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Relapsing fevers 

Relapsing fevers

Relapsing fevers

David A. Warrell



Taxonomy—molecular phylogenetic studies suggest that Borrelia recurrentis and B. duttonii are the same species.

Immunopathophysiology of the relapse phenomenon—IgM antibodies generated by the B1b cell subset control bacteraemia.

Treatment—azithromycin should be considered in future studies.

Updated on 31 May 2012. The previous version of this content can be found here.
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date: 30 March 2017

Louse-borne relapsing fever (LBRF) and tick-borne relapsing fevers (TBRF) are characterized by repeated episodes of high fever separated by afebrile period. They are caused by borrelia spirochaetes distinct from those responsible for Lyme borrelioses. Untreated patients may suffer as many as five (LBRF) or ten (TBRF) febrile relapses of decreasing severity.

Humans are the sole reservoir of epidemic LBRF caused by Borrelia recurrentis and transmitted by body lice (Pediculus humanus corporis). Endemic TBRFs are caused by at least 15 different borrelia species and have their own particular species of soft Ornithodoros tick vectors which also act as reservoirs. Transmission transplacentally, or by needlestick, blood transfusion, or laboratory accident is also possible.

LBRF is a classic historical epidemic disease of war, famine, and refugees, now largely confined to mountainous areas of the Horn of Africa and possibly Peru but still retaining its pandemic potential. TBRF is of increasing endemicity in sub-Sahelian West Africa and is common in Rwanda and Tanzania. It occurs sporadically in parts of North America, Europe, the Middle East, and central Asia.

The most distinctive feature of these infections, the relapse phenomenon, is explained by antigenic variation of borrelial outer-membrane lipoprotein (vmp). Starting 2–18 days after infection, there is acute fever, chills, headache, pain, and prostration. Petechial rash (thrombocytopenia), bleeding, jaundice, hepatosplenomegaly and liver dysfunction are common. In some forms of TBRF, there are neurological manifestations; lymphocytic meningitis, VII and other cranial nerve lesions, myelitis, radiculitis, etc.; and uveitis during relapses.

Dangerous complications are hyperpyrexia, shock, myocarditis causing acute pulmonary oedema, acute respiratory distress syndrome (ARDS), cerebral or massive external bleeding, ruptured spleen, hepatic failure, Jarisch–Herxheimer reactions (JHR), and typhoid or other complicating bacterial infections. Pregnant women are at high risk of aborting and perinatal mortality is high.

Diagnosis by microscopy of blood films is more difficult in TBRF than LBRF. Serology and polymerase chain reaction (PCR) are used increasingly. The most important differential diagnosis in residents and travellers from tropical endemic areas is falciparum malaria.

Untreated mortality, exceeding 40% in some epidemics, can be reduced to less than 5% by treatment with antibiotics such as penicillin, tetracycline, erythromycin, and chloramphenicol, but elimination of spirochaetaemia is often accompanied by a potentially fatal JHR.

Prevention of LBRF is by eliminating lousiness by sterilizing clothing, using insecticides, and improving hygiene. Improved house construction, control of peridomestic rodents, use of residual insecticides, protection of sleepers with impregnated bed nets, and a post-exposure course of doxycyline can reduce the risk of TBRF.

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