Important hepatic trematode infections

PREPARED BY : EYOB HABTAMU

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Schistosomiasis
SECTION 1

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 Introduction
• Schistosomiasis or bilharziasis is a primarily tropical parasitic disease caused by one or more
of five types of schistosome species(Schistosoma mansoni, S. haematobium, S. japonicum, S. intercalatum, &
S. mekongi).

• Second most common parasitic infection of humans after malaria, responsible for
approximately 200 million human infections and 200,000 deaths each year (over 90% in Africa).
• Infection may cause considerable morbidity in the intestines, liver, or urinary tract, and a small
proportion of affected individuals die.

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Epidemiology
• Disease due to schistosome infection is the consequence of parasitologic, host,
and associated viral infections and of nutritional and environmental factors.
• Overall, severe Schistosoma-specific disease manifestations are relatively rare
among persons infected with any of the intestinal schistosomes.
• In contrast, symptoms of urogenital schistosomiasis manifest clinically in most
S. haematobium–infected individuals.
• Schistosomiasis appears to be a cofactor in the spread and progression of
HIV/AIDS in areas where both diseases are endemic.

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Etiology

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Pathogenicity
•Cercarial invasion is associated with dermatitis arising from dermal and subdermal inflammatory
responses.
•As oviposition commences, acute schistosomiasis or Katayama syndrome may occur.
•In chronic schistosomiasis, most disease manifestations are due to eggs retained in host tissues.
•Chronic disease can affect the liver, urinary ducts, kidney, genitals, lung, spine and brain.

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Clinical features

“Swimmers itch Katayama fever/ Chronic

” Acute schistosomiasis
• Occurs 2-3 days schistosomiasis • Hepatosplenic phase
post contact • 4-8 weeks post within a year of
• Self limiting contact infection
• Usually benign but • Manifestations are
possibly lethal species specific

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Phase 1: swimmers itch
•Occurs most often with S. mansoni and S. japonicum infections
•Manifests 2 or 3 days after invasion as an itchy maculopapular rash on the
affected areas of the skin
•Cercarial dermatitis is a self-limiting clinical entity

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 Phase 2: Acute schistosomiasis
(Katayama fever)
•Acute schistosomiasis (Katayama fever) is common in areas of high transmission rates.
•history of contact with contaminated water 14 to 84 days before presentation is usual.
In its simplest definition fever + generalized lymphadenopathy + hepatosplenomegaly
•Common symptoms include fever, headache, generalized myalgias, right-upper-quadrant pain, and
bloody diarrhea.
•The distinguishing features from malaria include generalized urticaria, pruritic rash at the site of
cercarial penetration (often the legs), eosinophilia, and lymphadenopathy.
•Respiratory symptoms have been reported in up to 70 percent of persons infected with S. mansoni
but less frequently in those infected with S. haematobium.
•Tender hepatomegaly is usually present, and splenomegaly occurs in one third of cases.
•All patients have eosinophilia and most have positive serologic tests

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 Phase 3: Chronic schistosomiasis
The main clinical manifestations of chronic schistosomiasis are species-dependent.
The intensity and duration of infection determine the amount of antigen released and the
severity of chronic fibro-obstructive disease.
Most granulomas develop at the sites of maximal accumulation of eggs — the intestine and the
liver (S. mansoni) and the genitourinary tract (S. haematobium).
However, periovular granulomas have been found in many types of tissue, including the skin,
lung, brain, adrenal glands, and skeletal muscle.

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 Gastrointestinal and Liver Disease
• Eggs retained in the gut wall induce inflammation, hyperplasia, ulceration, microabscess
formation, and polyposis.
• Colicky hypogastric pain or pain in the left iliac fossa is frequent.
• Colicky abdominal pain, bloody diarrhea, and anemia may be the only symptoms. Patients may
also report fatigue and an inability to perform daily routine functions and may show evidence
of growth retardation and anemia.
• Diarrhea is common (especially in children) and may alternate with constipation.
• If there is an increase in the risk of colorectal cancer, it is small

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 Gastrointestinal and Liver Disease…
• The hepatosplenic phase of disease manifests early (during the first year of infection,
particularly in children) with liver enlargement due to parasite-induced granulomatous lesions.
• Hepatomegaly is seen in ~15–20% of infected individuals
• Bleeding from esophageal varices may, however, be the first clinical manifestation
• In late-stage disease, typical fibrotic changes occur along with liver function deterioration and
the onset of ascites, hypoalbuminemia, and defects in coagulation.
• Intercurrent viral infections of the liver (especially hepatitis B and C), toxic insults (excessive
ethanol ingestion or exposure to organic poisons or aflatoxin), or nutritional deficiencies may
well accelerate or exacerbate the deterioration of hepatic function.

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 Genitourinary Disease
• Urinary tract disease is a specific trait of infection with S. haematobium.
• The clinical manifestations of S. haematobium infection occur relatively early and involve a high
percentage of infected individuals.
• Up to 80% of children infected with S. haematobium have dysuria, frequency, and hematuria.
• Hematuria is the first sign of established disease, appearing 10 to 12 weeks after infection.
• Urine examination reveals blood and albumin as well as an unusually high frequency of
bacterial urinary tract infections and urinary sediment cellular metaplasia.

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 Genitourinary Disease
• Late manifestations also include proteinuria (often in the nephrotic range), calcifications in the
bladder, obstruction of the ureter, renal colic, hydronephrosis, and renal failure.
• Hydroureter and hydronephrosis, may be seen in 25–50% of infected children.
• S. haematobium is also classified as a human carcinogen.
• Involvement of the birth canal can cause cervical or vaginal wall polyps and friability leading to
contact bleeding, with an apparently increased risk of HIV transmission.
• Among men, S. haematobium infection can result in prostatic and testicular lesions with
hematospermia.
• Superficial cutaneous lesions of the perineum can occur in both sexes.

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 Female genital schistosomiasis
•FGS can be present without urinary schistosomiasis.
•FGS may be the most common gynecological condition in schistosomiasis-endemic areas.
•FGS remains undiagnosed in most cases and is associated with a risk of HIV and human
papillomavirus infections.
•Symptoms include: Vaginal discharge, Bloody discharge, Bleeding after intercourse or spotting,
Genital itching or burning sensation, Pelvic pain or pain during or after intercourse.
•Complications include: Bleeding during examination (contact bleeding), Infertility, Abortion or
ectopic pregnancy, Involuntary urination when coughing, laughing or jumping, etc., Genital
ulcers ,Tumours or swelling (vulva, vagina, cervix).
•FGS is diagnosed by visual inspection of characteristic lesions on the cervix and vaginal wall.
Visualization can be improved by using a digital camera or a colposcope. Current laboratory
techniques are inadequate for diagnosing FGS.

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 Female genital schistosomiasis
(diagnosis)

Fig: normal cervix

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 Neurologic and Other Manifestations
• In pulmonary schistosomiasis, embolized eggs lodge in small arterioles, producing acute
necrotizing arteriolitis and granuloma formation.
• Subsequent fibrous tissue deposition leads to endarteritis obliterans, pulmonary hypertension,
and cor pulmonale.
• The most common symptoms are cough, fever, and dyspnea.
• CNS disease occurs when migratory worms deposit eggs in the brain and induce a
granulomatous response.
• CNS disease can manifest with focal deficits, seizures and/or tranverse myelitis.
• Schistosome infection during childhood causes substantial growth retardation and anemia.
• Schistosome infection appears to have adverse effects on both maternal health and the fetus

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 Diagnosis
• History and clinical picture recognition are very important.
• Differential diagnosis of fever in returned travelers includes a spectrum of infections whose
etiologies are viral (e.g., dengue fever), bacterial (e.g., enteric fever, leptospirosis), rickettsial,
or protozoal (e.g., malaria).
• The differential diagnosis of schistosomal hepatomegaly must include viral hepatitis of all
etiologies, miliary tuberculosis, malaria, visceral leishmaniasis, ethanol abuse, and causes of
hepatic and portal vein obstruction.
• The differential diagnosis of hematuria in S. haematobium infection includes bacterial cystitis,
tuberculosis, urinary stones, and malignancy.

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 Diagnosis
• In cases of Katayama syndrome, diagnosis is based on clinical presentation, high-level
peripheral-blood eosinophilia, and a positive serologic assay for schistosomal antibodies.
• Falcon assay screening test (FAST-ELISA) and the confirmatory enzyme-linked
immunoelectrotransfer blot (EITB).
• Individuals with established infection are diagnosed by a combination of geographic history,
characteristic clinical presentation, and presence of schistosome ova in excreta +/- serology.
• In patients with a typical clinical presentation but negative urine and feces specimens, a biopsy
of bladder or rectal mucosa must be used for diagnosis

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 Treatment
• Treatment of schistosomiasis depends on the stage of infection and the clinical presentation.
• Cercarial dermatitis: no treatment indicated except for topical treatment to relieve itching.
• Acute schistosomiasis: needs to be adjusted appropriately for each case. Although
antischistosomal chemotherapy may be used, it does not have a significant impact on maturing
worms.
• Established infection: treatment to eradicate the parasite should be administered.
• Early hepatomegaly and bladder lesions are known to resolve after chemotherapy, but the late
established manifestations, such as fibrosis, do not recede.

Praziquantel: 40 or 60 mg/kg BID or TID for 1 day

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Fascioliasis
SECTION 2

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 Introduction
•Infections with Fasciola hepatica and F. gigantica are worldwide zoonoses that are particularly
endemic in sheep-raising countries.
•Humans acquire fascioliasis by ingestion of metacercariae attached to certain aquatic plants or
through consumption of freshly prepared raw liver containing immature flukes.
•Infection is initiated when metacercariae excyst, penetrate the gut wall, and travel through the
peritoneal cavity to invade the liver capsule.
•Adult worms migrate through the liver parenchyma and finally reach bile ducts, where they
produce large operculated eggs that are voided in bile through the gastrointestinal tract to the
outside environment.

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 Clinical manifestation
• After the larvae are ingested with contaminated food or water, a symptomless incubation
period starts, lasting for a few days to a few months, followed by an acute and a chronic
clinical phase.

• Up to 50% of Fasciola hepatica infections are asymptomatic and disease may appear anywhere
from a few days to several years after infection

• Eosinophilia is present with all infections at all stages and can be used as a diagnostic factor in
ectopic and early stage infections when eggs are not be present in the stool.

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 Clinical manifestation…
The Acute phase:

• lasts 2-4 months, and is rare in human beings.

• Begins when the immature worms penetrate the intestinal wall and the peritoneum (4-7 days
post ingestion)
• From here, they puncture the liver's surface and eat their way through its tissues until they
reach the bile ducts.
• This invasion kills the liver's cells and causes intense internal bleeding.
• Typical symptoms include fever, nausea, a swollen liver, skin rashes and extreme abdominal
pain.

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 Clinical manifestation…
The Chronic phase:
• The chronic phase begins when the worms reach the bile ducts, where they mature and start
producing eggs.
• These eggs are released into the bile and reach the intestine, where they are evacuated in
faeces.
• Symptoms include intermittent pain, jaundice and anaemia.
• Pancreatitis, gallstones and bacterial super-infections may also occur. Patients with chronic
infections experience liver fibrosis as a result of the long-term inflammation.

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Diagnosis
•Diagnosis of infection with any of the biliary flukes depends on
 A high degree of suspicion,
 elicitation of an appropriate geographic history,
 and stool examination for characteristically shaped parasite ova.
•Additional evidence may be obtained by documenting peripheral blood eosinophilia or imaging
the liver.
• Serologic testing is helpful, particularly in lightly infected individuals.

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 Treatment
•Treatment for fascioliasis has a 80-100% success rate
Praziquantel 25 mg/kg, 3 doses in 1 day
5-10 day course of oral bithionol at 30 mg/kg body weight
Triclabendazole 1-2 oral doses at 10 mg/kg body weight administered in a single 24
hour (virtually no side effects and has a success rate approaching 100%.)

•Surgery may be necessary in very extreme cases to clear the biliary tract.

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References
- Harrison's principles of internal medicine 19th edition.
- Allen G.P. Ross, PH.D. et.al Schistosomiasis review article; N Engl J Med,
Vol. 346, No. 16 · April 18, 2002
- J F Doherty, A H Moody, S G Wright; Katayama fever: an acute manifestation of
schistosomiasis: BAM 1996;313:1071-2
- https://emedicine.medscape.com/article/228392-clinical
- http://web.stanford.edu/group/parasites/ParaSites2001/fascioliasis/Fasciola.htm

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