Francisella tularensis Bone and Joint Infections: United States, 2004-2023.

Tularemia is caused by the highly infectious bacterium Francisella tularensis, which is recognized as a Tier 1 bioterrorism agent. Tularemia has a range of recognized clinical manifestations, but fewer than 20 bone or joint infections from 6 countries have been reported in the literature to date. This series includes 13 cases of F. tularensis septic arthritis or osteomyelitis in the United States during 2004-2023 and describes exposures, clinical presentation, diagnosis, and outcomes for this rare but severe form of tularemia. Clinicians should consider F. tularensis in patients with compatible exposures or a history of joint replacement or immunosuppression.

Body Lice among People Experiencing Homelessness and Access to Hygiene Services during the COVID-19 Pandemic-Preventing Trench Fever in Denver, Colorado, 2020.

Eight people with human body louse-borne Bartonella quintana infections were detected among people experiencing homelessness (PEH) in Denver during January-September 2020, prompting a public health investigation and community outreach. Public health officials conducted in-person interviews with PEH to more fully quantify body lice prevalence, transmission risk factors, access to PEH resources, and how the COVID-19 pandemic has affected resource access. Recent body lice exposure was reported by 35% of 153 interview participants. In total, 75% of participants reported reduced access to PEH services, including essential hygiene activities to prevent body lice, during Colorado's COVID-19 stay-at-home orders. Future pandemic planning should consider hygiene resource allocation for PEH populations to prevent emerging and reemerging infections such as B. quintana.

Impact of the US Two-dose Varicella Vaccination Program on the Epidemiology of Varicella Outbreaks: Data from Nine States, 2005-2012.

BACKGROUND: A routine 2-dose varicella vaccination program was adopted in 2007 in the US to help further decrease varicella disease and prevent varicella outbreaks. We describe trends and characteristics of varicella outbreaks reported to the Centers for Disease Control and Prevention (CDC) during 2005-2012 from 9 states. METHODS: Data on varicella outbreaks collected by 9 state health departments were submitted to CDC using the CDC outbreak reporting worksheet. Information was collected on dates of the outbreak, outbreak setting and number of cases by outbreak; aggregate data were provided on the numbers of outbreak-related cases by age group, vaccination status and laboratory confirmation. RESULTS: Nine hundred and twenty-nine outbreaks were reported from the 6 states, which provided data for each year during 2005-2012. Based on data from these 6 states, the number of outbreaks declined by 78%, decreasing from 147 in 2005 to 33 outbreaks in 2012 (P = 0.0001). There were a total of 1015 varicella outbreaks involving 13,595 cases reported by the 9 states from 2005 to 2012. The size and duration of outbreaks declined significantly over time (P < 0.001). The median size of outbreaks was 12, 9 and 7 cases and median duration of outbreaks was 38, 35 and 26 days during 2005-2006, 2007-2009 and 2010-2012, respectively. Majority of outbreaks (95%) were reported from schools, declining from 97% in 2005-2006 to 89% in 2010-2012. Sixty-five percent of outbreak-related cases occurred among 5-year to 9-year olds, with the proportion declining from 76% in 2005-2006 to 45% during 2010-2012. CONCLUSIONS: The routine 2-dose varicella vaccination program appears to have significantly reduced the number, size and duration of varicella outbreaks in the US.

Hepatocellular carcinoma in patients with chronic hepatitis C virus infection without cirrhosis.

AIM: To investigate and characterise patients with chronic hepatitis C virus (HCV) infection presenting with hepatocellular carcinoma (HCC) in the absence of cirrhosis. METHODS: Patients with chronic hepatitis C infection without cirrhosis presenting with HCC over a 2-year period were identified. The clinical case notes, blood test results and histological specimens were reviewed to identify whether additional risk factors for the development of HCC were present. RESULTS: Six patients (five male, one female) with chronic hepatitis C infection without cirrhosis presented to a single centre with HCC over a 2-year period. Five patients were treated by surgical resection and one patient underwent liver transplantation. Evaluation of generous histological specimens confirmed the presence of HCC and the absence of cirrhosis in all cases. The degree of fibrosis of the background liver was staged as mild (n = 1), moderate (n = 4) or bridging fibrosis (n = 1). Review of the clinical case notes revealed that all cases had an additional risk factor for the development of HCC (four had evidence of past hepatitis B virus infection; two had a history of excessive alcohol consumption; a further patient had prolonged exposure to immune suppression). CONCLUSION: HCC does occur in patients with non-cirrhotic HCV infection who have other risk factors for hepatocarcinogenesis.

Histological changes in HCV antibody-positive, HCV RNA-negative subjects suggest persistent virus infection.

UNLABELLED: It is unclear whether hepatitis C virus (HCV) has been eradicated or persists at a low level in HCV antibody-positive HCV RNA-negative individuals. The natural history and liver histology are not well characterized. One hundred seventy-two HCV antibody-positive, serum HCV RNA-negative patients underwent diagnostic liver biopsy between 1992 and 2000 and were followed a median 7 years (range, 5-12). Patients with any possible cause of liver injury other than HCV were excluded. A single histopathologist scored sections using Ishak criteria. Characterization of the inflammatory infiltrate in selected cases used a novel semiquantitative technique and compared with HCV RNA-positive patients and healthy controls. One hundred two patients were excluded because of a risk factor for liver injury other than HCV. Seventy patients met the study criteria; four (5.7%) became HCV RNA-positive during follow-up. Sixty-six cases remained HCV RNA-negative; five (7.5%) had a normal liver biopsy; 54 (82%) had fibrosis (stage 2 or 3 in 16 (24%)). Nonviremic cases revealed expanded portal tracts (P < 0.05), with fewer CD4+ (P < 0.05) and more CD8+ cells (P < 0.05) than healthy controls, but were indistinguishable from HCV RNA-positive cases for these parameters. Lobular CD4 staining, absent in healthy controls, was noted in both HCV RNA-negative and -positive cases and was more marked in the latter (P < 0.05) with a sinusoidal lining cell distribution. CONCLUSION: Nonviremic HCV antibody-positive patients have a liver biopsy that is usually abnormal. Fibrosis was present in most with similar inflammatory infiltrate to viremic cases. The presence of a CD8+ rich inflammatory infiltrate suggests an ongoing immune response in the liver, supporting the view that HCV may persist in the liver in the majority of HCV RNA-negative cases.

Bell's palsy associated with IFN-alpha and ribavirin therapy for hepatitis C virus infection.

First-line therapy for hepatitis C virus (HCV) infection comprises interferon-alpha (IFN-alpha) and ribavirin for 6 or 12 months. Mild complications of therapy are common, but more serious complications are rare. Three patients with chronic HCV infection, acquired through injecting drug use, developed idiopathic facial paralysis (Bell's palsy) during therapy, with spontaneous resolution after withdrawal of treatment. Large-scale cohort studies reveal that IFNs are associated rarely with neurologic complications, and only one previous report has linked IFN-alpha therapy and Bell's palsy. We postulate that IFN-alpha therapy led to a breakdown of peripheral tolerance to myelin sheath antigens, leading to neuropathy, just as IFN-alpha therapy can cause autoimmune thyroiditis through breakdown of tolerance to native thyroid antigens.