one type of extracellular vesicle, the exosome, has been implicated in HIV-1 transmission. HIV-1 also takes advantage of depolymerization of actin for spread between T-cells. Calpain-mediated depolymerization of the actin cytoskeleton, as a result of increases in intracellular calcium concentration during coxsackievirus infection, would result in a release of host cell-derived microvesicles. If so, we speculate that maybe such microvesicles, increasingly recognized as major vehicles mediating intercellular communication, could play a role in the intercellular transmission of non-enveloped viruses.
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PMID:Coxsackievirus B transmission and possible new roles for extracellular vesicles. 2335 1

Infection-induced acute hepatitis complicated with acute pancreatitis is associated with hepatitis A virus, hepatitis B virus or hepatitis E virus. Although rare, Epstein-Barr virus (EBV) infection should be considered also in the differential diagnosis if the patient has acute hepatitis combined with pancreatitis. We report a case of EBV infection with cholestatic hepatitis and pancreatitis with review of literature. An 11-year-old female was admitted due to 1-day history of abdominal pain and vomiting without any clinical symptoms of infectious mononucleosis. Diagnosis of reactivated EBV infection was made by the positive result of viral capsid antigen (VCA) IgM, VCA IgG, Epstein-Barr nuclear antigen and heterophile antibody test. We performed serologic tests and magnetic resonance cholangiopancreatography to exclude other viral or bacterial infection, autoimmune disorder, and structural problems. The patient's symptoms recovered rapidly and blood chemistry returned to normal with conservative treatment similar to previously reported cases.
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PMID:Epstein-barr virus infection with acute pancreatitis associated with cholestatic hepatitis. 2401 Jan 8

Infection with Ascaris lumbricoides is common in tropical and subtropical regions of the world. Prevalence of ascariasis is related to poverty, poor hygiene and poor fecal sanitation. This helminth usually lives harmlessly in small intestine but can also cause intestinal obstruction or perforation peritonitis which is common in childhood. Ascaris can also migrate through ampulla of vater to produce cholangitis, pancreatitis,cholecystitis and rarely hepatic abscess. Ascaris induced hepatic abscess can sometimes present with acute abdomen (like acute pyogenic abscess). We present a young adult with Ascaris induces hepatic abscess who presented and a case of acute abdomen in emergency department.
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PMID:Ascariasis presenting as acute abdomen-a case report. 2442 39

The treatment of infected necrotizing pancreatitis has evolved from time to time and the success of surgical intervention depends on the timing of necrosectomy. Bacterial infection occurs in 40-70% of patients with necrotizing pancreatitis. Infection is the main risk factor for mortality among patients with pancreatic necrosis. Timely intervention is generally required for pancreatic necrosis but is now deferred until four weeks after disease onset in order to permit encapsulation and demarcation of the necrotic material. Demarcation facilitates necrosectomy and reduces complications related to the drainage and debridement procedures. The approach to pancreatic necrosectomy has evolved from primary open necrosectomy to minimally-invasive radiologic, surgical and endoscopic procedures. Direct endoscopic necrosectomy is a minimally-invasive technique that was introduced in recent years for the treatment of walled-off necrosis. The pancreas is approached through the posterior wall of stomach and debridement is done.
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PMID:Extended Open Transgastric Necrosectomy (EOTN) as a Safer Procedure for Necrotizing Pancreatitis. 2517 3

Acute pancreatitis complicating fulminant viral hepatitis has been well recognized; however, acute pancreatitis occurring in nonfulminant hepatitis is very rare. The case presented describes moderate pancreatitis in a young male, manifesting during the course of nonfulminant acute hepatitis E infection. The diagnosis of acute viral hepatitis E was confirmed by serology and reverse transcriptase polymerase chain reaction (RT-PCR) to demonstrate Hepatitis E virus (HEV) RNA in both stool and serum. Patients with acute viral hepatitis presenting with severe abdominal pain should have a diagnosis of acute pancreatitis suspected and appropriate investigations including serum amylase, lipase, biliary ultrasonography and/or contrast-enhanced computed tomography of the abdomen should be undertaken. The identification of this unusual complication of Hepatitis E is important; however, the prognosis for patients with Acute Pancreatitis Complicating Acute Hepatitis E Virus Infection is good, and uncomplicated recovery with conservative treatment is expected.
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PMID:Acute pancreatitis complicating acute hepatitis e virus infection: a case report and review. 2537 21

Legionella-associated pancreatitis has been rarely reported. Since this condition is very rarely suspected and investigated in patients with Legionella pneumonia, its incidence is probably underestimated. Here we report a case of Legionella pneumonia-associated pancreatitis and review the relevant related literature.
Infection 2015 Jun
PMID:Pancreatic involvement in Legionella pneumonia. 2557 64

Infection with varicella zoster virus (VZV) causes varicella (chickenpox), which can be severe in immunocompromised individuals, infants and adults. Primary infection is followed by latency in ganglionic neurons. During this period, no virus particles are produced and no obvious neuronal damage occurs. Reactivation of the virus leads to virus replication, which causes zoster (shingles) in tissues innervated by the involved neurons, inflammation and cell death - a process that can lead to persistent radicular pain (postherpetic neuralgia). The pathogenesis of postherpetic neuralgia is unknown and it is difficult to treat. Furthermore, other zoster complications can develop, including myelitis, cranial nerve palsies, meningitis, stroke (vasculopathy), retinitis, and gastroenterological infections such as ulcers, pancreatitis and hepatitis. VZV is the only human herpesvirus for which highly effective vaccines are available. After varicella or vaccination, both wild-type and vaccine-type VZV establish latency, and long-term immunity to varicella develops. However, immunity does not protect against reactivation. Thus, two vaccines are used: one to prevent varicella and one to prevent zoster. In this Primer we discuss the pathogenesis, diagnosis, treatment, and prevention of VZV infections, with an emphasis on the molecular events that regulate these diseases. For an illustrated summary of this Primer, visit: http://go.nature.com/14xVI1.
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PMID:Varicella zoster virus infection. 2718 65

Infection with either mobilized colistin resistance-1 gene-positive gram-negative bacteria or invasive Candida lusitaniae occurs rarely throughout the United States. Here we report the existence of both invasive infections occurring in a single, complex patient who initially presented with necrotizing pancreatitis and gastrointestinal bleeding. We detail the patient's history and perioperative course for enterocutaneous fistulae takedown and ureteral stenting, describe a template of preventative steps taken in the perioperative environment to prevent nosocomial pathogen transmission, and provide a brief overview of both the mobilized colistin resistance-1 gene and C lusitaniae.
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PMID:Superbug Meets Opportunistic Infection: A Case Report of Mobilized Colistin Resistance-1-Positive Klebsiella pneumoniae and Candida lusitaniae in a Complex Surgical Patient. 3037 22

Coxsackie B viruses (CVB) cause a wide spectrum of diseases, ranging from mild respiratory syndromes and hand, foot, and mouth disease to life-threatening conditions, such as pancreatitis, myocarditis, and encephalitis. Previously, we and others found that the soluble virus receptor trap sCAR-Fc strongly attenuates CVB3 infection in mice. In this study, we investigated whether treatment with sCAR-Fc results in development of resistance by CVB3. Two CVB3 strains (CVB3-H3 and CVB3 Nancy) were passaged in HeLa cells in the presence of sCAR-Fc. The CVB3-H3 strain did not develop resistance, whereas two populations of CVB3 Nancy mutants emerged, one with complete (CVB3M) and one with partial (CVB3K) resistance. DNA sequence alignment of the resistant virus variant CVB3M with CVB3 Nancy revealed an amino acid exchange from Asn(N) to Ser(S) at position 139 of the CVB3 capsid protein VP2 (N2139S), an amino acid predicted to be involved in the virus's interaction with its cognate receptor CAR. Insertion of the N2139S mutation into CVB3-H3 by site-directed mutagenesis promoted resistance of the engineered CVB3-H3N2139S to sCAR-Fc. Interestingly, development of resistance by CVB3-H3N2139S and the exemplarily investigated CVB3M-clone 2 (CVB3M2) against soluble CAR did not compromise the use of cellular CAR for viral infection. Infection of HeLa cells showed that sCAR-Fc resistance, however, negatively affected both virus stability and viral replication compared to that of the parental strains. These data demonstrate that during sCAR-Fc exposure, CVB3 can develop resistance against sCAR-Fc by single-amino-acid exchanges within the virus-receptor binding site, which, however, come at the expense of viral fitness.IMPORTANCE The emergence of resistant viruses is one of the most frequent obstacles preventing successful therapy of viral infections, representing a significant threat to human health. We investigated the emergence of resistant viruses during treatment with sCAR-Fc, a well-studied, highly effective antiviral molecule against CVB infections. Our data show the molecular aspects of resistant CVB3 mutants that arise during repetitive sCAR-Fc usage. However, drug resistance comes at the price of lower viral fitness. These results extend our knowledge of the development of resistance by coxsackieviruses and indicate potential limitations of antiviral therapy using soluble receptor molecules.
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PMID:Single-Point Mutations within the Coxsackie B Virus Receptor-Binding Site Promote Resistance against Soluble Virus Receptor Traps. 3266 34


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