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Biomedical subjects

A M Lerner

Publications and source records attributed to A M Lerner.

At least 55 records · Page 3Linked to original sources
PubMed1980

Interferon in biopsy and autopsy specimens of brain. Its presence in herpes simplex virus encephalitis.

Quantitative virus and interferon titers were assayed in temporal lobe brain biopsy specimens (six patients); in various regions of the brain at autopsy (five of the six patients); and in serums and CSF during courses of herpes simplex virus, type 1 (HSV-1) encephalitis. Until the tenth day of neurologic disease, interferon (geometric mean titer, 25 units/mL) was present in each virus-positive brain biopsy specimen. The geometric mean HSV-1 titer at brain biopsy was 328 tissue culture dose (TCD)50/g. On the sixth day of disease, CSF from the sole survivor contained 160 units/mL, but five other samples of CSF contained no detectable interferon. No serums from any of the six patients contained interferon. At autopsies performed on the sixth to 19th day of neurologic disease, 13 of 35 of the regional areas of the brain retained HSV, but only a single specimen from a temporal lobe had measurable interferon. Early in the course of HSV-1 encephalitis, substantial interferon titers are present in areas of virus multiplication. This local brain interferon is insufficient alone to inhibit progression of a disease but could possibly be important in combination with antiviral chemotherapy.

Adult↗
PubMed1980

The gram-negative bacillary pneumonias.

With increasing age, chronic underlying disease, and debility, the oropharyngeal flora are colonized with aerobic gram-negative bacilli. In this debilitated population, gram-negative bacillary pneumonias (GNBP) are increasingly common. GNBP account for two of every three pneumonia deaths today. As a group, the mortality of GNBP is about 50%. Although the original epidemiologic surveys were done 15 years ago, there is little evidence for an improving case fatality rate despite the appearance of aminoglycoside antibiotics, carbenicillin, and cephalosporins. In susceptible patients, GNBP pneumonias occur both in the community and as nosocomial infections. Recognition of the dangers of contaminated reservoir nebulizers or other similar devices used in inhalation therapy has led to epidemiologic measures within hospitals that have markedly decreased the incidence of this nosocomial GNBP. The role of Gram stain and culture of expectorated sputum and similar examinations of specimens obtained by transtracheal aspiration, fiberoptic bronchoscopy, and lung biopsy in the diagnosis of GNBP are discussed in this review (see Criteria for Diagnosis). In the presence of pulmonary emphysema, congestive heart failure, mixed gram-negative bacillary infections, or the use of immunosuppressive drugs, typical characteristics of individual GNBP may not be apparent. Typical features of Pseudomonas aeruginosa, Escherichia coli, Enterobacter, Proteus, Hemophilus, and anaerobic pulmonary infections are described. Early recognition and institution of appropriate antibacterial agents are emphasized, particularly in GNBP caused by Pseudomonas aeruginosa, Escherichia coli, or Friedländer's bacillus, where the mortality approaches 70%. The mortality of GNBP, including Enterobacter, Proteus, Hemophilus, and anaerobic GNBP, is about 20%. The latter figure is the same as the mortality of pneumococcal pneumonia in similar patients.

Adolescent↗
PubMed1980

Age-dependent pathogenicity of group B coxsackieviruses in Swiss-Webster mice: infectivity for myocardium and pancreas.

Coxsackieviruses B1-B4 were inoculated intraperitoneally into 48-hr-old, 14-day-old, and three- to five-month-old Swiss-Webster mice. Immediate death occurred only among mice less than 48 hr old, which died from fulminant encephalitis. Older mice usually survived. Myocarditis ensued in mice less than 48 hr old that were infected with coxsackieviruses B1 and B4. Several of the surviving mice developed left ventricular aneurysms, which resulted from transmural necrotizing myocarditis. In this group (coxsackieviruses B1 and B4), pathologic changes in the heart were synchronous with maximal cardiac titers of virus. Fourteen-day-old mice infected with coxsackieviruses B2 and B3 developed nontransmural necrotizing myocarditis in which maximal pathologic changes followed peak cardiac titers of virus by several days, whereas three- to five-month-old mice infected with coxsackieviruses B1, B2, B3, or B4 showed maximal susceptibility to destructive lesions in the exocrine glandular pancreas. Therefore, specific susceptibilities to infection with coxsackieviruses group B vary with age of the mouse, virus type (and strain), and organ.

Aging↗
PubMed1980

Modified polyriboinosinic-polyribocytidylic acid complex: induction of serum interferon, fever, and hypotension in rabbits.

The purposes of this study were to determine whether the febrile and hypotensive reactions to the administration of polyriboinosinic-polyribocytidylic acid [poly (I)-poly (C)] complexed with poly-L-lysine and carboxymethylcellulose (poly ICLC) (9S) encountered in humans could be duplicated in rabbits, and when such duplication was demonstrated, to ascertain whether these untoward reactions could be avoided by (i) administration of hydrocortisone (HC), (ii) alteration of the route of delivery, or (iii) administration of poly ICLC (4S) an interferon inducer of lower molecular weight. Responses to intravenous poly ICLC (9S) in rabbits reproduced adverse reactions in humans, namely fever and hypotension, and were accompanied by high titers of serum interferon. Continuing investigations showed that (i) intravenous pretreatment of rabbits with HC ameliorated hypotensive responses but markedly diminished interferon induction. When HC was given after poly ICLC (9S), both interferon and hypotension induction were likewise depressed. (ii) Intramuscular or subcutaneous poly ICLC (9S) produced neither high titers of serum interferon nor toxic effects. (iii) Poly ICLC (4S) induced high titers of serum interferon and fever, but no hypotension. Poly ICLC (4S) warrants further study.

Animals↗
PubMed1980

Modified polyriboinosinic-polyribocytidylic acid complex: modulation of toxicity for rabbits by alterations in components.

In an earlier study the physiological effects encountered in humans of a modified complex of polyriboinosinic acid-polyribocytidylic acid [poly(I)-poly(C)] with carboxymethylcellulose and poly-L-lysine [poly(ICLC) (9S)], namely, the induction of high titers of serum interferon along with fever and hypotension, were reproduced in rabbits. In the present studies, also in rabbits, we evaluated effects of complexes with homopolymer polyribonucleotide sedimentation coefficients decreasing from 9S to 6S and 4S. Modified complexes of carboxymethylcellulose and poly-L-lysine with decreasing molecular weights were also tested. In several studies diphenhydramine and indomethacin were administered concomitantly. These experiments showed that at a daily intravenous dose of 0.2 mg/kg the various preparations of poly(I)-poly(C) (9S) and poly(I)-poly(C) (6S) induced falls in blood pressure, but stabilized complexes of poly(I)-poly(C) (4S) did not. Alterations in the molecular weights of carboxymethylcellulose and poly-L-lysine n the modified complex and the concomitant administration of diphenhydramine did not influence the occurrence or severity of untoward reactions. In rabbits, poly(ICLC) (4S) along with indomethacin induced high titers of serum interferon without fever or hypotension.

Animals↗
PubMed1980

Pyrogenic reactions after inadvertent infusion of endotoxin during cardiac catheterizations.

In April 1976 the attack rate of chills and fever with or without falls in blood pressure increased in association with cardiac catheterizations. Fevers were associated with coronary angiography and right and left heart catheterizations. Blood cultures were negative, and reactions did not correlate with amounts of contrast materials infused or with procedures done by a single operator. Significant numbers of Acinetobacter calcoaceticus (var. anitratus) and a Pseudomonas species were cultured from hospital-reservoir distilled water when it was flushed through a catheter before gas sterilization. This same water after ethylene oxide sterilization contained 2 x 10(5) ng/mL of endotoxin by limulus lysate test and was positive by rabbit pyrogen test. When washed reusable cardiac catheters were sterilized daily or when disposable catheters were substituted, febrile reactions ended. Pyrogenic reactions in patients undergoing cardiac catheterizations correlated with emptying retained endotoxin with injected contrast material from reused washed-sterilized catheters.

Acinetobacter↗
PubMed1979

Synergy between carbenicillin and an aminoglycoside (gentamicin or tobramycin) against Pseudomonas aeruginosa isolated from patients with endocarditis and sensitivity of isolates to normal human serum.

Isolates from the blood of 30 patients with endocarditis due to Pseudomonas aeruginosa were tested for synergy between carbenicillin and an aminoglycoside, either gentamicin or tobramycin, by in vitro checkerboard methods in modified (cation-supplemented) Mueller-Hinton broth. Twenty-five of the 30 isolates were affected synergistically. Whether given low (2.5--5 mg/kg) or high (8 mg/kg) doses of aminoglycoside along with 30 g of carbenicillin daily, all of the five patients infected with pseudomonads that were not synergistically affected were refractory to treatment with pseudomonads that were not synergistically affected were refractory to treatment with the carbenicillin-gentamicin combination, whereas the finding of synergy of carbenicillin with gentamicin (or tobramycin) did not assure a medical cure. Tests for synergy between carbenicillin and gentamicin yielded different results in Mueller-Hinton agar than in modified Mueller-Hinton broth. The majority (28) of 30 isolates of endocarditis-producing P. aeruginosa were resistant to the bactericidal effects of 50% pooled normal serum that had been freshly separated. One of the endocarditis-producing strains that was sensitive to 50% serum was resistant to 10% serum. However, sensitivity or resistance to freshly separated, pooled normal human serum did not predict the outcome of antibacterial therapy for pseudomonas endocarditis.

Aminoglycosides↗
PubMed1979

Modified polyriboinosinic-polyribocytidylic acid complex: sustained interferonemia and its physiological associates in humans.

Fourteen patients with severe viral illnesses were given intravenous infusions of a modified interferon inducer, polyriboinosinic-polyribocytidylic acid-poly-L-lysine complexed with carboxymethylcellulose [poly)I:C.LC)], during a phase 1 clinical trial. The first eight patients received 0.15 to 0.30 mg of poly(I:C.LC) per kg of body weight daily for 5 consecutive days, and another received two courses separated by 1 week. A second group of five patients was given single intravenous infusions of 0.10 to 0.15 mg of poly(I:C.LC) per kg. Interferon was detectable in the serum 8 to 16 h after injection. Titers ranged from 15 to 800 U/ml and varied directly with the dose of poly(I:C.LC). Interferonemias persisted for 12 to 48 h. In patients receiving 5-day courses of poly(I:C.LC), lower levels of serum interferon (0 to 160 U/ml) occurred on days 2 through 5, characteristic of a hyporesponsive state. An exception was a 69-year-old patient with disseminated varicella zoster, multiple myeloma, and renal insufficiency whose serum contained 3,150 U of interferon per ml on day 3 of 0.3 mg of poly(I:C.LC) per kg. Fever (39 to 40.5 degrees C, rectally; 13 of the 14 patients) peaked 3 to 8 h after completion of infusions. Other toxic effects included lymphopenia (10 of the 14 patients), hypotensive episodes (7 of the 14 patients), and minor elevations of serum glutamicoxalacetic transaminase and lactic dehydrogenase.

Adolescent↗
PubMed1979

Ventricular aneurysms complicating coxsackievirus group B, types 1 and 4 murine myocarditis.

Suckling Swiss Webster mice were inoculated with 10(4)TCD50 of coxsackieviruses, group B types 1 or 4. Virulent necrotizing myocarditis resulted in 185 infected mice. Of the latter group, three (14.3%) nurslings on the 17th and 23rd day after inoculations had left ventricular aneurysms postmortem. None of 61 concurrently matched control mice developed aneurysms. Ventricular aneurysm is a suggested but previously undocumented complication of murine, and possibly human necrotizing transmural coxsackievirus myocarditis.

Animals↗
PubMed1978

Simultaneous serum and CSF antibodies in herpes simplex virus encephalitis.

Serial concomitant paired sera (S) and CSF were taken from eight patients with biopsy-proved herpes simplex virus encephalitis (HSVE). These specimen pairs were compared with 28 others from patients with various neurologic conditions. Before and after reduction with 2-mercaptoethanol, a ratio of S/CSF antibody titers of less than or equal to 20 with either the passive hemagglutinating (PHA) or immune adherence hemagglutinating (IAHA) antibody tests occurred in every patient with HSVE. Diagnostic S/CSF ratios were noted in three patients before biopsy of the brain and in four patients by the tenth day of neurologic disease. Among control subjects, a ratio of S/CSF titers greater than 20 was observed in all but four patients. Each of the latter patients had neurologic diagnoses easily distinguishable from HSVE. The PHA or IAHA S/CSF ratio offers a rapid, reliable method for the diagnosis of HSVE (P less than .001).

Adult↗
PubMed1978

Coxsackievirus B4 myocarditis in mice: valvular changes in virus-infected and control animals.

Suckling, weanling, and adult HaM/ICR and Swiss-Webster mice were inoculated intraperitoneally with the TC631 and Dowell strains of coxsackievirus B4. Vero cell-inoculated and uninoculated control mice were also studied under code. An intense, necrotizing myopericarditis was produced in suckling mice; it was less severe in weanlings. Myocarditis did not occur when coxsackievirus B4 was inoculated into adult mice. Progressive sclerosis and thickening of all valves in both strains of mice were observed with equal frequency in infected and control mice. There was no evidence that coxsackievirus B4 induced a specific valvular or endocardial lesion.

Animals↗