Potential Infectious Causes Research Articles

Postencephalitic Parkinsonism in a Patient with Mumps Infection: A Case Report

In 1917, Von Economo described a disease named Encephalitis Lethargica which affected a large number of patients across the world in an epidemic between 1916 and 1927. It's spread paralleled with the spread of the pandemic influenza, but Von Economo and the contemporary authors did not believe it to be a post-influenzal sequela. Now parkinsonism is a well-known complication of acute infectious encephalitis. There are many potential infectious causes of parkinsonism reported in literature. In India, postencephalitic parkinsonism is commonly due to Japanese Encephalitis. Neurologic manifestations reported in Mumps include meningitis, encephalitis, deafness, facial neuritis, cerebellar ataxia, hydrocephalus, transverse myelitis and polyradiculitis. We describe a case of young girl who had Mumps parotitis and encephalitis and then subsequently developed parkinsonism as a sequela. Mumps was confirmed by positive serology and basal ganglia lesions were demonstrated by magnetic resonance imaging of the brain. To the best of our knowledge, this is the first case of postencephalitic parkinsonism following Mumps infection from India.

Cross-Roads in Research on Neurodegenerative Diseases

Alzheimer’s disease (AD) is the most prevalent of the neurodegenerative amyloid diseases and is characterized by accumulation of amyloid-β and tau. Recent studies have indicated that AD may be a brain infection. Although AD has not been shown to be transmissible, the burning issue is whether the potential infectious causes are the misfolded amyloid proteins themselves, or an unidentified microorganism. The idea of a replicating protein (prion) evolved from research on the transmissible spongiform encephalopathies (TSE) represented by Creutzfeldt-Jakob disease in humans. Prions are now suspect in all of the amyloid related neurodegenerative diseases. However, the popularized prion theory is controversial since there is convincing evidence that spiroplasma, a wall-less prokaryote, is involved in the pathogenesis of TSE, and may represent the trigger mechanism. Interest in bacterial involvement in AD has surfaced from discovery that most bacteria produce biofilm and that components of the biofilm experimentally induce misfolded amyloid proteins. The recent discovery of H. pylori in AD has brought this controversy to a head. In this review we will discuss involvement of bacteria as candidate causal agent/s for the neurodegenerative diseases, and relate the evidence to involvement of spiroplasma in the pathogenesis of the TSEs as a model for these neurodegenerative diseases.

Role of infectious agents in cutaneous T-cell lymphoma: Facts and controversies

The etiology of cutaneous T-cell lymphoma (CTCL) remains unknown, with potential infectious causes having been explored. This contribution evaluates the evidence suggesting an infectious etiology and pathogenesis of the disease, characterizes the relationships between various specific pathogens and CTCL, and discusses some of the difficulties in establishing a causal link between infectious agents and CTCL carcinogenesis. Researchers have evaluated CTCL specimens for evidence of infection with a variety of agents, including human T-lymphotropic virus, Epstein-Barr virus, human herpesvirus-8, and Staphylococcus aureus, although other pathogens also have been detected in CTCL. Although there is significant evidence implicating one or more infectious agents in CTCL, studies to date have not linked definitively any pathogen to disease development, and various studies have yielded conflicting results.

Atherosclerosis Induced byChlamydophila pneumoniae: A Controversial Theory

More than a century ago, inflammation and infection were considered to have atherogenic effects. The old idea that coronary heart disease (CHD) possibly has an infectious etiology has only reemerged in recent years. Atherosclerosis is the main pathological process involved in CHD and is, logically, the first place to look for infectious etiology. The process of atherosclerosis itself provides the first hints of potential infectious cause. Smooth muscle proliferation, with subsequent intimal thickening, luminal narrowing, and endothelial degeneration, constitutes the natural history of atherosclerosis, being with the severity and speed of these changes. Both viral and bacterial pathogens have been proposed to be associated with the inflammatory changes found in atherosclerosis. Recently, Chlamydophila pneumoniae (C. pneumoniae) has been implicated as a possible etiologic agent of coronary artery disease and atherosclerosis. New evidence which supports a role for C. pneumoniae in the pathogenesis of atherosclerosis has emerged. C. pneumoniae has been detected in atherosclerotic arteries by several techniques, and the organism has been isolated from both coronary and carotid atheromas. Recent animal models have suggested that C. pneumoniae is capable of inducing atherosclerosis in both rabbit and mouse models of atherosclerosis. Furthermore, human clinical treatment studies which examined the use of antichlamydial macrolide antibiotics in patients with coronary atherosclerosis have been carried out. The causal relationship has not yet been proven, but ongoing large intervention trials and research on pathogenetic mechanisms may lead to the use of antimicrobial agents in the treatment of CHD in the future.

Allogeneic Peripheral Blood Stem Cell Transplantation Significantly Increases the Risk of Chronic Graft-Versus-Host Disease of Lung Compared to Bone Marrow Transplantation

Chronic graft versus host disease (GVHD) of lung is associated with higher transplant related morbidity and mortality after allogeneic hematopoeitic cell transplant (HCT). Risk factors for lung GVHD are not yet fully elucidated in detail. We attempted to identify clinical risk factors for lung GVHD after allogeneic HCT based on single center experience. 401 patients were transplanted between year 2000 and 2007 at the Princess Margaret Hospital, Toronto, Canada. 280 (70%) and 121 (30%) patients received peripheral blood stem cell (PBSC) and bone marrow (BM) as a source of stem cells, respectively. Monitoring with pulmonary function tests (PFT) were performed prior to transplant, at day 180, then annually. PFT was also performed when indicated clinically. CT scan of lung was performed to confirm the diagnosis of lung GVHD and to exclude other infectious causes. Bronchoscopic lavage was performed to exclude potential infectious cause if needed. Potential clinical risk factors for lung GVHD were examined including conditioning, age, gender, source of stem cell, diagnosis, disease status and previous episode of acute GVHD. With median follow up of 1,122 days, 68 patients (16.9%) had a diagnosis of chronic GVHD of lung with median onset of 349 days (range 71-1,880 days; 95% CI [299-398 days]), 53(78%) of whom patients received myeloablative conditioning. Fifty one(75%) patients received matched sibling donor transplant versus 17(25%) patients received unrelated donor. Overall survival rates remained similar in both cohorts. In the univariate analyses, other clinical risk factors were not associated with the risk of chronic GVHD of lung: conditioning (p = 0.9), age with cut off of 60 years (p = 0.4), donor type (p = 0.5), grade II-IV acute GVHD (p = 0.7), grade III-IV acute GVHD(p = 0.4), development of CMV reactivation (p = 0.6). However, incidence of chronic GVHD lung was significantly higher in the group receiving PBSC (13.8± 2.4% at 1 year; 23.0±3.2% at 2 years) than in those receiving BM (6.8±2.5% at 1 year; 16±3.8% at 2 years; p = 0.02, hazard ratio 1.937, 95%CI [1.100-3.410]). Multivariate analyses also confirmed PBSC transplantation as an independent risk factor for chronic GVHD of lung (p = 0.005, hazard ratio 2.359, 95%CI [1.290-4.314]). The use of PBSC increases the risk of lung GVHD compared to the use of BM for allogeneic HCT. Closer monitoring is warranted to detect lung GVHD early after PBSCT.

Incidence, pattern and clinical relevance of microbial contamination of preservation fluid in liver transplantation

Transmission of pathogens via preservation fluid (PF) is a potential cause of infection among liver transplant recipients. Here, we evaluated the incidence and pattern of microbial contamination of PF and its impact on postoperative graft function after liver transplantation. This longitudinal study included data from 41 primary liver transplantations and 5 re-transplantations performed between December 2010 and September 2011. Results of microbiological analyses of 92 PF samples collected before and after the back-table procedure were evaluated in order to establish the incidence and pattern of contamination. The impact of positive PF cultures on early graft function and rate of pathogen transmission was assessed. Post-transplant antibiotic protocol was based on piperacillin/tazobactam administration for a minimum of 10 days. The incidence of contamination was 84.8% (39/46), both for samples collected before and after the back-table procedure. Gram-positive low-virulence organisms typical for superficial saprophytic flora, mainly coagulase-negative staphylococci, were predominant. There were no cases of pathogen transmission from PF to the recipient. Positive cultures of PF samples obtained after the back-table procedure were associated with significant elevation of aspartate (p=0.034) and alanine aminotransferase (p=0.048) on the first 5 postoperative days. No significant differences were found regarding serum bilirubin concentration (p=0.335) and international normalized ratio (p=0.137). Despite high incidence of PF contamination, infections caused by pathogens isolated from PF were not observed. However, presence of pathogens in PF might lead to temporary impairment of graft function.

Multiple potential infectious causes of hematuria complicate this diagnosis

Multiple potential infectious causes of hematuria complicate this diagnosis

Defects of camera covers after arthroscopic surgery

Arthroscopic cameras are used either sterilized or in an unsterile manner enveloped in a sterile cover. The goal of this investigation was to determine the integrity of camera covers after arthroscopic procedures, as defects of camera covers have been occasionally observed by us. Such defects might be a potential cause of infection. Six different types of camera covers were tested in a prospective randomized study involving 90 consecutive shoulder arthroscopies. After surgery, the covers were tested by filling them with water up to a level of 20 cm. Any water leaks were recorded. Of all tested camera covers, 74% had 1 to 9 holes involving all types of covers. Of the holes, 17% were larger than 1 mm. In addition, 37% of the covers leaked at the junction between the cover and the arthroscope. The type of cover with the lowest number of leaks had the largest diameter of all tested covers and included an arthroscope adapter, in contrast to the others, which were only sealed off from the arthroscope by adhesive tape. One cover with tape sealing leaked more frequently than the others at the junction (93% of cases, P < .003). The tested camera covers are fragile and tend to leak. This might be a potential risk factor for infection. Mechanically more resistant camera covers or sterilized cameras without the need for covers should be used instead.

Institute of Medicine Forum on Emerging Infections: Linking Infectious Agents and Chronic Diseases

Institute of Medicine Forum on Emerging Infections: Linking Infectious Agents and Chronic Diseases

Late shunt infection: incidence, pathogenesis, and therapeutic implications.

Shunt infections (SI) are a major concern in pediatric neurosurgery. Although SI occurs generally shortly after surgery, it can be very delayed in a number of cases. The incidence of late shunt infection (LSI) is not established, and the sources of contamination are poorly understood. We reviewed 1,793 pediatric cases from our database, with a mean follow-up of 9.12 years. We selected 40 cases of SI occurring more than one year after the previous shunt operation. These represented 12.7 % of SI, and the annual incidence of LSI was 0.28 % in our series. Peritonitis, generally due to appendicitis, was the cause of LSI in 11 cases. Hematogenous contamination was diagnosed in eight cases, because the germ was Haemophilus,Pneumococcus, or Listeria, or an ENT infection had preceded SI; the incidence of purulent meningitis was significantly higher in shunted patients than in the general population. LSI was due in seven cases to bowel perforation, and in four to direct inoculation, after abdominal surgery or traumatic exposure of the shunt. In the remaining 10 cases, no potential cause of infection was identified, and persistence of a germ since the previous shunt operation was suspected. SI represents a life-long threat after shunting, and may be unrelated to shunt surgery.

Antimicrobial resistance pattern and plasmid profile of Salmonella typhi isolated from an outbreak in Tehran province.

The antimicrobial resistance patterns and plasmid profiles of Salmonella typhi isolates from sporadic cases (n = 33) and an outbreak (n = 48) were compared. Of 28 sporadic drug-resistant isolates, 24 (85.7%) were multiply resistant. The predominant antibiotic resistance pattern was TeCmSmSxTAp, which was also the most common pattern of the outbreak isolates. 13 drug-resistant strains isolated before the outbreak (46.4%) were able to transfer the whole resistance pattern or part of it to Escherichia coli K 12 by conjugation. Although 20 of the sporadic strains contained plasmid DNA, transferable R plasmids were only detected in 13 (65%) of them. Among the outbreak strains, the rate of R plasmid transfer was 92.3%, with only the TeCmSmSxTAp pattern transferred. Plasmid profiling and Hind III endonuclease digestion of plasmid DNA identified a 91.2 megadaltons (Mda) plasmid that was recovered from most of the outbreak isolates and from 4 strains collected before the outbreak. This plasmid coded for TeCmSmSxtAp and transferred the pattern of resistance in toto. The results indicate multidrug-resistant S. typhi as a potential cause of infection in the region.

Mycobacterium asiaticum as the probable causative agent in a case of olecranon bursitis

Mycobacterium asiaticum was isolated from fluid aspirated from an olecranon bursa that had become inflamed following a superficial injury. Other possible causes of the inflammation were excluded. No specific antimycobacterial therapy was given. The infection responded to drainage, regular dressing, and immobilization. Our experience suggests that M. asiaticum is a potential cause of infection of the joints and surrounding tissues.

An unusual case of diabetic cellulitis due to pasturella multocida

Pasturella multocida is a well known potential cause of infection following bites or scratches by animals. The organism causes the usual clinical manifestations of a rapidly developing cellulitis at the site of injury. The resultant infection is dangerous and can progress on to a deep infection, osteomyelitis, and septicemia. In compromised patients, the source and etiology of the infection may be obscure making definitive diagnosis difficult. This paper reviews a very unusual case of a foot infection in a diabetic patient that was due to a domestic pet licking an excoriation on the foot.

Non-cryptosporidial diarrhoea in human immunodeficiency virus (HIV) infected patients.

Thirty of 81 consecutive HIV antibody positive patients referred with non-cryptosporidial diarrhoea had no potential infectious cause; most had AIDS related complex rather than the full blown syndrome. Opportunistic infections with cytomegalovirus (CMV), mycobacterium avium-intracellulare (MAI), and herpes simplex virus (HSV), which allowed a diagnosis of AIDS to be made, were found in 19 patients and were the presenting features of AIDS in five. Other potential pathogenic species included entamoeba, giardia, campylobacter, and salmonella (without septicaemia). Cytomegalovirus infection was often accompanied by abdominal pain. Severe weight loss (greater than 10 kg) at presentation was found in patients with CMV infection and MAI. Bloody diarrhoea was confined to the group with HSV procitis. Malignant causes of diarrhoea were rare. Two patients developed a squamous carcinoma of the anorectal margin and one a non-Hodgkin's lymphoma. In only two of 12 patients who had Kaposi's sarcoma was this considered as a cause of diarrhoea. Rigid sigmoidoscopy showed macroscopic abnormalities in over a third (32) of the 81 patients with non-cryptosporidial diarrhoea. Most commonly this was severe inflammation (17) or discrete ulceration (four) [three of whom had CMV colitis]. Kaposi's sarcoma was identified in 11 patients. Non-specific inflammation was seen histologically in 40 of the 60 patients with no sigmoidoscopic inflammatory changes. Barium enema only revealed an abnormality in a minority of the patients and a colonoscopy only revealed information additional to rigid sigmoidoscopy in two patients--one with CMV ulcers in the transverse colon and the other with evidence of Kaposi's sarcoma not seen in the rectum. Ten patients had a rectal biopsy examined by electron microscopy as no infective cause of diarrhoea was uncovered. In four of these microtubular structures which are commonly seen in viral infections were found and two had prelymphomatous changes and in one of these frank lymphoma has developed. We recommend multiple stool analysis, sigmoidoscopy and rectal biopsy as the initial investigations in these patients reserving tests of malabsorption, colonoscopy, and barium enema for the small number of more difficult cases.