PROF. DR. HJ. WAN OMAR ABDULLAH

1

1. 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

2

• 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

3
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.

4
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.

5

• 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

6
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.

7

• 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.
• 
  

8

• 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.

9

• 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.
• .

10

• 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.

11
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.

12
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)

13
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.
• 
  

14
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.

15

• 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.

16

• 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.