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Year : 2007  |  Volume : 17  |  Issue : 4  |  Page : 176--177

A sinister presentation of typhoid fever

P George1, B Pawar2,  
1 Department of Internal Medicine, Christian Medical College and Hospital, Ludhiana - 141 008, India
2 Department of Nephrology, Christian Medical College and Hospital, Ludhiana - 141 008, India

Correspondence Address:
P George
Department of Internal Medicine, Christian Medical College and Hospital, Brown Road, Ludhiana - 141 008, Punjab


Hemolytic uremic syndrome (HUS) is a recognized complication of E. coli O157:H7 and Shigella infection. It has been rarely associated with Salmonella typhi infection and has a high mortality, if the recognition and treatment of this disease is delayed. A fatal outcome of HUS following Salmonella typhi infection is described.

How to cite this article:
George P, Pawar B. A sinister presentation of typhoid fever.Indian J Nephrol 2007;17:176-177

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George P, Pawar B. A sinister presentation of typhoid fever. Indian J Nephrol [serial online] 2007 [cited 2022 Aug 19 ];17:176-177
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Typhoid fever is a systemic infection with Salmonella typhi ( S. typhi ). The occurrence of disease is high in developing countries due to poor sanitary conditions. The reported incidence may be higher than the currently estimated one in India due to the inadequate facilities for culture and predominantly outpatient empirical treatment with fluoroquinolones. Deaths are related to the complications of the disease which occur in 10-15% of patients. [1] Typhoid fever rarely presents as a renal manifestation.

 Case Report

A 56-year-old male presented with multiple episodes of loose, watery stools, vomiting and profound weakness. There was no blood or mucus in the stools, and he did not have fever. Three months earlier he had renal biopsy-proven acute interstitial nephritis, probably induced by a course of gatifloxacin. He was treated with oral prednisolone (1 mg/kg/day), which was tapered and stopped after 6 weeks. His renal functions improved during this period from a serum creatinine level of 4.5 to 0.9 mg/dl. An autoimmune and vasculitis work-up was normal.

During his admission, he had no other significant clinical signs besides dehydration. The urine output was normal. Investigations revealed a hemoglobin level of 15.6 gm/dl; total leucocyte count (TLC), 11200/mm 3 ; and platelet count, 40000/mm 3 . Peripheral blood film and reticulocyte count were normal. The blood urea and serum creatinine levels at admission were 62 mg/dL and 1.4 mg/dL, respectively. Urinalysis showed 1+ albumin and no active sediments. Stool analysis showed no cholera-like organisms, ova or cysts. A diagnosis of acute gastroenteritis and sepsis was made and treated with cefotaxime and metronidazole. On the third day in hospital, he developed fever, abdominal distension and drowsiness. The serum creatinine level increased up to 2.5 mg/dl, and he developed severe metabolic acidosis with hypokalemia necessitating urgent hemodialysis. He was anuric thereafter. The hemoglobin, TLC and platelet count decreased to 7 gm/dl, 5400/ mm 3 and 11000/mm 3 , respectively. The reticulocyte count was 1%, schistocytes were observed on the blood film and lactate dehydrogenase (LDH) increased up to 1192 IU/dl. The liver function was deranged with hyperbilirubinemia (total bilirubin, 2.8 mg/dL; and direct bilirubin, 1.6 mg/dL) and mildly raised transaminases (aspartate aminotransaminase, 407 IU/L; and alanine transaminase, 149 IU/L.) Direct Coomb's test was negative. Hemolytic uremic syndrome (HUS) was suspected, and plasmapheresis was initiated along with blood and platelet transfusion. He underwent two sessions of plasmapheresis, but died after this. His stool culture report that was available shortly after his death showed S. typhi . The blood culture was sterile.


Hemolytic uremic syndrome is a disease of nonimmune hemolytic anemia, low platelet count and renal impairment. Anemia is severe and microangiopathic in nature (schistocytes in the peripheral smear.) High LDH, circulating free hemoglobin, reticulocytes and a platelet count less than 60,000/mm 3 is observed in most of the cases. [2] However, this patient had a poor reticulocyte response explained by a possible lag in the bone marrow response to acute hemolysis. It is most commonly triggered by Shiga toxin (Stx)-producing Escherichia coli and Stx-producing Shigella dysenteriae serotype, [3] which has been commonly linked to Stx HUS in India. [4] S. typhi has been rarely described to be the cause for HUS and it may be fatal. [5] A case report found no evidence of Stx in the bacterial isolate of a patient with S. typhi -induced HUS. [6] The pathogenesis for HUS in typhoid is unclear, but the expression of S. typhi virulence factors and endothelial injury with oxidative and shear stress and resultant microvascular thrombosis may be a possible explanation.

The absence of specific symptoms or signs often makes the clinical diagnosis of typhoid difficult. Profound weakness, as described by the patient at admission, is a common symptom in HUS and appears to reflect more than just rapidly developing anemia. [7] Blood culture is positive in 60-80%, and the stool culture is positive in 30% of patients with acute typhoid fever. [1] Thrombocytopenia is generally found as a complication in typhoid fever, but may be encountered as a presenting sign on admission. [8] Leucocytosis could be a pointer to the development of HUS in typhoid fever. [9] While no studies on the role of plasmapheresis are available in typhoid fever-associated HUS, the decision to perform such a study was taken in the viewpoint of sudden deterioration of the patient and possible benefit, as demonstrated in an epidemic E. coli O157:H7 infection. [10]

The early recognition of clinical symptoms such as fever, diarrhea and profound weakness with laboratory parameters such as leucocytosis and thrombocytopenia may alert a physician to suspect HUS in typhoid fever. The close monitoring of nonimmune hemolytic anemia and renal impairment in such patients and the early institution of treatment with ceftriaxone may be life saving. More studies must be conducted on the role of plasmapheresis in typhoid fever-induced HUS to comment conclusively on its benefits.


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