Search

We isolated a novel coronavirus from a medical team member presenting with fever and malaise after travel to Haiti. The virus showed 99.4% similarity with a recombinant canine coronavirus recently identified in a pneumonia patient in Malaysia, suggesting that infection with this virus and/or recombinant variants occurs in multiple locations.

Four patients with adult-onset, disseminated mycobacterial infection had 5' UTR mutations in IKBKG without clear physical stigmata of NEMO deficiency. These mutations caused decreased levels of NEMO protein and Toll-like receptor driven cytokine production. Three patients died from disseminated disease. These mutations may be missed by whole exome sequencing.

Despite a regional decline in influenza A(H1N1)pdm09 virus infections during 2013–14, cases at a Florida hospital were more severe than those during 2009–10. Examined strains had a hemagglutinin polymorphism associated with enhanced binding to lower respiratory tract receptors. Genetic changes in this virus must be monitored to predict the effect of future pandemic viruses.

Influenza A(H3N2) strains isolated during 2014–15 in Alachua County, Florida, USA, belonged to hemagglutinin gene clade 3C.2a. High rates of influenza-like illness and confirmed influenza cases in children were associated with a decrease in estimated vaccine effectiveness. Illnesses were milder than in 2013–14; severe cases were concentrated in elderly patients with underlying diseases.

Multidrug-resistant (MDR) Gram-negative bacterial infections are a serious and ever-increasing threat for which limited therapeutic options exist. The bactericidal/permeability-increasing protein (BPI) is a cationic, neutrophil-derived, lipopolysaccharide (LPS)-binding protein that binds to Gram-negative bacteria (GNB) and LPS via its lipid A region. A recombinant fragment, rBPI-21, was studied extensively in clinical trials for meningococcal disease in the 1990s and exhibited no significant safety issues. In this report, a dose-dependent 1-2 log reduction of MDR Pseudomonas and Acinetobacter after 1h incubation with rBPI-21 using clinically achievable doses is described. Given the dearth of novel antimicrobials expected to emerge from the pharmaceutical pipeline in the near future, exploration of rBPI-21 to combat MDR GNB is now warranted.

Campylobacter jejuni is a major cause of food-borne gastroenteritis worldwide. While mortality is low, morbidity imparted by post-infectious sequelae such as Guillain-Barré syndrome, Reiter syndrome/reactive arthritis and irritable bowel syndrome is significant. In addition, the economic cost is high due to lost productivity. Food animals, particularly poultry, are the main reservoirs of C. jejuni. The over-use of antibiotics in the human population and in animal husbandry has led to an increase in antibiotic-resistant infections, particularly with fluoroquinolones. This is problematic because C. jejuni gastroenteritis is clinically indistinguishable from that caused by other bacterial pathogens, and such illnesses are usually treated empirically with fluoroquinolones. Since C. jejuni is naturally transformable, acquisition of additional genes imparting antibiotic resistance is likely. Therefore, an understanding of the antibiotic resistance mechanisms in C. jejuni is needed to provide proper therapy both to the veterinary and human populations.

Klebsiella pneumoniae is an opportunistic pathogen frequently associated with nosocomially acquired infections. Host cell adherence and biofilm formation of K. pneumoniae isolates is mediated by type 1 (T1P) and type 3 (MR/K) pili whose major fimbrial subunits are encoded by the fimA and mrkA genes, respectively. The E. coli common pilus (ECP) is an adhesive structure produced by all E. coli pathogroups and a homolog of the ecpABCDE operon is present in the K. pneumoniae genome. In this study, we aimed to determine the prevalence of these three fimbrial genes among a collection of 69 clinical and environmental K. pneumoniae strains and to establish a correlation with fimbrial production during cell adherence and biofilm formation. The PCR-based survey demonstrated that 96% of the K. pneumoniae strains contained ecpA and 94% of these strains produced ECP during adhesion to cultured epithelial cells. Eighty percent of the strains forming biofilms on glass produced ECP, suggesting that ECP is required, at least in vitro, for expression of these phenotypes. The fim operon was found in 100% of the strains and T1P was detected in 96% of these strains. While all the strains examined contained mrkA, only 57% of them produced MR/K fimbriae, alone or together with ECP. In summary, this study highlights the ability of K. pneumoniae strains to produce ECP, which may represent a new important adhesive structure of this organism. Further, it defines the multi-fimbrial nature of the interaction of this nosocomial pathogen with host epithelial cells and inert surfaces.

Introduction: Zika virus (ZIKV) and Chikungunya virus (CHIKV) can share the same mosquito vector, and co-infections by these viruses can occur in humans. While infections with these viruses share commonalities, CHIKV is unique in causing arthritis and arthralgias that may persist for a year or more. These infections are commonly diagnosed by RT–PCR-based methods during the acute phase of infection. Even with the high specificity and sensitivity characteristic of PCR, false negatives can occur, highlighting the need for additional diagnostic methods for confirmation. Case presentation: On her return to the USA, a traveller to Colombia, South America developed an illness consistent with Zika, Chikungunya and/or Dengue. RT-PCR of her samples was positive only for ZIKV. However, arthralgias persisted for months, raising concerns about co-infection with CHIKV or Mayaro viruses. Cell cultures inoculated with her original clinical samples demonstrated two types of cytopathic effects, and both ZIKV and CHIKV were identified in the supernatants. On phylogenetic analyses, both viruses were found to be related to strains found in Colombia. Conclusion: These findings highlight the need to consider CHIKV co-infection in patients with prolonged rheumatological symptoms after diagnosis with ZIKV, and the usefulness of cell culture as an amplification step for low-viremia blood and other samples.

Zika virus and dengue virus serotype 2 were isolated from a patient with travel to Haiti who developed fever, rash, arthralgias, and conjunctivitis. The infecting Zika virus was related to Venezuelan and Brazilian strains but evolved along a lineage originating from strains isolated in 2014 in the same region of Haiti.

To the Editor: Two recent articles (1,2) show that fluoroquinolone use in food animals is associated with infections by antimicrobial drug–resistant strains of Campylobacter in humans. These infections cause problems in treating illnesses as well as increased rates of illness and death (3). Despite a large body of scientific evidence and a judicial review (1–3) that show harmful results in many persons, some members of the poultry and pharmaceutical industries argue that fluoroquinolone use in food animals has no adverse effects in humans (4) and continue to supply these drugs for use in poultry (2,5). The use of these drugs has caused rapidly increasing resistance rates in most countries. In the United States, 19% of Campylobacter isolates from humans are now ciprofloxacin resistant (2), and resistance rates >80% are seen in Spain (5). By contrast, in Australia, where fluoroquinolones were never approved for use in food animals, domestically acquired infections with fluoroquinolone-resistant Campylobacter spp. are rarely found in humans (6). Drug-resistant Escherichia coli is also of concern. In Spain, humans frequently acquire fluoroquinolone-resistant E. coli associated with fluoroquinolone use in poultry (7). In the United States, better controls in meat and poultry slaughter and processing, as well as improved food-safety education campaigns, have resulted in 28% fewer Campylobacter infections annually since 1996 (8). However, ≈1.8 million persons (600 per 100,000) are likely to contract symptomatic Campylobacter infections per year (3,8), and fluoroquinolone resistance is now 19% (2). Thus, the risk of a person's contracting fluoroquinolone-resistant Campylobacter infection is 114 per 100,000 per year. If 80% of Campylobacter infections are foodborne (3), and 90% of these infections are acquired from poultry (9), then ≈82 of 100,000 persons per will contract ciprofloxacin-resistant Campylobacter infections from poultry each year. Most persons with Campylobacter infections would not benefit from antimicrobial drug therapy. However, if only 10% of infected persons would benefit from antimicrobial drug therapy, fluoroquinolone use in poultry could cause ≈82 persons per million to have a compromised response to therapy. In the United States (population 300 million), this number translates to >24,000 persons annually. Data on the number of animals that receive fluoroquinolones are difficult to find. Bayer (manufacturer of the only fluoroquinolone used in poultry in the United States) states that Baytril (enrofloxacin) is used in

The FilmArray blood culture identification (BCID) panel is a rapid molecular diagnostic test approved for use with positive blood culture material. We describe a fatal case of meningococcemia with central nervous system (CNS) involvement detected using the BCID test with culture-negative blood and cerebrospinal fluid.

The innate immune system plays a critical role in host defense against mucosal bacteria. Campylobacter jejuni is a major cause of human gastroenteritis that usually resolves spontaneously within several days, suggesting that innate mechanisms are important to control the infection. However, the specific means by which this occurs is not well understood. While diarrheal isolates of C. jejuni usually are susceptible to human serum, we found that a systemic strain of C. jejuni, isolated from the cerebrospinal fluid of an infant with meningitis, is relatively more resistant to human serum, the Bactericidal/Permeability-Increasing Protein (BPI), an endogenous cationic antimicrobial protein, and the cationic peptide antibiotic polymyxin B. To test the hypothesis that the surface properties of this strain contributed to its ability to withstand these innate host defenses, we constructed isogenic mutants in capsule (kpsM) and lipooligosaccharide (waaF) and complemented these mutants by insertion of the complementation construct in trans into hipO, a chromosomal locus. We found that capsule expression was essential for serum resistance, whereas lipooligosaccharide played no substantial role. In contrast, the lipooligosaccharide mutant showed increased sensitivity to polymyxin B, α-defensins, cathelicidins, and BPI. These findings suggest that the polysaccharides of C. jejuni strains contribute differently to resistance against host innate immunity; whereby capsule is more important for resisting human complement and lipooligosaccharide is more important for protection against killing mediated by cationic antimicrobial peptides and proteins.

Contamination of food with potentially dangerous human pathogens has been recognized since the time of Pasteur (1) and is well-documented in the modern era (2), but the development of antimicrobial agents has helped limit the consequences of such infections. Concomitantly, the widespread use of antimicrobial agents has also led to the emergence of antimicrobial drug–resistant organisms (3,4). Gupta et al. demonstrate the increasing prevalence in the United States of ciprofloxacin-resistant Campylobacter species isolated from humans and poultry from 1990 to 1997, and their studies implicate the prophylactic treatment of poultry with fluoroquinolones in this emerging problem (5). Their report indicates that the source of fluoroquinolone-resistant Campylobacter infections was consuming poultry colonized with resistant strains (Figure), rather than selection for Campylobacter resistance in the human gut after clinical fluoroquinolone use to treat the diarrheal illness (5). This work provides further evidence that fluoroquinolone use in poultry promotes the emergence of resistant Campylobacter strains that subsequently infect humans (6). That persons infected with these fluoroquinolone-resistant strains had 3 additional days of illness and were more likely to be hospitalized demonstrates the harm caused by such resistant stains (5). Figure Acquisition of fluoroquinolone (FQ)-resistant Campylobacter from poultry. Since campylobacters are normal enteric flora in many avian species, poultry represents a model system to test the hypothesis that prophylactic and growth-promoting use of antimicrobial agents in food animals selects for the emergence of antimicrobial drug–resistant organisms. In one study, chickens that were naturally colonized with fluoroquinolone-susceptible Campylobacter strains began to excrete resistant strains after 2 days of doses of enrofloxacin (7), which is commonly used for prophylaxis in the poultry industry. A single point mutation in gyrA encoding the bacterial DNA gyrase was sufficient to confer high-level resistance (7,8). This small genetic change apparently has a low "fitness cost" to the organism, as evidenced by fluoroquinolone-resistant strains' rapidly replacing susceptible Campylobacter in treated chickens (7). Developing an animal reservoir of fluoroquinolone-resistant Campylobacter has been the major factor behind transmission of quinolone resistance to humans (8,9). In contrast, among poultry treated therapeutically with enrofloxacin, no resistance was observed in the 13 C. jejuni isolates tested (9). Similarly, after the prophylactic and growth-promoting uses of macrolides in swine were banned in Denmark, the prevalence of macrolide-resistant C. coli declined (10). Thus, the major determinant of developing resistance appears to be use of subtherapeutic antimicrobial doses. The antimicrobial drug ban in Denmark did not decrease the amount of meat produced by the poultry and pig production industries, which removed a major concern (10). Evidence suggests that restricting fluoroquinolone use to therapeutic indications only in food animals could decrease rates of fluoroquinolone-resistant Campylobacter, and the Danish experience with macrolide restriction proves that such limitations need not harm the husbandry of food animals. The increased likelihood of foreign travel in persons infected with ciprofloxacin-resistant strains (5) illustrates the global threat posed by resistant strains. Appreciating such realities favors concerted efforts to limit use of fluoroquinolones (and other antimicrobial drugs) to therapy only in food animals. This view was supported by a recent (March 2004) landmark decision by Federal Drug Administration Administrative Law Judge Daniel J. Davidson, withdrawing approval for the new animal drug application to use enrofloxacin for prophylaxis or growth-promotion in poultry (11). This decision was the first occasion that a previously approved antimicrobial agent was removed from the U.S. veterinary market because of concerns about antimicrobial drug resistance. With this decision as precedent, we should follow the examples set in Europe and ban use of all antimicrobial agents in food animals, except when necessary for therapy of ill animals.

To the Editor: Iovine and Blaser (1) write, "This therapeutic use [of enrofloxacin] was withdrawn (2) but is now under appeal" and "Despite the restrictions on enrofloxacin use, emergence of fluoroquinolone-resistant Campylobacter species, with poultry as an important source, has been documented in the United States… Therefore, our conclusion remains: use of enrofloxacin in poultry materially contributed to increase in human infection by fluoroquinolone-resistant Campylobacter species." These claims propagate the following important errors. First, the therapeutic use of enrofloxacin was not withdrawn. Judge Davidson's order to withdraw the approval was an initial decision, to which exceptions were filed in 2004. A final decision rests with the US Food and Drug Administration Commissioner. Second, poultry has not been identified as an important source of fluoroquinolone resistance in human Campylobacter isolates. The raw data of the cited Smith et al. article (3) indicate a nonsignificant negative association between chicken consumption and fluoroquinolone resistance in human isolates. Substantial resistance levels in Northern Hemisphere countries with and without enrofloxacin use, which occurred well before fluoroquinolones were ever used in animals (3–5), also suggest that attribution of such resistance to enrofloxacin is simplistic. Finally, rational decision-making is based on probable future consequences of a decision, not past history or causes of the current situation. Iovine and Blaser's claim, "Thus the decision to withdraw therapeutic use of enrofloxacin (3) was warranted," is not implied, even if enrofloxacin use caused the emergence of fluoroquinolone resistance. If withdrawing enrofloxacin increases campylobacteriosis from airsacculitis-positive chickens, withdrawal may greatly harm human health. A rational withdrawal decision cannot be justified. In summary, Iovine and Blaser's view that enrofloxacin should be banned is not supported by the data that they have cited or by principles of sound risk management and decision-making.