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There are two
main types of relapsing fever:
Epidemic (louse-borne), for which man
is the reservoir, and Endemic (tick-borne), for which rodents and
other animals are the natural reservoir.
Louse-borne relapsing fever is
caused by spirochete Borrelia recurrentis.
Tick-borne relapsing fever
is caused by several species, the most common being B. turicatae , B.
hermsii , and B. parkeri in North America , B. hispanica in Spain , B. persica in Asia, and B. duttonii in Africa.
Borrelias are 0.2 micrometer
to 0.5 micrometer wide, 3 to 20 micrometer long, and they have three to ten
coarse irregular coils.
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Human body
louse, Pediculus humanus humanus becomes infected with B. recurrentis
when it feeds on an infected host.
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The borrelias cross the gut wall of
the louse into the haemolymph, where they multiply. Here they remain
unless the louse is crushed when feeding. If the louse is crushed, the borrelias escape and penetrate at the site of the bite or even through
the intact skin.
War, crowded migrant-worker camps, and heavy clothings during cold weather all favour mobilization of lice and the
spread of relapsing fever.
Furthermore, lice dislike the higher
temperatures of the feverish victims and seek new hosts, another
factor in the rapid spread of relapsing fever during epidemics.
In tick-borne
relapsing fever, ticks are infected while biting rats and other
animals. The borrelias grow in the hemocoelom of the tick and invade
other tissues including salivary glands. Man is infected by the saliva
or coxal fluid of the tick. Ticks are much more durable than fleas and
may harbour spirochetes 12 to 15 years without blood meal.
About I week
after inoculation, fever, headache, myalgia, arthralgia, and lethargy
begin suddenly.
The liver and spleen enlarge, and there are petechiae
of skin, conjunctival hemorrhages and abdominal tenderness.
In severe
cases a rash, coma, meningitis, myocarditis and liver failure may
ensue.
Three to nine days after onset the
fever ends abruptly, only to begin again seven to ten days later.
During the afebrile period the
spirochetes disappear from the blood and change their antigenic coats.
The symptoms are milder and the
duration of illness is shorter for each relapse.
In fatal
infections the spleen is enlarged and contains military microabscesses.
Spirochetes form entangled masses
around the necrotic centers.
The
lymphocytes and neutrophils infiltrate central and mid-zonal areas of
the liver, where spirochetes lie free in the sinusoids.
The pleura,
peritoneum, brain, stomach, and intestines exhibit focal hemorrhage.
Wright’s and Giemsa stained smears of blood, urine, and spinal fluid reveal
spirochetes within or outside of leukocytes.
Kelly’s broth medium
supports growth of borrelia.
Specimens from patients injected into
mice yield borrelia in blood of the animal.
Serologic tests for syphilis may also
be positive.
Antibodies in the serum of convalescent
patients agglutinize and immobilize spirochetes and fix complement.
Tetracycline
and erythromycin are effective.
Treatment can provoke a sudden drop of
blood pressure, headache, myalgia and sensation of cold.
This
reaction is thought to be related to the flooding of the blood by endotoxins when the spirochetes die, a process that activates fibrin
and complement factors.
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