PARASITOLOGY NOTES-MEDTECH EDITION PDF

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Liwanag Notes ———————————————————————————-Protozoa The science of the study of the protozoa is called Protozoology. Protozoans are the first group of organized but simplest animals in the animal kingdom. They are unicellular without any tissue grade of organization but multiply asexually by binary o...

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Liwa na g Notes ———————————————————————————-! Protozoa The science of the study of the protozoa is called Protozoology. Protozoans are the first group of organized but simplest animals in the animal kingdom. They are unicellular without any tissue grade of organization but multiply asexually by binary or multiple fission, by budding, and in some cases sexual reproduction by conjugation.! They are very minute and microscopic animals. The structure of a protozoan “cell” consists of cytoplasm body and nucleus. The cytoplasm is differentiated into two parts— the outer hyaline portion, ectoplasm; function is locomotive, protective and sensory and the inner granular portion, the endoplasm, function is nutritive and reproductive. Generally the protozoans possess definite locomotory organs, such as flagella, cilia or pseudopodia. In some of them cysts are formed during extreme condition. In protozoa free living, parasitic or symbiotic nature of animals is noticed. Contractile vacuole is present in many protozoans.! Protozoan can multiply by asexual method of reproduction for a long time. They may switch on to sexual method or undergoes cystic change to its host. In parasitic protozoa both asexual and sexual reproductions occur in a different host. This process is known as alternation of generation. Amoebae, intestinal flagellates, Balantidium coli, etc. are monogenetic i.e. require one host to complete their life cycles. The parasites may adopt in a different host as well and transfer themselves passively in cystic stage. Again some parasitic protozoa like Leishmania, Trypanosoma and Plasmodia, etc. are digenetic i.e. require two hosts to complete their life cycles. In Plasmodia infection (Malaria), man is the secondary or intermediate host but mosquito is the definitive or primary host. Tsetse fly is the intermediate host and man is the definitive host in Trypanosomiasis. In Leishmaniasis sand-fly is the intermediate host and man is the definitive host. General Characteristics unicellular/single celled eukaryotic microorganism! classified under the Kingdom protista! a single cell performs all the functions: reproduction, digestion, excretion etc.! cytoplasm: Protozoa! cytoplasm: with ectoplasm & endoplasm.! • amoebas -pseudopodia ! • Ciliate-cilia! • Flagellates-flagella/undulatinf membrane! • Sporozoa-none! • microsco sporidia/microspora - none Usual developmental stages of some protozoa

non-motile form! usually found in FORMED feces! usually INFECTIVE! usually smaller than trophozoite! usually multinucleated usually resistant to damage! best demonstrated in iodine iodine nakadestroy ng trophozoite remember????

CILIATE Balantidium coli • A common parasite of pigs (occupational hazard) and a tissue invader (it can produce lesions and ulcerations sa GIT; stool may contain blood)! • Parasitize the LARGE INTESTINE and regarded as the LARGEST INTESTINAL PROTOZOA! • can develop cyst and trophozoite! • largest intestinal protozoan in man and the only pathogenic ciliate causing balantidiasis or balantidial dysentery thru ingestion of food or water contaminated with faecal material containing B. coli cyst.! • MOT: ingestion (most parasites in GIT) • infective stage: cyst! • Lab Diagnosis: ! • DFS! • Concentration techniques! • rectal biopsies Cyst

Trophozoites

Size

45 - 64 um

50 x 70 um

Shape and motility

spherical or oval with thick wall

surrounded with hair-like cilia, exhibits a directional tumbling motility

Nuclei

macro - kidney-shaped! micro - spherical

macro - kidney-shaped! micro - spherical

Cytoplasm

cytoplasm with kidney or beans haped macronucleus; contractile vacuole and cilia

equipped with cytostome and a cytopyge; with 2 contractile vacuoles

Notes

Cyst

Trophozoite

motile form! usually found in liquid/diarrheic/watery feces! usually NOT INFECTIVE usually larger than cyst! usually uninucleated usually susceptible to damage! best demonstrated using permanent stains iron hematoxylin Gomori’s trichrome

Macronucleus - vegetation! micronucleus - reproduction! Cytostome - cell mouth; ingestion! Cytopage - cell anus; waste excretion

Morphology

LPO

1.2 Asymptomatic/ Chronic Usually (-) diarrhea, GIT disturbances and constipation! Stool consistency is NORMAL (formed or soft) with bloody and mucus stool may contain cyst Lab dx 1. DFS! 2. Iodine! 3. concentration techniques (not allowed in symptomatic) Extraintestinal - E. histolytica Extraintestinal lesions are formed from the primary intestinal lesions. Most common site is the liver that is why hepatic amebiasis is the most common extraintestinal complication of amebiasis.! Hepatic/ALA - Amebic liver abscess! pulmonary! cerebral! Lab Dx: Serologic tests (sp. blood)! Moan hemagglutination test, IFAT, etc. Extraintestinal amebiasis: hepatic (most common), pulmonary, cerebral

Amoeba Species

Effect to the host

Habitat

Impt. developmental stage

Infective stage

MOT

Sp. for diagnosis

Free-living/ Facultative Acanthamoeba spp.

E. histolytica

Pathogenic

E. coli Endolimax nana Iodamoeba butschlii Entamoeba gingivalis

NONPATHOGENI C/ COMMENS AL

COLON/ LARGE INTESTINE! (ex. e. histolytica also a tissue invader!!)

Cyst & trophozoite

CYST

Trophozoite

Trophozoite

Igestion/ fecal-oral route

Stool

ubiquitous (can be isolated ANYWHERE)! can develop cyst and trophozoite and both stages are infective Cyst have outer wrinkled wall, organ for locomotion “acanthopodia” — NOT PSEUDOPODIA! Pathogenic Causes! amebic keratitis (eye infxn; soft contact lens wearer from contaminated cleaning solutions)! granulomatous amebic encephalitis (quickly fatal; detection after DEATH; Naegleria fowleri (amoeboflagellate)

Buccal cavity/ gingival tissues/ pyorrheal pockets/ tartar of teeth

Intestinal - all exc. e. histolytica 1. Symptomatic/ Acute “Amebic Dysentery”! (+) diarrhea with necrotic mucosa and abdominal pain! stool is watery, bloody, and mucus filled stool may contain trophozoite Lab dx 1. Direct Fecal Smear! 2. Exam of permanently stained fecal smear

Oral contact i.e. kissing/ common use of utensils

Oral scrapings

an AMEBOFLAGELLATE! Thermophilic! may be acquired thru diving or swimming in stagnant water! enters the body via nasa mucosa (not ingestion; intranasal instillation) pathogenic PRIMARY AMEBIC MENINGOENCEPHALITIS (PAM) can develop cyst and trophozoite (like acanthamoeba) trophozoites in 2 forms: flagellated & ameboid (lobopodia) THREE STAGES: CYST > FLAGELLATED TROPHOZOITE > AMEBOID TROPHOZOITE (ONLY STAGE THAT IS BOTH DIAGNOSTIC AND INFECTIVE)

————————————— END ————————————-

HEMOFLAGELLATES ————————————————————————-!

TRICHOMONAS SPECIES Trichomonas vaginalis

Dientamoeba fragilis Habitat: LARGE INTESTINE Developmental stages: exist only as trophozoite, NO CYST! infective stage: trophozoite Diagnostic stage: trophozoite MOT: Ingestion/ fecal-oral rougte Lab diagnosis: stool exam (DFS or concentration technique) previously an amoeba, now a flagellate

Retortamonas intestinalis & Enteromonas hominis Rare intestinal flagellates! Habitat: LARGE INTESTINE! Developmental stages: CYST & TROPHOZOITE Infective stage: CYST Diagnostic stage: Cyst & Trophozoite MOT: Ingestion/ FOR Lab diagnosis: Stool exam (DFS, concentration technique)

Trichomonas tenax

Effect to the host

Pathogenic

Habitat

GUT

Large intestine

Buccal cavity

MOT

Sexual contact

Ingestion

Oral contact

Specimen for diagnosis

Urine! Vaginal secretion or urethral discharge

stool

oral scrappings

Notes

causes Trichomoniasis - a foul smelling vaginal discharge, burning sensation and intense itchiness

Morphology of trophozoite 80% are binucleated 20% are uninucleated Size: 5-12 u! Motility: multiple hyaline leaflike! Nucleus: with fragmented karyosome (tetrakaryosome)

Trichomonas hominis

Non-pathogenic/commensal

General characteristics Exist only as trophozoite, unable to develop cyst! infective stage: trophozoite! trophozoites are pear shaped/pyriform THE LARGEST trophozoite is produced by T. vaginalis! the smallest trophozoite is produced by T. tenax! Trophozoites are motile with fast jerking tumbling motility — allows rotatory movement (ikot) Equipped with 5 flagella and undulatin Leishmaniasis

(sandflies)

Lab Diagnosis

E. hominis CYST with 4 nucleus in BINUCLEATE CONDITION (2 nucleus lying at opposite ends)

R. intestinalis CYST uninucleated, with 2 fibrils on the top of the nucleus giving it a BIRD’S BEAK FIBRILLAR APPEARANCE

Notes

In Chilomastix, fibrils are on the side! In R. intestinalis, fibrils are on the top

1. demonstration of Leishmania/Amastigote forms in 1.1 skin biopsy - L. tropica 1.2 tissue biopsy - L. braziliense 1.3 Liver, spleen, Lymph node & bone marrow - L. donovani! 2. Serologic tests - ARE NOT DIAGNOSTIC although they may be employed! 2.1 Complement fixation test (CF)! 2.2 Immunofluorescent antibody test (IFAT)! 2.4 Counter current electrophoresis! 3. CULTURE using Novy, Mc Neal and Nicolle media (NMM)! 4. Montenegro intradermal test - tropica & braziliense! 5. Non-specific tests for the demonstration of IgM like Napier’s test and Chopra

Genus Trypanosoma (BRUCEI COMPLEX) tsetse ! Trypanosoma brucei gambiense Trypanosoma brucei rhodisiense Extracellular parasites of blood, lymph & CNS (blood -> lymph -> CNS!)! Arthropod borne; transmitted thru skin inoculation/bites Vector: Tse-tse flies of the genus GLOSSINA spp.! Trypomastigote is the stage that developes in MAN Epimastigote initially developes but later it becomes (2-3 days) METACYCLIC TRYPANOSOME in the salivary glands of the VECTOR Infective stage: metacyclic trypanosome! Diagnostic stage: Trypomastigote! parang natype ko na to Pathogenic: cause African Sleeping sickness or OLD WORLD TRYPANOSOMIASIS! T.b gambiense causes WEST african sleeping sickness (w/ longer course)! T.b. rhodesiense causes East African sleeping sickness (rapidly fatal; shorter course!) Clinical manifestations of Sleeping Sickness 1. 2. 3. 4.

• Trypanosome chancre – firm, tender, painful nodule at bite site! • Invasion of blood – characterized by remittent fever and headache! • Invasion of lymph nodes (Winterbottom sign) – enlargement of the lymph nodes ! • Invasion of CNS (Kerandal’s sign) – neurologic changes characterized by mental dullness, Severe headache, mental deterioration that may lead to coma and eventually death.

(lesion > fever > winterbottom > Kerandal (kendal jinnir)) • Gambian trypanosomiasis (West African) has a longer incubation period longer course (exhibit all the signs before fully leading to death) as compared with Rhodesian trypansomiasis - death after signs! • Rhodesian trypanosomiasis (East African) runs a rapid and fatal course/ quickly fatal/shorter course! symptoms develops more rapidly and patient usually dies before the full development of the CNS signs [death before signs]

Genus Trypanosoma Species: Trypanosoma cruzi INTRACELLULAR PARASITE! Causes chaga’s diseases/ South American trypanomiasis/new world trypanomiasis! SYMPTOMS: Acute: ROMANA’S SIGN (swelling of eyelids), chagoma (lesion @ bite site), Chronic: (malfunctioning of vital organs leading to death )! Transmitted thru skin inoculation or bites when the bug bites and defecates on the wound ! Vector: Kissing bug/ assassin bug/reduviid bug/triatoma bug! Infective stage to man: Metacyclic trypanosome! Diagnostic stage: Amastigote and Trypomastigote! Unique mode of transmission: the infective stage is transmitted when the bug bites & defacates on the wound made by its bite. Passed out in bugs feces is METACYCLIC TRYPANOSOME [NOT SALIVARY GLANDS UNLIKE OTHER VECTORS] complete cycle!

—— combine sporozoa & malaria life cycle pdf...