Unexplained Fever In Infectious Diseases: Section 2: Commonly Encountered Aerobic, Facultative Anaerobic, And Strict Anaerobic Bacteria, Spirochetes, And Parasites
Benedict Isaac, Serge Kernbaum, Michael Burke in Unexplained Fever, 2019
Babesiosis is a disease which often evolves with fever. It is caused by intraerythroeitic protozoan parasites of the genus Babesia. This infection is common in both domestic and wild animals. The parasite is transmitted from animal to man by the bite of ticks (of the genera Ixodes, Dermacentor, Rhipicephalus). The most important causative agents are bovine parasites (B. bovis, B. divergens) or rodent parasites (B. microti). Babesiosis should be considered in any patient with fever, a history of tick bite, a prior splenectomy, a blood transfusion, or sojourn in endemic areas (in U.S.: Nantucket, Massachusetts, New York, Long Island Sound; in Europe: Yugoslavia, USSR, France, Scotland, Ireland). An associated hemolytic anemia is very suggestive.117
Carrier Screening For Inherited Genetic Conditions
Vincenzo Berghella in Obstetric Evidence Based Guidelines, 2022
Alpha-thalassemia results from a gene deletion of two or more copies of the four alpha-globin genes on chromosome 16. It is common among individuals of Southeast Asian, African, West Indian, and Mediterranean ancestry. Deletion of two genes, alpha-thalassemia trait, causes a mild hemolytic anemia. The deletions may occur on the same chromosome (cis aa/-) or on two different chromosomes (trans a-/a-). Individuals of Southeast Asian descent are more likely to carry the cis configuration compared to their African counterparts. Individuals with alpha-thalassemia trait are at increased risk for having a child with a more severe form of alpha-thalassemia. Hemoglobin H disease is caused by the deletion of three alpha-globin genes. Affected individuals have mild to moderate hemolytic anemia. Alpha-thalassemia major (Hb Bart disease) results from the absence of functional alpha-globin genes. Fetal hydrops and intrauterine fetal demise is the expected outcome in these cases due to the inability to produce functional HbF. Hemoglobin Bart disease does not usually occur in fetuses of alpha-thalassemia carriers of African origin, since individuals of African descent usually have the trans-configuration genotype. See Chap. 14 in Maternal-Fetal Medicine Evidence Based Guidelines.
Anemia (Hemolytic)
Charles Theisler in Adjuvant Medical Care, 2023
Red blood cells carry oxygen for every cell (except cartilage and the cornea) throughout the entire body. Hemolytic anemia is a condition in which red blood cells are prematurely destroyed and removed from the bloodstream before their normal lifespan is over. When destruction of red blood cells outpaces the bone marrow’s production of these cells, hemolytic anemia occurs. Like other anemias, hemolytic anemia can cause pallor, fatigue, dizziness, and low blood pressure. Yellowing of the skin and whites of the eyes (jaundice), dark urine, shortness of breath, and a rapid heart rate or an enlarged spleen may also occur.1
Disordered bone metabolism in hereditary spherocytosis patients
Published in Hematology, 2019
Mahmut Cesur, Fatih Temiz, Can Acıpayam, Metin Kılınc, Nurten Seringec Akkececi
Chronic hemolytic anemia is a rare disease characterized by abnormal destruction of erythrocytes. Intrinsic hemolytic anemias divided into categories like membranopathy (Hereditary spherocytosis etc.), hemoglobinopathy (sickle cell anemia etc.), and enzyme deficiency (pyruvate kinase deficiency etc.). Extrinsic hemolytic anemias caused by autoimmunity and microangiopathy [1]. In patients with sickle cell anemia and thalassemia, the impairment in bone metabolism was demonstrated. In these patients there are changes in parameters related to bone metabolism and bone densities [2–4]. Vitamin D and growth hormone deficiency, chronic blood transfusion, iron toxicity, endocrine pathologies cause deterioration in bone metabolism [5]. In mouse studies, hemolytic anemia alone has been shown to cause bone health decline, decreased bone density, and a decrease in osteocalcin levels in the bone formation markers [6].
Management strategies for human babesiosis
Published in Expert Review of Anti-infective Therapy, 2020
Robert P. Smith, Klaus-Peter Hunfeld, Peter J Krause
Mild to moderate babesiosis is typical in those with mild immune suppression but who are otherwise in good health, such as those with well-controlled non-AIDS HIV or those on steroid treatment for another underlying condition [76]. Some of these patients can be managed as outpatients in a similar manner as immunocompetent patients but most will initiate treatment in a hospital setting. The combination of atovaquone and azithromycin given for 7 to 10 days is usually effective (Table 1). If gastrointestinal symptoms preclude oral administration, azithromycin may be given intravenously. The alternative regimen of clindamycin (intravenous or oral) and quinine (oral) can be used if needed but is more likely to cause side effects. Resolution of systemic inflammatory symptoms such as fever is expected during the first week of treatment. Hemolytic anemia, if present, stabilizes. Symptoms such as fatigue may persist for weeks despite resolution of parasitemia. Close monitoring during acute disease and follow up is advised for this group of patients until infection has cleared. Patients should be instructed to report any new symptoms suggestive of babesiosis to their physician, in which case a thin blood smear and PCR should be performed.
The first Chinese case of unstable Hemoglobin Santa Ana detected by capillary electrophoresis: a case report and literature review
Published in Hematology, 2022
Li Du, Danqing Qin, Jicheng Wang, Cuize Yao, Juan Zhu, Hao Guo, Tenglong Yuan, Jie Liang, Aihua Yin
Hemoglobin variants comprise a group of hereditary hemoglobin diseases caused by mutations in globin genes that lead to structural changes in the hemoglobin molecule. Hemoglobin variants with various clinical manifestations. Unstable hemoglobins are important causes of hemolytic anemia, which is rare and often undiagnosed. Hemoglobin Santa Ana, an unstable hemoglobin variant, was first reported in 1968 [1] and was later confirmed to be due to the HBB gene mutation c.266T > C [2]. In hemoglobin Santa Ana, the amino acid leucine at the 88th position of the normal β-globin chain is replaced by proline, which disturbs not only the heme contact but also the integrity of the F helix [3]. Several patients with hemoglobin Santa Ana have been described, but detection by capillary electrophoresis (CE) has never been reported [1–6]. The clinical manifestations of cases are very similar, including hemolytic anemia, jaundice, brown urine and splenomegaly.
Related Knowledge Centers
- Anemia
- Fatigue
- Jaundice
- Reticuloendothelial System
- Shortness of Breath
- Spleen
- Gallstone
- Blood Vessel
- Hemolysis
- Red Blood Cell
- Shortness of Breath