Prior statin use and 90-day mortality in Gram-negative and Gram-positive bloodstream infection: a prospective observational study.

In several studies on patients with bloodstream infection (BSI), prior use of statins has been associated with improved survival. Gram-positive and Gram-negative bacteria alert the innate immune system in different ways. We, therefore, studied whether the relation between prior statin use and 90-day total mortality differed between Gram-positive and Gram-negative BSI. We conducted a prospective observational cohort study of 1,408 adults with BSI admitted to Levanger Hospital between January 1, 2002, and December 31, 2011. Data on the use of statins and other medications at admission, comorbidities, functional status, treatment, and outcome were obtained from the patients' hospital records. The relation of statin use with 90-day mortality differed between Gram-negative and Gram-positive BSI (p-value for interaction 0.01). Among patients with Gram-negative BSI, statin users had significantly lower 90-day total mortality [odds ratio (OR) 0.42, 95 % confidence interval (CI) 0.23-0.75, p = 0.003]. The association remained essentially unchanged after adjusting for the effect of sex, age, functional status before the infection, and underlying diseases that were considered confounders (adjusted OR 0.38, 95 % CI 0.20-0.72, p = 0.003). A similar analysis of patients with Gram-positive BSI showed no association of statin use with mortality (adjusted OR 1.22, 95 % CI 0.69-2.17, p = 0.49). The present study suggests that prior statin use is associated with a lower 90-day total mortality in Gram-negative BSI, but not in Gram-positive BSI.

Impact of the World Health Organization's Surgical Safety Checklist on safety culture in the operating theatre: a controlled intervention study.

BACKGROUND: Positive changes in safety culture have been hypothesized to be one of the mechanisms behind the reduction in mortality and morbidity after the introduction of the World Health Organization's Surgical Safety Checklist (SSC). We aimed to study the checklist effects on safety culture perceptions in operating theatre personnel using a prospective controlled intervention design at a single Norwegian university hospital. METHODS: We conducted a study with pre- and post-intervention surveys using the intervention and control groups. The primary outcome was the effects of the Norwegian version of the SSC on safety culture perceptions. Safety culture was measured using the validated Norwegian version of the Hospital Survey on Patient Safety Culture. Descriptive characteristics of operating theatre personnel and checklist compliance data were also recorded. A mixed linear regression model was used to assess changes in safety culture. RESULTS: The response rate was 61% (349/575) at baseline and 51% (292/569) post-intervention. Checklist compliance ranged from 77% to 85%. We found significant positive changes in the checklist intervention group for the culture factors 'frequency of events reported' and 'adequate staffing' with regression coefficients at -0.25 [95% confidence interval (CI), -0.47 to -0.07] and 0.21 (95% CI, 0.07-0.35), respectively. Overall, the intervention group reported significantly more positive culture scores-including at baseline. CONCLUSIONS: Implementation of the SSC had rather limited impact on the safety culture within this hospital.

Severe consequences of healthcare-associated infections among residents of nursing homes: a cohort study.

The aim of this study was to identify the consequences of healthcare-associated infections in Norwegian nursing homes, to include debilitation, hospital transfer and mortality. We followed the residents of six nursing homes in two major cities in Norway during the period October 2004 to March 2005. For each resident with infection we randomly selected two controls among residents who did not have an infection. Cases and the controls were followed for 30 days as a cohort in order to measure the incidence of complications and risk ratio (RR) in the two groups. The incidence of infection was 5.2 per 1000 resident-days. After 30 days follow-up 10.9% of residents who had acquired infection demonstrated a reduction in overall physical condition compared with 4.8% in the unexposed group (RR: 2.3). Altogether 13.0% of residents with infections were admitted to hospital compared with 1.4% in the unexposed group (RR 9.2), and 16.1% residents with infections died in the nursing home during follow-up compared with 2.4% in the unexposed group (RR: 6.6). Residents with lower respiratory tract infections demonstrated higher morbidity and mortality. In conclusion, healthcare-associated infections cause severe consequences for people living in nursing homes, including debilitation, hospital admission and death.

Healthcare-associated infection among residents of long-term care facilities: a cohort and nested case-control study.

Knowledge of infection control measures in nursing homes is limited. This study aimed to assess the incidence of, and potential risk factors for, healthcare-associated infection in long-term care facilities in Norway. Incidence of healthcare-associated infection was recorded prospectively in six long-term care facilities located in two major cities in Norway between 1 October 2004 and 31 March 2005. For each resident with an infection we aimed for two controls in a nested case-control study to identify potential risk factors. Incidence of infection was 5.2 per 1000 resident-days. Urinary and lower respiratory tract infections were the most common. Patients confined to their beds [odds ratio (OR=2.7)], who stayed <28 days (OR=1.5), had chronic heart disease (OR=1.3), urinary incontinence (OR=1.5), an indwelling urinary catheter (OR=2.0) or skin ulcers (OR=1.8) were shown to have a greater risk for infection. Age, sex and accommodated in a two- versus single-bed room were not significant factors. Incidence of infection in nursing homes in Norway is within the range reported from other countries. This study identified several important risk factors for healthcare-associated infection. There is a need to prevent infection by implementing infection control programmes including surveillance in long-term care facilities.

Role of penicillin-binding protein 5 C-terminal amino acid substitutions in conferring ampicillin resistance in Norwegian clinical strains of Enterococcus faecium.

The importance of amino acid sequence differences in the C-terminal part and levels of mRNA expression of penicillin-binding protein 5 (PBP5) for ampicillin resistance in Enterococcus faecium was investigated. Seventeen isolates from Norwegian hospitalized patients (ampicillin MIC 0.064->256 mg/L) with different C-terminal pbp5 DNA sequences encoding 11 different amino acid sequences were analyzed with a 14C-radiolabeled penicillin- binding assay to PBP5 and with real-time PCR quantification of pbp5 mRNA expression. Using multiple logistic regression analysis the amino acid substitution Met 485 was linked to ampicillin MIC and levels of 14C-radiolabeled penicillin bound to PBP5; however, there were isolates with identical PBP5 alleles and different ampicillin MICs. There was no relation between the quantity of pbp5 mRNA transcripts and ampicillin resistance. The results cannot explain ampicillin resistance in Norwegian clinical strains of E. faecium and indicate that other factors besides the properties of the C-terminal part of PBP5 are most likely involved.

Outbreak of infection with high-level gentamicin-resistant Enterococcus faecalis (HLGRE) in a Norwegian hospital.

OBJECTIVES: To examine and characterize a suspected outbreak of high-level gentamicin-resistant Enterococcus (HLGRE) infection. METHODS: Eighty-nine patients with clinical infection diagnosed during hospital stay or within 30 days after discharge in the period from June 1995 to 31 December 1999 were included in the study. One control patient was assigned for each HLGRE patient according to localization in the hospital (same ward), time of admission (+/-3 months), and age (+/-10 years). Unadjusted risk analysis and multivariate logistic regression analysis were performed. Sixty-nine HLGRE strains were subjected to PCR amplification of the genes coding for aminoglycoside-3'-O-phosphoryltransferase-III (APH(3')-III) and aminoglycoside-6'-N-acetyltransferase/2"-O-phosphoryltransferase-III (AAC(6')/APH(2")). RESULTS: The gene aacA/aphD, associated with HLGRE, was detected by PCR in all isolates, and the gene aphA3, associated with high-level streptomycin, kanamycin and amikacin resistance, was detected in 56 of the 69 isolates. None of the 69 isolates was resistant to glycopeptides or ampicillin. Resistance to ciprofloxacin was found in 57 (82.6%). Pulsed-field gel electrophoresis analysis revealed 12 different genotypes, among which two major clusters dominated. CONCLUSIONS: Both clonal expansion and the emergence of unique strains contributed to the increased number of infections caused by HLGRE. Urinary catheterization, duration of hospital stay and antibiotic therapy were significant risk factors for HLGRE infection.

Prevalence of resistance to ampicillin, gentamicin and vancomycin in Enterococcus faecalis and Enterococcus faecium isolates from clinical specimens and use of antimicrobials in five Nordic hospitals.

We determined the species distribution and prevalence of ampicillin resistance, high-level gentamicin resistance (HLGR) and vancomycin resistance among clinical enterococcal isolates from five Nordic laboratories (Bergen, Tromsø, Uppsala, Aarhus and Reykjavik). Isolates represented three different groups: (i) all blood culture isolates from 1999; (ii) consecutive in-patient isolates (maximum 40); and (iii) consecutive outpatient isolates (maximum 40) collected during March to May 2000. Antimicrobial use data were collected at the national and hospital level. A high proportion (31.4%) of Enterococcus faecium was detected among blood culture isolates, in contrast to only 4.2% among isolates from outpatients. Ampicillin resistance was not found in Enterococcus faecalis, in contrast to 48.8% in E. faecium isolates. HLGR rates varied considerably between laboratories (1.1-27.6%). Acquired vancomycin resistance was not detected. There were no significant differences in the prevalences of HLGR between in-patient and outpatient isolates at individual hospitals. A cluster of clonally related ampicillin-resistant and HLGR E. faecium isolates was demonstrated in one of the hospitals. The lowest level of hospital antimicrobial use, the lowest proportion of E. faecium and the lowest prevalence of resistance were observed in Reykjavik. The study showed a relatively low level of resistance in enterococci, as compared with most European countries and the USA. However, there were large differences between hospitals with regard to the relative proportion of E. faecium isolates, their susceptibility to ampicillin and gentamicin, as well as the prevalence of HLGR in E. faecalis isolates. This indicates a potential for further improvement of antibiotic policies, and possibly hospital infection control, to maintain the low resistance levels observed in these countries.

The prevalence of faecal carriage of ampicillin-resistant and high-level gentamicin-resistant enterococci among inpatients at 10 major Norwegian hospitals.

From March to October 1999, 854 patients hospitalized at 10 major Norwegian hospitals were screened for rectal carriage of ampicillin-resistant enterococci (ARE) and high-level gentamicin-resistant enterococci (HLGRE). A total of 59 ARE carriers (prevalence 6.9%, range 0-22% among hospitals) and 28 HLGRE carriers (prevalence 3.3%, range 1-11%) were detected. All ARE or HLGRE strains were susceptible to vancomycin, whereas 77% of the ARE isolates were resistant to ciprofloxacin. All the ARE strains were identified as Enterococcus faecium, and 48% of these were genomically closely related as shown by PFGE. Specific point mutations in the pbp5 gene were associated with reduced susceptibility to ampicillin. The adjusted risk of becoming a carrier of ARE was related to the use of glycopeptides [odds ratio (OR) = 4.8], the use of any antimicrobial agent (OR = 3.1) and more than one hospital admission during the last six months (OR = 2.0). Twenty-five of 28 HLGRE isolates were Enterococcus faecalis. The aacA/aphD genes were detected in 26 (93%) and the aphA3 in 19 (68%) of the HLGRE isolates. Sixty-four percent of the HLGRE isolates belonged to two PFGE clusters. Consumption of antimicrobial agents was also a significant risk factor for HLGRE colonization (OR = 5.4), while prescription of penicillins was associated with reduced risk (OR = 0.28).

[Infection outbreaks caused by methicillin-resistant Staphylococcus aureus at Haukeland hospital]. / Infeksjonsutbrudd med meticillinresistente gule stafylokokker ved Haukeland Sykehus.

BACKGROUND: Nosocomial infections caused by methicillin-resistant Staphylococcus aureus (MRSA) represent an increasing problem worldwide. MATERIAL AND METHODS: We report two outbreaks of methicillin-resistant S. aureus at Haukeland University Hospital during 1998-99. RESULTS: During the fall of 1998, four patients in the dermatological ward and three of their relatives were infected or colonised with MRSA. The strain was probably introduced by an eczematous patient who had recently arrived from Japan. Three patients became chronic carriers. The second outbreak involved three other hospital departments in July-August 1999. The index patient, a multitraumatised japanese tourist, died 16 days after admission. Two other patients were infected, one of them became a chronic carrier. According to official guidelines, neither of the index patients needed MRSA screening. Pulsed field gel-electrophoresis of the MRSA isolates revealed two different strains at the first outbreak, both probably introduced from the index patient, and one single strain at the second outbreak. Nasal swabs of staff were negative. INTERPRETATION: Physicians need to know that recommended guidelines regarding MRSA screening do not cover all types of risk situations. MRSA carriage among healthcare workers is probably not an important source of MRSA spread in hospitals. Measures to prevent cross infection between patients should be emphasised.

[Outbreak of multiresistant Acinetobacter baumannii infection]. / Utbrudd av infeksjon med multiresistent acinetobacter baumannii.

BACKGROUND: Nosocomial infections caused by multiresistant gram-negative bacteria represent an increasing problem, especially among intensive care patients. A serious outbreak of infection caused by multi-resistant Acinetobacter baumannii occurred in four burn patients. Acinetobacter is a gram-negative coccibacilli which is widespread in nature, and has been reported as an increasing problem in critically ill patients. MATERIALS AND METHODS: The outbreak strain was introduced from Alicante, Spain, by a transferred patient. This strain was resistant to all commonly available systemic antibiotics (including the karbapenems and all aminoglycosides), and sensitive only to polymyxin B. Two patients were critically ill, one of them died in septic shock. RESULTS: The ward was closed for admission of new patients and hygiene precautions were strengthened. Extensive testing of staff and equipment revealed multi-resistant A baumannii on a shower trolley shared by several patients. The outbreak strain was also identified by restriction endonuclease analysis. The patients were kept strictly isolated until their burn wounds were sufficiently healed to allow them to be discharged to their homes. INTERPRETATION: Following discharge of the last patient and extensive cleaning and disinfection of the entire ward, the particularly resistant strain has not reoccurred. Still, this experience may warrant screening for multiresistant gram-negative rods in patients transferred from regions where broad resistance to antibiotics is a common problem.

Outbreak of ampicillin-resistant Enterococcus faecium--risk factors for faecal colonisation.

Since January 1995 there has been a nosocomial outbreak at Haukeland University Hospital involving more than 330 patients with clinical infections caused by ampicillin-resistant Enterococcus faecium (ARE) (minimum inhibitory concentration > or =32 mg/l). Rectal carriage of ARE was initially observed on two medical wards only. Here the ARE colonisation rate has remained high. To assess risk factors for ARE colonisation we performed a case-control study including 37 rectal carriers of ARE and 83 non-carriers on these wards. Significant differences were found between cases and controls with respect to the mean number of days on antimicrobial treatment (13.3 for carriers, 5.5 for non-carriers, p<0.001), mean number of different antibiotics prescribed (2.8 for carriers, 2.1 for non-carriers, p= 0.008) and mean number of days in hospital (18.4 vs 10.2, p=0.001). Unadjusted statistical analysis showed that several antibiotics were risk factors for ARE carriage. Logistic regression analysis showed that fluoroquinolone prescription (OR=3.5, p=0.01) and more than 10 days of antibiotic use (OR= 3.3, p=0.01) were significant risk factors. An additional follow-up screening of previous carriers revealed no colonisation 8 to 36 (median 9) months after discharge from hospital (n=17). Prolonged antimicrobial therapy and broad-spectrum antibiotics seem to facilitate nosocomial ARE colonisation.

Nosocomial outbreak of ampicillin resistant Enterococcus faecium: risk factors for infection and fatal outcome.

A nosocomial outbreak caused by ampicillin resistant Enterococcus faecium (ARE) was detected at a Norwegian university hospital in January 1995. Prior to this outbreak, ARE were not common in this hospital or other hospitals in Norway. During 1995 and 1996, a total of 149 cases with clinical ARE infection were detected prospectively. A case control study was performed by allocating controls matched for gender, age and ward of admission. Altogether, 123 case control pairs with mean age 70.1 years were included. Isolates from 89 (72. 4%) of the cases were identical or related to the defined outbreak strain as determined by pulsed-field gel electrophoresis (PFGE). In 75 of the patients (60.9%), ARE caused urinary tract infection, five (4.1%) had bacteraemia, 33 (26.8%) had wound infection and 10 (8.1%) had other infections. In a logistic regression model for 1:1 matched samples, the following factors were identified as significant risk factors for ARE infection: underlying neurological disease (OR=33.5), prescription of antimicrobial agents for more than 10 days (OR=8. 99), prescription of cephalosporins (OR=4.69), underlying gastrointestinal disease (OR=3.36) and length of hospital stay per day (OR=1.04). The intrahospital death rate for the cases was 18.7% compared with 8.9% for the controls, corresponding to an excess mortality attributable to ARE infection of 9.8%. A history of carbapenem prescription was the only independent factor contributing to death (OR=5.64) when comparing ARE patients dying in hospital to those surviving.

Vancomycin resistance emerging in a clonal outbreak caused by ampicillin-resistant Enterococcus faecium.

OBJECTIVES: To describe the first nosocomial outbreak of ampicillin-resistant Enterococcus faecium (ARE) in Norway, where a few vancomycin-resistant strains have also been identified. METHODS: All cases of ARE and vancomycin-resistant Enterococcus faecium (VRE) diagnosed by the medical microbiological laboratories in a region inhabited by approximately 1 million people were registered. Isolates obtained during the period 1 January 1995 to 31 December 1996 were characterized by pulsed field-gel electrophoresis and the clinical data were recorded. RESULTS: One hundred and forty-nine patients (64 males, 85 females, mean age 70.5 years) were infected with ARE. Isolates from 115 cases were genomically related to the outbreak strain. Infections included bacteremia (14), wound infections (31), urinary tract infections (97) and other infections (seven). Most had a severe underlying disease and 93% of the patients had received antibiotics for a mean time of 23 days. Twenty-four patients (16.1%) died during hospitalization. Four infections were caused by a vanB-type VRE that was genomically related to the ARE outbreak strain. The prescription rate for vancomycin was low, but an increase in vancomycin use paralleled the appearance of VRE. The highest monthly incidence rate was 2.5 per 1000 patient admissions in July 1996 declining to 0.5 in December 1996. CONCLUSIONS: The first nosocomial outbreak caused by ARE was observed in 1995 in Norway and is still ongoing. One year after the onset, VRE occurred in wards which had a relatively high consumption of vancomycin.

Treatment with interferon-alpha2a alone or interferon-alpha2a plus ribavirin in patients with chronic hepatitis C previously treated with interferon-alpha2a. CONSTRUCT Group.

BACKGROUND: Preliminary results from combination therapy with interferon-alpha and ribavirin (IFN/Rib) in patients with chronic hepatitis C have been promising, with up to 50% sustained hepatitis C virus (HCV) RNA response. The aim of this study was to investigate whether a sustained HCV RNA response could be obtained with combination therapy in patients who were non-responders or relapsers after IFN treatment. METHODS: In a multicenter study we randomized 53 HCV RNA-positive patients into 2 treatment groups. They all had biopsy-confirmed chronic hepatitis C, and all were recruited from a previous IFN study: 26 were previous non-responders and 27 responders with relapse. Group A received interferon-alpha2a, 4.5 MIU thrice weekly for 6 months, and group B received ribavirin, 1000-1200 mg/day, in combination with the same dose of interferon-alpha2a for 6 months. Median Knodell index was 5.0 in both groups. Genotype 1 was found in 24 (45%), type 2 in 3 (6%), and type 3 in 26 (49%). RESULTS: Sustained clearance of HCV viremia 6 months after interferon-alpha2a treatment stop was obtained in 12 of 53 patients (23%): 6 of 27 in the IFN group (22%) and 6 of 26 (23%) in the IFN/Rib group (NS). Nine of 27 (33%) former responders with relapse, compared with 3 of 26 (12%) non-responders, obtained a sustained HCV RNA response (P = 0.054). In previous relapse patients sustained loss of viremia was more frequent in genotype 3 (50%) than in genotype 1 (11%) patients (P = 0.022). CONCLUSIONS: In a group of previous IFN-alpha2a-treated chronic HCV patients we obtained a similar sustained clearance of viremia when retreated either with IFN-alpha2a alone or with a combination of IFN-alpha2a and ribavirin for 6 months. Previous relapse patients with HCV genotype 3 obtained sustained loss of viremia significantly more often (50%) than type-patients (11%). Previous IFN responders with relapse responded better than previous non-responders.

[Infections caused by multiresistant enterococci in Norway]. / Infeksjoner forårsaket av multiresistente enterokokker i Norge.

During the last decade antimicrobial resistant pathogens have become a major medical problem. Internationally, multiresistant enterococci have increased nosocomial morbidity and mortality. Such strains are often resistant to ampicillin, aminoglycosides, and glycopeptides such as vancomycin. The spread of these strains has been shown to correlate to the use of antibiotics and the practice of suboptimal infection control within health care facilities. The current situation in Norwegian hospitals is presented, including the only six cases with infections and the three carriers of vancomycin resistant enterococci found to date. Surveillance in the hospitals shows that such strains are uncommon in non-infected patients. To maintain this favourable situation it is necessary to continue to practice effective methods of infection control and to employ sound antibiotic policies.

The effect of treatment with alpha-interferon on hepatitis G/GBV-C viraemia. The CONSTRUCT Group.

BACKGROUND: Hepatitis G virus (HGV) or GBV-C is frequently detected in patients co-infected with hepatitis C virus (HCV). This study investigated host and virologic factors influencing the response to HGV/GBV-C to alpha-interferon treatment. METHODS: HGV/GBV-C was detected and quantified by nested polymerase chain reaction. The influence of variables such as liver biopsy appearance, liver function abnormalities, and response of HCV to interferon treatment was monitored. RESULTS: Fourteen of the 25 HGV/GBV-C-infected patients treated with interferon (3-6 MIU three times a week for 6 months) became non-viraemic during treatment, although all relapsed after treatment withdrawal at 6 months, with no net change in virus load between 0 and 12 months. CONCLUSIONS: Predictive factors for clearance of HGV/GBV-C viraemia by interferon were pre-treatment severity of liver disease (median Knodell score of 4, compared with 7 for non-responders; P = 0.030) and alanine aminotransferase levels (median, 114, 182 for non-responders; P = 0.039). Clearance was associated with the treatment response of HCV. Nine of 13 who cleared HGV/GBV-C also cleared HCV, compared with 3 of 11 HGV/GBV-C non-responders; P = 0.05). The shared susceptibility of HGV/GBV-C and HCV to interferon treatment suggests a link between the mechanism of clearance of the two viruses.

Low faecal carrier rate of vancomycin resistant enterococci in Norwegian hospital patients.

The faecal carrier rate of vancomycin resistant enterococci (VRE) was surveyed among 616 patients in selected departments of 7 Norwegian hospitals. One Enterococcus gallinarum isolate harbouring a vanB2 element was recovered from a child with malignant disease treated with vancomycin and ceftazidime. No vancomycin resistant Enterococcus faecalis or Enterococcus faecium were detected and no VRE isolates of the VanA type were identified. The low level of VRE carriage corresponds to the limited use of glycopeptide antibiotics for human therapeutic purposes in Norway. It indicates a low risk of acquiring VRE infections in Norwegian hospitals.

Genotype, viral load and age as independent predictors of treatment outcome of interferon-alpha 2a treatment in patients with chronic hepatitis C. Construct group.

Patients with chronic hepatitis C respond differently when treated with interferon. We randomized 116 patients with chronic hepatitis C in order to compare two dosage regimens of recombinant interferon alpha 2a:3 MIU x 3 per week for 6 months (arm A) or 6 MIU x 3 per week for 3 months and then 3 MIU x 3 per week for 3 months (arm B). There were no significant differences concerning outcome between the two dose regimens: sustained clearance of HCV viremia 6 months after the end of treatment was obtained in 12/59 (20%) in group A compared with 18/57 (32%) in group B (p = 0.24). In patients with genotype 1a, 4/31 (13%), in genotype 1b, none of 9 (0%), 9/15 (60%) in genotype 2, and 17/58 (29%) in genotype 3, showed sustained clearance of HCV viremia 6 months after the end of treatment (p = 0.002). In a stepwise logistic regression analysis, only pretreatment viral load (p = 0.0001), genotype (p = 0.001) and age (p = 0.04) were identified as independent predictors of sustained clearance of HCV viremia. Liver histology as assessed by Knodell index was significantly improved in patients with sustained HCV RNA response 6 months after the end of treatment (5.2 +/- 2.2 vs 2.6 +/- 2.2, p < 0.001), but not in responders with relapse or in non-responders. In conclusion, stepwise logistic regression analysis showed that viral load, HCV genotype and age were the only independent predictors for sustained HCV RNA response.

[Treatment of hepatitis C]. / Behandling av hepatitt C.

Hepatitis C virus (HCV) has been a major cause of post transfusion hepatitis, and is still an important cause of chronic liver disease throughout the world. How to treat patients with chronic HCV infection has been brought into focus in recent years, and a substantial amount of data has been obtained about the development of hepatitis C with and without treatment. This survey considers the diagnosis of hepatitis C, and present treatment modalities and their potential. The patients most likely to respond to treatment are described, and the authors finally discuss why treatment of hepatitis C still should take place in controlled studies.

Prevalence of hepatitis C genotypes among patients with chronic hepatitis C in Norway. Construct Group.

Among 116 patients with biopsy-confirmed chronic hepatitis C (Riba 2 or Riba 3 positive) in a multicenter study in southern Norway on interferon, we determined hepatitis C virus genotype by restriction fragment length polymorphism (RFLP) of the 5' NCR. The RFLP method was supplemented by and compared with a serological typing method based on the detection of type-specific antibody to peptide from the NS-4 region. A total of 102/106 (96%) patient sera showed detectable type-specific antibody to NS-4 peptides and corresponded in all cases, except two, to the genotype detected by polymerase chain reaction. Combining the results from RFLP genotyping and serotyping, genotype 1 was found in 40 (35%) (27 with 1a and 10 with 1b, 3 subtypes not determined), genotype 2 in 15 (13%) (subtype 2b in 14 and 1 subtype not determined), and genotype 3 in 58 (50%) of patients. The low mean age of the patients (34 years), the low prevalence of cirrhosis (3.5%), the short duration of the disease, and a high prevalence of intravenous-drug abusers may account for the low prevalence of infection with genotype 1b (9%). The epidemiological features of hepatitis C patients are markedly different from patient groups described in southern Europe in terms of risk factors, age, and genotype distribution.