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The Compu-pet 100 diluter/dispenser is a versatile and accurate instrument which can be employed for a wide variety of microbiological tests and techniques. Time in performing tests is often more than halved when the diluter is used. Large numbers of tests can be performed with minimal fatigue.
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SUMMARYIntra-amniotic infection is the main cause of spontaneous preterm birth and adverse maternal-fetal outcomes; therefore, rapid, robust, and accurate diagnosis remains a clinical priority. Conventional microbiological techniques, especially culture-based methods, are limited by long turnaround times and the inability to detect fastidious or unculturable organisms. This review summarizes the diagnosis, nomenclature, clinical significance, management, and laboratory approaches for diagnosing intra-amniotic infection. Targeted nucleic acid amplification methods, including species-specific polymerase chain reaction and broad-range 16S rRNA gene sequencing, have improved the detection of bacterial DNA and enabled the identification of organisms that evade routine culture in intra-amniotic infection. More recently, whole-genome sequencing and metagenomic next-generation sequencing have provided culture-independent strategies for comprehensive pathogen profiling, allowing simultaneous detection of bacteria, viruses, and fungi, as well as characterization of antimicrobial resistance determinants and virulence-associated genes. However, challenges remain, particularly in low-biomass samples such as amniotic fluid, where contamination, host DNA background, and data interpretation can compromise specificity. This review critically evaluates the advantages and limitations of each molecular modality and discusses pre-analytical, analytical, and bioinformatic considerations essential for reliable implementation. Integration of molecular diagnostics into clinical workflows holds promise for improving etiological diagnosis and guiding targeted therapy in intra-amniotic infection, thereby improving maternal and fetal outcomes.
Cotrimoxazole 4 tablets daily (1 tablet = trimethoprim 80 mg and sulphamethoxzole 400 mg) was given for a period of six to fourteen days to 13 inpatients, and serum-folate levels were measured before and one day after the course of treatment. The results were compared with those from 8 patients not receiving antibacterial therapy, tested on admission and one week later. Two assay techniques were used, one employing Lactobacillus casei and the other 125I-labelled folate isotope dilution. The microbiological technique showed a significant decline in folic-acid levels in the serum after cotrimoxazole, and this decline was not seen in controls. By contrast, the radioisotope technique showed no significant alteration in serum-folate levels compared with controls. This suggests that cotrimoxazole does not depress true serum-folate and that many low microbiological results obtained during cotrimoxazole therapy reflect interference with the assay organism. There is insufficient evidence to incriminate cotrimoxazole as a significant cause of blood dyscrasias in excess of those which might occur on sulphonamide alone or even with other antibacterials.
Patients may harbor cell-wall-deficient organisms or other aberrant bacterial forms (ABFs) in their eyes. In this survey of 400 cultures, we found the incidence of ABFs isolated from various ocular sites to be 13.2%. The rate of isolation of these forms from the eyes of patients with suspected bacterial infection differed greatly from that for noninfected eyes. We will describe the microbiological techniques employed and will present our analysis of the data obtained.
Listeria monocytogenes and a staphylococcus organism caused a catastrophic endophthalmitis in a patient despite appropriate local and systemic antimicrobial chemotherapy. Although L monocytogenes is widespread in nature and has produced a variety of clinical illnesses, it has only one previously been reported to cause endophthalmitis. If appropriate microbiologic techniques are not employed, the organism may go unrecognized as an ocular pathogen.
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1. An epizootic caused by Salmonella typhimurium var. copenhagen and occurring on the farms of one company was examined with the following factors in mind: the spread of the epizootic, the infection rate of the flocks and the role of the food, hatchery and parent stock. 2. A microbiological technique was used the aim of preventing infection on the farms. 3. The method of control was not as effective the field as in the laboratory; the possible reasons for this are discussed.
A simple method is described in which frozen sections are prepared from tissue cell suspensions with added microorganisms and then cultured. The enhanced growth of the organisms makes their indentification easier. A number of applications is suggested.
The microbiology laboratory's rapid and consistent identification of nosocomial pathogens is a keystone in the surveillance and control of hospital-acquired infections. In addition, the laboratory serves as a source of expert consultation for clinicians and infection control personnel and as an "early warning center" for infection problems. In making its contributions to infection control most effective, the laboratory must recognize its capabilities and limitations, must insure that the materials and methods it uses and the specimens it processes meet high standards, must provide retrievable records, and must have a good working knowledge of microbiologic technics used to evaluate both endemic and epidemic infections. Moreover, because laboratory workers come into contact daily with potentially infectious specimens and isolates, the laboratory's contributions to infection control should also include the prevention and surveillance of laboratory-acquired infections.
The component processes of phagocytosis (ingestion, inactivation, and destruction of bacteria) were studied in mice by histological and microbiological techniques after aerosol infection with Staphylococcus aureus. Rates of bacterial ingestion and inactivation were (respectively): 0 hr, 37.7% and 0; 1 hr, 64.5% and 45.8%; 2 hr, 75.9% and 67.9%; 4 hr, 82.4% and 84.1%; and 8 hr, 90.7% and 94.8%. Bacterial destruction began 2-4 hr after aerosol infection and affected 80% of the bacteria by 8 hr. Comparison of these processes indicated that bacterial ingestion occurred before inactivation and was 76% complete at 2 hr. Inactivation resulted in death of 84% of the bacteria at 4 hr, and 80% of the bacteria were at least partially destroyed by 8 hr. The mechanism of X-irradiation-induced depression of pulmonary bacterial inactivation was studied in syngeneic mice protected from lethal effects of X-irradiation by chest and pelvic shields or by transplantation of 2 times 10(6) bone marrow cells. Impairments in bacterial inactivation resulted from diminished ingestion of bacteria by macrophages.
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