The proportion of secondary transmissions of laboratory confirmed Shigella infection in high risk household contacts of primary cases reported in Amsterdam from 2002 to 2009 was 7.4%. Though not directly comparable to our study, similar intra-familial or household secondary transmission rates of Shigella have been reported in studies conducted in outbreak settings internationally [12, 13]. This rate is also similar to that of 8% reported by Vermaak et al. [8] in Amsterdam from 1992–1998. In our study, only households with contacts considered to be at high risk of secondary infection were included. As this represented a smaller denominator population than in Vermaak et al. [8], we had expected to find a relative increase in the rate of secondary infection. One explanation is that we underestimated the secondary attack rate and that (unscreened) positive asymptomatic cases in non-high risk households were missed. We consider this unlikely as in Vermaak et al. [8] this accounted for only 3 extra cases over 8 years. An alternative explanation is that hygiene standards in households in the Netherlands and abroad have improved over time, reducing the potential for secondary spread. The majority of Shigella infections are imported, but recent national research has shown that between 1995 and 2006 there was a significant reduction in the incidence of Shigella infection among travelers from the Netherlands which was related to improved hygiene standards in the countries visited [14]. Despite a doubling in the annual number of travelers to (sub)tropical countries from about 1 million in 1999 to 2 million in 2007 [15], the incidence of shigellosis in Amsterdam has remained relatively static at 8/100,000 in 1998 [8], and 7.7/100,000 annually from 2002–2009.
Where outbreaks of shigellosis have occurred in nurseries and schools, they have generally been attributable to children with diarrhoea who visited the institution or those who returned to school before being culture-confirmed negative [12, 16]. Outbreaks have been brought under control by excluding young shigellosis cases from school or daycare where supervision of a child’s hygiene may be inconsistent, pending microbiological clearance [17, 18]. In our first multivariable model, the only factor independently associated with Shigella positivity in a household contact was diarrhoea, irrespective of the age of the case or of the contact. The current policy, that all contacts with diarrhoea should be investigated for the presence of the bacterium Shigella, is therefore supported.
In the second multivariable model which examined predictors of secondary infection in contacts, preschool cases aged 0–3, those in junior classes in primary school aged 4–5 years, and those in large households were more likely to transmit (both symptomatic and asymptomatic) infection. Typically, young children who use the toilet independently but have limited understanding of good hand- and toilet-hygiene may be particularly susceptible to transmitting secondary infection. We did not find any increased risk among siblings of cases, or their mothers compared to other household contacts however, unlike similar research examining household transmission of E.Coli 0157 [19]. Based on our findings, screening of all contacts of cases who are under 6 years is also recommended. In fact, had faecal screening been limited to household contacts of cases who were under 6 years old and contacts with diarrhoea as we suggest, 96% of secondary cases would have been detected and only one asymptomatic adult carrier would have been missed. Additional faecal sampling of 164 contacts would not have been required.
The policy in the Netherlands of excluding all contacts under 6 years old pending a single negative faecal culture sample is generally not supported by our findings. In the multivariable models, the age of the contact was not independently associated with secondary Shigella infection and we found no association between young age of contact (<6 years old) and a risk of asymptomatic infection. In our study over the 8 year period, 70 asymptomatic children under 6 years old were potentially excluded from school or daycare pending microbiological clearance. This yielded only one asymptomatic infection. Although a formal cost-benefit analysis would be necessary to systematically compare costs, given considerable practical difficulties and low added value, the policy of excluding young children who are asymptomatic contacts of a case with shigellosis should be revisited.
There were a number of study limitations: firstly, we were unable to examine the risk of asymptomatic secondary transmission in low risk households, however among those at highest risk in these households who were screened (i.e. those who were symptomatic, or were care-workers or food-handlers) no secondary transmissions occurred. Secondly, we defined a secondary infection in a household contact as one that developed >1 day after the primary case. Had we used a more conservative definition (e.g. ≥3 days, based on the median incubation period), one additional case would have been reclassified, representing a secondary attack proportion of 7.2%. The associations at both univariable and multivariable level would not change however. Thirdly, there was a delay between date of onset of illness and date of notification of >3 weeks in 28% of cases. Recall bias is therefore likely, and cases and contacts may have reported estimated rather than precise dates of onset of illness. Ultimately, delay in reporting was not associated with secondary transmission of infection. Fourthly, culture was used for diagnosis of shigellosis, though it is recommended that the sample is submitted within 24 hours, false negatives may have occurred. The use of more sensitive molecular methods [20] might have revealed more cases of secondary transmission. Finally, given the low proportion of secondary transmissions, it is possible some differences may have been undetected due to insufficient power.
