West Visayas State University College of Medicine Batch 2020

MICRO-PARA
Lecture 4B
Block 11
Module 2
11/ 03/ 17
Dr. Melanie Jane Tendencia

TOPIC OUTLINE
I. Intestinal Protozoans (FECAL-ORAL) TRANSMISSION FACTORS
II. Types of Intestinal Protozoans 1. Poor personal hygiene
A. Flagellates a. Food handlers
B. Amoeba
C. Apicomplexa b. Institutions
III. Types of Diarrhea Caused by Intestinal Protozoans c. Children in day care centers
IV. Diagnosis 2. Developing Countries
V. Treatment
a. highly endemic
VI. Parasitic Enteritis
A. Human Coccidiosis b. poor sanitation
B. Isosporiasis c. Travelers Diarrhea
C. Cyclosporiasis 3. Water-borned epidemics
D. Giardiasis
E. Intestinal Amoebiasis
4. Male homosexuality
Supplementary Notes a. oral-anal contact
Review Questions
References
PREVENTION AND CONTROL
Appendices
Improve personal hygiene - especially in institutions
LECTURER BOOK REFERENCE OLD TRANS
Treat asymptomatic carriers - e.g. family members
Health education
Hand-washing
I. DEFINTION: INTESTINAL PROTOZOANS Sanitation
Unicellular eukaryotic organisms which includes Food handling
members from flagellates (e.g. Giardia lamblia), Protect water supply
Amoeba (e.g. Entamoeba histolytica, E. dispar, E. coli), Treat water if questionable
Apicomplexa (e.g. Cryptosporidium hominis, Boiling
Cryptosporidium parvum) and others (e.g. Balantidium Iodine
coli). Not chlorine

Figure 1. Typical fecal-oral life cycle of Intestinal Protozoans (Upclass Trans)

CCetC Group 25 1 of 10
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 II. TYPES OF INTESTINAL PROTOZOANS Possible Mechanisms
Mechanical irritation
FLAGELLATES Obstruction of absorption

GIARDIA LAMBIA
Worldwide distribution
Higher prevalence in developing countries (20%)
1-6% in temperate countries
Most common protozoa found in stools
~200 million clinical cases/year

Giardiasis
Often asymptomatic
Acute or chronic diarrhea
Fecal oral life cycle (*refer to Fig. 2)
Cyst - infective stage; passed in feces
Trophozoite replicating stage; found in small
intestine

Clinical Signs and Symptoms

Range of Outcomes
Asymptomatic/latent
Acute short-lasting diarrhea
Chronic/nutritional disorders

Subacute/Chronic Symptoms Figure 2. Life Cycle of Giardia sp. (Upclass Trans, CDC)
Recurrent diarrheal episodes
Cramps uncommon Life Cycle
Sulfuric belching, anorexia, nausea frequent Cysts are resistant forms and are responsible for
Can lead to weight loss and failure to thrive transmission of giardiasis. Both cysts and trophozoites
can be found in the feces (diagnostic stages) (1). The
Acute Symptoms cysts are hardy and can survive several months in cold
1-2 week incubation water.
Sudden explosive, watery diarrhea Infection occurs by the ingestion of cysts in
Characteristics: bulky, frothy, greasy, foul- contaminated water, food, or by the fecal-oral route
smelling stools (hands or fomites) (2).
No blood or mucus In the small intestine, excystation releases trophozoites
Upper gastro-intestinal uneasiness, bloating, (each cyst produces two trophozoites) (3).
flatulence, belching, cramps, nausea, vomiting, Trophozoites multiply by longitudinal binary fission,
anorexia remaining in the lumen of the proximal small bowel
Usually clears spontaneously (undiagnosed), but can where they can be free or attached to the mucosa by a
persist or become chronic ventral sucking disk. (4)
Encystation occurs as the parasites transit toward the
Pathogenesis colon. The cyst is the stage found most commonly in
Epithelial damage causing villus blunting, crypt cell nondiarrheal feces (5).
hypertrophy, cellular infiltration Because the cysts are infectious when passed in the
Malabsorption stool or shortly afterward, person-to-person
Enzyme deficiencies (e.g. lactase deficiency transmission is possible. While animals are infected with
causing lactose intolerance) Giardia, their importance as a reservoir is unclear.
Giardia adheres to the mucosal lining of the GIT
(masking effect) causing damage of the villus and Source: ( http://www.cdc.gov/dpdx/giardiasis/ )
malabsorption of nutrients

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 AMOEBA cysts can survive days to weeks in the external
environment and are responsible for transmission.
ENTAMOEBA HISTOLYTICA Trophozoites passed in the stool are rapidly destroyed
Cosmopolitan distribution once outside the body, and if ingested would not survive
Worldwide incidence : 0.2-50% exposure to the gastric environment.
No animal reservoirs In many cases, the trophozoites remain confined to
Typical fecal-oral life cycle (inhabits the large the intestinal lumen ([A] : noninvasive infection) of
intestine) individuals who are asymptomatic carriers, passing
Facultative virulent pathogen cysts in their stool.
Estimated 50 million cases/year In some patients the trophozoites invade the intestinal
100,000 deaths/year mucosa ([B] : intestinal disease), or, through the
bloodstream, extraintestinal sites such as the liver,
ENTAMOEBA DISPAR brain, and lungs ([C] : extraintestinal disease), with
Morphologically identical with E. histolytica. However, it resultant pathologic manifestations.
is non-pathogenic. It has been established that the invasive and
noninvasive forms represent two separate species,
Life Cycle (of both) respectively E. histolytica and E. dispar. These two
species are morphologically indistinguishable unless E.
histolytica is observed with ingested red blood cells
(erythrophagocystosis).
Transmission can also occur through exposure to fecal
matter during sexual contact (in which case not only
cysts, but also trophozoites could prove infective).

Source:
(http://www.cdc.gov/parasites/amebiasis/biology.html)

Pathogenesis
NON-INVASIVE
Amoeba colony on intestinal mucosa
Asymptomatic cyst passer
Non-dysenteric diarrhea, abdominal cramps, other GI
symptoms

INVASIVE
Necrosis of mucosa ulcers, dysentery
Ulcer enlargement dysentery, peritonitis
Metastasis extraintestinal amebiasis
Cessation of cyst production
Figure 3. Life Cycle of Entamoeba histolytica (Upclass Trans, CDC)
Presentation ulcers with raised borders with little
Cysts and trophozoites are passed in feces (1). Cysts
inflammation between lesions
are typically found in formed stool, whereas
Facultative Pathogenicity
trophozoites are typically found in diarrheal stool.
85-90% of infected individuals are symptomatic
Infection by Entamoeba histolytica occurs by ingestion
10% of the symptomatic will develop severe invasive
of mature cysts (2) in fecally contaminated food, water,
disease
or hands.
Excystation (3) occurs in the small intestine and
Histology
trophozoites are released (4), which migrate to the large
Flask-shaped ulcer
intestine.
Trophozoites at boundary of necrotic and healthy tissue
The trophozoites multiply by binary fission and produce
Trophozoites ingesting host cells
cysts (5), and both stages are passed in the feces (1).
Dysentery (blood and mucus in feces)
Because of the protection conferred by their walls, the

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 Figure 4. Amoebiasis (Upclass Trans)

Ulcer Enlargement and Disease Progression Cutaneous Amoebiasis

Amoeba expand laterally and downward into lamina
propria
Localized sloughing (ulcers coalesce)
Perforations of intestinal wall causing peritonitis
2nd bacterial infections
Local abscesses amebic granuloma also known as
ameboma
Ameboma is the inflammation thickening of the
intestinal wall around the abscess (can be
confused with tumor).
Intestinal or hepatic fistula
Mucosa bathed in fluids containing trophozoites
Perianal ulcers
Urogenital (e.g. labia, vagina, penis)
Mode of Action
Penetration of mucus layer
Contact-dependent killing of epithelial cells
Breakdown of tissues (extracellular matrix)
Contact-dependent killing of neutrophils, leukocytes,
etc.

Extraintestinal Amoebiasis APICOMPLEXA

Metastasis via blood stream
Primarily liver (portal vein) and sites are less frequent CRYPTOSPORIDIUM
Ameba-free stools common Fecal-oral transmission (coccidian type life cycle)
High antibody titers Two species infecting humans
1. parvum: cattle and other mammals
Amoebic Liver Abscess 2. C. hominis: only humans
Chocolate-colored pus (made up of necrotic material First human case reported in 1976
and bacteria free) Initially believed to be rare and exotic
Lesions expand and coalesce Now known to be common human pathogen
Further metastasis, direct extension or fistula Self-limiting diarrhea in immunocompetent persons
Profuse, water diarrhea associated with AIDS (life
Pulmonary Amoebiasis threatening)
Rarely primary
Rupture of liver abscess thru the diaphragm Life Cycle
Secondary bacterial infections are common Infectious form = oocysts
Fever, cough, dyspnea, pain, vomica Sporozoites invade the intestinal epithelial cells
(infective form)
Merogony
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 production of merozoites gastrointestinal tract or other tissues such as the
Gametogony respiratory tract. In these cells, the parasites undergo
produce micro and macrogametes asexual multiplication (schizogony or merogony) [d, e, f]
Sporogony and then sexual multiplication (gametogony) producing
Produce sporozoites microgamonts (male) [g] and macrogamonts (female)
Completed on host cell [h]. Upon fertilization of the macrogamonts by the
Thin (autoinfection) or thick walled oocysts microgametes [i], oocysts [j, k] develop that sporulate in
the infected host. Two different types of oocysts are
produced, the thickwalled, which is commonly excreted
from the host [j], and the thin-walled oocyst [k] , which is
primarily involved in autoinfection. Oocysts are infective
upon excretion, thus permitting direct and immediate
fecaloral transmission.

Source:
(http://www.cdc.gov/parasites/crypto/biology.html)

III. TYPES OF DIARRHEA CAUSED BY INTESTINAL

PROTOZOANS
A. Enterocyte malfunction (osmotic diarrhea)
Impaired absorption
Enhanced secretion
B. Inflammatory diarrhea
Mucosal invasion
Leukocytes in stools
C. Secretory diarrhea
Toxin associated
Watery

Pathogenesis: (Docs ppt lecture)

1. eneterocytes damaged or killed
a. villus atrophy
b. decreased Na absorption
c. increased intercellular permeability

Figure 5. Life Cycle of Cryptosporidium sp. (Upclass Trans)

2. crypt cell hyperplasia
(1) Sporulated oocysts, containing 4 sporozoites, are a. increased Cl secretion
excreted by the infected host through feces and possibly
other routes such as respiratory secretions 3. inflammation of lamina propria
(2) Transmission of Cryptosporidium parvum and C. a. cytokines, neurohormones
hominis occurs mainly through contact with contaminated b. enhanced secretion of antibodies
water (e.g., drinking or recreational water). Occasionally
food sources, such as chicken salad, may serve as IV. DIAGNOSIS
Suspect: acute or chronic GI symptoms
vehicles for transmission. Many outbreaks in the United
Confirmed: detection of parasite in feces
States have occurred in waterparks, community
Copro-antigens or molecular probes
swimming pools, and day care centers. Zoonotic and
Cryptosporidium
anthroponotic transmission of C. parvum and
Acid-fast stain
anthroponotic transmission of C. hominis occur through
Giardia
exposure to infected animals or exposure to water
3 non-consecutive days (inconsistent excretion)
contaminated by feces of infected animals.
Duodenal aspirates or biopsy
(3) Following ingestion (and possibly inhalation) by a
Presumptive treatment in chronic cases
suitable host , excystation [a] occurs. The sporozoites
Entamoeba
are released and parasitize epithelial cells [b,c] of the
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 Histolytica vs. dispar Etiologic agent:
Sigmoidoscopy (lesions. Aspirates, biopsy) unicellular sporozoan parasite
Extra-intestinal disease Undergoes schizogony in the intestinal epithelial cells
Merozoites are released
Additional notes from Docs lecture: Merozoites may then invade other cells and repeat
Diagnosis of Extraintestinal Diseases asexual schizogony cycle OR
symptoms associated with specific organ May mature into sexual gametocytes and form
history of dysentery zygocytes and then sporulated oocysts rupture to
hepatic sporozoites then restart the enterocyte cycle
RUQ pain
enlarged liver Isosporiasis Isospora belli sporulated oocysts
serology: current or past? (infective form)
imaging (CT, MRI, Ultrasound)
abscess aspiration Diagnosis
only select cases Careful examination of multiple serial sections of
reddish brown liquid intestinal biopsy specimens for any stage of the parasite
trophozoites at abscess wall Examination of the small bowel contents for oocysts
Modified acid-fast stain
V. TREATMENT To visualize stool oocyst
Table 1. Treatment options for the following Intestinal Protozoans Zinc sulfate flotation stool concentration technique
(Upclass Trans)

Treatment
Trimethoprim-sulfamethoxazole
Effective in AIDS patients
multiple courses of suppressive therapy

CRYPTOSPORIDIASIS - CRYPTOSPORIDIUM
Protozoan parasite
Severe chronic diarrhea in immunocompromised
patients
Typically self-limited 204 weeks in normal hosts
Usually infect only the surface of the mucosal epithelium
(process is less inflammatory)

Diagnosis
sugar flotation or modified acid fast stains of fecal
specimen

VI. PARASITIC ENTERITIS
HUMAN COCCIDIOSIS - ISOSPORA BELLI
Isospora belli
should be considered in patients (PWAs) with chronic
diarrhea of obscure origin and eosinophilia
Manifestations: weight loss, fever, headache, colicky
abdominal pain, steatorrhea, and malabsorption
CYCLOSPORIASIS - CYCLOSPORA
Persistent diarrhea in travelers, those living in tropical
areas, health care workers and AIDS patients
caused by infection with Cyclospora
cayetanensis, a pathogenic protozoan
transmitted by feces or feces-contaminated fruits
and vegetables
outbreaks have been reported due to contaminated
fruits and vegetables
it is not spread from person to person, but can be a
hazard for travelers as a cause of diarrhea
Tx: co-trimoxazole
GIARDIASIS - GIARDIA LAMBLIA
Severe infection, steatorrhea

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 Severe villous atrophy with dense plasma cell infiltration
and inflammation in the lamina propria
INTESTINAL AMOEBIASIS - ENTAMOEBA
HISTOLYTICA
Invasive syndrome with recurring pattern
May extend into Ulcerative Postdysenteric Colitis w/c
may no longer respond to antiamebic therapy
Doc Tendencia: Please read on the ff:
VIBRIO, CAMPYLOBACTER, HELICOBACTER
A. Morphology and Identification
a. Typical Characteristics
b. Culture Characteristics
c. Growth Characteristics
B. Antigenic Structure and Biologic Classification
C. Vibrio cholerae enterotoxin
D. Pathogenesis and Pathology
E. Clinical findings
F. Diagnostic Laboratory Tests
G. Specific Tests
H. Immunity
I. Treatment, Prevention and Control
J. Epidemiology
SUPPLEMENTARY NOTES
CHRONIC DIARRHEA
Chronic or persistent diarrhea last for >4weeks
3 or more stools per day
For healthy persons- chronic diarrhea can be a
nuisance, cause inconvenience
For immunocompromised patients, may represent a life-
threatening illness
Most of the causes are non-infectious
PEOPLE AT RISK
Persons with severely weakened immune systems
HIV/AIDS
Receiving chemotherapy or malignancy
Organ transplant recipients
Travelers to certain countries where water and food
supply may be contaminated
MAJOR CAUSES OF CHRONIC DIARRHEA
(ACCORDING TO PREDOMINANT MECHANISM)
A. Types
1. SECRETORY CAUSES
Due to derangements in F & E transport across the
enterocolonic mucosa
Characteristic-watery, large-volume fecal outputs;
typically painless and persist with fasting
Medications stimulant laxatives, etc
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Bowel resection mucosal disease or enterocolic
fistula
Certain bacterial infections
Hormones
Congenital defects in ion absorption
2. OSMOTIC CAUSES
Occurs when ingested, poorly absorbable,
osmotically active solutes draw enough fluid into the
lumen to exceed the reabsorptive capacity of the
colon
Ceases with fasting or with discontinuation of the
causative agent
Osmotive laxatives Mg-containing antacids, health
supplements or laxatives
Carbohydrate malabsorption lactase deficiency
3. STEATORRHEAL CAUSES
Fat malabsorption greasy, foulsmelling, difficult-to-
flush diarrhea associated with weight loss and
nutritional deficiencies
amino acids and vitamin malabsorption
intraluminal maldigestion
Mucosal malabsorption
Lymphatic obstruction
4. INFLAMMATORY CAUSES
Pain, fever, bleeding, other
manifestation of inflammation
Fecalysis reveals leukocytes or leukocyte-derived
proteins such as calprotectin
Idiopathic inflammatory bowel disease
Primary or secondary forms of immunodeficiencies
Infections invasive bacteria, viruses and parasites
Eosinophilic gastroenteritis
Others (radiation enterocolitis, chronic graft-versus-
host disease)
5. DYSMOLITY CAUSES rapid transit (e.g. irritable
bowel disease, hyperthyroidism)
6. FACTITIAL CAUSES eating disorders
DIARRHEA caused by an infection may result from:
1. Parasites (e.g, Cryptosporidium, Cyclospora,
Entamoeba, Giardia, Isospora, Microsporidia)
2. Bacterial toxins (e.g. Campylobacter, Clostridium
difficile, E. coli, Salmonella, Shigella, Cholera)
3. Viruses (e.g. rotavirus, CMV, HIV)
B. Diagnosis
Careful history
Onset, duration, pattern, aggravating (diet) and
relieving factors, stool characteristics
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 Fecal incontinence, fever, weight loss, pain, travel B. Antimicrobials
history, medications taken C. Judicious use of antidiarrheal medication
Perform a physical exam (loperamide) for symptomatic relief in some
The types of tests and orders will be based on the patients
symptoms and history D. Fluid and electrolytes replacement
The tests may include blood or stool tests (+) Blood E. Low fat diet for some patients
or leukocyte
Stool culture- bacteria, generally 3 or more stool are For DIARRHEA in which cause has not been determined,
collected and examined the following guidelines may help
Special tests may be required to diagnoses some relieve the symptoms:
parasites Remain well-hydrated and avoid dehydration
Additional tests may be done, including radiographs Serious health problems can occur if the body does not
(x-rays) and endoscopy/colonoscopy maintain proper fluid levels
Maintain a well-balanced diet - may help speed up the
C. Evaluation recovery
History Avoid beverages that contain caffeine - Tea, coffee and
Inquire about the diurnal variation, relationship to many soft drinks
meals, wt. loss
Character of stools E. Prevention
Foul or greasy; chronic bloody stools Infections that cause chronic diarrhea usually can be
Abdominal pain, tenesmus prevented by:
Physcial Exam 1. Always drink clean safe water that has been
Abdominal tenderness, distention properly treated
Organomegaly 2. Always use proper food handling and preparation
Anal fistulas, rectal mass techniques
Hyperactive bowel sounds 3. Always maintain good hand hygiene, including
Laboratory Exams and Analysis always washing hands properly with soap and
1. CBC & differential water before handling food and after using the
a. Anemia- chronic blood loss, infection, toilet or changing a diaper.
malabsorption or neoplasm
b. Eosinophilia parasitic disease or allergic ENTEROHEPATIC AND ENTERAGGREGATIVE
reaction E. COLI
c. Megaloblastic anemia- Vit B12 or folate
malabsorption EPEC
2. ESR, C-reactive protein may cause acute and chronic diarrhea
a. If elevated chronic inflammation insidious persistent or relapsing illness
3. Stool exam for occult blood, leukocytes, ova of E. coli organisms in O groups 1,2,4,7 and 75
parasites Produce hemolysin and necrotoxin
a. To detect parasites 3 or more stool samples Not present in healthy people or in patients with acute
diarrheal syndromes
are examined
b. Special stains to look for some parasites
EAEC
4. Stool Culture to test for bacteria
Cause of persistent diarrhea in India, Brazil and Mexico
5. X-rays plain abdominal radiography and Barium
Associated with intestinal inflammation and malnutrition
studies of the Upper GIT, small intestines and
even in the absence of diarrhea
colon
6. Endoscopy
OTHERS
a. Sigmoidoscopy/Colonoscopy to detect
inflammation of the colon or rectum,
SYPHILIS
neoplasms and parasites
Can also involve the GI tract upper part of the small
bowel or stomach
D. Treatment Late secondary syphilis
A. Should be directed towards the underlying cause
of the chronic diarrhea
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 Erosive and infiltrative gastritis with motile 2. An entamoeba histolytica trophozoite has the
spirochetes following characteristics:
(+) treponemal immunofluorescence test a. Central karyosome in the nucleus, ingested
Upper abdominal pain, vomiting, weight loss RBCs, clear pseudopodia
Late GI manifestation b. Ingested RBCs, clear pseudopodia, uneven
Pyloric obstruction, hourglass constriction chromatin on the nuclear membrane
Linitis plasctica of the stomach c. Ingested RBCs, clear pseudopodia, and large
Gumma may be seen in the small bowel or colon glycogen vacuoles in cytoplas
d. Large, blotlike karyosome, ingested white blood
GASTROINTESTINAL MYCOSIS cells (WBCs), granular pseudopods
3. Contains immature forms with only asexual
Candidiasis reproduction
causative agent: C/ albicans a. Definitive host
Pathogenecity: b. Intermediate host
Ulceration in any part of the GIT c. Ectoparasite
Immunocompromised patients especially neutropenic d. Endoparasite
patients 4. The motile, reproducing stage, feeding stage of
Ulcerations may be deeply invade and numerous; the protozoa is which of the following?
a. Cyst
these may become important entry sites for
b. Trophozoite
hematogenously disseminated candidiasis
c. Ova
HIV patients prone to esophageal candidiasis
d. Adult worm
Candida organisms
5. Which o the following organs of the body is most
may reach high concentration in stools of
often involved in extraintestinal amebiasis?
patients receiving antimicrobial agents
a. Lungs
may cause diarrhea
b. Kidneys
c. Pancreas
Phycomycoses
d. Liver
causative agents: Phycomycetes (Absidia, Rhizopus,
6. Which of the following is pathognomonic for G.
Mucor spp.)
lamblia and the stage it is found in?
Disseminated granulomatous disease
a. Spiral groove- trophozoite
Involve the predisposed host via GIT
b. Undulting membrane- cyst
By hematogenous spread
c. Cytostome-trophozoite
Manifestations include abdominal pain, diarrhea, GI
d. Ventral sucking disk- trophozoite
bleeding, peritonitis
7. 35 year old male, presents with bloodless, foul-
smelling bloating, watery diarrhea. He has not
Histoplasmosis had a full meal for 3 days. He was confirmed to be
causative agent: Histoplasma capsulatum HIV (+) 10 years ago. Stool exam revealed
May involve the GIT as a part of the disseminated parasitic cysts. Which of the ff parasites is the
infection most likely cause of the diarrhea?
Manifest as ulceration, bleeding, obstruction, rarely, a. Giardia lamblia
protein losing enteropathy b. E. histolytica
Lesions tend to be single and may be initially c. Balantidium coli
considered to be neoplastic d. Cryptosporidium hominis
8. Treatment for symptomatic E. histolytica infection
REVIEW QUESTIONS include:
1. Parasitic organisms that are most often a. Iodoquinol
transmitted sexually include: b. Metronidazole
a. Entamoeba gingivalis c. Paramomycin
b. Dientamoeba fragilis d. A and C only
c. Trichomonas vaginalis 9. A 95 year old woman living in Zone 1 Pala-Pala
d. D. latum presents with mild diarrhea and vague abdominal
pain. She has malaise, lassitude and low grade
fever. She has been febrile for 3 weeks already.
Which of the ff would you find in her stool if you
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 are suspecting a small intestinal sporozoan
infection?
a. Cysts
b. Oocytes
c. Sporozoites
d. Merozoites
10. The causative agent for human coccidiosis:
a. Isospora belli
b. Dientamoeba fragilis
c. C. hominis
d. Toxoplasma gondii

Answer: c, a, b, b, d, d, a, b, b, a

REFERENCES
Dr. Tendencias lecture
Upclass Notes

APPENDICES

Figure 6. Giardia life cycle - the cyst is the infective stage and the
trophozoite is the replicative state. (Dr. Tendencias lecture)

Figure 7. Typical Fecal-Oral life cycle of Intestinal Protozoans (Dr.

Tendencias lecture)

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