Infectious Disease Online
Pathology of Relapsing Fever
The term "Relapsing fever" includes a group of infectious disorders caused by blood spirochetes.
Synonyms: Carapata (Africa) ; Kimputu and Gorgoya (South America) ; Gharib Gez (Iran) ; Bilous Typhoid (Egypt) ; Fowl Nest Fever (China); Vagabond Fever (Spain).
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 Borrelia turicatae , Borrelia hermsii , and Borrelia parkeri in North America , Borrelia hispanica in Spain , Borrelia persica in Asia, and Borrelia 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.
Human body louse, Pediculus humanus humanus becomes infected with Borrelia recurrentis when it feeds on an infected host.
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 1 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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