Case presentation

1. Case presentation 盧主任/I2陳彥霖

2. Brief History • A 45-year-old man was seen in the emergency department for persistent night sweats, headache, intermittent fever, and severe chills, which occurred approximately every 48 h. The patient was born in Asia and had moved to the United States 5 years earlier. At that time, he had suffered a similar illness, was treated, and appeared to make a good recovery. Blood was drawn for laboratory studies including a hemoglobin determination and thick and thin blood smears for parasites.

3. Brief History • The patient was slightly anemic, with a hemoglobin level of 9.5 g/dl. Examination of Giemsa-stained blood films revealed the presence of enlarged red blood cells contain­ing trophozoite forms (Fig. 23.1). Several irregular ameboid trophozoites containing brown granules were seen. Eosinophilic stippling was visible in the cytoplasm of the erythrocytes. A few round to oval gametocytes were seen. Based on these findings, a diagnosis of infection with a blood parasite was made.

4. enlarged red blood cells contain­ing trophozoite forms (Fig. 23.1).

5. Plasmodium falciparum and P. malariae are encountered in all shaded areas of the map (with P. falciparum by far the most prevalent). Plasmodium vivax and P. ovale are traditionally thought to occupy complementary niches, with P. ovale predominating in Sub-Saharan Africa and P. vivax in the other areas; however these two species are not always distinguishable on the basis of morphologic characteristics alone; the use of molecular tools will help clarify their exact distribution.

9. Complications • Most complications are caused by P falciparum, and they may include the following: • Coma (cerebral malaria) • Defined as coma, altered mental status, or multiple seizures with P falciparum in the blood, cerebral malaria is the most common cause of death in malaria patients. If untreated, this complication is lethal. • Even with treatment, 15% of children and 20% of adults who develop cerebral malaria die. • The symptoms of cerebral malaria are similar to those of toxic encephalopathy. • Seizures • Renal failure: As many as 30% of nonimmune adults infected with P falciparum suffer acute renal failure. • Hemoglobinuria (blackwater fever) • Blackwater fever is the passage of dark, Madeira-colored urine. • Hemolysis, hemoglobinemia, and the subsequent hemoglobinuria and hemozoinuria cause this condition. • Noncardiogenic pulmonary edema: This affliction is most common in pregnant women and results in death in 80% of patients. • Profound hypoglycemia: Hypoglycemia often occurs in young children and pregnant women. It often is difficult to diagnose since adrenergic signs are not always present and since stupor already may have occurred in the patient. • Lactic acidosis: This occurs when the microvasculature becomes clogged with P falciparum. If the venous lactate level reaches 45 mg/dL, a poor prognosis is very likely. • Hemolysis resulting in severe anemia and jaundice • Bleeding (coagulopathy)

10. BABESIOSIS • SymptomsBabesiosis is associated with hemolytic anemia, jaundice, fever and hepatomegaly, usually 1-2 weeks after infection • DiagnosisDiagnosis is based on symptoms, patient history and detection of intraerythrocytic parasite in the patient or transfer of blood in normal hamsters which can be heavily parasitized.

11. Chloroquine (Aralen HCl, Aralen Phosphate) -- Inhibits parasite growth by concentrating within acid vesicles of the parasite and increasing its internal pH. In addition, inhibits hemoglobin utilization and metabolism by the parasite. Adult Dose10 mg base/kg PO, not to exceed 600 mg; then 5 mg base/kg PO; not to exceed 300 mg at 6-h, 24-h, and 48-h intervals (total 25 mg/kg)

12. QUESTIONS • Which infection does this patient have? Which parasite is infecting him? • Describe the typical appearance of this parasite in thick and thin Giemsa-stained smears. • Which blood protozoan parasite morphologically resembles this parasite? • Comment on the size of the erythrocytes. What do we call the eosinophilic stippling seen in these cells? Which other species causes this characteristic? • Describe the clinical illness caused by this parasite. Which serious complicationmay occur with this infection? • How does the life cycle of different species of this parasite vary? How does this fact relate to this patient's infection? • How would this patient be treated?