3. Learning objectives
❖At the end of this session students are able to understand
▪ Definition
▪ Ethologist
▪ Clinical presentation and diagnosis
▪ Management and prevention of
✓Amebiasis
✓Giardiasis
✓Visceral leishmaniosis
✓ Malaria
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4. Amoebiasis
▪ Amoebiasis is caused by Entamoeba histolytica.
▪ Cysts are transmitted by ingestion of contaminated food or water, or spread directly by
person-to-person contact.
▪ The incubation period of intestinal amoebiasis is highly variable and may be as short as
a few days or as long as several months
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5. Pathology
• Classic flask-shaped colon ulcer in the submucosa.
• The trophozoite toxin (cytolethal)
• If the trophozoite via portal circulation:
✓abscess and periportal fibrosis.
• Amebic ulceration sites:
✓colon, perineum, and genitalia
✓abscesses lung and brain.
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6. Clinical picture of Amoebiasis
▪ The usual course is chronic, with mild intermittent diarrhoea and abdominal discomfort.
▪ This may progress to bloody diarrhoea with mucus
▪ It is sometimes accompanied by systemic symptoms such as headache, nausea and
anorexia.
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7. Extraintestinal features
• Hematogenous spread may result in abscesses of the liver, spleen, lung or brain
• Hepatic amebiasis (abscess, hepatitis) is the most common :
✓ Enlarged, tender liver and upper abdominal pain
✓ Mild jaundice may be evident,
✓ Transaminases and alkaline phosphatase elevations may be seen.
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8. Diagnosis
▪ Stool examination:
✓Fresh stools specimens must be examined for
➢ trophozoites typical of E. hemolytica.
➢Cysts of both entamoeba species
▪ Entamoeba dispar or the invasive Entamoeba histolytica are very similar
✓therefore trophozoites that have ingested red blood cells are diagnostic of
E.hemolytica
• Microscopy of stools
✓E. histolytica vs. E. dispar)
• ELISA (antigen detection)
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9. Cont…
• Endoscopy
• Serology and liver scans
✓ultrasound or computed tomography) or magnetic resonance imaging.
• Leukocytosis (>10,000/mm3) and an elevated alkaline phosphatase concentration
(>75%)
• Needle aspiration
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10. Treatment Regimens
▪ Category of amebiasis:
✓asymptomatic cyst passers
✓intestinal amebiasis, and
✓amebic liver abscess
▪ Electrolyte replacement
▪ Antibiotic therapy
▪ Nutritional support
▪ Percutaneous catheter drainage
▪ Surgery
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11. Treatment of Amoebiasis
▪ Non pharmacologic
✓Hydration is impotent in patients who have severe dysentery
▪ Pharmacologic
▪ Treatment of invasive disease:
✓First line
➢Metronidazole, 500-750mg P.O., TID for 5-7 days
➢ For children: 7.5mg/kg P.O., TID for 5-7 days.
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12. Cont…
✓Alternative
➢Tinidazole, 2g P.O. QD for 3 consecutive days. For children: 50-60mg/kg daily for 3 days.
▪ Eradication of cysts:
✓First line
➢Diloxanide Furoate, Adult 500mg 3 times daily P.O., for 10 days.
✓Child over 25kg,
➢20mg/kg daily in 3 divided doses for 10 days; course may be repeated if necessary.
✓Alternative
➢Paromomycin, 25–35mg/kg/day P.O., divided in 3 daily doses for 7 days
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14. Cont…
▪ Asymptomatic cyst passers & patients with mild intestinal amebiasis
✓Paromomycin 25 to 30 mg/kg per day TID for 7 days
✓Iodoquinol 650 mg in three doses for 20 days
✓Diloxanide furoate 500 mg in three doses for 10 days
➢Cure rate: 84% and 96%
▪ The pediatric dose:
✓Iodoquinol: 30 to 40 mg/kg per day as TID for 20 days
✓Diloxanide furoate is 20 mg/kg per day as TID for 10 days.
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15. Cont,,,
▪ Pregnant patients: Paromomycin
▪ Severe intestinal disease or liver abscess:
✓Metronidazole 750 mg three times daily for 10 days,
✓followed by a course of one of the luminal agents
✓Tinidazole 800 mg three times daily for 5 days
▪ Pediatric patient:
✓metronidazole is 50 mg/kg per day in divided doses
✓followed by a luminal agent
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16. Monitoring
▪ Evaluation Of Therapeutic Outcomes
✓Response: 3 to 5 days to 7 to 10 days
✓Repeat stool examination, serology
✓Colonoscopy: Colitis
✓Computed tomography (CT): Liver abscess
✓Day #5 and 7, at the end of the course of therapy, and
✓a month after the end of therapy
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17. Prevention
▪ Wash your hands often
▪ Avoid eating raw food
▪ Avoid eating raw vegetables or fruit that you did not wash and peel yourself
▪ Avoid consuming milk or other dairy products that have not been pasteurized
▪ Drink only bottled or boiled water or carbonated (bubbly) drinks in cans or bottles
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18. Giardiasis
• Giardia intestinalis or Giardia duodenalis
• Most common intestinal parasite responsible for diarrheal syndromes throughout the
world.
• G. Lamblia (children): 15% and 30%.
• Two stages in the life cycle:
✓G. lamblia: the trophozoite and the cyst
• Fecal contamination, lack of potable water, education, and housing
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19. Cont…
▪ Giardia lamblia infects humans through ingestion of as few as 10 cysts
▪ The infection is more prevalent in children than adults
▪ Asymptomatic infection occurs in approximately 60% of people exposed to Giardia.
▪ The most common presentation is diarrhoea
✓which is foul smelling with fatty stools(steatorrhea)
✓Flatulece
✓weight loss
✓crampy
✓abdominal pain with bloating and failure to thrive
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20. Cont…
Clinical Presentation of Giardiasis
Acute onset
• Diarrhea, cramp-like abdominal pain, bloating, and flatulence
• Malaise, anorexia, nausea, and belching
Chronic
• Diarrhea: foul-smelling, copious, light-colored, fatty stools; weight loss
• Periods of diarrhea alternating with constipation
• Steatorrhea, lactose intolerance, vitamin B12, and fat-soluble vitamin
deficiencies
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21. Diagnosis
• Type of stool examination
✓Fresh stool (trophozoites) or
✓Preserved specimen (cysts)
• Duodenal aspiration and biopsy (AIDS patients and in patients with
hypogammaglobinemia)
• Enzyme-linked immunosorbent assay (ELISA) or immunofluorescence or identification
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22. Pathology
• Ingestion of G. lamblia cysts in fecally contaminated water or food
• The protozoan excysts release the trophozoite (low pH)
✓Mucosal invasion, localized edema, and flattening of the villi, resulting in
malabsorption states in the host.
✓Lactose intolerance
✓Achlorhydria
✓hypogammaglobinemia, or deficiency in secretory immunoglobulin A (IgA)
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23. Treatment
▪ Goal of therapy
✓Prevent and treat dehydration
✓Stop diarrhoea as promptly as possible
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24. Cont…
▪ Medicine Treatment
✓First line
➢Tinidazole, single oral dose of 2g
➢ For children, 50-75mg/kg as a single dose
❑may be repeated once if necessary
✓Alternative
➢Metronidazole, 250-500mg TID or 15 mg/kg per day three times PO for five days
➢Furazolidone 100 mg or suspension 6 mg/kg per day four times
➢Paromomycin 25 to 30 mg/kg per day in divided doses for 1 week.
✓Pregnancy:
• Paromomycin 25 to 30 mg/kg per day in three doses for 7 days
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25. Visceral leishmaniosis
▪ Leishmaniasis is a parasitic disease found in parts of the tropics, subtropics, and
southern Europe
▪ Leishmaniasis is a vector-borne disease caused by protozoan parasite of the genus
Leishmania
▪ Leishmaniasis has several different forms
▪ This section focuses on visceral leishmaniasis (VL)
✓ which affects some of the internal organs of the body (such as the spleen, liver, and
bone marrow).
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26. Cont…
▪ VL a vector-borne disease is caused by obligate intracellular protozoan parasites,
particularly by the species
✓Leishmania donovani and L. infantum/L. chagasi
▪ Visceral leishmaniasis, also known as kala-azar
✓It is the severe form of the disease.
✓The incubation period typically ranges from 2–6 months
✓ but it can also range from a few weeks to years.
✓If the disease is not treated, the fatality rate in developing countries can be as high as
100% within 2 years.
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27. Transmission
▪ Bite of an infected female phlebotomine sand fly
▪ Congenital and parenteral transmission (through blood transfusions and needle sharing)
have been reported.
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28. Clinical presentation
▪ Among symptomatic people, the incubation period typically ranges from weeks to
months.
▪ The onset of illness can be abrupt or gradual
▪ Stereotypical manifestations of VL include fever, weight loss, hepatosplenomegaly
(especially splenomegaly), and pancytopenia (anemia, leukopenia, and
thrombocytopenia).
▪ If untreated, severe (advanced) cases of VL typically are fatal.
▪ Latent infection can become clinically manifest years to decades after exposure in
people who become immunocompromised for other medical reasons (such as HIV
infection).
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29. Cont….
▪ weight loss
▪ weakness
▪ cough
▪ fever that lasts for weeks or months
▪ enlarged spleen
▪ enlarged liver
▪ decreased production of red blood cells
(RBCs)
▪ bleeding
▪ other infections
▪ night sweats
▪ thinning hair
▪ scaly skin
▪ Dark
▪ ashen skin
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30. Diagnosis
▪ Clinicians should consider VL in people with a relevant travel history (even in the
distant past) and a persistent, unexplained febrile illness, especially if accompanied by
other suggestive manifestations (such as splenomegaly and pancytopenia).
▪ Laboratory confirmation of the diagnosis is achieved by detecting Leishmania parasites
(or DNA) in infected tissue (such as in bone marrow, liver, lymph node, or blood),
through light-microscopic examination of stained specimens, culture techniques, or
molecular methods.
▪ Serologic testing can provide supportive evidence for the diagnosis.
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31. VL case definition
▪ A person who presents with fever for more than two weeks and
✓an enlarged spleen (splenomegaly) and/or enlarged lymph nodes
(lymphadenopathy), or
✓ either loss of weight, anemia or leucopenia
➢while living in a known VL endemic area or having travelled to an endemic area
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32. Laboratory Investigation
▪ Non-Leishmanial Tests
✓Hematologic data
▪ Parasite Detection
✓Definitive diagnosis of VL is made by visualization of the amastigote form of the
parasite by microscopic examination of aspirates
▪ Antibody Detection
✓direct agglutination test (DAT)
✓rK39 strip test
➢39-amino acid repeat of a kinesin-related protein cloned from Leishmania
chagasi and conserved in L. donovani complex
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33. Cont…
▪ Antigen Detection Test
✓A urine latex agglutination
▪ Molecular Techniques
✓The polymerase chain reaction (PCR) based assays currently constitute the main
molecular diagnostic approach of Leishmaniasis
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34. Treatment
▪ The objectives of VL treatment are to
✓Reduce the parasite burden,
✓Prevent drug resistance,
✓Avoid toxic drug effects, and
✓Improve the clinical condition of patients and to manage complications
➢anemia, malnutrition and secondary infections
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35. Treatment
▪ Supportive treatment is important
✓Patients should be properly hydrated
✓ given nutritional therapy before starting the VL treatment
✓ Severe anemia should be corrected with blood transfusions
✓ Concomitant infections should be treated with appropriate anti-infective agents
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36. First-Line Regimens for Primary VL
❖Combination Therapy: Sodium Stibogluconate (SSG) and Paromomycin
▪ In the combination therapy, sodium stibogluconate (20mg/kg body weight/day), and
paromomycin (15mg/kg body weight/day) injections are given intramuscularly for 17
days
▪ The advantage of combination
✓Shortening duration of treatment, thereby increasing compliance
✓ Reducing the overall dose of drugs, thereby reducing toxic effects of drugs and cost
✓ Reducing the probability of selection of drug resistant parasites, thereby prolonging
the effective life of the available drug
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37. Treatment
❖Sodium Stibogluconate or Meglumin Antimoniate (Monotherapy)
▪ SSG in monotherapy is administered as intramuscular injection of 20mg/kg/day for 30 days
▪ possible shift of treatment to AmBisome
✓Acute pancreatitis with abdominal pain and vomiting
✓Jaundice developing while on treatment
✓Elevated liver function tests (5 times of the normal value)
✓Elevated creatinine level
✓Evidence of cardio-toxicity
✓Uninterrupted severe vomiting
✓Declining hematologic parameters, and
✓Failure to respond to treatment after two weeks of drug treatment
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38. Treatment
❖Liposomal Amphotericin B (LAmB, AmBisome)
▪ Liposomal Amphotericin B is recommended in those patients with
✓Pregnancy
✓HIV-co-infection
✓severe illness
✓ severe anemia
✓ severe malnutrition
✓ extremes of age (below 2 years or above 45 years).
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39. Second-Line Treatment for Primary Visceral Leishmaniasis
❖Liposomal Amphotericin B (AmBisome)
▪ The recommended dose of AmBisome for treatment is 5mg/kg/day over a period of 6 days
(i.e. 30mg/kg in total)
✓It is administered by reconstitution with 5% D/W
✓with a volume of 100ml of D/W for 50mg of AmBisome (for 100mg or 2 vials of
AmBisome 200ml of D/W, for 3 or more vials use all the 500ml D/W)
▪ The infusion can run over 30 to 60 minutes
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40. Treatment
❖Miltefosine
✓originally developed as an oral anticancer drug that has shown to have anti-
leishmanial activity
✓This is the only oral anti-leishmanial drug taken at a dose of 2-3mg/kg per day
(100mg/day for patients weighting more than 25kg) for 28 days
✓Miltefosine commonly induces gastrointestinal side effects, such as anorexia,
nausea, vomiting (38%) and diarrhea (20%)
✓Miltefosine is potentially teratogenic and, thus, it is contraindicated during
pregnancy
❖Paromomycin (Aminosidine)
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41. Treatment Regimens for First VL Relapse
▪ Liposomal amphotericin B 5mg/kg/day for a period of 6 days
✓ The treatment period can be extended up to 14 doses for better therapeutic advantages
▪ SSG 20 mg/kg/day for 40 days until 2 consecutive weekly aspirates for parasitology are
negative
✓ If TOC is still positive, SSG should be given for a total of 60 days with close monitoring
of drug toxicity and TOC checked again, if positivity persists, then 2nd line treatment
must be used.
▪ .SSG/PM combination: SSG (30 days) and Paromomycin (17 days) can be used for VL
relapse treatment
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42. Treatment of VL by Drug Interruption
▪ The treatment of VL after drug interruption depends on the duration of the interruption
✓If the duration of treatment interruption is less than 5 days, continue the same treatment
until the full course without compensating the missed treatment days.
✓If the duration of treatment interruption is between 5–10 days, continue the same
treatment until the full course but with compensation.
✓If the duration of treatment interruption is more than 10 days, restart treatment as day
one.
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43. Prevention
▪ No vaccines or drugs to prevent infection are available.
▪ Preventive measures are aimed at reducing contact with sand flies
▪ Protection against Mosquitoes, Ticks, & Other Arthropods; and Prevention in the
previous section,Cutaneous Leishmaniasis).
▪ Preventive measures include minimizing outdoor activities, to the extent possible,
especially from dusk to dawn, when sand flies generally are the most active; wearing
protective clothing; applying insect repellent to exposed skin; using bed nets treated with
a pyrethroid-containing insecticide; and spraying dwellings with residual-action
insecticides
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44. Prevention
▪ Vector Control
▪ Insecticide Application
▪ Use of Long-Lasting Insecticide Treated Nets (LLITN)
▪ Repellents (Chemical or Natural)
▪ Integrated Control
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