Bacillary dysentery / by Sudhir Chandra Pal

Bacillary dysentery by Sudhir Chandra Pal uring the first half of 1984, a severe epidemic of bacillary dysentery swept through the districts of West Bengal and a few other eastern Indian States, affecting over 350,000 people and leaving about 3,500, mostly children, dead. It was like a nightmare as the disease stubbornly refused to respond to con- ventional treatment, and its galloping spread could not be contained by all available public health measures. People became confused and panicky, not knowing what to do. Bacillary dysentery, characterised by frequent passage of blood and mucus in the stools accompanied by excruciating abdominal pain, fever and intense weakness, has been afflict- ing mankind since recorded history began. It has been responsible for millions of deaths and disabilities dur- ing wars, floods, famines and other human catastrophes. Infection is caused by bacteria be- longing to the genus Shigella, and hence the disease is known as shigel- losis. The genus Shigella comprises four subgroups-S. dysenteriae, S. flexneri, S. boydii, S. sonnei-and 34 serotypes. Of the various types of shigellosis, infections caused by S. dysenteriae type 1 are the most severe and often occur in epidemic form. This type is also known as Shiga bacillus after the Japanese scientist Dr Kiyoshi Shiga who discovered the organism in 1890. Bacillary dysentery has a global dis- tribution but the highest prevalence is in countries where hygiene and sanita- tion are poor. There, endemic shigel- losis still remains a significant cause of morbidity and mortality, especially among pre-school children. In the de- veloped countries, bacillary dysentery is a mild disease mostly caused by the less virulent S. sonnei. Man is both the reservoir and natur- al host of shigella. Infection is by the faecal-oral route and the most com- mon mode of spread is by person-to- person transmission owing to the low 14 infectious dose. It requires only 10 to 100 shigella bacteria to produce dys- entery, whereas one million to ten million germs may need to be swal- lowed to cause cholera. By 1920, dysentery due to the most virulent variety, the Shiga bacillus, had almost disappeared from Europe and North America. However, it con- tinued to be reported from the de- veloping countries in the form of local- ised outbreaks. During the late sixties, Shiga's bacillus reappeared with a big bang as the main culprit of a series of devastating epidemics of dysentery in a number of countries in Latin America, Asia and Africa. In 1967 it was first detected on the border between Mexico and Guatema- la and then spread into most parts of Guatemala, Belize, El Salvador, Hon- duras, Nicaragua and Costa Rica. An estimated half million cases with 20,000 deaths (including 13,000 chil- dren) were reported during 1967 to 1971 from these countries. The case- fatality rate was as high as 15 per cent in some villages. Delayed diagnosis and improper treatment might have been the cause of the high death rate, particularly among children. An addi- tional disturbing feature was that the causative agent was resistant to the commonly used antibacterial drugs such as sulfonamides, tetracycline, chloramphenicol and streptomycin. During 1970 to 1972, the disease spread to the United States but could not get a firm foothold and was limited to only 140 cases. The next devastating epidemic oc- curred in Bangladesh in 1972 and continued with undiminished ferocity up to 1978. The cases were uniformly severe and the case-fatality rate in a well-equipped Dhaka hospital was as high as 10 per cent by contrast with only 0.5 per cent in cholera. The death rate was highest among infants (41 per cent) and elderly persons (22 per cent). In addition, several uncommon serious complications such as toxic megacolon, haemolytic uraemic syn- drome and leukaemoid reactions were also reported. Similar epidemics due to the multiple-drug-resistant S. shigae have also occurred in Somalia (1976), three villages in South India (1976), Sri Lanka (1978-80), Central Africa (1980-82), Eastern India, Nepal, Bhu- tan and the Maldives (1984) and Bur- ma (1984-85). The pattern was more or less the same everywhere. The disease spread with terrific speed in spite of all available public health measures, attacking over 10 per cent of the population and killing between two and 10 per cent even of the hospitalised cases, but mostly infants and children. In Central Africa it spread 800 kilometres in the first year and attacked several countries. The State of West Bengal (as well as the rest of India) has been endemic for bacillary dysentery, but the propor- tion of cases always remained less than five per cent of the total acute diarrhoea cases referred to hospital. But clinical dysentery cases with fre- quent passage of blood and mucus in the stool, abdominal cramps and fever started occurring in large numbers in northern districts of West Bengal from early 1984. The disease spread rapidly to the southern part of the State, and a team from the National Institute of Cholera and Enteric Diseases inves- tigated an outbreak in a village 70 kilometres from Calcutta in March that year. The village of Dhamasin had 91 acute dysentery cases with two deaths among its 937 population during a one-month period, giving an attack rate of 9.7 per cent and a case-fatality rate of 2.2 per cent. The attack rate was highest (22.7 per cent) in the below-one-year age group. Seven pa- tients were admitted to the local health centre, of whom a boy and a girl aged two years died. Shigella shigae was isolated from six out of 22 stool samples examined. All these bac- teria were resistant to the commonly used drugs and similar to those re- W oRLD HEALTH, April 1986 parted from neighbouring Bangladesh and elsewhere. The matter was promptly brought to the notice of the State as well as of the central government for early initiation of control measures. Information on the epidemic was flashed by newspapers, radio and television to raise public awareness, and health functionaries at the district level were alerted. As a result, the State Health Directorate started receiving reports of dysentery cases from one district after another. The numbers started increasing shar- ply, with the addition of 2,000 to 3,000 new cases and 100 to 150 deaths per day. The public started to panic, and the clinicians felt frustrated because the conventional treatment regimen proved ineffective. The epidemic also spread to Calcut- ta, and the number of clinical dysen- tery cases started increasing at the local Infectious Diseases Hospital from the middle of April. A total of 3 ,493 W oRLD HEALTH, April 1986 Simple prevention-washing hands with soap and water before eating and after going to the toilet. Photo W HO/S. C. Pal cases were admitted to the hospital by the end of May, and there were 70 deaths (two per cent). Samples of stool from 382 patients revealed different species of shigella germs in 52 per cent and Shigella shigae in 35 per cent of cases. These germs were sensitive to nalidixic acid (96.7 per cent), gen- tamycin (83 per cent) and furazo- lidone (77.7 per cent) , and moderately sensitive to ampicillin (42.2 per cent), kanamycin (37.4 per cent), neomycin (21.8 per cent) and co-trimoxazole (23.2 per cent), but were resistant to other commonly available antibiotics and drugs. For most of the clinicians, this was the first encounter with an epidemic of severe bacillary dysentery and there was terrible confusion over the choice of antibacterial drugs and other treat- ment. Nalidixic acid was found to be the drug of choice, but its high cost precluded its common use. Oral rehy- dration, the magic therapy for watery diarrhoea, was effective in only 10 per cent of these cases since 90 per cent had no dehydration. The sudden appearance of the large- scale epidemic took the public health authorities by surprise. But soon pre- ventive measures were undertaken at all levels of health care. The mass media undertook a vigorous prop- aganda campaign for public aware- ness, advocating boiling or chlorinat- ing drinking water, covering faeces with soil, protecting food from flies, avoiding eating exposed raw veget- ables and cut fruits, and washing hands with soap and water before eating and after going to the toilet. However, the efficacy and feasibili- ty of such methods of prevention are questionable. For example, the total production of halogen tablets-used for purifying drinking water-was only enough to meet the requirements for one or two days in the State of West Bengal alone. Similarly the scarcity of fuel restricted its use for boiling water for drinking. There is convincing evi- dence that washing hands with soap and water reduces transmission of the pathogen, but people cannot be edu- cated overnight to practise this simple procedure. As a result the epidemic took its own course and subsided only gradually, traumatising both the pub- lic and physicians in the process. Epidemics of bacillary dysentery which had been thought a thing of the past have emerged once again as a major threat to the poverty-stricken people of developing countries. The disease has already spread to as many as seven out of 11 countries in the South-East Asian region. The cause of this resurgence is not yet understood. Further alarming features are that the causative agent, Shiga's bacillus, has become resistant to most of the anti- bacterial drugs and the case-fatality rate is unbelievably high. Scientific knowledge about the dis- ease and the · germ is still inadequate. More needs to be known about the exact mode of transmission of the pathogen, about the mechanisms of pathogenicity, or even about the actu- al cause of death due to the disease. This would help in formulating more effective and practicable control measures, including development of an effective vaccine. • 15