673 Pattern A shows that the current nutrition of all family members is
adequate. The parents and older children
may be small in stature, but their present
reflecting undernutrition in early childhood,’° nutritional status is satisfactory.
In pattern B the adults, infant, and older children
are
all
adequately nourished, but the pre-school children show evidence of present undernutrition. This is
a
very
common
pattern in poor
communities, where infants are generally protected for the first
few months of life by breastfeeding, but from the later months of infancy to about four years of age the children are undernourished with resulting decrease in height-for-age, weight-for-age, and weight-for-height. By the time these children reach school age, they can cope adequately with their environment. From then on their current nutrition, as indicated by weight-for-height, approaches normal, but they are left with a deficit in height-for-age and weightfor-age. This pattern of malnutrition does not reflect an absolute deficiency of food in the family home, rather it suggests either a lack of satisfactory foods for young children or else other deficiencies in their care. These are common causes of malnutrition in developing countries, where young children are expected to eat the same foods as adults and where both parents may spend their days in the fields, leaving the care of young children to older siblings. Pattern Csuggests poor practices of infant and child care, perhaps with a working mother who cannot feet and care for her infant and younger children during the day. In pattern D, poor nutrition or disease in the mother is almost certainly the primary factor leading to secondary effects in the younger children. The school-age children can fend for themselves. Pattern E indicates an absolute lack of food in the family. Pattern F with isolated "malnutrition" of a school-age child is much more likely to result from disease than malnutrition. Many other family patterns are possible and each could be interpreted as a result of specific family problems. Malnutrition and disease tend to cluster in problem families. When such families are identified and the pattern of their needs determined, intervention can be targetted more accurately and efficiently. Anthropometry has its limitations and cannot detect all diseases, but it will increase the efficiency in the use of field data for action programmes. Human Nutrition Research Group, c/o Department of Child Health,
University of Queensland, St Lucia, Queensland 4067, Australia
Ig titres to Sflexneri during dysentery after accidental infection. Titres are expressed relative to preinfection levels±SD. For ELISA Sflexneri 2a was harvested from blood agar plates and adsorbed onto ’Immulon’ 96-well micro-ELISA plates (Dynatech) over 24 h at 37°C (0- 5 mg dry weight per well). Plates were rinsed thrice with phosphate buffered saline (PBS) containing 0-5% ’Tween-80’. Serial serum dilutions in PBS containing 1 % bovine serum albumin (essentially Ig free; Sigma were incubated in quadruplicate at 37°C for 1 h. After rinsing thrice in PBS-tween, anti-humanIg peroxidase conjugates (Tago) were incubated for 1 h at 37°C and, after rinsing five times, fresh substrate was added. The reaction was stopped after 15 mm and optical absorbance measured with a multiscan reader (Flow Laboratories). Each plate contained a row of substrate controls and a calibration
curve.
later. 4 days after infection and 1 day after severe dysentery had developed, titres were still at baseline. IgA and IgG titres had increased sharply 18 days after infection, especially IgA, which rose to 50 times the pre-infection value. Titres had returned to baseline
after about 1 year. A. E. DUGDALE
Waterlow JC. Classification and definition of protein-calorie malnutrition. Br Med J 1972; ii: 566-69. 2. Waterlow JC. Note on the assessment and classification of protein-energy malnutrition in children. Lancet 1973; ii: 87-89. 3. Jelliffe DB. WHO Monogr Ser 1966, no 53, Geneva. 4. Keys A. Overweight, obesity, coronary heart disease and mortality. Nutr Rev 1980; 38: 1.
297-307. 5. Andres R. Effect of obesity on total mortality. Int J Obesity 1980; 4: 381-86. 6 Measuring change in nutritional status. Geneva: WHO, 1983. 7. Dugdale AE. Nomograms for monitoring nutritional status. Ecol Food Nutrit 1984; 14: 59-62. 8. Garrow JS. Desirable weight. Br Nutr Found J 1983; 8: 149-153. 9. Bray GA. Definition, measurement and classifications of syndromes of obesity. Int J Obesity 1978; 2: 99-112. 10. Anderson MA. Comparison of anthropometric measures of nutritional status in preschool children in five developing countries. Am J Clin Nutr 1979; 32: 2339-45.
IgA RESPONSE DURING ACCIDENTAL INFECTION WITH SHIGELLA FLEXNERI
SIR,-Bacillary dysentery due to Shigella flexneri is a major disease
in the tropics,1 but outbreaks also occur in temperate climates, often after consumption of contaminated imported food.Since most patients with shigellosis have positive stool cultures for only a few days,3 a sure diagnosis cannot always be made on bacteriological findings alone; serological support would be convenient. Furthermore, serology requires less laboratory back-up. Unfortunately, little information is available about the serological response in bacillary dysentery. We have found a major IgA response. The figure shows serum immunoglobulin titres to Sflexneri as determined by ELISA in a 25-year-old male laboratory worker who was accidentally infected by mouth and who had dysentery 3 days
Assay IgA antibody to S flexneri may assist in the diagnosis of shigellosis, and this can conveniently be done by ELISA. The finding of a clear serum IgA response to Sflexneri might be useful in the development of immunisation schemes to counter bacillary dysentery. Department of Medical Microbiology, University of Amsterdam, 1105 AZ Amsterdam, Netherlands
Ch. G. VAN BOHEMEN
A. J. J. M. NABBE H. C. ZANEN
1.
Khan MU. Interruption of shigellosis by hand washing. Trans Roy Soc Med Hyg 1982;
2.
van
3.
post-dysenteric arthropathies. Immunology (in press). Sharp JT. Reiter’s syndrome: a review of current status and a hypothesis regarding its pathogenesis. Curr Probl Dermatol 1973; 5: 157.
76: 164. Bohemen CG, Lionarons RJ, van Bodegom P, et al. Susceptibility and HLA-B27 in
TEST FOR &bgr;-LACTAMASE PRODUCTION
SIR,-The case described by Dr Black and colleagues (Aug 10, p 331) is the latest of several reports of multiple &bgr;-lactamase resistance emerging after therapy with one of the newer cephalosporins. We have had a similar experience with a burns patient and found that a simple techniques 1,2 can avoid the problem. A 39-year-old man with 40% burns was given ceftazidime for a clinically diagnosed septicaemia with a presumed Pseudomonas aeruginosa (ceftazidime sensitive) known to be present on his burns. He improved clinically. Swabs from burns 10 days later grew P aeruginosa resistant to ceftazidime and other &bgr;-Iactams. No organism was isolated from blood cultures and the resistant strain did not cause further infection. Multiple -lactam resistance has been shown to arise in certain groups of organism, Enterobacter spp, P aeruginosa, Citrobacter spp,