1. CHRONIC MALNUTRITION (STUNTING) Presenters: Dr Nkhoma, Dr Zimba Moderator: Dr Amadi

2. ACUTE MALNUTRITION Acute malnutrition Diarrhoea

3. MALNUTRITION  Acute 1. by weighing a child and measuring his or her height (wasting); 2. by measuring the circumference of the mid-upper arm; or 3. by checking for oedema in the lower legs or feet  Chronic 1. by takina height of child against his or her age (stunting)

4. STUNTING MAGNITUDE Of the 555 million children in developing countries: 32% stunted Consequences  > 20 % of all <5 year mortality  Fewer years of school and poorer performance while there  Long-term cognitive defects  Lower adult productivity  For girls: increased risk of stunted children

5. WHAT CAUSES STUNTING?  Malnourished mothers? Meta-analysis shows 20-30% of stunting is due to intra-uterine factors  Poor feeding? The average deficit in African children is -2 HAZ but the best studies of complementary feeding improve growth only 0.7 HAZ (about 30% of the deficit)  Diarrhea? Five studies suggest that 5% to 20% of stunting is associated with diarrhea  Environmental enteropathy? A study from the Gambia showed that all young children are affected and attributed 40-60% of stunting to this condition

7. ENVIRONMENTAL ENTEROPATHY (EE)  EE also called tropical enteropathy is a subclinical disorder that occurs among inhabitants of environments with poor sanitation and hygiene, such as those often found in developing countries  Chronic exposure to faecal pathogens is hypothesized to cause inflammation and structural changes in the small bowel, which ultimately result in functional changes

9. IMPACT AND COURSE OF EE  EE explained 43% of growth faltering in the Gambia with a range from ~40-60% based on different measures – No association with frequency of diarrhoea – Little impact of supplementary feeding on growth  EE first occurs at ~2 mo; affects 50% of infants at 6 mo; and 96% at 10 mo  During the first yr of life, EE present >75% of the time compared with diarrhoea for 7-10% of the time  Of over 400 infants studied, all had EE at some point before 15 mo of age (Lunn PG. Proceedings of Nutr Society, 2000)

10. PATHOPHYSIOLOGY OF EE  Flattening of villi in gut mucosa –villous atrophy – modest malabsorption – Reduced lactase enzyme – functional lactose intolerance – Increased permeability, absorption of pathogens and chronic inflammation  Measuring EE – Decreased mannitol uptake & increased lactulose uptake measured by ratio of the two in a 5 hr urine sample

11. MECHANISM OF EE Chronic immune activation ↑ pro-inflammatory cytokines Immunosenescence (premature aging) of adaptive cell- mediated immune system Anemia ↑ Hepcidin ↓ Growth Factor (IGF-1) Stunting Impaired response to vaccines and infections

12. TODDLERS CONSUME POULTRY FECES  Peruvian shantytown families: – Households who owned free-range poultry: Average ingestion of poultry faeces by toddlers per 12-hour observation period was 3.9 times – Marquis GM et al., Am J Public Health 1990  Rural Zimbabwe: – Not selected for poultry ownership: 3 of 7 toddlers directly ate chicken faeces during a 6- hour observation period. – Ngure F et al., submitted, 2012

13. MICROBIAL CONTENT OF CHILD EXPOSURES:ZIMBABWE %HH with E coliE coli/ per gramAverage E Coil Per “ serving size” Infant Food0%00 Drinking Water54%2800 Soil in laundry area 60-80%702,100 Chicken feces100%10,000,000

14. Baby WASH: Potential Interventions to Prevent EE  Protective play space  Limit child exposure in high risk areas  Keep animals out of house  Latrines/safe disposal of feces (adult & infant)  Infant handwashing  Clean water  Community developed solutions

15.  Thank you for Listening