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Is Relapsing Fever one of the Hanta Virus names?

Posted By: CrystalRiver
Date: Saturday, 24-Feb-2018 10:02:54

In Response To: LYME SCI: B. miyamotoi has been in California ticks for a long time (closely related to relapsing fever Borrelia) (CrystalRiver)

Dear RM Agents and Readers,

From The Pages of the CDC (also wonder if it will be on semantics that the corrupt doctors and their scientists will be released from responsibility regarding Lyme and Lyme like conditions from the phrase: "It's all in you head". Perhaps the realization that it spreads to the entire body will be enough to hold them accountable?

https://wwwnc.cdc.gov/eid/article/21/2/14-1276_article

Many Blessings,
CrystalRiver
------------------------------------------

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Volume 21, Number 2—February 2015

Research

Tickborne Relapsing Fever, Bitterroot Valley, Montana, USA


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Case-Patient Materials and Methods Results Discussion Cite This Article
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Joshua Christensen, Robert J. Fischer, Brandi N. McCoy, Sandra J. Raffel, and Tom G. SchwanComments to Author
Author affiliations: St. Patrick Hospital, Missoula, Montana, USA (J. Christensen); University of Montana College of Health Professionals and Biomedical Sciences, Missoula (J. Christensen); National Institute of Allergy and Infectious Diseases, Hamilton, Montana, USA (R.J. Fischer, B.N. McCoy, S.J. Raffel, T.G. Schwan)
Cite This Article

Abstract

In July 2013, a resident of the Bitterroot Valley in western Montana, USA, contracted tickborne relapsing fever caused by an infection with the spirochete Borrelia hermsii. The patient’s travel history and activities before onset of illness indicated a possible exposure on his residential property on the eastern side of the valley. An onsite investigation of the potential exposure site found the vector, Ornithodoros hermsi ticks, and 1 chipmunk infected with spirochetes, which on the basis of multilocus sequence typing were identical to the spirochete isolated from the patient. Field studies in other locations found additional serologic evidence and an infected tick that demonstrated a wider distribution of spirochetes circulating among the small mammal populations. Our study demonstrates that this area of Montana represents a previously unrecognized focus of relapsing fever and poses a risk for persons of acquiring this tickborne disease.

Seminal research on tickborne diseases of humans in North America began more than a century ago with the discovery in 1906 that an illness locally called black measles, which affected persons in the Bitterroot Valley of western Montana, USA, resulted from the bite of a bacteria-infected Rocky Mountain wood tick (1,2). What soon followed was the establishment of a multidisciplinary public health program to control this newly identified disease, now called Rocky Mountain spotted fever, which was caused by Rickettsia rickettsii, and a search was conducted for other diseases in nature that resulted from the bite of pathogen-infected ticks. These programs were based at a newly funded state laboratory in Hamilton in the Bitterroot Valley, a facility that was soon incorporated into the US Public Health Service and is now the Rocky Mountain Laboratories (RML) of the National Institute of Allergy and Infectious Diseases.

One of the many diseases studied at the RML since the early 1930s has been tickborne relapsing fever (RML, unpub. data) (3,4). In North America, this zoonosis is associated with 3 species of spirochetes, but most human cases are caused by Borrelia hermsii, which is found in scattered foci in the western United States and southern British Columbia, Canada (5,6). The specific vector of this spirochete is the Ornithodoros hermsi tick (7), which is found in higher-elevation coniferous forests where its preferred rodent hosts, primarily squirrels and chipmunks, are also found (6). In spite of the many decades of intensive research on ticks and tickborne diseases in the Bitterroot Valley, the tick O. hermsi, the spirochete B. hermsii, or an autochthonous human case of relapsing fever has not been observed in this region of Montana, until now. We report a case of tickborne relapsing fever in a person in this region.

Case-Patient

The patient was a previously healthy 55-year-old man who sought care in July 2013 after a week of fevers. He had traveled widely over the previous months, including trips to Antarctica, New Zealand, Spain, Italy, and eastern Washington State, before returning to his home in the Bitterroot Valley of Montana. A week before his symptoms developed, he had moved part of a woodpile and noted rodent feces among the cut logs. He came to the emergency department of a local hospital because of fever, chills, night sweats, fatigue, nausea, vomiting, diarrhea, and malaise.

At initial evaluation, he had a temperature of 37.3°C; other vital signs were within reference ranges. Initial laboratory values included mildly increased levels of bilirubin, alkaline phosphatase, and aspartate aminotransferase, and mild transaminitis with an increased level of alanine aminotransferase (Table 1). A complete blood count showed thrombocytopenia (platelet count 51,000/mL). Hemoglobin level and leukocyte count were within reference ranges. He was given a presumptive diagnosis of an acute viral infection and discharged from the emergency department.

He returned 2 days later with confusion, tachycardia, hypoxemia, and a measurable fever (temperature 38.7°C). A physical examination identified a bilateral conjunctival suffusion, more notable in the right eye; cervical lymphadenopathy, tachypnea, tachycardia, splenomegaly, and major confusion. Additional laboratory tests showed a leukocyte count of 9,400 cells/mm3with 23% bands and a further reduced platelet count of 29,000/mL. Levels of bilirubin, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, serum lactate with lactic acidosis, procalcitonin, and total creatine kinase were all highly increased above reference values (Table 1). Urinalysis showed a 2+ protein level, and a chest radiograph showed diffuse bilateral pulmonary infiltrates.

He was admitted to the hospital and given intravenous ceftriaxone and oral doxycycline pending further examination. A peripheral smear was prepared, which showed thrombocytopenia and multiple extracellular spirochetes. A coded diagnostic specimen of the patient’s whole blood was sent to the RML for identification of the spirochetes. His hospital course was notable for acute respiratory failure caused by acute respiratory distress syndrome, metabolic encephalopathy, and uveitis of the right eye. His sepsis and acute respiratory distress syndrome resolved, and his condition rapidly improved after treatment with ceftriaxone and doxycycline. On hospital day 5, he was discharged and given a 14-day course of oral doxycycline.

He was seen as an outpatient and showed resolution of abnormalities and symptoms, except for decreased visual acuity of the right eye that ultimately required a corrective lens. Results of serologic tests performed at a commercial diagnostic laboratory were negative for antibodies against Coxiella burnetii, Brucella spp., Francisella tularensis, Leptospira interrogans, Treponema pallidum, hantavirus (Sin Nombre virus), Colorado tick fever virus, cytomegalovirus, Epstein-Barr virus, and hepatitis A, B, and C viruses. An IgM test result for Lyme disease was equivocal but was probably cross-reactive because of the B. hermsii infection. A convalescent-phase serum sample obtained 6 weeks after onset of symptoms was sent to the Centers for Disease Control and Prevention (Fort Collins, CO, USA). This sample was positive for B. hermsii by enzyme immunoassay and Western blotting.





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