Acute Coinfection Research Articles

Co-infection of Primary Syphilis and HIV after a Single Exposure - a Case Report

Abstract Human immunodeficiency virus type 1- infected patients with syphilis are among the most important transmitters of HIV-1 infection due to biological effects of genital ulcerations, and aggravation due to their continued risky behavior. The association between primary syphilis and acute HIV-1 co-infection is not well documented, and reports on isolated cases are raising special interest and indicate that this double primary co-infection may occur. We present a case of a 31-year-old man with no past medical history who presented with fever, papular rash on the face which lasted for a few days, and a single genital ulcer. He was diagnosed with primary syphilis and primary HIV-1 infection after a single exposure with an infected female sex worker. Male-to-female HIV transmission during vaginal intercourse is significantly more likely than female-to-male HIV transmission. However, high prevalence of sexually transmitted diseases among female sex workers contributed to high HIV transmission probability, as in our case. As far as the available world literature is concerned, this is the first case of co-infection of primary syphilis and HIV.

Does EBV alter the pathogenesis of malaria?

Plasmodium falciparum infections have been implicated in immune deficiencies resulting in ineffective control of Epstein-Barr virus, thereby increasing the risk of endemic Burkitt lymphoma in children. However, the impact of Epstein-Barr virus infections on the development of immunity to P.falciparum has not been studied in depth. In this review, we examine novel findings from animal co-infection models and human immuno-epidemiologic studies to speculate on the impact of acute gammaherpesvirus co-infection on malarial disease severity. Children are often concurrently or sequentially infected with multiple pathogens, and this has implications for understanding the development of protective immunity as well as in the evaluation of vaccine efficacy.

PTU-108 A UK single centre experience of management of hepatitis C virus genotype 4 infection with pegylated-interferon and ribavirin

<h3>Introduction</h3> New direct acting antiviral agents are revolutionising hepatitis C virus (HCV) treatment. However, to date published phase 3 clinical trial data in genotype 4 (GT4) HCV patients is limited. GT4 HCV is more common in Africa, the Middle East and Asia. In the UK, the mainstay of treatment has been pegylated interferon and ribavirin but limited data exists on outcomes in patients treated in Europe. We report the first “real-life’ sustained virological response (SVR) outcomes using pegylated interferon and ribavirin for HCV GT4 in the UK, and the largest European single centre cohort. <h3>Method</h3> HCV GT4 patients treated at a London, UK centre between 2002 and 2014 were assessed for SVR outcomes. Patient age, sex, region of origin, co-infection with HIV, pre-treatment liver biopsy histological assessment, genotype subtyping, treatment duration and dose reductions were compared against SVR outcomes on univariate analysis. Multivariate analysis was performed on results with P &lt; 0.1. <h3>Results</h3> During the study period 219 patients were diagnosed with HCV GT4. Of these 118 (54%) were treated with pegylated interferon and ribavirin and 57 achieved SVR (48%). The median age at the start of treatment was 48 years (range 6 to 66 years) and 72% were male. Six patients were intolerant, 25 were non responders, 3 developed breakthrough, 18 were relapsers, 3 are currently undergoing treatment and 6 lost to follow-up. Five out of 6 patients with acute HCV and HIV co-infection achieved SVR. Three HCV monoinfected patients were treated while on renal dialysis, with 2 achieving SVR. On univariate analysis age ≥ 45 (P &lt; 0.0001), high viral load (P &lt; 0.0001), Ishak staging 5–6 (P &lt; 0.0001) and non-Egyptian Africans (P = 0.0059) were all negatively associated with SVR. Eastern Europeans appeared to have higher rates of SVR (P &lt; 0.0001). Using multivariate correlation viral load (P = 0.0005); Ishak staging (P = 0.0031) and age (P = 0.0003) were associated with SVR but not country of origin (P = 0.0645). <h3>Conclusion</h3> Outcomes with pegylated interferon and ribavirin for HCV GT4 in this “real-life” setting were sub-optimal especially in the context of newer regimens. Patients with older age, high viral loads and advanced disease need prioritisation for alternative treatments. <h3>Disclosure of interest</h3> N. Selvapatt Conflict with: Gilead, BMS, M. Habibi: None Declared, A. Brown Speaker Bureau of: Abbvie, BMS, Gilead, Janssen, Merck.

A Case of Acute Co-infection with Human Immunodeficiency Virus and Cytomegalovirus

A Case of Acute Co-infection with Human Immunodeficiency Virus and Cytomegalovirus

A comparison of seminal hepatitis C virus (HCV) RNA levels during recent and chronic HCV infection in HIV-infected and HIV-uninfected individuals.

We aimed to characterize seminal hepatitis C virus (HCV) RNA dynamics in human immunodeficiency virus (HIV)-positive men with acute HCV infection given its potential role in sexual transmission of HCV. Men with acute HCV infection (duration, ≤12 months) or chronic HCV infection (duration, >12 months) were prospectively recruited. Paired semen and blood samples were assayed for HCV RNA levels. Results were analyzed using χ(2), Fisher exact, Mann-Whitney U, and Kruskal-Wallis tests. Eighteen men (27.3%) had acute HCV and HIV coinfection, 22 (33.3%) had chronic HCV infection and HIV coinfection, and 26 (39.4%) had chronic HCV monoinfection. HCV RNA was detected in semen specimens from 29 of 66 men (43.9%). The median HCV RNA level in blood was 4.0 log IU/mL higher than that in semen. HCV RNA levels were correlated in semen and blood (r(2) = 0.142). Neither HIV positivity nor acute HCV infection was associated with an increased frequency of seminal HCV RNA detection. Among men with acute HCV and HIV coinfection, the median HCV RNA level in blood specimens from those with seminal HCV RNA was higher than that in blood specimens from those without seminal HCV RNA (P = .001). Seminal HCV RNA was detected in ≥1 sample for 26 of 35 men (74.3%) attending follow up. HCV RNA was detected in semen during both acute and chronic HCV infection. This was unaffected by HIV positivity or the phase of HCV infection. Elevated seminal HCV RNA levels could contribute to sexual transmission of HCV, but other factors, including high-risk behaviors, may be the main drivers for HCV transmission in HIV-infected individuals.

Acute Appendicitis and Coinfection with Enterobiasis and Taeniasis: A Case Report

Parasites are rarely associated with inflammation of the appendix. Generally, parasites cause acute abdominal pain via blocking the gut lumen. In this article, we presented a case of appendicitis where Enterobius vermicularis was detected in the surgical specimen and Taenia was detected in the stool. A 31 year old male patient was admitted to the emergency room with severe abdominal pain, which has begun two days ago. On physical examination, tenderness was positive on palpation of the right lower abdominal quadrant and the patient was operated on with the diagnosis of acute appendicitis. Histopathological examination of the patient's appendectomy material revealed numerous parts of parasites resembling Enterobius vermicularis and slight mucosal erosion. On parasitological examination of the patient's stool, Taenia eggs and adult forms were determined. Antiparasitic therapy was started with niclosamide for taeniasis and albendazole for enterobiasis. Parasitic infections can mimic acute appendicitis clinically. Radiological and laboratory findings do not help to distinguish the diagnosis of acute appendicitis. In the histopathological examination of the appendix, the findings of acute inflammation of the appendix wall may not be defined. For patients with normal histopathological examination, screening for parasites should be done, and anti-parasitic treatment should be started after appendectomy.

Community-associated methicillin-resistant Staphylococcus aureus necrotizing pneumonia without evidence of antecedent viral upper respiratory infection.

USA300 community-associated (CA) methicillin-resistant Staphylococcus aureus (MRSA) strains causing necrotizing pneumonia have been reported in association with antecedent viral upper respiratory tract infections (URI). A case series of necrotizing pneumonia presenting as a primary or coprimary infection, secondary to CA-MRSA without evidence of antecedent viral URI, is presented. Cases were identified through the infectious diseases consultation service records. Clinical and radiographic data were collected by chart review and electronic records. MRSA strains were isolated from sputum, bronchoalveolar lavage, pleural fluid or blood cultures and confirmed using standard laboratory procedures. MRSA strains were characterized by susceptibility testing, pulsed-field gel electrophoresis, spa typing, agr typing and multilocus sequence typing. Testing for respiratory viruses was performed by appropriate serological testing of banked sera, or nucleic acid testing of nasopharyngeal or bronchoalveloar lavage specimens. Ten patients who presented or copresented with CA necrotizing pneumonia secondary to CA-MRSA from April 2004 to October 2011 were identified. The median length of stay was 22.5 days. Mortality was 20.0%. Classical risk factors for CA-MRSA were identified in seven of 10 (70.0%) cases. Chest tube placement occurred in seven of 10 patients with empyema. None of the patients had historical evidence of antecedent URI. In eight of 10 patients, serological or nucleic acid testing testing revealed no evidence of acute viral coinfection. Eight strains were CMRSA-10 (USA300). The remaining two strains were a USA300 genetically related strain and a USA1100 strain. Pneumonia secondary to CA-MRSA can occur in the absence of an antecedent URI. Infections due to CA-MRSA are associated with significant morbidity and mortality. Clinicians need to have an awareness of this clinical entity, particularly in patients who are in risk groups that predispose to exposure to this bacterium.

Prevalence of hepatitis B and hepatitis D coinfection in asymptomatic blood donors in Iran

Hepatitis delta virus (HDV) is a satellite virus that needs hepatitis B virus (HBV) surface antigen for amplification and transition. HDV appears in HBsAg carriers as acute coinfection and superinfection in patients with chronic hepatitis B. This coinfection leads to chronic hepatitis, cirrhosis, and liver carcinoma. The aim of this study was to detect the prevalence of coinfection and superinfection of HBVs and HDVs in blood donor individuals in Iran. Sera from 854 asymptomatic blood donors from the Bank of positive samples storage at the National Blood Transfusion Organization of Iran that were positive for hepatitis B surface antigen were analysed. The presence of antibody against HDV in blood donors was detected using ELISA followed by conventional PCR, seminested PCR and real-time PCR to determine coinfection and/or superinfection. Restriction fragment length polymorphism was used for HDV genotyping. All 854 samples were HBsAg and anti-HBc positive whereas only 18 (2%) of them were positive for anti-HDV. Of the 854 samples, 154 (18%) were HBV-DNA positive. HDV-RNA was detected in 0.6% of the total samples by seminested PCR and real-time PCR and the two PCR methods produced similar results. Moreover, 16.6% and 83.4% of anti-HDV-positive samples exhibited coinfection and superinfection with HBV, respectively. Genotype I of HDV was determined in positive samples.

A 3-month-old Boy With Concomitant Respiratory Syncytial Virus Bronchiolitis and Infant Botulism

To the Editors: A 3-month-old boy with respiratory failure was admitted to the pediatric intensive care unit of a Northern California medical center in February 2011. The illness began 3 days earlier with progressively worsening lethargy, cough and stridor, decreased oral intake and decreased urine output. A review of systems was notable for decreased bowel movements in the past week and the presence of copious clear secretions from the infant’s nose and oropharynx. The infant was born at term with no complications, was exclusively breastfed other than a dropperful of chicken broth given when the child was ill in the days before admission and had received no vaccines. A nasal aspirate polymerase chain reaction was positive for respiratory syncytial virus. Over the next 4 days, ventilatory settings were weaned as oxygenation normalized. The child was extubated twice, but each time developed hypercapnia requiring reintubation. Seven days after admission, the infant remained intubated and ventilated with poor respiratory effort. Neurologic examination revealed a nearly complete bilateral ptosis; facial diplegia with tears produced under stimulation and no facial grimace. Infant botulism was suspected. Stool was sent for Clostridium botulinum toxin, and botulism immune globulin was administered empirically. Two days later, stool tests revealed C. botulinum toxin type A and the diagnosis of infant botulism was confirmed. During the next 3 weeks, the child received nasogastric feeds and ventilatory support and slowly regained bulbar strength. He was extubated 9 days after botulism immune globulin administration and was discharged to home 1 month after admission with a mixed breastfeeding/tubefeeding regimen. He required supplemental oxygen by nasal cannula until 2 days before discharge. On discharge, the child was still noted to have decreased tone, a weak cry and mildly uncoordinated feeding mechanics. Infant botulism results from ingestion of spores of Clostridium species, which germinate and colonize the infant intestine, producing botulinum toxin. This toxin is absorbed and causes a descending, symmetric paralysis. Constipation is almost always the first sign of illness and is often overlooked (as in the case above).1 Diagnosis is confirmed by identification of C. botulinum organisms in the feces of an infant with a presentation consistent with the disease. Supportive care forms the cornerstone of therapy, though specific treatment has been available in the form of intravenous human botulism immune globulin since 1992, through the California Department of Public Health. Botulism immune globulin should be initiated as early as possible in the course of illness and should not be delayed for laboratory confirmation. Acute coinfection with respiratory syncytial virus and Clostridium spp. has not previously been described. This case serves to demonstrate the necessity to maintain an open differential diagnosis even when presented with laboratory confirmation of an apparent causative etiology. Kevin K. Quinn, MD James D. Cherry, MD, MSc Division of Pediatric Infectious Diseases UCLA David Geffen School of Medicine Neeta R. Shah, MD Laura J. Christie, MD Department of Pediatrics Kaiser Permanente Northern California Oakland, CA

A Deterioration of Anemia in Hemoglobin E Disease caused by Cholestatic Hepatitis A

ABSTRACT Patients with hemoglobin E disease usually have mild hemolytic anemia and mild splenomegaly. Acute infection including acute inflammatory disease of the liver caused by hepatitis A viral, which attacks patients with previous hemolytic anemia, may result in deterioration of anemia. A 17-year-old female patient was admitted with chief complaint of having jaundiced body and non-specific prodromal symptoms within one week prior to admission. Physical examination revealed jaundiced skin and sclera as well as tenderness in right upper quadrant of the abdomen. Laboratory tests revealed microcytic hypochromic anemia with hemoglobin (Hb) level of 6.3 g/dL, increased reticulocyte count and abnormal morphology of erythrocyteson blood smear. Hemoglobin electrophoresis indicated hemoglobin E disease and serologic tests suggested a positive anti-HAV immunoglobulin M (IgM) with increased level of liver enzymes and functions. Abdominal ultrasound showed hepatosplenomegaly without extra-hepatic cholestasis. The working diagnosis was hepatitis A with intrahepatic cholestasis and hemoglobin E disease. The patient was treated with hepatoprotector and ursodeoxycholic acid. Anemia was not treated specifically. It was assumed that hemolytic anemia was worsened by acute infection of hepatitis A viral. The assumption had been proven to be right since there was improvement of anemia after the acute infection had recovered. Patients with hemoglobin E disease usually have mild anemia; however, in this case, the hemoglobin level decreased significantly due to the acute co-infection. Keywords: hemoglobin E disease, anemia, acute infection, acute hepatitis A infection

Autochthonous Hepatitis E Co-Infection Causing More Severe Acute Hepatitis B Infection

Introduction: Acute hepatitis E is caused by an RNA virus (HEV) endemic in many parts of the developing world usually producing a brief icteric illness, similar to Hepatitis A. In Western countries, acute HEV is rare and usually seen in subjects that have recently traveled to endemic areas (Central and Southeast Asia, North and West Africa and Mexico). However, there have been multiple case reports of autochthonous (locally acquired) HEV in the United Kingdom, Japan, Holland, and France of unknown sources. Hepatitis B Virus (HBV) is transmitted by percutaneous and mucous membrane exposure to infectious body fluids and in adults it is likely to cause clinically apparent acute HBV infection. Less than 1% of the cases of acute HBV progress to fulminant liver failure although the disease may be more severe in patients with other hepatitis viruses. We describe a rare case of dual acute HBV and HEV in the USA with severe clinical manifestations. Case Presentation: A 70-year-old male developed generalized myalgias, headache, nausea, and fatigue. Six weeks prior while in Florida, he had a sexual encounter with a sex worker. The patient had no history of previous hepatic disease and was found to have icteric hepatitis with ALT/AST >1500 U/L and bilirubin of 4.1 mg/dl. He had detectable HBV surface antigen (HBsAg) and anti-HBc IgM consistent with acute HBV with a HBV viral load of >1.1x108 IU/ml. Further laboratory work-up at that time for other etiologies was negative and the patient denied any new medications or recent acetaminophen intake. Supportive care was initiated but the patient began to show evidence of hepatic synthetic dysfunction with prolonged prothrombin time and continued worsening of aminotransferases and bilirubin. Further laboratory analysis revealed detectable anti-HEV IgM consistent with acute HEV infection. Biopsy showed marked hepatitis (Scheuer Grade 4) and early bridging fibrosis (Scheuer Stage 3) and with bile ductular proliferation characteristic of HEV supporting the impression of co-infection by both HBV and HEV. Antiviral therapy with entecavir was initiated and the patient slowly improved. One year later, the patient is negative for HBs Ag, anti-HBc IgM, HBV DNA and anti-HEV. He is asymptomatic. Discussion: This is a unique case of acute HEV in a patient without travel to an endemic area consistent with an autochthonous infection in the United States. This case is also unique due to the severity of the acute co-infection with HBV and HEV. Practitioners should be aware of this viral hepatitis that can worsen other hepatitides and consider screening for HEV in cases of acute hepatitis.

Acute HCV/HIV Coinfection Is Associated with Cognitive Dysfunction and Cerebral Metabolite Disturbance, but Not Increased Microglial Cell Activation

BackgroundMicroglial cell activation and cerebral function impairment are described in both chronic hepatitis C viral (HCV) and Human-Immune-Deficiency viral (HIV) infections. The aim of this study was to investigate the effect of acute HCV infection upon cerebral function and microglial cell activation in HIV-infected individuals.MethodsA case-control study was conducted. Subjects with acute HCV and chronic HIV coinfection (aHCV) were compared to matched controls with chronic HIV monoinfection (HIVmono). aHCV was defined as a new positive plasma HCV RNA within 12 months of a negative RNA test. Subjects underwent neuro-cognitive testing (NCT), cerebral proton magnetic resonance spectroscopy (1H-MRS) and positron emission tomography (PET) using a 11C-radiolabeled ligand (PK11195), which is highly specific for translocator protein 18 kDA receptors on activated microglial cells. Differences between cases and controls were assessed using linear regression modelling.ResultsTwenty-four aHCV cases completed NCT and 1H-MRS, 8 underwent PET. Of 57 HIVmono controls completing NCT, 12 underwent 1H-MRS and 8 PET. Subjects with aHCV demonstrated on NCT, significantly poorer executive function (mean (SD) error rate 26.50(17.87) versus 19.09(8.12), p = 0.001) and on 1H-MRS increased myo-inositol/creatine ratios (mI/Cr, a marker of cerebral inflammation) in the basal ganglia (ratio of 0.71(0.22) versus 0.55(0.23), p = 0.03), compared to subjects with HIVmono. On PET imaging, no difference in 11C-PK11195 binding potential (BP) was observed between study groups (p>0.10 all cerebral locations), however lower BPs were associated with combination antiretroviral therapy (cART) use in the parietal (p = 0.01) and frontal (p = 0.03) cerebral locations.DiscussionPoorer cognitive performance and disturbance of cerebral metabolites are observed in subjects with aHC,V compared to subjects with HIVmono. Higher 11C-PK11195 BP was not observed in subjects with aHCV, but was observed in subjects not on cART.

Lack of TGF-β production by hepatitis C virus-specific T cells during HCV acute phase is associated with HCV clearance in HIV coinfection

Immunity and genetic factors govern the recovery from acute hepatitis C virus (HCV) infection. No predictive factors have been yet identified in patients coinfected with the human immunodeficiency virus (HIV). We investigated whether early T cell responses to HCV producing transforming-growth-factor beta (TGF-β) predict the outcome of acute HCV coinfection, independently of the IL-28B gene polymorphism. Intracellular cytokine staining assays against HCV-core, E1, NS2, and NS4 overlapping peptides were used for the analysis of peripheral HCV-specific TGF-β-producing T cells. Patients were genotyped for IL-28B polymorphisms. Healthy donors' samples were tested as controls. Twenty-four acute hepatitis C-HIV+ patients were followed-up for 15 months defining two groups: (A) Recovered (n=16, 5 spontaneous recoveries, 11 sustained virologic response after treatment), (B) Chronic HCV (n=8, 4 spontaneous chronic course, 4 therapeutic failures). During the acute pretreatment phase, core/NS2-specific TGF-β-producing CD4+ and/or CD8+ T cells were detected in 8/24 (33%) patients. Lack of anti-HCV TGF-β+ cells was characteristic of healthy donors and Group A, except for 2 cases, with frequencies significantly lower than in Group B (p=0.04 and 0.01), and was associated with recovery in 14/16 cases. Presence of anti-HCV TGF-β+ cells was associated with persistent viremia in 6/8 cases (p=0.005). This profile remained stable over time. Such TGF-β production was independent of the rs129679860 SNP (p=1.0) which was not associated with recovery (p=1.0). During acute hepatitis C, pre-therapeutic HCV-specific TGF-β-producing T cells are a new marker independent of the IL-28B gene polymorphism, predicting the lack of spontaneous or therapeutic HCV clearance.

Serum complement C4 in chronic hepatitis C: Correlation with histopathologic findings and disease activity

Hepatitis C virus leads to chronic liver disease, cirrhosis and hepatocellular cancer. Viral markers and other laboratory tests used in the diagnosis and follow-up of chronic hepatitis C do not correlate well with disease activity and liver histopathology. Therefore, alternative tests that indicate disease activity and relate with liver biopsy findings are needed. We aimed to investigate the relationship between serum complement levels and biopsy findings in patients with chronic hepatitis C. One hundred cases (70 patients, 30 healthy controls) were included in the study. Patients were divided into two groups: chronic hepatitis C patients with high transaminase levels were evaluated as the first group and patients with normal transaminase levels as the second group. Patients with a high transaminase level were biopsied and activity scores were evaluated against complement C3c and C4 levels. In addition, demographic data and laboratory tests were evaluated. Patients with chronic hepatitis C without proteinuria, acute phase response, cirrhosis, or coinfection with another hepatitis virus were included in the prospective study. Serum complement C3c (p<0.01) and C4 (p<0.01) levels were significantly lower in the first group than the second group. Serum complement C3c levels did not correlate with laboratory tests, hepatitis C virus-RNA levels, histological activity index, or fibrosis scores in patients with high transaminase levels, whereas complement C4 levels showed significant correlation with alanine aminotransferase (r: -0.368, p: 0.001) and histological activity index (r: -0.639, p: 0.001). We could not find any relation between serum complement C4 level and fibrosis. Serum complement C4 levels correlate with the histological activity index of the Knodell scoring system.

Stability of Yellow Fever Virus under Recombinatory Pressure as Compared with Chikungunya Virus

Recombination is a mechanism whereby positive sense single stranded RNA viruses exchange segments of genetic information. Recent phylogenetic analyses of naturally occurring recombinant flaviviruses have raised concerns regarding the potential for the emergence of virulent recombinants either post-vaccination or following co-infection with two distinct wild-type viruses. To characterize the conditions and sequences that favor RNA arthropod-borne virus recombination we constructed yellow fever virus (YFV) 17D recombinant crosses containing complementary deletions in the envelope protein coding sequence. These constructs were designed to strongly favor recombination, and the detection conditions were optimized to achieve high sensitivity recovery of putative recombinants. Full length recombinant YFV 17D virus was never detected under any of the experimental conditions examined, despite achieving estimated YFV replicon co-infection levels of ∼2.4×106 in BHK-21 (vertebrate) cells and ∼1.05×105 in C710 (arthropod) cells. Additionally YFV 17D superinfection resistance was observed in vertebrate and arthropod cells harboring a primary infection with wild-type YFV Asibi strain. Furthermore recombination potential was also evaluated using similarly designed chikungunya virus (CHIKV) replicons towards validation of this strategy for recombination detection. Non-homologus recombination was observed for CHIKV within the structural gene coding sequence resulting in an in-frame duplication of capsid and E3 gene. Based on these data, it is concluded that even in the unlikely event of a high level acute co-infection of two distinct YFV genomes in an arthropod or vertebrate host, the generation of viable flavivirus recombinants is extremely unlikely.

Peginterferon ALPHA-2A (40KD) Plus Ribavirin for the Treatment of Patients With Chronic Hepatitis C (CHC) and Compensated Liver Cirrhosis in Japan

Introduction: Known predictors of response to combination pegylated interferon (PEG-IFN) and ribavirin (RBV) for treatment of chronic hepatitis C (CHC) include genotype, race, rapid virologic response, early virologic response and recently identified interleukin-28B polymorphism. There has been conflicting data regarding the relationship between weight loss during antiviral therapy and sustained virologic response (SVR). Purpose: To determine if weight loss during antiviral therapy correlates with SVR to PEG-IFN and RBV therapy in CHC patients. Methods: We conducted a retrospective chart review of approximately 500 randomly selected CHC patients treated with combination PEG-IFN and RBV therapy from 2004 to 2009 in our urban academic hepatology practice. Random selection was accomplished by electronically randomizing an alphabetical list of CHC patients seen in our practice. Patients with acute HCV infection, HBV or HIV co-infection, liver transplant recipients, patients on experimental protocols or extended treatment courses, with unavailable weight data or lost to follow up were excluded. Both treatment-naive and treatment-experienced patients were included. Univariate and multivariate analysis, including chi-square testing, t-test and logistic regression modeling using SAS 9.2, was completed to assess for association between weight loss and achieving SVR. Results: Data on 194 patients (68% genotype 1; 43% with advanced fibrosis) were analyzed after exclusion criteria applied. 37% of patients had SVR (including treatment-naive and prior non-responders and relapsers). Baseline characteristics for SVR and non-SVR groups were similar except for genotype (40% in SVR group were genotype 1 vs 84% in non-SVR group) and fibrosis scores (SVR group had lower scores). Overall, 68% had weight loss >1 kg, with 40% SVR in those with weight loss vs 24% SVR among those with no weight loss. Overall, the majority of weight loss (67%) occurred in the first 12 weeks, but for those with weight loss >10kg (10% of patients), only 40% of weight loss occurred by week 12. In multivariate analysis, weight loss > 5kg (28% of patients) was associated with SVR (aOR 2.9, CI 1.04-8.30). Consistent with previous studies, genotypes 2/3 (aOR 7.1, CI 2.94-17.28), lower stage of fibrosis (aOR 1.7, CI 1.162.44) and lower baseline weight (aOR 1.03, CI 1.01-1.06) were also associated with SVR. Conclusions: Our study found an association between SVR and weight loss while controlling for other known predictors of SVR. Our data suggests that weight trend during treatment of CHC patients with combination PEG-IFN and RBV should be monitored as weight loss may be used as a surrogate marker of SVR to the current standard of care.

Atypical bacterial pathogen infection in children with acute bronchiolitis in northeast Thailand

Atypical bacterial pathogens--including Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Chlamydia trachomatis--are important infectious agents of the respiratory system. Most current information pertains to adults and little is known about the role of these organisms in lower respiratory tract infections among young children with acute bronchiolitis. This study detected these pathogens in the nasopharyngeal secretions of children between 1 month and 2 years of age admitted with acute bronchiolitis to hospitals in Khon Kaen, northeast Thailand. The M pneumoniae and C pneumoniae in the nasopharyngeal secretions were detected using multiplex and nested-polymerase chain reaction (PCR), whereas PCR and restriction fragment length polymorphism were used to investigate C trachomatis. These samples were also tested by multiplex reverse transcriptase PCR for respiratory viruses, including respiratory syncytial virus (RSV), influenza A, influenza B, and human metapneumovirus. Of the 170 samples taken from hospitalized children with acute bronchiolitis, 12.9% were infected with atypical bacteria and 85.3% with respiratory viruses. RSV was the most common causative viral agents found in 64.7% of the samples. M pneumoniae was the most common atypical bacterial pathogen (14/170, 8.2%) and most of the patients infected with it were between 6 and less than 12 months of age (71 cases). Of the infected cases in this age group, 7 of 14 were infected with M pneumoniae and 4 of 4 with C pneumoniae. Both M pneumoniae (13/14) and C pneumoniae (4/4) had etiologies indicating viral coinfections. Four (2.4%) of all of the cases had C trachomatis infections and all of these were infected with RSV, including three patients less than 6 months of age. These results suggest that in children with virus-induced acute bronchiolitis coinfection with M pneumoniae, C pneumoniae, or C trachomatis can be expressed differently in each age group. These atypical bacteria may be the important infectious agents that induce severe illness of acute bronchiolitis.

Leptospirosis and dengue co-infection in a Brazilian Amazon patient

Leptospirosis and dengue are two major urban health problems associated with high mortality. Acute co-infection with leptospirosis and dengue is an extremely rare event. The aim of the present report is to describe the first case of leptospirosis and dengue co-infection in a patient from the Brazilian eastern Amazonia.

Plasmodium falciparum malaria and Parvovirus B19; a case of acute co-infection

BackgroundCo-infection with Plasmodium falciparum malaria and Parvovirus B19 in adults is an extremely rare occurrence and, apparently, only one case has been previously reported. Herein we describe a case of acute co-infection with severe anemia and renal failure.Case presentationThe patient was a 34-year-old African man presenting myalgia, fatigue, headache, anemia and hepatosplenomegaly. A thin peripheral smear showed Plasmodium falciparum trophozoites and the patient was treated with oral mefloquine. After an initial amelioration, fever, fatigue and myalgia reappeared, the anemia worsened and there was evidence of acute renal failure. No malarial parasites were found with a blood smear. A bone marrow aspiration showed marked erythroid hypoplasia. Parvovirus B19-specific IgM and IgG and viremia were positive. The patient was treated with steroids and blood cell transfusions. After ten days, anemia and renal failure progressively decreased. When last seen, the patient was asymptomatic and the blood values were within the normal range.ConclusionsThe diagnosis of Parvovirus B19 acute infection should be considered in any case of persistent severe anemia and/or renal failure, even in clinical conditions that are well-known causes of anemia and renal failure, such as malaria.

HHV‐6 IgG4 isotype response following measles infection

Human herpesvirus 6 (HHV-6) is widespread in the human population by infecting most individuals in early childhood. After primary infection, HHV-6 establishes a latent infection by remaining in circulating mononuclear cells of healthy individuals. The HHV-6 antibody titer increases after primary infection with measles virus. The present study was undertaken to determine the specific antiviral IgG1, IgG2, IgG3, and IgG4 subclass response patterns to HHV-6 in HHV-6-seropositive individuals with natural measles virus infection, measles vaccination, and rubella virus infection. The purpose of this study was to examine HHV-6-specific IgG isotype response in patients with acute virus coinfection. Serum samples were obtained from individuals who were seropositive for HHV-6 after natural primary infection with measles virus during an outbreak, measles vaccination, or rubella virus infection, and from healthy individuals. Sera were examined by indirect immunofluorescence assays for detection of HHV-6-specific IgG1, IgG2, IgG3, and IgG4 antibodies. A high percentage (69%) of those infected with measles virus had an HHV-6 IgG1 and IgG4 response (P < 0.001, chi(2) test), whereas persons vaccinated against measles, those infected with rubella, and healthy individuals showed an HHV-6 IgG1 response. These results demonstrate that natural measles virus infection induces an HHV-6 IgG isotype response, which suggests a shift in immune activity from a Th1 to a Th2 response. J. Med. Virol. 82:396-399, 2010. (c) 2010 Wiley-Liss, Inc.