Liver abscess and parasitic liver disease

• A liver abscess is a pocket of pus or necrosis inside the liver parenchyma. Most are pyogenic (bacterial), produced either by spread from the biliary tree and gut or by bloodstream seeding.
• In industrialised settings pyogenic abscess accounts for over 80% of cases, while Entamoeba histolytica accounts for up to 10%, with higher rates in tropical and subtropical regions and among migrants and travellers.^[1]
• An amoebic liver abscess is the most common extraintestinal form of amoebiasis. It can appear months or years after travel to an endemic region, often as a single right-lobe lesion with "anchovy paste" pus.^[4]
• A hydatid cyst is the larval stage of Echinococcus granulosus in the liver. It is a parasitic cyst, not a bacterial abscess, and its treatment depends on ultrasound stage rather than on drainage.
• The curative strategy for a pyogenic abscess is broad-spectrum antibiotics plus drainage; an amoebic abscess is usually cured by metronidazole without drainage; a small active hydatid cyst may be treated with albendazole alone, while larger cysts need PAIR or surgery. ^[1]
• Fever is present in 90-95% of pyogenic cases, and ultrasound or CT detects an abscess with sensitivity 96-100%.^[1]

By the end of this page you should be able to:

1. Name the three common causes of a focal liver lesion in this topic and state how their frequencies differ by setting.^[1][2]
2. Explain how a pyogenic liver abscess forms and why Klebsiella pneumoniae is a special concern.
3. Recognise the clinical picture of an amoebic liver abscess, interpret serology and imaging, and know when drainage is and is not indicated.^[4][5]
4. Plan empiric antibiotic therapy for a pyogenic abscess, including drug choice, dose, duration and when to add antifungal cover.^[5]
5. Explain the WHO-IWGE ultrasound staging of a hydatid cyst and match each stage to treatment.^[6][7]
6. Give the dose, duration and monitoring of albendazole, and the peri-procedural rules around PAIR.^[6][7]
7. Adapt the whole pathway to a low-resource setting.^[3]

• Pyogenic (bacterial) liver abscess. The commonest form in industrialised regions. It may be monomicrobial or polymicrobial, and organisms usually reflect gut flora (Escherichia coli, Klebsiella species, enterococci, anaerobes such as Bacteroides).^[1][5]
• Amoebic liver abscess. The most common extraintestinal form of amoebiasis. It follows invasion of the colonic mucosa by E. histolytica trophozoites with spread via the portal circulation.^[1][4]
• Hydatid (echinococcal) cyst. A cystic echinococcosis lesion, usually from Echinococcus granulosus. It contains viable protoscolices in earlier stages and becomes inactive and calcified in later stages.^[6][7]
• Other causes of an apparent liver abscess include fungal infection (usually in immunosuppressed or neutropenic hosts), mycobacterial disease, and malignant or iatrogenic necrosis. These are mentioned so that "liver abscess" is not assumed bacterial.^[2]

Because a hydatid cyst is a living parasite rather than a bacterial collection, treating it like a pyogenic abscess (for example routinely draining it) can spill protoscolices and cause secondary echinococcosis. Staging comes before treatment.^[6]

Pyogenic abscess. In the USA the incidence is 8-15 per 100,000 inhabitants per year, and over 80% of liver abscesses in industrialised areas are pyogenic.^[1] Before the 1980s E. coli was the most common pathogen; highly virulent Klebsiella pneumoniae strains (capsular serotypes K1 and K2) are now predominant in Asia, with spread to the USA, Europe and Australia.^[1] Middle-to-older adults are most affected, with peak incidence at 50-65 years, male-to-female ratio about 1.5-2.5, and paediatric cases are rare.^[1] Mortality, formerly 5-26%, is now under 10% because of improved diagnosis and treatment.^{[1] [5][6]}

Amoebic abscess. E. histolytica infects an estimated 50 million people per year worldwide. About 90% of carriers remain asymptomatic and roughly 10% develop invasive disease, usually amoebic colitis or liver abscess.^[4][3] Amoebic liver abscess is the most common extraintestinal manifestation and affects about 1% of infected individuals.^[4] It causes an estimated 55,000 deaths per year, mainly in low-income countries and especially in children under 5 years.^[4] Endemic areas include Central and South America, Asia and Africa, with the highest burdens in countries such as India, Mexico, Colombia, Brazil, Egypt, Turkey and South Africa.^[4] Men are affected far more often than women (up to 72-76% of adult cases), probably due in part to alcohol-related liver injury increasing susceptibility.^{[4] [1][7]}

Hydatid cyst. Cystic echinococcosis is endemic wherever humans live close to dogs and sheep. It is rare in the USA and most cases are diagnosed in immigrants or travellers.^[5][7] Most infection is silent for years; symptoms usually appear only once a cyst reaches 10 cm.^[2][7]

• Pyogenic abscess most often arises from biliary infection (up to 50% of cases), followed by portal spread (intra-abdominal sepsis, diverticulitis), arterial seeding (bacteraemia) and contiguous spread (cholecystitis, local abscess). Many are cryptogenic.^[1][5]
• Risk factors include diabetes, cirrhosis, immunosuppression or neutropenia, older age, male sex and proton-pump inhibitor use.^[5]
• K. pneumoniae invasive syndrome. These strains colonise the gut; translocation and portal spread (or biliary spread) are favoured. Diabetes, especially with poor glycaemic control, is a strong risk factor. Metastatic spread to the eye, meninges, central nervous system and lungs occurs in 10-45% of patients, and abscess size over 5 cm is a predictor.^[1]
• Amoebic abscess follows penetration of the colonic mucosa. Most patients have no bowel symptoms at presentation and stool microscopy is usually negative. A travel history can be months or years old and disease may appear over 20 years after exposure.^[1][4]
• Risk factors for amoebiasis include travel or residence in an endemic area, male sex (especially for liver abscess), men who have sex with men, postmenopausal women, corticosteroid or other immunosuppressant use, and alcohol-related liver disease.^[4]
• Hydatid cyst follows ingestion of Echinococcus granulosus eggs from dog faeces in sheep-rearing areas. The released oncosphere travels to the liver, where most cysts form.^[6][7]

Pyogenic. Bacteria arriving via the portal vein, hepatic artery, biliary tree or lymphatics establish microabscesses that coalesce into a larger necrotic cavity. The right lobe is involved in about 75% of cases because of portal venous drainage patterns.^[5] The inflammatory wall may be thin or thick; a thin-walled, gas-forming abscess is more likely to rupture.^{[1] [7]}

Amoebic. Trophozoites that breach the colonic mucosa enter the portal circulation and lodge in hepatic sinusoids. They kill hepatocytes by contact-dependent cytotoxicity and enzymatic damage, producing a single, well-defined cavity containing chocolate-brown necrotic material ("anchovy paste") with few visible organisms.^[1][4]

Hydatid. The parasite cyst grows slowly, producing an inner germinal layer and an outer laminated wall, with host fibrous tissue outside (pericyst). Daughter cysts and brood capsules containing protoscolices may form. When a cyst becomes inactive it solidifies and calcifies and no longer contains viable parasites.^[6]

Pyogenic abscess. The presentation is non-specific. Fever and chills occur in 90-95% of cases, right upper quadrant pain in about 72%, nausea in about 43%, vomiting in about 32% and weight loss in about 26%. Jaundice occurs in roughly 21%.^[1] Hepatic tenderness and hepatomegaly are common. Diarrhoea, cough, right pleural effusion and headache can mislead. Symptoms may be acute or insidious over weeks.^[1][5]

A vignette: a 62-year-old man with diabetes presents with 10 days of fever, rigors and dull right upper quadrant pain. He had been well before this. His white cell count is raised. This could be acute cholecystitis, cholangitis or a right lower lobe pneumonia; the decisive step is imaging of the liver.^[5]

Amoebic abscess. Onset is usually 8-20 weeks after travel (median about 12 weeks), but may be years later.^[4] Symptoms are fever and a dull or aching right upper quadrant pain that may radiate to the epigastrium, chest or shoulder; cough and right-sided pleural pain suggest diaphragmatic abutment. Jaundice is uncommon and raises suspicion of another diagnosis. Only about 38% of patients report concurrent diarrhoea. Physical examination shows hepatic tenderness and hepatomegaly in about 50% of cases. Hepatomegaly may be the main finding in a chronic, subclinical presentation with weight loss.^{[4] [5]}

Hydatid cyst. Most cysts are found incidentally. When symptoms occur they come from mass effect: right upper quadrant discomfort, a palpable mass, hepatomegaly, or cholestasis and portal hypertension with very large cysts. Symptoms generally do not appear until a cyst reaches 10 cm.^[2][7]

A focal liver lesion with fever is not always a pyogenic abscess.

Other conditions that mimic liver abscess clinically are cholecystitis, cholangitis, right basal pneumonia and subphrenic abscess. After imaging, the differential also includes hepatocellular carcinoma, metastases and benign cysts.

Imaging is the cornerstone. Ultrasound or CT has 96-100% sensitivity for a liver abscess.^[1] CT is usually more sensitive than ultrasound and better defines biliary obstruction and extrahepatic spread. A pyogenic abscess is usually hypoechoic with a thick wall and internal echoes or septa; CT shows a hypodense lesion with rim enhancement.^[1] Amebic abscesses are most commonly solitary, right-lobe and subcapsular; CT shows a non-enhancing centre with an inflammatory ring.^[4] Ultrasound is usually enough for hydatid staging. ^[2]

Microbiology. Blood cultures are positive in up to 50% of patients with pyogenic abscess.^[5] Culture of drained pus should include aerobic and anaerobic organisms, and mycobacterial or fungal stains when the clinical picture suggests them. Do not stop anaerobic cover even when cultures are negative, because anaerobes are difficult to grow.^[5]

Laboratory. Leukocytosis, raised C-reactive protein and erythrocyte sedimentation rate, anaemia, hypoalbuminaemia and raised alkaline phosphatase are common in both pyogenic and amoebic disease; bilirubin may be high in pyogenic disease. No blood test is diagnostic.^[1][4]

Amebic diagnosis. Amebic serology is highly sensitive (over 94%) and highly specific for amebic liver abscess (over 95% by ELISA for liver abscess; over 90% for serology overall), but may be falsely negative in the first 7-10 days (Lübbert) (antibodies are usually positive within 7-14 days per Cooney).^[1][4] Serology can remain positive for years, so it is most useful in non-endemic areas. PCR on stool or aspirate is the most reliable test where available. Liver aspirate microscopy is unhelpful, showing trophozoites in under 20% of cases.^[4] Stool microscopy has under 60% sensitivity.^[4]

Hydatid cyst. Serology sensitivity for liver cysts is 85-98%, with limited specificity.^[5] Imaging determines the stage. Puncture, when indicated, shows protoscolices on microscopy.

There is no universal severity score for liver abscess. The useful stratifiers are:

• Size and number of cavities: abscesses over 5 cm (or over 6 cm by the Lübbert drainage criterion), or multiple abscesses, have higher rates of complications, failure of simple aspiration and need for catheter drainage or surgery.^{[1][5] [4]}
• Biliary obstruction or multiple lesions often indicate the need for surgical or endoscopic source control, not only antibiotics.
• Klebsiella (invasive syndrome) predictors: for invasive K. pneumoniae syndrome, abscess size over 5 cm, diabetes, and serotype K1 infection predict metastatic complications.^[1]
• Left-lobe amebic abscess or diameter over 10 cm predicts risk of rupture (including into the pericardium) and lower threshold for drainage.^[4][5]
• Hydatid stage by WHO-IWGE ultrasound classification: CE1 (pure fluid, active), CE2 (multiple daughter cysts, active), CE3a (detached endocyst, "water lily" sign, transitional), CE3b (daughter cysts in solid matrix, transitional), CE4 (heterogeneous, inactive), CE5 (calcified, inactive).^[6][7]

Start broad-spectrum antibiotics as soon as microbiological specimens (blood cultures and, when drainage is done, aspirate) have been obtained. Empiric coverage must include Enterobacterales, enterococci and anaerobes.^[5] Most pathogens are now resistant to ampicillin; resistance against fluoroquinolones can reach about 30% in E. coli and K. pneumoniae. Therefore third-generation cephalosporins (ceftriaxone or cefotaxime) plus metronidazole, or piperacillin/tazobactam (which also partly covers enterococci), are the favoured initial regimens.^[1][5]

One guideline-style empiric choice is cefotaxime 2.0 g intravenously every 8 hours or ceftriaxone 2.0 g intravenously once daily, plus metronidazole 0.5 g intravenously every 8 hours; or piperacillin/tazobactam 3.375 g intravenously every 6 hours.^[5] The older "triple" regimen was ampicillin 2.0 g intravenously every 6 hours plus gentamicin 1.7 mg per kilogram intravenously every 8 hours plus metronidazole 0.5 g intravenously every 8 hours.^[5]

• For patients who are stable, antibiotics may be deferred until after aspiration to improve culture yield.^[5]
• Carbapenems are reserved for ESBL-producing organisms or severe sepsis; their use (mainly imipenem/cilastatin) has been associated with lower mortality than other agents in those settings.^[1]
• In documented or suspected K. pneumoniae meningitis or endophthalmitis, use high-dose third-generation cephalosporins: cefotaxime up to 2 g intravenously every 4 hours, or ceftriaxone 2 g intravenously twice daily, for 3 weeks. Intravitreal plus intravenous therapy is used for endophthalmitis.^[1]
• Good glycaemic control in diabetic patients reduces the risk of metastatic complications.^[1]
• Antifungal cover (for example amphotericin B or fluconazole) is added when the host is neutropenic or immunosuppressed and candidiasis is a possibility.^[5]
• Because anaerobes are hard to grow, anaerobic cover should not be withdrawn just because cultures are negative.^[5]
• Duration is usually 14-42 days in total when adequate drainage and defervescence occur; without adequate drainage, treatment may be needed for several months. Follow-up imaging often lags behind clinical improvement.^[5]
• Studies from Taiwan used 3 weeks of intravenous therapy followed by 1-2 months of oral therapy, while shorter courses of 2-3 weeks intravenous and 1-2 weeks oral therapy have been associated with mortality under 5%.^[1] Guidelines differ on duration, so local practice and clinical response should guide the decision, supported by repeated ultrasound.

Drainage is needed for most pyogenic abscesses. CT- or ultrasound-guided percutaneous aspiration, with or without catheter placement, is the initial method of choice, with success rates up to 90%.^[5] Catheter placement (usually a 6-8 French catheter for standard catheterization, or 12-14 French for modified catheterization, with a pigtail catheter) is preferred for abscesses over 5 cm, multiloculated collections or those with thick pus; simple aspiration is reasonable for smaller abscesses but repeat aspiration is needed in about 50% of cases.^{[5] [7]} Drainage is ideally 1 week or longer with CT follow-up.

Surgical drainage is reserved for patients who fail percutaneous therapy, or who have rupture, complex or inaccessible abscesses, multiple abscesses, abscesses over 5 cm not amenable to a catheter, or concurrent intra-abdominal pathology needing operation. Laparoscopic drainage is a useful minimally invasive option.^[1][5] In one series of multiple abscesses, percutaneous transhepatic drainage gave similar effectiveness to surgical drainage but shorter hospitalisation, so percutaneous drainage should be attempted before surgery.^[1]

An amoebic abscess is treated with a tissue agent followed by a luminal agent. Metronidazole is the key drug. Regimens include metronidazole 800 mg by mouth 3 times daily for 5-10 days, or tinidazole 2 g once daily for 3-5 days depending on guideline (3 days for intestinal disease in the MSF protocol; 5 days for liver abscess in Cooney; 3-5 days in Johns Hopkins) where available, followed by paromomycin 25-35 mg per kilogram per day in 3 divided doses for 7 days (Johns Hopkins lists paromomycin 500 mg 3 times daily for 7 days in adults) to clear cysts.^[4][5] MSF protocols use metronidazole 500 mg by mouth 3 times daily for 5-10 days, or tinidazole for 5 days in adults, for liver abscess.^[3] Johns Hopkins lists metronidazole 750 mg by mouth 3 times daily for 7-10 days.^[5] The exact adult dose therefore varies between references; local protocol should be followed.^[4][5]

• Most abscesses are cured by drug treatment alone, even when they are large. Surgical drainage of an uncomplicated amoebic abscess is unnecessary and should be avoided.^[1]
• About 70-80% of amoebic abscesses are solitary right-lobe lesions; drainage does not shorten recovery in uncomplicated disease.^[2]
• Clinical response (loss of fever and pain) usually occurs within 72-96 hours.^[1]
• Drainage is reserved for diagnostic uncertainty, failure to respond after 3-4 days, left-lobe abscess (risk of pericardial rupture), imminent rupture, or severely ill patients with large abscesses.^[1][4]
• For empyema after rupture or pericarditis, percutaneous catheter or surgical drainage can be life-saving.^[1]
• Treat immunosuppressed patients early for amoebiasis before starting steroids, because disseminated disease can be fulminant.^[4]

Treatment is stage-specific and follows the WHO-IWGE classification. The newest guidance in common practice is the WHO guidelines for the treatment of patients with cystic echinococcosis, issued 16 June 2025, alongside the expert consensus of the WHO-IWGE (2010) cited in Medscape.^[6]

• Active small cysts (CE1 and CE3a under 5 cm): albendazole alone is usually sufficient.^[6]
• CE1 or CE3a cysts 5-10 cm: percutaneous treatment, usually PAIR, under albendazole cover is preferred.^[6]
• Complex or multivesicular cysts (CE2, CE3b): larger-bore catheterisation or surgery, because standard PAIR has a higher relapse rate.^[6]
• Complicated cysts (biliary communication, rupture, secondary infection, high-risk site): surgery, often with preoperative albendazole.^[6][7]
• Inactive cysts (CE4, CE5): watch and wait. Cysts that have undergone natural death need no treatment; surveillance is usually annual and more frequent for high-risk sites. Reactivation prompts treatment.^[6]

Drug therapy. Albendazole is the drug of choice because of better tissue penetration. The standard adult dose is 400 mg by mouth twice daily (10-15 mg per kilogram per day, maximum 800 mg in two doses); the paediatric dose is 10-15 mg per kilogram per day in two doses. Treatment lasts 1-6 months, given continuously rather than in 28-day cycles. It should be taken with a fatty meal, which can increase bioavailability up to 5 times. Mebendazole 40-50 mg per kilogram per day in three divided doses is an alternative. Praziquantel may be added perioperatively or after rupture to reduce secondary echinococcosis.^[6][7] About one third of patients are cured by drug treatment alone and 30-50% show significant cyst regression and symptom relief.^[7]

PAIR procedure. Performed under ultrasound or CT guidance: puncture, aspiration of cyst fluid, injection of a scolicidal agent (usually 95% ethanol or 20% hypertonic saline), 5-30 minutes of dwell (commonly at least 15 minutes in published protocols), then reaspiration. Albendazole cover is used around the procedure (preoperative therapy is mandatory). The risk of lethal anaphylactic shock is about 0.03%, so an anaesthetist and resuscitation capacity must be present. Contrast injection after aspiration excludes cystobiliary communication; if a communication exists, scolicidal agents can cause cholangitis, and surgery becomes preferable.^[6]

Surgery. Radical procedures (total pericystectomy or partial hepatectomy) carry lower recurrence than conservative ones. Mortality is up to 2% and recurrence ranges 2-25% in surgical series (up to 2-40% in the reviewed literature).^[6][7] Preoperative albendazole is mandatory to inactivate protoscolices. Laparoscopic surgery suits peripheral, unilobar cysts.^[6]

Monitoring during benzimidazole therapy. Check aminotransferases, white cell count and haemoglobin, along with monthly haematology and liver function. Screen women of childbearing age before starting; albendazole is not recommended in the first trimester. Ultrasonographic reassessment begins at 3 months and continues for 5-7 years.^[6][7]

• Spontaneous rupture of a pyogenic abscess, especially K. pneumoniae, with gas-forming or thin-walled cavities over 5 cm.^[1]
• Metastatic K. pneumoniae infection: endophthalmitis (often irreversible vision loss), meningitis, brain abscess, septic pulmonary emboli.^[1]
• Rupture of an amoebic abscess into the peritoneum, pleura, pericardium or lung.^[4]
• Superinfection or bacterial contamination of a hydatid cyst.
• After surgery for hydatid disease, recurrence 2-25% in surgical series (up to 2-40% in the reviewed literature) and spillage leading to secondary echinococcosis.^[6][7]
• Recurrence of amoebiasis from untreated intestinal carriage if only a tissue agent is given.^[4]

• Untreated pyogenic abscess is almost uniformly fatal. With treatment, mortality is under 15% in many series, and modern combination therapy is associated with mortality under 5%.^[1][5]
• Amoebic abscess mortality is 1-3% in uncomplicated cases; prognostic markers include encephalopathy, hyperbilirubinaemia, hypoalbuminaemia and large abscess size.^[1][4]
• Hydatid disease has a favourable prognosis for inactive cysts; active treatment cures a minority outright, but controls most disease, with long survival after surgery.

• Pyogenic abscess has no specific vaccine. Reducing risk means controlling biliary disease, diabetes and immunosuppression, and careful asepsis at biliary procedures.
• Amoebiasis prevention rests on safe water, sanitation, food hygiene and sexual health. There is no licensed vaccine; the Gal/GalNAc lectin remains a research target.^[4]
• Hydatid prevention is control of dogs, safe disposal of sheep offal, education in endemic areas and no feeding of dogs with raw offal.^[6][7]
• Screen returning travellers with unexplained right upper quadrant pain and fever, and screen intestinal amoebiasis before immunosuppression for inflammatory bowel disease.^[4]

Pregnancy. Metronidazole for amoebiasis and albendazole for echinococcosis should be weighed for fetal risk; albendazole is generally avoided in the first trimester. Individualised specialist care is required.^[6]

Children. Amoebiasis is an important cause of parasitic death in children under 5 in endemic areas.^[4] Hydatid cysts occur in children in endemic regions and are treated with paediatric albendazole dosing; cystic echinococcosis in children may need surgery. Pyogenic abscess is uncommon but not impossible. Use paediatric doses throughout.

Immunocompromised hosts. Bacterial and fungal abscesses are more likely; add antifungal cover where neutropenia is present.^[5] Immunosuppression worsens amoebiasis dramatically. Corticosteroids should not be started for possible inflammatory bowel disease until amoebiasis has been excluded.^[4]

• Ultrasound is often the only imaging available. A trained clinician can identify many abscesses with basic views; MSF guidance specifically describes a focused liver ultrasound examination for amoebic lesions.^[3]
• The clinical clues matter: fever, right upper quadrant pain and hepatomegaly in a patient from an endemic area should raise suspicion for amoebic abscess even without travel in the recent past.^[3][4]
• Amoebic abscess can be treated with oral metronidazole (or tinidazole where available), without drainage, in most patients, even in large abscesses.^[1][3]
• Drainage, when essential for pyogenic or complicated amoebic abscess, can be done under ultrasound guidance with simple aspiration needles; surgery is a last resort.
• Hydatid cysts in remote settings may be managed with long-term albendazole and watchful waiting, with surgery or PAIR at a referral centre for large or complicated cysts. Community control of dogs and slaughter hygiene reduces new cases.^[6][7]

• Most liver abscesses in industrialised settings are pyogenic; E. histolytica causes up to 10%, and hydatid cyst is a parasitic, not bacterial, lesion.^[1][2]
• Fever occurs in 90-95% of pyogenic cases; ultrasound or CT has 96-100% sensitivity.^[1]
• K. pneumoniae invasive syndrome is an increasingly common cause in Asia and carries a 10-45% rate of metastatic infection; abscess size over 5 cm is predictive.^[1]
• An amoebic abscess is usually a solitary right-lobe lesion, serology becomes positive in most patients, and it is cured by metronidazole plus a luminal agent; most do not need drainage.^[1][2][4]
• Uncomplicated hydatid cysts are staged first; CE1-CE3a lesions under 5 cm take albendazole, 5-10 cm lesions take PAIR plus albendazole, and inactive CE4/CE5 cysts are watched.^[6][7]
• Albendazole 400 mg twice daily for 1-6 months (10-15 mg per kilogram per day in children, maximum 800 mg) with monitoring of blood counts and liver function is the main drug therapy for hydatid disease.^[6][7]
• Drainage of a hydatid cyst is not routine; if PAIR is performed, scolicidal agents must be kept out of the biliary tree and anaesthetic support must be ready.^[6]
• Empiric pyogenic therapy should cover Enterobacterales, enterococci and anaerobes, usually with a cephalosporin plus metronidazole or piperacillin/tazobactam, for 14-42 days when drainage is adequate.^[1][5]
• Corticosteroids for possible inflammatory bowel disease should wait until amoebiasis is excluded.^[4]
• Prevention of hydatid disease depends on dog control, safe offal disposal and patient education.^[6]

No verified MedGrasp liver topics are linked yet. Planned follow-ons include biliary tract infection, amoebic dysentery, echinococcosis and neglected tropical diseases.