Bacterial sepsis precipitating jaundice is a well-recognized phenomenon particularly in the newborn and young infants [1]. The exact pathogenesis of hepatic insult is not known, but may be multifactorial, including direct invasion of liver parenchyma by blood-borne pathogens and nonspecific injury due to hypoxia or endotoxin-mediated paralysis of biliary canaliculi inducing cholestasis. Implicated bacteria include ‘coliforms’, pseudomonads, Salmonella spp., anaerobes, Haemophilus influenzae, streptococci and Staphylococcus aureus. In patients with jaundice, serum bilirubin is usually between 5 and 10 mg/dl. Hepatomegaly is found in 50 % of cases, and liver enzymes usually mildly elevated. Clinical evaluation and microbiological investigation may identify the source of sepsis and antimicrobial therapy usually results in complete resolution.

Pyogenic liver abscess (PLA) in infancy and childhood is uncommon, with incidence ranging from 3 to 25 per 100,000, but carries a high mortality [2–4]. The oetiology of PLA is variable. Though PLA in healthy children is a rare entity, up to 40–50 % has occurred among immunocompromised children [2]. Pyogenic bacteria can reach the liver through various routes: (i) portal: secondary to gut pathologies such as appendicitis, inflammatory bowel disease or diverticulitis, sometimes complicated by portal pyelophlebitis and portal vein system thrombosis; (ii) biliary: caused by extrahepatic biliary tract disease such as stricture, calculus or malignancy; (iii) blood borne from an infected focus anywhere in the body via hepatic artery; (iv) contiguous extension from gallbladder or perinephric abscess; (v) following penetrating wounds of liver and (vi) cryptogenic [2, 5].

PLA may present as single large lesion or multiple abscesses, the latter often secondary to biliary tract infection. The importance of the portal venous route has fallen with better diagnosis and management of appendicitis . In most reviews, more than 60 % abscesses are in the right lobe, 20–25 % bilateral, and less than 15 % in the left lobe [4, 5].Predisposing factors include immunosuppression, quantitative or qualitative granulocyte abnormalities like chronic granulomatous disease, trauma, umbilical vein catheterization, omphalitis, sickle-cell disease, biliary tract surgery, hepatic artery thrombosis (post liver transplantation), liver biopsy, percutaneous or endoscopic biliary drainage, diabetes, worm infestation and protein-energy malnutrition especially in developing countries [4, 5].

Multiple abscesses complicate biliary diseases such as bacterial cholangitis, sclerosing cholangitis , congenital biliary anomalies (Caroli’s disease) and gallstones with higher mortality. S. aureus is the most common isolate in children, but Gram-negative aerobes, anaerobes and microaerophilic streptococci are also common [2, 4, 5]. Less frequent causes include Pseudomonas spp., Clostridium spp., Salmonella typhi, Yersinia enterocolitica and Pasteurella multocida. The classic presentation is pyrexia, chills, right upper quadrant (RUQ) tenderness, abdominal pain, hepatomegaly and leucocytosis but may be nonspecific. The diagnosis must be entertained in any pyrexia of unknown origin (PUO). Unusual presentations include an abdominal mass or acute abdomen secondary to rupture in to the peritoneal cavity or portal hypertension secondary to portal pyemia and portal vein thrombosis. Liver function tests may be unhelpful with nonspecific changes. Ultrasonography (USS), computerized tomography (CT) and magnetic resonance imaging (MRI) are all sensitive but cannot always differentiate abscesses from other lesions such as cysts, tumours or haemorrhage. USS or CT-guided drainage of as much pus as possible (from as many abscesses as possible) confirms diagnosis, and is central to the management. Initial treatment is conservative with broad-spectrum antibiotics (e.g. cefotaxime plus metronidazole or clindamycin) and should be adjusted when culture results are available [5, 6]. Duration of treatment is usually 3–6 weeks. Patients with multiple abscesses have to be on conservative treatment after a diagnostic tap, and up to 3–4 months of antibiotic therapy has been recommended to prevent relapses [5, 7]. Prognosis is worse in multiple abscesses. Most reports emphasize the good outcome after percutaneous drainage, which should be USS or CT guided. Contraindications to drainage include ascites and inaccessible lesions. Complications of aspiration include haemorrhage, hepatic laceration, fistula formation, peritonitis and additional abscess formation. Indications for open drainage procedure are biliary obstruction, loculated or highly viscous abscesses, persistence of fever for more than 2 weeks despite percutaneous catheter drainage and appropriate antimicrobial therapy. Predisposing immunodeficiency conditions should be managed with appropriate expert opinion from immunologists or infectious diseases experts.

The normal biliary tract is sterile and, in children, acute cholangitis rarely occurs in the absence of congenital abnormalities or interventions in the biliary tract [8]. The children at highest risk include those with portoenterostomy or choledochal cyst, and those who have nonoperative biliary manipulations such as transhepatic cholangiography or endoscopic retrograde cholangiography with stent placement. Risk of cholangitis in children after Kasai operation has been reported to be 40–50 % [8]. Partial biliary obstruction encourages bacterial growth , with increased intraductal pressure and reflux of bacteria into blood vessels and perihepatic lymphatics leading to bacteremia. Infection may ascend from the duodenum or an infected gallbladder, or via lymphatics or bloodstream [9].

Cholangitis is a clinical diagnosis based on fever, abdominal pain, jaundice, pale stools or hepatic tenderness. However, the spectrum encompasses mild disease to severe sepsis, or shock, with bacteraemia [8]. Although Escherichia coli, Klebsiella spp., Enterobacter spp. and Pseudomonas spp. are usually implicated, infection may be polymicrobial and include anaerobes [8]. Leucocytosis is common, but changes in liver function tests are nonspecific; the serum bilirubin may be normal. In recurrent cholangitis, liver biopsy may be indicated for confirmation and microbiological examination. Treatment requires supportive care and an urgent USS or CT will help establish whether obstruction requires drainage. Broad-spectrum antibiotics should be administered—such as an acylureidopenicillin (piperacillin, mezlocillin or piperacillin-tazobactam) or a late generation cephalosporin (e.g. ceftazidime), plus an aminoglycoside [10]. Single agents, such as piperacillin, piperacillin-tazobactam, ciprofloxacin and imipenem or meropenem, appear safe and effective if an aminoglycosides is contraindicated. Duration of treatment is generally 3 weeks for acute cholangitis, but prolonged therapy may be necessary for recurrent cholangitis and multiply resistant bacteria [11]. Three months of intravenous antibiotics through central line has been helpful in treating recurrent cholangitis in biliary atresia children with portoenterostomy. Prolonged antimicrobial therapy in recurrent cholangitis only helps in preventing the bacteraemia by preventing bacterial overgrowth in biliary tract. There is always risk of development of resistant organisms and therefore more serious infection.

Tuberculosis (TB) of the liver is almost invariably a complication of miliary disease and occurs in 50 and 75 % of patients with pulmonary or extrapulmonary TB, respectively. The site of primary focus usually dictates presentation. Rarely the liver appears to be the sole site of infection such as in congenital TB acquired via the ductus venosus [12, 13]. Congenital TB may present in first few weeks of life with failure to thrive, hepatosplenomegaly and jaundice . In older children, hepatic TB presents with PUO, weight loss, abdominal discomfort and hepatomegaly [12, 13]. In areas of low incidence a positive tuberculin skin test is diagnostically useful.However, confirmation requires liver biopsy, histology and culture confirmation. Caseating granulomata on liver biopsy are highly suggestive of TB, but may be absent; a granulomatous hepatitis can complicate Bacille Calmette–Guerin (BCG) administration. The diagnosis of TB should be sought by specific staining and culture of material from other sites, including bronchoalveolar lavage, lymph node or pleural biopsy, marrow aspirate, lumbar puncture or early morning gastric aspirates, as clinically indicated. Polymerase chain reaction (PCR)-based tests may be helpful but require further evaluation. Standard antituberculous therapy is effective, but expert advice should be sought in areas with a high incidence of drug resistant TB or in compromised patients, including those with concurrent HIV infection.

It is a multisystem infection caused by Brucella melitensis, B. suis, B. abortus and B. canis; B. melitensis causes more severe disease with a higher risk of chronicity. In endemic areas, transmission is often by ingestion of unpasteurized dairy products or raw meat. Granulomatous hepatitis may occur in acute or chronic disease and manifests as nonspecific changes in liver function tests [14]. Diagnosis requires clinical suspicion, blood and bone marrow cultures, serology and histopathological examination. PCR-based tests for brucellosis are available. The recommended treatment for children under 9 years of age with uncomplicated brucellosis is trimethoprim–sulphamethoxazole. For the treatment of serious infection, the addition of gentamicin or streptomycin is recommended for the first 1–2 weeks. Older children should receive doxycycline (6 weeks) plus rifampicin or streptomycin (2 weeks).