Parasitic Infestations

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Parasitic Infestations Liver & Biliary tract

Dr Kapil K Agrawal TATA MAIN HOSPITAL, JSR

Parasitic Infestations Parasitic diseases: Caused by Protozoa or Helminths Endoparasitic protozoa: A diverse group of >10,000 eukaryotic unicellular organisms Endoparasitic helminths of humans: Two phyla – (1) Platyheminths (Flatworms) (2) Nematoda (Round-worms)

• Global problem – more in third world countries • Commonly undiagnosed and neglected health problem • Un-noticed cause of malnourishment & deficiency disorders

Why Don’t We Know They Are There? • A smart parasite lives without being detected – as the symptoms are mild and nonspecific • They are intelligent in their ability to survive and reproduce • No organ is immune from their infestation

Symptoms of Parasites • • • • •

Forgetfulness Slow reflexes Gas and bloating Loss of appetite Increase in appetite but still feel hungry after eating • Yellowish face • Grinding of teeth

• Pain in back, thighs shoulders • Lethargy • Burning in the stomach • Indigestion • Dry lips during the day • Semisolid stools, mucus • Jaundice • Non sp. Abd pain

What Parasites Do?

• Eat

: Nutrients

• Secrete

: Toxins

• Reproduce

: Cycling

• Parasitic infestations include mainly : Hydatid disease Amoebiasis Ascariasis Fascioliasis Schistosomiasis Trichuris Necator Ancylostoma Toxocara

Hydatid disease of the liver

Carnivores (dog, dingo) definitive host, lives in the small intestine Sheds ova into faeces Sheep, cattle (kangaroos, pigs) intermediate host

• • • • •

Liver (most common) Lungs Brain Bone Secondary spread

Pathology • Migration via portal circulation • Essentially creates a cyst (mucopolysaccharide) • lined by inflammatory reaction of the host tissue

Ectocyst (laminated membrane) Endocyst (Germinal Membrane)

Scoleces (400,000 scoleces per 1 ml of ‘hydatid sand’)

Natural course • Growth rate 1-2 cm / year • Eventually reach the capsular surface of liver – rupture - intraperitoneally - intrathoracic - biliary system - pericardium (Lt lobe)

Presenting symptoms • • • • • • •

Asymptomatic Abdominal pain (RUQ mass) – Liver being pushed down Jaundice Acute abdomen/ Rupture Cholangitis Secondary infection chest pain / cough / haemoptysis / bilioptysis 2013 patients - uncomplicated 82% - biliary complications 12% - thoracic complications 2.2% - other rarer complications Zaouche et al Tunisienne de Chirurgie 1997

Diagnosis • History of exposure • Clinical examination - Abdominal lump/Ac abdomen - Jaundice - Chest symptoms • Imaging • Blood tests

CT scan findings

Laboratory diagnosis of hydatid disease • ELISA

- very sensitive - cross reactive with other parasites

• IEP • Immuno HaemAglutination - Has replaced the others over last 3 years - Approx 98% accurate

Treatment • Symptomatic vs Aysmptomatic 1. Medical Rx only 2. Surgery

3. PAIR

- open - laparoscopic

Benzimidazoles • Albendazole, Mebendazole • Albendazole - most commonly used - 1-month oral doses(10-15mg/Kg/day) - ± Praziquantal • Anti-helminthic – direct effect on the parasite and perhaps on the cyst wall • Side effect – Hepatic enzyme disturbances, Alopecia, Glomerulonephritis, Neutropaenia

• Current role of Albendazole ± Praziquantal 1. Perioperatively 2. Widely disseminated disease 3. Poor surgical risk 4. Alveolar echinococcosis 5. Small deep seated hydatids

EBM review • • • • • • •

Three available RCTs showed that ABZ had a better effect on hydatid cysts than placebo [17, 21] or MBZ[20]. One prospective controlled trial compared ABZ and praziquantel versus ABZ alone [24] and concluded that the combined treatment was more effective than ABZ alone. However, complete disappearance of all cysts was not reached according to these data. Therefore chemotherapy is not the ideal treatment for hydatid cyst of the liver when used alone (level II evidence, grade B recommendation). Dzeri et al WJS 2004

Surgery • Principles – Remove all the hydatid scolicoles – complete removal of laminated membrane • Prevent - Abscess / sinus formation - Biliary leak • Avoid intra-operative anaphylaxis • Avoid peritoneal spillage and dissemination

• Definitve surgical options • Conservative • Radical 1) Excision of cyst and Pericyst 2) Partial hepatectomy

• Pack behind liver and pack-off the cyst • Scolicidal agents - 15-20% saline (Most effective) - 75% ethanol - 0.1-0.5% cetrimide - 1% povidone

• Avoid Formalin & 0.5% Silver Nitrate

Communication with the biliary tree • Clinical or biochemical suspicion • Visual inspection • Cholangiogram - identifies communication - cysts in ducts • Biliary communications closed off with sutures if small, peripheral ducts • Larger duct communication is (US/CT) predictable on pre-op imaging ( close to ducts) LFTs • consider: CBD Stenting, T-tube

Percutaneous Aspiration, Injection & Reaspiration (PAIR) • Scolicidal agents - Ethanol, Hypertonic saline, Providone used in conjunction with Albendazole • < 5% incidence of anaphylaxis • Safe and effective • Uncomplicated small cysts

Percutaneous aspiration, injection and reaspiration (PAIR) • Meta-analysis 769 patients with PAIR + Albendazole vs 952 era matched patients treated surgically ↑ clinical efficacy • PAIR & Alb ↓ morbidity, mortality, recurrence ↓ LOS

Smego Clin infect Dis 2003

According to our systematic review, PAIR with or without benzimidazole coverage may be comparable or superior to surgery or medical treatment with benzimidazoles alone for uncomplicated hepatic hydatid cysts, but the data are not sufficient to draw definite conclusions. Therefore, we cannot recommend the use of PAIR with or without benzimidazole coverage outside randomised clinical trials for treating patients with uncomplicated hepatic hydatid cyst Cochrane Collaboration 2006

Parasitic infestations Hydatid disease

Amoebiasis Ascariasis Fascioliasis Schistosomiasis Trichuris Necator Ancylostoma Toxocara

Amebiasis Entamoeba histolytica • Pseudopod, non-flagellated protozoa • Only member that causes: Amebic colitis & liver abscess • Life Cycle consists of: (1) Infectious cyst (2) Invasive trophzoite Trophozoites adhere to colonic mucin and epithelial cells  kill host epithelial & immune cells  tissue destruction

Amebiasis Entamoeba histolytica trophozoite

Entamoeba histolytica mature cyst

Amebiasis Infection of Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands (2). Feco-oral route trophozoites released in the small intestine (3)  migrate to the large intestine (4). Trophozoites multiply by binary fission and produce cysts (5) passed in the feces. Cysts are responsible for the transmission. In many cases, trophozoites remain confined to the intestinal lumen (noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients trophozoites invade the intestinal mucosa (intestinal disease), or, through the bloodstream,

extraintestinal sites such as the liver, brain, and lungs (extraintestinal disease), with resultant pathologic manifestations.

Trophozoites of Entamoeba histolytica (Trichrome stain) Two diagnostic characteristics: ingested erythrocytes nuclei have a small, centrally located karyosome & uniform peripheral chromatin.

Entamoeba histolytica Epidemiology



Greatest morbidity/mortality in the developing countries of Central & South America, Africa, and India



Disease more severe in: The very young, Elderly, Pregnant women



Worldwide: 40-50 million symptomatic infections/year 100,000 deaths annually

Entamoeba histolytica C linical Manifestations Amebic colitis Sign or Symptom % of Patients Affected Symptoms > 1 wk Most patients Diarrhea 94-100 Dysentery 94-100 Abdominal pain 12-80 Weight loss 44 Fever >38oC 10 Heme (+) stool 100 Immigrant from or traveler to endemic area >50 Prevalence (male/female) 50/50

Entamoeba histolytica C linical Manifestations Amebic colitis Patients with chronic, non-dysenteric intestinal amebiasis may complain for months to years of abdominal pain, flatulence, intermittent diarrhea, mucus in the stools, and weight loss Chronic non-dysenteric intestinal amebiasis has been mistakenly diagnosed as ulcerative colitis

Amebic Colitis:

Severe dysentery with multiple flask shaped ulcers in the large bowel, and a bloody diarrhoea

Histopathology of a typical flask-shaped ulcer of intestinal amebiasis

Entamoeba histolytica Clinical Manifestations

Amebic Liver Abscess • Develops in about 10% of patients with invasive E. histolytica infections • Few patients have concurrent dysentery – most report dysentery within the preceding year • Occurs in any age group • Patients with a more chronic illness (2-12 weeks of symptoms) commonly present with hepatomegaly and weight loss

Entamoeba histolytica Clinical Manifestations

Amebic Liver Abscess Sign or Symptom Symptoms > 4 wks Fever Abdominal tenderness Hepatomegaly Jaundice Diarrhea Weight loss Cough 1 Immigrant from or traveler to endemic area Prevalence (male/female)

% of Patients Affected 21-51 85-90 84-90 30-50 6-10 20-33 33-50 0-30 >50 50/50 in children; 90/10 in adults

Gross pathology of liver containing amebic abscess

Gross pathology of amebic abscess of liver. Tube of "chocolate" pus from abscess.

Entamoeba histolytica

Laboratory Findings and Diagnosis • Diagnostic Tests: – EIA is best for specific diagnosis of amebiasis (Sensitivity & specificity of assay on stool >95%) – Colonoscopy remains important to evaluate for other causes – Serology for antibodies: IHA – Positive in: 88% amebic dysentery, 70-80% liver abscess, 50% of general population

Entamoeba histolytica

Laboratory Findings and Diagnosis • Diagnostic Tests: – Ultrasonography – CT Scan – MRI None differentiate amebic from pyogenic abscess Diagnosis is frequently a diagnosis of exclusion

IHA: Acutely, E. Histolytica antibody can be detected in serum in 70-80% of cases EIA: Can detect E. histolytica antigen in serum in ~96% of patients with abscess

Amebic liver abscess

Amebic liver abscesses

Entamoeba hystolityca Prevention

Asymptometic amebiais: Luminal agent (Paromomycin, Diloxanide furoate) Amebic Colitis: Metronidazole & a luminal agent Amebic Liver Absces: Metronidazole & a luminal agent

Entamoeba Histolityca Prevention Prevention of E. hisolytca transmission requires disruption of the fecal-oral spraed of amebic cysts Individuals should be advised regarding: • Risk of traveling to endemic areas • Safeguards to prevent ingesting colonic organisms Because humans and primates are the only known reservoirs of E. histolytica, a successful vaccine Could potentially eliminate this disease

Parasitic infestations Hydatid disease Amoebiasis

Ascariasis Fascioliasis Schistosomiasis Trichuris Necator Ancylostoma Toxocara

Intestinal Nematodes Round Worms • The most common parasitic infections in humans; affect one quarter of the world population • Remain a major cause of physical growth delay, cognitive delay, and malnutrition throughout the world • In certain endemic populations, children are disproportionately affected • Being increasingly encountered in the developed world. In the USA, groups at increased risk include: international travelers, recent immigrants, refugees, and international adoptees

Ascaris lumbricoides • The most common helminthic infection in humans • 1.2 billion infected worldwide • 51 million children are currently estimated to be infected • Commonly affects children living in economically week communities • Young children seem to be affected more severely than adults (larger worm burden, parasite-induced malnutrition)

Ascaris lumbricoides

Ascaris lumbricoides Transmission - Feco-oral Route Embryonated eggs Poverty, Overcrowding Unhygienic living conditions Human excreta as fertilizer Unsafe water supply Pickling of vegetables

Ascaris lumbricoides Clinical Manifestations • Ascariasis usually have a benign course but it can lead to – • Chronic infection  malnutrition due partly to malabsorption (proteins, fat & vitamin A) • Heavy infestation  intestinal obstruction

• Some times it goes to biliary tract and causes obstructive symptoms with jaundice Adult worm

Biliary Ascariasis Bile Duct

Jejunum

Via the Ampulla

Excessive worm load

Propensity to explore openings

Abnormal mobility

Intestinal infections (viruses,bacteria,parasites) . Fasting

Common Bile DuctBiliary Colic,Cholangitis, Pigment stones

Bile Duct

Intrahepatic DuctsCholangitis,Pigment stones Strictures, Hepatoliathiasis Gall Bladder

Acute Cholecystitis, Empyema,Stones

Liver

Hepatic Abscess, Hepatoliathiasis

Pancreas

Acute Pancreatitis

Ascaris lumbricoides Diagnosis

• • • • • •

Characteristic ova in stools Eosinophilia LFT pulmonary infiltrates on chest radiograph USG abdomen Cholangiogrm- ERCP/MRCP

Aim

Modalities

Treat Cholangitis Paralysis of worms in intestines by Drugs Expulsion

o Conservativ e-Majority o EndoscopicFailures

Ascaris lumbricoides treatment • Mebendazole (100 mg twice daily X 3 days) or • Albendazole (400 mg as a single dose) (The above are not generally given to children < 1 yr) • Pyrantel pamoate (11 mg/kg up to 1 gm/day, X 3 days)

Ascaris lumbricoides Prevention • Safe disposal of excreta • Wash hand, Wash eatables • Diagnosis, effective treatment • In endemic areas (infection rate is >50%), antihelmenthic agents administration to school-age children has been recommended as part of a targeted deworming program • Sustained economic growth is most effective means of long-term parasite control

Hydatid disease Amoebiasis Ascariasis

Fascioliasis Schistosomiasis Trichuris Necator Ancylostoma Toxocara

• F hepatica (most common) • F. gigantica (Africa)

• Infective stage • Excystation

• Migration

• Diagnostic stage

• Fasciola species inhabit the hepatobiliary system causing considerable human morbidity dependent on the • number of worms and stage of infection

• The course of infection passes through three phases: • The acute phase : Immature flukes penetrates liver capsule and reaches to bile channels- Toxic & Allergic (3-4 months) • The chronic phase : Flukes in bile ducts, relatively free of symptoms (10-13 yrs) • The obstructive phase :epithelial and parenchymatic changes, recurrent cholangitis, cholecystitis, jaundice, calcification, fibrosis Ectopic fascioliasis

Complications 1. 2. 3. 4. 5.

Liver abscess and haematoma (subcapsular) (acute stage) Biliary cirrhosis :due to the peri-ductal fibrosis Obstructive jaundice : Obstruction of the common bile duct by Fasciola adults + Biliary sludge and stones Hemobilia

Diagnosis • Clinical • Parasitological • Immunodiagnosis – – – – –

ELISA Indirect haemagglutination test (IHA) Counter immuno electrophoresis (CIEP) Indirect fluorescent antibody test (IFA)

• Imaging- USG/CT/MRI/ERCP/PTC • Liver biopsy

Treatment • Chemotherapeutic agents in common use in human fascioliasis:  Effective with no or little side effects: Triclabendazole, bithionol, Mirazid  Effective with side effects: severe (dehydroementine), or moderate (Metronidazole)  Controversial therapeutic results (Praziquantel)

THANK YOU!

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