The anus will excrete feces that is thought to attract male fleas for mating, described in a later section. The hypertrophic zone between tergites 2 and 3 in the abdominal region begins to expand a day or two after penetration and takes the appearance of a life belt. During this time, the flea begins to feed on the hosts blood.Stage 3 is divided into two substages, 3a and 3b. Stage 3a is 2–3 days after penetration is complete. In substage 3a, the fleas midsection swells, balloon-like, to the size of a pea. This expansion of the flea causes its integument to be stretched thin, a process called physogastrism. The swelling ends in the condition of physogastry, and results in the appearance of a white halo around a black dot at the center of the lesion. That dot is the rear end of the flea. In substage 3b, the chitin exoskeleton of tergites 2 and 3 increase in thickness, which gives the structure the look of a miniature caldera. Egg release is common in substage 3b, as are fecal coils. The eggs tend to stick to the skin.At about the 3rd week after penetration, stage 4 begins, which is also divided into two substages. In 4a, the flea loses its signs of vitality and appears near death. As a result, the lesion shrinks in size, turns brown, and appears wrinkled.
Boutonneuse fever (also called, Mediterranean spotted fever, fièvre boutonneuse, Kenya tick typhus, Indian tick typhus, Marseilles fever, or Astrakhan fever) is a fever as a result of a rickettsial infection caused by the bacterium Rickettsia conorii and transmitted by the dog tick Rhipicephalus sanguineus. Boutonneuse fever can be seen in many places around the world, although it is endemic in countries surrounding the Mediterranean Sea. This disease was first described in Tunisia in 1910 by Conor and Bruch and was named boutonneuse (French for "spotty") due to its papular skin-rash characteristics. Presentation
After an incubation period around seven days, the disease manifests abruptly with chills, high fevers, muscular and articular pains, severe headache, and photophobia. The location of the bite forms a black, ulcerous crust (tache noire). Around the fourth day of the illness, a widespread rash appears, first macular and then maculopapular, and sometimes petechial. Diagnosis
The diagnosis is made with serologic methods, either the classic Weil–Felix test, (agglutination of Proteus OX strains), ELISA, or immunofluorescence assays in the bioptic material of the primary lesion. The Weil–Felix test demonstrated low sensitivity (33%) in diagnosing acute rickettsial infections and low specificity, with a positive titre of 1:320 seen in 54% of healthy volunteers and 62% of non-rickettsial fever patients. Therefore, the use of the WFT should be discouraged in the diagnosis of acute rickettsial infections. Treatment
The illness can be treated with tetracyclines (doxycycline is the preferred treatment), chloramphenicol, macrolides, or fluoroquinolones. See also
Rocky Mountain spotted fever

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