General

Parasitology
Human parasites are divided as-
I.Protozoa

II. Helminths

Subkingdom protozoa is further divided into 4 Phylum-

I. Sarcomastigophora Consists of Amobebae and Flagellates

II. Apicomplexa-Coccidian parasite and piroplasmida
III. Ciliophora- Balantidium
IV. Microspora Microsporida

Ameoeba
A) Parasitic Amoeba(Amoeba of alimentary canal)Consists -
Entamoeba histolytica
Entamoeba coli
Entamoeba dispar
Endolimax
Lodamoeba

Characteristics E.histolytica/E.dispar E.coli

Trophozoites Actively motile Sluggishly
with finger motile,
shaped Blunt
pseudopodia pseudopodia
Cytoplasm
Presence of
RBC

Cysts 10-20um 20-25um

Nucleus- Four Nucleus Eight
nuclei, nuclei
fine granular Coarsely
granules, granular
evenly unevenly
 distributed arranged

Similarities:
Spread through ingestion of infectious cysts.
Cysts- morphologically identical
Both species colonize the large intestine.
Differences:
Only E.histolytica- causes invasive disease
Differentiated by Zymodeme analysis(Distinct surface Ag and isoenzyme
markers)
Gal/N Acetyl Gal lectin
PCR
B) Free living Amoeba consists of-
Naegleria fowleri
Acanthamoeba spp.
Balamuthia spp.

Flagellates
A) Intestinal and Genital flagellates
Giardia lamblia
Trichomonas
B) Haemoflagellates
Trypanosoma
Leishmania
A) Coccidian parasites

Isopora
Toxoplasma gondii
Sarcocystis
Cryptosporidium parvum

B) Piroplasmida

Plasmodium
Babesia
 Intestinal amoebae,Free-Living Amoeba and
Balantidium Coli
Intestinal Amoebae
Habitat- Trophozoites of Entamoeba histolytica live mucosa and sub mucosa of
Large intestine of man.

Morphology- 3 stages
Trophozoites Feeding stage of the parasite, which is actively motile in
freshly passed dysenteric stool, contains phagocytosed RBCs.
Pre-cystic stage-It secrets highly refractile cyst wall around it and becomes
cyst.
Cystic stage- Mature cyst contain 4 nuclei and its cytoplasm 1-4
chromatoid bodied and glycogen mass.

Life Cycle
Definitive host- Man

Infective form-Mature quadrinucleate cyst

Mode of infection-Food or water contaminated with cyst
Mode of transmission Faeco-oral route and sexual transmission(20-30%
in homosexuals)
Reservoir of infection- Asymptomatic carriers

Culture Media
Polyaxenic Bacterial supplement(for diagnosis)

Boeck and Drbohlavs Media

Locks egg serum/egg albumin
Nelsons Medium
Craigs Medium

Monoxenic Medium Diamond

Cultivating E.histolytica with Trypanosoma cruzi

For study of pathogenesis,antiamoebic susceptibility,preparation of Ag

Virulence factors

Lectin Ag(galactose inhitable adherence lectin)

Helps in binding of Trophozoite to mucosa which is the pathogenic form

Cysteine proteinase/enterotoxin/Cytotoxin-assists organism in digesting the extra

cellular matrix and invading tissues.

Host factors influencing course of infection

Stress, Malnutrition, Alcoholism, Corticosteroid therapy and immune deficiency

Clinical Syndromes

Incubation period -4 days to a year

1) Asymptomatic infection-most frequent

2) Symptomatic infection-
Uncomplicated intestinal infection-diarrhae,cramps and flatulence
Acute Amoebic Dysentry
Chronic Amoebic Dysentry
Amoeboma- Localised tumor-like lesion results from chronic ulceration
Hapatic Amoebiasis
3) Metastatic Infections
Pulmonary Amoebiasis
Cerebral Amoebiasis
Splenic Abscess
Cutaneous amoebiasis

Entamoeba coli, E.dispar, E. hartmanni, E. polecki, lodamoeba butschlii and

Endolimax nonpathogenic intestinal amoeba.

Lab diagnosis:

Light Microscopy of Stool

Identification of trophozoites / cysts in fresh stool

Demonstration of Trophozoite in faeces Active infection.

Colonoscopy / Sigmoidoscopy

Colonoscopy preferable
 Wet preps of material from ulcer-base can show trophozoites

Stool antigen-detection test or PCR

Sensitive and Specific

ELISA-Best method to detect Ab against Lectin Ag

PCR

Zymodeme analysis(Distinct surface Ag and isoenzyme markers)- Have

identified 7 pathogenic and 11 non pathogenic species

FREE LIVING AMOEBA

CHARACTERS Naegleria.fowleri Acanthamoeba-
castellani,culbertsoni,israelii

Disease Primary amoebic Granulomatous amoebic

Meningoencephalitis meningoencephalitis- Ulcerative
keratitis

Portal of entry Nose- olfactory Nasal route URT- Hematogenous route

Pre disposing Swimming in contm water Imm def

factor
Clinical course Acute Sub acute chronic

Pathology Acute suppurative changes Granulomatous inflammation

Morphological Trophozoite,cyst,flagellated form Cyst and trophozoites-CSF
form
Culture Frequently positive-non nutrient Negative,Brain biopsy often
agar required
Trophozoites Single pseudopodium Thorn like
pseudopodium(Acanthopodia)
Leukocytes in CSF Neutrophils Lymphocytes

Ciliate Parasites-
 Balantidium coli- only ciliate parasite of humans.
Inhabiting the large intestine, caecum, and terminal ileum, feeding on
bacteria.
The parasite may also invade the intestinal mucosa causing ulceration.
Morphology-Trophozoites and cysts.
Extra intestinal spread to the liver, lungs and urogenital tract is rarely
observed.
Infection occurs by ingestion of cysts in contaminated food or drink.
Pigs represent the source of infection for humans.
Symptoms of the disease-Balantidiasis- may range from mild colitis and
diarrhea to clinical manifestations resembling severe dysentery.

Flagellates
 A)Intestinal flagellates
Giardia Lamblia
Habitat- Mucosa of duodenum and upper ileum of man.
Morphology 2 forms

Trophozoites Tear drop shaped/ racket shaped / piriform shaped

It has 2 nuclei, 4 pairs of flagella, 2 Axostyles, 2 parabasal body and

ventral sucking disk
Cyst- Mature cyst consists of 4 nuclei and cysts are passed in faeces.

Life cycle

Infective stage Cyst

Route of infection- Faeco- oral route
Trophozoite has falling Leaf like motility

Susceptibility to infection

Children
Immunocompromised individual
Individuals with Achlorhydria and Hypochlorhydria (Gastric acidity weakens
the cyst wall and excystation is completed in duodenum)

Pathogenesis

It causes abnormalities of villous structure and causes malabsorption(lipids

and lipid soluble vitamins)

Clinical Disease

Symptomatic children- watery diarrhea with malabsorption

Older patients Epigastric pain, flatulence, low grade fever, diarrhea with foul
smelling stool.
Travellers diarrhea
Gall bladder infection Biliary colic and jaundice

Lab diagnosis

Sample collected Stool sample and duodenal contents

Microscopy Iodine and saline wet mount-Demonstrates either trophozoites or
cyst
 String test/Entero test-Bile stained mucus is collected for examination of
Trophozoites.
Serology- Antigen or Antibody detection by ELISA and Immuno-fluorecent
method

Treatment

Metranidazole/ Tinidazole

B) Genital Flagellates Trichomonas

Vaginalis
Habitat

Urethra, vagina and prostate

Morphology

Only trophozoite form, which is pear- shaped consists of 5 flagellas. No cystic

stage.

Life Cycle

Mode of transmission Sexual route

Reservoir of infection-Women
Infective stage-Trophozoites

Clinical disease

Incubation period-4-28 days

In women Asymptomatic or vaginitis and UTI
In men Asymptomatic or Urethritis, Prostatitis and cystis.

Lab diagnosis
Sample collected vaginal and urethral discharge, prostatic secretions or
urine sediments
Microscopy (Wet mount)- Actively motile (Jerky motility) trophozoites
observed
Staining Giemsa and papanicolaou staining used.
Culture more sensitive (93 %)
Serology- Indirect haemagglutination, gel diffusion
Gene probes DNA probes used
PCR
Treatment-Drug of choice -Metronidazole
 C) Haemoflagellates
Lie in the blood or tissue of man, who serves as definitive hosts.

A) Trypanosoma spp.

B)Leishmania spp.

Parasite Epidemiolog Location Mode Symptoms

y

Leishmania Mediterranean Skin Sand fly Skin lesions-Cut L

tropica area,Asia (Phlebotomous (Orientalsore/Delhi
) boil/Aleppo,button,Baghdad
)
L.Brasiliensi Central and Skin Sand fly Skin lesion,Espundia
s South &Muco (Lutzomyia)
America cutaneous

L.Donovani Asia,Africa Skin & Sand fly Skin lesion,liver and spleen
somatic (Phlebotomous
organs )

L.mexicana America Muco- -------- Chiclero ulcer

cutaneous

There are three forms of leishmaniasis :

1- Cutaneous

2- Mucocutaneous

3- Visceral

PKDL- 2yr after treatment with Antimony

3% African ; 10% Indians

 Non ulcerative hypopigmented lesions

Lab diagnosis:

Specimens:

Spleen( Most Sn)

Bone marrow asp ( Mc preferred)

Demon. Of LD bodies (Amastigote)

Lymph node asp( Not useful in Indians)

Novy MacNeal and Nicolle Medium ( Promastigotes grown)

(Splenic,Liver ,Lymph node puncture )

Napiers Aldehyde test

Chopras Antimony test

ELISA Sensitive and specific

Leishmania( Montenegro) skin test - Delayed hypersensitivity

Negative in Ac cases of Kala azar

Leishmanin ( Montenegro) skin test
Treatment- Pentavalent antimonials (Sodium stibogluconate) and
Amphotericin B.

Trypanosoma Cruzi
Clinical spectrum of disease
Acute stage of infection
Incubation period -1-2 weeks
Chagoma Dusky-red swelling at site of entry of T.cruzi
Conjunctival swelling, unilateral swelling of lids (Romanas sign)
Generalized lymphadenopathy, enlargement of liver and spleen

Chronic stage of infection

 Heart- thinning of the ventricular walls, biventricular enlargement, apical
aneurysms, atrophy of myocardial cells and conduction system
involvement.
GIT-varying degrees of dilatation (mega disease) of esophagus and colon

Laboratory Diagnosis
Acute Chagas disease- requires the detection of parasites.
Microscopic examination of fresh anticoagulated blood or of the buffy coat-
demonstrates motile organisms.
Giemsa-stained thin and thick blood smears.
Microhematocrit tubes containing acridine orange QBC examination useful.
PCR or hemoculture in special media- when repeated attempts to visualize
the organisms are unsuccessful.
Hemoculture- takes several weeks to give positive results.
Serologic testing plays no role in diagnosing acute Chagas disease

Chronic Chagas disease

Detection of specific antibodies that bind T. Cruzi antigens.

Demonstration of the parasite is not of primary importance.
The radioimmune precipitation assay (Chagas RIPA) is a highly sensitive and
specific confirmatory method for detecting antibodies to T. Cruzi
The use of PCR assays to detect T. Cruzi DNA in chronically infected persons
has been studied extensively

Treatment -Nifurtimox and benznidazole- drugs used.

Parasite Epidemiolog Location in Mode Symptoms

y Host

T.Cruzi S.America Cardiac Reduvid Chagoma,Muscle

muscle,Bd and bug pain,LN,Myocarditis
Chagas other tissues (Kissing bug Meningoencephalitis
disease triatomine bug Romanas sign Eye
assassin bug) edema

Trypanosoma brucei Sleeping sickness

Comparision West African East African

Organism T. b. gambiense T. b.rhodesiense

Vectors Tse tse fly( palpalis gp) Tse tse fly ( morsitans)

Primary reservoir Humans Antelope and cattle

Human illness Chronic CNS disease- Kerandels Acute ( early CNS disease) < 9m
sign-Pressure on palm /over ulnar
Nr is followed by severe pain after
pressure is removed.
Lymphadenopathy Prominent post cerv LN Minimal axially and inguinal
( Winter bottom sign)

Parasitemia Low High,FATAL

Ag variation +/- +

Plasmodium species and Babesia

Malaria is caused by a parasite called Plasmodium, which is transmitted via
the bites of infected Anopheline mosquitoes. In the human body, the
parasites multiply in the liver, and then infect red blood cells. Plasmodium
spp. Causing malaria as follows-

Life Cycle
 Man- Intermediate host.
Mos quito-Definitive host
Sporozoites are infective forms
Present in the salivary gland of female anopheles mosquito
After bite of infected mosquito sporozoites are introduced into blood
circulation.

Clinical features of malaria

Fever
Sweating
Anemia
Splenomegaly (enlarged spleen)
Irritability
Coma, Retinal Hemorrhages
Algid Malaria (a shock like syndrome)
Respiratory distress syndrome
Complications
Cerebral malaria
Back water fever
Malarial hyperpyrexia
Gastrointestinal disorders.
Algid malaria
Recrudescence-P.falciparum infection
Relapse P. vivax infection
Nephrotic syndrome-P. malariae infection
 Species Colour of pigment No of merozoites/Mature schizont

P.Falciparum Dark brown 18-24(Not demon. In PBS)

P.Vivax Yellowish- brown 12-24

P.Ovale Dark yellowish -brown 8

P.malariae Dark - brown 8

Laboratory Diagnosis
Microscopy- for demonstration of parasites and for speciation
Stained peripheral blood smear examination (thick and thin smears)-Gold
standard method
Quantitative Buffy Coat examination- Rapid method for detection of parasites

The QBC method is the simplest and most sensitive method for diagnosing the
following diseases

Malaria
Babesiosis
Trypanosomiasis (Chagas disease, Sleeping Sickness)
Filariasis (Elephantiasis, Loa-Loa)
Relapsing Fever (Borreliosis)
Antigen Deection (pLDH and HRP-2 Ag detection)- Immunochromatographic
tests- Rapid and simple
Serology-antibodies against malaria parasite detected by indirect
Immunofluorescence (IFA) or enzyme-linked immunosorbent assay(ELISA)
Molecular Diagnosis Parasite nucleic acids are detected using polymerase
chain reaction(PCR)

Treatment
Choroquine Drug of choice in all forms of susceptible in all forms of Acute malaria
Radical cure-Primaquin

Other Alternatives
Quinine plus Doxycycline or Tertracycline
Quinine plus Clindamycin

Newer Alternatives
Mefloquine
 Halofantril.

Species Disease Periodicity

(hours)

P.Vivax(Most common) Benign tertian 48

P.falciparum Malignant tertian 24-48

P. Ovale Ovale tertian 48
(Orissa,W.bengal,Assam,Delhi,Gujurat)
P. malariae Quartan 72
P. knowlesi 24-48

Characteristi P.falciparum P.vivax P.ovale P.malariae

c

Red cell All age RBC Reticulocytes Reticulocytes Older cells

preference and young RBC and young RBC
Morphology Ring forms- Irregularly Erythocytes Band form
Multiple shaped large enlarged and Schizont and
Double dot rings and fimbrinated late
Accolle form trophozoites Schizont and trophozoites
Banana shaped Shizont and late late also are seen
gametocytes trophozoites trophozoites
also are seen also are seen
 Relapses No Yes Yes No

Recrudescence Yes No No Yes

Babesia
Texas cattle fever,Red water fever,Tick fever,Nantucket fever

Not found in India

Tick borne malaria like illness in animal

Lymes disease may co-exist in same pt

Treatment Clindamycin with oral quinine and atovaquone and azithromycin

Inf form: Sporozoite Man,Gametocyte Mosquito

Reservoir- Tick

Intraerythrocytic protozoa

Maltese cross form seen Ring in tetrad in merozoites

Severe infection on splenectomised pt.

Mode of transmission- Ticks, Packed RBC cell transfusion,Organ transplantation

Species B.microti B.bovis//divergens

Distribution North America Europe

Host Rodent Cattle

Immunity of host Spleen is usually normal Seen in spleenectomised and

Immcomp pt
Clinical feature Asymptomatic /mild fever Severe,but no cerebral
involvement
Clinical course Self limiting Severe,fulminant
Coccidian
Parasite
Toxoplasma gondii
It is a coccidian protozoan worldwide distribution
Infects a wide range of animals and birds but does not appear to cause
disease in them. The normal final hosts are strictly the cat and in which the
oocyst-producing sexual stage of toxaplasma can develop.
Morphological forms
o Oocyst- each oocyst has 2 sporocysts and each sporocyst containing 4
sporozoites.
o Tachyzoites- rapidly multiplying crescentic cells, which intiate the acute
stage of disease

Congenital infection develops only when nonimmune mothers are infected
during pregnancy (first time) is usually of great severity.

o Prenatal toxoplasmosis is a major cause of blindness and other

congenital defects.
o Congenital infection leads to stillbirths, chorioretinitis, intracerebral
calcifications, psychomotor disturbances and hydrocephaly or
microcephaly.
Postnatal toxoplasmosis is less severe.

Culture

T gondii may be cultured only in the presence of living cell, in cell culture or
eggs.
Optimal are relatively resistant, but low-grade lymph node infection
resembling infectious mononucleosis may occur.
Laboratory Diagnosis-

Specimens
o Blood, sputum, bone marrow, cerebrospinal fluid, and exudates; lymph
node, tonsillar and striated muscle biopsy material; and ventricular
fluid(in neonatal infections) may be required.
Microscopic Examination
o Smears and sections stained with Giemsas or other special stains,
such as the periodic acid Schiff technique, may show the organisms.
o The densely packed cysts, in the brain or other parts of CNS, suggest
chronic infection.
Animal Inoculation
o Commonly used for definitive diagnosis.
o A variety of specimens are inoculated intraperitoneally into groups of
mice that are free from infection.
o If no deaths occur, the mice are observed for about 6 weeks, and tail or
heart blood is then tested for specific antibody.
o The diagnosis is confirmed by demonstration of cyst in the brains of
the inoculated mice.
Tissue culture-
o Infection of cells in tissue culture is also useful and rapid (3-6 days)
Molecular methods- polymerase chain reaction will amplify T. gondii DNA
Serology
o Sabin-Feldman dye test- depends upon the appearance of
antibodies (in 2-3 weeks), that will render the membrane of laboratory-
cultured living T. gondii impermeable to alkaline methylene blue..
Interpretation If organisms are unstained indicates presence of
antibodies in serum.
o IFA and ELISA tests are useful
Treatment
o Acute infections- Combination of pyrimethamine and sulfadiazine or
trisulfapyrimidines.
o Alternatives spiramycin, clindamycin, trimethoprim-
sulfamethoxazole.
o In pregnancy spiramycin (Rovamycine) is recommended.

Other Coccidian parasites

Cryptosporidium parvum
Cyclospora cayetanensis
Isospora belli
Sarcocystis hominis, S. suihominis and S. lindermanii
Microsporidia
 Cryptosporidium
2 genotypes-C.hominis and C.felis that can infect humans

Others-C.muris(rodents),C.meleagridis

Transmission- Feco-oral

Located in brush border of epithelial cells of small intestine,

mainly in jejunum .

2 l/day- watery diarrhoea to 25 l/day

CD4 count > 200cu mm-disease either asymp or resolves

CD4 count < 100 cu mm chronic spreads beyond intestine

Cholangitis,Biliary cryptosporiodosis,Cholecystitis.

Cyclospora - Recent outbreaks of disease ingestion of contaminated

Raspberries,mesclun,basil.

Microsporidium-

Characterized by a unicellular spore containing a coiled spring-like tubular

polar filament through which the sporoplasm is forcibly discharged into a host
cell.
A modified trichrome blue stain may detect microsporidia in urine, stool,
and nasopharyngeal specimens.
Transmission is chiefly by ingestion of spores in food or water.
 Transplacement transmission is common.
Non pathogenic in immunologically intact persons but a continuing threat to
the immunocompromised.
They often occur along with cryptosporidium in AIDS patients.

Property Cryptosporidium Cyclospora Isospora

catayensis

Size 4-6um 8-10um 10-20um

Shape Round Round Oval

Cyst contains 4 sporozoites 2 sporoblast, each 2 sporoblast,each with 4

with 2 sporozoites sporozoites
Acid fastness Uniformly AF Variable AF Uniformly AF

Autofluorescence No,but can be +++ AF +/-

stained with F dye
Treatment Co T Co T Spiramycin,Nitazoxanide

Cestodes and
Trematodes
 Cestodes

Cestodes, or tapeworms, are segmented worms.

Habitat- adults reside in the GIT and larvae can be found in any organ.

Intestinal Cestodes- Humans are definitive host

Tania saginata and T. solium

Diphyllobothrium,
Hymenolepis,
Dipylidium caninum.

Tissue cestodes (Larval stage) Humans are intermediate host

Echinococcus granulosus
Sparganum
Multiceps spp.

Taenia solium- human may be either the definitive or the intermediate host

Taenia saginata and T.solium

Both Taenia saginata and T.solium causes intestinal Taeniasis.

T.solium in addition causes Cysticercosis in humans, when they act as
intermediate hosts.

Man acquires cysticercosis by

Ingestion of food and water contaminated with eggs.

Auto infection through anus- hand- mouth transfer of eggs.
Reverse peristalsis of eggs throwing back the eggs duodenum where
they hatch and cause tissue infection.

Cysticercosis

Potentially dangerous systemic disease.

 Most commonly found in subcutaneous and intramuscular tissue
followed by the eye and then the brain.

Neurocysticercosis

Most serious form of cysticerosis.

Two types :
o Parenchymal
o Extra- Parenchymal
Convulsions, intracranial hypertension and psychiatric disturbance are
three important manifestations.

Characters Taenia saginata Taenia solium/Armed/pork

Length 5-10 mt 2-3 mt

Scolex Large & Quadrate,no hooklets Small & globular with hooklets
Neck Short Long

Proglattid 1000-2000 Less than 1000

Larva Cysticercus bovis Cysticercus cellulosae

Characters Intestinal taeniasis Cysticercosis

Infective stage Cysticercus cellulosae T.Solium egg

Cysticercus bovis
Cl. Symptoms Ints symptoms only Depending on location of the cyst
Diagnosis Demon of eggs in faeces Demon of larvae in tissues(C.cellulosae)
Serological tests are of great value

Echinococcus
Echinococcus granulosus- hydatid tape worm or dog tape warm.
Hydatid cyst is the larval stage.
Causes cystic echinococcosis or hydatid in man and other herbivorous
animals

Life cycle:
 Definitive host Dog and other carnivores

Int host- Man and other herbivores animals

Man is an accidental host

Eggs- infective stage of the parasite

Clinical feature:

Hepatomegaly with or without palpable abdominal mass

Bone rapid erosion leading to fractures

Other sites-tumor like condition or an abscess

Parasitic diagnosis:

Hydatid fluid microscopy-Protoscolices on wet mount

Acid fast stain of centrifuge deposit Hooklets

Casoni skin test-Imm HSN reaction,Intradermal inoculation -wheal in

30min

IHA,CIEP,ELISA and Western blot used for detection of Ab.

Detection of Ag- ELISA,CIEP

Imaging methods-USG,MRI,X-Ray are of immense help to show the size

and condition and to pinpoint the exact location of the cysts.

Water lily sign inX ray,.

Treatment:

Surgery is the mainstay

Albendazole and mebendazole useful in cystic echinococcosis

Percutaneous aspiration injection respiration (PAIR) of the cyst

Echinococcus multilocularis- 2nd MC

Lungs-mistaken as a malignant tumor(Alveolar

Echinococcosis/Multilocular Hy Disease)
 Has ability to metastasize(Liver-lung-brain-kidney)

Hymenolepis nana-Dwarf tape worm

Only cestode of humans that doesnt require an intermediate host.

Hymenolepis diminuta- Rat tapeworm

Trematodes
Schistosomiasis and other Trematode Infections

Trematodes, or flatworms- belong to the phylum plathelminthes.

All human parasitic trematodes are hermaphroditic (except for

schistosomes)

Life cycle

Definitive host- mammal/ human

Intermediate host- snails or for some trematodes more than one
intermediate host may be
Metacercariae-infective stage.

Blood Flukes : Schistosomiasis

5 Species infecting humans :

Eggs with a terminal spine- Schistosoma haemetobium, Schistosoma

intercalatum
Eggs with lateral spine- Schistosoma mansoni,
Eggs with a rudimentary knob- Schistosoma japonicum, Schistosoma
mekongi
Habitat

S. hematobium- vesicle plexus

S. mansoni- inferior mesenteric plexus
S. japonicum- superior mesenteric plexus

Clinical spectrum of disease

Acute schistosomiasis

Most cases are asymptomatic

Schistosomal dermatitis- swimmers itch
Migration of Schistosomule may be associated with inflammatory and
mechanical effects in liver and lung.
Katayama fever- serum sickness like illness

Intestinal schistosomiasis

S. mansoni, S. japonicum, S. mekongi

Intermediate diarrhea with constipation

Haepatosplenic schistosomiasis

S. haematobium, S. japonicum
Massive splenomegaly
Hyper splenism- anemia

Genito urinary disease

Intermittent hematuria, dysuria, urinary frequency

Hydronephrosis, pyelonephritis, UTI-d/t persistant obstruction

Malignancy

S. haematobium- squamous cell carcinoma of bladder

Drug Therapy for Human Trematode Infections- Praziquantel

Laboratory diagnosis

Urine diagnosis

S. haematobium eggs are passed with diurnal frequency

Sedimentation or filtration methods-concentration techniques

Stool diagnosis:

Useful for S.mansoni,S.japonicum,S.intercalatum

Conc techniques should be used

Formol ether sedimentation technique

Kato Katz thick smear preparation

Biopsy:

Rectal biopsy is much sensitive than Kato Katz thick smear preparation

Liver biopsy may be useful in ruling out co morbid conditions like Hepatitis B
and C.

Serology:

Antibody detection systems

Antigen detection detects Ag in blood and other body fluids

Circulating Anodic Ag(CAA) and Circulating cathodic Ag(CCA)

 TIPS

Same life cycle ovum-miracidium-snail-cercaria aq veg

Fasciola hepatica

Fasciolopsis

Lung fluke 2nd intm crab/cray fish

Chinese liver fluke -2nd intm - FISH

FORKED TAILED CERCARIA

Schistosomes

STRAIGHT TAILED CERCARIA / METACERCARIA

Liver flukes,Fasciolopsis,Lung flukes

REDIA

Liver flukes,Fasciolopsis,Lung fluke.

NEMATODES
Unsegmented,enlongated and cylindrical
Separate sexes
Buccal capsule
GIT is complete
Body cavity is present

According to egg/larva producing capacity:

Viviparous:
Filarial worms
Trichinella
D.medinensis
Oviparous:
Ascaris
Trichiuris
Hook worm
Enterobius

Oviviviparous:
S.stercoralis

Classification based on mode of infection

INGESTION (EAT)
E.vermicularis
Ascaris
T.trichura
D.medinensis( larva with Itm host)
T.spiralis( Encysted larva in muscle)

SKIN PENETRATION / CUTANEOUS ( ANS)

A.duodenale
Necatar americanus
S.stercoralis
Schistosoma sp

SEXUAL CONTACT
T.vaginalis
E.histolytica
 G.lamblia

INSECTS
W.bancrofti
B.malayi
Loa loa
O.volvulus

AUTO-INFECTION( HETS)
H.nana
E.vermicularis
T.solium
S.stercoralis

INHALATION OF DUST- Ascaris,Enterobius

PARASITES TRANSMITTED CONGENITALLY
T.gondii
Plasmodium sp
Microsporidia
T.cruzi
Only protozoan parasite found in human small intestine-Giardia lamblia

Dogs are responsible for transmission of-

Hydatid cyst,Toxocara canis,L.donovani infantum

PARASITES INFECTING DIFFERENT TISSUES

Infecting Intestine: Lung:

E.histolytica Paragonimus
westermanii
G.lamblia
B.coli
Cyclospora
Isospora belli
Affecting Liver: Infecting
Lymphatic system
E.histolytica W.bancrofti
E.granulosus B.malayi
F.hepatica
 Infecting Brain:
P.falciparum
Free living Amoeba
Trypanosoma
Toxoplasma gondii
E.histolytica
E.granulosus
T.solium

Feature A.lumbricoide Hook S.stercoralis T.trichiura E.vermiculari

s worm s

Inf stage Egg Filariform Filariform Egg Egg

larvae larvae
Route of Oral Percut Percut/Auto Oral Oral
infection inf
GI Jejunal lumen Jejunal Small bowel Caecum,col Caecum,
location mucosa mucosa onic mucos appendix
of worms
Pulm Yes Yes Yes No No
passage
of larvae
Principal Rarely GI/ Fe def GI GIsymp, Perianal
symptom Biliary obstr Anaemia symp;malabso anemia pruritis
s r sepsis in Rectal
Hyperinf prolapse
Diagnosti Eggs in stool Eggs in Rhabd larvae Eggs in Eggs from
c stage stool in stool/duod stool perianal skin
asp,sputum in
hyperinf

TISSUE NEMATODES
TRICHINELLA SPIRALIS

Smallest nematode infecting man

Ingestion of the raw flesh containing viable encysted larvae

 Man is dead end--Pig is reservoir

Diagnosis Demonstration of larvae in muscle biopsy/autopsy

specimen

Site- tendinous insertion of deltoid/gastrocnemius muscle

Serology-CFT,Betonite flocculation test/latex with Trichinella

X-Ray-Calcified cyst

Skin test- Bachmans Ag

TREATMENT:

Thiabendazole

PROPHYLAXIS:

Proper cooking of pig with proper inspection of slaughter house

Trichiuris trichura
Adult worm Caecum,appendix

Brown,bile stained egg

Contains an unsegmented ovum

Floats in saturated solution od common salt.

Embryonated egg is infectious

Asymptomatic except when there is heavy load of worms.

Disease results Mech effects or allergic reaction

Intimate contact Whipworm dysentry

Rectal prolapse

Fe def anemia

On sigmoidoscopy- Coconut cake rectum

Treatment: Thiabendazole and Mebendazole

Ascaris lumbricoides
Largest intestinal nematode parasite of humans

Most infected individuals have low worm burdens and are asymptomatic

Adult worm resides in small intestine

Source- Contaminated food and water

Important features:

Chest X ray- Eosinophilic pneumanitis(Loefflers syndrome)

Hook worm
Most Hookworm infections are asymptomatic

Ground Itch at the site of penetration

Chronic infection- Fe def Anemia

Hypochromic microcytic anemia,occasionally with eosinophilia or

hypoalbunemia is characteristic of Hookworm disease.

Strongyloides stercoralis
Dwarf thread worm

Smallest pathogenic nematode causing human infection

Has both parasitic and free living stages.

Has potential for Autoinfection and multiplication within infected host.

Female adult worm is parthenogenetic(Able to produce female

egg/larvae without mating with male

Larva currens-Intradermal migration of filariform larva

Loefflers syndrome

Acute Watery or mucoid diarrhea

Chronic- Diffuse abdominal pain,nausea,vomiting diarrhea

Hyperinfection syndrome Corticosteroides,tacrolimus,chemotherapeutic

agents,radiation therapy etc

Larval demonstration in stool low sensitivity

Atleast three specimens to be examined

Formalin ethyl acetate conc techq

For isolation of larvae

Baemann method

Harada mori fiter paper method - Not very sensitive

Agar plate method 96% sensitive

Serology- IgG ELISA 85-95% SENSITIVE

IVERMECTIN Drug of choice

Thiabendazole/Albendazole can also be given

 F IL A R IA

H u m a n F ila r ia s is

L Y M P H A T IC SUBC UTANEO US S E R O U S C A V IT Y

W u c h e r e r ia b a n c r o f t i L o a lo a M a n s o n e lla o z z a r d i
B r u g ia m a la y i O n c o c e r c a v o lv u lu s M a n s o n e lla p e r s t a n s
M a n s o n e lla s t r e p t o c e r c a
Organis Periodici Vector Location of adult Microfilar Sheat
m ty ia h
location

W.Bancro Nocturnal Culex Lymphatic tissue Blood +

fti , Anophel Lymphatic tissue Blood +
Subperiod es, Aedes
ic
B.malayi Nocturnal Mansoni Lymphatic tissue Blood +
, a, Lymphatic tissue Blood +
Subperiod Anophel
ic es
B.timori Nocturnal Anophel Lymphatic tissue Blood +
es
Loa loa Diurnal Chrysops Sub cut tissue Blood +
Mango/ Calabar swelling
Deerfly
O.Volvulu None Simuliu Sub cut Skin,eye -
s m tissue(firm,nontendermobile,no
River Black fly dule)
blindness Buffalo
gnats
M.Ozardd None Culicoid Undermined site Blood -
i es
(Midges)
M.Perstan None Culicoid Bodycavities,mesentry,Perirena Blood -
s es l tissue
(Midges)
M. None Culicoid Sub cut tissue Skin -
streptocer es
ca (Midges)

Non bile stained eggs

Hook worm

Pin worm

Strongyloides stercoralis

Hymenolepis nana

Necatar americanus

Dog tape worm

Bile stained eggs

Ascaris

Taenia sp

Trichiuris trichura

Do not Float in Sat salt

solution:
Un fertilized egg Of Ascaris

Larva of Strongyloides Stercoralis

Taenia egg

Eggs of all intestinal flukes

Float in Sat salt solution :

E.granulosus

H.nana

AlL nematodes except Unfertz egg of Ascaris

Premunition-Immunity to
reinfection
Syphilis
 Cut leishmaniasis

Holoendemic malarial area

Parasites causing Dysentry

E.Histolytica

B.Coli

S.Japonicum

Trichiuris trichura

Parasites causing Malignancy

S.haematobium

Squamous cell carcinoma of urinary bladder

Clonorchis sinensis

Cholangiocarcinoma of liver,bile duct& Adenocarcinoma of pancreas

Opisthorchis viverrini

Cholangiocarcinoma of bile duct

Autoinfection
Cryptosporidium

H.nana

Echinococcus

Taenia solium

S.stercoralis

E.vermicularis

Obligate Intracellular Parasites

Plasmodium sp

Babesia sp
 Leishmania sp

Toxoxplasma sp

Trypanosoma cruzi ,Microsporidia

Parasites
associated with Anemia
Hookworm-Fe def anemia

Diphyllobothria latum- Megaloblastic anemia

Malaria-Haemolytic anemia

Trichiuris trichiuria- Prolonged massive inf Fe Def Anemia