What viruses affect the liver

Other findings during this phase include modest elevation of transaminases, leukopenia and lack of jaundice. Patients may recover from this phase and develop lifelong immunity. During this phase, patients may have fever, emesis, abdominal pain, jaundice, coagulopathy with bleeding diathesis, and renal failure. Transaminase levels peak and are directly proportional to the severity of disease.

Liver pathology typically reveals mid-zonal hepatocyte necrosis and injury often with sparing of the central vein and portal tracts, minimal inflammatory cell infiltrates, and preserved reticulin framework.

Infected hepatocytes undergo apoptosis with characteristic eosinophilic condensed nuclear chromatin called Councilman bodies. The pathogenesis of severe disease is not fully understood. Proposed mechanisms include undetermined host genetic factors that confer susceptibility to infection, direct viral cytopathic effect and host cytokine dysregulation. Direct viral infection of hepatocytes and ischemia contribute to liver injury observed in yellow fever. Diagnosis is usually established on clinical grounds in persons with an appropriate travel history.

Other febrile illnesses that cause jaundice include bacterial sepsis, acute HSV hepatitis, leptospirosis, severe malaria, relapsing fever from Borrelia recurrentis infection, dengue hemorrhagic fever, and acute hepatitis A, B, or E infection although fever is less likely with these hepatotropic viruses.

There are no specific antiviral therapies available for yellow fever. A 17D live-attenuated vaccine is available for travelers to endemic regions, but is contraindicated in pregnancy, and immunosuppressed persons. Reports of serious infection with the attenuated vaccine strain have been reported but are exceedingly rare and occur in less than one per a million vaccinations. The World Health Organization estimates that Dengue virus infects 50 million people annually.

The incubation period ranges from several days to 1—2 weeks. The symptoms and severity of disease vary with age. Infections are often asymptomatic in children. Classic Dengue presents with fever, severe myalgias, arthralgias, headache, retro-orbital pain, gastrointestinal symptoms and rash. Minor bleeding from mucosal surfaces, hemoptysis and gastrointestinal hemorrhage can occur. The enzyme elevations peak on day 9 and return to normal levels within 2—3 weeks. The differential diagnosis of dengue is very similar to that of yellow fever.

There is no effective antiviral treatment at this time and treatment is supportive. Although there are vaccine candidates in development, there are currently no approved vaccines for dengue.

Systemic bacterial infections can have an impact on many organ systems including the liver. The indirect impact of these infections that is seen with syndromes such as sepsis are discussed elsewhere in this issue. Formation of abscesses in the liver is a complication of many bacterial infections.

Although not a focus of this review, Table 2 describes the pathogens that have been reported to cause liver abscesses. This topic has also been reviewed in depth elsewhere. Salmonella enterica serotype typhi is the causative agent of typhoid fever which is an enteric fever syndrome characterized by acute onset of fever and abdominal pain.

There are approximately 16 million cases of typhoid fever and , deaths annually. In addition to fever and abdominal pain, other clinical features of typhoid fever are variable and non-specific and include headache, relative bradycardia, leukopenia, hepatomegaly, splenomegaly. Constipation may occur as frequently as diarrhea in otherwise healthy adults whereas diarrhea occurs more frequently in children and patients infected with HIV.

A severe form of disease with jaundice can occur in 0. The elevations in serum transaminases are usually 3—5 times the upper limit of normal with AST usually being higher than the ALT. Twenty-three percent of cases have elevations in serum bilirubin and alkaline phosphatase levels are normal to slightly elevated.

Bone marrow cultures have a higher yield and may remain positive even after initiation of antibiotics. There are a variety of clinical manifestations of hepatic tuberculosis prompting some investigators [ 44 ] to further classify the various forms as miliary, granulomatous, and localized hepatic tuberoculosis. Localized hepatic tuberculosis may occur either with or without biliary involvement.

Another review of 14 cases noted a median time from the onset of symptoms to presentation for medical evaluations of over 40 days. On computed tomography, both solitary and multiple lesions were found, and were often difficult to distinguish from malignancy, amebic or pyogenic abscesses. Chalky hepatic and bile duct calcifications have also been described. The role of adjunctive drainage is debated and instances of biliary involvement may necessitate ERCP and stent placement.

Brucellosis is a systemic febrile illness caused by zoonotic infection with Brucella species, which are small, intracellular gram negative diplococci. The four species responsible for disease in humans and their main domestic animal hosts include B. The majority of human infections are caused by B. Exposure to domestic animals is the usual mode of transmission. Infection can occur through direct contact with infected animal hides and carcasses, inhalation of aerosols and ingestion of contaminated milk or milk products.

The incubation period is variable and may be up to several months. Apart from fevers, chills and constitutional symptoms, clinical manifestations of brucellosis can vary widely as multiple organ systems may be involved.

Hepatitis associated with brucella appears to be mild, with no reports of acute liver failure. In its more severe form, brucella can cause hepatic abscesses, traditionally associated with B. A correlation with cirrhosis has been observed but is not definitive. Histopathology also varies, with the most common finding being hepatic granulomas, inflammatory cell infiltrates and mild, localized parenchymal necrosis.

Diagnosing brucellosis is challenging, Serological assays are the most common diagnostic test used to make the diagnosis. Titers generally remain high for prolonged periods.

However this test does not detect B. ELISA may offer improved sensitivity and specificity, and PCR from blood and tissue specimens is promising but not yet widely available. Modern blood culture systems appear to have a higher yield. Bone marrow cultures have a higher yield of organisms. In both cases, laboratory personnel should be alerted to the suspicion of brucellosis. The WHO recommends treatment with doxycycline mg daily for 6 weeks combined with either rifampin — mg daily for 6 weeks or IM streptomycin 1 gm daily for 2 weeks.

Q fever is a worldwide zoonotic infection caused by Coxiella burnetii , an intracellular gram-negative coccobacillus formerly classified as a rickettsiae. Many animals are reservoirs of infection with cattle, goats and sheep being the most frequent sources of human infection. Infection typically arises after inhalation of aerosolized infectious particles, usually from parturient livestock or carcasses, although animal contact is notably absent in some cases.

The clinical spectrum of illness caused by this pathogen varies from asymptomatic infection to acute and chronic Q fever. Acute Q fever may manifest as a flu—like illness, hepatitis, and pneumonia. Illness is characterized by the acute onset of high fever, headache, and myalgias. Pneumonia, when present is usually mild without characteristic chest X-ray findings.

Hepatitis typically manifests as fever and mild asymptomatic elevations 2—3 xULN of transaminases. Chronic Q fever may also present as endocarditis, osteomyelitis , arteritis with aneurysm formation and hepatitis. It may be difficult to distinguish Q fever hepatitis from other cases of acute hepatitis save for the presence of severe headache and fever.

As with other self-limited illnesses with abnormal liver function, biopsy may not be performed, but it can prove quite useful. The diagnosis of Q fever is usually established by positive serology, usually indirect immunofluorescent assays.

Leptospirosis, caused by spirochetes of the genus Leptospira. Human infection is usually acquired through contact with urine from infected animals, most commonly rodents and other small mammals. The clinical presentation of the disease is variable. Subclinical infection occurs in a majority of cases, which, in general, do not seek medical attention. The acute phase can last 5—7 days and then is followed a brief period of improvement. A second or immune phase is characterized by recurrence of the symptoms and signs seen in the acute phase and may last from 4—30 days.

Notably, the headache may be severe and throbbing. Other symptoms and signs include: nausea, vomiting, abdominal pain and diarrhea. In this form, jaundice may occur in the acute phase and last for weeks. The immune phase follows without the period of brief improvement. This phase presents with high fever, hepatic failure, and renal failure. Hemorrhagic complications, likely a result of immune complex mediated capillary injury, are common and thrombocytopenia may occur in the absence of disseminated intravascular coagulation.

Hepatic histology is usually non-specific but may reveal intrahepatic cholestasis, hypertrophy of Kupffer cells, and, in severe cases, erythrophagocytosis. The disease is diagnosed by blood or urine cultures and serologies are used for confirmation of the diagnosis. Doxycycline is effective in mild disease or when utilized as disease prophylaxis. Penicillin or ceftriaxone are generally utilized in more severe disease. Hepatic involvement during the various stages of syphilis is a rare event in the postantibiotic era.

Hepatic architecture remains intact with cirrhosis occurring very rarely. Lyme disease, caused by Borrelia burgdorferi may also be accompanied by hepatitis, usually manifesting as incidental, asymptomatic elevations in aminotransferases.

Evaluation of parasitic infections requires a careful clinical history including travel and exposures in order to direct further work-up. Many parasitic infections may cause liver pathology as outlined in Table 3. Schistosoma and malaria are two of the most common parasitic infections globally and will be discussed in more detail in this section. Schistosomiasis is a parasitic infection caused by trematode blood flukes referred to as schistosomes.

The four main species capable of producing hepatic complications during human infection include S. The fifth major species, S. Approximately, 20 million suffer from more severe disease which causes an estimated , deaths annually.

Schistosomes have a complicated life cycle with snails as an intermediate host and humans as the definitive host. Infected humans excrete eggs of the parasite in feces and urine, which can contaminate fresh, warm water, especially in areas with poor sanitation. The eggs hatch, releasing miracidia which infect susceptible snails, reproduce asexually and emerge as cercariae. The cercariae then penetrate through the human skin and transform into schistosomula. The schistosomula traverse through blood and lymph making their way to the left side of the heart and eventually into mesenteric and portal vessels where the maturing worms take up residence about 3—6 weeks after initial infection.

The subsequent sexual reproduction with egg deposition in various organs elicits an immune response responsible for tissue damage and disease. Most infections occur in inhabitants of endemic regions and the severity of infection is generally proportional to the organism burden.

Infections in travelers to endemic regions with brief freshwater exposures have been reported. Most patients with the chronic form will have eosinophilia. Chronic schistosomiasis can present with as intestinal or hepatosplenic disease. Hepatic disease is usually caused by S. The spectrum and severity of liver disease seen in schistosomiasis varies according to duration of infection and organism load.

Early in the disease, egg deposition in portal vein tributaries elicits an immune response with granuloma formation, hepatomegaly and splenomegaly. This inflammatory hepatic form of schistosomiasis is usually seen in children. Five-ten percent of infected young and middle aged adults who have been infected for a number of years develop periportal or Symmers pipestem fibrosis as a consequence of the chronic inflammation.

Hepatic parenchymal perfusion is usually preserved, thus hepatocyte dysfunction is generally not observed, and lobular architecture remains intact. Nonetheless, the fibrosis can progress leading to clinical sequelae of portal hypertension including splenomegaly , bleeding esophageal varices and, with decompensated disease, encephalopathy and ascites.

Stigmata of chronic liver disease are noticeably absent. Diagnosis is based on clinical findings in patients with appropriate exposure history and microscopic examination of feces or urine for eggs. Malaria is caused by one of four species of the protozoan parasite, Plasmodium: Plasmodium falciparum, Plasmodim vivax, Plasmodium malariae and Plasmodium ovale. The WHO estimates that there were million cases of malaria in which led to close to one million deaths.

The life cycle of all of the Plasmodium species is composed of 2 phases. The bite of the anopheline mosquito introduces sporozoites into the bloodstream which after circulating for a short period of time invade hepatocytes in the liver. The sporozoites then mature into tissue schizonts, a hepatocyte infected by a sporozoite, which can each produce thousands of merozoites.

When the hepatocyte ruptures to release the merozoites, each merozoite can invade a human erythrocyte and produce an additional 20—30 merozoites through asexual replication. Infected erythrocytes then rupture to release the merozoites which are able to repeat this cycle which is termed erythrocytic schizogony.

In Plasmodium vivax and ovale, which can cause relapsing malaria, sporozoites also can become dormant hypnozoites when they invade hepatocytes. These hypnozoites may remain dormant for months after an initial infection, without any symptoms of disease, before they mature to tissue schizonts and produce symptomatic infection. The classic presentation of malaria is cyclic fever occurring every 48 to 72 hours. Shaking chills usually precede the high fever.

Fever coincides with schizont rupture and can be accompanied by cough, headache, nausea, vomiting, abdominal pain, diarrhea, backache, and tachycardia. After several hours, the febrile phase is followed by severe diaphoresis and fatigue. Severe cases of Plasmodium falciparum can also present with hypotension, altered consciousness and CNS complications, hypoglycemia, renal failure, pulmonary edema and, occasionally, hepatic failure.

Although the exact pathogenesis of all of these complications is not clear, obstruction of the microvasculature related to cytoadherence of falciparum to vessel endothelia, binding of infected erythrocytes to noninfected erythrocytes, reduced erythrocyte deformability and platelet-mediated clumping of infected erythrocytes of parasitized erythrocytes are thought to be the central process.

Moderate elevations of serum aminotransferase levels are commonly seen in malaria. However, severe falciparum malaria may mimic hepatic failure with marked transaminase elevations usually accompanied by multi-organ dysfunction. Hepatocyte necrosis, portal inflammation, steatosis and cholestasis may also be observed especially in fatal cases.

Peripheral blood smears thick and thin can be diagnostic for malaria however, in many cases, the number of organisms may be very low, especially in mild cases. Evaluation by an experienced examiner is recommended in these situations. Clinical history and physical examination are also important in making the diagnosis of malaria. Treatment for malaria depends on the species and the prevalence of antimalarial drug resistance in the region malaria was acquired.

For chloroquine sensitive malaria, the treatment is usually chloroquine mg base initially followed by mg base at 6, 24 and 48 hours. Other agents utilized in the treatment of uncomplicated malaria include: mefloquine, quinine plus doxycycline, atovaquone-proguanil, and artemether plus lumefantine. For patients infected with Plasmodium vivax or ovale, chloroquine treatment is followed by 14 days of primaquine to eradicate hypnozoites.

Note that primaquine is contraindicated in patients with G6PD deficiency. Liver infection with Candida species usually manifests as hepatosplenic candidiasis, a complication of disseminated candida infection that is usually seen among patients with hematologic malignancies who are recovering from a prolonged severe neutropenia.

Clinically, the classic symptom of hepatosplenic candidiasis is prolonged fever despite broad spectrum antibiotics in a patient with recovering neutropenia.

Diagnosis is usually made on clinical grounds, precluding the need for more invasive measures. When performed, liver biopsy may reveal granulomatous inflammation with characteristic fungal elements demonstrated with special staining techniques.

What causes it? Number of U. About 22, new infections in Estimated , people living with hepatitis B. About 50, new infections in Estimated 2. Key facts Hepatitis A Hepatitis B Hepatitis C Effective vaccine available Outbreaks still occur in the United States; currently there are widespread person-to-person outbreaks Recent foodborne outbreaks in US traced to imported food Common in many countries, especially those without modern sanitation. S are Asian Hepatitis B is a leading cause of liver cancer.

How long does it last? How is it spread? Hepatitis A Hepatitis B Hepatitis C Hepatitis A is spread when a person ingests fecal matter—even in microscopic amounts—from contact with objects, food, or drinks contaminated by feces or stool from an infected person. The hepatitis B virus can also be transmitted from: Birth to an infected mother Sex with an infected person Sharing equipment that has been contaminated with blood from an infected person, such as needles, syringes, and even medical equipment, such as glucose monitors Sharing personal items such as toothbrushes or razors Poor infection control has resulted in outbreaks in health care facilities.

The hepatitis C virus can also be transmitted from: Sharing equipment that has been contaminated with blood from an infected person, such as needles and syringes Receiving a blood transfusion or organ transplant before when widespread screening virtually eliminated hepatitis C from the blood supply Poor infection control has resulted in outbreaks in health care facilities Birth to an infected mother. Who should be vaccinated? All infants All children and adolescents younger than 19 years of age who have not been vaccinated People at risk for infection by sexual exposure including: people whose sex partners have hepatitis B, sexually active people who are not in a long-term, mutually monogamous relationship, people seeking evaluation or treatment for an STD, and men who have sex with men People at risk for infection by exposure to blood including: people who inject drugs, people who live with a person who has hepatitis B, residents and staff of facilities for developmentally disabled people, health care and public safety workers at risk for exposure to blood or blood-contaminated body fluids on the job Hemodialysis patients and predialysis, peritoneal dialysis, and home dialysis patients People with diabetes aged 19—59 years; people with diabetes aged 60 or older should ask their doctor.

International travelers to countries where hepatitis B is common People with hepatitis C People with chronic liver disease People with HIV People who are in jail or prison All other people seeking protection from hepatitis B virus infection. There is no vaccine available for hepatitis C. How serious is it? Hepatitis A Hepatitis B Hepatitis C People can be sick for a few weeks to a few months Most recover with no lasting liver damage Although very rare, death can occur.

Who should be tested? CDC recommends hepatitis C testing for: All adults aged 18 years and older All pregnant women during each pregnancy People who ever injected drugs and shared needles, syringes, or other drug preparation equipment, including those who injected once or a few times many years ago.

Regular testing is recommended for people who currently inject and share needles, syringes, or other drug preparation equipment. People with HIV People who have ever received maintenance hemodialysis. Regular testing is recommended for people who currently receive maintenance hemodialysis. ABC Table What causes it? Let us understand the details of each types and sub-types of liver infections.

These viruses are unrelated to each other. Viral inflammation is mostly caused by Hepatitis A, B and C viruses.

These three types of viruses cause acute hepatitis. However, B and C can cause chronic hepatitis which lasts for a long time. Patients with liver infection due to hepatitis B or C have severe liver damage due to cirrhosis.

Although each type is transmitted in a different way, the symptoms for all hepatitis viruses are nearly similar which includes:. Hepatitis A virus HAV enters the body through intake of water or food contaminated with faeces of patient infected with hepatitis A and consumption of raw fish food. This virus is observed in developing countries where there is poor sanitation.

It is most likely contracted while travelling to such countries. HAV causes acute and short term liver inflammation. It causes mild hepatitis which resolves within two months. In some rare cases it progresses to cause liver failure. Hepatitis A virus is detected by blood test where antibodies to HAV indicate presence of infection. It is a short term disease hence only bed rest is recommended. The infection clears on its own within one or two months.

Patients are advised to take rest, drink plenty of liquids, eat healthy diet and avoid intake of alcohol. Hepatitis B virus is seen all over the world and is endemic in South East Asian countries. It is responsible for most of the liver inflammations and liver damage. It enters the body through use of contaminated needles, due to contact with infected blood and other body fluids such as vaginal discharge and semen.

In addition, the risk is increased while having unprotected sex with HBV infected partner and using HBV infected razors and needles. It is also transmitted from infected mother to her baby. It causes both acute and chronic liver infections.

Acute infection is short term where the infection lasts for few weeks since the body is able to fight off the infection. Healthy adults and children are able to recover from HBV infections without any medication.

Chronic infection is a long lasting infection and is dangerous. It causes severe inflammation which hinders the normal functioning of the liver. If left untreated, it leads to further complications such as cirrhosis, liver failure and liver cancer.

The patient has to undergo physical examination. Further, both medical history of the patient and his family is noted. Regular blood tests Liver function tests are done.