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Salmonella Hepatitis: a Review Farzana Shafqat, Anwaar A

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Salmonella Hepatitis: a Review Farzana Shafqat, Anwaar A Editorial Review Proceeding S.Z.P.G.M.I vol: 8(3-4) 1994, pp. 78-88. II II Salmonella Hepatitis: A Review Farzana Shafqat, Anwaar A. Khan, Zafar Iqbal Department of Medicine and Gastroenterology, Shaikh Zayed Hospital, Lahore INTRODUCTION the identification of salmonella typhi in the laboratory and also for the serological diagnosis of he clinical picture of typhoid is extremely infection. These are O antigen, H antigen and Vi variable with increasing reports of atypical antigen. T 1 6 features · • Toxic manifestations like headache, step Somatic or O antigen is present within the ladder temperature, coated furred tongue, cough, bacterial cell wall. This is lipopolysaccharide, protein abdominal symptoms, malaise etc. may be observed and lipid complex. This constitutes the endotoxin. in only 50% of cases5. A special problem is the Group classification is done on the basis of this occurrence of typhoidhepatitis. antigen, Salmonella typhi belongs to 'Group D'. Typhoid hepatitis is one of the atypical Fu1ther typing of S. typhi is done on the basis of presentations of typhoid fever and can be defined as flagellar antigen called 'H' antigen. Surface antigen reversible involvement of liver during the course of which covers O antigen, is called Vi antigen. Vi typhoid fever. antigen increases the virulence of the organism. This Diagnosis of typhoid should always be antigen is also present in Paratyphi C, though their considered in patients presenting with fever and group factor and flagellar antigen are different. features of liver involvement especially in endemic These bacteria are readily killed by heat in one areas, because it can mimick other diseases hour at 55 ° C, in 15-20 minutes at 60 ° C and within occurring commonly in these areas, like acute viral 5 minutes by boiling. Baking also kills these hepatitis, amoebic hepatitis or malaria. organisms and other salmonellae. Growth stops below 55 ° C but survival is possible. Contamination Epidemiology during preparation of food or after cooking may not Involvement of liver in typhoid is more be harmful if the food is quickly cooled and kept af commonly seen in endemic areas but has also been refrigerator temperature below 5 ° C but if leftfor an reported from non-endemic areas7• hour or two before cooling, bacteria may multiply No age is exempt from typhoid hepatitis, but it rapidly and food becomes contaminated for safe is commonly seen between second and fourth consumption before it is put in the refrigerator. S. decade5 and in patients belonging to lower socio­ typhi and other Salmonellae can be destroyed by a economic class4• Complications like hepatitis occur number of chemicals including phenols, mercuric more in patients with depressed cellular immunity chloride, formaldehyde and quaternary ammonium and in those with relapse of typhoidfever1· 8•9 . compounds. Chlorine and potassium permanganate can be used for treating food. Bacteriology I,nfection in India and Pakistan occurs more Pathogenesis of salmonella hepatitis commonly with salmonella typhi as compared to The exact mechanism of hepatic damage in paratyphi A, B and C4• 10 • Similarly, liver involvement typhoid fever is not clear. It has been seen that this occurs more commonly with salmonella typhi complication, like other complications occurring in infection 11• Salmonella group of organisms belong to typhoid, is more commonly seen in malnourished the family enterobacteriaceae. Salmonella typhi are people belonging to lower socio-economic group4• gram negative, actively motile organisms. They do Bacteremia may be the cause of liver damage as not ferment lactose, sucrose and salicin. Salmonella bacteremia occurs in most patients with typhoid typhi only produce acid but no gas from dextn;>se and fever3. It definitely has a diagnostic significance but other carbohydrates. Their colonies stand out pale clinical severity and development of complications of against the coloured colonies of lactose fermenters in the disease have no significant association with the media containing lactose and a pH indicator. There concentration of bacteria in blood 12• are three groups of antigens that are important for Salmonella endotoxin has beeP implicated in 78 causing salmonella hypatitis like other features of hyperreactivity to catecholamines during typhoid typhoid fever. When these bacilli enter the fever is not clearly understood but it may represent a circulation after considerable multiplication in contributing mechanism to the pathogenesis of the lymphoid tissue of intestine, they undergo focal necrotic lesions and arteritis that occur m destructionwith the result of liberation of endotoxin typhoid11. 13 which produces the symptoms of typhoid fever • But Immune complexes and high ratio of rapid development of tolerance to endotoxin in an4trypsinto C3 have been seen in typhoidfever and volunteers can not explain the protracted course of more frequently in patients with complications 14 18 the disease . including hepatitis • Cell mediated immune Human volunteer studies showed that response (CMIR) appeared to play an important role 9 endotoxins did not play much role in the production in typhoid and its complications . It can be measured of sustained pyrexia and toxemia of typhoid by leucocyte migration test and delayed fever14, 15 • While evidence continues to accumulate hypersensitivity8. Recovery of the complicated cases that endotoxins do not play a major role in the was associated with change of negative L.M.T to 8 9 pathogenesis of typhoid fever and its complications, positive , • Mebel and Paniker19 found increased but in fact there are indicators favouring its local incidence of typhoid and severe toxemia in patients effectin the vicinityof the salmonella typhiinfection. with negative L.M. T cell mediated immune At these local sites, where salmonella typhi are response. Rajagopalan et al.9 also found intact CMIR multiplying, the highest concentration of endotoxins in uncomplicated cases of typhoid fever as compared might be expected14_ to complicated cases. The ratio of T lymphocyte sub­ Salmonella endotoxin is a potent inflammatory populations was grossly imbalanced in typhoid agent and is chemotactic for polymorphonuclear patients, the number of T lymphocytes and their leucocytes. Very minute concentration as low as 1 sub-population was further altered m the ng/ dl can produce local dermal responses during complicated cases as compared to uncomplicated .." , typhoid fever15. Therefore, sustained pyrexia and cases. Increased proportions of T suppressor cells toxemia may be explained by the ability of S. typhi and reduced population of T helper cells especially in and its endotoxin component to stimulate the complicated cases suggest that high levels of synthesis and release of endogenous pyrogens from suppressor T cells and circulating immune mononuclear cells and polymorphs accumulated at complexes may be responsible for a negative L.M.T. the site of inflammation.in tissues. Simultaneous presence of these two factors is to be­ Demonstration of salmonella bacilli within the expected since it has been reported that immune liver by indirect immunoflurescencestrongly favours complexes stimulate the formation of suppressor T the possibility of damage caused by locally released cells and other suppressor factors. Further endotoxins by the proliferating organisms and by confirmation of the involvement of circulating 16 ..... invoking local inflammatory reactions • Hepatic immune complexes and suppressor T cells in damage seen in patients with gut perforation and producing immunological abnormalities in typhoid peritonitis was considered to be due to ascending fever would help in deciding therapeutic approach to cholangitis17 • correct these abnormalities. Thus, there is found to Hornick et al.14 also considered the possibility of be a close correlation between the development of localized intravascular coagulation and arteritis in leucocyte migration test (L.M. T), recovery and the pathogenesis of dinical features of typhoid fever. inverse correlation with complications and a Hepatic injury in typhoid fever could be due to prolonged illness in typhoidfever. vascular hyperreactivity to catecholamines. In man '·-· and animals, intestinal mucosa possesses high Clinical features of salmonella hepatitis serotonin concentrations and a variety of Clinical features would be both of typhoid fever inflammatory lesions of the intestine cause vascular and that of hepatic involvement. Onset of fever in hyperactivity to catecholamines in man. Therefore, typhoid is slow and insidious in most of the cases3 release of serotonin from the inflammed intestinal but rapid onset "':ith or without chills has also been mucosa could be responsible for the vascular observed 17. hyperreactivityto the catecholamines. The most common prodromal symptoms which The clinical significance of the vascular precede the actual onset of fever were headache, 79 Shafqat et al. Salmonella Hepatitis: A Review Table 1: Reports of liver involvement in typhoid fever (in percentage) � No. of' Jaundice Hrpalome11aly Abnormal Abnormal liver Study patirnts LFTs (t;I) histoloJ!y Sluarl and Pullen ]!)4(i :mo :u; 20 NR' NR Rowland l m; l fi30 I.I NR NR NR Gulati <'Lal. IDGS !JS 0 () NR NR \Vic.:ks <'l al. 1!)71 243 l.(i NR NR NR Rarnaehundran E'L al. 197-1 iiS 7.H 2!l Di Pm l'l al. I !l7G Iii 2(i.(i 10 !"13.3 100 Sa man lray PL al. I !)77 iiOO 0 18 NR NR Singhrlal.1!)78 4GO l NR NR NR Nasrallah and Nassar 1!)78 10-l 23 3:1 17 NR Johm,on and AderelP l !)8 I 117 (i 27 ii NR Guplu Pl al. 1!)85 125 fi.G 8.8 S.G NR Khnsla <'l al. I !l88 :m 8.:1 !iii fl:i ,10 bhaq PL al. I !)!JO :iO 0 (i:1 NR NR Arif ('l al. l !l!)O !) (i(i 77 100 1-1 Shafqal ('t al71'. ( HJ!l1) 31 ·l'l 70 NR :12 'Not n·rordPd. 3 17 malaise and anorexia • • Abdominal pain, benign course and may even be missed by the constipation, diarrhoea abdominal distension, body physician or it can be severe presenting with severe aches and pains and symptoms pertaining to chest bleeding syndrome, haematemesis, or hepatic 7 e.g.
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