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Medical parasitology

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					 I.   Introduction to Medical Parasitology &
      Entomology and Luminal Protozoa

PROF. DR. HJ. WAN OMAR ABDULLAH
            Medical Parasitology Unit,
       Faculty of Medicine and Health Sciences,
              Universiti Putra Malaysia




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I. Zoological Normenclature:
Entamoeba histolytica
     (Genus), (Species)
Causative agent of the disease
 -- amebiasis
II. Epidemiology – distribution; endemic;
III. Morphology
IV. Life cycle – Environment, Human, Animals
Developmental stages in environment & human
body . Infective forms to man
V. Symptomatology
VII. Pathology
VIII. Diagnosis
IX. Treatment
X. Prevention and Control




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           Module: Medical Parasitology & Entomology

PARASITOLOGY- science that deals with organisms that seek shelter
and nourishment on or within other living organisms.
Helmintology – helminths/worms - Metazoa
ENTOMOLOGY – science that deals with
arthropods of medical importance
Protozoology – PROTOZOA – unicellular
STAGES IN LIFE CYCLE OF PROTOZOA
Infective stage – Cysts, Oocysts, Sporozoites, Spores- dormant stages and
Resistant;
Vegetative stage – Trophozoites – take nourishment
from the hosts; invasive causing pathology; most are motile.




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                                      PROTOZOA
•   According to degree of pathogenicity, protozoa can be categorized into – (I) pathogenic;
    (2) Non-pathogenic (commensals); (3) whose pathogenicity are debatable.
• 4 types according types of organs for locomotion– Amoebae - pseudopodia; Flagellates -
    flagella; Ciliates - cilia and Sporozoa – absence of locomototion.
                                    LUMINAL PROTOZOA
- COLONIZE THE LUMINAL ORGANS- intestinal tract and the urogenital tract
- TWO STAGES – i) Trophozoite (vegetatative/invasive); ii) Cyst (infective)
• Entamoeba histolytica – AMOEBIASIS, AMEBIC DYSENTRY; AMOEBIC LIVER
    ABSCESS
Life cycle: inhabit the large intestine; the cyst is the infective stage. On ingestion – excyst
    into amoebulae – trophozoites which is the vegitative stage – invade the mucosa to
    absorb nourishment from tissues dissolved by its cytolytic enzymes and also ingest
    RBCs.




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•   Pathology and Symptomatology: primary lesion is ULCER - invasion of the wall of
    large intestine – ulcer is flask shaped. Complications – amoebic granuloma (amoeboma);
    appendicitis, stricture, intestinal perforation
•   Secondary lesions occur as a result of METASTASIS of trophozoites to extraintestinal
    organs – liver is most frequently affected – Hepatic amoebiasis; pulmonary amebiasis;
    cerebral ameobiasis; cutaneous amebiasis; spleenic abscess.
•   Symptoms: : Diarrhea; dysentery – stool containing blood, mucous and shreds of
    necrotic mucosa, acute abdominal pain, tenderness and fever. Chronic ameobiasis –
    recurrent attacks of dysentery. Abdominal tenderness, HEPATOMEGALY; weight loss
    and emaciation.
•   Ulcer of large intestine        Amoebic ulceration               Amebic liver abscess




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                    GIARDIA LAMBLIA (INTESTINALIS)
•   Disease – giardiasis
•   Life cycle: trophozoites in duodenum and proximal jejunum;
    and biliary duct.. Attach to intestinal mucosa – Not invasive.
•   PATHOLOGY AND SYMPTOMATOLOGY
•   Principal lesion – atrophy and shortening of the villi- Factors are still unknown.
    Possibily the mucosal abnormalities are due to mechanical, toxicity effect – impaired
    absorption of carotene, folate and vitamin B 12. Production of disaccharidases and other
    mucosal enzymes are greatly reduced; uptake of bile salts by Giardia inhibits the
    digestion of fats by pancreatic lipase – Collectively these lead to Malabsorption
    syndrome. greasy stool clinically refer as STEATORRHEA
•   Main symptom is diarrhoea; others are abdominal distension, flatulence, bulky stool and
    weight loss.




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ISOSPORA BELLI - Isosporiasis
Man is definitive host- sexual and asexual multiplication takes place in intestinal mucosa.
Oocyst are discharged in the stool- infectious to man.
An opportunistic infection in patients with AIDS thru ingestion of sporulated oocysts.
serious disease characterize by malabsorption syndrome, wt. loss, and even fatal outcome.
Int. biopsies – shortened villi, hypertrophied crypts, lamina propria infiltrated with
eosinophils, polymorphs and round cells.
Atropy (blunting; shortening) of the villi as in in severe giardiasis


CRYPTOSPORIDIUM PARVUM
Cryptosporidiasis is often the cause of profuse watery diarrhoea in AIDS patients. Produce
disease in immunocompetent hosts as well- outbreaks of diarrhoea in veterinary workers
dealing with calves; common cause of diarrhoea among travelers and day care centers.
Sexual and asexual multiplication in the enterocytes. Oocysts are excreted in patients stool.
Clinical symptoms: Diarrhoea, nausea, vomitting, abdominal cramps and fever. Severe fluid
loss (dehydration) from diarrhoea and vomitting can lead to a fatal outcome in children.




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CYCLOSPORA CAYETANENSIS

Diarrhoeal diseases among travelers and children in slump areas. Most cases are
reported in immunodeficient patients. Bowel biopsies revealed intracellular
organisms in jejunal enterocytes. Infective form is the oocyst but detail of the life
cycle not yet known.

MICROSPORIDIA sp.

Enterocytozoan bieneusi – most common microsporidium
causing entritis in AIDS patients, an opportunistic pathogen
but can also cause disease in immunocompetent patients. A
characteristic feature of microsporidium is the spore with coiled
organelle- polar filament, which is extruded from the spore to
inject infectious material, the sporoplasm into the host cell to initiate infection.
Within an infected cell, a complex process of multiplication takes place, resulting
in the production of new spores- 1 to 4 microns in size– require electron
microscopy to examine. Excreted via feces and urine.

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•   BALANTIDIUM COLI
•   Largest protozoa and only pathogenic ciliate of man. Causing balantidiasis, balantidial
    dysentery.

•   Lives in the lumen, mucosa and submucosa of the large intestine. Cyst is the the
    infective form. Trophozoites invade and multiply in the intestinal wall but do not
    metastasis therefore no extraintestinal complication. Form nests and necrotic ulcers of
    the large intestine (bigger than the ulcer of E.h). In acute infection, bowel movement is 6
    to 15 times of liquid stools per day, with mucus, blood and pus.

•   Chronic disease- intermittent diarrhoea alternating with constipation, tender colon,
    anemia and cachexia. Most infections are asymptomatic.

•   .




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BLASTOCYSTIS HOMINIS
Lack cell wall, strictly anaerobic and have a variety of
morphologic forms. Sometimes B. h is found in large numbers
in fecal specimen of patients with diarrhoea especially in AIDS
patients. No morphologic or physiologic evidence of pathology
can be attributed to this organism; Bh has been associated
with Irritable Bowel Syndrome (IBS)

DIENTAMOEBA FAGILIS
Amoeboflagellate of the intestinal tract that is found only as
trophozoite (No cyst). Has two nuclei; resembles trichomonads
antigenically and ultrastructurally. Sometimes may ingest
RBCs and produces a moderate, persistent diarrhoea and other
 gastrointestinal symptoms.




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         DIAGNOSIS OF INTESTINAL INFECTIONS WITH PROTOZOA

Clinical dx is based on history of travel to or residence from an endemic area with
GIT signs.
Parasitological diagnosis- microscopy identification of parasite in feces;
Concentration technique – formalin ether; increase the chance of detection
especially in very light infection
sigmoidoscope useful in obtaining materials from the
intestine microscopy.
Intestinal biopsy - Demonstrating intracelluar stages in mucosa
and sub mucosa.
For Giardiasis (1) Duodenal aspiration – examine the contents;
(2) Enterotest (string test) for Giardia- weighted gelatin tied to
string- “fish” for giardia
Lab. Culture – grow the parasite in media – increase chance of
detection.
Serological tests – detection of specific antibodies to parasite
antigens; detection of parasite antigens e.g ELISA.
Hepatic amoebiasis – exploratory puncture and examine for
E.h trop.in liver abscess.

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      CONTROL AND PREVENTION OF INTESTINAL INFECTIONS WITH
                          PROTOZOA
•   In general, the prevention of intestinal protozoal infectionsis largely a problem of
    sanitation and hygiene.
•   Infections can be reduced or even eliminated in a community by:
•   (1) sanitary disposal of fecal wastes;
•   (2) the protection of susceptible individuals,
•   (3) treatment of infected individuals;
•   (4) wash hands and vegetables;
•   (5) Screened toilets and latrines from flies, cockroaches – mechanical vectors
•   Cryptosporidium – for vet., med. and lab personnel, contact with infected material must
    be avoided by use of gloves, gowns and hand-washings. Instruments and equipments
    should be autoclaved. Disinfect with common bleach (chlorox)




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        TREATMENT OF INTESTINAL INFECTIONS WITH PROTOZOA

•   Amoebiasis
•   Carriers should be treated with luminal amoebicide to reduce risk of
    transmission and protect patient from invasive amoebiasis –
    Diloxanide;
•   Invasive amoebiasis – systemic amoebicide – Metronidazole plus
    tetracycline in severe cases of amoebic dysentery to lessen the risk of
    superinfection, int. perforation and peritonitis. Or Chloroquine in
    combination with metronidazole.
•   Giardiasis – Tinidazole in a single dose; Albendazole- also a broad
    spectrum anthelminthic is currently the drug of choice.
•   Cryptosporidium – Spiramycine, 1 gm t.i.d for 2 weeks.




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                          TRICHOMONAS VAGINALIS
Flagelate of the lumen of the urogenital tract- vagina, urethra, epididymis and
prostate. Only trophozoite stage known to exist i. e absence of cyst stage.
Epidemiology: incidence is about 10 – 20 % in women. Higher among women
with poor feminine hygiene. One seventh of female patients complaint of
symptoms; but detection rate in their husbands are low.
Mode of transmission: sexual contact, direct contact with infected female,
contaminated toilet articles eg towels, toilet seats and infection acquired in babies
while passing the birth canal at birth.




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Pathology and Symptoms:
Bacterial flora, physiological status of the vagina eg pH are some of the
determining factors.
Causing persistent vaginitis, complain of itching and burning sensation; vaginal
wall is injected, tender, hyperemia, petechial haemorrhage and some areas become
granular – strawberry vagina. The surface is covered with frothy, seropurulent,
creamy or yellowish discharge – leucorrhoea. In males, there may be urethritis
and protato vesiculitis.




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Diagnosis: 1. Clinically, symptoms of burning sensation, frothing discharge,
punctate lesions of the vagina; 2. Parasitological-microscopic examination of
motile trichomonads in fresh vaginal discharge and prostate secretion;
3. Laboratory culture- allowing the trichomonads to multiply in numbers and
increase chance of detection.
Treatment:
1.Metronidazole (Flagyl) (note: carcinogenic and mutagenic)
2. Insufflation (powder) or suppositories (pills)
i) silver picrate; ii) furazolidone, iii) iodochlorhydroxyquin
3. Vinegar douches: 1 ounce vineger in a quart of water- trichomonads does
        poorly at pH below 5.




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posted:11/9/2011
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