Kyasanur forest disease: a state-of-the-art review.

Kyasanur forest disease (KFD) virus is a flavivirus that can be transmitted to humans from monkeys or other mammals through hard ticks (Haemaphysalis spinigera). The disease is endemic to 16 districts in 5 states of Southern India and is reported in the dry season, most commonly in humans travelling to the forests in these areas. The aim of this systematic review is to raise awareness of the clinical and laboratory manifestation of KFD among physicians and travel medicine practitioners. A total of 153 articles were screened of which 16 articles that met the inclusion and exclusion criteria were included for qualitative analysis. KFD is an acute haemorrhagic fever with a biphasic component in some individuals. The second phase is usually marked by neurological symptoms. Leucopoenia, thrombocytopenia and elevated transaminases are the hallmarks of the first phase of KFD. The diagnostic modality of choice in the first few days of illness is polymerase chain reaction assay, whereas serology is used in the late phase. In the absence of a specific antiviral treatment, the clinical management of patients is limited to supportive care. Avoidance of exposure and vaccination is recommended to prevent this infection.

TB disease patterns by HIV and diabetes status.

BACKGROUND: TB is commonly categorised as pulmonary (PTB) or extrapulmonary TB (EPTB). Knowledge of TB disease patterns (PTB and/or EPTB) and determining risk factors remains limited.METHODS: This was a prospective cohort study using point-of-care ultrasound (POCUS) in Indian patients with presumed TB. Clinical and imaging data were used to develop refined case definitions for PTB, concurrent PTB and EPTB (PTB + EPTB) and EPTB without PTB (EPTB). These groups were analysed by HIV (HIV+/-) and diabetes mellitus (DM+/-) status.RESULTS: Of 172 HIV-/DM- patients with TB, 48% had PTB, 23% PTB + EPTB and 29% had EPTB, totalling 52% with any EPTB (PTB + EPTB or EPTB). In HIV+/DM- patients with TB (n = 35), 6% had PTB, 40% had PTB + EPTB and 54% had EPTB, accounting for 94% with EPTB. In HIV-/DM+ patients with TB (n = 61), 61% had PTB, 28% had PTB + EPTB and 11% had EPTB, representing 39% with EPTB.CONCLUSION: Refined case definitions revealed high proportions of EPTB even without HIV or DM. HIV further altered the TB disease pattern towards EPTB and DM towards PTB. Therefore, the dichotomy between PTB or EPTB does not represent the actual spectrum of TB disease. EPTB should receive higher priority in research and clinical practice.

Thrombocytopenia in vivax and falciparum malaria: an observational study of 131 patients in Karnataka, India.

BACKGROUND: Thrombocytopenia has been reported in the majority of malaria studies. Some but not all studies suggest the possible role of platelets in the pathology of severe malaria. We assess the association of admission platelet count with malaria complications and mortality in vivax and falciparum malaria. METHODS: This is a prospective, observational study of patients aged 18 years and above admitted in a tertiary care teaching hospital from August 2004 to July 2006 in Manipal, India. Malaria was diagnosed based on clinical features along with positive Quantitative Buffy Coat method (QBC MP) or thin blood smear examination (Giemsa stain). Platelet counts were measured using Coulter LH 756 Analyser. Thrombocytopenia was defined as a platelet count <150×10(9)/l. RESULTS: A total of 131 consecutive patients were included. Sixty patients (46%) were infected with Plasmodium vivax and the rest with Plasmodium falciparum. Forty-six (35%) patients had non-severe and 24 (18%) had severe falciparum infection. The prevalence of thrombocytopenia was similar in vivax and falciparum malaria. Patients with severe falciparum malaria had a statistically significant lower platelet count (P = 0·01) compared to non-severe falciparum malaria. Severe malaria patients with renal failure (P = 0·02) or hyperparasitaemia (P = 0·03) had a statistically significant lower mean platelet count compared to non-severe falciparum malaria. Patients with involvement of more than one organ system had a lower mean platelet count compared to those with single organ involvement. CONCLUSIONS: The incidence of thrombocytopenia was similar in vivax and falciparum malaria. The admission platelet count is significantly lower in patients who have hyperparasitaemia and acute renal failure compared to patients without complications.

Melioidosis in southern India: epidemiological and clinical profile.

Melioidosis, which is mainly prevalent in Thailand and Australia, has shown an increasing trend in India in the last few years. We carried out a retrospective study of 25 culture-proven adult cases of melioidosis who were admitted to a tertiary care hospital in southern India during June 2001 to September 2007. There was a six-fold increase in the number of cases in 2006 and 2007 as compared to 2001. Diabetes mellitus was the predisposing factor in 68% of cases, followed by alcoholism (28%). The clinical presentations were fever (80%), pneumonia and/or pleural effusion (48%), hepatomegaly (56%), joint involvement, and/or osteomyelitis (48%), splenomegaly (40%), splenic abscess (24%) and septicemia (28%). The organism, Burkholderia pseudomallei, was sensitive to co-amoxiclav, cotrimoxazole, ceftazidime, and carbapenem. The study suggests that melioidosis is an emerging infectious disease in the southwestern coastal belt of India, and it is likely to happen at much higher incidence.

Immune thrombocytopenia secondary to tuberculosis: a case and review of literature.

Immune thrombocytopenia (ITP) is an auto-immune condition that results in isolated thrombocytopenia associated with possibly lethal haemorrhage. In its secondary form, ITP can be triggered by many infectious and non-infectious conditions. Secondary ITP associated with tuberculosis (TB) has rarely been described in the literature. We report on a 22-year-old patient presenting with hypermenorrhoea and petechiae due to ITP secondary to tuberculous lymphadenitis. Normalisation of thrombocytopenia was only achieved after initiation of anti-tuberculosis treatment following failure of thrombocyte substitution and immune-modulatory treatment. A search of the literature available on TB-associated ITP identified 50 cases published between 1964 and 2016. We reviewed all cases using suggested case definitions on the likelihood of association between ITP and TB. A broad spectrum of TB sites was reported to be associated with ITP, and anti-tuberculosis treatment was the most effective therapy for platelet count normalisation. Time from initiation of anti-tuberculosis treatment to platelet count recovery ranged from 2 days to 3 months. In endemic regions, TB should be considered as an underlying cause of ITP. Early diagnosis of TB and initiation of anti-tuberculosis treatment appears crucial for rapid platelet count recovery, and can reduce the risks associated with long-term immunosuppression, transfusions and the time at risk for haemorrhage.

Near-fatal amlodipine poisoning.

Amlodipine poisoning is very rare and only few cases have been reported in English literature. We report here a case of severe amlodipine poisoning with non-cardiogenic pulmonary edema.

Emphysematous pyelonephritis.

Emphysematous pyelonephritis is a rare life-threatening suppurative necrotising infection of the renal parenchyma and perirenal tissue producing abscess formation and intrarenal gas. It is almost always seen in diabetics, making it a concern of the physician. A high index of suspicion is required for diagnosis and a combined approach has significantly reduced the mortality.

Gerbode's defect--a rare type of ventricular septal defect.

We report on an elderly lady in the sixth decade of life with congenital Gerbode's defect who refused surgery. She has atrial fibrillation, massive cardiomegaly and repeated episodes of lower respiratory tract infection.

Recurrent pseudomonal pneumonia in a young immunocompetent adult - something fishy?

Community-acquired pneumonia due to Pseudomonas aeruginosa typically occurs in patients with pre-existing lung disease and immunocompromised individuals. We report the case of a previously healthy young adult who presented with recurrent episodes of pneumonia due to Pseudomonas aeruginosa complicated by pleural effusion. Careful and extensive evaluation ultimately revealed the unusual reason behind the patient's illness.

Pulmonary melioidosis in febrile neutropenia: the rare and deadly duet.

We present the first two fulminant cases of pulmonary melioidosis in febrile neutropenic patients with acute and varied presentations seen in our institution and their fatal outcome. A high index of suspicion coupled with microbiological confirmation can facilitate the administration of the appropriate therapy in cases of melioidosis that differ from other bacterial infections in terms of presentation and the response to antimicrobials.

False-positive widal in melioidosis.

Enteric fever is endemic in this part of the world, and Widal test is one of the time-honored laboratory tests that are being used for years to diagnose the disease. On the other hand, melioidosis is a newly emerging disease from this region, which is most often misdiagnosed or underdiagnosed by clinicians. It is well accepted that false-positive Widal reactions following certain non-typhoid Salmonella infections may occur commonly. Three cases of high titers of Widal test are described, where melioidosis was the actual diagnosis in every occasion and was never suspected until diagnosed microbiologically. All the patients had shown a partial response to ceftriaxone. Blood and pus cultures grew Burkholderia pseudomallei, whereas Salmonella typhi was not isolated from blood in any patient. With appropriate antibiotics, the patients showed clinical and microbiological improvement with lowering of Widal titers. These 3 cases show that high Widal titer in any patient may mislead the diagnosis of melioidosis, and further laboratory workup should always be done to rule out melioidosis, especially in cases with nonresponsiveness to treatment.

Drug use in porphyria: a therapeutic dilemma.

One of the most frequent precipitating factors for attacks of porphyria is the administration of drugs. Use of drugs with porphyrinogenic potential often worsens the condition and often poses a therapeutic dilemma. A 23-year-old female patient presented to the casualty room with abdominal pain, chest pain and vomiting. Her past medical history was significant with episodes of generalised abdominal pain. The patient was initially treated for her abdominal pain and vomiting. She developed seizures and was treated with diazepam and phenytoin. Based on the positive investigation reports (positive urine porphyrins, elevated urine ALA and positive porphobilinogen) and symptoms, a diagnosis of acute intermittent porphyria (AIP) was done. Before the diagnosis of AIP was made, the patient was treated with drugs which are not considered to be safe in porphyric patients, such as phenytoin, metoclopramide, and diclofenac. The use of these drugs probably contributed to the initial worsening of the patient's clinical condition. After the diagnosis of AIP was made, the patient was treated with safer alternatives; gabapentin as the antiepileptic agent, promethazine as antiemetic, and propanalol as the antihypertensive agent. Withdrawal of the unsafe agents and symptomatic management with the safer alternatives contributed to the recovery of the patient. Along with the case report and the observations made on the various drugs used in the patient, the importance of the various information sources available on the safety potential of these agents is discussed. The observations with the drugs used in our case will be a useful addition to the existing information on the safety of these agents.