Biomedical subjects
Publications and source records attributed to R Khatib.
An outbreak of gastroenteritis at a large teaching hospital affected at least 52 workers. Investigation implicated a tuna salad, and the circumstances suggested Clostridium perfringens as the etiologic agent. The risk of such outbreaks may be reduced by cooling of ingredients prior to mixing and refrigeration in small steel containers.
Coxsackievirus B (CB) 4 causes transmural myocarditis in suckling mice with ensuing development of focal ventricular thinning or aneurysms. We studied whether subsequent infection with another cardiotropic virus influences the expression of CB4 disease. CB4 infection was established in 2-day-old CD1 mice by intraperitoneal (IP) inoculation. Three weeks later, surviving animals were randomized to receive CB3 or saline IP. They were then killed over a 45-day period. CB4 neutralizing antibody (NA) titres were comparable in both groups (31 +/- 23 vs 37 +/- 19). CB3 NA were detected in CB3 infected animals only (72 +/- 86 versus 0). The incidence of myocarditis was comparable (67.4% vs 55.2%). The indices of histopathological changes (assessed according to a semiquantitative grading scale from 0-4) were greater among CB3 recipients on day 9 post CB3 challenge (1.38 +/- 0.43 vs 0.46 +/- 0.4, P < 0.001) and to a lesser extent, on day 13 (0.56 +/- 0.56 vs 0.19 +/- 0.38, P > 0.1). On days 30, and 45, these indices became similar in both groups. Focal thinning was noted on days 45 in 6/11 animals with CB4 infection alone and in 0/11 mice with subsequent CB3 infection (P = 0.006). These findings show that CB3 myocarditis can be expressed in mice with prior CB4 disease, that sequential infections do not lead to cumulative cardiac injury, and that subsequent CB3 infection suppresses the formation of CB4 induced ventricular aneurysms.
Candida albicans meningitis developed in a 55-year-old diabetic female, 1 year after catheter-associated candidemia. It was characterized by a protracted course, lack of meningeal signs, and the presence of an intradural filling defect within the caudal canal. Complete resolution of this filling defect with antifungal therapy implies that it probably represented an inflammatory mass. The development of meningitis after self-limiting candidemia and similar intradural filling defects have not been reported previously.
All consecutive patients with positive blood culture for Candida species over a 6-year period were evaluated to define recent epidemiologic characteristics of candidemia, and to assess the prevalence of late complications. We encountered 106 cases; medical records were available for 99 of them. The rate of candidemia was increasing until 1990, after which it declined. C. albicans was the most common species, but in the last 2 years, C. tropicalis and C. parapsilosis were emerging. Overall mortality rate was 54.5% without significant variation during the study period. Antifungal therapy was withheld in 24/99 cases (24.2%). Decision to withhold treatment was taken in 19/59 cases (32.2%) before the availability of fluconazole in 1990, compared with 5/40 cases (12.5%) afterward (p < 0.05). Follow-up was possible in 35 instances for an average period of 17.1 months (range: 1-48 months); 7 of these individuals, all with transient candidemia, were untreated. None of the survivors developed late complications. These findings demonstrate that candidemia appears to be declining since 1990, with a noticeable decrease in the prevalence of C. albicans but an increase in that of C. tropicalis and C. parapsilosis, that fewer patients are left untreated since fluconazole became available, and that the risk of late complications among the survivors is low.
A case of multifocal cystic tuberculosis is presented, affecting the clavicle and the iliac bones with considerable soft tissue involvement. It was found in a 34-year-old male, an immigrant from Yemen. The extensive cystic nature of both lesions and the lack of systemic manifestations despite multifocal disease are unusual.
During the period 1982-1990, 544 patients with clinical evidence of liver disease were admitted to King Fahd University Hospital, Al-Khobar, Saudi Arabia. Besides routine laboratory and sonographic investigations, all were subjected to either a needle liver biopsy, laparoscopy or a laparotomy. The tissue diagnoses were as follows: liver cirrhosis 17.3%, periportal fibrosis 14.3%, metastatic cancer 12.9%, primary hepatoma (hepatocellular carcinoma: HCC) 12.1%, hepatic granuloma 11.2%, chronic active hepatitis 7.7%, chronic persistent hepatitis 2.2%, fatty liver 7.2%, hydatid liver disease 4.6% and others 2.8%. In 7.7% the histology was normal. These results will be discussed and compared with results reported in local and international literature.
An 81-year-old man, previously a shepherd in Italy, presented with recurrent Escherichia coli empyema over an 8-month period. His empyema was caused by an infected, nonviable hepatic Echinococcus cyst that eroded the diaphragm and led to intermittent spillage and pleural seeding. This case demonstrates that when dealing with Escherichia coli empyema, a subdiaphragmatic source ought to be suspected, and among immigrants from areas with prevalent hydatid disease, infected hepatic Echinococcus cyst might rarely be the cause.
OBJECTIVES: To define the clinical characteristics of acyclovir neurotoxicity and to outline how to distinguish it from viral encephalitis. DESIGN: Case series of acyclovir neurotoxicity. SETTING: All cases reported in Index Medicus or in bibliographic reviews of acyclovir neurotoxicity plus two representative studies of Varicella zoster and Herpes simplex virus encephalitis. SUBJECTS: Thirty-five patients who developed neuropsychiatric symptoms during acyclovir therapy. INTERVENTIONS: Analysis of the patients' demographics, risk factors, acyclovir dosages and duration, clinical and laboratory findings and outcome. MAIN OUTCOME MEASURES: All clinical and laboratory findings that were statistically significantly different from viral encephalitis. RESULTS: The median age was 53.3 years. The most common predisposing factors were the use of other potentially neurotoxic medications (17 cases) and acute or chronic renal failure (15 cases). Acyclovir levels were frequently found above the therapeutic range. The characteristic manifestations were confusion (15 cases), hallucination or delirium (9 cases), agitation (8 cases) and lethargy (10 cases). Few patients had associated tremors (11 cases). Fever, headache, seizures and focal neurologic findings were distinctly rare. Cerebrospinal fluid and computed tomography were normal except in patients with other central nervous system disorders. Symptoms appeared within 2 days of therapy in the majority and resolved completely within several days of discontinuing acyclovir. CONCLUSIONS: Acyclovir neurotoxicity is a self-limiting, dose-dependent phenomenon which is more common in the elderly, in patients with renal failure or in association with other neurotoxic medications. It is distinguished from viral encephalitis by its sudden onset, absence of fever or headache, lack of focal neurologic findings and normal cerebrospinal fluid.
OBJECTIVE: To assess the expression of coxsackievirus B3 (CB3) myocarditis in mice with pre-existing CB4 myocardial disease. DESIGN: Double blind comparative study of CB3 myocarditis in CD1 mice with or without prior CB4 induced cardiac damage. INTERVENTIONS: Antecedent myocardial injury was produced by CB4 infection intraperitoneally at age two days. Two to three weeks later, when CB4 myocarditis was established, infected and control animals were inoculated intraperitoneally with CB3. They were then sacrificed over a 45-day period. Virus and neutralizing antibody titres were measured on days 3 and 13 after CB3 infection, respectively. The incidence of myocarditis and the intensity of histopathological changes (assessed according to a semiquantitative grading scale from 0 to 4) over a 45-day period were compared. MAIN RESULTS: Among animals with prior CB4 disease, CB3 titres were lower (2.3 +/- 1.7 versus 3.6 +/- 0.8, tissue culture infective dose 50, P = 0.05) and neutralizing antibody response was slightly higher. The incidence of myocarditis was diminished (59.1 versus 89.3%, P = 0.01) and the indices of pathological changes were lower but the differences were not significant (0.68 +/- .54 versus 1.10 +/- 0.20, 1.38 +/- 0.43 versus 1.50 +/- 0.25, 0.56 +/- 0.56 versus 1.26 +/- 0.75, 0.38 +/- 0.58 versus 1.30 +/- 0.78, 0.12 +/- 0.28 versus 0.47 +/- 0.2 on days 3, 9, 13, 30 and 45 post infection, respectively, P > 0.1). CONCLUSION: These results demonstrate that prior exposure to CB4 offers some protection from subsequent CB3 infection. Moreover, they show that antecedent CB4 myocardial damage does not predispose to a worsened expression of CB3 myocarditis.
A case of group B streptococcal meningitis in an adult is presented with a review of 42 other cases reported in the English literature since 1940. Their median age was 58 years (72.5% were older than 45 years). Male/female ratio was 0.9:1, with male predominance in patients older than 60 years (76.5%). Predisposing illnesses were common but 13.9% of cases reported had no identifiable risk factor. Encephalopathy and bacteremia were frequent (81.3% and 94.4% respectively) and many patients (30%) had other foci of infection. Gram stain of cerebrospinal fluid was positive in 75% of cases. Mortality was 18.4% and 9.7% of survivors had bilateral hearing loss. Thus, this review illustrates that group B streptococcal meningitis in adults is a rare disease which occurs among high risk individuals. It is characterized by frequent encephalopathy, prevalence of other foci of infection and bacteremia with an outcome similar to other types of purulent meningitides.
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Indomethacin has been shown to increase virus titers and to worsen cardiac injury in the acute phase of coxsackievirus B4 murine myocarditis. The authors evaluated the effects of indomethacin on the histopathologic changes in a later phase of this disease after virus clearance. Two-day old CD1 mice were infected with coxsackievirus B4. Ten days later, surviving animals were randomized to receive indomethacin or saline intraperitoneally for 10 days. They were then euthanatized, and their hearts were examined for the presence of inflammation, necrosis, scarring, and focal thinning. Mortality was slightly higher among treated animals (7/15 versus 2/12, p = 0.3). The index of inflammation (0.6 +/- 0.5 versus 0.7 +/- 0.5) necrosis and scarring (0.4 +/- 0.5 versus 0.3 +/- 0.5) among treated and control animals, respectively, was not significantly different, but the size of involved myocardium (149742 +/- 201982 versus 35300 +/- 45413 microns2) was remarkably larger (p less than 0.05), and focal ventricular thinning (5/12 versus 0/10, p = 0.03) was encountered among indomethacin recipients exclusively. These findings indicate that indomethacin treatment in the late phase of coxsackievirus B4 myocarditis enhances myocardial damage and increases the incidence of focal ventricular thinning.
The effect of captopril on coxsackievirus B3 murine myocarditis was investigated. Thirty-two, 3-week-old mice were infected with coxsackievirus B3 on day 0 of the study, then randomized into a placebo group or a captopril group starting on day 3 of infection. On day 9 of infection, the mice were put to death. Hearts were weighed and processed for light microscopic examination. Heart weight was 125 +/- 19 mg in the control group versus 102 +/- 14 mg in the captopril group (p less than 0.0003). Amount of necrosis as a percentage of left ventricular section was 3.5% (2.0% to 7.5%) in the placebo group versus 2.0% (0.0% to 5.0%) in the captopril group (p less than 0.01). The amount of dystrophic calcification was 5.0% (0.0% to 27.5%) in the placebo group versus 1.3% (0.0% to 20.0%) in the captopril group (p less than 0.01). The extent of the histopathologic involvement by planimetry was 10.2% in the placebo group versus 5.4% in the captopril group (p = 0.052). We conclude that captopril is beneficial in decreasing left ventricular mass and the amount of myocardial necrosis and calcification in the short term in the murine myocarditis model.
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To date, there is no universally accepted therapy for viral myocarditis. We investigated the effect of the angiotensin converting enzyme inhibitor captopril on both early and late phases of coxsackievirus murine myocarditis. Mice were infected with coxsackievirus B3 and were divided into two main protocols. Mice in the early treatment protocol (n = 30) were treated on day 1 after infection with either captopril or saline through day 6 of infection and euthanized on day 6 of infection. In the late treatment protocol, mice (n = 60) were treated starting on day 10 of infection through day 30 of infection with either captopril or saline. Mice were killed on days 20 and 30 of infection. In the early treatment protocol, heart weight was 67 +/- 14 mg in the captopril-treated group versus 98 +/- 17 mg in the control group (p less than 0.0001). The degree of inflammation, necrosis, and dystrophic calcification assessed with a semiquantitative histological score was significantly less in the captopril-treated group. The degree of pathological involvement determined by planimetry of histological sections was 8.1 +/- 7.2% for the captopril-treated group versus 22.5 +/- 10.0% for the saline-treated group (p less than 0.0001). In the late treatment protocol, captopril also caused a reduction in heart weight as compared with controls at day 20 (116 +/- 21 mg in captopril-treated group vs. 166 +/- 34 mg in controls, p less than 0.0001) and also at day 30 (136 +/- 23 mg in captopril-treated group vs. 185 +/- 48 mg in controls, p less than 0.004). On days 20 and 30 of infection, the degree of inflammation, necrosis, and dystrophic calcification was similar in both groups. We conclude that captopril is beneficial in acute coxsackievirus B3 murine myocarditis because it reduces heart weight and necrosis when administered early and reduces heart weight when administered in a delayed manner.
The safety of nonsteroidal anti-inflammatory agents in viral infections was assessed in a mouse model of coxsackievirus B4 neonatal myocarditis. Two-day-old mice were infected intraperitoneally with 10(4) TCID50 coxsackievirus B4 and then randomized to receive indomethacin or saline for 7 days. A number of them were killed on designated days. Mortality, viral titers, antibody, and interferon levels plus histopathologic changes in the heart were compared. Among treated animals, mortality was greater (22/45 vs 7/27; p = 0.07) and viral titers were higher on days 4 and 7 (p = 0.038 and 0.028, respectively). Interferon levels were lower on days 4 and 7 (p = 0.028 and 0.008, respectively), and histopathologic changes were more extensive on days 7 and 21 (p = 0.008 and 0.028, respectively). These findings show that indomethacin decreased interferon production, increased coxsackievirus4 titers, and enhanced the virulence of coxsackievirus B4. These results raise significant concerns about the safety of indiscriminate use of nonsteroidal anti-inflammatory agents during severe viral infections.
The effects of T lymphocyte suppression on coxsackievirus B3 (CB3) myocarditis and its augmentation by exercise were determined in this study. Three-week-old male C3H/HeN mice were divided into four groups. Group 1 mice were infected intraperitoneally (IP) on day 0 with CB3 10(2.5) TCID50, were made to swim daily from days 1 to 9, and were immunosuppressed with daily doses of cyclosporine A (25 mg/kg IP) from days -2 to 8, plus 0.1 ml antithymocyte 1.2 IgG 2a monoclonal antibody IP on day 0. Mice in group 2 were infected and made to swim daily from days 1 to 9. Mice in group 3 were infected and immunosuppressed as outlined. Mice in group 4 were infected IP with CB3. Mortality rates during the acute phase of infection (days 1 to 9) were as follows: group 1, 4% (1/25); group 2, 52% (13/25); groups 3 and 4, 0. Overall mortality rates through day 21 were as follows: group 1, 67% (17/25); group 2, 72% (18/25); group 3, 40% (10/25); and group 4, 4% (1/25). Mean viral titers in serum were highest in the immunosuppressed groups throughout the study. Myocardial viral titers (mean log10 TCID50) were higher in group 2 mice than in group 1 on days 6 (10(6.9) vs 10(4.6)) and 9 (10(8.4) vs 10(7)); however, these titers peaked in group 1 mice on day 13 (10(9.7)). Myocardial inflammation, necrosis, and mean heart weight/body weight ratios were lower in group 1 compared with group 2 on days 6 and 9 but were maximal on day 13 in group 1. Neutralizing antibody titers were lower in immunosuppressed mice on days 6 and 9; however, a rebound increase occurred on day 13.(ABSTRACT TRUNCATED AT 250 WORDS)
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