Prevalence:
Sd1 has caused epidemics of dysentery throughout the world. It caused a 4-year epidemic in
Central America beginning in 1968 that resulted in more than 500 000 cases and at least 20 000
deaths. No epidemics have occurred in the region since then, but Sd1 continues to occur
sporadically in the Western hemisphere. In Africa, epidemic dysentery due to Sd1 appeared in
eastern Zaire in 1979 and has subsequently been confirmed in Angola, Burundi, Equatorial
Guinea, Ethiopia, Kenya, Malawi, Mozambique, Rwanda, Sao Tomé and Principe, South
Africa, Swaziland, Tanzania, Uganda, Zambia, and Zimbabwe.
Transmission:
Few studies have been done to determine how dysentery is spread. The most likely modes of
transmission are person-to-person contact, and contaminated water and food. Epidemics of Sd1
usually occur in impoverished areas. They affect people of all ages, with the highest
age-specific incidence occurring among adults and the highest case fatality rates occurring
among children.
Antimicrobial Resistance:
A major obstacle to the control of Sd1 is its resistance to many antimicrobial drugs. In one
central African country the bacillus was resistant to all oral antibiotics that were locally
available. Furthermore, Sd1 can quickly develop resistance. Antibiotics are often effective
against it for only one or two years after being introduced; resistance has even been observed
to develop during the course of an epidemic. As resistance to commonly available antibiotics
becomes more prevalent, alternative antibiotics are needed which are more expensive and more
difficult to procure.
Treatment:
During an epidemic, all dysentery patients should receive an antibiotic to which Sd1 from
local cases has been shown to be sensitive. Dehydration should be treated with oral
rehydration salts or, if severe, with intravenous fluids. Urgent efforts should be made to
obtain enough antimicrobials to treat all patients, but if in short supply they should be
reserved for those at highest risk of secondary complications and death. These would include
children under five years of age, adults older than 50 years, patients presenting with
dehydration, and those with serious underlying conditions such as malnutrition. Patients
should be identified as early as possible so that treatment can be initiated with a minimum of
delay.
Epidemic Control and Preventive Measures:
Early detection and notification of epidemic dysentery, especially among adults, allows for
timely mobilization of resources needed for appropriate case management and control. National
and peripheral-level laboratories should be strengthened so they can reliably confirm Sd1 as
the cause of an outbreak. Rectal swabs from suspected cases should be collected and shipped to
laboratories in an appropriate medium (preferably refrigerated) for culture to confirm the
diagnosis of Sd1.
Laboratories should also be able to determine antimicrobial sensitivity patterns of Sd1 so that rational policies for the use of antimicrobials may be developed. Such policies should consider the antimicrobial sensitivity of local Sd1 strains and the availability and cost of effective antimicrobials. Testing of Sd1 isolates for antimicrobial sensitivity should be done at regular intervals to determine whether treatment guidelines remain appropriate.
Health education efforts should promote improved personal, domestic, and environmental hygiene. This includes hand washing with soap after defecation and before handling food, use of clean drinking water, safe practices for preparing and storing food, and safe disposal of faeces.