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Biomedical subjects

D L Paterson

Publications and source records attributed to D L Paterson.

At least 55 records · Page 3Linked to original sources

Infective endocarditis in solid organ transplant recipients.

Infective endocarditis, defined as pathologically or clinically definite by the Duke criteria, was observed in 14 transplant recipients at our institutions. In addition, we reviewed 32 previously reported cases in solid organ transplant recipients. The spectrum of organisms causing infective endocarditis was clearly different in transplant recipients than in the general population; 50% of the infections were due to Aspergillus fumigatus or Staphylococcus aureus, but only 4% were due to viridans streptococci. Fungal infections predominated early (accounting for six of 10 cases of endocarditis within 30 days of transplantation), while bacterial infections caused most cases (80%) after this time. In 80% (37) of the 46 cases in transplant recipients, there was no underlying valvular disease. Seventy-four percent (34) of the 46 cases were associated with previous hospital-acquired infection, notably venous access device and wound infections. Three patients with S. aureus endocarditis had had an episode of S. aureus bacteremia > 3 weeks prior to the diagnosis of endocarditis and had received treatment for the initial bacteremia of < 14 days' duration. The overall mortality rate was 57% (26 of 46 patients died), with 58% (15) of the 26 fatal cases not being suspected during life. Endocarditis is an underappreciated sequela of hospital-acquired infection in transplant recipients.

Adult↗

Zoonotic disease in Australia caused by a novel member of the paramyxoviridae.

Twenty-three horses and three humans in Queensland, Australia, were infected with a novel member of the Paramyxoviridae family of viruses in two geographically distinct outbreaks. Two of the humans died-one died of rapid-onset respiratory illness, and the other died of encephalitis. The third infected human developed an influenza-like illness and made a complete recovery. All infected humans had close contact with sick horses. Since the two outbreaks occurred at sites 1,000 km apart and no known contact between the two groups of humans and horses occurred, extensive testing of animals and birds common to the two areas was conducted. Fruit bats (Pteropus species) were found to carry a virus identical to that found in the infected humans and horses. Although there was no contact between the infected humans and the bats, some form of close contact between the horses and bats is the likely mode of infection.

Adult↗

Mycobacterium tuberculosis infection in solid-organ transplant recipients: impact and implications for management.

Tuberculosis is a serious opportunistic infection in transplant recipients. On the basis of the compilation of published reports in the literature, the incidence of Mycobacterium tuberculosis infection in organ transplant recipients worldwide ranged from 0.35% to 15%. Nonrenal transplantation (P = .004), rejection within 6 months before the onset of tuberculosis (P = .02) and type of primary immunosuppressive regimen (P = .007) were predictors of M. tuberculosis infection occurring within 12 months after transplantation. Thirty-three percent (155) of 476 transplant patients with tuberculosis had disseminated infection; receipt of OKT3 or anti-T cell antibodies (P = .005) was a significant predictor of disseminated tuberculosis. Overall, the mortality rate among 499 patients was 29%; disseminated infection (P = .0003), prior rejection (P = .006), and receipt of OKT3 or anti-T cell antibodies (P = .0013) were significant predictors of mortality in patients with tuberculosis. Clinically significant hepatotoxicity due to isoniazid occurred in 2.5%, 4.5%, and 41% of renal, heart and lung, and liver transplant recipients, respectively. The diagnosis and effective management of tuberculosis after transplantation warrant recognition of the unique epidemiological and clinical characteristics of tuberculosis in transplant recipients.

Adolescent↗

Disseminated donovanosis (granuloma inguinale) causing spinal cord compression: case report and review of donovanosis involving bone.

Donovanosis is a genital ulcer disease that occasionally has extragenital manifestations. This report describes a case of disseminated donovanosis in a 54-year-old woman from northern Australia who had subsequent thoracic vertebral osteomyelitis and spinal cord compression. Malignancy and vertebral tuberculosis were the major differential diagnoses. The patient had no genital lesions at the time of diagnosis of extragenital donovanosis but had undergone a hysterectomy, thus raising the possibility of prior disease of the uterine cervix (most previous cases have been associated with primary cervical disease). Despite treatment with doxycycline, she had no significant neurological improvement. Donovanosis disseminated to bone has been reported in 18 cases in the last 55 years. Awareness of donovanosis in the differential diagnosis of osteomyelitis and prompt pelvic examinations enabling early diagnosis of occult cervical disease are the most important measures in preventing morbidity and mortality due to disseminated donovanosis.

Bone Diseases↗

Pulmonary nodules in liver transplant recipients.

Pulmonary nodules present a diagnostic dilemma in liver transplant recipients because of the broad differential diagnosis involved. Eleven of 155 (7.1%) liver transplant recipients at the Veterans Affairs Medical Center, Pittsburgh, developed pulmonary nodules. The underlying etiology included aspergillosis (3 cases), cryptococcosis (2), metastatic hepatocellular carcinoma (1), posttransplant lymphoproliferative disorder (1), Staphylococcus aureus (1), squamous cell carcinoma (1), adenocarcinoma of unknown primary site (1), and undifferentiated carcinoma (1). A review of the literature revealed 22 other liver transplant recipients with pulmonary nodules. There appears to be a definite relationship between time since transplantation and etiology of the nodule. Aspergillosis and bacterial infections appear early (within the first month), whereas nocardiosis, coccidiomycosis, tuberculosis, and cryptococcosis occur from 3 to 24 months posttransplantation. Metastatic hepatocellular carcinoma is a relatively common cause of pulmonary nodule and appears from 2 months to 2 years posttransplantation. Detection of skin lesions (indicating nocardiosis or cryptococcosis) and positive serologic tests may further narrow the diagnosis. However, radiographic appearances of nodules of differing etiology are relatively nonspecific, necessitating biopsy in virtually all cases.

Adult↗

Bacillus Calmette-Guerin (BCG) immunotherapy for bladder cancer: review of complications and their treatment.

BACKGROUND: Intravesical bacillus Calmette-Guerin (BCG) is widely used in the management of bladder cancer but because it is a living organism, local and disseminated infection may result. METHODS: A prospective assessment of complications of this therapy in 200 patients in Queensland was performed. A review of management of complications of intravesical BCG was also carried out. RESULTS: Major side effects were rare. Cystitis was the most common side effect, being seen to some degree in all patients, although only forcing cessation of BCG therapy in two patients. Two patients developed persistent cystitis necessitating institution of isoniazid and rifampicin. Two patients had culture-proven bladder infection that presented several months after the BCG treatment. These patients also responded to two-drug antituberculous therapy. While low-grade fever is very common with this therapy, seven patients (3.5%) had fevers of > 39 degrees C within 48 h of receiving BCG. Fevers may be an indication of severe disseminated mycobacterial infection, which has a high mortality, so it needs to be treated aggressively. Alternatively bacterial sepsis with gram-negative bacterial pathogens or a hypersensitivity reaction to BCG may cause this degree of fever, and cannot be rapidly distinguished from fulminant mycobacterial infection. One patient in the present series developed pneumonia attributed to mycobacterial dissemination. CONCLUSIONS: The key to appropriate management of complications of BCG therapy is awareness of their possibility, even months or years after the therapy has been given. Appropriate empirical therapy in acute situations and mycobacterial culture in chronic situations can then be performed.

Administration, Intravesical↗

Invasive aspergillosis in liver transplant recipients in the 1990s.

Invasive aspergillosis occurred in 26 liver transplant recipients since 1990 at five liver transplant centers. The median time to onset was 17 days after transplantation. Twenty-seven percent of the patients had undergone retransplantation. Invasive aspergillosis occurred significantly earlier after transplantation in smokers than in nonsmokers (P=0.017). Patients with late-onset aspergillosis (occurring after posttransplant day 90) were more likely to have had prior cytomegalovirus infection than those with early-onset aspergillosis (occurring within 90 days of transplantation) (67% vs. 10%, respectively, P=0.013). Only 8% of the patients had received additional corticosteroids or OKT3, which suggests that augmented immunosuppression may not be a relevant risk factor for invasive aspergillosis in the 1990s due to less frequent use of these agents. The median serum bilirubin level of the patients was 21.8 mg/dl, 85% of the patients had renal insufficiency, and 54% were on dialysis before the onset of invasive aspergillosis, which suggest that overall severity of illness, including poorly functioning hepatic allograft and renal failure may be the major determinants of disease occurrence. Overall mortality was 92% (24/26). No difference in mortality could be shown for the patients who received amphotericin B versus liposomal amphotericin B preparations (100% vs. 89%); however, the mean time to death after the initiation of therapy was 20 days in patients who received amphotericin B and 43 days in those who received liposomal amphotericin B preparations.

Adolescent↗

Fatal encephalitis due to novel paramyxovirus transmitted from horses.

BACKGROUND: In September, 1994, an outbreak of severe respiratory disease affected 18 horses, their trainer, and a stablehand in Queensland, Australia. Fourteen horses and one human being died. A novel virus was isolated from those affected and named equine morbillivirus (EMV). We report a case of encephalitis caused by this virus. FINDINGS: A 35-year-old man from Queensland had a brief aseptic meningitic illness in August, 1994, shortly after caring for two horses that died from EMV infection and then assisting at their necropsies. He then suffered severe encephalitis 13 months later, characterised by uncontrolled focal and generalised epileptic activity. Rising titres of neutralising antibodies to EMV in the patient's serum at the time of the second illness suggested an anamnestic response. Distinctive cortical changes were shown on magnetic resonance neuroimaging and histopathological examination of the brain at necropsy. Immunohistochemistry and electronmicroscopy of brain tissue revealed pathology characteristic of the earlier cases of EMV infection. PCR on cerebrospinal fluid taken during the second illness, brain tissue, and serum retained from the original illness resulted in an amplified product identical to that previously described from EMV. INTERPRETATION: The results of serology, PCR, electronmicroscopy, and immunohistochemistry strongly suggest that EMV was the cause of this patient's encephalitis, and that exposure to the virus occurred 3 months before the fatal illness.

Adult↗

Interactions between tacrolimus and antimicrobial agents.

Tacrolimus is being increasingly used as an immunosuppressive agent in transplant recipients. The drug is metabolized by the cytochrome P-450 3A system, thus antimicrobials that inhibit or induce these enzymes can alter levels of tacrolimus in the bloodstream. Tacrolimus is potentially nephrotoxic and neurotoxic; the likelihood of toxicity rises as blood levels of the drug increase. Increased tacrolimus levels and subsequent toxicity have been produced by a number of antimicrobial agents that inhibit the cytochrome P-450 3A system. Conversely, drugs with the potential to induce the cytochrome P-450 3A system can reduce the levels of tacrolimus in the blood, leading to increased risk of acute rejection in transplant recipients. Antimicrobial agents that can have adverse effects on renal function may add to the nephrotoxicity of tacrolimus. The potential for drug interactions should be reviewed before antimicrobial agents are prescribed to patients treated with tacrolimus.

4-Quinolones↗