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BACKGROUND:Bone marrow examination is the gold standard test in determining the cause of thrombocytopenia; whether it is of hypoproductive or hyperdestructive nature. However, this process has distinct disadvantages such as being invasive, not feasible in critical situations and is often not preferred by clinicians and patients alike. The introduction of platelet indices in automated hematology analyzers has provided a small window into the cause of thrombocytopenias in the recent years. Mean platelet volume (MPV) has evoked much interest in this regard. This study aimed at assessing the predictive value of MPV in determining the aetiology of thrombocytopenia. MATERIALS AND METHODS:We analyzed 100 cases of thrombocytopenia (platelet count < 100x10 3 / cu.mm) on a retrospective basis for a period of one month. The cases were divided into 2 groups: with and without bone marrow diseases; based on individual pathophysiology. A statistical analysis was done to assess predictive values, odds ratio and confidence intervals and also to elicit a cut-off value for MPV. RESULTS: The mean MPV in the group with marrow disease was 8.95fl while the group without marrow disease was 9.42fl. The difference in MPV between the 2 groups was not statistically significant (P value: 0.088). The sensitivity and specificity scores as tabulated by the receptor operating characteristic (ROC) curve at a cut-off of 9.35fl were 69% and 55% respectively. CONCLUSIONS: The study concluded that although MPV may provide a small initial insight into the aetiology of thrombocytopenia, it is limited by insufficient sensitivity and specificity. A bone marrow examination continues to be the gold standard to differentiate the hypoproductive and hyperdestructive thrombocytopenias.

A 30-year-old manual laborer from Karnataka, India presented with intermittent low grade fever and diffuse headache for 1 month. On examination, patient had enlarged supraclavicular and cervical lymph nodes. Patient had positive Kernig's sign and neck stiffness. Motor, sensory and cranial nerve examinations were within the normal limits. Abdominal, cardiovascular and chest examination did not yield any positive findings. Contrast enhanced computed tomography head was normal. Patient was suspected to have extrapulmonary tuberculosis. Patient was started on antitubercular drugs. Diagnostic lumbar puncture was performed. Wet mount and Giemsa smear preparation of cerebrospinal fluid (CSF) showed trophozoites suggestive of Acanthamoeba. CSF was cultured onto non-nutrient agar with an overlay of Escherichia coli. Wet mount made from the culture media yielded cysts and trophozoites of Acanthamoeba spp. Patient was diagnosed with Acanthamoeba meningitis and was started on specific therapy with Rifampicin 600 mg once a day, Cotrimoxazole 960 mg twice-a-day and Fluconazole 400 mg once daily for 2 weeks. Patient had a complete recovery and was discharged from the hospital.

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Primary amoebic meningoencephalitis (PAM) caused by free-living amebae Naegleria fowleri is a rare and fatal condition. A fatal case of primary amoebic meningoencephalitis was diagnosed in a 5-month-old infant who presented with the history of decrease breast feeding, fever, vomiting, and abnormal body movements. Trophozoites of Naegleria fowleri were detected in the direct microscopic examination of CSF and infant was put on amphotericin B and ceftazidime. Patient condition deteriorated, and he was discharged against medical advice and subsequently expired. We also reviewed previously reported 8 Indian cases of primary amoebic meningoencephalitis (PAM) and observed that for the last 5 years, none of the patients responded to amphotericin B. Has an era of amphotericin B-resistant Naegleria fowleri been emerged? Management strategy of PAM needs to be reviewed further.

Background:Stool microscopy and concentration techniques are the two most important and necessary aspects of diagnostic parasitology. In an era when there is increased disease burden due to intestinal parasites, an early and appropriate diagnosis is warranted. Direct microscopy is usually labor intensive and tedious.Materials and Methods:Thirty-two fresh fecal specimens from patients presenting with eosinophilia and/or anemia (hemoglobin levels <10 g%), HIV-positive patients, and in patients clinically suspected of harboring parasites, were collected for the study. All the positive samples were processed by both the standard methodology, i.e., formalin-ethyl acetate sedimentation technique and Mini Parasep® SF method, by the standard operating procedure of our laboratory and the manufacturer's instruction. Stool pellet concentrates were subjected to saline/iodine wet mount, modified acid fast staining for intestinal coccidian parasites and trichrome staining for Blastocystis hominis. The average number of organisms counted in 0.5 ml of pellet was used for comparison of the two techniques.Results:The morphology of eggs was maintained in both the techniques; however, the wet mount prepared from the sedimentation technique had more background fecal debris in comparison to the Parasep® technique. The parasite yield was equal for both the techniques while Mini parasep had the advantage of less distortion of parasite morphology.Conclusion:We found that Parasep® offered a better parasitic yield, a better workflow capacity, and a reduced turnaround time, which would further benefit resource-restrained laboratories and those with a high sample turnover.

A 52-year-old male patient, who was a known case of retroviral illness since eight years and an old case of pulmonary tuberculosis treated eight years ago, was admitted with a chief complaint of easy fatigability for three weeks duration. The patient complained of tiredness and fatigability present throughout the day. This was associated with a decrease in appetite and occasional dysphagia. The patient also complained of retrosternal chest pain present intermittently throughout the day. There was no associated history of fever, breathlessness, palpitations or abdominal pain.On examination, the patient's vital signs were stable. There was conjunctival pallor and no lymphadenopathy. The rest of general physical examination was normal. Systemic examination of all systems was unremarkable. Blood investigations revealed a haemoglobin of 7.2 g/dl, platelet count of 259,000 cells/ml, total leucocyte count of 5100 cells/ml, ESR of 101 mm/hour, serum urea of 34 mg/dl, serum creatinine of 1.0 mg/dl, serum sodium of 136 mmol/l and serum potassium of 4.1 mmol/l. Peripheral smear showed normocytic normochromic anaemia and red blood cells with anisocytosis, polychromasia and occasional spherocytes. Total bilirubin was 0.2 mg/dl, direct bilirubin was 0.1 mg/dl, aspartate aminotransferase was 37 IU/ml, alanine transaminase was 34 IU/ml, alkaline phosphatase was 98 IU/ml, serum albumin was 3 gm/dl and serum globulin was 5 gm/dl. Serum lactate dehydrogenase levels were elevated (417 U/l). Serum iron, total iron binding capacity and vitamin B12 levels were found to be normal. Antinuclear Antibody (ANA) and ANA profile were negative. Stool routine and microscopy was negative for opportunistic organisms (e.g., Crytosporidia, Isospora, etc.,) and occult blood.

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