Compared Methods for Reducing Stress in ROP Exams; Stake-Holding Examiner Perspective.

Purpose: To better understand the sensory impact of retinal exam components typically experienced by infants undergoing various retinopathy of prematurity staging examinations, adults concerned for infant welfare and exam quality underwent similar exams to compare their perceived stress. Patients and Methods: Adults directly involved with ROP exams and infant stress reduction had cardiac monitoring and concomitant ordinal self symptom-score (1-10 Likert) during 15 components of the exam including lid speculum, various scleral depressors, indirect ophthalmoscopy, goniolens and direct ophthalmoscopy and retinal photography (Phoenix ICON) with or without topical anesthesia. Results: Nine adults provided impressions and cardiac rhythm gathered supine over 15 minutes. Pain score for topical anesthetic 2 was less than for tropicamide 4. Lid specula numb scored a median 2 level (from 1 to 10) pain but without anesthetic scored 6. The goniolens numb scored 3. Scleral depression numb scored 3-4 but increased to 7 without topical anesthesia. Direct ophthalmoscope scored 3 through the goniolens and the retinal camera scored 4 pain. Brightness with low 350 Lux indirect scored 6-8 numb and 9 brightness without anesthetic. Full bright indirect, direct ophthalmoscope and the retinal camera all had Lux of 3000-4000 and were scored brightness 9, 7 and 10, respectively. Adults had minimal oculocardiac reflex during on-globe retinal examination methods (range 98% to 102%). Conclusion: Topical anesthesia provided a moderate reduction in pain during on-globe lid-speculum, scleral depressed indirect examination. There was a synergistic augmented sensory response between pain and brightness. Adults did not show the bradycardia typically elicited by retinal examinations in premature infants.

Escherichia coli and TNF-alpha modulate macrophage phagocytosis of Candida glabrata.

BACKGROUND: The incidence of systemic nonalbicans Candida (especially C. glabrata) infections is increasing dramatically in intensive care units, but relatively little is known about the pathogenesis or host defenses associated with these life threatening infections. MATERIALS AND METHODS: The course of systemic C. glabrata infection was assessed as the fungal burden in the kidneys and livers of mice sacrificed 1, 8, and 15 d after intravenous C. glabrata. Sixteen hours before each sacrifice, half of the mice were injected intraperitoneally with intact viable or nonviable E. coli cells, or with E. coli lipopolysaccharide (LPS), or with tumor necrosis factor (TNF)-alpha. To clarify the effect of LPS and TNF-alpha on phagocytosis, resident (unstimulated) mouse peritoneal macrophages were harvested, cultivated ex vivo, and some cultures were treated with LPS or TNF-alpha prior to 30 min incubation with C. glabrata. RESULTS: Compared with mice injected with vehicle, each agent (intact E. coli cells or E. coli LPS or TNF-alpha) was consistently associated with decreased numbers of tissue C. glabrata, and some of these decreases were significant (P < 0.05). Compared with untreated macrophages, phagocytosis of C. glabrata was increased with LPS-treated macrophages (P < 0.01), and phagocytosis was also increased in the presence of TNF-alpha (P < 0.01). CONCLUSION: E. coli LPS and TNF-alpha may participate in host defense against C. glabrata by a mechanism involving increased macrophage phagocytosis, suggesting that stimulation of inflammatory cytokines may facilitate host clearance of C. glabrata.

Candida glabrata colonizes but does not often disseminate from the mouse caecum.

Candida glabrata is the second or third most frequent cause of candidaemia. The gastrointestinal tract is considered to be a major portal of entry for systemic candidiasis, but relatively few studies have investigated the pathogenesis of C. glabrata. Experiments were designed to clarify the ability of C. glabrata to disseminate from the mouse intestinal tract. Following oral inoculation, C. glabrata readily colonized the caeca [approx. 10(7) cells (g caecum)(-1)] of antibiotic-treated mice, but extraintestinal dissemination was not detected. Superimposing several mouse models of trauma and/or immunosuppression known to induce dissemination of Candida albicans and other intestinal microbes did not cause C. glabrata to disseminate often, although one exception was mice given high doses of dexamethasone for 4 days. These data support the hypothesis that the antibiotic-treated mouse intestine may be an epidemiological reservoir for C. glabrata and that this yeast tends to disseminate under specific clinical conditions.