not-yet-known not-yet-known not-yet-known unknown Outcome and Follow-up The patient’s condition gradually improved. Following 48 hours in the ICU and three pints of blood transfusion, the child was moved to the general pediatric ward with improved hemoglobin (6.5 g/dL), haematocrit (20%), yellowish urine, and stable vital signs. The following six days were uneventful, with no fever and urine returning to a clear and transparent state (Figure 2). The child was called for follow up after twelve weeks post-discharge with G6PD enzyme level test, which revealed a level of 3.06 U/g Hb. The patient’s guardians were counselled about their child’s disease, future diet, precautions, and possible genetic transmissions. Discussion : The presence of clinical features such as pallor, icterus, and dark-colored urine, along with laboratory findings of rapidly increasing anemia (in the absence of bleeding) and indirect hyperbilirubinemia, indicate hemolysis. A dipstick positive for heme protein, with no RBCs and negative myoglobin, suggests hemoglobinuria. The presence of anemia, indirect bilirubin-predominant hyperbilirubinemia, markedly elevated LDH, and hemoglobinuria are suggestive of intravascular hemolysis.5,6,7 Additional features of hemolysis include decreased serum haptoglobin and increased reticulocyte count. Haptoglobin binds free hemoglobin released from lysed red blood cells, and its decline is a significant indicator of hemolysis.8 An elevated reticulocyte count reflects a bone marrow response to anemia, though in this case, the initial count was 1.1%, which is within the normal range. The peak reticulocyte response typically occurs 4-7 days after the insult, 9-11 explaining the initially normal count and subsequent increase of reticulocyte count in our case. Hemoglobin levels generally begin to recover 8 to 10 days after the offending agent is removed.9 Common clinical features of scrub typhus include fever, headache, myalgia, and often an eschar at the site of chigger bite. An eschar, a painless cutaneous necrosis up to 1 cm with a black center resembling a cigarette burn, is observed in 50-80% of cases and has high diagnostic value [4,12]. Laboratory diagnosis of scrub typhus can be done using various methods, including molecular assays, Indirect Immunofluorescence Assay (IFA), Immunochromatographic Tests (ICT), Weil-Felix test, and Enzyme-Linked Immunosorbent Assay (ELISA). IFA is considered the gold standard.13,14 An IgM density > 0.5 by ELISA also confirms the infection.1 In our case, rapid diagnostic serology kit was used for blood serum, which employs rapid immunochromatography to qualitatively detect IgM and IgG antibodies. This kit has demonstrated high reliability, with relative sensitivities and specificities for IgG and IgM antibodies of 95.45%, 96.81%, and 96.15%, 97.69%, respectively, compared with ELISA. After confirmation, for treating scrub typhus in young children, azithromycin is preferred over doxycycline due to its safety and better tolerability. 15-17 Tropical diseases, disseminated intravascular coagulation (via ISTH scoring), hemolytic uremic syndrome, and immune hemolysis as causes of acute extensive intravascular hemolysis were excluded based on laboratory findings. Heeding to medical literature and our clinical experience, only scrub typhus positive status was not convincing as the cause of this presentation. Furthermore, a normal G6PD level during an acute crisis does not rule out G6PD deficiency, as G6PD tests may be negative during or immediately after a hemolytic episode due to the destruction of old, G6PD-deficient red blood cells and the higher G6PD content in newly formed cells, which may yield falsely normal results.18 Suspecting this, the patient was advised for G6PD spectrometry, the gold standard for measuring G6PD activity19, three months after hospital discharge. The report showed a G6PD level of 3.06 U/gm Hb, while the normal laboratory reference range is 4.6-13.5 U/gm Hb and mild deficiency is defined as 2.76-4.5 U/gm Hb. This suggests that scrub typhus can precipitate an episode of extensive intravascular hemolysis in the patients of mild G6PD enzyme deficiency. Infections such as viral hepatitis, typhoid fever, pneumonia, and upper respiratory and gastrointestinal infections are known triggers for hemolytic episodes in individuals with G6PD deficiency.20 However, in this case, aside from the scrub typhus infection, no other potential triggers for hemolysis could be identified. Scrub typhus infection in human hosts with G6PD deficiency has a worse prognosis than healthy individuals.21,22 There is limited statistical data on the frequency of scrub typhus presenting with hemolytic anemia in patients with G6PD deficiency, possibly due to under-reporting of the cases and the disease being endemic to resource-limited settings where empirical antibiotic use is more common. We hope that this report will enhance awareness of the coexistence of these conditions in a single case. The distinctive features of scrub typhus, such as the presence of a typical skin eschar, specific clinical symptoms, and its occurrence in well-defined endemic areas, may not always present together in clinical practice. Therefore, scrub typhus should be considered in cases of unexplained fever in individuals from endemic and neighboring regions. Also, often overlooked tropical diseases such as scrub typhus should be considered as a differential diagnosis for infection-induced hemolysis in G6PD deficiency, so that clinical judgement and laboratory investigations can be used to diagnose and treat.