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Aspergillosis ofthe nose and paranasal sinuses is being recognised more and more, and it has been found that four forms of the infection occur each of which has its own distinct histopathological features. Allergic Aspergillus sinusitis and aspergilloma are benign saprophytic infections; invasive aspergillosis is a slowly progressive but destructive infection. Fulminant aspergillosis is a rapidly progressive infection which carries a high mortality and usually affects immunocompromised patients. The histological picture shows infiltrating Aspergillus hyphae with little inflammatory response. We describe here a patient in whom two forms of the disease could be identified concomitantly after a detailed investigation of the paranasal sinuses at necropsy using a special method. As an accurate histological diagnosis of the disease is important for its specific treatment we review the pathological features of the four types of aspergillosis.Case report A 49 year old Nigerian brewery controller was referred from Nigeria with a three month history of pronounced right proptosis, periorbital swelling, and nasal obstruction. He had lost 16 kg in weight over the preceding six months and had periods of confusion and unsteadiness. He was a non-insulin dependent diabetic, well controlled on chlorpropramide. He had hepatomegaly and a liver biopsy performed three years previously showed cirrhosis, although the exact histology was not known and was unavailable for review. Investigations showed an anaemia of 8-4 g/dl

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The encephalopathy resulting from direct infection of the brain by human immunodeficiency virus (HIV), which correlates clinically with the AIDS dementia complex, has been reported as being localized to the white matter where it induces myelin loss, gliosis and perivascular infiltration by mononuclear macrophages and multinucleated giant cells. Damage to the cortical grey matter in HIV encephalopathy was investigated in nine randomly selected HIV-positive cases with or without clinical or morphological evidence of encephalopathy and in five age-matched controls, using routine histology and immunohistochemical methods [glial fibrillary acidic protein (GFAP), microglia and HIV antibodies]. Increased numbers of GFAP-expressing astrocytes and Ricinus communis agglutinin 1-120-expressing microglial cells were found in all the HIV-positive cases (including asymptomatic) and their severity could be correlated with the severity of the encephalopathy in the white matter; the increase in number of cells expressing GFAP was diffuse and the intensity of the staining higher than that of microglial cells. The subpial region was the most severely involved. It is suggested that involvement of the cortical grey matter is more common in HIV infection than previously suspected and that clinical evidence of a dementing process in AIDS is not necessarily due only to white matter lesions.

Eight patients with AIDS and Pneumocystis carinii infection were studied. Protean manifestations were a feature not untypical of disseminated pneumocystosis. Aerosolised pentamidine as prophylaxis against P carinni pneumonia was ineffective at suppressing dissemination. The knowledge that extrapulmonary infection can occur has implications for the detection and treatment of, and prophylaxis against, P carinji infection. The survival of patients with disseminated pneumocystosis is particularly poor, and may be due to a lack of clinical awareness and consequent delay in diagnosis. A 26 year old homosexual man presented with severe abdominal pain. A chest x ray picture on admission showed bilateral pulmonary infiltrates suggestive of P carinii pneumonia. He had been found to be HIV antigen and antibody positive two years previously (November 1988). Mycobacterium malmoense had been isolated from sputum samples in June 1990 and at that time he had started quadruple anti-tuberculous treatment. He had developed an enlarged non-tender thyroid six weeks before admission and was found to be hypothyroid for which he was being treated with thyroxine. Auto-antibodies were not detected. He had received aerosolised pentamidine (300 mg fortnightly) as prophylaxis against P carinii pneumonia for six months. At laparotomy a perforation of the small bowel was found and repaired, but he died seven days later. CASE 32A 33 year old homosexual man presented with a history of weight loss, anorexia, dry cough, fever and night sweats. He had been found to be HIV-1 antibody positive three years previously and had developed P carinii pneumonia two years and again 10 months before admission. Since his first episode ofP carinii pneumonia he had been maintained on aerosolised pentamidine (300 mg fortnightly). He was feverish (39-4°C) and cachectic. His chest and abdomen were clinically normal, as were chest x ray picture and arterial blood gas analysis. Bronchoscopy

We report a case of a patient with a rapidly progressive dementing illness and gait disturbance, in whom initial screening demonstrated a high methylmalonic acid level only, suggestive of a functional vitamin B(12) deficiency. Despite B(12) replacement therapy, he continued to decline. Further investigations demonstrated extensive signal change on magnetic resonance imaging involving grey and white matter within the corpus callosum, deep grey matter, brainstem and cerebellar peduncles, and patchy post-contrast enhancement. Laboratory testing revealed a raised erythrocyte sedimentation rate, raised anti-nuclear, intrinsic factor and lupus anticoagulant antibody titres, and a IgG kappa paraprotein. Cerebrospinal fluid was unremarkable. Bone marrow trephine biopsy showed monoclonal gammopathy of unknown significance. The patient initially responded to steroids, and underwent a brain biopsy, which was uninformative. However, 3 weeks following admission, he died due to an aspiration pneumonia. Autopsy findings were consistent with a diffuse primary central nervous system small cell B-cell lymphoma. This has been rarely reported in the medical literature, but our case exhibits typical clinical features, although patchy enhancement on imaging and the high methylmalonic acid have not been previously described. We hypothesise that his functional B(12) deficiency may have resulted from rapid cell turnover, perhaps in conjunction with the presence of intrinsic factor antibodies.

Introduced into clinical practice in the 1960s, the analgesic fentanyl is 100 times more potent than morphine. Various methods of administration exist including the transdermal Duragesic patch system, widely used in chronic pain and palliative care settings. Numerous, often imaginative methods of abuse of fentanyl patches have been reported; the majority of fatal fentanyl overdose cases resulting from deliberate abuse or suicide. We describe the accidental overdose of a young black male with sickle cell/beta-thalassemia who had been using the Duragesic system for almost 2 years.At autopsy the macroscopic findings were of nonspecific opiate overdose with congested heavy lungs. Histopathological examination revealed severe sickling of red blood cells in the lungs (acute chest syndrome). Toxicological examination revealed blood and urine fentanyl levels of 40 microg/L and 400 microg/L (10 fold and 100 fold higher than therapeutic levels). The mast cell tryptase was also significantly elevated at 76 microg/L, (Normal 2-14 microg/L). We discuss the relevance of these findings with regard to the cause of death, and stress the need to consider fentanyl when confronted with nonspecific signs of opiate overdose as it is not detected in routine toxicological drug screens.