ABSTRACT
The environmental mold Aspergillus fumigatus is the primary cause of invasive aspergillosis. In patients with high-risk conditions, including stem cell and organ transplant recipients, mortality exceeds 50%. Triazole antifungals have greatly improved survival (1); however, triazole-resistant A. fumigatus infections are increasingly reported worldwide and are associated with increased treatment failure and mortality (2). Of particular concern are resistant A. fumigatus isolates carrying either TR34/L98H or TR46/Y121F/T289A genetic resistance markers, which have been associated with environmental triazole fungicide use rather than previous patient exposure to antifungals (3,4). Reports of these triazole-resistant A. fumigatus strains have become common in Europe (2,3), but U.S. reports are limited (5). Because of the risk posed to immunocompromised patients, understanding the prevalence of such isolates in patients is important to guide clinical and public health decision-making. In 2011, CDC initiated passive laboratory monitoring for U.S. triazole-resistant A. fumigatus isolates through outreach to clinical laboratories. This system identified five TR34/L98H isolates collected from 2016 to 2017 (6), in addition to two other U.S. isolates collected in 2010 and 2014 and reported in 2015 (5). Four of these seven isolates were reported from Pennsylvania, two from Virginia, and one from California. Three isolates were collected from patients with invasive pulmonary aspergillosis, and four patients had no known previous triazole exposure. A. fumigatus resistant to all triazole medications is emerging in the United States, and clinicians and public health personnel need to be aware that resistant infections are possible even in patients not previously exposed to these medications.
Subject(s)
Antifungal Agents/pharmacology , Aspergillus fumigatus/drug effects , Aspergillus fumigatus/genetics , Drug Resistance, Multiple, Fungal/genetics , Environmental Exposure/adverse effects , Fungicides, Industrial/toxicity , Mutation , Adult , Aged , Aged, 80 and over , Aspergillosis/drug therapy , Aspergillosis/epidemiology , California/epidemiology , Female , Humans , Male , Middle Aged , Pennsylvania/epidemiology , Virginia/epidemiology , Young AdultABSTRACT
BACKGROUND: During 2009 and 2010, 2 clusters of organ transplant-transmitted Balamuthia mandrillaris, a free-living ameba, were detected by recognition of severe unexpected illness in multiple recipients from the same donor. METHODS: We investigated all recipients and the 2 donors through interview, medical record review, and testing of available specimens retrospectively. Surviving recipients were tested and treated prospectively. RESULTS: In the 2009 cluster of illness, 2 kidney recipients were infected and 1 died. The donor had Balamuthia encephalitis confirmed on autopsy. In the 2010 cluster, the liver and kidney-pancreas recipients developed Balamuthia encephalitis and died. The donor had a clinical syndrome consistent with Balamuthia infection and serologic evidence of infection. In both clusters, the 2 asymptomatic recipients were treated expectantly and survived; 1 asymptomatic recipient in each cluster had serologic evidence of exposure that decreased over time. Both donors had been presumptively diagnosed with other neurologic diseases prior to organ procurement. CONCLUSIONS: Balamuthia can be transmitted through organ transplantation with an observed incubation time of 17-24 days. Clinicians should be aware of Balamuthia as a cause of encephalitis with high rate of fatality, and should notify public health departments and evaluate transplant recipients from donors with signs of possible encephalitis to facilitate early diagnosis and targeted treatment. Organ procurement organizations and transplant centers should be aware of the potential for Balamuthia infection in donors with possible encephalitis and also assess donors carefully for signs of neurologic infection that may have been misdiagnosed as stroke or as noninfectious forms of encephalitis.
Subject(s)
Amebiasis , Balamuthia mandrillaris , Encephalitis , Kidney Transplantation/adverse effects , Liver Transplantation/adverse effects , Adult , Amebiasis/diagnostic imaging , Amebiasis/pathology , Amebiasis/transmission , Brain/diagnostic imaging , Brain/parasitology , Brain/pathology , Child , Child, Preschool , Encephalitis/diagnostic imaging , Encephalitis/pathology , Female , Humans , Male , Middle Aged , Tissue Donors , Transplant RecipientsABSTRACT
The first outbreak of Ebola hemorrhagic fever (EHF) due to Bundibugyo ebolavirus occurred in Uganda from August to December 2007. During outbreak response and assessment, we identified 131 EHF cases (44 suspect, 31 probable, and 56 confirmed). Consistent with previous large filovirus outbreaks, a long temporal lag (approximately 3 months) occurred between initial EHF cases and the subsequent identification of Ebola virus and outbreak response, which allowed for prolonged person-to-person transmission of the virus. Although effective control measures for filovirus outbreaks, such as patient isolation and contact tracing, are well established, our observations from the Bundibugyo EHF outbreak demonstrate the need for improved filovirus surveillance, reporting, and diagnostics, in endemic locations in Africa.
Subject(s)
Disease Outbreaks , Hemorrhagic Fever, Ebola/epidemiology , Population Surveillance/methods , Hemorrhagic Fever, Ebola/diagnosis , Hemorrhagic Fever, Ebola/mortality , Humans , Uganda/epidemiologyABSTRACT
Marburg hemorrhagic fever was detected among 4 miners in Ibanda District, Uganda, from June through September, 2007. Infection was likely acquired through exposure to bats or bat secretions in a mine in Kamwenge District, Uganda, and possibly human-to-human transmission between some patients. We describe the epidemiologic investigation and the health education response.
Subject(s)
Disease Outbreaks , Marburg Virus Disease/epidemiology , Mining , Occupational Exposure , Adult , Animals , Chiroptera , Humans , Male , Uganda/epidemiology , Young Adult , ZoonosesABSTRACT
In July and September 2007, miners working in Kitaka Cave, Uganda, were diagnosed with Marburg hemorrhagic fever. The likely source of infection in the cave was Egyptian fruit bats (Rousettus aegyptiacus) based on detection of Marburg virus RNA in 31/611 (5.1%) bats, virus-specific antibody in bat sera, and isolation of genetically diverse virus from bat tissues. The virus isolates were collected nine months apart, demonstrating long-term virus circulation. The bat colony was estimated to be over 100,000 animals using mark and re-capture methods, predicting the presence of over 5,000 virus-infected bats. The genetically diverse virus genome sequences from bats and miners closely matched. These data indicate common Egyptian fruit bats can represent a major natural reservoir and source of Marburg virus with potential for spillover into humans.
Subject(s)
Chiroptera/virology , Marburg Virus Disease/virology , Marburgvirus/genetics , Animals , Antibodies, Viral/blood , Antigens, Viral/blood , Chiroptera/blood , Enzyme-Linked Immunosorbent Assay , Female , Humans , Immunohistochemistry , Liver/chemistry , Liver/virology , Male , Marburg Virus Disease/blood , Marburgvirus/isolation & purification , Phylogeny , Reverse Transcriptase Polymerase Chain Reaction , UgandaABSTRACT
The first known Ebola hemorrhagic fever (EHF) outbreak caused by Bundibugyo Ebola virus occurred in Bundibugyo District, Uganda, in 2007. Fifty-six cases of EHF were laboratory confirmed. Although signs and symptoms were largely nonspecific and similar to those of EHF outbreaks caused by Zaire and Sudan Ebola viruses, proportion of deaths among those infected was lower (≈40%).
Subject(s)
Disease Outbreaks , Ebolavirus , Hemorrhagic Fever, Ebola/diagnosis , Hemorrhagic Fever, Ebola/mortality , Adult , Aged , Diarrhea/diagnosis , Diarrhea/virology , Fatigue/diagnosis , Fatigue/virology , Female , Fever/diagnosis , Fever/virology , Headache/diagnosis , Headache/virology , Humans , Male , Middle Aged , Uganda/epidemiologyABSTRACT
Hantaviruses are rodent-borne viruses capable of causing human disease. The Seoul virus is a hantavirus that causes hemorrhagic fever with renal syndrome in East Asia. To our knowledge, we report the first domestically acquired case of hemorrhagic fever with renal syndrome caused by the Seoul virus, confirmed by serology testing, reverse-transcriptase polymerase chain reaction, and nucleotide sequence analysis. The patient presented with myalgias and fever, and developed acute renal failure.
Subject(s)
Hemorrhagic Fever with Renal Syndrome/diagnosis , Seoul virus/isolation & purification , Antibodies, Viral/blood , Hemorrhagic Fever with Renal Syndrome/pathology , Hemorrhagic Fever with Renal Syndrome/physiopathology , Hemorrhagic Fever with Renal Syndrome/virology , Humans , Male , Maryland , RNA, Viral/blood , RNA, Viral/genetics , Sequence Analysis, DNA , Young AdultSubject(s)
Internationality , Population Surveillance , Respiratory Syncytial Virus Infections/epidemiology , Respiratory Syncytial Virus, Human/isolation & purification , Adult , Child , Child, Preschool , Humans , Infant , Infant, Newborn , Population Surveillance/methods , Respiratory Syncytial Virus Infections/mortality , Respiratory Syncytial Virus Infections/prevention & control , Respiratory Syncytial Virus Infections/virology , Respiratory Syncytial Virus, Human/geneticsSubject(s)
Centers for Disease Control and Prevention, U.S. , Communicable Diseases, Emerging/epidemiology , International Cooperation , Population Surveillance/methods , Program Development , Respiratory Tract Infections/epidemiology , Aged , Child, Preschool , Communicable Diseases, Emerging/prevention & control , Developing Countries/statistics & numerical data , Humans , Respiratory Tract Infections/prevention & control , United StatesABSTRACT
BACKGROUND: In December 2010, a case of West Nile virus (WNV) encephalitis occurring in a kidney recipient shortly after organ transplantation was identified. METHODS: A public health investigation was initiated to determine the likely route of transmission, detect potential WNV infections among recipients from the same organ donor, and remove any potentially infected blood products or tissues. Available serum, cerebrospinal fluid, and urine samples from the organ donor and recipients were tested for WNV infection by nucleic acid testing and serology. RESULTS: Two additional recipients from the same organ donor were identified, their clinical and exposure histories were reviewed, and samples were obtained. WNV RNA was retrospectively detected in the organ donor's serum. After transplantation, the left kidney recipient had serologic and molecular evidence of WNV infection and the right kidney recipient had prolonged but clinically inapparent WNV viremia. The liver recipient showed no clinical signs of infection but had flavivirus IgG antibodies; however, insufficient samples were available to determine the timing of infection. No remaining infectious products or tissues were identified. CONCLUSIONS: Clinicians should suspect WNV as a cause of encephalitis in organ transplant recipients and report cases to public health departments for prompt investigation of the source of infection. Increased use of molecular testing and retaining pretransplantation sera may improve the ability to detect and diagnose transplant-associated WNV infection in organ transplant recipients.
Subject(s)
Kidney Transplantation/adverse effects , Public Health , Tissue Donors , West Nile Fever/transmission , Aged , Female , Humans , Male , Middle AgedABSTRACT
From September through early December 2005, an outbreak of yellow fever (YF) occurred in South Kordofan, Sudan, resulting in a mass YF vaccination campaign. In late December 2005, we conducted a serosurvey to assess YF vaccine coverage and to better define the epidemiology of the outbreak in an index village. Of 552 persons enrolled, 95% reported recent YF vaccination, and 25% reported febrile illness during the outbreak period: 13% reported YF-like illness, 4% reported severe YF-like illness, and 12% reported chikungunya-like illness. Of 87 persons who provided blood samples, all had positive YF serologic results, including three who had never been vaccinated. There was also serologic evidence of recent or prior chikungunya virus, dengue virus, West Nile virus, and Sindbis virus infections. These results indicate that YF virus and chikungunya virus contributed to the outbreak. The high prevalence of YF antibody among vaccinees indicates that vaccination was effectively implemented in this remotely located population.
Subject(s)
Disease Outbreaks , Yellow Fever/epidemiology , Adolescent , Adult , Child , Child, Preschool , Family Characteristics , Female , Humans , Infant , Infant, Newborn , Male , Seroepidemiologic Studies , Sudan/epidemiology , Yellow Fever/blood , Young AdultABSTRACT
An outbreak of Rift Valley fever (RVF) occurred in Kenya during November 2006 through March 2007. We characterized the magnitude of the outbreak through disease surveillance and serosurveys, and investigated contributing factors to enhance strategies for forecasting to prevent or minimize the impact of future outbreaks. Of 700 suspected cases, 392 met probable or confirmed case definitions; demographic data were available for 340 (87%), including 90 (26.4%) deaths. Male cases were more likely to die than females, Case Fatality Rate Ratio 1.8 (95% Confidence Interval [CI] 1.3-3.8). Serosurveys suggested an attack rate up to 13% of residents in heavily affected areas. Genetic sequencing showed high homology among viruses from this and earlier RVF outbreaks. Case areas were more likely than non-case areas to have soil types that retain surface moisture. The outbreak had a devastatingly high case-fatality rate for hospitalized patients. However, there were up to 180,000 infected mildly ill or asymptomatic people within highly affected areas. Soil type data may add specificity to climate-based forecasting models for RVF.
Subject(s)
Disease Outbreaks , Rift Valley Fever , Rift Valley fever virus , Adolescent , Adult , Aged , Aged, 80 and over , Antibodies, Viral/blood , Child , Child, Preschool , Climate , Female , Forecasting , Humans , Kenya/epidemiology , Male , Middle Aged , Population Surveillance/methods , Rift Valley Fever/epidemiology , Rift Valley Fever/mortality , Rift Valley Fever/prevention & control , Rift Valley Fever/virology , Rift Valley fever virus/genetics , Rift Valley fever virus/immunology , Rift Valley fever virus/isolation & purification , Soil/analysis , Young AdultABSTRACT
Vaccination against yellow fever is effective, but available live virus vaccines are not recommended for use in immunocompromised or elderly patients. We report the successful and uneventful immunization of a 62-year-old man with a history of allogeneic bone marrow transplant and discuss evidence for this recommendation.
Subject(s)
Bone Marrow Transplantation , Yellow Fever Vaccine/administration & dosage , Contraindications , Ecuador , Humans , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/therapy , Male , Middle Aged , Transplantation, Homologous , Yellow Fever/prevention & controlABSTRACT
From September through December 2005, an outbreak of hemorrhagic fever occurred in South Kordofan, Sudan. Initial laboratory test results identified IgM antibodies against yellow fever (YF) virus in patient samples, and a YF outbreak was declared on 14 November. To control the outbreak, a YF mass vaccination campaign was conducted and vector control implemented in parts of South Kordofan. Surveillance data were obtained from the Sudan Federal Ministry of Health. Clinical information and serum samples were obtained from a subset of patients with illness during the outbreak. Nomads, health personnel and village chiefs were interviewed about the outbreak. Mosquitoes were collected in 11 villages and towns in North and South Kordofan. From 10 September to 9 December 2005 a total of 605 cases of outbreak-related illness were reported, of which 45% were in nomads. Twenty-nine percent of 177 patients seen at clinics in Julud and Abu Jubaiyah had illness consistent with YF. Five of 18 unvaccinated persons with recent illness and 4 of 16 unvaccinated asymptomatic persons had IgM antibodies to YF virus. IgM antibodies to chikungunya virus were detected in five (27%) ill persons and three (19%) asymptomatic persons. These results indicate that both chikungunya and YF occurred during the outbreak.
Subject(s)
Alphavirus Infections/epidemiology , Chikungunya virus , Disease Outbreaks , Yellow Fever/epidemiology , Adolescent , Adult , Aedes/virology , Aged , Aged, 80 and over , Alphavirus Infections/blood , Alphavirus Infections/virology , Animals , Antibodies, Viral/blood , Chikungunya virus/immunology , Child , Child, Preschool , Dengue/epidemiology , Humans , Immunoglobulin G/blood , Immunoglobulin M/blood , Infant , Infant, Newborn , Insect Vectors/virology , Middle Aged , Sudan/epidemiology , Yellow Fever/blood , Yellow Fever/virology , Yellow fever virus/immunology , Young AdultABSTRACT
BACKGROUND: In February 2006, poultry outbreaks of highly pathogenic avian influenza A (H5N1) virus were confirmed in Nigeria. A serosurvey was conducted to assess H5N1 transmission among poultry workers and laboratory workers in Nigeria. METHODS: From 21 March through 3 April 2006, 295 poultry workers and 25 laboratory workers with suspected exposure to H5N1 virus were administered a questionnaire to assess H5N1 exposures, medical history, and health care utilization. A serum specimen was collected from participants to test for H5N1 neutralizing antibodies by microneutralization assay. RESULTS: The 295 poultry workers reported a median of 14 days of exposure to suspected or confirmed H5N1-infected poultry without antiviral chemoprophylaxis and with minimal personal protective equipment. Among 25 laboratory workers, all handled poultry specimens with suspected H5N1 virus infection. All participants tested negative for H5N1 neutralizing antibodies. CONCLUSIONS: Despite widespread exposure to poultry likely infected with H5N1 virus, no serological evidence of H5N1 virus infection was identified among participants. Continued surveillance for H5N1 cases in humans and further seroprevalence investigations are needed to assess the risk of avian-to-human transmission, given that H5N1 viruses continue to circulate and evolve among poultry.