The disease is classically a five-day fever of the relapsing type, rarely exhibiting a continuous course. The incubation period is relatively long, at about two weeks. The onset of symptoms is usually sudden, with high fever, severe headache, pain on moving the eyeballs, soreness of the muscles of the legs and back, and frequently hyperaesthesia of the shins. The initial fever is usually followed in a few days by a single, short rise but there may be many relapses between periods without fever. The most constant symptom is pain in the legs. Recovery takes a month or more. Lethal cases are rare, but in a few cases "the persistent fever might lead to heart failure". Aftereffects may include neurasthenia, cardiac disturbances and myalgia.

"Bartonella quintana" is transmitted by contamination of a skin abrasion or louse-bite wound with the faeces of an infected body louse ("Pediculus humanus corporis"). There have also been reports of an infected louse bite passing on the infection.

A symptom complex characterised by the clinical features of a high intermittent fever of septic type, constantly recurring exanthema, transient arthralgia, carditis, pleurisy, neutrophil leukocytosis, and increased erythrocyte sedimentation rate.

Wissler's syndrome (or Wissler's disease or Wissler-Fanconi syndrome) is a rheumatic disease that has a similar presentation to sepsis. It is sometimes considered closely related to Still's disease. It is named for Guido Fanconi and Hans Wissler It was first described by Wissler in 1944 and Fanconi in 1946. Single observations by E. Uhse in 1943 («Febris maculosa intermittens»), Fykow in 1929 and Nowak in 1942.

Hypochromic anemia occurs in patients with hypochromic microcytic anemia with iron overload. The condition is autosomal recessive and is caused by mutations in the SLC11A2 gene. The condition prevents red blood cells from accessing iron in the blood, which causes anemia that is apparent at birth. It can lead to pallor, fatigue, and slow growth. The iron overload aspect of the disorder means that the iron accumulates in the liver and can cause liver impairment in adolescence or early adulthood.

It also occurs in patients with hereditary iron refractory iron-deficiency anemia (IRIDA). Patients with IRIDA have very low serum iron and transferrin saturation, but their serum ferritin is normal or high. The anemia is usually moderate in severity and presents later in childhood.

Hypochromic anemia is also caused by thalassemia and congenital disorders like Benjamin anemia.

Hypochromic anemia is a generic term for any type of anemia in which the red blood cells (erythrocytes) are paler than normal. ("Hypo"- refers to "less", and "chromic" means "color".) A normal red blood cell will have an area of pallor in the center of it; it is biconcave disk shaped. In hypochromic cells, this area of central pallor is increased. This decrease in redness is due to a disproportionate reduction of red cell hemoglobin (the pigment that imparts the red color) in proportion to the volume of the cell. Clinically the color can be evaluated by the Mean Corpuscular Hemoglobin (MCH) or Mean Corpuscular Hemoglobin Concentration (MCHC). The MCHC is considered the better parameter of the two as it adjusts for effect the size of the cell has on its color. Hypochromia is clinically defined as below the normal MHC reference range of 27-33 picograms/cell in adults or below the normal MCHC reference range of 33-36 g/dL in adults.

Red blood cells will also be small (microcytic), leading to substantial overlap with the category of microcytic anemia. The most common causes of this kind of anemia are iron deficiency and thalassemia.

Hypochromic anemia was historically known as chlorosis or green sickness for the distinct skin tinge sometimes present in patients, in addition to more general symptoms such as a lack of energy, shortness of breath, dyspepsia, headaches, a capricious or scanty appetite and amenorrhea.