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Species down, disease up - Study shows biodiversity loss drives human infections

The extinction of plant and animal species can be likened to emptying a museum of its collection, or dumping a cabinet full of potential medicines into the trash, or replacing every local cuisine with McDonald’s burgers.

But the decline of species and their habitats may not just make the world boring. New research now suggests it may also put you at greater risk for catching some nasty disease.

“Habitat destruction and biodiversity loss,”—driven by the replacement of local species by exotic ones, deforestation, global transportation, encroaching cities, and other environmental changes—”can increase the incidence and distribution of infectious diseases in humans,” write University of Vermont biologist Joe Roman, EPA scientist Montira Pongsiri, and seven co-authors in BioScience.

Their study, “Biodiversity Loss Affects Global Disease Ecology,” will appear in the December issue of the journal, available on-line on December 7, 2009.

Diseases Go Global

“Lots of new diseases are emerging, and diseases that were once local are now global,” says Roman, a wildlife expert and fellow at UVM’s Gund Institute for Ecological Economics. “Diseases like West Nile Virus have spread around the world very quickly.”

This is not the first time humans have faced a raft of new diseases. About 10,000 years ago, humans invented farming. This move from hunting to agriculture brought permanent settlements, domestication of animals, and changes in diet. It also brought new infectious diseases, in what scientists call an “epidemiologic transition.”

Another of these transitions came with the Industrial Revolution. Infectious diseases decreased in many places while cancer, allergies and birth defects shot up.

Now, it seems, another epidemiologic transition is upon us. A host of new infectious diseases—like West Nile Virus—have appeared. And infectious diseases thought to be in decline—like malaria—have reasserted themselves and spread.

“Ours is the first article to link the current epidemiological transition,” says Pongsiri, an environmental health expert in EPA’s Office of the Science Advisor, “with biodiversity change, decline and extinction.”

“People have been working on this in individual diseases but no one has put all the studies together to compare them,” says Roman. In 2006, he and Pongsiri gathered a group of scientists and policy analysts with expertise in a range of the new diseases being observed—including West Nile virus as well as malaria, the African parasitic disease schistosomiasis, hantavirus pulmonary syndrome, and several others. From that meeting, the forthcoming BioScience study developed.

“We’ve reviewed all those studies and show that emergence or reemergence of many diseases is related to loss of biodiversity,” says Pongsiri.

“We’ve taken a broad look at this problem to say that it’s not just case-study specific,” she says. “Something is happening at a global scale.”

Of Mosquitoes and Mice

One of the studies that Pongsiri and Roman’s team examined was a 2006 investigation in Amazonian Peru. It was the first to demonstrate that malaria transmission can rise in response to deforestation. Though the mechanisms are complex and not fully worked out, it appears that loss of the structural diversity provided by trees led to higher density of Anopheles darlingi mosquitoes, a potent transmitter of malaria, as well as to higher biting rates.

“Or think about Lyme disease,” says Roman, calling from Connecticut.

People get this disease from ticks infected with a bacterium, Borrelia burgdorferi. The ticks, in turn, usually get the bacterium by feeding on small mammals—particularly white-footed mice.

“Historically, Lyme disease was probably rare, because you had a large range of mammals, everything from pumas all the way down to a widespread community of rodents,” says Roman. Ticks feed on different species, and, since many are poor hosts for the bacterium, only a limited number of ticks would carry the disease to people. But fragmentation and reduction of forests has led to deep declines in the number of mammals—and white-footed mice tend to thrive in species-poor places, like small patches of forest on the edge of neighborhoods.

“In fact, white-footed mice appear to be the most competent animal host reservoir of Lyme disease in the northeastern U.S.,” Pongsiri notes on an EPA blog, “So, the more white-footed mice that are in the forest, the greater chance more ticks will be infected, and the greater chance you have of getting bitten by an infected tick.”

In other words, if you’re worried about catching Lyme disease, it’s a good idea to wear long pants—but it might be a better idea to join your conservation commission or zoning board since “protecting large forested areas in the vicinity of residential areas may reduce the risk of Lyme disease,” the BioScience paper notes.

Eco-epidemiology

It is new to think about biodiversity—and therefore, species and land conservation—as integral to public health. Until recently, almost no epidemiologists, nor medical schools, were framing questions of human infectious disease prevention in terms of, say, habitat structure, promoting genetic diversity in non-human species, or protecting animal predators as ecosystem regulators. Human diseases, goes the conventional thinking, are best understood and treated by looking at humans.

“Now there is the beginning of a movement to bring epidemiology and ecology together,” says Pongsiri.

“We’re not saying that biodiversity loss is the primary driver for all of these emerging diseases,” says Roman, “but it appears to be playing an important role.”

“We’re trying to make the case that all of these environmental changes we’re making, because they are anthropogenic, can be managed, can be controlled,” says Pongsiri. “We may be able to actually reduce or prevent these diseases by managing for biodiversity from the genetic level to the habitat level.”

A third of the bird species on the planet are at risk of extinction and a quarter of the mammals, Roman says, “and we have an incredible amount of habitat being destroyed, along with climate change. We should expect to see the impacts of these changes occurring now, to people—and we do.”

“The standard argument for protecting biodiversity is often that, well, there are medicines out there and you don’t want to destroy a forest where you might have a cure for cancer,” he says, ” and that’s true—but I don’t think that’s as compelling as the argument that if you cut down the forest you or your kids are more prone to infectious diseases.”

Contact: Joshua Brown
joshua.e.brown@uvm.edu
802-656-3039
University of Vermont

http://www.eurekalert.org/pub_releases/2009-12/uov-sdd120309.php

Authors: Paul D. Haemig a;  Stefan Lithner a;  Sara Sjstedt de luna b;  ke Lundkvist c;  Jonas Waldenstrm de;  Lennart Hansson f;  Malin Arneborn c; Bjrn Olsen g
Affiliations:    a From the Section for Zoonotic Ecology and Epidemiology, School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar
 b Department of Mathematics and Mathematical Statistics, Ume University, Ume
 c Department of Virology, Swedish Institute for Infectious Disease Control (SMI), Solna
 d Section for Zoonotic Ecology and Epidemiology, School of Pure and Applied Natural Sciences, University of Kalmar,
 e Kalmar and Department of Animal Ecology, Lund University, Lund
 f Department of Conservation Biology, Swedish University of Agricultural Sciences, Uppsala
 g Section of Infectious Diseases, Department of Medical Sciences, Uppsala University Hospital, Uppsala and Section for Zoonotic Ecology and Epidemiology, School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden

DOI: 10.1080/00365540701805446
Publication Frequency: 10 issues per year
Published in:  Scandinavian Journal of Infectious Diseases, Volume 40, Issue 6 & 7 2008 , pages 527 - 532
First Published: 2008
Subject: Infectious Diseases;
Abstract
Analysing datasets from hunting statistics and human cases of tick-borne encephalitis (TBE), we found a positive correlation between the number of human TBE cases and the number of red fox (Vulpes vulpes). Time lags were also present, indicating that high numbers of red fox in 1 y translated into high numbers of human TBE cases the following y. Results for smaller predators were mixed and inconsistent. Hares and grouse showed negative correlations with human TBE cases, suggesting that they might function as dilution hosts. Combining our findings with food web dynamics, we hypothesize a diversity of possible interactions between predators and human disease - some predators suppressing a given disease, others enhancing its spread, and still others having no effect at all. Larger-sized predators that suppress red fox numbers and activity (i.e. wolf, Canis lupus; European lynx, Lynx lynx) were once abundant in our study area but have been reduced or extirpated from most parts of it by humans. We ask what would happen to red foxes and TBE rates in humans if these larger predators were restored to their former abundances. 

http://www.informaworld.com/smpp/content~db=all~content=a788554272

By Mark Macaskill, December 6, 2009

The Prince of Wales is backing plans to use deer as “tick mops” in countryside frequented by walkers to curb the spread of Lyme disease, a deadly infection.

Prince Charles discussed the technique with researchers at the Macaulay Land Use Research Institute, Aberdeen, who are looking for an environmentally-friendly way to curb the soaring number of ticks.

The prince, who farms sheep and cattle at his organic Duchy Home Farm at Highgrove, Gloucestershire, has said he is concerned about Lyme disease but does not support the use of chemical pesticides.

The Aberdeen team is considering lacing deer with a natural pesticide; the creatures would be allowed to roam close to areas frequented by visitors or used by rural workers.

They believe such “tick mops” would not only reduce the number of parasites but would be a more humane way to tackle the disease than culling or fencing in the animals.

“It is encouraging that [Prince Charles] is taking an interest in the issue,” said Dr Lucy Gilbert, from the Macaulay Institute.

In the UK each year, some 3,000 people are infected by Lyme disease and about 60 die. Symptoms include a rash, fever, headache and fatigue. The infection can be treated with antibiotics.

http://www.timesonline.co.uk/tol/news/uk/scotland/article6946028.ece

Published: 07:00 p.m., Tuesday, March 16, 2004

Researchers at the Connecticut Agricultural Experiment Station in New Haven have uncovered proof Babesia microti, which causes the malaria-like ailment babesiosis, is established in Fairfield County.

“It’s not a surprise it’s expanding,” Dr. John Shanley, a professor of medicine at the University of Connecticut Health Center in Farmington said Tuesday . “I predict it will spread.”

“It’s something doctors should be aware of,” said Louis Magnarelli, an entomologist at the experiment station.

Magnarelli and John Anderson, director of the experiment station, found the protozoa in two mice. The station captured the mice in the yards of two Greenwich residents who were diagnosed with babesiosis in 2002. The Centers for Disease Control and Prevention’s monthly report, “Emerging Infectious Diseases,” published their findings in its March edition.

Magnarelli said finding the protozoan in the mice is “hardcore evidence” the parasite is in the most westernmost town in the state. Previously, he said, researchers had found the same evidence of the disease only in New London County, with most of the state’s cases located there.

Humans contract babesiosis the same way they get Lyme disease - from the bite of a black-legged tick, a.k.a. the deer tick. Magnarelli and Anderson’s report points out that, with such a high incidence of Lyme disease in Fairfield County, “the number of cases of babesiosis is likely to increase appreciably in the future.”

Thomas Forschner, executive director of the Lyme Disease Foundation in Hartford, said the same ticks can carry at least two other diseases in the state - human granulocytic ehrlichiosis and bartonella, or cat scratch fever.

In “Everything You Need to Know About Lyme Disease” Karen Vanderhoof-Forschner, the foundation’s co-founder, wrote that a 2000 study of babesiosis found 22 percent involved co-infection with Lyme disease.

Magnarelli and Anderson’s report said 290 cases of babesiosis were diagnosed in Connecticut between 1991 and 2000, with 230 found in New London County. Because babesiosis is more common in vacation spots along the East Coast - Nantucket, Martha’s Vineyard, Cape Cod, Rhode Island - the report said doctors have assumed many of these patients were infected elsewhere.

But, with the finding of the Babesia microti protozoa in the mice in Greenwich, the report said it’s clear the parasite also can be found in the western corner of the state.

“We’ve found it in Fairfield County, right next to New York,” Magnarelli said. “We believe it’s spreading.”

In Fairfield County, where Lyme disease is widespread, co-infection with babesiosis isn’t new. Maggie Shaw of Newtown, one of the founders of the Newtown Lyme Disease Task Force, has tangled with babesiosis. So has Mary Beth Olah,� another task force member.

“It’s been four years, and I’m still being treated for both,” Olah said. “The doctors think, with co-infection, it’s harder to diagnose and treat the two diseases.”

“The physicians around here know so little about Lyme disease,” Shaw said. “They know even less about babesiosis.”

The Babesia microti protozoa attaches to human red blood cells, feeds on them and kills them. Symptoms of the disease include chills, fatigues, night sweats, muscle aches and headaches.

“The headaches were the worst,” said Shaw, who is still being treated for babesiosis.

Like malaria, it can be a hard disease to cure. Shaw is on a combination of Mepron, an anti-parasitic drug, and antibiotics.

“It helps, but it’s very tricky,” Shaw said. “I’m fine until I go off them. Then a few weeks later, I slowly begin to get sick again.”

Like Lyme disease, babesiosis probably is under-reported. People can mistake it for a summer flu. But unlike the bacteria that causes Lyme disease, doctors can do a blood test that can find the ring-shaped Babesia microti in red blood cells.

“You look at the labs, and if you have a low red blood cell count, you have to consider babesiosis,” said UConn’s Shanley.

The disease is most serious for the elderly, those who have compromised immune systems, or those who have had their spleens removed.

“Spleens are big filters,” Shanley said. “People without them are prone to infections. With something like babesiosis, they have trouble fighting it off.”

Contact Robert Miller

at bmiller@newstimes.com

http://www.newstimes.com/news/article/Scientists-fear-rise-of-tick-borne-disease-47751.php

Med Vet Entomol. 2009 Dec;23(4):393-8.
Márquez FJ, Millán J, Rodríguez-Liébana JJ, García-Egea I, Muniain MA.

Departamento Biología Animal, Biología Vegetal y Ecología, Universidad de Jaén, 23071 Jaén, Spain. jmarquez@ujaen.es

A total of 559 fleas representing four species (Pulex irritans, Ctenocephalides felis, Ctenocephalides canis and Spilopsyllus cuniculi) collected on carnivores (five Iberian lynx Lynx pardinus, six European wildcat Felis silvestris, 10 common genet Genetta genetta, three Eurasian badger Meles meles, 22 red fox Vulpes vulpes, 87 dogs and 23 cats) in Andalusia, southern Spain, were distributed in 156 pools of monospecific flea from each carnivore, and tested for Bartonella infection in an assay based on polymerase chain reaction (PCR) amplification of the 16 S-23 S rRNA intergenic spacer region. Twenty-one samples (13.5%) were positive and the sequence data showed the presence of four different Bartonella species. Bartonella henselae was detected in nine pools of Ctenocephalides felis from cats and dogs and in three pools of Ctenocephalides canis from cats; Bartonella clarridgeiae in Ctenocephalides felis from a cat, and Bartonella alsatica in Spilopsyllus cuniculi from a wildcat. DNA of Bartonella sp., closely related to Bartonella rochalimae, was found in seven pools of Pulex irritans from foxes. This is the first detection of B. alsatica and Bartonella sp. in the Iberian Peninsula. All of these Bartonella species have been implicated as agents of human diseases. The present survey confirms that carnivores are major reservoirs for Bartonella spp.

PMID: 19941605 [PubMed - in process]

Written by Susan Wolf
Tuesday, 01 December 2009 00:00

The results of last fall’s tick study in four Fairfield County towns, including Redding, shows that 90% of the adult ticks that were collected were infected with Lyme bacteria, compared to 60% in 2007. Lyme disease is considered a major health issue in Redding.

Overall, the study found 90% of ticks tested were infected with the Lyme bacteria, with the range from 98% in Newtown to 88% in Redding.

The latest results mark the end of the second phase of a study coordinated by the Fairfield County Municipal Deer Management Alliance. As part of the study, deer tick populations in the four Fairfield County towns — Redding, Ridgefield, Newtown and Bethel — were examined in the fall 2008 and spring 2009. Then Dr. Eva Sapi, the molecular biologist and tick-borne disease expert from the University of New Haven who led the study, analyzed both the number of ticks found in each of the participating towns and the proportion of ticks that carry the bacteria that cause Lyme disease and the parasite of babesiosis, a malaria-like illness. Dr. Sapi is an expert in the collection and analysis of deer ticks.

Symptoms of Lyme disease can range from fever, chills and body aches to joint swelling, weakness, severe fatigue, trouble concentrating and temporary paralysis. Some, but not all, who have the disease will see a bull’s-eye rash between three and 30 days after infection.

Previous studies have reported a rise over the last 10 or more years in the percentage of ticks found in Connecticut that carry not only the infectious agents that cause Lyme, but also ehrlichiosis and babesosis, the alliance said in the press release it issued last week.

Newtown, Bethel, Ridgefield and Redding had ticks analyzed for the Babesia microti parasite in 2008 and with an infection rate of 30%, were found to be well above previously reported levels of 5% to 8%, said Dr. Georgina Scholl, research chair for the alliance. She set up the tick study.

The three sites in Redding are Fox Run Road Trail, Topstone Park and John Read Middle School in the vicinity of the Project Adventure area Dr. Sapi collected 224 ticks in hour-long drags at these sites. Of 181 Redding ticks tested for the Lyme bacteria, 159, or 88%, were positive. Of 153 tested for babesiosis, 44, or 29%, were positive.

Combining results from all towns on the babesiosis parasite, the study found a 30% infection rate with a range from 28% in Newtown to Ridgefield’s 33%.

Ms. Scholl said the alliance’s study is the first systematic study of ticks from specific locations across Fairfield County, which has had had the highest number of Lyme disease cases in the state for many years.

“This information will help towns understand better how to protect their residents from these infections, and will reinforce the need for vigilance in controlling ticks. This study will also serve as a baseline for future studies of changes in tick populations that may result from various intervention programs such as deer population reduction programs,” Dr. Scholl said.

Another important aspect of the study, she added, is that it has collected ticks from parts of town that are in close proximity to school play areas, ball fields, parks and trails.

“Ongoing studies by others have used ticks submitted by individuals with unknown places of origin,” Dr. Scholl said.

In the third phase of the tick study, which began this week, ticks will be collected, counted and analyzed for the presence of co-infections borrelia, babesia and ehrlichiosis in the same tick. Rates will be compared with the first two years to see if the high rates of infection previously found in the 17-town alliance are an indication of an overall trend or are indicative of local conditions.

Dr. Scholl said on Friday that she expects to get results sooner from the third phase of the study.

She also pointed to a recent study by Columbia University Center for Infection and Immunity on ticks collected in nearby Westchester County, N.Y., where 65% of ticks were infected with the Lyme bacteria, and a total of 72% were infected with either Lyme or one of four other tick-borne diseases. The New York study found 32% of ticks infected with more than one pathogen.

In its press release, the alliance pointed to a new program in Redding, BeSafeRedding.org, that matches homeowners to volunteer hunters. The program “acknowledges the direct correlation between high numbers of deer and higher numbers of ticks,” the release said. Tick experts now know, the release said, that ticks need deer to complete their breeding cycle; if there are fewer deer, then fewer ticks will lay eggs successfully.”

In Newtown, a committee is discussing how best to reduce tick infection risk. A regional HVCEO (Housatonic Valley Council of Elected Officials) Lyme Task Force is also educating the public on the need to reduce the source of ticks (www.hvceo.org/lymemain.php).

The Fairfield County Municipal Deer Management Alliance is a 17-town appointed deer study group. Its role is to educate communities “on the role of high deer numbers in supporting the breeding of ticks and their diseases.”

More information is available on the alliance Web site at www.deeralliance.com and on the state health department Web site, www.ct.gov/dph/

The tick study is funded by the participating towns and their tick-borne disease task forces.

http://acorn-online.com/joomla15/thereddingpilot/news/localnews/43000-tick-study-results-infection-rate-stands-at-90.html

Release Date: 12-02-2009
Author: Joshua E. Brown1
Email: Joshua.E.Brown@uvm.edu2

The extinction of plant and animal species can be likened to emptying a museum of its collection, or dumping a cabinet full of potential medicines into the trash, or replacing every local cuisine with McDonald’s burgers.

But the decline of species and their habitats may not just make the world boring. New research now suggests it may also put you at greater risk for catching some nasty disease.

“Habitat destruction and biodiversity loss,” — driven by the replacement of local species by exotic ones, deforestation, global transportation, encroaching cities, and a litany of other environmental woes — “can increase the incidence and distribution of infectious diseases in humans,” write University of Vermont biologist Joe Roman, EPA scientist Montira Pongsiri, and seven co-authors in BioScience3.

Their study, “Biodiversity Loss Affects Global Disease Ecology,” will appear in the December issue of the journal, available online on Dec. 7.

Diseases go global
“Lots of new diseases are coming up and diseases that used to be local are now global,” says Roman, a wildlife expert and fellow at UVM’s Gund Institute for Ecological Economics, “diseases like West Nile Virus now spread around the world very quickly.”

This is not the first time humans have faced a raft of new diseases. About 10,000 years ago, humans invented farming. This move from hunting to agriculture brought permanent settlements, domestication of animals, and changes in diet. It also brought new infectious diseases, in what scientists call an “epidemiologic transition.”

Another of these transitions came with the Industrial Revolution. Infectious diseases decreased in many places while cancer, allergies and birth defects shot up.

Now, it seems, another epidemiologic transition is upon us. A host of new infectious diseases — like West Nile Virus — have appeared. And infectious diseases thought to be in decline — like malaria — have reasserted themselves and spread.

“Ours is the first article to link the current epidemiological transition,” says Pongsiri, an environmental health expert in EPA’s Office of the Science Advisor, “with biodiversity change, decline and extinction.”

“People have been working on this in individual diseases but no one has put all the studies together to compare them,” says Roman. In 2006, he and Pongsiri gathered a group of scientists and policy analysts with expertise in a range of the new diseases being observed — including West Nile virus as well as malaria, the African parasitic disease schistosomiasis, hantavirus pulmonary syndrome, and several others. From that meeting, the forthcoming BioScience study developed.

“We’ve reviewed all those studies and show that emergence or reemergence of many diseases is related to loss of biodiversity,” say Pongsiri.

“We’ve taken a broad look at this problem to say that it’s not just case-study specific,” she says, “we’re saying something is happening at a global scale.”

Of mosquitoes and mice
One of the studies that Pongsiri and Roman’s team examined was a 2006 investigation in Amazonian Peru. It was the first to demonstrate that malaria transmission can rise in response to deforestation. Though the mechanisms are complex and not fully worked out, it appears that loss of the structural diversity provided by trees led to higher density of Anopheles darlingi mosquitoes, a potent transmitter of malaria, as well as to higher biting rates.

“Or think about Lyme disease,” says Roman, calling from Connecticut.

People get this disease from ticks infected with a bacterium, Borrelia burgdorferi. The ticks, in turn, usually get the bacterium by feeding on small mammals — particularly white-footed mice.

“Historically, Lyme disease was probably rare, because you had a large range of mammals, everything from pumas all the way down to a widespread community of rodents,” says Roman. Ticks would happily feed on dozens of these animals, and, since many of them were unlikely or unable to transmit the bacterium to the tick, only a limited number of ticks would carry the disease to people. But fragmentation and reduction of forests has led to deep declines in the number of mammals — and white-footed mice tend to thrive in species-poor places, like small patches of forest on the edge of neighborhoods.

“In fact, white-footed mice appear to be the most competent animal host reservoir of Lyme disease in the northeastern U.S.,” Pongsiri notes on an EPA blog, “So, the more white-footed mice that are in the forest, the greater chance more ticks will be infected, and the greater chance you have of getting bitten by an infected tick.”

In other words, if you’re worried about catching Lyme disease, it’s a good idea to wear long pants — but it might be a better idea to join your conservation commission or zoning board since “protecting large forested areas in the vicinity of residential areas may reduce the risk of Lyme disease,” the BioScience paper notes.

Eco-epidemiology?
It is new to think about biodiversity — and therefore, species and land conservation — as integral to public health. Until recently, almost no epidemiologists, nor medical schools, were framing questions of human infectious disease prevention in terms of, say, habitat structure, promoting genetic diversity in non-human species, or protecting animal predators as ecosystem regulators. Human diseases, goes the conventional thinking, are best understood and treated by looking at humans.

“Now there is the beginning of a movement to bring epidemiology and ecology together,” say Pongsiri.

“We’re not saying that biodiversity loss is the primary driver of all of these diseases emerging,” says Roman, “it could be the major factor, or it could be one of many factors.”

“We’re trying to make the case that all these environmental changes we’re making, because they are anthropogenic, can be managed, can be controlled,” say Pongsiri. “We may be able to actually reduce or prevent these diseases by managing for biodiversity from the gene level to habitat level.”

A third of the bird species on the planet are at risk of extinction and a quarter of the mammals, Roman says, “and we have an incredible amount of habitat at risk and climate change. We should expect to see the impacts of these changes occurring now, to people — and we do.”

“The standard argument for protecting biodiversity is often that, well, there are medicines out there and you don’t want to destroy a forest where you might have a cure for cancer,” he says, “and that’s true — but I don’t think that’s as compelling as the fear that if you cut down the forest you or your kids are more prone to infectious diseases.”

http://www.uvm.edu/~uvmpr/?Page=News&storyID=15531

Emerg Infect Dis. 2008 July; 14(7): 1147–1150.
doi: 10.3201/eid1407.071599.

Janet E. Foley,* Nathan C. Nieto,* Jennifer Adjemian,* Haydee Dabritz,† and Richard N. Brown‡

*University of California, Davis, California, USA
†California Department of Public Health, Richmond, California, USA
‡Humboldt State University, Arcata, California, USA
Corresponding author.
Address for correspondence: Janet E. Foley, Department of Medicine and Epidemiology, University of California, Davis, California 95616, USA; email: jefoley@ucdavis.edu 

Abstract
A total of 2,121 small mammals in California were assessed for Anaplasma phagocytophilum from 2006 through 2008. Odds ratios were >1 for 4 sciurids species and dusky-footed woodrats. High seroprevalence was observed in northern sites. Ten tick species were identified. Heavily infested rodent species included meadow voles, woodrats, deer mice, and redwood chipmunks.

Conclusions
We show that a strong distinction can be made in possible reservoir capacity among rodent species, with many, such as deer mice and voles, only contributing to the ecology of granulocytic anaplasmosis through their support of ticks but not A. phagocytophilum infection. Others, including tree squirrels and woodrats, are frequently infected, in addition to supporting ticks. Considerable similarities exist between the ecology of A. phagocytophilum and B. burgdorferi in the West, although the large diversity of genospecies that exists for B. burgdorferi has not been reported for A. phagocytophilum. These data provide a starting point for future work to clarify the reservoir competence of small mammals for A. phagocytophilum and to determine how ecologic interactions among small mammals, other vertebrate hosts, multiple possible vectors, and both B. burgdorferi and A. phagocytophilum could affect the enzootic persistence of these pathogens and risk to humans and animals.

To read full article: CLICK HERE

Volume 15, Number 12–December 2009

Letter

Robert J. Fischer, Tammi L. Johnson, Sandra J. Raffel, and Tom G. Schwan
Author affiliations: National Institutes of Health, Hamilton, Montana, USA (R.J. Fischer, T.L. Johnson, S.J. Raffel, T.G. Schwan); and The University of Montana, Missoula, Montana, USA (T.L. Johnson)

To the Editor: On August 5, 1994, a northern spotted owl, Strix occidentalis caurina, was found dead in Kittitas County, Washington, USA (1). A thorough investigation and necropsy identified the probable cause of death to be a spirochete infection. The organisms were seen in sections of the bird’s liver with use of modified Steiner silver stain and microscopy. DNA was extracted from the infected liver, and PCR–DNA sequencing of the 16S ribosomal RNA (rRNA) locus identified the bacterium as a relapsing fever spirochete related most closely to Borrelia hermsii (1). The lack of additional data surrounding this case precluded Thomas et al. from concluding that this spirochete infecting the owl was B. hermsii. Yet, in a subsequent analysis using the intergenic spacer region, the owl spirochete was included with isolates of B. hermsii (2).

To investigate the distribution and prevalence of B. hermsii , during the summer of 2008, we began a study at Flathead Lake, Lake County, Montana, USA, where 9 persons have contracted relapsing fever since 2002 (3–5). A blood smear from 1 pine squirrel (Tamiasciurus hudsonicus) captured July 9 at Yellow Bay on the east shore of the lake (elevation 887 m; geographic coordinates 47°52´35´´N, 114°01´54´´W) contained spirochetes detected when stained with Giemsa and examined by microscopy (600× brightfield with oil immersion). Whole blood from the squirrel contained live spirochetes visible by dark-field microscopy, and ≈50 μL of this blood was injected intraperitoneally into a laboratory mouse. The next day, a few spirochetes were observed in the peripheral blood of the mouse, and during the next 3 days, the density of spirochetes increased. We used intracardiac puncture to collect blood from the mouse for spirochete isolation in BSK-H medium (Sigma-Aldrich, St Louis, MO, USA) and for analysis by PCR and DNA sequencing of multiple bacterial loci as described elsewhere (4,6).

The spirochetes observed in the squirrel’s blood failed to grow in BSK-H medium after passage in the laboratory mouse; however, we acquired DNA sequences from infected squirrel and mouse blood from PCR amplicons for 6 spirochete loci including 16S rDNA, flaB, gyrB, glpQ, IGS, and vtp. Sequences for the loci were each aligned with homologous sequences from other borrelia in our collection, and each locus grouped the spirochete within the 2 genomic groups of B. hermsii described previously (4,6). The unique squirrel spirochete differed from all other B. hermsii identified in our previous studies; deep branches in each phylogram grouped the spirochete more closely with B. hermsii genomic group I than with genomic group II (data not shown).

Next, we compared the sequences from the squirrel spirochete with those available in the National Center for Biotechnology Information database (www.ncbi.nlm.nih.gov), including those sequences reported for the spirochete found in the spotted owl (AY515269.1, AF116903.1, AF116904.1) (1,2). The 3 trimmed and aligned sequences for the 16S rDNA (1,290 bases), flaB (467 bases), and IGS (665 bases) from the squirrel spirochete were identical to those of the owl spirochete; no base differences were found among the 2,422 bases compared. We also examined DNA extracted from the spotted owl’s liver during the first investigation (1) (provided by Alan G. Barbour). We successfully PCR amplified most of the 16S rDNA and the complete flaB, gyrB, glpQ, and vtp genes from the owl spirochete DNA and determined their sequences. The complete sequences of the first 4 loci from the owl and squirrel spirochetes were identical and differed from all other B. hermsii sequences. A phylogram of the concatenated sequences totaling 5,188 bases demonstrated that the owl and pine squirrel spirochetes were identical and were divergent members of B. hermsii genomic group I (Figure).

Finding the same strain of B. hermsii, separated by ≈525 km, in a pine squirrel and a spotted owl demonstrates a broader geographic distribution and host range for this spirochete than what could have been envisaged previously. The possible role of birds as hosts for the vector Ornithodoros hermsi ticks has been demonstrated elsewhere (4). Given the ecologic overlap of pine squirrels and coniferous forest-dwelling birds, we believe that the previous finding of the infected spotted owl is likely not an isolated event. Instead, it may represent a tick–spirochete cycle for B. hermsii that includes a broader host range for this group of relapsing fever spirochetes than previously appreciated.

Acknowledgments
We thank Jake Beldsoe and Michaela Ponce for their help in the field, Colleen Miller for arranging all travel, Kerry Foresman for advice and equipment, and staff of the University of Montana Flathead Lake Biological Station.

This work was supported by the Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health.

References
1.Thomas NJ, Bunikis J, Barbour AG, Wolcott MJ. Fatal spirochetosis due to a relapsing fever–like Borrelia sp. in a northern spotted owl. J Wildl Dis. 2002;38:187–93.
2.Bunikis J, Tsao J, Garpmo U, Berglund J, Fish D, Barbour AG. Typing of Borrelia relapsing fever group strains. Emerg Infect Dis. 2004;10:1661–4.
3.Schwan TG, Policastro PF, Miller Z, Thompson RL, Damrow T, Keirans JE. Tick-borne relapsing fever caused by Borrelia hermsii, Montana. Emerg Infect Dis. 2003;9:1151–4.
4.Schwan TG, Raffel SJ, Schrumpf ME, Porcella SF. Diversity and distribution of Borrelia hermsii. Emerg Infect Dis. 2007;13:436–42. PubMed DOI
5.Uhlmann EJ, Seed PC, Schwan TG, Storch GA. Polymerase chain reaction of tick-borne relapsing fever caused by Borrelia hermsii. Pediatr Infect Dis J. 2007;26:267–9. PubMed DOI
6.Porcella SF, Raffel SJ, Anderson DE Jr, Gilk SD, Bono JL, Schrumpf ME, et al. Variable tick protein in two genomic groups of the relapsing fever spirochete Borrelia hermsii in western North America. Infect Immun. 2005;73:6647–58. PubMed DOI

Figure
Phylogram based on the alignment of the concatenated DNA sequences containing the 16S rDNA, flaB, gyrB, and glpQ loci for 6 isolates…

Suggested Citation for this Article
Fischer RJ, Johnson TL, Raffel SJ, Schwan TG. Identical strains of Borrelia hermsii in mammal and bird [letter]. Emerg Infect Dis [serial on the Internet]. 2009 Dec [date cited]. Available from http://www.cdc.gov/EID/content/15/12/2064.htm

DOI: 10.3201/eid1512.090792

http://www.cdc.gov/eid/content/15/12/2064.htm