Typhoid fever is endemic across sub-Saharan Africa. However, estimates of the burden of typhoid are undermined by insufficient blood volumes and lack of sensitivity of blood culture. Here, we aimed to address this limitation by exploiting pre-enrichment culture followed by PCR, alongside routine blood culture to improve typhoid case detection. We carried out a prospective diagnostic cohort study and enrolled children (aged 0–4 years) with non-specific febrile disease admitted to a tertiary hospital in Blantyre, Malawi from August 2014 to July 2016. Blood was collected for culture (BC) and real-time PCR after a pre-enrichment culture in tryptone soy broth and ox-bile. DNA was subjected to PCR for invA (Pan- Salmonella ), staG ( S . Typhi), and fliC ( S . Typhimurium) genes. A positive PCR was defined as invA plus either staG or fliC (CT<29). IgM and IgG ELISA against four S . Typhi antigens was also performed. In total, 643 children (median age 1.3 years) with nonspecific febrile disease were enrolled; 31 (4.8%) were BC positive for Salmonella (n = 13 S . Typhi, n = 16 S . Typhimurium, and n = 2 S . Enteritidis). Pre-enrichment culture of blood followed by PCR identified a further 8 S . Typhi and 15 S . Typhimurium positive children. IgM and IgG titres to the S. Typhi antigen STY1498 (haemolysin) were significantly higher in children that were PCR positive but blood culture negative compared to febrile children with all other non-typhoid illnesses. The addition of pre-enrichment culture and PCR increased the case ascertainment of invasive Salmonella disease in children by 62–94%. These data support recent burden estimates that highlight the insensitivity of blood cultures and support the targeting of pre-school children for typhoid vaccine prevention in Africa. Blood culture with real-time PCR following pre-enrichment should be used to further refine estimates of vaccine effectiveness in typhoid vaccine trials.
Context: Primary hyperparathyroidism (PHPT) is commonly associated with reduced bone mineral density (BMD) presenting with osteoporosis, increasing the risk of bone fragility fractures in these patients. Bisphosphonates, due to their anti-resorptive action, are known to improve the BMD and reduce the risk of bone fragility fractures. Therefore, bisphosphonates are considered as an alternative to surgical treatment in managing osteoporosis in PHPT patients. Aim: The aim of this observational study was to assess the effect of long term bisphosphonate therapy on BMD, bone fragility fracture and biochemical markers of bone metabolism in patients with PHPT. Methodology: Fifty patients (mean age 74 years) with PHPT who were treated with long term bisphosphonate therapy were studied retrospectively. The mean baseline (before commencing bisphosphonate therapy) BMD T-scores for lumbar spine (L2-L4) and left femoral neck were −2.5 and −2.1, respectively. Fourteen patients had bone fragility fractures before initiation of bisphosphonate therapy. Results: After an average of 5 years of bisphosphonate treatment, there was a significant increase in lumbar BMD T-score (−2.5 to −2.1, p = 0.013) and a non-significant change in left femoral neck BMD T-score (−2.1 to −2.2, p = 0.497). There was no increase in bone fragility fracture rate (p = 0.167). Serum corrected calcium reduced from 2.74 mmol/L to 2.60 mmol/L (p < 0.001) and urine calcium to creatinine ratio from 0.70 to 0.55 (p < 0.0001), both within the reference range. Conclusions: Our study suggests that long term bisphosphonate therapy improves lumbar BMD and prevents increase in bone fragility fracture rate. Additionally it improves hypercalcaemia in PHPT.
BackgroundAs control interventions are rolled out, the burden of malaria may shift from young children to older children and adults as acquisition of immunity is slowed and persistence of immunity is short-lived. Data for malaria disease in adults are difficult to obtain because of co-morbid conditions and because parasitaemia may be asymptomatic. Regular surveys of adult admissions to a hospital in Malawi were conducted to characterize the clinical spectrum of malaria and to establish a baseline to monitor changes that occur in future.MethodsIn 2011–2012, at Queen Elizabeth Hospital, Blantyre, four separated one-week surveys in the peak malaria transmission period (wet season) and three one-week surveys in the low transmission period (dry season) were conducted using rapid diagnostic tests (RDT) with confirmation of parasitaemia by microscopy. All adults (aged ≥15) being admitted to the adult medical wards regardless of the suspected diagnosis, were enrolled. Participants with a positive malaria test underwent a standardized physical examination and laboratory tests. Malaria syndromes were characterized by reviewing charts and laboratory results on discharge.Results765 adult admissions were screened. 63 (8.2%) were RDT-positive with 61 (8.0%) positive by microscopy. Over the course of the seven study weeks, two patients were judged to have incidental parasitaemia, 31 (4.1%) had uncomplicated malaria and 28 (3.7%) had severe malaria. Both uncomplicated and severe malaria cases were more common in the rainy season than the dry season. Prostration (22/28 cases) and hyperparasitaemia (>250,000 parasites/μl) (9/28) were the most common features of severe malaria. Jaundice (4/28), severe anaemia (2/28), hyperlactataemia (2/28), shock (1/28) and haemoglobinuria (1/28) were less commonly seen, and no patient had severe metabolic derangement or organ failure. There were no deaths attributable to malaria.ConclusionIn this study of adults admitted to hospital in southern Malawi, an area with year-round transmission of Plasmodium falciparum, classical metabolic and organ complications of malaria were not encountered. Prostration and hyperparasitaemia were more common indicators of severity in patients admitted with malaria, none of whom died. These data will provide a baseline for monitoring trends in the frequency and clinical patterns of severe malaria in adults.
MalawiOn the 23rd of January 2011, we admitted a 46-year-old man to Queen Elizabeth Central Hospital (QECH) with a 5-month history of recurrent vomiting. This was associated with nausea. He would vomit at least 5 times per day. The vomitus was non-projectile, would usually take the colour of the food eaten and was never bilious. There was no history of abdominal pain, dysphagia, fever or headache. The colour of stools was normal but he had complained of constipation for 6 days prior to admission. He also admitted to weight loss, which could not be quantified. Prior to attending QECH he had been seen in several health facilities and had been treated with promethazine, but had had no relief of his symptoms. An endoscopy done at another hospital was documented as follows: 'endoscopy shows reflux oesophagitis and lax lower oesophageal sphincter' There was no comment on whether there were structural abnormalities at the level of the pylorus or duodenum. He had been diagnosed with type 2 diabetes mellitus in December 2010 on the basis of high random blood glucose readings. He had been prescribed glibenclamide but stopped as he felt it was making him vomit more, and was now only taking metformin. Blood glucose measurements since the start of treatment were not available so we do not know how well the diabetes had been controlled. He had a history of moderate alcohol consumption (< 20 units per week) but had not taken alcohol since the symptoms started. He had no history of smoking. He was HIV negative. He used to work as a foreman for a construction company but had stopped work owing to the severity of his symptoms. He was married with 3 children. There was no family history of diabetes. On examination, he was moderately cachexic and dehydrated. His blood pressure (BP) was 130/80 mmHg, temperature 37oC, pulse 92/minute, respiratory rate 28/minute. His conjunctivae were pink, there were no oral lesions and he had no lymphadenopathy, including Virchow's node. Chest examination was normal. Abdominal examination was normal except there were hard stools in the rectum. His fundoscopy showed dot and blot haemorrhages, consistent with background diabetic retinopathy. His random blood glucose concentration was 252mg/dl and there were no ketones in his urine. Blood potassium and sodium were 3.1 mmol/L (3.6 -5.0) and 127 mmol/L (135 -145) respectively. He had a normal blood creatinine and no proteinuria. Discussion 1) Causes of vomiting can be divided into gastrointestinal causes, central causes and metabolic causes. In this case the causes of vomiting that should be considered include gastrointestinal causes such as achalasia, gastric malignancy, pyloric stenosis, gastric or duodenal ulcer, gastroparesis and generalized motility disorders such as intestinal myopathies and neuropathies. Central causes include migraine, cyclical vomiting, psychogenic vomiting, space occupying lesions and labyrinthitis. Metabolic causes such as drugs, hypercalcaemia and hyponatraemia should also be considered. 2)A careful history and examination ar...
We assessed the effect of fluconazole 1200 mg/day on the QT interval in cryptococcal meningitis patients. Mean corrected QT (QTc) change from baseline to day 7 was 10.1 ms (IQR: −28 to 46 ms) in the fluconazole treatment group and −12.6 ms (IQR: −39 to 13.5 ms) in those not taking fluconazole (P = 0.04). No significant increase in QTc measurements over 500 ms was observed with fluconazole. Nevertheless, it remains important to correct any electrolyte imbalance and avoid concomitant drugs that may increase QTc.
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