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Malaysian Journal of Medical Sciences
School of Medical Sciences, Universiti Sains Malaysia
ISSN: 1394-195X
Vol. 13, Num. 2, 2006, pp. 64-65

Malaysian Journal of Medical Sciences, Vol. 13, No. 2, July 2006, pp. 64-65

CASE REPORT

TYPHOID AND MALARIA CO-INFECTION - AN INTERESTING FINDING IN THE INVESTIGATION OF A TROPICAL FEVER

Wahinuddin Sulaiman

Department of Medicine, Hospital Taiping, Jalan Taming Sari, 34000 Taiping, Perak , Malaysia
Correspondence: Dr. Wahinuddin Sulaiman M.B.B.S (Malaya), M.Med (Internal Medicine)(USM) Department of Medicine, Hospital Taiping, Jalan Taming Sari 34000 Taiping, Perak, Malaysia, Malaysia Tel : 609+05-808 3333 Direct : 609+05-840 8025 Fax : 609+05-808 0930 E-mail : wahin@hotmail.com

Submitted-20-02-2004, Accepted-03-12-05

Code Number: mj06025

Malaysia is endemic for both these diseases and one should not be too surprised when faced with a diagnosis of co-infection of typhoid and malaria, as have been described in India and Canada. Here we describe one such case of Salmonella typhi and Plasmodium vivax infection.

Key words : typhoid, malaria, co-infection

Introduction

In the investigation of fever in the tropics, two important diagnoses to be ruled out are typhoid and malaria. Both cause significant morbidity, mortality and economic loss. An estimated 17 million cases of typhoid are reported worldwide each year, resulting in 0.6 million deaths. Seventy five to eighty percent of these cases occur in Asia alone. Malaria affects 1 billion people each year; out of which 1-3 million die. Although caused by very different organisms - one Gram negative bacilli, the other a protozoa, and transmitted via different mechanisms - ingestion of contaminated food and water and via the bite of an insect vector respectively, both typhoid and malaria share rather similar symptomatology and epidemiology.

Case report

A 41-year old Malay man, working as a logger, presented with two weeks of fever, myalgia and abdominal pain. He had been diagnosed and treated for malaria 20 years ago. He remained asymptomatic until now. He had no other history of traveling to any malaria endemic country and taking any malarial chemoprophylaxis. On examination, he was febrile with his body temperatures swinging between 37°C and 39.3°C and relative bradycardia. He was not jaundiced and neither were any rashes noted. There was no hepatosplenomegaly on physical examination.

His full blood count showed normal Hb (14.2g/dl) and platelet count (201 x 109 /l). The white cell count, was within normal range (5.2 x 109 /l) with neutrophil predominance. Serum albumin was 34.9 g/l, alkaline phosphatase 178 IUl, aspartate transaminase 63 IU/l, alanine transaminase 63.9 IU/ l and total bilirubin 9.4 umoll/l.

Ultrasonography of the abdomen showed hepatomegaly with a mildly echogenic parenchyma. The spleen was at the upper limit of normal (13.8 cm). Blood cultures isolated Salmonella typhi. The first Widal test was not significant (T(O) 1:50 and T(H) 1:50). The second Widal test taken nine days later showed T(O) 1:100 and T(H) 1:200. Serial blood smears for malaria parasites was positive for Plasmodium vivax (160/ul blood) on the fifth smear. He was treated with chloramphenicol 500mg qid for 14 days and a course of chloroquine and primaquine with an uneventful recovery.

Discussion

Typhomalaria was first described by an army doctor, J J Woodward (1833-1884) in 1862 among young soldiers during the American Civil War who were suffering from febrile illness that seemed to be typhoid (including intestinal lesions found at postmortem) but with fever patterns also suggestive of intermittent fever. He believed that it might be a hybrid rather than a new species of disease (1 - 3). However, by the end of 19th century, laboratory tests had eliminated this theory as they found that it was either one thing or the other, or in rare instances, co-infection with both S. typhi and the plasmodium of malaria.

Both typhoid and malaria share social circumstances which are imperative to their transmission. Therefore, a person living in such an environment is at risk of contracting both these diseases, either concurrently or an acute infection superimposed on a chronic one. A high index of suspicion is necessary to diagnose a co-infection as most clinicians are used to linking every symptom and sign to a single pathology.

In co-infections, the diagnosis of typhoid should be made from a culture specimen as false positives and overestimation occur with the use of the Widal test (4). Ammah A, et al reported that in 200 patients with fever, 17% had concurrent malaria and typhoid fever based on bacteriological proven diagnosis as compared with 47.9% based on the Widal test. This is to be expected as the Widal test being a serological test, only proves exposure to a certain antigen. It does not tell if an infection is recent or not. Samal KK, et al, described 52 patients with malaria positive in the peripheral blood smear (cases consisted of vivax, falciparum or mixed vivax and falciparum), out of whom eight cases had a positive Widal test but blood cultures were negative for S. typhi in all. All of the cases were cured with antimalarial therapy (5). There were no complications attributed to these infections documented in the previous reported cases. Nevertheless, complications may occur even if patient received adequate treatment. Hence monitoring for the complications is essential especially for travelers who traveling to endemic areas.

The actual and precise underlying mechanisms to explain the association between malaria and Salmonella species infection is still uncertain. However, there are few postulation which may explain why malaria may predispose to salmonella bacteremia and sepsis. It has been shown that antibody response to O antigen of S. typhi was markedly reduced in acute episode of malaria compared with that in controls where humoral immunity is transiently impaired (6). It has been demonstrated in a murine model of infection with Salmonella murium that hemolysis which occur in malaria may predispose to gram-negative organism as what has been seen in hemolytic disease caused by sickle cell disease and bartonellosis (7).

In the case illustrated above, the diagnosis was from a blood smear and a blood culture, both providing objective evidence of the on-going dual infection. Fortunately, he did not developed any complications such as hemolysis.

Although cases which had been reported were common among travelers, certain areas in our country is still considered endemic for both malaria and typhoid infections and our patient demonstrated that although he is not a traveler, these co-infection may still occur. Thus, in malarial patient with persistent fever in spite of therapy, one should consider drug resistant as well as concomitant gramnegative infection such as typhoid fever.

References:

  1. Bynum B. Typhomalaria. Lancet 2002; 360: 1339.
  2. Smith DC: The rise and fall of typhomalarial fever : I. Origins. J Hist Med Allied Sci 1982; 37: 182-220.
  3. Smith DC: The rise and fall of typhomalarial fever: II. Decline and fall. J Hist Med Allied Sci 1982; 37: 287- 321.
  4. Ammah A, Nkujo-Akenji T, Ndip R, Deas JE. An update on concurrent malaria and typhoid fever in Cameroon. Trans R Soc Trop Med Hyg. 1999; 2: 127- 129.
  5. Samal KK, Sahu CS. Malaria and Widal reaction. J Assoc Physicians India. 1991; 10: 745-747.
  6. Greenwood BM, Bradley-Moore AM, Palit A, Bryceson ADM. Immunosuppression in children with malaria. Lancet 1972; 1: 169-172.
  7. Kaye D, Hook EW. The influence of hemolysis or blood loss on susceptibility to infection. J Immunol 1963; 91: 65-75.

© Copyright 2006 - Malaysian Journal of Medical Science

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