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May 1997, Volume 47, Issue 5

Case Reports

Shigella Septicaemia in An Infant

Javaid Usman  ( Department of Microbiology, Armed Forces Institute of Pathology, Rawalpindi Cantt. )
Shahid Aziz  ( Combined Military Hospital, Kharian Cantt. )
K. A. Karamat  ( Department of Microbiology, Armed Forces Institute of Pathology, Rawalpindi Cantt. )
Tariq Butt  ( Department of Microbiology, Armed Forces Institute of Pathology, Rawalpindi Cantt. )


Shigellosis has a global distribution and is one of the importantpathogens responsible for bacterial dysentery which is a common diarrhoeal disease of the developing countries1. The infection is transmitted by faecal oral route. The prevalence of the disease is highest in the developing countries withbad hygiemc conditions and poor sanitation2. The disease isusually ushered inwithfeverfollowedby the onsetofwatery diarrhoeawhichtums to bloody withorwithout the othersigns and symptoms of dysentery. Local or systemic manifestations may complicate the illness. Systemic complications include bacteremia and septicemia with the infecting strain especially in malnourished, young. weaned infants. Shigella septicemia is not a common complication. We observed a case of shigella septicemia which is presented hem.

Case Report

A 10 months old child, resident of rural area of Tehsil Kharian, presented with loose motions, vomiting, fever and fits off and on of one month duration. The frequency of stools was 5-6 times per day without blood. The child was bottle fed. On examination, the child was lethargic, pale dehydrated, had a temperature of 100°F and pulse rate of 140/mm. His chest was clinically clear and abdomen was soft. At the time of admission, his blood urea was 26.4 mmol/l, Na 132 mmoLfl, potassium 5.2 mmoIIl, creatinine 308 umol/l, blood glucose 4.1 mmoLfl, serum calcium 7.6 mg/dl, Hb 8.1 g/dI, TLC 13.5x109/l, differential Count with neutrophils 80%, lymphocytes 16%, monocytes 1%, eosinophils 03% and plain X-ray chest was. nonnal. His stool and blood revealed on culture, Shigella flexnerii serotype 2. The Shigella flexnerii was resistant to ampicillin, cotrimoxazole andtetracycine and sensitive to chloramphenicol, ciprofloxacin, cephmdine and ceftizbxime. The child was administered Ringer’s solution and Glucose 5% alongwith chlorainphenicol 175 mg 1/V 6 hourly. Six days after admission he became afebrile and after 7 days all the laboratory tests became normal. He was discharged from the hospital with advice to continue oral chloramphenicol for further 7 days.


Shigellosis is an acute inflammation of the intestinal tract caused by species of Gram negative genus Shigella. The transmission of Shigella species normally occurs by the direct anal-oral route, although waterand food supplies are involved in some outbreaks of bacterial dysentery. Extra-intestinal presentations of shigellosis is quite rare. Systemic complications include bacteremia with the infecting stain especially in malnourished young weaned infants and occasionally resulting in disseminated intravenous coagulopathy3,4. Leukemoid reaction5, or the haemolytic syndrome6. Infants and children are more prone to develop shigellosis and its complications, presumably because of lack of pre-existing immunity and greater likelihood that the children will transfer the organism via the faecal-oral route7. Although bactemmia and septicemia may not be a common feature of shigcllosis but it is reported by many workers3,6. Struelens et al , isolated shigellae from blood in 4.1% (n=82) from patients with shigellosis. The prevalence of all bacteremia was highest in the first year of life. Patients at the highest risk of death from shigella bactemmia were less than orte year old, non-breast fed, malnourished and febnle6. The disease is self-limiting in many cases and antimicrobial usage does not seem to shorten the duration of symptoms or hospital stay8, but when the child develops bacteremia and septicemia, antimicrobials may play a role in controlling the infection and reducing the mortality rate. Although the isolate was sensitive to chloramphenicol butitwas resistant to many antibiotics like ampicillin, cotrimoxazole and tetracycline. The resistance of shigellae in our set-up is constantly changing9 and we may find no choice of antimicrobial, particularly for such serious situations.


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2. Christie, AD. Bacillary dysentery. Br. Med.J, 1968;2:285-8.
3. Struelens, Mi., Patte, D., Kabir, I. et a!. Shigella septicemia: Prevalence, presentation, risk factors and outcome.J. Infect. Dis., 1985;152:784-90.
4. Bennish, ML., Harris, J.R., Wojtyniak, B.J. etal. Death in shigellosis: incidence and risk factors in hospitalized patients. J.Infect.Dis., 1990;1 61:500-506.
5. Butler, T., Islam, M.R., Bardhan, P.K. Leukemoid reaction in shigellosis. Ain.J.Dis.Child., 1984;138:162-64.
6. Koster, F., Levin, 3., Walker, L. et al. Haemolytic-uremic syndrome after shigellosis. N. Engi. 3. Med., 1978;298:927-933.
7. Keusch, G.T. and Bennish, ML. Shigellosis: Recent progress, persisting problems and research issues. Pediatr.Infect. Dis. J., 1989;8:713-716.
8. Daoud, A.S., Zaki, M., Al-Matairi, G. et a!. Childhood shigellosis: Clinical and bacteriological study. J. Trop. Med. Hyg., 1990;93:275-9.
9. Butt,T.,Karamat,K.A., Qamar,R.H. et al. Is nalixidic acid the drug of choice for shigellosis? JCPSP., 1996;6:24-27.

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