Spontaneous Infection Research Articles

Immunopathology of Airway Surface Liquid Dehydration Disease.

The primary purpose of pulmonary ventilation is to supply oxygen (O2) for sustained aerobic respiration in multicellular organisms. However, a plethora of abiotic insults and airborne pathogens present in the environment are occasionally introduced into the airspaces during inhalation, which could be detrimental to the structural integrity and functioning of the respiratory system. Multiple layers of host defense act in concert to eliminate unwanted constituents from the airspaces. In particular, the mucociliary escalator provides an effective mechanism for the continuous removal of inhaled insults including pathogens. Defects in the functioning of the mucociliary escalator compromise the mucociliary clearance (MCC) of inhaled pathogens, which favors microbial lung infection. Defective MCC is often associated with airway mucoobstruction, increased occurrence of respiratory infections, and progressive decrease in lung function in mucoobstructive lung diseases including cystic fibrosis (CF). In this disease, a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene results in dehydration of the airway surface liquid (ASL) layer. Several mice models of Cftr mutation have been developed; however, none of these models recapitulate human CF-like mucoobstructive lung disease. As an alternative, the Scnn1b transgenic (Scnn1b-Tg+) mouse model overexpressing a transgene encoding sodium channel nonvoltage-gated 1, beta subunit (Scnn1b) in airway club cells is available. The Scnn1b-Tg+ mouse model exhibits airway surface liquid (ASL) dehydration, impaired MCC, increased mucus production, and early spontaneous pulmonary bacterial infections. High morbidity and mortality among mucoobstructive disease patients, high economic and health burden, and lack of scientific understanding of the progression of mucoobstruction warrants in-depth investigation of the cause of mucoobstruction in mucoobstructive disease models. In this review, we will summarize published literature on the Scnn1b-Tg+ mouse and analyze various unanswered questions on the initiation and progression of mucobstruction and bacterial infections.

FXR modulates the gut-vascular barrier by regulating the entry sites for bacterial translocation in experimental cirrhosis

Pathological bacterial translocation (PBT) in cirrhosis is the hallmark of spontaneous bacterial infections, increasing mortality several-fold. Increased intestinal permeability is known to contribute to PBT in cirrhosis, although the role of the mucus layer has not been addressed in detail. A clear route of translocation for luminal intestinal bacteria is yet to be defined, but we hypothesize that the recently described gut-vascular barrier (GVB) is impaired in experimental portal hypertension, leading to increased accessibility of the vascular compartment for translocating bacteria. Cirrhosis was induced in mouse models using bile-duct ligation (BDL) and CCl4. Pre-hepatic portal-hypertension was induced by partial portal vein ligation (PPVL). Intestinal permeability was compared in these mice after GFP-Escherichia coli or different sized FITC-dextrans were injected into the intestine. Healthy and pre-hepatic portal-hypertensive (PPVL) mice lack translocation of FITC-dextran and GFP-E. coli from the small intestine to the liver, whereas BDL and CCl4-induced cirrhotic mice demonstrate pathological translocation, which is not altered by prior thoracic-duct ligation. The mucus layer is reduced in thickness, with loss of goblet cells and Muc2-staining and expression in cirrhotic but not PPVL mice. These changes are associated with bacterial overgrowth in the inner mucus layer and pathological translocation of GFP-E. coli through the ileal epithelium. GVB is profoundly altered in BDL and CCl4-mice with Ileal extravasation of large-sized 150 kDa-FITC-dextran, but only slightly altered in PPVL mice. This pathological endothelial permeability and accessibility in cirrhotic mice is associated with augmented expression of PV1 in intestinal vessels. OCA but not fexaramine stabilizes the GVB, whereas both FXR-agonists ameliorate gut to liver translocation of GFP-E. coli. Cirrhosis, but not portal hypertension per se, grossly impairs the endothelial and muco-epithelial barriers, promoting PBT to the portal-venous circulation. Both barriers appear to be FXR-modulated, with FXR-agonists reducing PBT via the portal-venous route. For intestinal bacteria to enter the systemic circulation, they must cross the mucus and epithelial layer, as well as the gut-vascular barrier. Cirrhosis disrupts all 3 of these barriers, giving bacteria access to the portal-venous circulation and thus, the gut-liver axis. Diminished luminal bile acid availability, cirrhosis and the associated reduction in farnesoid x receptor (FXR) signaling seem, at least partly, to mediate these changes, as FXR-agonists reduce bacterial translocation via the portal-venous route to the liver in cirrhosis.

Neorickettsia helminthoeca associated lymphoid, enteric, and pulmonary lesions in dogs from Southern Brazil: An immunohistochemical study.

Neorickettsia helminthoeca (NH), the agent of salmon poisoning disease or canine neorickettiosis (CN), is a bacterial endosymbiont of the nematode Nanophyetus salmincola, and infections are spreading among specific fish-eating mammalians. This article describes the pathologic and immunohistochemical findings associated with spontaneous NH-induced infections in dogs from Southern Brazil. The principal pathologic findings were hypertrophy of Peyer patches and lymphadenopathy with lymphocytic proliferation, chronic interstitial pneumonia, and chronic enteritis associated with positive intralesional immunoreactivity to antigens of NH within macrophages and histiocytes. Positive immunoreactivity against canine parvovirus-2 (CPV-2) or/and canine distemper virus was not detected in the evaluated intestinal segments or in the samples from the cerebellum and lungs, respectively, from the dogs evaluated. These findings demonstrated that NH was involved in the enteric, pulmonary, and lymphoid lesions herein described, and provide additional information to confirm the occurrence of this bacterial endosymbiont within this geographical location. It is proposed that chronic pneumonia should be considered as a pathologic manifestation of NH-induced infections. Additionally, our results show that the occurrences of CN seem to be underdiagnosed in Southern Brazil due to the confusion with the incidence of CPV-2.

Advanced age promotes colonic dysfunction and gut‐derived lung infection after stroke

Bacterial infection a leading cause of death among patients with stroke, with elderly patients often presenting with more debilitating outcomes. The findings from our retrospective study, supported by previous clinical reports, showed that increasing age is an early predictor for developing fatal infectious complications after stroke. However, exactly how and why older individuals are more susceptible to infection after stroke remains unclear. Using a mouse model of transient ischaemic stroke, we demonstrate that older mice (>12 months) present with greater spontaneous bacterial lung infections compared to their younger counterparts (7–10 weeks) after stroke. Importantly, we provide evidence that older poststroke mice exhibited elevated intestinal inflammation and disruption in gut barriers critical in maintaining colonic integrity following stroke, including reduced expression of mucin and tight junction proteins. In addition, our data support the notion that the localized pro‐inflammatory microenvironment driven by increased tumour necrosis factor‐α production in the colon of older mice facilitates the translocation and dissemination of orally inoculated bacteria to the lung following stroke onset. Therefore, findings of this study demonstrate that exacerbated dysfunction of the intestinal barrier in advanced age promotes translocation of gut‐derived bacteria and contributes to the increased risk to poststroke bacterial infection.

Infected Baker’s cyst, diagnosed in the emergency department using POCUS

Baker’s cyst is a closed collection of fluid that forms in the posterior aspect of the knee. Usually, it appears as a non-painful inflammation in the popliteal fossa. In adults, its aetiology is secondary to problems that cause distension of the knee joint. It is often associated with rheumatoid arthritis and osteoarthritis. Occasionally, the cyst may become oversized and rupture with the consequent leakage of synovial fluid into adjacent tissues, presenting a clinical course similar to acute thrombophlebitis. Infection of a popliteal cyst is an uncommon complication and is associated with septic arthritis. In this paper, we present the case of a patient, an intravenous drug user (IVDU), who developed a spontaneous infection of a Baker’s cyst secondary to Staphylococcus aureus, which was diagnosed in the emergency department (ED) using point-of-care-ultrasound (POCUS).
 
 Figure 1. Within the posterior aspect of the left calf on the medial aspect there is an extremely large cystic lesion measuring 18.7 cm in length and 4 cm in width with no adverse features. The cystic lesion is communicating with the semimembranosus/medial head gastrocnemius bursa more proximally in the knee where it demonstrates internal echoes and synovial thickening and a single septation.

Long-time dynamics of an SIRS reaction-diffusion epidemic model

In this paper, we first deal with a diffusive SIRS epidemic system in spatially heterogeneous and time periodic environment with no flux boundary condition. We establish the uniform persistence if the basic reproduction number R0>1. When the diffusion rates are equal and the system parameters are constant, we obtain the global stability of the unique endemic equilibrium if R0>1, and that of the diseases-free equilibrium if R0≤1. We also study the SIRS epidemic system with spontaneous infection, in addition to disease transmission. Our results show that spontaneous infection enhances the persistence of disease. The uniform bounds of solutions, which are derived by a feedback argument, play a fundamental role in our analysis.

CD200-CD200R1 inhibitory signaling prevents spontaneous bacterial infection and promotes resolution of neuroinflammation and recovery after stroke

BackgroundIschemic stroke results in a robust inflammatory response within the central nervous system. As the immune-inhibitory CD200-CD200 receptor 1 (CD200R1) signaling axis is a known regulator of immune homeostasis, we hypothesized that it may play a role in post-stroke immune suppression after stroke.MethodsIn this study, we investigated the role of CD200R1-mediated signaling in stroke using CD200 receptor 1-deficient mice. Mice were subjected to a 60-min middle cerebral artery occlusion and evaluated at days 3 and 7, representing the respective peak and early resolution stages of neuroinflammation in this model of ischemic stroke. Infarct size and behavioral deficits were assessed at both time points. Central and peripheral cellular immune responses were measured using flow cytometry. Bacterial colonization was determined in lung tissue homogenates both after acute stroke and in an LPS model of systemic inflammation.ResultsIn wild-type (WT) animals, CD200R1 was expressed on infiltrating monocytes and lymphocytes after stroke but was absent on microglia. Early after ischemia (72 h), CD200R1-knockout (KO) mice had significantly poorer survival rates and an enhanced susceptibility to spontaneous bacterial colonization of the respiratory tract compared to wild-type (WT) controls, despite no difference in infarct or neurological deficits. While the CNS inflammation was resolved by day 7 post-stroke in WT mice, brain-resident microglia and monocyte activation persisted in CD200R1-KO mice, accompanied by a delayed, augmented lymphocyte response. At this time point, CD200R1-KO mice displayed greater weight loss, more severe neurological deficits, and impaired motor function compared to WT. Systemically, CD200R1-KO mice exhibited signs of persistent infection including lymphopenia, T cell activation and memory conversion, and narrowing of the TCR repertoire. These findings were confirmed in a second model of acute neuroinflammation induced by systemic endotoxin challenge.ConclusionThis study defines an essential role of CD200-CD200R1 signaling in stroke. Loss of CD200R1 led to high mortality, increased rates of post-stroke infection, and enhanced entry of peripheral leukocytes into the brain after ischemia, with no increase in infarct size. This suggests that the loss of CD200 receptor leads to enhanced peripheral inflammation that is triggered by brain injury.

The role of medical thoracoscopy in the management of empyema

BackgroundEmpyema thoracis is defined as accumulation of pus in the pleural space. Despite advanced medical diagnostic and therapeutic methods, thoracic empyema remains a common clinical entity and a serious problem all over the world with significant associated morbidity and mortality.AimThe aim of this work was to study the efficacy and safety of medical thoracoscopy (MT) in the management of empyema.Patients and methodsThis study included 30 inpatients with empyema. Included patients had frank pus on aspiration (turbid purulent fetid fluid) with or without positive Gram stain smear and microbiological culture findings or pH less than 7.20, with signs of sepsis. Patients were managed by MT. MT using rigid thoracoscopy was performed with evacuation of the purulent fluid, visualization of the pleural space, assessment of adhesions and purulent material, forceps adhesiolysis, and irrigation by normal saline with partial debridement of accessible parietal pleural surface.ResultsThe present study included 30 patients with empyema (17 men, 13 women with a mean age of 47.4±14.5 years; range, 18–70 years); 19 (63.3%) patients had free-flowing empyema (by computed tomography/ ultrasonography) and 11 (36.7%) patients had multiloculated empyema. The etiology of empyema included pneumonia (parapneumonic effusion) (33.3%), malignancy (23.3%), tuberculosis (6.7%), lung abscess (6.7%), and no cause was identified in nine patients (spontaneous pleural infection) (30%). MT was considered successful without subsequent interventional procedures in 26 of 30 (86.7%) patients, including all patients with free-flowing empyema (19 patients), 63.6% of patients with multiloculated empyema (seven patients), and four (13.3%) patients required surgical intervention (surgical decortication). No procedure-related mortality or chronic morbidity occurred in this study.ConclusionMT is a simple, safe, minimally invasive, and effective modality in the management of empyema.

Case report of cutaneous nodule caused by Gordonia bronchialis in an immunocompetent patient after receiving acupuncture

Gordonia species were recently found to cause human infection. Most Gordonia bronchialis infections are associated with sternal wounds and foreign bodies. Here, we present a case of a firm cutaneous nodule caused by G. bronchialis on an immunocompetent patient's lower extremity after receiving acupuncture. Our present case indicates that spontaneous cutaneous infection of G. bronchialis can develop even in a healthy patient. With the popularity of complementary and alternative medicine, physicians should be aware that G. bronchialis infection can be associated with Oriental medicine similar to mycobacterial infection. Recognizing the diverse clinical features of newly emerging Gordonia species will facilitate appropriate diagnosis and management of future patients.

Treatment algorithm for spontaneous spinal infections: A review of the literature.

Background:Primary spinal infections are rare pathologies with an estimated incidence of 5% of all osteomyelitis. The diagnosis can be challenging and this might result in a late identification. The etiological diagnosis is the primary concern to determine the most appropriate treatment. The aim of this review article was to identify the importance of a methodological attitude toward accurate and prompt diagnosis using an algorithm to aid on spinal infection management.Methods:A search was done on spinal infection in some databases including PubMed, ISI Web of Knowledge, Google Scholar, Ebsco, Embasco, and Scopus.Results:Literature reveals that on the basis of a clinical suspicion, the diagnosis can be formulated with a rational use of physical, radiological, and microbiological examinations. Microbiological culture samples can be obtained by a percutaneous computed tomography-guided procedure or by an open surgical biopsy. When possible, the samples should be harvested before antibiotic treatment is started. Indications for surgical treatment include neurological deficits or sepsis, spine instability and/or deformity, presence of epidural abscess and failure of conservative treatment.Conclusion:A multidisciplinary approach involving both a spinal surgeon and an infectious disease specialist is necessary to better define the treatment strategy. Based on literature findings, a treatment algorithm for the diagnosis and management of primary spinal infections is proposed.

Cytokines and immunoglobulin g response in donkeys with spontaneous Setaria equine infection

Setaria equina (S. equina) is a filarial worm that exists in peritoneal cavity of equines. This study aimed to evaluate cytokine mediators tumour necrosis factor alpha (TNF-α), interleukin-4 (IL-4) and immunoglobulin G (IgG) responses in spontaneously S. equina infected and non-infected donkeys with emphasis on choosing the best antigen that could be used in diagnosis of such filarial infection. A total of 87 donkeys were examined. Two S. equina antigens: crude somatic S. equina antigen (CSS) and excretory secretory S. equina antigen (ESS) were prepared. They were evaluated in diagnosis of the infection using indirect ELISA and electrophoretically characterised through sodium dodecyl sulphate poly acrylamide gel electrophoresis (SDS-PAGE) and western blotting technique. The results indicated that both TNF-α and IL-4 in the serum of infected donkeys were significantly higher compared with the non-infected group at P<0.05 and P<0.01, respectively. However, the IL-4 level of infected donkeys was significantly higher than that of TNF-a (P<0.01). Apparent prevalence, specificity and positive predictive values (96.55%, 100%, and 100% each) of CSS showed higher diagnostic accuracy than that of ESS. In addition, electrophoretic protein profile and IgG reactivity of CSS antigen via western blot presented a prominent reactive protein band at 28 kDa. It was concluded that the CSS antigen was the best antigen that could be used in serodiagnosis of S. equina infection. The cytokine responses were explored in order to differentiate infected from non-infected donkeys.

Morphological and immunohistochemical characteristics of spontaneous distemper infection in the brains of red foxes in Serbia

Morphological and immunohistochemical characteristics of spontaneous distemper infection in the brains of red foxes in Serbia

Current Evaluation of Sepsis among Patients with Liver Cirrhosis

Background and study aim: patients with liver cirrhosis have high incidence of sepsis. Spontaneous bacterial peritonitis and urinary tract infections are the most common infections among patients with livercirrhosis.New criteria including quick qSOFA and sepsis-3 criteria are used for diagnosing sepsis in patients with liver cirrhosis. These criteria appear to be more accurate than SIRS. The aim of this study is to evaluate the existing scoring systems in our patients with liver cirrhosis to identify patients with sepsis. Patients and Methods: This prospective study included 288 consecutive patients previously diagnosed to have liver cirrhosis and suspected to have bacterial/fungal infections. Quick Sequential (sepsis-related) organ failure assessment (qSOFA) criteria and sepsis-3 criteria were used to identify patients with organ dysfunction due to sepsis. Results: qSOFA and sepsis-3 criteria are more accurate than SIRS in detecting sepsis among patients with cirrhosis (The area under the receiver operating characteristic curve (AUROC) value for a model with qSOFA and sepsis-3 was AUROC: 0.77 and 0.76), while AUROC for SIRS was 0.66. Conclusion: Sepsis-3 and qSOFA are more accurate than SIRS criteria in early detection of sepsis among patients with cirrhosis. Patients with positive criteria need intensive management due to high risk of in-hospital mortality.

Antibiotic-Resistant Spondylodiscitis With Canal Invasion and Aggressive Evolution to Epidural Abscess: A Case Series of Spontaneous Occurrence in 16 Patients.

The study aimed to assess the effectiveness of antibiotic treatment for spondylodiscitis, its failure rates, and the need for surgical intervention. This is a retrospective study of patients who presented with spontaneous deep spinal infections and spondylodiscitis between 2011 and 2013. Clinical, bacteriologic, and radiographic data during hospitalization were analyzed. A total of 16 patients presented with deep spinal infections during the study period; 15 of them presented with spontaneous pyogenic spondylodiscitis, and 1 presented with epidural abscess. Median age was 68 years (range, 50-80 years), and 6 (38%) were healthy young laborers. None of the patients were immunocompromised. On admission all patients presented with pain, there was fever in 3 patients (19%), and there was elevated blood C-reactive protein, white blood cell count and erythrocyte sedimentation rate, with a mean of 147 ± 83.1 mg/L, 11.65 ± 5.6 × 103/μL, 93.6 ± 35.1 mm/h, respectively. A total of 15 patients (94%) developed infections that were refractory to appropriate culture-specific intravenous antibiotic treatment (mean, 10.2 days); 8 patients (50%) deteriorated neurologically and required wide surgical decompression. Complications included widespread epidural free gas in 2 patients (12%), multiple bilateral psoas abscesses in 2 patients (12%), kyphotic segmental instability in 4 patients (25%), and inferior vena cava septic thrombi in 1 patient (6%). A total of 3 patients (19%) died within 6 months; 7 of 13 surviving patients still had residual neurologic deficits at the 6-month follow-up. Spondylodiscitis may be resistant to antibiotic treatment and may evolve into epidural abscess via extension of the infection and pus into the spinal canal, necessitating repetitive surgical treatment due to neurologic and clinical deterioration, and expansion of the persistent infection with a mass effect. Increased vigilance for this condition and its misleading initial presentations is warranted.

Prevalence of osteochondral lesions in the fetlock and hock joints of Standardbred horses that survived bacterial infection before 6\u2009months of age

BackgroundYoung Standardbred horses frequently develop fragments in joints. Some fragments represent osteochondrosis; others are considered developmental, but it is uncertain whether they result from preceding osteochondrosis. Osteochondrosis occurs as a consequence of failure of the cartilage canal blood supply and ischaemic chondronecrosis. In heritably predisposed foals, failure was associated with incorporation of vessels into bone. However, bacterial vascular failure was also recently documented in foals suffering spontaneous infections, proving that bacteria can cause osteochondral lesions in foals up to 150 days old. The aim was to determine prevalence of fetlock and hock lesions at screening age in Standardbred horses that survived infections before 6 months of age, and compare this to prevalence reported in the literature.MethodsThe material consisted of 28 Standardbred horses; 17 males and 11 females that presented and were diagnosed clinically with bacterial infections from 1 to 150 days of age (average: 41.3 days). A screening set of 8 radiographic projections was available from all 28 horses at 7–85 months of age (average: 23.6 months). Lesion prevalence was compared to three previously reported Standardbred cohorts.ResultsOsteochondral lesions were detected in one or more joints of 19/28 horses (67.9%); in the fetlock joint of 14/28 horses (50%) and the hock joint of 11/28 horses (39.3%). These prevalences were ≥ 2 x higher than the corresponding prevalences in the comparison cohorts, and statistically significantly so in 5:6 comparisons (p-values from < 0.00001 to 0.01). In the sepsis cohort, there were an average of 2.3 affected joints and 2.5 lesions per affected horse, whereas there in the one comparable literature cohort were an average of 1.5 affected joints and 1.7 lesions per affected horse.ConclusionsStandardbred horses that survived bacterial infections before 6 months of age had more osteochondral lesions than literature comparison cohorts at screening age. The implication was that some of the lesions in this group were caused by bacteria. It may become necessary to develop methods for differentiating between acquired, septic and aseptic, heritably predisposed lesions.

Paropisthorchis caninus Stephens, 1912: Synopsis of identity and pathological findings due to spontaneous infection in the liver of a street dog in Assam, India.

The present study describes a small liver fluke recovered at post-mortem and the pathological alteration produced by the parasite in the liver of a street dog from Assam, India. The spatulate parasite measured 3-4 mm in length and 1.0-1.25 mm in width with spiny body surface and showed a grossly visible peduncle projecting from the ventral surface at the anterior portion. The eggs of the parasite contained well developed miracidia. The parasite was identified as Paropisthorchis caninus. Identity of the parasite is discussed in the light of available literature and found to be morphologically different from other reported species of dog Opisthorchis. Pathological lesions observed in the liver included degeneration of hepatic parenchyma, hyperplasia of bile duct epithelium, fibrous tissue proliferation and formation of pseudo lobule which were the characteristics of chronic proliferative inflammation.

Staphylococcus aureus meningitis in adults: A comparative cohort study of infections caused by meticillin-resistant and meticillin-susceptible strains

Staphylococcus aureus meningitis is an uncommon nosocomial infection usually associated with neurosurgical procedures, but spontaneous infections may occasionally appear. To compare the features of meningitis caused by meticillin-resistant (MRSA) and meticillin-susceptible (MSSA) S.aureus and examine the prognostic factors for mortality, including MRSA infection and combined antimicrobial therapy. Retrospective cohort study of 350 adults with S.aureus meningitis admitted to 11 hospitals in Spain (1981-2015). Logistic regression and propensity score matching were used to analyse prognostic factors. There were 118 patients (34%) with MRSA and 232 (66%) with MSSA. Postoperative infection (91% vs 73%) and nosocomial acquisition (93% vs 74%) were significantly more frequent in MRSA than in MSSA meningitis (P<0.001). Combined therapy was given to 118 (34%) patients. Overall 30-day mortality rate was 23%. On multivariate analysis, mortality was associated with severe sepsis or shock (odds ratio (OR) 9.9, 95% confidence interval (CI) 4.5-22.0, P<0.001), spontaneous meningitis (OR 4.2, 95% CI 1.9-9.1, P<0.001), McCabe-Jackson score rapidly or ultimately fatal (OR 2.8, 95% CI 1.4-5.4, P=0.002), MRSA infection (OR 2.6, 95% CI 1.3-5.3, P=0.006), and coma (OR 2.6, 95% CI 1.1-6.1, P<0.029). In postoperative cases, mortality was related to retention of cerebrospinal devices (OR 7.9, 95% CI 3.1-20.3, P<0.001). Clinical and epidemiological differences between MRSA and MSSA meningitis may be explained by the different pathogenesis of postoperative and spontaneous infection. In addition to the severity of meningitis and underlying diseases, MRSA infection was associated with increased mortality. Combined antimicrobial therapy was not associated with increased survival.

Pathologic and molecular findings associated with atypical porcine pestivirus infection in newborn piglets

Atypical porcine pestivirus (APPV) has been associated with congenital tremor (CT) type A-II in newborn piglets. Although the number of APPV-based studies is increasing, the associated pathologic findings in infected piglets are underreported. This study describes the histopathologic features of spontaneous APPV infection in CT-affected piglets and complements a previous report by our group. Four two-day-old piglets with CT were evaluated by histopathology, immunohistochemistry (IHC), and molecular assay. The main histopathologic findings at the brain and spinal cord included neuronal necrosis, gliosis, neuronophagia, satellitosis, demyelination, Wallerian degeneration, and Purkinje cell necrosis. An IHC assay designed to detect the proliferation of glial fibrillary acidic protein (GFAP) in affected areas of the brain and spinal cord revealed that the proliferation of GFAP + cells and fibers was predominant in APPV-infected piglets relative to asymptomatic piglets of the same age group. The RT-nested-PCR assays identified APPV RNA in the cerebrum, cerebellum, and brainstem of all piglets; other viruses known to produce similar manifestations were not detected. These results suggest that the APPV-induced histopathologic findings are predominantly degenerative and necrotic and correlate with our previous findings. Consequently, it is proposed that neuronal necrosis, gliosis, neuronophagia, and satellitosis should be considered as important histologic features of APPV-induced infection in symptomatic CT piglets.

Metastatic Gastric Adenocarcinoma Diagnosed Following Spontaneous Bacterial Peritonitis: A Rare Complication of Malignant Ascites

Spontaneous bacterial peritonitis (SBP) complicating malignant ascites without evidence of liver disease or portal hypertension is a rare clinical presentation. We report a case of non-cirrhotic SBP leading to a new diagnosis of metastatic gastric cancer. A 51-year-old male presented with a one-month history of diffuse abdominal pain, early satiety, nausea and non-bloody, non-bilious emesis. On exam, the patient's abdomen was notably distended and diffusely tender to palpation. Admission laboratory data were significant for a mild leukocytosis of 12,700 WBC/mm3 with a neutrophilic predominance of 83% and mild anemia of 13.1 g/dl. Liver function tests showed a serum total bilirubin of 0.5 mg/dl, aspartate aminotransferase of 28 U/L, alanine aminotransferase of 16 U/L, protein of 6.7 g/dl, and albumin of 3.8 g/dl. Computed tomography of the abdomen and pelvis revealed new large volume abdominal ascites without radiological evidence of cirrhosis, portal vein thrombosis, or portal hypertension. A diagnostic paracentesis revealed 2843 WBC/ mm3, 40% neutrophils, 25% lymphocytes, fluid protein of 4.8 g/dl, and fluid albumin of 2.9 g/dl with a serum ascites albumin gradient (SAAG) of 0.9 g/dl. The patient was started on ceftriaxone for five days. Fluid culture remained negative, but repeat fluid studies showed 1475 WBC/mm3 with 25% neutrophils indicating ceftriaxone treated SBP. Upper endoscopy revealed a 10 mm, oozing, cratered gastric ulceration with surrounding congested mucosa. Biopsies later confirmed undifferentiated gastric adenocarcinoma. In addition, ascitic fluid cytology was positive for metastatic signet ring cells. SBP is an established diagnosis that has been known to complicate at least 8-10% of the cirrhotic patient population. However, spontaneous infection of ascites fluid in malignancy has not been well-described in the literature. Other cases of SBP complicating malignant ascites reported were in patients with hepatic involvement of their primary malignancies. One other case of SBP complicating gastric cancer without liver disease has been reported in the literature; this patient had hematemesis with severe anemia thought to result in bowel ischemia and bacterial gut translocation. Our patient did not report a history of gastrointestinal bleed and had a stable hemoglobin on presentation. In conclusion, this patient's diagnostic course represents a unique presentation of a rare complication of malignant ascites in gastric cancer.2681_A Figure 1. Computed tomography of abdomen revealing diffuse abdominal ascites2681_B Figure 2. Upper endoscopy revealing ulceration with surrounding congested mucosa of the greater curvature of the gastric body

Robustness and fragility of the susceptible-infected-susceptible epidemic models on complex networks.

We analyze two alterations of the standard susceptible-infected-susceptible (SIS) dynamics that preserve the central properties of spontaneous healing and infection capacity of a vertex increasing unlimitedly with its degree. All models have the same epidemic thresholds in mean-field theories but depending on the network properties, simulations yield a dual scenario, in which the epidemic thresholds of the modified SIS models can be either dramatically altered or remain unchanged in comparison with the standard dynamics. For uncorrelated synthetic networks having a power-law degree distribution with exponent , the SIS dynamics are robust exhibiting essentially the same outcomes for all investigated models. A threshold in better agreement with the heterogeneous rather than quenched mean-field theory is observed in the modified dynamics for exponent . Differences are more remarkable for , where a finite threshold is found in the modified models in contrast with the vanishing threshold of the original one. This duality is elucidated in terms of epidemic lifespan on star graphs. We verify that the activation of the modified SIS models is triggered in the innermost component of the network given by a -core decomposition for while it happens only for in the standard model. For , the activation in the modified dynamics is collective involving essentially the whole network while it is triggered by hubs in the standard SIS. The duality also appears in the finite-size scaling of the critical quantities where mean-field behaviors are observed for the modified but not for the original dynamics. Our results feed the discussions about the most proper conceptions of epidemic models to describe real systems and the choices of the most suitable theoretical approaches to deal with these models.