Non Viral Liver Infections Flashcards
What are the signs, symptoms and complications of bacterial liver abscesses? Prognosis?
- Clinical manifestations
a. Symptoms
(1) abdominal pain in the right or left upper quadrant depending on the location of the abscess in the liver is
common
(2) diffuse abdominal pain occurs if peritonitis has developed
(3) diarrhea, weight loss due to anorexia
(4) fever, chills, diaphoresis (non-specific symptoms of bacterial infection)
(5) occasional cough, pleuritic chest pain, right shoulder pain
b. Signs
(1) enlarged liver
(2) RUQ (right upper quadrant) abdominal tenderness in most patients
(3) jaundice is uncommon
c. Complications
(1) local extension
(a) contained rupture under the diaphragm can cause subdiaphragmatic abscess; erosion through the diaphragm causes empyema (pus in the pleural space)
(2) rupture
(a) causes acute diffuse abdominal pain due to peritonitis; this happened in 15% of patients in one series of 73 patients
d. Natural history
(1) death is likely without treatment
(2) the use of antibiotics has helped reduce mortality
(3) biggest improvement in mortality followed the use of CT-guided drainage of abscesses
What is the most common predisposing factor for a liver bacterial abscess? Does it occur as a single abscess or multiple abscesses? Which bacteria typically cause it?
e. Pathophysiology
(1) the most common predisposing factor is intraabdominal infection: appendicitis, biliary obstruction with cholangitis (bacterial infection within the bile ducts), cholecystitis, perforated peptic ulcers, pelvic infections, infected pancreatitis, inflammatory bowel disease; non-abdominal infections can also be causative such as pneumonia, endocarditis
(2) single abscesses and multiple abscesses occur with equal frequency; multiple abscesses are more commonly associated with biliary tract infection
(3) the bacteria are typically aerobic and anaerobic enteric flora (see Table) which makes sense given the predisposing condition is usually an abdominal infection
How is the diagnosis made for a liver bacterial abscess? What is the treatment?
f. Diagnosis
(1) Leukocytosis (elevated white blood count), elevated alkaline phosphatase, and anemia are common
(2) Most patients will have negative blood cultures
(3) Imaging with CT scan or ultrasound is essential to establish the diagnosis
(4) CT or ultrasound-guided needle aspiration with culture of the fluid helps with identifying appropriate antibiotics
(5) Amebic abscess should be ruled out by obtaining serology for amebic infection before drainage if an obvious source of bacterial infection is not identified (e.g. cholangitis, appendicitis)
g. Treatment
(1) Drainage
(a) radiologic or surgical
(2) Antibiotics
(a) broad spectrum enteric aerobic and anaerobic coverage until the causative organisms are identified and their antibiotic sensitivities are known
What is Fitz-Hugh-Curtis Syndrome? Which microbe typically causes it? In what setting does it occur? What are the symptoms? Treatment?
Elevated liver enzymes are commonly observed in patients with gonococcal bacteremia. Most patients have elevated alkaline phosphatase levels and 30-40% have
elevated AST levels.
Direct spread of infection from the pelvis leads to “perihepatitis” and adhesions to the liver. This is called “Fitz-Hugh-Curtis” syndrome and typically causes sudden sharp right upper quadrant abdominal pain in young women with pelvic inflammatory disease caused by gonorrhea. Gallbladders have been unnecessarily
removed for this syndrome because the symptoms can mimic acute cholecystitis. Diagnosis is established by vaginal swab for gonorrhea and the symptoms respond to appropriate antibiotics.
Describe Entamoeba histolytica. Describe its life cycle.
A. Entamoeba histolytica (amebic) liver abscess
. About this organism
a. “Trophozoites” are the relatively big blobs
that we think of as ameba.
b. Trophozoites measure 10-50 um in diameter and contain a single nucleus with a central karyosome, reside in the lumen of the colon, where they adhere to the colonic mucosa
c. Life cycle
(1) two stages: cysts and trophozoites
(2) cysts measure 10-15 um in diameter and typically contain four nuclei
(3) cysts are spread via the ingestion of fecally contaminated food or water
(4) during excystation within the small intestine, division of one cyst leads to eight trophozoites
(5) re-encystation of the trophozoites occurs within the lumen of the colon
(6) excretion of cysts in the feces perpetuates the life cycle
(7) the trophozoites can also invade the colonic epithelium, causing amebic colitis (this occurs in only 10% of infected people)
Describe various presentations of an amebic liver abscess. What are the clinical signs in the different presentations? What are some complications? Natural history?
a. Symptoms
(1) 90% of individuals infected with E. histolytica are asymptomatic (ie, “colonized”)
(2) Acute presentation:
(a) fevers, chills, pleuritic (ie, with pain with inspiration) right-sided pain referred to right shoulder if right lobe abscess, epigastric pain radiating to left shoulder if left lobe abscess
(b) anorexia, nausea, vomiting are common
(c) non-productive cough is common
(3) Insidious presentation:
(a) anorexia, weight loss
(b) no abdominal pain or only mild and vague abdominal pain
(c) sometimes low grade fevers (clinically, this is often a “fever of unknown origin”, or FUO since nobody thinks of amebic liver abscess during the workup)
b. Signs
(1) Acute presentation:
(a) tender liver, leukocytosis
(b) normal or near normal liver enzymes
(c) usually no anemia
(d) cough
(2) Insidious presentation:
(a) tender enlarged liver is common
(b) minimal elevation of white blood count
(c) normal ALT but elevated alkaline phosphatase in 90%
c. Complications
(1) direct extension
(a) pleuropulmonary: empyema, lung abscesses, hepatobronchial fistulae
(b) pericarditis
(2) rupture
(a) acute peritonitis and gradual seepage with abdominal abscess formation can occur
d. Natural history
(1) hepatic abscesses may not develop for years after travel to an endemic area
(2) mortality after developing a liver abscess is 13% if untreated
Describe the pathophys of E. Histolytica. Who is at risk for amebic abscess?
- Pathophysiology
a. Not all strains are invasive; some just reside in colon
b. E. histolytica can spread in the bloodstream (hematogenously) after it has
penetrated the colonic epithelium to establish extraintestinal infections, most
commonly amebic liver abscesses
c. Half of patients with amebic liver abscesses have no history of known intestinal involvement
AT RISK
c. Those living in and traveling to tropical regions are at highest risk
d. Compared to natives, travelers to endemic areas seem to be more susceptible to invasive disease
e. Males are ten times more likely to develop amebic liver abscesses than females (nobody knows why)
What is the diagnostic approach to an amebic liver abscess? Treatment approach? Preventative measures?
- Diagnostic approach
a. Differentiate from pyogenic abscess, malignancy, echinococcal cyst by serology and imaging
b. Serologic testing (ie, tests for antibodies in the blood)
(1) Usually fairly sensitive but may remain positive years after infection
c. Imaging: CT and ultrasound both useful
d. Aspiration
(1) typically sterile of bacteria
(2) trophozoites can be difficult to find in the necrotic debris of the abscess
(3) can help exclude bacterial abscess
- Treatment
a. Metronidazole (Flagyl) 750-1000 mg tid (three times daily) po or IV x 5-10 days is 95% effective in treating the abscess(es)
b. Also need to eliminate luminal (ie, in the colon) ameba: paromycin or diloxanide furoate or iodoquinol is essential to prevent recurrent abscess formation
c. Percutaneous or surgical drainage may be needed when not responding totherapy or risk of rupture is present
d. Complete resolution after treatment is slow and can take 6 months to 2 years(this means it doesn’t make sense to repeat imaging just after treatment because the abscess will still be there (although the bugs will be dead)) - Preventive measures in endemic regions
a. Environmental sanitation (keep stool out of the water supply)
b. Identification and treatment of infected individuals
c. Health education (don’t drink contaminated water)
Describe the lifecycle of schistomiasis. What is the mode of transmission and mechanism of injury?
- The organism
a. Different species with slightly different
geographic distribution
b. Life cycle requires both humans and snails.
(1) Humans shed eggs in stool.
(2) Eggs that are deposited in fresh water develop into miracidia.
(3) Miracidia infect snails and develop into cercaria.
(4) Cercaria are released and live in fresh water until finding human skin which they penetrate.
(5) After penetration of the skin, they ultimately lays eggs in intestinal mucosa and the cycle continues.
c. There are 5 major species of schistosomiasis; S. hematobium does not cause liver disease whereas the others do.
5. Pathophysiology
a. Mode of transmission
(1) Cercaria, the free-living form in sewage contaminated fresh water, penetrate the skin and enter the blood.
b. Mechanism of injury
(1) eggs elicit a severe granulomatous reaction in the liver and in the intestine
Describe the symptoms, signs, and complications of acute schistomiasis disease.
- Clinical manifestations of acute disease
a. Symptoms of acute infection
(1) immunologic response to worms and eggs: redness at skin penetration
(2) symptoms begin 2-4 weeks after exposure and subside after 1-2 months
b. Signs
(1) tender hepatomegaly, splenomegaly, lymphadenopathy, eosinophilia
c. Complications
(1) major complication is the development of chronic infection site(s), headache, fever, chills, cough, anorexia, abdominal pain and other constitutional symptoms
Describe the symptoms, signs, and complications of chronic schisto disease.
- Clinical manifestions of chronic disease
a. Symptoms of chronic infection
(1) relatively asymptomatic until overt liver failure or variceal bleeding develops
b. Signs
(1) hepatomegaly, splenomegaly
(2) eosinophilia
c. Complications
(1) liver involvement is the major manifestion of chronic schistosomiasis
(2) presinusoidal obstruction of portal blood flow in the liver causes portal hypertension, ascites, esophageal varices and hypersplenism
What is the diagnostic approach with schisto? Treatment approach? Prevention techniques?
- Diagnostic approach
a. Stool examination for eggs is generally not helpful during the early acute phase
b. Colonoscopy with biopsy of the rectal mucosa has a better yield than stool studies
c. Serologies are available that detect acute infection
- Treatment
a. Praziquantel given in 2 or 3 doses in one day is effective - Prevention, societal issues
a. Education to avoid fecal contamination of water is essential
b. Widespread treatment of infected individuals to reduce water contamination
c. Travelers to endemic areas should avoid contact with fresh water
Describe the lifecycle of echniococcus granulosis. Describe the mechanism of injury.
- The organism
a. Echinococcus granulosis causes human liver cystic disease (other species of Echinococcus don’t)
b. The worm form (scolex) is a 5-10 mm long tapeworm that lives in domestic dogs (and also wolves, coyotes, jackels and dingos). Sheep serve as the major intermediate host for the egg and cyst development (and also goats, cattle, pigs, buffalo, horses, camels).
c. Humans become an accidental intermediate host by ingesting eggs, usually from infected dogs, food, water, or soil that has been contaminated by dog feces
d. Ingested eggs hatch in small intestine to form oncopheres
(1) Oncospheres migrate through lymphatics and form cysts
(2) Protoscolices develop in the cysts
(3) Don’t crowd your brain with the terms oncopheres and protoscolices; just remember that people can ingest the eggs and develop cysts
- Pathophysiology
a. Mechanism of injury
(1) “hydatid disease” is the name given to the single or multiple liver cysts that develop in intermediate hosts (such as humans) after unintentionally ingesting eggs from dog feces
(2) Most cysts develop in the liver, but they can develop in just about any other organ
Describe the signs, symptoms, complications, and natural history of echinococcus granulosis.
- Clinical manifestations
a. Symptoms
(1) liver cysts are typically asymptomatic for years as they slowly grow at a rate of 1-5 cm per year
(2) abdominal pain, nausea, vomiting can develop
b. Signs
(1) hepatomegaly
(2) only mild elevations of liver enzymes
c. Complications
(1) spontaneous or traumatic rupture of the cyst(s) can cause an allergic reaction with urticaria (hives), or even anaphylaxis and death
(2) erosion into the biliary tract allows bacterial infection of the cyst leading to combined hydatid pyogenic liver abscess
d. Natural history
(1) slowly progressive disease; outcome depends on the location of the cysts (brains cysts are bad)
What is the diagnostic approach, treatment approach, and prevention strategies for echinococcus?
- Diagnostic approach
a. Obtain careful history for exposure (e.g. sheep ranching, exposure to dogs that have access to sheep or other furry four-footed animals)
b. CT and ultrasound
(1) cyst septations help distinguish a hydatid cyst from common benign/non-infectious liver cysts
c. Serologic tests for antibodies are helpful
d. Cyst aspiration can lead to intraperitoneal seeding of the organism
- Treatment
a. Careful surgical drainage without peritoneal contamination is generally recommended
b. Drug options include mebendazole and praziquantel - Prevention, societal issues
a. Good handwashing is essential in endemic areas, especially by children
