https://imcjms.com/public Ibrahim Medical College Journal of Medical Science https://imcjms.com/public/registration/journal_full_text/87 Mon, 19 Sep 2016 15:09:54 +0000 Abstract Introduction Based on DNA studies, all salmonellae are now considered a single species (S choleraesuis), separated into 7 distinct subgroups. Multiple serotypes of Salmonella cause the syndrome of enteric fever, of which typhoid fever is the best studied and described4,5.  Caused by Salmonella typhi and occurring only in humans, typhoid fever is a severe multisystem illness and potentially fatal if untreated. Death may occur from overwhelming toxemia, myocarditis, intestinal hemorrhage, or perforation.   In September 2005, a 22 year old febrile man was admitted in the department of internal medicine, BIRDEM with the complaints of productive cough and exertional dyspnoea. He was febrile for last 10 days; fever was high grade intermittent in nature, associated with mild headache and myalgia. Highest temperature recorded was 105°F. For the last 5 days he developed cough, first mucoid then becoming productive along with progressive dyspnoea later on orthopnoea. He gave history of loose motions 2-3 times a day for the last 3 days but there was no vomiting. He was non-smoker, non asthmatic. He refused any recent travel abroad, or to the hill-tracts. He took a course of oral ciprofloxacin 500mg bid for 5 days. Systemic examination revealed fine crepitations in mid and lower zone of both lung fields with vesicular breath sound. Right hypochondrium was mildly tender. Liver, spleen and lymph nodes were not palpable. On routine investigations, complete blood count showed total count of WBC was at lower normal range with normal distribution and thrombocytopenia. (TC-4100, P/C-33000, DC-N=79%, L=15%, M=6%, E=1%). Liver enzymes were slightly raised. SGPT-68 U/L, SGOT-72 U/L and serum bilirubin 3.2 mg/dl. Blood urea and s. creatinine were normal. On the 10th day blood, urine and sputum samples were sent for culture along with blood for triple antigen and viral markers. Bedside urine examination was normal. ECG showed nonspecific ST change. There was bilateral patchy opacities on CxR in mid and lower zone. But on the 3rd day of admission, i.e. 13th day of the onset of fever, patient was still febrile, respiratory distress worsened. He also complained of palpitation. On examination there was undue tachycardia (142 b/min) and tachypnoea (34 breath/min). On auscultation fine basal crepitations were found on both lungs. Urgent chest X-ray showed cardiomegaly with evidence of pulmonary edema along with the previous radiological findings. Arterial blood gas analysis revealed Type I respiratory failure. (PO2=55 mm of Hg, PCO2=23 mm of Hg, SaO2=76%, pH=7.45, HCO3=20 mmol/L). Viral markers for hepatitis were negative. Then investigations supported the clinical suspicion. Echocardiography revealed global hypokinesia with ejection fraction only 37%. CPK- 583u/l, CK-MB 70u/l, S. LDH-1510 u/l. Troponin-I was found normal. Diuretic was continued. On the 4th day patient was not dyspnoeic any more but fever still persisting with cough. So we reached our final diagnosis-Enteric fever with myocarditis with  acute left ventricular failure.   Myocarditis is used to describe simply as an inflammatory process with necrosis involving myocardium. According to Dallas criteria, the diagnosis of active myocarditis is defined as an inflammatory infiltrate of the myocardium with injury to the adjacent myocyte not typical for ischaemic damage associated with coronary artery disease. It usually forms part of a generalized  infection, so far most commonly initiated by viral infection but can also be due to  drugs, toxin, hypersensitivity reaction, collagen vascular disease and autoimmune reaction and less commonly with other infections like bacteria, rickettsia, spirochete, fungi, protozoa. ECG changes of myocarditis are often nonspecific usually appearing only in the first two weeks of illness. Commonest ECG abnormality was Q-Tc prolongation (29%) followed by ST-T changes (20%), bundle branch block (7%), first degree A-V Block and arrhythmia (2%)6. Other evidence for myocarditis include myocardial imaging, cardiac catheterization. Endomyocardial biopsy is considered the gold standard. But according to the ‘Myocarditis Treatment Trial’ it is no longer mandatory in the evaluation of unexplained heart failure. This was a case of myocarditis due to enteric fever which was confirmed by blood culture sensitivity report. Usually diagnosis of enteric fever is suggested by assays that identify Salmonella antibodies, antigens, or DNA and is then confirmed by isolation of the organism. The most sensitive method of isolating S typhi is obtaining a bone marrow aspirate (BMA) culture, positive in 90% cases7. Blood, urine, and stool cultures are still frequently used but the yield is only about 70%8. Rectal swab and bile from duodenal string test can also be used8,9. The Widal reaction is indicative in only 40-60% of patients during  admission10. Although not commercially available, DNA probes have been developed for identifying S typhi from bacterial culture isolates and directly from blood11. Our patient improved with ceftriaxone, diuretics and bed rest. He did not respond to oral ciprofloxacin though this drug combines a lower documented resistance rate with excellent penetration into macrophages and the biliary system12. Since 1989, S typhi strains with simultaneous plasmid-mediated resistance to chloramphenicol, ampicillin, and co-trimoxazole have emerged and spread rapidly in the Indian subcontinent and parts of Southeast Asia13,19. Between 10% and 20% of patients treated with antibiotics have a relapse after initial recovery. Thus now the fluoroquinolones and the third-generation cephalosporins are the antibiotics of choice to treat these multidrug-resistant (MDR) strains, both in children and adults14-16. Furazolidone and Azithromycin are also used to treat typhoid in children in some parts of the developing world17,18. Case fatality rates of 10-50% have been reported from endemic countries when diagnosis is delayed or in cases of severe typhoid fever not treated with high-dose corticosteroid therapy and antibiotics20.. The two most common complications of enteric fever are intestinal hemorrhage and perforation 21. Among other complications, pancreatitis and simultaneous acute renal failure and hepatitis, cholangitis, meningism, encephalomyelitis, subclinical disseminated intravascular coagulation, osteomyelitis, arthritis have been reported22-26. Early antibiotic therapy has reduced the rate of these systemic complications transforming a previously life threatening illness into a short time febrile illness with negligible fatality.  Parenteral corticosteroid is recommended in severe typhoid fever with shock or depressed level of consciousness. As far our case is concerned, supportive treatment for myocarditis included absolute bed rest and diuretics. Judicious use of corticosteroids is indicated in selected cases of severe myocarditis. In conclusion, our case again emphasizes the utmost importance of early and proper use of antibiotic therapy in determining the prognosis of disease. 1. World Health Organization: Background document: the diagnosis, treatment, and  prevention of typhoid fever. Geneva, Switzerland: 2003. 3. Ryan CA, Hargrett-Bean NT, Blake PA: Salmonella typhi infections in the States, 1975-1984: increasing role of foreign travel. Rev Infect Dis 1989: 11(1): 1-8. 5. Farmer JJ: Enterobacteriaceae: introduction and identification. In: Murray PR, Baron EF, Pfaller MA, eds. Manual of Clinical Microbiology. 6th ed. Washington, DC: American Society for Microbiology; 1995: 438-49. 7. Hoffman SL, Edman DC, Punjabi NH, et al: Bone marrow aspirate culture superior to streptokinase clot culture and 8ml 1:10 blood-to-broth ratio blood culture for diagnosis of typhoid fever. Am J Trop Med Hyg 1986 Jul; 35(4): 836-9. 9. Duodenal string-capsule culture compared with bone-marrow, blood, and rectal- swab cultures for diagnosing typhoid and paratyphoid a fever. J Infect Dis 1984 Feb; 149(2): 157-61. 11. Rubin FA, McWhirter PD, Punjabi NH, et al: Use of a DNA probe to detect Salmonella typhi in the blood of patients with typhoid fever. J Clin Microbiol 1989 May; 27(5): 1112-4. 13. Butler T, Rumans L, Arnold K: Response of typhoid fever caused by Chloramphenicol-susceptible and chloramphenicol-resistant strains of Salmonella typhi to treatment with trimethoprim-sulfamethoxazole. Rev Infect Dis 1982 Mar-Apr; 4(2): 551-61. 15. Tran TH, Bethell DB, Nguyen TT, et al: Short course of ofloxacin for treatment of multidrug-resistant typhoid. Clin Infect Dis 1995 Apr; 20(4): 917-23. 17. Carcelen A, Chirinos J, Yi A: Furazolidone and chloramphenicol for treatment of typhoid fever. Scand J Gastroenterol Suppl 1989; 169: 19-23. 19. Fever in Anand AC, Kataria VK, Singh W, Chatterjee SK: Epidemic  multiresistant enteric eastern India. Lancet 1990 Feb 10; 335 (8685): 352. 21. Rowland HA: The complications of typhoid fever. J Trop Med Hyg 1961; 64: 143-8. 23. Khan M, Coovadia Y, Sturm AW: Typhoid fever complicated by acute renal    failure and hepatitis: case reports and review. Am J Gastroenterol 1998 Jun; 93(6): 1001-3 25. Baker NM, Mills AE, Rachman I, Thomas JE: Haemolytic-uraemic syndrome in Typhoid fever. Br Med J 1974 Apr 13; 2(910): 84-7. 27. Hanel RA, Aravjo JC, Antoriuk A, et al: Multiple brain abscesses caused by solmonella typhi: Case report. Surg Nevrol 2003; 53(i): 86-90. 28. Julia J, Canet JJ, Lacasa XM, et al: Spantoneous spleen rupture during typhoid fever. Int J Intect Dis 2000; 4(2): 108-9. 2026 Ibrahim Medical College. All rights reserved.