Year : 2012 | Volume
: 5 | Issue : 5 | Page : 551--552
Co-existence of typhoid fever and hepatitis A
Syed Ahmed Zaki, Preeti Shanbag
Department of Pediatrics, Lokmanya Tilak Municipal General Hospital and Medical College, Sion, Mumbai, India
Syed Ahmed Zaki
Room no. 509, New RMO Quarters, Sion, Mumbai - 400 022, Maharashtra
Typhoid fever and viral hepatitis are endemic in many developing countries. Both are transmitted by the feco-oral route and are associated with poor sanitation. Co-existence of both the infection is possible posing a diagnostic dilemma for the treating physician. We report a 7-year-old boy, who had co-existent typhoid fever and hepatitis A infection and was managed successfully. An aim of this report is to discuss the clinical scenario and presentation when typhoid fever and hepatitis A occur concurrently in a patient.
|How to cite this article:|
Zaki SA, Shanbag P. Co-existence of typhoid fever and hepatitis A.Ann Trop Med Public Health 2012;5:551-552
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Zaki SA, Shanbag P. Co-existence of typhoid fever and hepatitis A. Ann Trop Med Public Health [serial online] 2012 [cited 2021 Jan 19 ];5:551-552
Available from: https://www.atmph.org/text.asp?2012/5/5/551/105163
Both, typhoid fever and viral hepatitis are endemic in developing countries. As typhoid hepatitis can clinically mimic an acute viral hepatitis, their differentiation assumes significance in clinical practice since the former has definitive treatment in the form of antimicrobials.  In addition to above, sometimes both can co-exist in the same patient as the transmission routes of both the infection are feco-oral and have an association with poor sanitation.  This can give rise to diagnostic dilemma resulting in delayed diagnosis and treatment. We report a 7-year-old boy, who had co-existent typhoid fever and hepatitis A infection and was managed successfully.
A 7-year-old Indian boy was admitted with fever, vomiting, abdominal pain for 5 days and yellowish discolouration of eyes for 3 days. Fever was high grade, continuous and associated with chills and rigors. An abdominal pain was dull aching in the right hypochondriac region. Vomiting was non-bilious, non-projectile, containing ingested food particles. There was also history of loss of appetite and passing high colored urine for two days. There was no history of blood transfusion, jaundice or hospitalisation in the past. There was no headache, dysuria, diarrhea or bleeding from any site. His family and developmental history was normal. On admission, he was conscious, febrile with a heart rate of 120/min, respiratory rate 26/min, blood pressure 100/78 mmHg and deep icterus was present. The liver was tender and palpable 6 cm below the costal margin with a span of 9 cm, and the spleen was palpable 2 cm. Other systems were normal. With a provisional diagnosis of typhoid fever, an empirical treatment with intravenous ceftriaxone, intravenous fluids and antipyretics were started. Investigations revealed: hemoglobin 9.8 gm/dL, total leukocyte count 5800/cumm (neutrophils 60%, lymphocyte 40%) and platelet count 2.9 lac/cumm. Erythrocyte sedimentation rate was 60 mm at 1 hr. peripheral blood smear and OptiMal test was negative for malarial parasites. The total serum bilirubin concentration was 4.8 mg/dL with a conjugated fraction of 2.3mg/dL. The serum concentrations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were 4260 U/L (N: 10-40), 4625 U/L (N: 5-40), 458 IU/L (N: 225-450 IU/L), respectively. His serum ALT/LDH was 10.09. Prothrombin time was 22 sec (control: 12 sec). Serum electrolytes, renal function tests, and random blood sugar were normal. Glucose-6-phosphate dehydrogenase test was normal. Urine bile salts and bile pigments were positive. As the liver enzymes were highly elevated, serological test for viral hepatitis was done. It was positive for HAV-IgM: 1.2 (N # 0.4) and negative for hepatitis B, C, and E viruses. Serological tests for dengue, leptospirosis and HIV were negative. The blood culture was reported positive for Salmonella Typhi, sensitive to ceftriaxone. A final diagnosis of typhoid fever with co-existent hepatitis A infection was made. After 4th day of starting ceftriaxone, the general condition and an appetite of the child started showing improvement. The fever spikes were still persistent. However, ceftriaxone was continued as the child had shown an improvement in his general condition. He became afebrile on the 13th day of admission. The child was discharged on the 15 th day of admission, and is well on follow-up after 2 months. His liver enzyme tests done on follow-up were normal.
The presence of highly elevated liver enzymes and deranged prothrombin time alerted us to the possibility of co-existent viral hepatitis. , Fever with jaundice can be seen in both, typhoid hepatitis and viral hepatitis. In 1899, Osler first described the hepatic complications in typhoid fever.  Although the liver is commonly involved in patients with typhoid fever, severe hepatic derangement simulating an acute viral hepatitis is rare. The pathogenesis of typhoid hepatitis has been attributed to typhoid endotoxemia, cytotoxin, or direct bacterial invasion. Additionally arteritis, immune complexes and consumption of complement are believed to contribute to hepatic insult. ,, Other causes of jaundice in typhoid fever include cholangitis, cholecystitis, salmonella liver abscess and hemolysis.  Presentation of an acute viral hepatitis is similar to typhoid hepatitis, but with a few differences: In viral hepatitis, the fever usually subsides with an appearance of jaundice, and the period between onset of fever and jaundice is usually 1-7 days.  However, in typhoid fever, jaundice usually occurs at the peak of fever.  Also, the fever persists after an appearance of jaundice. , In children, serum aminotransferase levels are markedly elevated in viral hepatitis (8-10 times normal) as compared to typhoid hepatitis, and the ratio of AST/LDH is more than 9 in viral hepatitis. ,,
Balasubramanian et al. found that, on admission, children with typhoid hepatitis had ALT: LDH values below 9, and those with an acute viral hepatitis had the values above 9. 
Other differentiating clinical features in typhoid fever include high grade fever, toxic appearance, relative bradycardia, relative lymphocytosis with leucopenia and an absence of deep jaundice.  The coagulation profile is usually normal in typhoid fever even in the presence of elevated hepatic enzymes. A study was done by Jagadish et al. on the hepatic manifestations of typhoid. They found that, although the hepatic enzymes were elevated in more than 60% of cases, prolonged prothrombin time was observed in only 9.7% of cases.  Hence, an abnormal coagulation profile in a patient with typhoid hepatitis should alert one to an underlying infection with a hepatotropic virus or disseminated intravascular coagulation associated with sepsis. Normally, in cases of typhoid fever with an onset of treatment, the fever spikes should come down by day 4-5 of illness.  However, it may be delayed in patients having co-existing other infections, as seen in our patient.  The interaction of infections such as typhoid and viral hepatitis is unknown but may be synergistic, and thus lead to more severe liver damage than when the infections act separately. 
In conclusion, dual infections can present diagnostic dilemmas, severe complications, and prolonged course; hence, it is important that they are diagnosed early in the course of the disease.
We would like to thank the Dean of our institution for permitting us to publish this manuscript.
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