Intestinal Protozoa Flashcards
List medically important protozoa and their diseases
(a) Amoebas: Entamoeba histolytica, Naegleria,
Acanthamoeba.
(b) Flagellates: Trypanosoma cruzi
(c) Sporozoa: Toxoplasma gondii
Protozoa - classify by motility
(a) Mastigophora (flagella) - Trypanosoma cruzi, Giardia lamblia
(b) Sarcodina (pseudopodia) - Amoebas
(c) Apicomplexa (microtubule complex, commonly
referred to as sporozoa) - Toxoplasma gondi, Plasmodium
(d) Ciliophora (ciliates) - Balantidium coli
Ciliophora spp
Balatidium coli
Apicomplexa spp
Split into two categories Coccidia Isospora belli Toxoplasma gondii Sarcocystis spp. Cryptosporidium parvum Pneumocystis carinii
Piroplasma Plasmodium falciparum Plasmodium vivax Plasmodium malariae Plasmodium ovale Babesia microti
Kinetoplastida spp
(Flagellated) Trypanosoma gambiense Trypanosoma rhodiense Trypanosoma cruzi Leishmania spp
Amoebic abscess (amoebiasis, amoebic dysentery) agent, epidemiology
Agent: Entamoeba histolytica
E. dispar (non invasive)
Epidemiology Contaminated water Poor sanitation - daycares Close proximity places - military barracks, nursing home, prisons Human waste as fertilizer
Entamoeba coli, E. hartmanii, Endolimax nana, Iodamoeba bütschlii non pathogenic to humans (T/F)
True
Amoebic abscess - transmission
–faeco-oral, food and water contaminated by flies/roaches, oral-anal sex
All cases of amoebic abscess are symptomatic
False
Amoebic abscess - Pathogenesis
- Cysts pass in stool of infected person
- Cysts ingested
- Cysts pass through stomach ->
Gastric acid promotes trophozoite release in small intestine. - Trophozoites multiply
((may cause necrosis + ulceration in the large intestine))
- Flask shaped ulceration = secondary bacterial infection/peritonitis due to damage to intestinal wall
If parasite moves to peritoneal cavity = goes to bloodstream -> goes to diff organs
(intermittent diarrhoea with abdominal pain and weight loss).
Virulence factor of amoebiasis, explain
Trophozoites invade BVs of the portal system,
surviving lytic complement & neutrophils.
Result: Gain access to the liver parenchyma.
What is second leading cause of mortality due to parasites?
Entamoeba histolytica
Possible parasitic cause of diarrhea in infants
E. moshkovskii
E. histolytica - host range
Mainly humans.
But: higher primates, dogs, cats and some rodents
Which Trophozoite has the foll description:
Trophozoites are round with large,
lobular pseudopodia and a clock-face nucleus.
E. histolytica
- Central nucleus (most times)
- Erythrocytes seen in cytoplasm means digested erythrocytes
Active, feeding stage
Describe cyst stage of E. histolytica
Cysts are smaller than trophozoites.
They have 4 nuclei and chromatoid bars (tightly
packed mRNA with rounded ends).
-Infective stage
What do E. histolytica and Entamoeba coli have in common?
They look alike
Why is it important to distinguish between E histolytica and E coli?
E coli is not pathogenic in the GIT but E histolytica is; need to know if treatment is necessary
E coli vs E histolytica
E. coli-coarser chromatin, eccentrically located
endosome (protein trafficking) and the absence of erythrocytes in the cytoplasm
-ingested erythrocytes appear as dark
inclusions.
Entamoeba coli cyst
-8 nuclei (compared to 4 nuclei seen in E. histolytica)
and
-smaller chromatid bodies that are often filamentous
E. histolytica - life cycle
- Ingestion of cysts
- Excystation in small intestine
- Division of quadrinucleate cyst
into 4 and then 8 trophozoites - Trophozoites move to colonize the colon
- Encystation
- Excretion of cysts
- Ingestion of cyst by the patient
Epidemiologic factors
Events, characteristics, or other definable entities that have the potential to bring about a change in a health condition.
Epidemiologic factors - Amoebiasis
(i)Strain virulence - classic strain, non-classic strain; Laredo , Huff; pathogen zymodemes (ii) Susceptibility of the host (iii) Nutrition status (iv) Immune-system. • Breakdown of immunologic barrier (tissue invasion)
Virulence factors
Virulence factors:
- assist and promote colonization of the host e.g. adhesins, invasins, antiphagocytic factors.
- Bring damage to the host e.g. toxins, hemolysins, proteases
Virulence factors - Amoebiasis
-Secreting proteolytic enzymes (histolysin)
and cytotoxic substances.
• Contact-dependent cell killing
• Cytophagocytosis
Necrosis in amoebiasis is caused by trophozoite division and cytotoxin produced by E histolytica.
Amoebic killing target cell: • Receptor-mediated adherence of amoebae to target cell • Amoebic cytolysis of target cell • Amoebic phagocytosis of killed target cell
Intestinal and Extraintestinal Amoebiasis symptoms
Intestinal amoebiasis - Diarrhea or dysentery, abdominal
pain, cramping , anorexia, weight loss, chronic fatigue
Extraintestinal amoebiasis - Systemic signs - fever, leukocytosis, abscess formation in right lobe, pain over liver, hepatomegaly
Liver abscess - due to Amoebiasis - causation
- seeding of infection from the bowel
- infectious agents are carried to the liver
from the portal venous circulation. - Necrosis of hepatocytes due to toxins
of lysed neutrophils - liver abscess pus = chocolate brown -‘anchovy paste’.
- Amoebas are to be found in the wall
of the abscess
Complications of liver abscess Secondary bact infection Rupture into pleural space - Empyema Rupture into pericardium - Pericarditis Rupture into peritonium - Peritonitis
Lab ID - Amoebiasis
microscopy, culture, serologic testing, and (PCR) assay
Microscope and culture ID - Amoebiasis
Parasites concentrated in intestinal ulcers - one stool sample not as effective (need multiple stool samples)
Microscopic identification using:
Wet Mount (with or w/o iodine)
– a mature cyst has 4 nuclei, immature 1 – 3.
Trichrome stain
– Cysts, trophozoites can be stained for the location
of chromatoid bodies of the nucleus.
Culture: Using modified Locke-egg media
• culture less sensitive than microscopy
Antigen detection - Amoebiasis
EIA kits.
Ag detection may be useful as an adjunct to microscopic
diagnosis in detecting parasites and to distinguish between pathogenic and nonpathogenic infections.
Molecular tests - Amoebiasis
Conventional and Real time PCR, LAMP
Intestinal Amebiasis: Treatment
Asymptomatic amoebiasis (cyst passer): Diloxanide furoate ( furamide) 500 mg tid/ 10 days
• Symptomatic amebiasis - Iodoquinol , 650 mg tid/ 20 days or Metronidazole , 750 mg tid/ 10 days; Paramomycin.
Amebic colitis: Chloroquine, 250 mg bid
• Acute amebic dysentery: Emetine hydrochloride, 1mg/kg od IM or SC
Extraintestinal Amebiasis: Amebic liver abscess,
Ameboma:
Metronidazole, as above plus dihydroemetine / 10 days or Metronidazole or dihydroemetine as above plus Chloroquine ,
500 mg bid/ 2 days. Tinidazole, Ornidazole.
Surgical drainage – Drip and suck
Giardiasis
Giardia intestinalis / Giardia lamblia / Lamblia intestinalis / Giardia duodenalis.
Amitochondriate
Lacking mitochondria
G lamblia - features
Amitochondriate flagellated protozoan
Bilaterally symmetrical
Most primitive eukaryotes in existence
Protozoa
Single celled eukaryote
Protozoa represent a unique type of evolution, how?
Organelles are structures performing the same functions as tissue and organs in “higher organisms“. Locomotion and feeding: cilia, flagella, pseudopodia. Osmoregulation: pulsatory vesicle, contractile vacuole
Virulence factors - G lamblia
Infraciliature (skeleton): coordinating system of cilia. Rhoptries: penetration of cells (Apicomplexa).
Cell covered in 3-layered Plasma membrane
Giardia - transmission
Main host reservoir: Humans
Zoonotic transmission is possible but contraversial for Giardia spp
Epidemic form - drinking water
-Cysts infectious right after excretion
-Spread from person to person / oral-anally (carried to colon and encyst along the way)
Giardia - Trophozoite morphology
8 flagella.
No mitochondria, or organelles for energy metabolism
This parasite is generally tear-drop shaped with two
visible nuclei.
Anterior region contains structure for epithelial cell attachment
Cyst - Trophozoite morphology
Cysts (protective, infective stage)
• Cysts is ellipsoid; slightly smaller than trophozoites
- have 4 visibly distinct nuclei.
-median rod (axostyles), visible down the centre
Giardiasis is common in children and hikers (T/F)
True
Cysts susceptibility
Desiccation and direct sunlight
Mild to severe gastrointestinal signs
of Giardiasis
• Sudden onset diarrhea; Foul-smelling stools
• Abdominal cramps
• Bloating, flatulence
•Nausea, fatigue
• Weight loss
-Lactose intolerance up to six months afterward
Lab ID - Giardiasis
•Direct observation in feces
-Trophozoites
“Tear drop” shape
Two nuclei and tumbling mobility
-Cysts
Approximately 13μ long
Oval, with 2-4 nuclei
- Immunofluorescence
- ELISA, PCR
Giardiasis - Treatment
Anti-protozoal drugs
• Metronidazole
• Tinidazole
•Ornidazole
Chronic cases
• May be resistant
• Prolonged therapy may be necessary
Giardiasis - Prevention
Treat potential contaminated water -Boil water, filter (pore size 1 uL), chlorinate Wash fruits and veg Hand washing No swimming wks after exposure
Trichomonas vaginalis
Euprotista
Small flagellates
Only exist as trophozoites
T vaginalis - hosts
Hosts and Host Range: Humans (men & women)
Karyomastigont
Protozoa giving rise to 2 pairs of flagella
T vaginalis - morphology
Karyomastigont - 2 pairs flagella
Parabasal - very Small cells accompanying T vaginalis
Axostyle- runs diagonally through organism
Life Cycle - T vaginalis
- Trophozoite
- Binary fission
- Direct transmission through sexual intercourse
T vaginalis - pathogenesis
- Remain and multiply in vagina and cause
inflammation of the epithelium. - Excessive production of mucus; pain.
Can invade other organs such as kidney
T vaginalis - lab ID
•Wet preparation: Microscopic examination of
vaginal swab or urethral swabs observing for
tumbling
Balantidium coli
Euprotista
Phyllum: Ciliophora
Largest protozoan parasite of humans
Heterokaryotic (i.e. two kinds of nuclei)
B. coli - trophozoite reproduction
Trophozoites multiply by asexual binary fission or sexual conjugation (with the exchange of nuclear material).
Balantidiosis is common in areas near swine (T/F)
True
Trophozoites - B coli features
- oblong
- kidney shaped macronucleus and smaller micronucleus.
Cysts - B coli features
-round with a rounder and thicker macronucleus
B coli - life cycle
(1) Cyst
(2) Cyst ingested, swallowed
(3) Excysts (emerge from cyst), Trophozoites
(4) Division: Binary fission in small intestine. Trophozoite colonize large intestine, where they live in the
lumen and feed on the intestinal flora.
Some trophozoites invade the wall of the colon using proteolytic enzymes and multiply, and some of them return to the lumen.
(5) Form cysts -> feces
Clinical features - Balantidiosis
Acute disease
-explosive diarrhea may occur as often as
every twenty minutes. Perforation of the colon may also
occur -> lead to life- threatening situations.
Diagnosis - Balantidiosis
Microscopic examination of stool: Trophozoites and Cysts
