A Quality Improvement Approach to Reducing the Caesarean section Surgical Site Infection Rate in a Regional Hospital.

Surgical site infection (SSI) rates are used extensively by hospitals as a basis for quality improvement. A 30-day post-discharge SSI programme for Caesarean section operations has been implemented in Our Lady of Lourdes Hospital since 2011. It has been shown that skin antisepsis and antibiotic prophylaxis are key factors in the prevention of SSI. Using quality improvement methodology, an infection prevention bundle was introduced to address these two factors. Skin antisepsis was changed from povidone-iodine to chlorhexidine-alcohol. Compliance with choice of antibiotic prophylaxis increased from 89.6% in 2014 to 98.5% in 2015. Compliance with timing also improved. The SSI rate of 7.5% was the lowest recorded to date, with the majority of SSIs (64%) diagnosed after hospital discharge. The level of variation was also reduced. However, the continued presence of variation and possibility of lower infection rates from the literature imply that further improvements are required.

Twenty four-hour helpline access to expert management advice for food-allergy-triggered anaphylaxis in infants, children and young people: a pragmatic, randomized controlled trial.

BACKGROUND: Anaphylaxis is a life-threatening emergency. If promptly administered, adrenaline is potentially life-saving. Many food-allergic-children/carers are unsure when to use their adrenaline autoinjectors, contributing to a low quality of life and worse outcomes in the setting of an acute allergic reaction. OBJECTIVES: The aim of this study was to assess the effectiveness of 24-hour telephone access to specialist clinical advice on disease-specific quality of life. METHODS: A pragmatic two-arm, parallel-group randomized control trial was conducted. Children/carers (<16 years) with food allergy, trained in adrenaline auto-injector use, were recruited from a hospital-based paediatric allergy clinic. Baseline disease-specific quality of life was ascertained using the validated Food-Allergy-Related Quality-of-Life Questionnaire (FAQLQ), either Parent Form, Child Form or Teenager Form depending on child's age. Participants were then centrally randomized for a 6-month period to 24-hour telephone specialist support line or to usual care. The primary outcome measure was a change in FAQL scores, at one and 6 months postrandomization, compared with baseline. The minimum clinically important difference (MCID) in score is 0.5. RESULTS: Fifty two children/carers were recruited. FAQL scores remained static in the control group across the three time points. Scores gradually improved in the intervention group, with a significant difference seen at 6 months (T1-T3 Mean difference = -1.5, (CI 0.87-2.25) P < 0.005] Follow-up questionnaires, 6 months after the intervention was removed, T4, showed sustained significant difference between the groups (control M = 3.0; intervention M = 1.1[t = -4.113, P < 0.05]). CONCLUSION: The 24-hour helpline improved food-allergy-specific quality of life in children. Six-month intervention support resulted in sustained benefits for at least a further 6 months.

Improving otoscopy education and diagnostic accuracy: A prospective interventional study.

OBJECTIVE: To assess and improve otoscopy examination skills across various medical specialities who perform otoscopy during their professional practice. METHODS: A pre-intervention survey was created using www.surveymonkey.com, which included several preliminary questions to clarify the participant's speciality and training level, followed by 25 individual otoscopy images. The participants were given 12 possible diagnoses for each otoscopy image and asked to choose the single best answer. After completing the survey, participants were asked to watch an otoscopy teaching session. This teaching session was created with multidisciplinary feedback, and the content included a demonstration video and a didactic lecture. Finally, a post-intervention survey was circulated four weeks later to the same cohort of doctors to assess improvement. RESULTS: A total of 79 pre-intervention surveys were collected with an average score of 53% (range 20-100%). The spectrum of medical specialities that completed the pre-intervention survey included paediatrics, ear, nose, and throat (ENT), emergency medicine, and general practice. The largest cohort of surveys came from senior house officers (SHO). In addition, 78.5% of responses were completed by doctors who had not worked in ENT before. After completing the otoscopy teaching session and at least four weeks after the initial survey, 23 post-intervention surveys were completed with an average score of 66% (range 32-100%), a 13% improvement. CONCLUSIONS: The results of the pre-intervention survey show that many doctors have difficulty diagnosing ear conditions. The implementation of a 25-min teaching session achieved a 13% improvement in the otoscopy knowledge of doctors across a variety of specialities.

Death in the neonatal intensive care unit: changing patterns of end of life care over two decades.

BACKGROUND: Death remains a common event in the neonatal intensive care unit, and often involves limitation or withdrawal of life sustaining treatment. OBJECTIVE: To document changes in the causes of death and its management over the last two decades. METHODS: An audit of infants dying in the neonatal intensive care unit was performed during two epochs (1985-1987 and 1999-2001). The principal diagnoses of infants who died were recorded, as well as their apparent prognoses, and any decisions to limit or withdraw medical treatment. RESULTS: In epoch 1, 132 infants died out of 1362 admissions (9.7%), and in epoch 2 there were 111 deaths out of 1776 admissions (6.2%; p<0.001). Approximately three quarters of infants died after withdrawal of life sustaining treatment in both epochs. There was a significant reduction in the proportion of deaths from chromosomal abnormalities, and from neural tube defects in epoch 2. CONCLUSIONS: There have been substantial changes in the illnesses leading to death in the neonatal intensive care unit. These may reflect the combined effects of prenatal diagnosis and changing community and medical attitudes.

The effects of lipid fluidity on the rotational diffusion of complex I and complex III in reconstituted NADH-cytochrome c oxidoreductase.

NADH-ubiquinone oxidoreductase (Complex I) can be recombined with ubiquinol-cytochrome c oxidoreductase (Complex III) to reconstitute NADH-cytochrome c oxidoreductase. Two modes of interaction have been found. In one, the Complexes interact stoichiometrically in one to one molar ratios to give a binary Complex I-III unit. In the other, the kinetics of NADH-cytochrome c oxidoreductase are characteristic of 'Q-pool' behaviour seen in intact mitochondria and submitochondrial particles in which the Complexes need not interact directly but can do so via a pool of mobile ubiquinone. Stoichiometric behaviour is found when only boundary layer or annular lipid is present or the lipid is in the gel phase. The lipid is immobile on the ESR time scale and protein rotational diffusion, measured by saturation transfer ESR, is very slow. Q-pool behaviour is found when mobile extra-annular lipid phase is also present. Protein rotational diffusion is rapid and characteristic of a fully disaggregated state. We have also used freeze-fracture electron microscopy of reconstituted NADH-cytochrome c oxidoreductase to monitor protein aggregation and lateral phase separation of lipids and proteins under various conditions. We discuss our findings in relation to models for lateral interactions between respiratory chain enzymes.

Increased sodium appetite stimulates c-fos expression in the organum vasculosum of the lamina terminalis.

The relation between c-fos expression in the forebrain of Lister hooded rats and water and NaCl intakes was examined in response to systemic injection of angiotensin II, desoxycorticosterone, angiotensin II and desoxycorticosterone together, frusemide or low sodium diet, all treatments that induce a sodium appetite. Angiotensin II (1 mg/kg subcutaneously) caused significant increases in the 1-h intakes of water and 1.8% NaCl compared to controls, the effect on water intake being the greater. There was a similar increase in NaCl intake after four days' treatment with desoxycorticosterone (20 mg pellet subcutaneously) but water intake was not increased. The NaCl intake of rats given angiotensin II following desoxycorticosterone treatment was approximately the sum of the intakes after angiotensin II or desoxycorticosterone alone, but the water intake was slightly less than after angiotensin II alone. Frusemide pretreatment (4 mg/kg subcutaneously) caused an NaCl intake similar to that following angiotensin II and desoxycorticosterone but water intake was little affected. Low dietary sodium also increased salt appetite, as expected. These treatments were repeated in rats that were not allowed to drink NaCl, after which the brains were processed for c-fos immunocytochemistry. This showed intense staining of the subfornical organ, median preoptic nucleus, organum vasculosum of the laminal terminalis, paraventricular nucleus and supraoptic nucleus after subcutanous angiotensin II. Animals given angiotensin II following desoxycorticosterone pretreatment showed patterns of c-fos expression that did not differ from those of angiotensin II alone. Treatment with desoxycorticosterone alone produced intense staining in the organum vasculosum of the laminal terminalis and some staining in the median preoptic nucleus. Frusemide gave a similar pattern of staining to desoxycorticosterone, stimulating c-fos expression in the same regions but to a lesser extent. A low salt diet resulted in increased c-fos expression only in the organum vasculosum of the laminal terminalis. Therefore, five different treatments that induced increased sodium appetite evoked distinct patterns of c-fos expression in the anteroventral region of the third ventricle of the rat forebrain. Since the common feature was induction of c-fos in the organum vasculosum of the laminal terminalis, these results suggest a key role for this structure in the development of increased sodium appetite.

The association of thirst, sodium appetite and vasopressin release with c-fos expression in the forebrain of the rat after intracerebroventricular injection of angiotensin II, angiotensin-(1-7) or carbachol.

The effect intracerebroventricular injections of angiotensin II (0.1 nm), angiotensin-(1-7) (1 or 100 nm) and carbachol (500 ng) on c-fos expression was examined in the forebrain of Lister hooded rats. Intense staining of the c-Fos protein was found in the median preoptic nucleus, organum vasculosum of the lamina terminalis, subfornical organ, paraventricular nucleus and supraoptic nucleus after angiotensin II and carbachol Angiotensin II caused significantly more c-fos expression in the ventral median preoptic nucleus and organum vasculosum of the lamina terminalis than carbachol, whereas in the paraventricular and supraoptic nuclei this was reversed, with carbachol having a greater effect on c-fos expression in these areas. Angiotensin-(1-7), however, only induced c-Fos protein in the organum vasculosum of the lamina terminalis and median preoptic nucleus with the number and the intensity of staining of the nuclei significantly less in both areas than after angiotensin II or carbachol. Separate groups of Lister rats were given i.c.v. injections of the same substances at the same doses, but excluding the lower dose of angiotensin-(1-7), and the intakes of water and 1.8% NaCl over 60 min were measured. Angiotensin II stimulated intakes of both water and NaCl. The effect on water intake was almost immediate (<1 min), whereas NaCl intake did not usually start until at least 5 min after injection. Over 60 min, water (12.4 +/- 1.0 ml) and NaCl (4.2 +/- 0.9 ml) intakes were significantly greater than water (1.1 +/- 0.2 ml) and NaCl (0.6 +/- 0.5 ml) intakes of the controls. Carbachol caused less drinking than angiotensin II, the water intake over 60 min being significantly less (4.8 +/- 0.7 ml) and the latency of response greater (>5 min). Carbachol, unlike angiotensin II, had little effect on NaCl intake (0.7 +/- 0.4 ml). Angiotensin-(1-7) had no effect on water (1.1 +/- 0.3 ml) or NaCl (0.3 +/- 0.3 ml) intakes. The plasma levels of vasopressin were measured after i.c.v. injection of the same three substances in the same doses, again excluding the lower dose of angiotensin-(1-7), in further groups of rats. Angiotensin II and carbachol caused an approximate five-fold increase in plasma vasopressin levels compared to cerebrospinal fluid-injected rats, but angiotensin-(1-7) had no effect on vasopressin release. Therefore, three compounds with widely differing effects on thirst, sodium appetite and vasopressin release induce distinctive patterns of c-fos protein expression in the forebrain. By combining experimental approaches in this way it is possible to determine areas of the brain which are involved in certain behavioural and endocrine responses.

Dependence of spontaneous and angiotensin-induced drinking in the rat upon the oestrous cycle and ovarian hormones.

The influence of the oestrous cycle on spontaneous and dipsogen-induced drinking was studied in female rats. Spontaneous fluid intake was lowest on the day of oestrus. Drinking induced by subcutaneous isoprenaline, and by angiotensin II (injected into the preoptic area), also showed marked cyclical variation, being lower at pro-oestrus and oestrus than at other stages of the cycle. Drinking induced by subcutaneous hypertonic NaCl or by intracranial carbachol did not vary with the oestrous cycle. Cyclicity of spontaneous and of angiotensin-induced water intake was not apparent in rats before puberty or after ovariectomy. Ovariectomy reduced drinking in response to isoprenaline. Treatment with oestradiol benzoate (20 micrograms) caused a reduction in spontaneous water intake, but a marked increase in the drinking response to isoprenaline. Treatment with oestradiol benzoate and progesterone (2.5 mg) caused a larger decrease in spontaneous water intake and an insignificant increase in isoprenaline-induced drinking. Water intake induced by subcutaneous hypertonic saline was unaffected by gonadal steroids. The results provide further evidence for the view that the thirst of extracellular origin, in which the renin-angiotensin system is involved, is brought about by mechanisms different from those that respond to cellular dehydration. Only drinking caused by activation of extracellular mechanisms appeared to be sensitive to the ovarian cycle and to ovarian hormones.

Increased sodium appetite in adrenalectomized or hypophysectomized rats after intracranial injections of renin or angiotensin II.

Rats given free access to food, water and 2.7% NaCl and injected with either renin or angiotensin II into the preoptic area showed an immediate increase in water intake followed by an increase in intake of 2.7% NaCl. The rats continued to drink the hypertonic NaCl solution throughout the test session of 18 h. Intracranial injections of the dipsogen, carbachol, caused thirst but no sodium appetite. Bilateral adrenalectomy had no effect on either the initial water intake or the delayed intake of NaCl that was induced by intracranial injections of renin or angiotensin II. However, the increased water intake during the 18 h after the administration of renin was reduced to normal levels in adrenalectomized rats. Similar results were obtained with hypophysectomized rats. These results demonstrated that the delayed sodium appetite induced by renin or angiotensin II is not secondary to the stimulation of release of hormones from the pituitary gland or adrenal cortex.

The effects of centrally administered porcine relaxin on drinking behaviour in male and female rats.

Of the reproductive hormones it has been suggested that relaxin may play an important role in the increased sodium appetite of pregnancy. ICV injection of porcine relaxin caused water-replete male and female Wistar rats with access to water and 0.9% or 2.7% NaCl to drink on average about 3 to 8 ml of water within 1 h of injection. By 24 h the cumulative intake of water was no different from the control intake. The amounts of water drunk were similar after doses of 50, 100, 250 and 500 ng of relaxin. A dose of 5 ng was ineffective. Male rats generally drank more water than female rats after ICV injection of angiotensin or relaxin. Male SH rats which drink more water than male WKY rats in response to ICV angiotensin also drank more after ICV relaxin. Intakes of 0.9% or 2.7% NaCl were unaffected for up to 24 h after injection of relaxin, whereas angiotensin-injected rats showed a significant increase in 0.9% NaCl 1 h after injection though this difference was no longer evident in the 24 h cumulative intake. Relaxin did not cause any increase in NaCl intake in SH rats. Insulin, which is similar in structure and molecular weight to relaxin, was without effect on drinking when doses comparable to dipsogenically effective doses of relaxin were injected ICV. In male Wistar rats treated with DOCA for 5-15 days, relaxin retained its weak stimulatory action on water intake but did not affect NaCl intake despite the increased baseline NaCl intake during DOCA. These results indicate that relaxin is a dipsogen in the rat but that it seems to have little short-term effect on sodium appetite.

Increased sodium appetite and thirst in rat induced by the ingredients of liquorice, glycyrrhizic acid and glycyrrhetinic acid.

In the rat, blocking 11 beta-OHSD with the active ingredient of liquorice, glycyrrhizic acid (GZA) or its hydrolytic product, 18 beta-glycyrrhetinic acid (GTA), caused potassium loss, increased water intake and a primary increase in salt appetite that was specific for sodium and not secondary to sodium loss. Intracerebroventricular injection of angiotensin II enhanced the sodium appetite but carbachol did not. The stimulating effects of GZA or GTA on intakes of water and NaCl resembled those caused by the administration of excessive amounts of mineralocorticoid. The results suggest that GZA- or GTA-induced drinking behaviour is mediated by circulating glucocorticoids. After liquorice blockade of 11 beta-OHSD, the peripheral and central mineralocorticoid receptors are no longer protected from glucocorticoid action.

Eledoisin, substance P and related peptides: intracranial dipsogens in the pigeon and antidipsogens in the rat.

The undecapeptide eledoisin caused vigorous and copious drinking within a minute or two of injection into the pigeon forebrain. Systemic injections of the same doses were ineffective. The relative efficacy of eledoisin and angiotensin II as dipsogens in the pigeon was similar to that of carbachol and angiotensin II in the rat. The related peptides eledoisin hexapeptide, physalaemin and substance P also caused some drinking, but they were less effective than eledoisin. In the rat none of these substances caused drinking. On the contrary eledoisin and substance P were found to depress angiotensin-induced drinking, but carbachol-induced drinking was not depressed to the same extent by these peptides. The preferential depression of angiotensin II-induced drinking resembles the effects of other vasoplegic drugs on this response in the rat, and may be related to the potent vasodilator properties of these peptides.

Petide antagonists of the renin-angiotensin system in the characterisation of receptors for angiotensin-induced drinking.

The two naturally occurring analogues of angiotensin II (AII), Asp1-Val5-AII and Asp1-Ile5-AII, were equally effective as intracranial dipsogens in the water-replete rat. Renin, synthetic tetradecapeptide renin substrate (SRS) and angiotensin I (AI) also produced copious drinking when injected into the brain, but the naturally occurring renin substrate of rat caused little drinking and was much less effective than SRS. Prior intracranial injection of pepstatin, a competitive antagonist of the renin-angiotensinogen reaction, reduced drinking in response to renin and SRS but not to AI and AII. Renin-, SRS- and AI-induced drinking were inhibited by the converting enzyme inhibitor SQ 20881 injected through the same intracranial cannula in antagonist to agonist ratio of 1000:1, whereas the AII response was enhanced, although not significantly so, and the carbachol response was unaffected. Finally, position 8 aliphatic substituted analogues of AII were competitive antagonists of AII-induced drinking, and also inhibited drinking induced by renin, SRS and AI injected through the same intracranial cannula, but they did not inhibit carbachol-induced drinking. In conclusion, the angiotensin-sensitive receptor for thirst does not accept SRS or AI. It responds best to AII.

Structure and ultrastructure of the testis and sperm formation in goodeid teleosts.

Testis structure in four species of goodeid teleosts is described. Testicular tubules terminate blindly at the testis periphery where spermatogonia are located. In goodeid teleosts, development of sperm takes place synchronously within cysts whose periphery is made up of a single layer of Sertoli cells. Upon completion of spermiogenesis, spermiation ensues wherein sperm are shed, as spermatozeugmata, into the testis efferent duct system. Subsequently, Sertoli cells, which comprised the cyst periphery, transform into efferent duct cells. Sertoli cells phagocytize residual bodies and are involved in the formation of spermatozeugmata. The structure of the goodeid spermatozeugmatum is quite different from that observed in the related poeciliids. It is concluded, in view of this and other considerations, that the goodeids and poeciliids have independently evolved solutions to the problems of internal fertilization and gestation.

The use of thiamine and thiamine antagonists to investigate the etiology of early mortality syndrome in lake trout (Salvelinus namaycush).

Early mortality syndrome (EMS) is a non-infectious disease affecting lake trout and other salmonids in the Great Lakes and in inland lakes. It is characterised by loss of equilibrium, hyperexcitability, anorexia, and eventually death. EMS is associated with low thiamine and treatment of eggs or fry with thiamine-HCl eliminates symptoms and mortality. To verify the role of the active form of the vitamin as the prophylactic agent, we used thiamine pyrophosphate (TPP) to reverse EMS symptoms. We also investigated the ability of specific thiamine antagonists that either block TPP production or interfere with its function to induce EMS. When graded doses of TPP were administered to EMS-susceptible sac-fry, there was a dose-dependent reduction in EMS. The egg concentration of TPP that was associated with reduced EMS was similar to the threshold thiamine concentration found in feral lake trout stocks where EMS occurs. A thiamine deficient stock from Lake Ontario was very sensitive to the thiamine antagonist oxythiamine (OXY) with total mortality associated with developmental arrest occurring at an antagonist to thiamine molar ratio (ATR) above 7:1. The threshold ATR with OXY for development of EMS-like neurological signs in this stock was 1.6:1. In addition to EMS-like neurological signs, OXY caused dose-dependent increases in hydrocephalus, developmental arrest, and vitelline congestion in the Lake Ontario stock. These signs are consistent with those observed in feral fish exhibiting EMS. Much higher doses of antagonists were required (both pyrithiamine (PT) and OXY) to induce EMS-like clinical signs in the thiamine replete Lake Manitou stock. PT was a more potent inducer in this stock as the ATR associated with development of clinical signs was 111:1 for PT compared with 892:1 for OXY. These data provide experimental evidence supporting the hypothesis that a thiamine deficiency in the natural environment is the cause of EMS.

Carcinogenic and genotoxic activity of extracts from contaminated sediments in western Lake Ontario.

In order to investigate the putative association between chemical contamination in western Lake Ontario and high prevalences of fish tumors, sediments from Hamilton Harbour and Oakville Creek in Lake Ontario and reference sites in non-polluted areas of Ontario, Canada were collected and extracted for organic contaminants. Sediment extracts from Hamilton Harbour had the highest concentrations of polychlorinated biphenyls and organochlorine insecticides (ppb) and contained very high concentrations of polynuclear aromatic hydrocarbons (ppm); although the levels of these compounds varied widely with sampling location in the harbor. A sediment extract from Hamilton Harbour was mutagenic in the Ames bacterial assay, both with and without microsomal activation. High levels of aromatic DNA adducts were induced in cultured mouse C3H1OT1/2 cells after in vitro exposure to Hamilton Harbour sediment extract. In two separate carcinogenicity experiments involving a sac fry microinjection assay with rainbow trout (Oncorhynchus mykiss), Hamilton Harbour sediment extract induced hepatocellular carcinomas in fish. No hepatic neoplasms were observed in fish that had been treated with sediment extract from Oakville Creek, or with extract from a reference sediment. The significance of these results is discussed in relation to the distribution of neoplasms in feral fish within western Lake Ontario.

Control of ovine gastrointestinal helminthiasis by the use of 'clean' grazing and strategic dosing in the field.

Despite the widespread adoption of clean grazing systems in lowland sheep flocks, detailed parasitological investigations had not previously been carried out on such flocks. A trial was therefore conducted on two commercial flocks: a traditional permanent pasture flock (A) and one operating a system of clean grazing (B), and on an East of Scotland College flock (C) which had operated a clean grazing system for eight years. Ewe and lamb worm egg output, pasture larval levels and lamb liveweight gains were monitored and tracer lambs were grazed during July and August on each farm. Under clean grazing conditions on farm C all parasitological parameters were lower than on both commercial farms. However, in the commercial flocks comparable contamination was evident from midsummer onwards and tracer lambs grazed during August on farm B had significantly greater worm burdens than on the other two farms. The differences observed between the flocks were thought to be due to greater residual contamination by overwintered larvae in both commercial flocks while the higher worm burdens in August on farm B probably resulted partly from incomplete control of the periparturient rise in ewe faecal egg output and partly to autoinfection of the lamb crop. It was concluded that farm C grazing was the cleanest. Considerable contamination was present on farm A while farm B occupied an intermediate position which resulted in considerable worm burdens in lambs grazing during the latter part of the season.

Comparative study of gastrointestinal helminthiasis in sheep on 'clean' grazing and permanent pasture under field conditions.

An investigation of sources of helminth infection was carried out on three flocks: a traditional permanent pasture flock (A), one operating a 'clean' grazing system (B), and an East of Scotland College flock (C) which had operated a clean grazing system for nine years. Ewe and lamb worm egg output and pasture larval levels were recorded and tracer lambs were grazed during July and August on each farm. Considerable contamination was present on farm B fields compared with farms A and C, which resulted in higher worm burdens in late summer in farm B tracer lambs and lower weight gains. The main source of this infection was thought to be ewe periparturient egg output, as 21 per cent of ewes had positive worm egg counts over the lambing period. Differences in management practices between farms B and C, eg, earlier stocking of farm B fields, were also considered contributory factors.

Epidemiology of Nematodirus battus infection in eastern Scotland.

A field investigation was carried out from 1981 to 1983 on the prevalence of Nematodirus battus under different systems of lowland sheep management. Pasture larval counts, ewe and lamb worm egg counts, and tracer lamb worm counts were carried out. As expected, contamination was generally greater on permanent pasture than on new leys as measured by pasture larval counts and lamb worm egg counts. However significant contamination was also recorded on young grass fields for which alternate grazing with young calves may have been partly responsible. It is suggested that the 1983 hatch was delayed because of a drop in soil temperature in late March which may have increased subsequent scour problems involving N battus seen in May.

Colostrum production by ewes and the amounts ingested by lambs.

Studies involving 49 ewes which were well nourished during the last eight weeks of pregnancy indicated that ewe weight loss during pregnancy and lamb birth weights followed the recognised pattern and were within acceptable "normal" limits. Colostrum production ranged from 1238 to 4593 g per ewe during the 48 h following the first suckling and there was evidence that production levels were related to demand by the lambs. Colostrum consumption by individual lambs was related to litter size. The smaller the litter size the greater was the amount ingested during the first 48 h of life. No clear relationship was established between the amount of colostrum consumed and the level of immunoglobulin in a lamb's circulation. Possible reasons for this are discussed.