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 Table of Contents  
Year : 2014  |  Volume : 11  |  Issue : 2  |  Page : 149-152

Salmonella paratyphi A endocarditis complicating chronic rheumatic heart disease: A case report with review of literature

1 Department of Medicine, Government Medical College, Srinagar, India
2 Department of Medicine, Disrict Hospital, Anantnag, Jammu and Kashmir, India

Date of Web Publication3-Oct-2014

Correspondence Address:
Ishrat H Dar
P. O. Box 90, GPO Srinagar - 190 001, Jammu and Kashmir
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0189-7969.142144

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Infective endocarditis is a rare complication of salmonellosis. The most commonly observed species in endemic areas is Salmonella typhi as a cause of enteric fever associated with various complications. Endocarditis caused by Salmonella paratyphi is very rare and so far only seven cases have been reported in medical literature. We report a case of Salmonella paratyphi A endocarditis in a 20 year old young man who had an underlying chronic rheumatic heart disease with aortic and mitral valve involvement. These rare cardiac complications should always be considered especially in persons with underlying congenital or acquired cardiac diseases with unrelenting fever particularly if they reside in an endemic area of enteric fever or during outbreak of the disease. The case is highlighted not only for its rarity but also to keep in mind the importance of looking minutely for uncommon organisms like Salmonella paratyphi in cases of PUO and complicated chronic rheumatic heart disease.

Keywords: Ceftriaxone, chloramphenicol, infective endocarditis, rheumatic heart disease, Salmonella paratyphi A

How to cite this article:
Dar IH, Kamili MA, Dar SH, Mir SR. Salmonella paratyphi A endocarditis complicating chronic rheumatic heart disease: A case report with review of literature. Nig J Cardiol 2014;11:149-52

How to cite this URL:
Dar IH, Kamili MA, Dar SH, Mir SR. Salmonella paratyphi A endocarditis complicating chronic rheumatic heart disease: A case report with review of literature. Nig J Cardiol [serial online] 2014 [cited 2023 Feb 7];11:149-52. Available from: https://www.nigjcardiol.org/text.asp?2014/11/2/149/142144

  Introduction Top

Enteric fever is a serious health problem in most regions of the world, particularly in the under developed countries. The causative organisms are  Salmonella More Details typhi, Salmonella non-typhi and Salmonella paratyphi A, B, and C. Paratyphoid fever is relatively uncommon and so are its complications. Endocarditis, a rare complication of  Salmonellosis More Details occurs mostly during or after a concomitant infection like gastroenteritis in predisposed patients such as HIV patients and individuals with underlying heart disease who have prosthetic valves (15%), congenital heart disease (5%) and less frequently in patients with other valvular abnormalities. [1]

  Case report Top

Mr. K a 20-year-old male student was admitted to the emergency department of our hospital with 7 days history of high-grade fever associated with chills, loose motions, vomiting, and breathlessness. The patient was a known case of chronic rheumatic heart disease (RHD) with aortic and mitral valve involvement (aortic regurgitation [AR], mitral regurgitation [MR]) since the age of 5 years. He was receiving procaine penicillin at 1.2 million units every 3 weeks intramuscularly. No history of instrumentation like catheterization, upper or lower gastrointestinal endoscopy, proctoscopy, bronchoscopy, dental extraction, scaling of the teeth, a major or minor surgical procedure was forth coming.

The clinical examination revealed a tall, lean, and thinly built man with marfanoid habitus with arm span greater than the height, a high arched palate without evidence of subluxation or dislocation of the lens, no flat feet, but with long tapering fingers and toes. The patient appeared pale, ill-looking and toxic with a temperature of 102°F and had no rash or spots on the body. No jaundice or lymphadenopathy was noted. Examination of the nails revealed splinter hemorrhages, and Osler's nodes were palpable in the finger pulps. Jugular venous pressure was raised as evidenced by pulsatile nature of the neck vessels. Blood pressure was 110/40 mm Hg and pulse was 104 beats/min, collapsing type. Cardiovascular examination revealed a heaving apex 2 cm away from the anterior axillary line with a pan systolic murmur in the tricuspid and mitral area radiating to the axilla and a long early diastolic murmur in the aortic area suggesting tricuspid (TR), mitra (MR) and aortic regurgitation (AR). Almost all clinical signs of severe AR were present. Chest examination revealed a respiratory rate of 36/min with fine crepitations at the bases. Abdominal examination revealed mild ascites, palpable tender liver and splenomegaly 4 cm below the left costal margin. Fundus examination did not show the presence of Roth's spots. A provisional diagnosis of infective endocarditis on an underlying chronic RHD was made.

Routine baseline investigations, including three blood cultures were done. Laboratory investigations revealed mild anemia (Hb - 9 g/dL), leucocytosis (total leukocyte count - 12 × 10 3 /μL), differential leukocyte count (polymorphs 65%, lymphocytes 31% and mixedcells 4%), thrombocytopenia (platelets - 33 × 10 3 /μL), normal kidney functions, blood sugar and electrolytes, mild-transaminitis on liver function tests and elevated C-reactive protein. Urine examination revealed microscopic hematuria and microalbuminuria without casts. Ultrasonography of abdomen revealed a congested liver, splenomegaly with free fluid in the peritoneal cavity and bilateral pleural effusion with normal kidneys/urinary bladder, pancreas and gall bladder. Electrocardiogram was suggestive of left ventricular hypertrophy with strain pattern in the lateral leads [Figure 1]. A chest radiograph (posterior-anterior view) showed left ventricular type of cardiomegaly [Figure 2]. Transthoracic echocardiography (TTE) revealed thickened aortic and mitral valve leaflets with doming anterior mitral leaflet (AML) and flat posterior mitral leaflet with poor coapting. A vegetation measuring 5 × 7 mm was attached to the AML tip [Figure 3] which was ascertained on transesophageal echocardiography (TEE) as well. Initial blood culture at 48 h of incubation failed to grow any organisms. Widal and  Brucella More Details serology was negative. An empirical treatment of infective endocarditis with intravenous ceftriaxone and amikacin was started along with diuretics. Initially the patient's response was favorable, but after 5 days he developed increasing ascites with abdominal pain and worsening fever. An abdominal paracenticis was done and straw colored ascitic fluid obtained was subjected to cytology, Gram's and acid-fast bacilli (AFB) staining, culture, sugar, protein and adenosine deaminase (ADA) estimation and polymerase chain reaction (PCR) for tuberculosis (TB). Ascitic fluid was lymphocytic exudative type, no organisms were found on Gram's or AFB staining or culture, ADA levels were 23 U/L and PCR for TB was negative. One week later following the initial negative blood culture the microbiology laboratory reported the growth of S. paratyphi A, which was sensitive to ceftriaxone, chloramphenicol, cefaperazone/sulbactum, ciprofloxacin and resistant to ofoxacin/sparfloxacin [Figure 4]. A repeat Widal test confirmed the presence of S. paratyphi A with a high rising titer of 1:320. Considering that the patient had not responded to a combination of drugs including amikacin and the widespread resistance to ciprofloxacin it was decided to institute treatment with ceftriaxone and chloramphenicol for 6 and 4 weeks, respectively. At the end of the 2 weeks with this treatment the fever disappeared, blood cultures became sterile repeatedly until 6 weeks, ascites and pleural effusion disappeared and the general condition of the patient improved by way of normal counts, defervescence, regression of splenomegaly and disappearance of the vegetation on echocardiography. The patient was discharged after 6 weeks of treatment and continues to be on regular follow-up with a plan for aortic and mitral valve replacement.
Figure 1: Electrocardiogram of the patient depicting left ventricular hypertrophy with strain pattern

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Figure 2: X-ray chest posterior-anterior view of the patient depicting cardiomegaly

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Figure 4: Microbiology report of the blood culture showing Salmonella paratyphi A and the sensitivity to various drugs

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{Figure 4}

  Discussion Top

Salmonellae are Gram-negative, flagellated, facultative anaerobic bacilli comprising more than 2500 serotypes capable of infecting humans and the organisms causing enteric fever in humans comprise S. typhi and S. paratyphi serotypes A, B and C and have no other hosts except humans. Particular serovars show a strong propensity to produce particular syndromes: S. typhi, S paratyphi A and S. schottmuelleri produce enteric fever, S. choleraesuis produces septicemia or focal infections, S. typhimurium and S. enteritidis produce gastroenteritis.

Food borne or water borne transmission results commonly from fecal contamination by ill or asymptomatic chronic carriers. The infection may take several clinical forms, the most common being gastroenteritis typically presenting with fever, diarrhea and cramping abdominal pain. Most patients have a self-limiting illness without complications, but transient bacteremia may occur in 10% of patients and lead to metastatic complications at a number of sites. [2]

Bacteremia is more common in the young, elderly and immunocompromised patients. Depending on the serotype and the effectiveness of the host defenses some organisms may infect the liver, spleen, gall bladder, bones, meninges, heart valves, myocardium and other organs like the normal arterial intima causing endothelial infection in presence of atherosclerosis. [2]

Endocarditis is a rare complication of salmonellosis with an incidence of 0.2-0.4% occurring mostly during or after a concomitant Salmonella infection like gastroenteritis. [3] Nontyphoidal Salmonella endocarditis is a distinct rare clinical entity. Saphra and Winter reported 20 cases of Salmonella endocarditis among 7779 cases of Salmonella infections and none of these was caused by S. paratyphi. [4] From 1939 to 1967, only 23 confirmed cases have been recorded, most of which were caused by S. choleraesuis. There were no cases of endocarditis caused by S. paratyphi. [5] Johnson et al. were the first to report a case of endocarditis caused by S. paratyphi. [6] Different authors from different countries have at various points of time depicted the presence of S. paratyphi A in both native valves and in those with underlying structural heart disease (congenital as well as rheumatic). From all these cases including our case, the most common valve involved was the mitral followed by aortic, tricuspid and one case of interventricular septum involvement. There was no preexisting disease in four out of eight cases, one case each with ventricular septal defect and tetralogy of fallot, two cases with RHD and mitral valve involvement that includes our case as well. Interestingly, both the cases with RHD and mitral valve involvement with infective endocarditis related to S. paratyphi A have been from India [Table 1]. [7],[8],[9],[10],[11],[12] All cases excluding the one reported by Johnson et al. had complete recovery. Our case is the second reported case of S. paratyphi A endocarditis after Yadav et al. in an underlying setting of chronic RHD with valvular involvement.

Salmonella endocarditis is an invasive and destructive process with valve ring abscess, valve perforation and rupture of the cusps occurring during the illness in a significant number of patients. Mortality associated with endocarditis and aortitis caused by Salmonella remains exceedingly high between 40% and 45%, respectively. [13] New or changing murmurs, cardiac failure or peripheral embolic manifestations appear during the course of endocarditis in most patients and normal leukocyte count should be interpreted carefully in selected patients. Elevated leukocyte count occurs in a minority of patients with Salmonella infection and patients with positive blood cultures with fever and back/abdominal pain should undergo workup for aortitis and aneurysm formation or vascular infection. [2] The diagnosis of Salmonella endocarditis requires a high degree of suspicion and TTE is the first choice among noninvasive methods of diagnosis though TEE is more conclusive as reported in a case series by Fukushima et al. [14] Computed tomography and magnetic resonance imaging should be performed to look for organ involvement, including the aorta, myocardium, lungs, brain and bones. Early surgical intervention is described to have increased survival and is therefore the treatment of choice in many patients. [15]
Table 1: Confirmed cases of endocarditis worldwide caused by S. paratyphi

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  Conclusion Top

The diagnosis of Salmonella endocarditis requires a high level of suspicion particularly in the setting of a congenital, RHD or valvular heart disease. TTE is inadequate for diagnosis and should be supplemented by TEE along with blood, urine and stool cultures. Multisystem involvement is usually common contributing to mortality and morbidity. Intensive antibiotic therapy based on culture and early surgical intervention hold the key to survival of these patients.

  References Top

1.Rodriguez C, Olcoz MT, Izquierdo G, Moreno S. Endocarditis due to ampicillin-resistant nontyphoid Salmonella: Cure with a third-generation cephalosporin. Rev Infect Dis 1990;12:817-9.  Back to cited text no. 1
2.Nielsen H, Gradel KO, Schønheyder HC. High incidence of intravascular focus in nontyphoid Salmonella bacteremia in the age group above 50 years: A population-based study. APMIS 2006;114:641-5.  Back to cited text no. 2
3.Mutlu H, Babar J, Maggiore PR. Extensive Salmonella enteritidis endocarditis involving mitral, tricuspid valves, aortic root and right ventricular wall. J Am Soc Echocardiogr 2009;22:210.e1-3.  Back to cited text no. 3
4.Saphra I, Winter JW. Clinical manifestations of salmonellosis in man; an evaluation of 7779 human infections identified at the New York Salmonella Center. N Engl J Med 1957;256:1128-34.  Back to cited text no. 4
5.Schneider PJ, Nernoff J 3 rd , Gold JA. Acute Salmonella endocarditis. Report of a case and review. Arch Intern Med 1967;120:478-86.  Back to cited text no. 5
6.Johnson DH, Rosenthal A, Nadas AS. Bacterial endocarditis in children under 2 years of age. Am J Dis Child 1975;129:183-6.  Back to cited text no. 6
7.Gupta S, Singh B, Kapoor H, Minocha SK, Jain AK. Ventricular septal defect with endocarditis caused by Salmonella paratyphi A. Trop Doct 1994;24:40.  Back to cited text no. 7
8.Yadav P, Duggal G, Walia M, Wardhan H, Chugh S. Infective endocarditis. J Indian Acad Clin Med 2000;1:163-70.  Back to cited text no. 8
9.Pancharoen C, Thisyakorn C, Thisyakorn U. Endocarditis and pericarditis caused by Salmonella paratyphi A: Two case reports and review of the literature. Southeast Asian J Trop Med Public Health 2002;33:161-3.  Back to cited text no. 9
10.Vaisbein E, Melamed-Snapiri Y, Nassar F. Salmonella paratyphi endocarditis. Acta Cardiol 2006;61:191-2.  Back to cited text no. 10
11.Subasinghe S, Indrakumar J. An uncommon complication of Salmonella paratyphi A infection. Ceylon Med J 2010;55:56-7.  Back to cited text no. 11
12.Sibly AJ, Tissera WA. A case of Salmonella paratyphi endocarditis; a rare complication of paratyphoid fever. Galle Med J 2011;16:39-40.  Back to cited text no. 12
13.Fernández Guerrero ML, Aguado JM, Arribas A, Lumbreras C, de Gorgolas M. The spectrum of cardiovascular infections due to Salmonella enterica: A review of clinical features and factors determining outcome. Medicine (Baltimore) 2004;83:123-38.  Back to cited text no. 13
14.Fukushima N, Ishikawa N, Shimazaki Y, Taniguchi K, Tanemura M, Matsuyama A, et al. Salmonella prosthetic valve endocarditis. J Thorac Cardiovasc Surg 1996;112:840-2.  Back to cited text no. 14
15.Soravia-Dunand VA, Loo VG, Salit IE. Aortitis due to Salmonella: Report of 10 cases and comprehensive review of the literature. Clin Infect Dis 1999;29:862-8.  Back to cited text no. 15


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1]

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