Legionnaires' Disease Outbreak Caused by Endemic Strain of Legionella pneumophila, New York, New York, USA, 2015

Abstract

During the summer of 2015, New York, New York, USA, had one of the largest and deadliest outbreaks of Legionnaires' disease in the history of the United States. A total of 138 cases and 16 deaths were linked to a single cooling tower in the South Bronx. Analysis of environmental samples and clinical isolates showed that sporadic cases of legionellosis before, during, and after the outbreak could be traced to a slowly evolving, single-ancestor strain. Detection of an ostensibly virulent Legionella strain endemic to the Bronx community suggests potential risk for future cases of legionellosis in the area. The genetic homogeneity of the Legionella population in this area might complicate investigations and interpretations of future outbreaks of Legionnaires' disease.

Keywords: Bronx; Legionella; Legionella pneumophila; Legionnaires’ disease; New York; New York City; PCR; United States; bacteria; cooling towers; endemic strain; legionellosis; outbreak; outbreak investigation; pulsed-field gel electrophoresis; water; whole-genome sequencing.

Figure 1

Legionnaires’ disease outbreak caused by an endemic strain of Legionella pneumophila, New York City, New York, USA, 2015. Timeline shows all diagnosed cases linked to the July 2015 South Bronx and August 2015 East Bronx outbreaks. Each orange square represents the time at which a person was given a diagnosis of the disease. Annotations of some of the key actions taken by the authorities are listed above their corresponding days. DOHMS, Department of Health and Mental Hygiene.

Figure 2

Pulsed-field gel electrophoresis (PFGE) of case-patient and environmental isolates from a Legionnaires’ disease outbreak caused by an endemic strain of Legionella pneumophila, New York City, New York, USA, 2015. One clinical isolate with the outbreak PFGE pattern (Clinical isolate−outbreak pattern) shows matches to cooling tower (CT A and CT B) isolates from a South Bronx hotel (SB), a homeless shelter (HS), and East Bronx College (EBC). Molecular typing patterns of Legionella pneumophila serogroup 1 isolates from CT from the SB hotel, HS, and EBC were indistinguishable from 26 clinical isolates associated with the Legionnaires’ disease cluster in the South Bronx. Samples that were not linked to the outbreak had major differences in patterns when compared with the outbreak pattern.

Figure 3

Minimum spanning tree of 77 isolates related to the 2015 South Bronx Legionnaires’ disease outbreak caused by an endemic strain of Legionella pneumophila, New York City, New York, USA, 2015. The tree was created by using single-nucleotide polymorphism (SNP) differences found across all isolates. Sizes of circles are proportional to number of isolates having identical genomic backgrounds, numbers adjacent to lines indicate number of polymorphism differences between each node, and numbers in parentheses indicate years. Strains 07-304 and 15-215 contain the same plasmid and differ greatly from the plasmid present in all East Bronx isolates. These plasmids have only partial identity with known plasmids in other Legionellaceae. *East Bronx outbreak samples contain 1,030 additional SNP differences caused by the presence of suspected homologous recombination events that were omitted from the final SNP analysis; †Plasmids are present in these isolates. EBC, East Bronx college; env., environmental; HS, homeless shelter; NH, nursing home.

Figure 4

Blast ring genome comparison of Legionella pneumophila strains from investigation of Legionnaires’ disease outbreak caused by an endemic strain of L. pneumophila, New York City, New York, USA, 2015. Comparison is shown between South Bronx outbreak strain (F4469) and other sequenced strains (Philadelphia 1, Corby, Alcoy, Paris, and Lens). The 2 innermost circles indicate G + C content and G + C skew, respectively, of the outbreak strain genome. Gaps in outer circles indicate genome areas in strain F4469 that are either absent or of low identity in compared genomes. Most of these regions are composed of virulence factor–associated genes, such as an F-type IVA secretion system, effector protein genes, toxin/antitoxin loci, and genes with unknown functions. Hip, hippurate hydrolysis gene; Lub, Legionella U-box gene; RTX, repeats in structural toxin gene; Sid; substrate of macrophage killing/defective organelle trafficking transporter gene.