ABSTRACT
Plasmodium knowlesi was known as a plasmodium of macaques until P. knowlesi transmission to humans was recognised in Borneo and later throughout South-East Asia. We describe here a case of a P. knowlesi infection imported to Germany from Thailand. The patient had not taken antimalarial chemoprophylaxis and suffered from daily fever attacks. Microscopy revealed trophozoites and gametocytes resembling P. malariae. P. knowlesi malaria was confirmed by PCR.
Subject(s)
Malaria/diagnosis , Plasmodium knowlesi/isolation & purification , Travel , Acute Kidney Injury/complications , Acute Kidney Injury/diagnosis , Antimalarials/therapeutic use , Artemether , Artemisinins/therapeutic use , Ethanolamines/therapeutic use , Female , Fluorenes/therapeutic use , Germany , Humans , Lumefantrine , Malaria/drug therapy , Malaria/transmission , Microscopy , Middle Aged , Plasmodium knowlesi/genetics , Polymerase Chain Reaction , Thailand , Treatment OutcomeSubject(s)
Embolization, Therapeutic , Esophageal and Gastric Varices/therapy , Gastrointestinal Hemorrhage/therapy , Hypertension, Portal/complications , Liver Cirrhosis/complications , Portasystemic Shunt, Transjugular Intrahepatic , Splenic Vein , Thrombocytopenia/complications , Thrombosis/therapy , Aged , Angiography , Esophageal and Gastric Varices/diagnosis , Female , Follow-Up Studies , Gastrointestinal Hemorrhage/diagnosis , Gastroscopy , Humans , Image Interpretation, Computer-Assisted , Radiographic Image Enhancement , Retreatment , Risk Factors , Secondary Prevention , Splenic Infarction/diagnosis , Splenic Infarction/therapy , Thrombosis/diagnosis , Tomography, X-Ray ComputedABSTRACT
Urea cycle defects belong to the most common metabolic disorders with a cumulative incidence of 1:8000. A common trait of urea cycle defects is a disturbed detoxification of ammonia leading to hyperammonemia in the event of a high nitrogen load. Most patients develop symptoms in the neonatal period or in infancy, e. g. vomiting, seizures and disturbed consciousness. Depending on the affected enzyme and its residual activity, patients differ in the age at first presentation, the character and severity of symptoms and in the susceptibility to metabolic derangement. The presence of hyperammonemia and an altered plasma amino acid profile give the essential diagnostic clues. Since modern therapeutic measures have prolonged the life expectancy of these patients and provided the possibility of a first presentation in adulthood, patients with urea cycle defects have become an increasing challenge in internal medicine. The reported case series illustrates the heterogeneous clinical course of these disorders from childhood to adulthood.
