[ MODES OF TRANSMISSION ] [ TERMS RELATED TO PARASITOLOGY ]

 Oral – most common, contaminated food & water (most common source  Epidemiology: the study of patterns, distribution, and occurrence of
of infection) disease
 Examples  Incidence
 Taenia solium, Taenia saginata, and Dibothriocephalus latus  Prevalence
(formerly Diphyllobothrium latum)  Intensity of Infection/Worm Burden: refers to burden of infection
 Entamoeba histolytica and Giardia duodenalis (G. lambia) which is related to the number of worms per infected person
 Clonorchis, Opistorchis, and Haplorchis  Morbidity
 Skin penetration  Mortality
 Hookworms, Strongyloides: Filariform larvae (IS)  Deworming: the use of anthelminthic drugs in an individual or a public
 Schistosoma sp. enter skin via water: Cercariae (IS) health program

 Arthropod bites (Vector-borne) ֍ Disease Eradication: defined as a permanent reduction to zero of the
 Mosquito worldwide incidence of infection caused by a specific agent, as a result
o Malaria of deliberate efforts
o Filariasis ֍ Disease elimination: a reduction to zero of the incidence of a specified
 Fly disease in a defined geographic area as a result of deliberate efforts
o Leishmaniasis
o African
trypanosomiasis
 Sporadic: a disease that occurs infrequently and irregularly.
o Onchocercosis  Endemic: refers to constant presence and/or prevalence of a disease or
o Loiasis an infectious agent in the population within a geographic area.
 Tick  Epidemic: refers to an increase, often sudden, in the number of cases
o Babesiosis of a disease often above what is normally expected in that population
 Bug (Reduviid) in that area
o Chagas’ Disease  Pandemic: refers to an epidemic that has spread over several countries
or continents
 Congenital Transmission
o Toxoplasma gondii
 Transmammary
o Ancylostoma and Strongyloides

 Enterobius vermicularis: inhalation of airborne eggs

 Trichomonas vaginalis: sexual intercourse
[ EFFECTS OF PARASITES ON HOSTS ] [ PARASITE EVASION MECHANISM ]
Mechanisms by which parasites cause injury: Resistance to Infection
 Creation of enzymes  Permits survival of parasites upon entering blood and tissues
 Invasion and destruction of host tissue  Cuticle and integument > resist macrophage
 Depriving the host of essential nutrients and substances Immune Suppression
 Parasites can reduce immune function of macrophages > lower
[ EFFECTS OF HOST ON THE PARASITES ] action of macrophages and defective processing of antigen
Several Factors that affect outcome of Infection in the host Antigenic Variation
 Genetic make-up of the host  Trypanosoma brucei infection:
 Nutritional Status of the host  variant surface glycoproteins (VSG)
 Immunity of the host  Plasmodium: antigenic diversity

[ IMMUNOLOGY OF PARASITIC INFECTIONS ] Host Mimicry

Possible outcomes of parasite to host interactions:
1. Parasite fails to become established in the host.
2. Parasite becomes established and the host eliminates the infection.
3. Parasite becomes established, and the host begins to overcome the
infection but is not totally successful.
4. Parasite becomes established and the host, in trying to eliminate the
organism, becomes damaged itself.
5. Parasite becomes established and kills the host.
 Echinococcus granulosus larval stages carry P blood group antigens
 Schistosoma sp. Can acquire antigenic molecules from host
 Body could not differentiate self from non-self
Intracellular Sequestration
 Intracellular parasites: Leishmania, Plasmodium

[ HOST PARASITE INTERACTIONS ]

Physical barriers (1st line of defense against pathogens)
 Skin
 Mucous membranes
 Components of body fluids
 Physiologic functions of the body

[ HOST IMMUNE RESPONSE ]

Innate immune response
 body detects and eliminates pathogens through non-specific
mechanisms [ ADVERSE EFFECTS OF IMMUNE RESPONSE ON THE HOST ]
 Ex. Phagocytosis by macrophage and dendritic cells  Dysfunction of any of the host defense systems can result in damage
Acquired immune response to host tissue and produce clinical disease:
 host exposed to the parasite antigens > stimulate an immune  Types of Reaction:
response 1. Type 1 (Immediate type hypersensitivity)
 T and B Cells 2. Type 2 (Immune complex formation)
3. Type 3 (Cytotoxic reactions of antibody)
4. Type 4 (Delayed-type hypersensitivity).
[ TAXONOMY OF MEDICALLY IMPORTANT PARASITES ] [ OVERVIEW OF PARASITE CLASSIFICATION ]
 Protozoans – unicellular eukaryotic organisms
o Phylum Sarcomastigophora
 Ameba, Atrial Flagellates and Hemoflagellates
o Phylum Ciliophora
 Ciliates
o Phylum Apicomplexa
 Plasmodium, Babesia, Intestinal Coccidians, Tissue
Coccidians
o Microspora – now under Fungi
o Helminthes – “worms”; metazoan parasites
 Nematodes (Roundworms)
 Cestodes (Tapeworms)
 Trematodes (Flukes)

[ PROTOZOANS ]

[ SARCODINA ]
 Pathogenic: Entamoeba histolytica
 Commensals:
 E. dispar
 E. moshkovskii
 E. hartmanni
 E. coli
[ OVERVIEW OF PARASITE CLASSIFICATION ]  Endolimax nana
 Iodamoeba butschlii

[ Entamoeba histolytica ]
 Most invasive of the Entamoeba parasites
 Only member to cause colitis and liver abscess
Classification:
o Subphylum Sarcodina
o Superclass Rhizopoda
o Class Lobosea
o Order Amoebida
o Family Entamoebidae
o Genus Entamoeba
- Pseudopod-forming non-flagellated protozoan parasite.
 [ Entamoeba histolytica ]

-Eukaryotic organism but has several unusual features, including the lack of
organelles that morphologically resemble mitochondria.
o Nuclear-encoded mitochondrial genes such as pyridine nucleotide
transhydrogenase and hsp60 are present, E. histolytica, at one time
may have contained mitochondria.
o No rough endoplasmic reticulum or Golgi apparatus.
o Cell surface and secreted proteins contain signal sequences.
o Tunicamycin inhibits protein glycosylation.
o Ribosomes form aggregated crystalline arrays in the cytoplasm of the
trophozoite.
o Some differences in biochemical pathways from higher eukaryotes:
 Lack of glutathione metabolism.
 Use of pyrophosphate instead of ATP at several steps in
glycolysis.
 Inability to synthesize purine nucleotides de novo.
o Glucose is actively transported into the cytoplasm, where the end
No host other than humans is implicated in the life cycle, although natural products of carbohydrate metabolism are ethanol, carbon dioxide,
infection of primates has been reported. and under aerobic conditions, acetate.
o Infection occurs when cysts are ingested from fecally- contaminated
material. Trophozoite
o Other modes of transmission: ▪ Highly motile.
 Venereal transmission through fecal-oral contact. ▪ Possess pseudopodia.
 Direct colonic inoculation through contaminated enema • Hyaline.
equipment. • Formed when the clear, glasslike ectoplasm
- Excystation is extruded and the granular endoplasm flows
 Occurs in the small or large bowel. into it.
 Cyst undergoes nuclear followed by cytoplasmic division to
form eight trophozoites
▪ From 12 to 60 μm in diameter (about 20 μm in average). Life cycle consists of two stages:
▪ Ingested red blood cells are observed as pale, greenish, refractile bodies ▪ Infective Cyst
in the cytoplasm of the ameba. ▪ Invasive Trophozoite Form
▪ Microscopic examination of fully passed stool specimens reveals the
characteristic progressive and directional movement of trophozoites with [ PATHOGENESIS ]
pseudopodia as locomotory organelles. Mechanisms for virulence:
▪ Ability to colonize and/or invade the large bowel.  production of enzymes or other cytotoxic substances
▪ Multiply by binary fission.  contact-dependent cell killing
▪ Encyst producing uninucleate cysts which then undergo two successive  cytophagocytosis
nuclear divisions to form the characteristic quadrinucleate cysts.
o In vitro, amebic killing of target cultivated mammalian cells involve:
Cyst ▪ Receptor-mediated adherence of ameba to target cells.
▪ Quadrinucleated. ▪ Amebic cytolysis of target cells.
▪ Usually spherical. ▪ Amebic phagocytosis of killed or viable target cells.
▪ From 10 to 20 μm. o Trophozoites adhere to the colonic mucosa through a galactose-
▪ Highly refractile hyaline cyst wall. inhibitable adherence lectin (Gal lectin).
▪ One to four nuclei. o Amebae kill mucosal cells by activation of their caspase-3, leading to
▪ Rod-shaped/cigar-shaped chromatoidal bars. their apoptotic death engulfment.
▪ Resistant to gastric acidity and desiccation. o Susceptibility of humans to E. histolytica infection is associated with
▪ Can survive in a moist environment for several weeks. specific alleles of the HLA complex.
[ PATHOGENESIS ]
Cases may manifest as:
1. Asymptomatic
2. Amebic Colitis
3. Ameboma
4. Amebic Liver Abscess
1. Present as asymptomatic infections with cysts being passed out in the stools (cyst carrier state).

[ AMEBIC COLITIS ]
 abdominal pain + diarrhea +/- blood & mucus in the stools
 Children may develop fulminant colitis (severe bloody diarrhea + fever
+ ab pain)
▪ Most serious complication:
• Perforation
• Secondary Bacterial Peritonitis
▪ Acute amebic colitis should be differentiated from bacillary dysentery of the
following etiology:
• Shigella
• Salmonella
• Campylobacter
• Yersinia
• Enteroinvasive Escherichia coli
[ AMEBOMA ]  E. dispar and E. moshkovskii
 A mass-like lesion with abdominal pain and a history of dysentery  Morphologically similar to E. histolytica
 Can be mistaken as a carcinoma  Non-pathogenic
 May be asymptomatic E. moshkovskii (previously known as the Laredo strain).
[ AMEBIC LIVER ABSCESS ] o Differentiated through:
▪ Isoenzyme analysis polymerase chain reaction (PCR).
 most common extra-intestinal form of amebiasis
▪ Restriction fragment length polymorphism (RFLP)
 Usually presents with fever and right upper quadrant pain ▪ Typing with monoclonal antibodies.
▪ Differential diagnoses of ALA:
 Entamoeba coli
• Pyogenic liver abscess.
• Tuberculosis of the liver. • Cosmopolitan in distribution.
• Hepatic carcinoma. • More common than other human amebae.
[ DIAGNOSIS ] • Cyst may be differentiated from E. histolytica by:
 DFS o Larger size (10 to 35 μm in
 Concentration techniques (FECT) diameter).
 PCR o More nuclei (eight).
o More granular cytoplasm.
 Serological tests (ELISA): for ALA
o Splinter-like chromatoidal bodies.
 Ultrasound, CT scan, MRI • Trophozoites measure 15 to 50 μm in diameter.
[ TREATMENT ] • Differentiated from E. histolytica trophozoite by the following
 Metronidazole features:
 Diloxanide furoate o More vacuolated or granular endoplasm with bacteria and debris
Metronidazole: drug of choice for the treatment of invasive amebiasis. but no red blood cells.
Diloxanide furoate o Narrower, less-differentiated ectoplasm.
▪ Drug of choice for asymptomatic cyst passers. o Broader and blunter pseudopodia used more for feeding than
▪ Given after a course of metronidazole for invasive amebiasis. locomotion.
o More sluggish, undirected movements.
[ EPIDEMIOLOGY ] o Thicker, irregular peripheral chromatin with a large, eccentric
karyosome in the nucleus.
 Amebiasis: 1-5% worldwide
 3rd most important parasite (malaria, schistosomiasis)
Amebiasis
 Entamoeba hartmanni
▪ Second to malaria as the top cause of mortality
• Appearance is relatively similar to E. histolytica
among parasitic protozoans. apart from its smaller size.
[ PREVENTION AND CONTROL ] • Mature cysts
o Measure 4 to 10 μm.
 Proper sanitation
o Quadrinucleated.
 Safe water supply o Have rod-shaped
 Good personal hygiene chromatoid material with
 Proper food preparation rounded or squared ends.
 Vaccines • Does not ingest red blood
Candidate vaccine molecules: cells.
▪ Serine-rich E. histolytica protein (SREHP).
▪ Adherence lectin (Gal/GalNAc lectin).
▪ 29 kDa cysteine-rich amebic antigen.
  Iodamoeba butschlii
 Ameba of swine (pigs)
• Trophozoites  Prominent Feature:
measure from 3 to – Uninucleated with a large eccentric karyosome; with achromatic
12 μm in granules
diameter.
 “Basket of Flowers”
– Large Glycogen Vacuole
• Trophozoite averages 9 to 14 μm in diameter (ranging from 4-20 μm).
• Large, vesicular nucleus with a large, *central karyosome, surrounded by
achromatic granules.
 Entamoeba polecki • No peripheral chromatin granules on the nuclear membrane.
• Cyst
• Found in the intestines of pigs and o About 9 to 10 μm in diameter (ranging from 6-16 μm).
o Uninucleated.
monkeys.
o Has a large glycogen body which stains dark brown with iodine.
• Rarely infects humans.

• Motility of trophozoites is sluggish.

• Small karyosome is centrally located in the
nucleus.
• Cyst is consistently uninucleated.
• Chromatoidal bars are frequently angular
or pointed.
• In stained fecal smears, the nuclear
membrane and karyosome are very  Entamoeba gingivalis
prominent.
 Endolimax nana
• Occurs with the same frequency as Entamoeba coli.
• Trophozoites
o Small.
o Diameter of 5 to 12 μm.
o Exhibit sluggish movement.
o Blunt, hyaline pseudopodia.
o Nucleus has a large, irregular karyosome.
o Food vacuoles found in the cytoplasm may
contain bacteria.
▪ Cysts
o Measure about the same size as trophozoites.
o Quadrinucleated when mature. • Found in the mouth.
• Lives on the surface of gum and teeth, in gum pockets, and sometimes in the
Blot like karyosome tonsillar crypts.
• Abundant in cases of oral disease.
• No cyst stage.
• Transmission is most probably direct: through kissing, droplet spray, or by
sharing utensils.
 • Trophozoite measures 10 to 20 μm.
o Moves quickly.
o Has numerous blunt pseudopodia.
o Food vacuoles that contain cellular
debris (mostly leukocytes) and bacteria are
numerous.

[ FREE LIVING PATHOGENIC AMEBAE ]

 Found Inhabiting Lakes, Pools, Tap Water, Air Conditioning Units and
Heating Units
 Acanthamoeba
 Balamuthia
 Naegleria

 Naegleria fowleri
 Important Stages
 Cyst
 Trophozoite

Naegleria fowleri
▪ Only the one reported to cause disease in humans.
▪ Three stages:
• Feeding trophozoite stage.
o Two forms of Naegleria fowleri trophozoites:
▪ Ameboid Trophozoite
• Size: 10 to 35 μm or 10 to 15 μm when
rounded, may get up to 40 μm in culture.
• Cytoplasm: granular and contains
many vacuoles.
• Nucleus: single and large.
 Entry into the body: Olfactory Epithelium, Respiratory Tract, Skin and
• Structures: Sinuses
o Dense karyosome. o Multiple mechanisms involve in the cytopathology of the host-tissues including:
o Lacks peripheral chromatin. ▪ Lytic enzymes secretion.
▪ Ameboflagellate ▪ Membrane pore-forming proteins.
• Dormant cyst stage. ▪ Factors that induce secretion.
o Dormant cyst form is produced when conditions are not ▪ Direct feeding on cells by the amebae.
favorable. o PAM presents as:
• Transitional flagellate stage. ▪ Fever
o Thermophilic organisms thriving best in hot springs and ▪ Nausea
warm aquatic environment. ▪ Headache
▪ Nuchal rigidity
▪ Mental status changes
▪ Rapid progression to coma and death
  Treatment and Prevention
 Amphotericin B with Clotrimazole
o Amphotericin B and Clotrimazole: successfully used to treat PAM.
o Azithromycin and Voriconazole: active against N. fowleri.

 Acanthamoeba spp.
 Free-living Ameba
 Morphologic Forms:
 Cyst
 Trophozoite
o Ubiquitous, free-living ameba.
o Reported as possible reservoir hosts for medically important
 Disease Manifestation and Pathology bacteria such as Legionella spp., mycobacteria, and gram-negative
 Primary Amebic Meningoencephalitis bacilli such as E. coli.
o Survives even in contact lens cleaning solutions.
o CSF findings:
- Acanthamoeba was first described in 1974 as an
▪ Elevated WBC with neutrophilic predominance. opportunistic ocular surface pathogen causing keratitis.
▪ High protein. o No flagellated stage.
▪ Low glucose.
o Postmortem examination:
▪ Hemorrhagic necrosis.
▪ Inflamed and congested leptomeninges.

o Microscopic examination:
fibrinopurulent exudate
o Death: result of cerebral or
cerebellar herniation

 Diagnosis
 Wet Mount Examination of CSF
 Smears stained with Wright’s or Giemsa
 Biopsy
 CSF Analysis
 Culture
 Molecular Methods
N. fowleri is identified through the presence of blunt, lobose pseudopodia and
directional motility. o Entry can occur through the eye, the nasal passages to the lower respiratory tract, or
ulcerated or broken skin.
 Acanthamoeba ▪ Known species that have caused AK are:
 Cyst • A. castellani
• A. culbertsoni
• A. hutchetti
o Cyst stage: highly resilient which
• A. polyphaga
transforms when environmental
• A. rhysoides
conditions are not favorable
▪ Associated with the use of improperly disinfected soft contact lenses.
▪ Symptoms include severe ocular pain and blurring of vision.
▪ Progression of infection may cause scleritis and irititis, and may lead to vision loss.
 Diagnosis
 Trophozoite  Usually diagnosed after death (GAE)
▪ Characteristic prominent “thornlike”  Biopsy
appendages called acanthopodia.
 Corneal Scrapings
▪ Characteristic single large nucleus
with a centrally located, densely  Culture
staining nucleolus.  Molecular Methods
▪ Large endosome.  Treatment
▪ Finely granulated cytoplasm.  Very fatal once cerebral manifestations appear
▪ Large contractile vacuole.  Fluorocystine, ketoconazole, amphotericin B
▪ Replicate by mitosis.
▪ Infective stage.
o Acanthamoeba Keratitis
▪ Surgical excision of the infected cornea with subsequent corneal
 Disease Manifestation and Pathogenesis transplantation.
 Causes Granulomatous Amebic Encephalitis ▪ Clotrimazole combined with pentamidine, isethionate, and Neosporin.
 Chronic; slow in progression ▪ Other agents used: • Polyhexamethylene biguanide • Propamidine •
▪ Systemic manifestations: Dibromopromadine isethionate • Neomycin • Paromomycin • Polymyxin B •
• Fever Ketoconazole • Miconazole • Itraconazole.
• Malaise ▪ Topical corticosteroids should be avoided.
• Anorexia ▪ Deep lamellar keratectomy is the procedure of choice.
▪ Neurologic symptoms: o Granulomatous Amoebic Encephalitis
• Increased sleeping time ▪ Combinations of Amphotericin B, pentamidine isethionate, sulfadiazine,
• Severe headache flucytosine, fluconazole, or itraconazole.
• mental status changes
• epilepsy • Coma
▪ Likely route of invasion is hematogenous. [ CILIATES ]
▪ Incubation from initial inoculation is approximately 10 days. Balantidium Coli
▪ Clinical manifestations: • largest protozoan parasite affecting humans (the only ciliate th at causes
• Decreased sensorium
human disease –attacks intestinal epithelium causing bloody diarrhea like
• Altered mental status
• Meningitis the amebic dysentery)
• Neurologic deficits • normal host: pigs (primary host), man
▪ Natural course of disease eventually results in coma and death. • mot: ingestion of cysts
• habitat: colon (cecum)
 Disease Manifestation
• reproduction-asexual through asymmetric binary fission
 Amebic Keratitis
Acanthamoeba

• cyst: cilia within a cyst wall, micronucleus, macronucleus
• trophozoite: motile stage
• cytostome-mouth
• cilia-confers thrown ball motility (rolling motion)
• macronucleus-kidney/bean-shaped)
• micronucleus-lies in the concavity of themacronucleus
• cytopyge-anus
• contractile vacuole-osmoregulatory organelle-maintains osmotic
pressure of the parasites fuids
Pathogenesis
• attacks intestinal epithelium
• ulcers: rounded base and wide neck (in contrast to the flask-shaped,
narrow necked ulcers of amebiasis)
• ulcerations are due to hyaluronidase (lytic enzyme secreted by the
trophozoite)
Balantidiasis has 3 forms of clinical manifestations:
• asymptomatic
 asymptomatic carriers are those who do not present with
diarrhea or dysentery, but may serve as parasite reservoir in the
community
• fulminant balantidiasis/balantidial dysentery
 “balantidial dysentery” - diarrhea with bloody and mucoid stools,
which is sometimes indistinguishable from amebic dysentery
 acute cases may have 6 to 15 episodes of diarrhea per day
accompanied by abdominal pain, nausea, and vomiting.
 often associated with immunocompromised and malnourished
states
• chronic form
 diarrhea may alternate with constipation, and may be
accompanied by nonspecific symptoms such as abdominal pain
or cramping, anemia, and cachexia
Note:
• B. Coli can spread to extraintestinal sites including the mesenteric
nodes, appendix, liver, genitourinary sites, pleura, and lungs.
• cases of mortality related to balantidiasis - associated with intestinal
hemorrhage and shock, intestinal perforation, or sepsis
Diagnosis
• DFS
• Concentration Techniques
• Biopsy
• Bronchoalveolar Washings (In Case of Pulmonary Infections)
Note:
• repeated stool examinations may be done to increase sensitivity.
Treatment
• tetracycline or metronidazole
• alternative treatment: doxycycline and nitazoxanide
Epidemiology
Prevalent In:
• areas with poor sanitation
• abbatoir, farms (close contact w/ pigs)
• overcrowded institution
• warm/humid climates
Prevention and Control
• proper sanitation
• safe water supply
• good personal hygiene
• proper food preparation
• cysts are easily inactivated by heat and 1% sodium hypochlorite
Flagellates
Subphylum Mastigophora
Class Zoomastigophora
• Intestinal and Urogenital Flagellates
• Hemoflagellates
• habitat: duodenum and jejunum
Intestinal/Urogenital Flagellates
• excystation occurs in duodenum
Generalities
G. Lamblia Cyst G. Lamblia Trophozoite
• all inhabit the large intestine except Giardia Lamblia, Trichomonas
Vaginalis, Trichomonas Tenax
• all undergo encystation except Trichomonas species
• all are commensals except Giardia Lamblia, Dientamoeba Fragilis
And Trichomonas Vaginalis

Giardia Duodenalis
• Other names: G. Intestinalis, G, Lamblia, Cercomonas Intestinalis
• MOT: ingestion of infective cysts
• causative agent of Giardiasis, Traveller’s Diarrhea, Backpacker’s
Diarrhea, Beaver Fever
Pathogenesis Epidemiology
• parasite attaches to the intestinal cells via an adhesive sucking disc • Prevalent worldwide
located on its ventral side • Areas with poor sanitation and poor hygiene
• once attached, the parasites cause villous flattening and crypt • Direct oral-anal sexual contact among MSM increase the risk
hypertrophy
Prevention and Control
• half of the patients may be asymptomatic
• Proper or sanitary disposal of human excreta
• acute cases: excessive flatus with rotten egg (due to hydrogen
• Normal water chlorination will not affect cysts, but usual water
sulfide) odor, diarrhea, malaise, abdominal pains, anorexia
treatment modalities should be adequate.
• chronic cases: steatorrhea, weight loss, profound malaise, low-grade
fever Dientamoeba fragilis
• Originally described as ameba
Diagnosis
• Trophozoite and Cyst (newly discovered)
• DFS
• Concentrations techniques: cysts • 1 or 2 nuclei (rosette-shaped)
• Nuclear membrane has no peripheral
• Duodenal-jejunal aspiration
• Enterotest - may demonstrate Giardia trophozoites; the patient chromatin
• Karyosome: 4-6 discrete granules
swallows a gelatin capsule attached to a nylon string, with one end
of the string attached to the patient’s cheek; after about 4 to 6 hours,
the string is removed, and any adherent fluid is placed on the slide • MOT: fecal-oral route or via transmission of helminth eggs (observed
for microscopic examination in the lumen of Enterobius adults and eggs present in the intestines)
• lives in the mucosal crypts of the appendix, cecum and the upper
• Antigen detection test - detect the presence of Giardia antigen in
stool; cyst wall protein 1 (CWP1) is one of the antigens used for these colon
diagnostic tests
• Direct fluorescent Ab test - have been considered by many
laboratories as the gold standard in diagnosis as such assays have the
highest combination of sensitivity and specificity

Treatment
• Metronidazole
• Alternative drugs : tinidazole, furazolidone, albendazole

Note: Although not available in the Philippines, nitazoxanide has been used
effectively in drug-resistant cases.
Pathogenesis • exists only in the trophozoite stage
• Usually asymptomatic • has a pyriform shape with four free anterior flagella that appear to
• In symptomatic individuals, the onset of infection is usually arise from a simple stalk, and a fifth flagellum embedded in the
accompanied by loss of appetite, colicky abdominal pain, and undulating membrane (membrane extends to about half the
intermittent diarrhea with excess mucus, abdominal tenderness, a organism’s length)
bloating sensation, and flatulence • has a median axostyle and a single nucleus
Note:
• does not invade tissues, but its presence in the intestines produces
irritation of the mucosa with secretion of excess mucus and
hypermotility of the bowel
• Chronic infection of this organism can mimic the symptoms of
diarrhea-predominant irritable bowel syndrome (IBS).
Treatment
• Iodoquinol
• Tetracycline and metronidazole

Diagnosis
• DFS (observation of binucleate trophozoites)
• Not detected by concentration techniques
• Prompt fixation of fresh stool w/ PVA fixative or Schaudinn’s fixative
has been helpful.
Trichomonas vaginalis
• Causes trichomoniasis
• Habitat: urogenital area
• MOT: intimate contact; infant delivery; contaminated towels and
underwear
Pathogenesis
• Common symptoms: vaginal discharge (green/yellow color), vulvitis,
dysuria, postpartum endometritis, strawberry cervix (2% of the
cases)
• Males: asymptomatic, some cases: urethritis, prostatitis

Note:
• vaginal secretions are very irritating and may cause intense itchiness
and burning sensation
Strawberry cervix Prevention and Control
• Reduce the risk of exposure
• Proper use of protective devices such as condoms and spermicidal
foams
• Simultaneous treatment of infected sexual partners - to prevent
“pingpong” or recurrent infections

Note:
• Prompt follow-up of patients and their contacts, as well as health and
sex education about venereal disease are also important.

Diagnosis NON-PATHOGENIC FLAGELLATES

• Saline preparation of vaginal fluid - quickest and most inexpensive • Pentatrichomonas (Trichomonas) hominis
way but the sensitivity of this technique is low at 60 to 70% • Trichomonas tenax
• Culture: gold standard (takes 2 to 5 days) • Chilomastix mesnili
• Pap’s smear (unstained wet drop preparations may be fixed and Trichomonas hominis
stained by Giemsa, Papanicolau, Romanowsky, and acridine orange
stains)
• Ag detection test
• PCR

Note:
• Trichomonas can also be cultured using Diamond’s modified medium,
and Feinberg and Whittington culture medium.

Treatment
• Metronidazole
• Tinidazole

Note:
• In pregnancy, metronidazole remains the drug of choice for • Transmission occurs rapidly through fecal contamination of food and
trichomoniasis. drinks
• habitat is the cecal area of the large intestine of human and other
Epidemiology primates
• Occurs worldwide • noninvasive
• High prevalence is associated with greater sexual activity with • trophozoites pass out with diarrheic stools
multiple partners
 • has five anterior flagella and a • characteristic boring and spiral forward movement is made possible by the
posterior flagellum projecting three anterior free flagella and a more delicate one within the prominent
from an undulating membrane cytostome
• cytostome and the nucleus are Chilomastix mesnili – cyst
situated at the anterior end
• an axostyle extends from anterior
to posterior along the mid-axis

Trichomonas tenax
• pyriform flagellate which has been observed only in the trophozoite stage
• smaller and more slender than T. vaginalis
• has four free equal flagella and a fifth one on the margin of an undulating
membrane which does not reach the posterior end of the body, and lacks a
• cyst is pear- or lemon-shaped
free posterior extension
• broadlyrounded at one end and somewhat bluntly conical at the other end
• has a single nucleus and a cytostome
which has a knob-like protruberance that is visible occasionally
• multiplies by binary fission and thrives on the microorganisms found in its
• hematoxylin and eosin stained films clearly demonstrate the single large
environment
vestibular nucleus and the cytostome, which is almost as long as the
• exposure results from droplet spray from the mouth, kissing, or common
encysted organism
use of contaminated dishes and drinking glasses
• good preparations reveal a fibril on either side of the cytostome
• pulmonary trichomoniasis has been reported among those with underlying
chronic pulmonary disease, entering the lungs most probably by aspiration
Chilomastix mesnili
• inhabits the cecal region of the large intestine

• has well-defined trophic and cystic stages

• trophozoite is asymmetrically pear-shaped as a result of a spiral groove
extending through the middle half of the body
 • non-pathogenic, but if present in sufficient numbers cause diarrhea; • All forms are found in Trypanosoma cruzi infections
intestinal problems • Only the epimastigote and trypomastigote are seen in Trypanosoma
• transmission occurs through ingestion of cysts in food and drinks brucei infections
• harmless commensal diagnosed by microscopic examination of feces • Only the amastigote and promastigote are seen in Leishmania
and demonstration of either trophozoites or cysts infections
• no treatment is indicated • Diagnostic Stages (found in humans) include amastigote and or
• preventive and control measures include improved sanitation and trypomastigote
personal hygiene
Trypanosoma cruzi
BLOOD AND TISSUE FLAGELLATES • Causative agent of Chagas disease or American trypanosomiasis
• Flagellates that are found in the blood and other fluids (CSF) and in • Habitat: RES, cardiac muscle, CNS
tissues • Intermediate host Vector: Reduviid Bug, (kissing bug)
• Vector borne parasites • MOT: Feces of vector entering bite wound; blood transfusion, organ
• Medically important genera transplants; transplacentally
1. Trypanosoma
2. Leishmania
GENERALITIES
• Only Trypanosoma and Leishmania infect humans
• Transmitted by a bite of an infected vector
• There are four morphological forms:
• Amastigote – (Donovan Leishman)
• Promastigote – (Leptomonas)
• Epimastigote – (Crithidia)
• Trypomastigote
 • Humans Treatment
• Trypomastigotes: bloodstream Acute Phase
• Amastigotes: tissue cells • Nifurtimox
• Benznidazole
Chronic Phase – symptom specific management
• Pacemakers
• Antiarrhythmic drugs (amiodarone)
• Megasyndromes are managed w/ special diets, laxatives, surgery

Epidemiology
• Most cases : Latin America
• Other cases reported in Mexico, USA, Canada, France, Switzerland,
Pathogenesis Japan, and Australia
• Acute phase Prevention and Control
• Non specific S/S: fever, malaise, nausea, • Vector control
vomiting,lymphadenopathy, cutaneous inflammation • Blood transfusion regulations
• Chagomas • No vaccines available
• Romaña’s sign
• Chronic phase Trypanosoma brucei complex
• Enlargement of vital organs (myocardium, megaesophagus) • Etiologic Agents of African Sleeping Sickness

Diagnosis o Trypanosoma brucei rhodesiense

Acute Phase  Causes Rhodesian or East African Sleeping Sickness
• Thick and thin blood smear using Giemsa  Endemic in East and South Africa
• CSF, tissue samples, lymph examination o Trypanosoma brucei gambiense
• Concentration methods  Causes Gambian or West African Sleeping Sickness
• Blood culture  Endemic in West and Central Africa
• PCR o Trypanosoma brucei brucei
• Xenodiagnosis  affects wild and domestic animals
Chronic Phase
• ELISA • Vector: Tsetse fly (Glossina sp.)
• Indirect hemagglutination • Only epimastigote and trypomastigote are exhibited
• Indirect immunofluorescence
• PCR
 • IFA
• Indirect hemagglutination
• Mini-anion exchange centrifugation technique
• PCR
• CATT

Treatment
• Intravenous suramin solution: first stage of the disease
• Intravenous melarsoprol: if w/ CNS involvement

Prevention and Control

• Vector control
• Protective clothing
• Regulation and treatment of reservoir host (cattle and game
animals)

Leishmania spp.
Pathogenesis • Divided into:
• Initial lesion: local, painful, pruritic, erythematous chancre • Old World: L. tropica, L. aethiopica, L. major
• Early HAT • New World: L. mexicana, L. amazonensis, L.
• Hemolymphatic stage guyanensis, L. braziliensis, L. chagasi
• Fever, joint and muscle pain, malaise • Vector-borne
• Winterbottom’s sign • Old World: Phlebotomus sandfly
• Late HAT • New World: Lutzomyia
• Meningoencephalitic stage • Obligate intracellular parasite
• Neurologic symptoms • Primarily a zoonotic disease
• Convulsions, tremors, speech and reflexes defects, paralysis • MOT: congenitally, blood transfusion,contamination of bite
• Kerandal’s sign wounds, direct contact with contaminated specimens
• Death
Pathogenesis
Diagnosis 4 categories
• Demonstration of trypomastigote in chancre, lymph node aspirate, • Cutaneous Leishmaniasis (CL)
CSF • Diffuse Cutaneous Leishmaniasis (DCL)
• Thick and thin blood smear (Giemsa) • Mucocutaneous Leishmaniasis (MCL)
• Buffy coat concentration • Visceral Leishmaniasis (VL)
• ELISA
Cutaneous leishmaniasis • Immunologic assays
o ELISA
o rk39 Ag test (for VL)
o Direct agglutination
o Urine Ag test
o Flow cytometry
o PCR
o RFLP analysis

Treatment
• Antimony compounds: IM or IV for up to 4 weeks; primary treatment

Epidemiology
• Primarily a disease of poverty
Mucocutaneous leishmaniasis • VL is an important opportunistic infection in AIDS

Prevention and Control

• Use of insect repellant (DEET & permethrin)
• Insecticide-treated clothing
• Fine-mesh bed nets
• Screens and sprays in houses
• Regulation of reservoir hosts

Visceral Leishmaniasis (VL)

• L. donovani complex (L. donovani, L. chagasi, L. infantum)
• Acute phase: may be mistaken for malaria
• Post- Kala-azar dermal leishmaniasis: cutaneous eruption resulting in
hypopigmented macules, malar erythema, nodules, and ulcerations

Diagnosis
• Microscopic demo of Leishmania form lesions and tissue scrapings,
aspirates, and biopsy
• Culture: NNN medium, Schneider’s medium
• Animal inoculation (hamster)
• Montenegro skin test