RELAPSING FEVER

References: eMedicine Online: Tick Borne Diseases, Relapsing Fever. (http://www.emedicine.com/emerg/topic590.htm)

Endemic relapsing fever: Is caused by at least 15 different Borrelia species. Soft ticks of the genus Ornithodorus spread the tick-borne variety. The responsible Borrelia species are identified closely with its tick vector and they share parallel nomenclature. (For example, Borrelia parkeri infects Ornithodoros parkeri; Borrelia hermsii is the agent transmitted by tick bite by Ornithodoros hermsii.)

Epidemic relapsing fever: Is caused by B. recurrentis. It is the only agent of louse-borne disease. Pediculus humanus, is the specific vector (Pediculus pubis is not a vector). Louse-borne relapsing fever is more severe than the tick-borne variety.

EPIDEMIOLOGY

Undoubtedly, many cases occur that either are misdiagnosed or go unreported.

Epidemic relapsing fever is spread between humans by body lice, when crushed into the bite-wound. Distribution is limited to situations of overcrowding, war, and poverty; presently limited to Africa, China, and Peru.  Large outbreaks of louse-borne relapsing fever have occurred throughout the past century. These outbreaks usually occur following man-made breakdowns in public health, as typified by the epidemic following World War II that involved about 10 million people. Epidemic relapsing fever has not been reported in the U.S. since 1906. It is not endemic in the U.S. however, an occasional traveler will present with an imported case.

Epidemic relapsing fever: No animal reservoir exists. Lice that feed on infected humans acquire the Borrelia that then multiplies in the gut of the louse. When an infected louse feeds on an uninfected human, the organism gains access when the victim crushes the louse or scratches the area where the louse is feeding. B. recurrentis infects the patient via either abraded or intact skin (or mucous membranes) and then invades the bloodstream.

Following transmission a massive spirochetemia develops. Symptoms develop in about 3-18 days (incubation period; average 7-8 days).

Regardless of the mode of transmission, a spirochetemia develops. The Borrelia then invade the endothelium. This can produce a low-grade disseminated intravascular coagulation and thrombocytopenia. The relapses occur because of genetically programmed shifting of outer surface proteins of the Borrelia that allows a new clone to avoid destruction by antibodies directed against the majority of the original infecting organisms. Thus, the patient clinically improves until the new clone multiplies sufficiently to cause another relapse. Tick-borne disease tends to have more relapses (average of 3) compared to the louse-borne variety (often just 1).

Specific immunoglobulin-complement-mediated lysis and the release of endotoxin accounts for some of the symptoms.

Periodic relapses continue until the infection runs out of antigenic variations.

Most organs of the body are invaded, but mortality is usually associated with myocarditis.

SYMPTOMS include : Abrupt onset of symptoms which include: High fever, rigors, severe headache, muscle pains, weakness, anorexia, weight loss, cough, Pulse is rapid in proportion to the fever, a point of differential value with typhoid fever with which louse-borne relapsing fever can be confused, systemic complications which include: nausea, vomiting, upper abdominal pain due to liver and spleen involvement, a dry cough.

The primary febrile episode typically ends after 3-6 days by crisis that can culminate in fatal shock. About 7-10 days later, the first relapse occurs abruptly. Subsequent relapses tend to be less severe. In tick-borne disease, relapses average 3, and there can be more than 10. The febrile period terminates abruptly with the induction of the immune response.

Usually, 1-2 (epidemic form), or 3-4 (endemic form) relapses occur.

Other Symptoms that can occur are: Splenomegaly, hepatomegaly and jaundice, rash, respiratory symptoms, CNS involvement.

Blood smear stained with Giemsa or Wright stain. 70% of patients will show spirochetes in their blood during the febrile period.

Mortality rate is 1% with treatment; 30-70% without treatment. Poor prognostic signs include severe jaundice, severe change in mental status, severe bleeding, and prolonged QT interval on ECG.

Tetracycline is very effective, but may, within 2 h, induce a Jarisch-Herxheimer reaction, which can be fatal. This reaction produces apprehension, diaphoresis, fever, tachycardia, and tachypnea with an initial pressor response followed rapidly by hypotension. The Jarisch-Herxheimer reaction can be fatal. Recent studies have shown that tumor necrosis factor (TNF) alpha may be partly responsible for the reaction.

Tetracycline or Doxycycline- not recommended for pregnant women or for children.

Erythromycin or Chloramphenicol- can be used for the treatment of pregnant women and children (chloramphenicol can cause serious and fatal blood dyscrasias (eg, aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) and should only be used in seriously ill children)

Delousing and improved hygiene for epidemic disease.