Relapsing fever in epidemic form is caused by Borrelia recurrentis, which is transmitted by the human body louse; it does not occur in the United States. Endemic relapsing fever is caused by borreliae transmitted by ticks of the genus Ornithodoros. The species name of the Borrelia genus is often the same as that of the tick. Borrelia hermsii, the cause of relapsing fever in the western United States, is transmitted by Ornithodoros hermsi. In recent years, Borrelia miyamotoi, a relapsing fever spirochete, has been recognized in the United States as the cause of an acute febrile, Lyme disease-like illness. B. miyamotoi is transmitted by the same hard-bodies ticks, namely Ixodes scapularis, that transmit B. burgdorferi and other Borrelia species that cause Lyme disease (see discussion below).

Morphology and Identification

A. Typical Organisms The borreliae form irregular spirals 10–30 μm long and 0.3 μm wide. The distance between turns varies from 2 to 4 μm. The organisms are highly flexible and move both by rotation and by twisting. Borreliae stain readily with bacte riologic dyes as well as with blood stains such as Giemsa stain or Wright stain (Figure 1).

Fig1. Borrelia (arrow) in a peripheral blood smear of a patient with relapsing fever. Original magnification ×1000.

 B. Culture

The organism can be cultured in fluid media containing blood, serum, or tissue, but it rapidly loses its pathogenicity for animals when transferred repeatedly in vitro. Multiplication is rapid in chick embryos when blood from patients is inoculated onto the chorioallantoic membrane.

C. Growth Characteristics

 Little is known of the metabolic requirements or activity of borreliae. At 4°C, the organisms survive for several months in infected blood or in culture. In some ticks (but not in lice), spirochetes are passed from generation to generation.

D. Variation

The only significant variation of Borrelia species is with respect to its antigenic structure.

Antigenic Structure

 Antibodies develop in high titer after infection with borreliae. The antigenic structure of the organisms changes in the course of a single infection. The antibodies produced initially act as a selective factor that permits the survival only of antigenically distinct variants. The relapsing course of the disease appears to be caused by the multiplication of such antigenic variants, against which the host must then develop new antibodies. Ultimate recovery (after 3–10 relapses) is associated with the presence of antibodies against several antigenic variants.

 Pathology

 Fatal cases show spirochetes in great numbers in the spleen and liver, necrotic foci in other parenchymatous organs, and hemorrhagic lesions in the kidneys and the gastrointestinal tract. Spirochetes have occasionally been demonstrated in the spinal fluid and brain of persons who have had meningitis. In experimental animals (guinea pigs, rats), the brain may serve as a reservoir of borreliae after they have disappeared from the blood.

Pathogenesis and Clinical Findings

 The incubation period is 3–10 days. The onset is sudden, with chills and an abrupt rise of temperature. During this time, spirochetes abound in the blood. The fever persists for 3–5 days and then declines, leaving the patient weak but not ill. The afebrile period lasts 4–10 days and is followed by a second attack of chills, fever, intense headache, and malaise. There are 3–10 such recurrences, generally of diminishing severity. During the febrile stages (especially when the temperature is rising), organisms are present in the blood; during the afebrile periods, they are absent.

Antibodies against the spirochetes appear during the febrile stage, and the attack is probably terminated by their agglutinating and lytic effects. These antibodies may select out antigenically distinct variants that multiply and cause a relapse. Several distinct antigenic varieties of borreliae may be isolated from a single patient’s sequential relapses even after experimental inoculation with a single organism. Infection with the recently emerging pathogen B. miyamotoi typically presents as a febrile illness, with high fever (≥40°C), fatigue, headache, myalgia, arthralgia, and nausea. In some patients, leukopenia, thrombocytopenia, and elevated transaminases have also been reported. In contrast to Lyme dis ease, the typical skin lesions (erythema migrans) are absent with B. miyamotoi infection. Symptoms of infection usually resolve within 1 week of starting antibiotic therapy. In severely immunocompromised patients, meningoencepha litis has been described as a complication of B. miyamotoi infection. Infection with B. miyamotoi should be considered in patients with an acute febrile illness following the exposure to Ixodes ticks in areas where Lyme disease is also present.

Diagnostic Laboratory Tests

 A. Specimens

Blood specimens are obtained during the rise in fever for smears and animal inoculation.

B. Smears

Thin or thick blood smears stained with Wright or Giemsa stain reveal large, loosely coiled spirochetes among the red cells.

 C. Animal Inoculation

 White mice or young rats are inoculated intraperitoneally with blood. Stained films of tail blood are examined for spirochetes 2–4 days later.

 D. Serology

Spirochetes grown in culture can serve as antigens for CF tests, but the preparation of satisfactory antigens is difficult. Patients with epidemic (louse-borne) relapsing fever may develop a positive VDRL test result.

 E. Other tests

There are currently no FDA-approved tests for the diagnosis of B. miyamotoi infection. No serologic tests are currently available, and in some cases cross-reactivity with serologic tests for B. burgdorferi has been reported. However, several PCR tests have been described for the detection of B. miyamotoi from whole blood, plasma, CSF, and tissue.

 Immunity

 Immunity following infection is usually of short duration.

Treatment

The great variability of the spontaneous remissions of relapsing fever makes evaluation of chemotherapeutic effectiveness difficult. Tetracyclines, erythromycin, and penicillin are all believed to be effective. Treatment for a single day may be sufficient to terminate an individual attack.

Epidemiology, Prevention, and Control

 Relapsing fever is endemic in many parts of the world. Its main reservoir is the rodent population, which serves as a source of infection for ticks of the genus Ornithodoros. The distribution of endemic foci and the seasonal incidence of the disease are largely determined by the ecology of the ticks in different areas. In the United States, infected ticks are found throughout the West, especially in mountainous areas, but clinical cases are rare. In the tick, Borrelia species may be transmitted transovarially from generation to generation.

 Spirochetes are present in all tissues of the tick and may be transmitted by the bite or by crushing the tick. The tick borne disease is not epidemic. However, when an infected individual harbors lice, the lice become infected by sucking blood; 4–5 days later, they may serve as a source of infection for other individuals. The infection of the lice is not trans mitted to the next generation, and the disease is the result of rubbing crushed lice into bite wounds. Severe epidemics may occur in louse-infected populations, and transmission is favored by crowding, malnutrition, and cold climate.

 In endemic areas, human infection may occasionally result from contact with the blood and tissues of infected rodents. The mortality rate of the endemic disease is low, but in epidemics, it may reach 30%.

Prevention is based on avoidance of exposure to ticks and lice and on delousing (cleanliness, insecticides).

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