Diseases of the Liver and Biliary System - part 8 ppt

Pyogenic liver abscess Over the past 30 years there has been a marked change in the aetiology of pyogenic liver abscess (fig. 29.1) [7]. Abscesses secondary to biliary disease, particularly malignant, have continued to increase. The immunosuppressive states have increased the number due to opportunistic infections. Earlier diagnosis has followed increased use of scanning and cholangiographic techniques. Aetiology Underlying biliary disease is the most frequent cause. Septic cholangitis can complicate any form of biliary obstruction, especially if partial. More cases are related to surgical or invasive non-surgical treatment of hepatobiliary disease, despite the use of prophylactic antibiotics. Biliary stenting for malignant biliary and pancreatic disease is a particular association. Abscess may follow sclerosing cholangitis and congenital biliary anomalies, especially Caroli’s disease. Portal pyaemia may follow pelvic or gastrointestinal infection resulting in portal pylephlebitis or septic emboli. It can follow appendicitis, empyema of the gallbladder, diverticulitis, regional enteritis [14], Yersinia ileitis [9], perforated gastric or colonic ulcers, leaking anastomoses, pancreatitis [1] or infected haemorrhoids. Neonatal umbilical sepsis may spread to the portal vein with subsequent liver abscesses. Injury to the hepatic arterial system may lead to liver abscesses. This can follow cholecystectomy. In liver transplant patients, abscess may be diagnosed 2 weeks post- operatively associated with technical complications, particularly hepatic arterial thrombosis. Abscesses may follow local treatment of liver tumours by trans-hepatic chemo-embolization or percutaneous tumour injections [5]. Abscess may follow therapeutic hepatic arterial catheterization to treat colonic cancer metastases [15]. Increase in liver abscesses may also be related to the numbers of severely immunosuppressed patients. These include those post-transplant, with HIV infection or with leukaemia receiving chemotherapy [3]. Traumatic causes include penetrating wounds or blunt trauma from automobile accidents. A solitary liver abscess may follow direct spread from an adjacent septic focus such as a perinephric abscess. Diabetics may develop a liver abscess with gas-forming organisms (Klebsiella) [16]. 495 Chapter 29 The Liver in Infections 70 60 50 40 30 20 10 0 Biliary 1952–72 1973–93 *p<0.05 vs 1952–72 Percentage of patients (%) Cryptogenic Portal vein Direct extension Trauma Hepatic artery Benign Benign Malignant Malignant * * Fig. 29.1. Aetiology of pyogenic hepatic abscesses from 1952 to 1993 (from [7]). About one half of abscesses are cryptogenic. This is especially so in the elderly. Infecting agents The commonest are Gram-negative Escherichia coli, Strep- tococcus faecalis, Klebsiella and Proteus vulgaris. Recurrent pyogenic cholangitis may be due to Salmonella typhi. Streptococcus milleri, which is neither a true anaerobe nor a micro-anaerobe is a very common cause [13]. Anaerobes are particularly important. Infections are liable to be mixed and often antibiotic resistant. Super- infection is common. Liver abscesses associated with biliary stents are often due to resistant Klebsiella, enterobacter and Pseudomonas, Candida may be found in the bile. Fungal infections may be associated with underlying malignancy. Staphylo- cocci, usually resistant, are found especially in those who have received chemotherapy. Klebsiella pneumoniae, Pseudomonas and Clostridium welchii may also be found. Rare causes include Yersinia enterocolitica [9] and septicaemic melioidosis. The abscess may be sterile, but this is usually due to lack of adequate, particularly anaerobic, culture techniques or to previous antibiotics. Pathology The enlarged liver may contain multiple yellow abscesses, 1cm in diameter or a single abscess encased in fibrous tissue and usually found in the right lobe. With pylephlebitis, the portal vein and its branches contain pus and blood clots. There may be peri-hepatitis or adhe- sion formation. A chronic liver abscess may persist for as long as 2 years before death or diagnosis. In biliary- associated cases, multiple foci correspond to the bile duct system. Small pyaemic abscesses may be found in lung, kidney, brain or spleen. Direct extension may lead to sub-phrenic or pleuro-pulmonary suppuration. Exten- sion to the peritoneum or rupture of a sinus pointing under the skin are rare. Asmall amount of ascites may be present. Histologically, areas remote from the abscess show portal zone infection and surrounding disintegrating hepatocytes being infiltrated by polymorphs. Clinical features Features such as diabetes, biliary disease, malignancy or immunosuppressive states are recorded. Presentation is with abdominal pain and fever with features of a space-occupying lesion in the liver. The onset may be insidious and diagnosis delayed for at least 1 month. A single abscess is often insidious and cryptogenic especially in the elderly. Multiple abscesses are more acute and the cause is more often identified. Sub-diaphragmatic irritation or pleuro-pulmonary spread leads to right shoulder pain and to an irritable cough. The liver is enlarged and tender and the pain is accentuated by percussion over the lower ribs. Jaundice is late unless there is biliary disease. It is more common than with amoebic abscess. Recovery may be followed by portal hypertension due to thrombosis of the portal vein. Serum alkaline phosphatase is usually raised. Poly- morph leukocytosis is usual. Blood cultures may show the causative organism or organisms [2]. Localization of the abscess Ultrasound (US) distinguishes a solid from a fluid-filled lesion (fig. 29.2). CT scanning is particularly valuable although false negatives can be due to lesions near the dome of the liver and to micro-abscesses (figs 29.3–29.5). Multiple small abscesses aggregate, suggesting the beginning of coalescence into single larger abscesses (cluster sign) [8]. Endoscopic or percutaneous cholangiography may be used to diagnose cholangitic abscesses. MRI shows a raised lesion with sharp borders, hypo- intense on T 1 -weighting, and hyper-intense on a T 2 - weighted image. Appearances are not specific or diagnostic of biliary or haematogenous origin [11]. Aspirated material is positive in 90% [2]. It should be cultured aerobically, anaerobically and in carbon dioxide-enriched media for Streptococcus milleri. Treatment Management has been revolutionized by the wide- 496 Chapter 29 A B Fig. 29.2. US of a pyogenic liver abscess shows a low-density lesion (A) containing echogenic material which is pus and necrotic tissue. Acoustic enhancement (B) beyond the lesion is characteristic. spread use of imaging, especially US, allowing localization and easy aspiration for both diagnostic and therapeutic purposes (fig. 29.4). The majority of abscesses can be managed by systemic antibiotics and aspiration, which may need to be repeated [4]. Intravenous antibiotics are rarely effective alone. Drainage is indicated if signs of sepsis persist. Open surgical drainage is rarely indicated. However, solitary left-sided abscess may require surgical drainage, especially in children [12]. With multiple abscesses, the largest is aspirated and the smaller lesions usually resolve with antibiotics. Occasionally, percutaneous drainage of each is necessary. If amoebiasis is suspected, metronidazole should be given before aspiration [6]. Biliary obstruction must be relieved, usually by ERCP, papillotomy and stone removal. If necessary, a biliary stent is inserted (Chapter 32). Even with eventual cure, fever may continue for 1–2 weeks [2]. Prognosis Needle aspiration and antibiotic therapy have lowered the mortality [3]. The prognosis is better for a unilocular abscess in the right lobe where survival is 90%. The outcome for multiple abscesses, especially if biliary, is very poor. The prognosis is worsened by delay in diagnosis, associated disease, particularly malignant [17], hyperbilirubinaemia, hypo-albuminaemia, pleural effusion and old age [10]. The Liver in Infections 497 Fig. 29.3. Thalassaemic Greek patient post-splenectomy. CT scan shows a filling defect in the right lobe of the liver with marker over it (labelled 1). Fig. 29.4. Same patient as in fig. 29.3 with directed puncture of the abscess which resolved without surgery. Fig. 29.5. CT shows a large pyogenic abscess with thick shaggy walls in the inferior part of the right lobe of the liver (arrowhead). The abscess contains gas. References 1 Ammann R, Münch R, Largiadèr F et al. Pancreatic and hepatic abscesses: a late complication in 10 patients with chronic pancreatitis. Gastroenterology 1992; 103: 560. 2 Barnes PF, DeCock KM, Reynolds TN et al. A comparison of amebic and pyogenic abscesses of the liver. Medicine (Baltimore) 1987; 66: 472. 3 Branum GD, Tyson GS, Branum MA et al. Hepatic abscess. Changes in aetiology, diagnosis, and management. Ann. Surg. 1990; 212: 655. 4 Ch Yu S, Hg Lo R, Kan PS et al. Pyogenic liver abscess: treatment with needle aspiration. Clin. Radiol. 1997; 52: 912. 5 De Baere T, Roche A, Amenabar JM et al. Liver abscess formation after local treatment of liver tumours. Hepatology 1996; 23: 1436. 6 Giorgio A, Tarantino L, Mariniello N et al. Pyogenic liver abscesses: 13 years of experience in percutaneous needle aspiration with US guidance. Radiology 1995; 195: 122. 7 Huang CJ, Pitt HA, Lipsett PA et al. Pyogenic hepatic abscess. Changing trends over 42 years. Ann. Surg. 1996; 223: 600. 8 Jeffrey RB Jr, Tolentino CS, Chang FC et al. CT of small pyogenic hepatic abscesses: the cluster sign. Am. J. Roentgenol. 1988; 151: 487. 9 Khanna R, Levendoglu H. Liver abscess due to Yersinia enterocolitica: case report and review of the literature. Dig. Dis. Sci. 1989; 34: 636. 10 Lee K-T, Sheen P-C, Chen J-S et al. Pyogenic liver abscess: multivariate analysis of risk factors. World J. Surg. 1991; 15: 372. 11 Méndez RJ, Schiebler ML, Outwater EK et al. Hepatic abscesses: MR imaging findings. Radiology 1994; 190: 431. 12 Moore SW, Millar AJ, Cywes S. Conservative initial treatment for liver abscesses in children. Br. J. Surg. 1994; 81: 872. 13 Moore-Gillon JC, Eykyn SJ, Phillips I. Microbiology of pyogenic liver abscess. Br. Med. J. 1981; 283: 819. 14 Vakil N, Hayne G, Sharma A et al. Liver abscess in Crohn’s disease. Am. J. Gastroenterol. 1994; 89: 1090. 15 Wong E, Khadori N, Carrasco CH et al. Infectious complications of hepatic artery catheterization procedures in patients with cancer. Rev. Infect. Dis. 1991; 13: 583. 16 Yang CC, Chen CY, Lin XZ et al. Pyogenic liver abscess in Taiwan: emphasis on gas-forming liver abscess in diabetics. Am. J. Gastroenterol. 1993; 88: 1911. 17 Yeh TS, Jan YY, Jeng LB et al. Pyogenic liver abscesses in patients with malignant disease: a report of 52 cases treated at a single institution. Arch. Surg. 1998; 133: 242. Other infections Giardiasis is rarely associated with hepatic granulomas and cholangitis [3]. Campylobacter colitis can be related to a non-specific acute hepatitis [2]. Cat scratch disease is due to Bartonella henselae. It causes hepatic nodules, biopsy of which reveals necrotizing granulomas containing the organism [4]. CT shows focal hepatic defects and mediastinal and peri-portal lymphadenopathy. Listeria monocytogenes can cause hepatic abscesses [1]. References 1 Jenkins D, Richards JE, Rees Y et al. Multiple listerial liver abscesses. Gut 1987: 28: 1661. 2 Reddy KR, Farnum JB, Thomas E. Acute hepatitis associated with Campylobacter colitis. J. Clin. Gastroenterol. 1983; 5: 259. 3 Roberts-Thomas JC, Anders RF, Bhathal PS. Granulomatous hepatitis and cholangitis associated with giardiasis. Gastroen- terology 1982; 83: 480. 4 Tompkins LS. Of cats, humans and Bartonella. N. Engl. J. Med. 1997; 337: 1916. Hepatic amoebiasis Entamoeba histolytica exists in a vegetative form and as cysts, which survive outside the body and are highly infectious. The cystic form passes unharmed through the stomach and small intestine and changes into the vegetative, trophozoite form in the colon. Here, it invades the mucosa, forming typical flask-shaped ulcers. Amoebae are carried to the liver in the portal venous system. Occa- sionally, they pass through the hepatic sinusoids into the systemic circulation with the production of abscesses in lungs and brain. Amoebae multiply and block small intra-hepatic portal radicles with consequent focal infarction of liver cells. They contain a proteolytic enzyme which destroys the liver parenchyma. The lesions produced are single or multiple and of variable size. The amoebic abscess is usually about the size of an orange. The most frequent site is in the right lobe, often supero-anteriorly, just below the diaphragm. The centre consists of a large necrotic area which has liquefied into thick, reddish-brown pus. This has been likened to anchovy or chocolate sauce. It is produced by lysis of liver cells. Fragments of liver tissue may be recognized in it. Initially, the abscess has no well-defined wall, but merely shreds of shaggy, necrotic liver tissue. Histologi- cally, the necrotic areas consist of degenerate liver cells, leucocytes, red blood cells, connective tissue strands and debris. Amoebae may be identified in scrapings. Hepato- cyte death is by apoptosis, but not proceeding through Fas or tumour necrosis factor as pathways [6]. Small lesions heal with scars, but larger abscesses show a chronic wall of connective tissue of varying age. The lesion is focal and liver away from the abscess or micro-abscesses is normal. Only 10% of those harbouring the parasite develop invasive amoebiasis. Two species of entamoebae are found and one is non-pathogenic. The pathogenic may be distinguished from the non-pathogenic by DNA markers for antigens on the surface of the amoeba [4]. 498 Chapter 29 Secondary bacterial infection of the abscess occurs in about 20%. The pus then becomes green or yellow and foul smelling. Epidemiology Colonic amoebae have a worldwide distribution, but hepatic amoebiasis is a disease of the tropics and sub- tropics. Endemic areas are Africa, south-east Asia, Mexico, Venezuela and Colombia. In temperate climates, symptomless carriers of toxic strains are found but colonic ulcers are not seen. It is a frequent commensal in homosexual men [3]. In the tropics a new arrival is heavily exposed, especially when sanitation is poor. Locals are less prone, presumably because of partial immunity induced by repeated contact. The latent period between the intestinal infection and hepatic involvement has not been explained. Clinical features Residence in tropical or subtropical areas is noted. Amoebic dysentery is found in only 10% and cysts in the stool in only 15%. Past history of dysentery is rare. Hepatic amoebiasis has been recorded as long as 30 years after the primary infection. It is most frequent in young males. Multiple abscesses are frequent in such areas as Mexico and Taiwan. The onset is usually sub-acute with symptoms lasting up to 6 months. Rarely it may be acute with rigors and sweating and a duration of less than 10 days. Fever is variously intermittent, remittent or even absent unless an abscess becomes secondarily infected; it rarely exceeds 40°C. Deep abscesses may present simply as fever without signs referable to the liver. Jaundice is unusual and, if present, mild. Bile duct compression is rare. The patient looks ill, with a peculiar sallowness of the skin, like faded suntan. Pain in the liver area may commence as a dull ache, later becoming sharp and stabbing. If the abscess is near the diaphragm, there may be referred shoulder pain accentuated by deep breathing or coughing. Alcohol makes the pain worse, as do postural changes. The patient tends to lean to the left side; this opens up the right intercostal spaces and diminishes the tension on the liver capsule. The pain increases at night. A swelling may be visible in the epigastrium or bulging the intercostal spaces. Hepatic tenderness is vir- tually constant. It may be elicited over a palpable liver edge or by percussion over the lower right chest wall. The spleen is not enlarged. The lungs may show consolidation of the right lower zone, pleurisy or an effusion. Pleural fluid may be blood stained. Examination of faeces. Cysts and vegetative forms are rare. Serological tests The fluorescent antibody test is positive and remains so for some time after clinical cure. Amoebic abscess is unlikely if the test is negative. Current tests do not dis- tinguish acute from chronic amoebiasis. This may be possible using antibody responses to recombinant E. histolytica antigens [8]. Biochemical tests In chronic cases, serum alkaline phosphatase values are usually about twice normal. Increases in transaminases are found only in those who are acutely ill or with severe complications. A rise in serum bilirubin is unusual except in those with superinfection or rupture into the peritoneum. Radiological features Achest X-ray may show a high right diaphragm, obliter- ation of the costophrenic and cardiophrenic angles by adhesions, pleural effusions or right basal pneumonia (fig. 29.6). A right lateral abscess may cause widening of the intercostal spaces. The liver shadow may be enlarged with a raised immobile right diaphragm. The abscess commonly causes a bulge in the antero-medial part of the right diaphragm. The Liver in Infections 499 Fig. 29.6. Amoebic abscess of liver. Note the elevated right diaphragm with overlying reaction in the lung field. An abscess in the left lobe of the liver may show a crescentic deformity of the lesser curve of the stomach. US is the most useful (fig. 29.7). CT shows the abscess with a somewhat irregular edge and low attenuation. It is more sensitive than US for small abscesses. It may show extra-hepatic involvement, for instance in the lung [5]. MRI can be used for diagnosis and to follow treatment [2]. Liquefaction of the cavity may be shown as early as 4 days after starting treatment [2]. Diagnostic criteria • History of residence in an endemic area. • An enlarged tender liver in a young male. • Response to metronidazole. • Leucocytosis without anaemia in those with a short history, and less marked leucocytosis and anaemia with a long history. • Suggestive postero-anterior and lateral chest X-ray. • Scanning showing a filling defect. • Apositive amoebic fluorescent antibody test. Complications Rupture into the lungs or pleura causes empyema, hepato-bronchial fistula or pulmonary abscess. The patient coughs up pus, develops pneumonitis or lung abscess or a pleural effusion. Rupture into the pericardium is a complication of amoebic abscess in the left lobe. Intra-peritoneal rupture results in acute peritonitis. If the patient survives the initial effect, long-term results are good. Abscesses of the left lobe may perforate into the lesser sac. Rupture into the portal vein, bile ducts or gastrointestinal tract is rare. Secondary infection is suspected if prostration is particularly great, and fever and leucocytosis high. Aspiration reveals yellowish, often fetid, pus and culture reveals the causative organism. Treatment Metronidazole, 750mg three times a day for 5–10 days, has a 95% success rate. An intravenous preparation is available. The time to defervescence is 3–5 days [1]. Failures may be related to the persistence of intestinal amoebiasis, drug resistance or inadequate absorption. The time taken for the abscess to disappear depends on its size and varies from 10 to 300 days [7]. Aspiration is rarely necessary even with very large abscesses. It should be done under US or CT guidance. A tense abscess in the left lobe that is likely to rupture into the peritoneum demands aspiration. The mortality from amoebic liver abscess should be zero [1]. A course of oral amoebocide should be given to cover amoebae persisting in the gut. References 1 Barnes PF, De Cock KM, Reynolds TB et al. A comparison of amebic and pyogenic abscess of the liver. Medicine 1987; 66: 472. 2 Elizondo G, Weissleder R, Stark DD et al. Amebic liver abscess: diagnosis and treatment evaluation with MR imaging. Radiology 1987; 165: 795. 3 Goldmeier D, Sargeaunt PG, Price AB et al. Is Entamoeba histolytica in homosexual men a pathogen? Lancet 1986; i: 641. 4 Katwinkel-Wladarsch S, Lascher T, Rinder H. Direct amplifi- cation and differentiation of pathogenic and nonpathogenic Entamoeba histolytica DNA from stool specimens. Am. J. Trop. Med. Hyg. 1994; 51: 115. 500 Chapter 29 Fig. 29.7. Amoebic liver abscess. US demonstrates an amoebic abscess (1) in the liver (2), lying posteriorly against the diaphragm (3). The anterior abdominal wall (4) is also shown. 32 4 1 5 Radin DR, Ralls PW, Colletti PM et al. CT of amebic liver abscess. Am. J. Roentgenol. 1988; 150: 1297. 6 Seydel KB, Stanley SL Jr. Entamoeba histolytica induces host cell death in amoebic liver abscess by a non-Fas-dependent, nontumour necrosis factor alpha-dependent pathway of apoptosis. Infect. Immun. 1998; 66: 2980. 7 Simjee AE, Patel A, Gathiram V et al. Serial ultrasound in amoebic liver abscess. Clin. Radiol. 1985; 36: 61. 8 Stanley SL Jr, Jackson TF, Foster L et al. Longitudinal study of the antibody response to recombinant Entamoeba histolytica antigens in patients with amoebic liver abscess. Am. J. Trop. Med. Hyg. 1998; 58: 414. Tuberculosis of the liver Abdominal tuberculosis is suspected in immigrants from developing countries and also increasingly in patients with AIDS [4]. The liver may be involved as part of miliary tuberculosis or as local tuberculosis where evidence of extra-hepatic disease is not obvious. Rarely, hepatic tuberculosis can cause fulminant liver failure [5]. The basic lesion is the granuloma which is very frequent in the liver in both pulmonary and extra- pulmonary tuberculosis (fig. 29.8) (Chapter 28). The lesions usually heal without scarring but sometimes with focal fibrosis and calcification. Pseudo-tumoral hepatic tuberculomasare rare [1]. There may be no evidence of extra-hepatic tuberculosis [2]. The tuberculomas may be multiple, consisting of a white, irregular, caseous abscess surrounded by a fibrous capsule (fig. 29.9). Their naked eye distinction from Hodgkin’s disease, secondary carcinoma or actinomycosis may be difficult. Occasionally, the necrotic area calcifies. Tuberculous cholangitis is extremely rare, resulting from spread of caseous material from the portal tracts into the bile ducts. Biliary stricture is a rare complication [3]. Tuberculous pylephlebitis results from rupture of caseous material. It is usually rapidly fatal although chronic portal hypertension can result [8]. Tuberculous glands at the hilum may lead rarely to biliary obstruction. Clinical features These may be few or absent. The condition may present as a pyrexia of unknown origin. Jaundice may appear in overwhelming miliary tuberculosis, particularly in the racially susceptible. Rarely, multiple caseating granulomas lead to massive hepatosplenomegaly and death in liver failure [5]. Biochemical tests Serum globulin is increased so that the albumin/globulin ratio is reduced. Alkaline phosphatase is dispropor- tionately elevated [2]. Diagnosis This is difficult. Tuberculomas in liver and spleen are difficult to differentiate from lymphoma. Liver biopsy is essential. The indications are unexplained fever and weight loss with hepatomegaly or hepatosplenomegaly. A portion of the biopsy should be stained for acid- fast bacilli and cultured. Positives are obtained in about 50%. A plain X-ray of the abdomen may reveal hepatic calcification. This may be multiple and confluent in tubercu- The Liver in Infections 501 Fig. 29.8. Miliary tuberculosis: a caseating granuloma contains lymphocytes, epithelial cells and numerous giant cells (arrow). There is central caseation. Fig. 29.9. Hepato-splenic tuberculosis. CT scan showing scattered filling defects in the liver and spleen. Aspirate showed acid-fast bacilli and the culture was positive. loma, discrete and scattered and of uniform size, or large and chalky adjoining a stricture in the common bile duct [6]. CT may show a lobulated mass or multiple filling defects in liver and spleen (fig. 29.9). Extra-hepatic features of tuberculosis may not be obvious. Treatment is that for haematogenous tuberculosis. The effect on the liver of tuberculosis elsewhere Amyloidosis may complicate chronic tuberculosis. Fatty change is due to wasting and toxaemia. Drug jaundice may follow therapy, especially with isoniazid, rifam- picin and pyrazinamide. Other mycobacteria Atypical mycobacteria can produce a granulomatous hepatitis, particularly as part of the AIDS syndrome (see p. 26). Mycobacterium scrofulaceum can cause a granulomatous hepatitis, characterized by a rise in alkaline phosphatase, tiredness and low-grade fever. Liver biopsy culture produces the organism [7]. References 1 Achem SR, Kolts BE, Grisnik J et al. Pseudotumoral hepatic tuberculosis. Atypical presentation and comprehensive review of the literature. J. Clin. Gastroenterol. 1992; 14: 72. 2 Chien R-N, Lin P-Y, Liaw Y-F. Hepatic tuberculosis: comparison of miliary and local form. Infection 1995; 23: 5. 3 Fan ST, Ng IOL, Choi TK et al. Tuberculosis of the bile duct: a rare cause of biliary stricture. Am. J. Gastroenterol. 1989; 84: 413. 4 Guth AA, Kim U. The reappearance of abdominal tuberculosis. Surg. Gynecol. Obstet. 1991; 172; 432. 5 Hussain W, Mutimer D, Harrison R et al. Fulminant hepatic failure caused by tuberculosis. Gut 1995; 36: 792. 6 Maglinte DDT, Alvarez SZ, Ng AC et al. Patterns of calcifica- tions and cholangiographic findings in hepatobiliary tuberculosis. Gastrointest. Radiol. 1988; 13: 331. 7 Patel KM. Granulomatous hepatitis due to Mycobacterium scrofulaceum: report of a case. Gastroenterology 1981; 81: 156. 8 Ruttenberg D, Graham S, Burns D et al. Abdominal tuberculosis—a cause of portal vein thrombosis and portal hypertension. Dig. Dis. Sci. 1991; 36: 112. Hepatic actinomycosis Hepatic involvement due to Actinomyces israeli is a sequel to intestinal actinomycosis, especially of the caecum and appendix. It spreads by direct extension or, more often, by the portal vein, but can be primary. Large greyish-white masses, superficially resembling malignant metastases, soften and form collections of pus, sep- arated by fibrous tissue bands, simulating a honeycomb. The liver becomes adherent to adjacent viscera and to the abdominal wall, with the formation of sinuses. These lesions contain the characteristic ‘sulphur granules’, which consist of branching filaments with eosinophilic, clubbed ends. Clinical features The patient is toxic, febrile, sweating, wasted and anaemic. There is local, sometimes irregular, enlarge- ment of the liver with tenderness of one or both lobes. The overlying skin may have the livid, dusky hue seen over a taut abscess that is about to rupture. Multiple irregular sinus tracks develop. Similar sinuses may develop from the ileo-caecal site or from the chest wall if there is pleuro-pulmonary extension. Diagnosis The diagnosis is obvious at the stage of sinus tracts, because the organism can be isolated from the pus. If actinomycosis is suspected before this stage, percutaneous liver biopsy may reveal sulphur granules with organisms [1]. Early presentation is as pyrexia, hepatosplenomegaly and anaemia. It may be months before multiple abscesses are detected, often by US, CT [3] or MRI [4]. Anaerobic blood cultures may be positive. Treatment Intravenous penicillin is given in massive doses. Because of the thick capsule, the penicillin may reach the abscess with difficulty. Surgical resection may be necessary [2]. References 1 Bhatt BD, Zuckerman MJ, Ho H et al. Multiple actinomycotic abscesses of the liver. Am. J. Gastroenterol. 1990; 85: 309. 2 Kasano Y, Tanimura H, Yamaue H et al. Hepatic actinomycosis infiltrating the diaphragm and right lung. Am. J. Gastroen- terol. 1996; 91: 2418. 3 Mongiardo N, De Rienzo B, Zanchetta G et al. Primary hepatic actinomycosis. J. Infect. 1986; 12: 65. 4 Nazarian LN, Spencer JA, Mitchell DG. Multiple actinomycotic liver abscesses: MRI appearances with aetiology sug- gested by abdominal radiography. Case report. Clin. Imaging 1994; 18: 119. Other fungal infections These usually affect the immunocompromised, includ- ing sufferers from AIDS, acute leukaemia [6], cancer [10] and following liver transplant. The liver is involved, together with other organs, particularly kidney, spleen, heart, lungs and brain. Fever 502 Chapter 29 with a raised serum transaminase or alkaline phosphatase indicates needle liver biopsy. US shows multiple hypoechoic areas throughout the liver and spleen, often with a target (bull’s eye) configu- ration [8]. CT shows multiple, non-enhancing, low- attenuation lesions [6]. The scanning appearances are not diagnostic. The histological picture is usually granulomatous and the causative organism can be identified by appropriate stains and cultures, so allowing selection of appropriate antifungal treatment [4, 5]. Candidiasis. The liver is affected in up to three-quarters of those with disseminated Candida albicans infection who come to autopsy [5]. Hepatic granulomas and micro-abscesses are the commonest histological lesions. Candida can be demonstrated in the liver [2]. The treatment is with fluconazole. Disseminated aspergillosis may attack the immunocompromised patients with respiratory, renal or hepatic failure [7]. Hepatic cryptococcosis usually affects the immunocompromised but sometimes it may be seen in the otherwise normal. Liver biopsy shows granulomas with yeast-like organisms. The picture may resemble sclerosing cholangitis when bile is positive for the fungus (Chapter 15). Disseminated coccidioidomycosis may involve the liver and be diagnosed by liver biopsy [3]. Torulopsis glabrata hepatic abscesses and fungaemia have developed in a severely diabetic patient with biliary stricture due to chronic pancreatitis [1]. Blastomyces dermatitidis can cause cholangitis in the elderly or immunocompromised [9]. References 1 Friedman E, Blahut RJ, Bender MD. Hepatic abscesses and fungemia from Torulopsis glabrata. Successful treatment with percutaneous drainage and amphotericin B. J. Clin. Gastroenterol. 1987; 9: 711. 2 Gordon SC, Watts JC, Veneri RJ et al. Focal hepatic candidiasis with perihepatic adhesions: laparoscopic and immunohistologic diagnosis. Gastroenterology 1990; 98: 214. 3 Howard PF, Smith JW. Diagnosis of disseminated coccidioidomycosis. Arch. Intern. Med. 1983; 143: 1335. 4 Korinek JK, Guarda LA, Bolivar R et al. Trichosporon hepatitis. Gastroenterology 1983; 85: 732. 5 Lewis JH, Patel HR, Zimmerman HJ. The spectrum of hepatic candidiasis. Hepatology 1982; 2: 479. 6 Maxwell AJ, Mamtora H. Fungal liver abscesses in acute leukaemia—a report of two cases. Clin. Radiol. 1988; 39: 197. 7 Park GR, Drummond GB, Lamb D et al. Disseminated aspergillosis occurring in patients with respiratory, renal and hepatic failure. Lancet 1982; i: 179. 8 Pastakia B, Shawker TH, Thaler M et al. Hepatosplenic candidiasis: wheels within wheels. Radiology 1988; 166: 417. 9 Ryan ME, Kirchner JP, Sell T et al. Cholangitis due to Blastomyces dermatitidis. Gastroenterology 1989; 96: 1346. 10 Thaler M, Pastakia FB, Shawker TH et al. Hepatic candidiasis in cancer patients: the evolving picture of the syndrome. Ann. Intern. Med. 1988; 108: 88. Syphilis of the liver Congenital The liver is heavily infected by any trans-placental infection. It is firm, enlarged and swarming with spirochaetes. Initially, there is a diffuse hepatitis, but gradually fibrous tissue is laid down between the liver cells and in the portal zones, and this leads to a true peri-cellular cirrhosis. Since hepatic involvement is but an incident in a wide- spread spirochaetal septicaemia, the clinical features are seldom those of the liver disease. The fetus may be still- born or die soon after birth. If the infant survives, other manifestations of congenital syphilis are obvious, apart from the hepatosplenomegaly and mild jaundice. Syphilis nowadays rarely causes neonatal jaundice. In older children who have survived without this florid neonatal picture, the hepatic lesion may be a gumma. Diagnosis can be confirmed by blood serology which is always positive. Secondary In the secondary septicaemic stage, spirochaetes produce miliary granulomas [1]. Fifty per cent of sufferers have raised serum enzyme levels [4]. Clinical hepatitis is rare. However, sometimes the picture is of severe cholestatic jaundice [2]. Serology is positive. Serum alkaline phosphatase levels are high. The M1 cardiolipin fluorescent anti- mitochondrial antibody is positive and becomes normal with recovery [2]. Liver biopsy shows non-specific changes with moder- ate infiltration with polymorphs and lymphocytes, and some hepato-cellular disarray, but cholestasis is absent or mild except in the severely cholestatic patients [2]. Portal-to-central zone necrosis can be seen (fig. 29.10). Spirochaetes are sometimes detected in the liver biopsy. Tertiary Gummas may be single or multiple. They are usually in the right lobe. They consist of a caseous mass with a fibrous capsule. Healing is followed by deep scars and coarse lobulation (hepar lobatum). Hepatic gummas are usually diagnosed incidentally, by US or CT, at surgery or at autopsy. US-guided biopsy The Liver in Infections 503 [...]... Cloning of TH 0- and TH2type helper lymphocytes from liver granulomas of Schistosoma mansoni-infected mice Infect Immun 1994; 62: 994 Malaria [1] In the erythrocytic stage, the parasite is engulfed by reticulo-endothelial cells The liver suffers from the general effects of the toxaemia and pyrexia [2] The Liver in Infections 511 In the pre-erythrocytic (exo-erythrocytic) stage, schizogony takes place in the. .. to the liver cells to initiate the exo-erythrocytic or relapse cycle In malignant tertian this does not happen and there are no true relapses So far only Plasmodium falciparum and P vivax have been found in the liver of man The tissue stage of human malaria is confined to the liver cells Pathology The liver shows reticulo-endothelial proliferation, both of Kupffer cells and in zone 1 Focal, non-specific... mucosa and is carried by the portal vein to the liver, where it develops into an adult cyst Seventy per cent of hydatid cysts form in the liver A few ova pass through the liver and heart, and are held up in the lungs causing pulmonary cysts A few ova reach the general circulation causing spleen, brain and bone cysts Development of the hepatic cyst (fig 29. 18) The adult cyst develops slowly from the ovum and. .. Relapsing fever This arthropod-borne infection is caused by spirochaetes of the species Borrelia recurrentis It is encountered throughout the world except in New Zealand, Australia and some parts of the west Pacific The Borrelia multiply in the liver, invading liver cells and causing focal necrosis Just before the crisis the Borrelia roll up and are ingested by reticulo-endothelial cells This effect is... Gastroenterol 1 988 ; 83 : 323 2 Simson JNL Chlamydial perihepatitis (Curtis–Fitz Hugh syndrome) after hydrotubation Br Med J 1 984 ; 289 : 1146 Hepato -biliary disease in HIV infection HIV does not seem to exert any direct effect on the liver Many diseases, however, affect the immunodeficient and provide a confusing picture [23, 31] All parts of the hepato -biliary system can show changes and may be involved... the liver and within them the Leishman–Donovan bodies may be identified (fig Biology (fig 29.17) Man is infected by the excreta of dogs, often during childhood The dog is infected by eating the viscera of sheep, which contain hydatid cysts Scolices, contained in the cysts, adhere to the small intestine of the dog and become adult worms which attach to the intestinal wall Each worm sheds 500 ova into the. .. in 40% of sufferers Jaundice appears between the fourth and seventh day in 80 % of patients It is a grave sign, for the disease is never fatal in the absence of icterus The liver is enlarged, but not the spleen The urine shows albumin and bile pigment The stools are well coloured There is a leucocytosis of 10 000–30 000/mm3 with a relative increase in polymorphs Thrombocytopenia may be profound The second... pathogenic than S mansoni and produces hepatosplenic schistosomiasis more often and faster In the liver, the ova penetrate and obstruct the portal branches and are deposited either in the large radicles, producing the coarser type of bilharzial hepatic fibrosis, or in the small portal tracts, producing the fine diffuse form The granulomatous reaction to the Schistosoma ovum is of delayed hypersensitivity... project into the lumen of the cyst as brood capsules Scolices develop from the brood capsules and eventually indent it The attachment of the brood capsules to the germinal layer becomes progressively thinner until the capsule bursts, releasing the scolices into the cyst fluid These fall to the bottom and are termed hydatid sand All hydatid cysts start as purely cystic type I structures [10] When they develop... deposits of hydatid antigen [7] Endemic regions The disease is common in sheep-raising countries, where dogs have access to infected offal These include South Australia, New Zealand, Africa, South America, southern Europe, especially Cyprus, Greece and Spain, and the Middle and Far East The disease is rare in Britain, apart from some areas in Wales Clinical features These depend on the site, the stage and . 1 989 ; 96: 1346. 10 Thaler M, Pastakia FB, Shawker TH et al. Hepatic candidiasis in cancer patients: the evolving picture of the syndrome. Ann. Intern. Med. 1 988 ; 1 08: 88 . Syphilis of the liver Congenital The. enter the intra-hepatic portal system, where they grow rapidly. The extent and severity of chronic liver disease corre- lates with the intensity and duration of egg production and hence with the. encountered throughout the world except in New Zealand, Australia and some parts of the west Pacific. The Borrelia multiply in the liver, invading liver cells and causing focal necrosis. Just before the crisis the

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