Acalculous cholecystitis occurring in the context of Plasmodium malariae infection: a case report.

INTRODUCTION: Acalculous cholecystitis has been shown to occur in the context of malarial infection with Plasmodium vivax and Plasmodium falciparum and requires prompt diagnosis and treatment to prevent complications. To the best of our knowledge this is the first reported case of the disease occurring in a patient infected with Plasmodium malariae. CASE PRESENTATION: We report the first case of acalculous cholecystitis associated with Plasmodium malariae in a 59-year-old male Nepalese ex-Gurkha soldier. He presented with fever and vomiting and later developed right upper quadrant pain. Abdominal ultrasound and computed tomography scans confirmed acalculous cholecystitis for which he was treated medically with chloroquine, gentamicin and metronidazole. He made a full recovery. CONCLUSIONS: Physicians should be aware that in addition to Plasmodium vivax and Plasmodium falciparum infections, acalculous cholecystitis can occur in the context of Plasmodium malariae infection. Mechanisms for this are discussed but further studies are needed to establish the etiology of this association.

Chronic Q fever: different serological results in three countries--results of a follow-up study 6 years after a point source outbreak.

BACKGROUND: Acute and chronic Q fever/Coxiella burnetii infection is diagnosed principally by serology. The management of patients who have serological evidence of chronic Q fever but no other manifestation of chronic infection is challenging. METHODS: This paper describes a follow-up study of individuals 6 years after a point source outbreak. The study compares serological and polymerase chain reaction (PCR) results between 3 international reference laboratories in a well-defined cohort of Q fever patients. RESULTS: Concordance in microimmunofluorescence result interpretation from the 3 centers was only 35%. Australian and UK results had the greatest concordance and French and UK results the lowest. Serological testing revealed no chronic serological profiles when tested in either France or Australia but 10 when tested in the UK. Serological results from a patient with treated Q fever endocarditis suggested treated (France), chronic (UK), and borderline chronic (Australia) infection. PCR results on blood were universally negative. CONCLUSIONS: This study has shown that the results from Q fever micro-immunofluorescence vary according to the center in which they are carried out. This has implications for the interpretation of such tests, raises questions regarding the validity of using serological criteria alone as a means of diagnosing chronic Q fever, and affects the interpretation of epidemiological studies. We recommend that all results are interpreted according to the clinical picture and particular caution is applied in the interpretation of chronic serological profiles. In order to further our understanding of Q fever infection we propose that an international standard of Q fever serological investigation be developed.

Chronic treatment with modafinil may not be beneficial in patients with chronic fatigue syndrome.

Fourteen patients (7 male, 7 female, 22-63 years), classified as having chronic fatigue syndrome (CFS), but without concurrent major depression, significant sleepiness or use of psychoactive medication, completed a double-blind, placebo-controlled, crossover study of the effects of the selective wakefulness-promoting agent, modafinil (200 and 400mg/day). The treatment periods were each 20 days, with washout periods of 2 weeks. The primary aim was to determine effects on cognition and the secondary aim was to determine effects on self-ratings of fatigue, quality of life and mood. Modafinil had mixed effects in two cognitive tasks. In a test of sustained attention, treatment with 200mg reduced the latency to correctly detect sequences, but 400mg increased the number of missed targets. In a test of spatial planning, the 200mg dose resulted in a slower initial thinking time for the easiest part of the task, whereas 400mg reduced the initial thinking time for the hardest part of the test. Lastly, in a test of mental flexibility and one of motor speed, patients performed worse whilst on modafinil (400mg), compared with the placebo period. No effects were observed on the performance of other psychometric tests or on self-ratings of fatigue, quality of life or mood, but this may have been due to insufficient statistical power. It is discussed whether the limited and mixed cognitive effects that we observed could have occurred by chance, or whether a subgroup of CFS patients with daytime sleepiness would have shown greater benefits.

Heterogeneity of serum tryptophan concentration and availability to the brain in patients with the chronic fatigue syndrome.

We assessed the serotonin status of patients with the chronic fatigue syndrome (CFS). Tryptophan (Trp) availability to the brain, expressed as the ratio of concentration of serum Trp to the sum of those of its five competitors (CAA), and other parameters of Trp disposition were compared in 23 patients with the CFS and 42 healthy controls. The serum [free Trp]/[CAA] ratio was 43% higher in CFS patients, due to a 48% higher [free Trp]. [Total Trp] was also significantly higher (by 19%) in CFS patients, and, although the [total Trp]/[CAA] ratio did not differ significantly between the control and patient groups, the difference became significant when the results were co-varied with age and gender. [CAA] was not significantly different between groups, but was significantly lower in females, compared to males, of the CFS patient group. We have established normal ranges for Trp disposition parameters and propose criteria for defining the serotonin-biosynthetic status in humans. We have provisionally identified two subgroups of CFS patients, one with normal serotonin and the other with a high serotonin status. The relevance of our findings to, and their implications for, the pharmacological and other therapies of the chronic fatigue syndrome are discussed.

A comparison of the sites at which pentazocine and morphine act to produce analgesia.

Sites in the brain stem at which microinjected morphine can produce analgesia have been investigated for sensitivity to microinjections of pentazocine, which has been proposed to act at receptors different to those mediating the effects of morphine. Microinjection of 10 micrograms of pentazocine into the periaqueductal grey matter (PAG), the nucleus reticularis gigantocellularis (NRGC) and nucleus reticularis paragigantocellularis (NRPG) produced analgesia as determined by the tail flick response to noxious heat. Microinjection of pentazocine into nucleus raphe magnus (NRM) did not produce any discernible change in the nociceptive threshold measured with the tail flick test. Using the pain pressure test, analgesia was observed following microinjections of pentazocine into NRGC and NRPG, but not following microinjections into PAG or NRM. Morphine (3 and 5 micrograms) microinjected into PAG, NRM, NRGC or NRPG produced analgesia as determined by both heat and pressure tests. The analgesia produced by injection of pentazocine into the NRGC or NRPG was comparable to the analgesia produced by microinjection of 3 micrograms of morphine into these areas. The analgesia produced by injection of pentazocine into PAG was significantly less than that produced by 3 micrograms of morphine injected into PAG. Pretreatment with naloxone did not affect the analgesia produced by microinjection of pentazocine into NRGC or NRPG, but did antagonize the analgesia produced by injection of pentazocine into PAG. Naloxone blocked the analgesic effects of microinjected morphine. Analgesia produced by systemically given pentazocine was significantly reduced following microinjection of naloxone into PAG or NRM but not into NRGC or NRPG. The present data provide further evidence that the effects of pentazocine, a kappa agonist drug may be mediated by mechanisms different to those mediating the action of morphine, a mu agonist.

The contribution of nucleus reticularis paragigantocellularis and nucleus raphe magnus to the analgesia produced by systemically administered morphine, investigated with the microinjection technique.

Intracerebral administration of morphine into either nucleus reticularis paragigantocellularis (NRPG) or nucleus raphe magnus (NRM) of rats produced analgesia, as measured by the tail flick test. NRPG was more sensitive to morphine and the effect was dose dependent. The narcotic antagonist naloxone blocked these analgesic effects of morphine. The effect of intracerebral injection of naloxone on the analgesia produced by systemically administered morphine was examined. Morphine was administered subcutaneously (2.86 mg/kg) and naloxone was microinjected 35 min later. Microinjection of 5 micrograms of naloxone into NRM was found to be more effective in reversing in analgesia produced by morphine than naloxone microinjected into more lateral sites, including NRPG. Lesions of NRPG did not attenuate the analgesia produced by systemically administered morphine, whereas lesions of NRM did attenuate this analgesia. The analgesia produced by morphine administered into NRPG was blocked by lesions of NRM. Cinanserin, a serotonergic blocker, blocked the effects of morphine microinjected into NRM but not effects of morphine injected into NRPG. Phenoxybenzamine partially blocked the effects of morphine injected into NRPG but not the effects of morphine injected into NRM. These results show that both nuclei are sensitive to morphine, exert their effects by different synaptic mechanisms and that NRPG does not make an appreciable contribution to the analgesia produced by systemically administered morphine.