Opportunistic coccidian parasites

Coccidian Parasites
UNDER GARADUATE STUDENT’S LECTURE ON
BY
GUNJAL PN
ASSIST. PROF.
DEPT OF MICROBIOLOGY
DVVPF’S MEDICAL COLLEGE & HOSPITAL
AHMENDAGAR
7/8/2021 Department of Microbiology 1

Aims and Objectives
At the end of the session, the students will be able to
understand:
• Classification of Coccidian parasites
• Toxoplasma gondii
• Cryptosporidium parvam
• Cyclospora cayetanesis
• Isospora belli
• Pathogenicity and Clinical features of coccidian
parasites.
• Laboratory Diagnosis of coccidian parasites
• Treatment and prevention.

Introduction
• Coccidian parasites can be divided into three orders
• Eimeriida
• Haemosporida
• Piroplasmida
• Order- Eimeriida – has - 5 genera
• Toxoplasma,
• Cryptosporidium,
• Cyclospora,
• Isospora,
• & Sarcocystis

Introduction
• Toxoplasma gondii is an intracellular parasite
affecting a wide range of mammals and birds
including humans.
• Cryptosporidum, Isospora and Cyclospora are
acid fast parasites that causes opportunistic
infections in HIV infected patients.
• Sarcocystis spp is rare parasite infecting man
and forms cystic lesions in muscles.
• Microsporidium obligate intracellular parasite
responsible to cause opportunistic infections in
HIV infected pts.
ISOSPORA
CYCLOSPORA
CRYPTOSPORIDIUM
MICROSPORIDIUM

CRYPTOSPORIDIUM PARVAM
• It is an intestinal coccidian parasite affecting
many animals and humans.
• Can cause self limiting diarrhea in helathy
individuals.
• Can be an opportunistic pathogen in
immunocompromised patients (HIV) causing chronic
persistent life threatening diarrhea.
• Tyzzer (1907), was first to describe it in gastric crypts of
laboratory mice.
• The first human case was reported in 1976.

CRYPTOSPORIDIUM PARVAM
• Belongs to family Cryptosporidiidae.
• Different from other coccidian parasites- does not go into
deep host cells, but confined to an intracellular extra
cytoplasmic location.
• All sexual and asexual stages of development takes place
within a parasitophorous vaculoe
• That lies just below the cell membrane of the brush border
epithelium of the small intestine.
• Cryptosporidium parvam is the most common species
affecting humans.
• Other species infect wide range of mammals and reptiles.

CRYPTOSPORIDIUM PARVAM – MORPHOLOGY
• OOCYST:
• Infective form for humans.
• Diagnostic form.
• Excreted in the feces.
• Round, small, 4-6 um, surrounded by a cyst wall and bears four
sporozoites.
• Each sporozoite is crescentic shaped with pointed anterior end, blunt
posterior end and a nucleus located posteriorly .
• Two types of oocysts are demonstrated
• 1. thick walled
• 2. thin walled
Fig: Sporulated oocysts of A: Cryptosporidium B: Cyclospora C: Isospora

CRYPTOSPORIDIUM PARVAM – MORPHOLOGY
• 1. Thick-walled Oocyst:
• Contains two electrodense cyst wall.
• Outer – uniformly thick, moderately coarse.
• Inner – Fine granular with a suture point at one pole.
• In between two walls, lies an electroluscent middle zone containing
two oocyst membranes.
• 2. Thin-walled Oocyst :
• Surrounded by a single layered membrane.
• The oocysts are acid fast in nature but don’t stain by iodine.
• Extremely resistant to routine chlorination, heat and other
disinfectants.

Life cycle
• Host: Cryptosporidium parvam completes
its life cycle (both sexual and asexual stages)
in single host (human or animal).
• Infective stage: Sporulated oocyst.
• Thick-walled oocyst is infectious to other person.
• Thin-walled oocyst can cause autoinfection (through contaminated
fingers).
• Mode of transmission : Feco-oral route – ingestion of thick wall
oocyst.
Sporulated oocyst

Life cycle
• DEVELOPMENT IN HUMAN:
• EXCYSTATION:
• In small intestine, the suture present in the inner wall of the oocyst
gets dissolved and 4 slender crescent shaped sporozoites are
released from each oocyst.
• Various factors like pancreatic enzymes are bile salts help in
excystation.
• INVASION:
• Sporozoites invade the brush border epithelium of the small intestine
and lie inside a parasitophorous vaculoe near the microvilli surface,
within which all the stages of development take place.

Life cycle
• EXCYSTATION - SCHIZOGONY:
• The sporozoites – differentiated into - trophozoites – which
undergo – asexual multiplication (Schizogony) to produce -
Type I Meronts.
• Each type I meront undergoes – schizogony – releases 8
merozoites – again invade the adjacent enterocytes and
undergo repeated schizogony to produce - Type II meronts.

Life cycle
• EXCYSTATION - GAMATOGONY:
• Merozoites undergo – Gametogony – transformed – sexual forms –
Micro and Macrogamont.
• Each microgamont releases 16 microgamets
• only ONE – Macrogamet is produced from each macrogamont.
• SPOROGONY:
• Fertilization takes place – micro and macrogamete fuses to produce
– zygote.
• Subsequently, about 80% of zygote transform into highly resistant
doubled layered thick-walled oocyst.
• 20% transformed into single layered thin-walled oocyst.

Life cycle
• EXCYSTATION - SPOROGONY:
• Within host cell , oocyst undergo- Sporogony – sporozoites.
• Sporulated oocysts are excreted in feces.
• Thick-walled oocyst infects the new hosts where as the thin-
walled oocysts – infects – the same host (autoinfection).
• Prepatent period:
• Period from the time of ingestion of oocyst to completion of
the life cycle and release of new oocysts in environment
through human feces (4-22 days approx.).

Epidemiology
• Cryptosporidiosis is a zoonotic disease.
• PREVALENCE RATE OF CRYPTOSPORIDIOSIS:
• In immunocompetent people – prevalence – India (developing
countries) – 2.4 -15%, Whereas in Western Countries (1.4-6%).
• In immunocompromised hosts (HIV positive pts) – 12-46% in
developing countries, 7-21% in developed countries.

Epidemiology
• RISK FACTOR’S CONTRIBUTING TO DISEASE INCLUDE:
• Low infective dose of C. parvam (10-100 oocysts ) can initiate
infection.
• Large multiplication capacity (> 1010) in single host.
• Resistant to the available drugs and disinfectants.
• Large animals and humans are the reservoirs.
• Lack of appropriate immune response, poor sanitation, travel to
underdeveloped countries, zoonotic contact.
• Peak age of Infection: Infants and Children.

Pathogenesis and Clinical Features
• ATTACHMENT:
• Sporozoites attach to the brush border epithelium of the small
intestine with the help of a unique protein called as CP47
(47kDa C. parvam protein).
• PENETRATIO:
• Discharge from the apicomplex present in the anterior end of
the sporozoites help in invasion.
• Following penetration, parasite forms a parasitophorous
vacuole near microvilli surface of the host cells (intracellular
extra cytoplasmic location).

• Then parasite activates host cell kinase signalling pathway that
liberates pro-inflammatory cytokines like tumor necrosis factor (TNF)
– α, Interleukin (Ic)- 8, prostaglandins, etc.
• Cytokines released from the inflammatory site can activate the
phagocytes; attract fresh leukocytes which in turn liberate soluble
factors.
• These factors increase intestinal secretion of chloride and water and
decreases the sodium absorption coupled to glucose transport . But
sodium-glutamine transport is not affected.
• So, glutamine transport based ORS (Oral Rehydration Solution) are
more effective in treatment.

Cryptosporidiosis in Immunocompetent Hosts
• Usually infection – asymptomatic.
• Sometimes, pts. develops self-limiting watery non-bloody
diarrhea.
• Other features like – abd. Pain, nausea, anorexia, fever, and/or
weight loss.
• Symptoms develop after an incubation period of 1 wk. and
subside within 1-2 wks.
• C. parvam accounts for 2-6% of cases of Traveler's Diarrhea.

Cryptosporidiosis in Immunocompromised Hosts
• More severe disease in IC pts with AIDS having CD4+ T cells
count less than 100/ul.
• Produces chronic, persistent remarkably profuse diarrhea (1-25
L/day), leading to significant fluid and electrolyte loss
(resembling cholera and diarrhea).
• Severe weight loss, wasting and abdominal pain may be seen.
• Autoinfection by thin-walled oocysts is key factor for the
chronic diarrhea which maintains the infection.

• Involvement of sites other than small
intestine – like – pharynx, stomach,
large intestine and respiratory tract is
quite common in HIV positive pts.
• Involvement of biliary tract can cause
papillary stenosis - is a disturbance of
the sphincter of Oddi, a muscular
valve, that prevents the opening and
release of bile or pancreatic fluids
into the duodenum
• In response to food entering the
duodenum.
• Obstruction of the valve can cause:
pancreatic pain. jaundice - bile
leaking back into the blood stream.

• Sclerosing cholangitis - Along-term
progressive disease of the liver and
gallbladder characterized by
inflammation and scarring of the
bile ducts which normally allow
bile to drain from the gallbladder.
• OR Cholecystitis - is inflammation
of the gallbladder.
• Can cause mid-epigastric or right-
upper-quadrant pain.

Laboratory Diagnosis
• Direct Microscopy:
• Stool Examination:
• 3 consecutive stool samples should be screened.
• Rarely (in HIV pts) –
• Sputum,
• Bronchial wash,
• Duodenal or
• Jejunal aspirates can be collected.

• DIRECT WET MOUNT:
• Direct mounting - From mucus plug of the stool sample is done.
• Can demonstrate highly refractile, round, double walled 4-6um sized
oocyst.
• Concentration Techniques:
• If oocyst load is less – conc. tech can be used –
• 1. Flotation technique –
• Sheather’s Sugar Floatation Technique – widely used for coccidian
parasites.
• Zinc Sulfate Flotation technique or Saturated Salt Flotation technique.
• 2. Sedimentation technique like –
• Formalin Ether or Formalin Ethyl Acetate Sedimentation technique.

• STAINING PROCEDURES:
• ACID FAST STAINING :
• Oocysts of C. parvam are acid fast to 1%
sulfuric acid or acid alcohol and appear as
round, 4-6 um red colored against blue
background.
• Sensitivity of AF staining is low and requires
minimum conc of more than 50,000
oocysts/mL of stool.

STAINING PROCEDURES:
• Commonly used modified ZN staining
methods: Kinyoun’s method (Cold AF
staining)
• Rapid Safranin Methylene blue method -
Oocysts of Cryptosporidium often (but not
always) stain a bright reddish-orange color.
• This method, advocated for Cyclospora, is not
widely used for Cryptosporidium because the
Cryptosporidium oocysts may not always
properly stained.
• Carbol Fuchsin negative staining method.
Kinyoun’s method
Rapid Safranin Methylene
blue method

STAINING PROCEDURES:
• Direct Fluorescent Antibody Staining –
• Done to detect C. parvam oocyst by using
fluorescent labelled monoclonal Abs
directed against cyst wall Ags.
• More sensitive (10 times) and specific than
Acid Fast staining.
• Useful to detect oocyst from water and
other environmental samples.
• Currently Gold Standard for
Cryptosporidiosis.

Antigen detection from stool :
• ELISA has been developed to detect C. parvam specific
coproantigen from stool shows a sensitivity ranging from 66 –
100% with excellent specificity.
• Immunochromatographic test (ICT) is also available for
simultaneous detection of Ag of C. parvam, Giardia and E.
histolytica.

Principal methods used for the detection of
Cryptosporidium in stool samples.

Antibody detection :
• ELISA has been developed to detect C. parvam specific antibodies
from serum (IgM and IgG) – seroepidemiological purpose.
• Indirect Immunofluorescent Antibody detection tests are also
available for detecting C. parvam specific antibodies against
oocyst antigens.
• MOLECULAR TECHNIQUES:
• PCR is available for detection of specific C. parvam genes from
both clinical and environmental specimens.
• HISTOPATHOLOGY-
• Parasites can be demonstrated in intestinal biopsy specimens.

Treatment
• Mild Cases: Self limited – Require – Fluid replacement – ORS,
lactose free glutamine supplemented diet.
• Severe Cases -
• Nitazoxanide – adult dose – 500 mg BD 3 days
• Paromomycin – alternative.
• Macrolide antibiotics – Spiramycin, Azithromycin and
Clarithromycin – have some activity against Cryptosporidium
• Prevention
• Requires minimizing exposure to infectious oocysts in human or
animal feces.
• Proper hand washing, using of submicron water filters, improved
personal hygiene are some of the efforts to prevent transmission.

CYCLOSPORA CAYETANENSIS

History
• Cyclospora cayetanensis is the most recently
described coccidian parasite as human
intestinal pathogen.
• Named by Schneider (1881).
• Human infection – described by Ashford in
1979.

Life cycle
• Host: Humans are only know host.
• Infective Form: Sporulated Oocyst
• Mode of Transmission: Feco-oral Route
• Life cycle is not fully understood but believed to be similar to
that of C. parvam except following points:
• Oocysts released in feces are not sporulated.
• Sporulation takes place in soil unlike C. parvam in which it
takes place in human intestine.

Life cycle of Cyclospora cayetanensis

Morphology of Sporulated Oocyst
• Mature oocyst is
round, 8-10um in
size.
• Contains 2
sporocysts .
• Each sporocysts
has 2 sporozoites.

Epidemiology
• Prevalent in Central America and South Asia.
• 11% of AIDS related diarrhea reported from Haiti.
• Children of Nepal 32%
• Traveler’s coming to India, Pakistan and Morocco.
• Less common in African countries.

• DIRECT DEMONSTRATION METHODS:
• STOOL EXAMINATION:
• 3 consecutive days sample should be screened
• Cyclospora oocysts are approx. twice the size of the
Cryptosporidium oocysts.
• It is round, 8-10um size and variably acid fast (i.e. 50%
of oocyst are acid fast, rest are non acid fast).
• Auto-fluorescence – The oocyst under ultraviolet
epifluorescence microscopy is both rapid and sensitive,
but not specific.
• Additional stains includes – Auramine, Safranin and
Lactophenol cotton blue stains.

Treatment
• Cotrimoxazole : Trimethoprim 160mg/ Sulphamethoxazole
800mg BD for 7 days.
• HIV pts may experience – relapse and may require long
term suppressive maintenance therapy.
• Pts who cannot tolerate cotrimoxazole may be treated with
Ciprofloxacin or Nitazoxanide.

ISOSPORA BELLI

Introduction
• Isospora more than 200 species are identified.
• Isospora belli is the only human pathogenic
species.
• No other animal reservoir known.
• It belongs to family – Sarcocystiidae.
• First described by Virchow in 1860 and was
named by Wenyon (1923).

Morphology
• OOCYST:
• Sporulated oocyst is oval/elliptical.
• Measuring 23-36um x 12-17um in
size.
• Contains 2 sporocysts.
• Each with 4 sporozoites.
• The oocyst is surrounded by a thin,
smooth, two layered cyst wall.

Life cycle – Isospora belli
• Host: Man.
• Infective form: Sporulated oocyst.
• Mode of Transmission: Feco-oral Route.

Life Cycle
• Man acquires infection after consumption of contaminated
food or water with the sporulated oocyst of Isospora belli.
• In the proximal small intestine – eight sporozoites are
released from each oocyst.
• Invade – duodenal and jejunal epithelium and transform into
trophozoites.
• Trophozoites multiply and transform into schizont that
undergoes asexual multiplication (Schizogony) to produce
merozoites.

Life Cycle
• Merozoites again attack fresh enterocytes to repeat the asexual cycle.
• Some of the merozoites transform into microgametocyte and
Macrogametocyte (Gametogony).
• Eventually, they form macrogametes and microgametes which fuse to
form the zygote (Fertilization).
• Zygote secrete the cyst wall and develops into immature oocysts,
excreted in the feces.
• In the soil, the sporulation occurs within 3-4 days and immature
oocyst transform into sporulated oocyst which bears two sporocysts
each containing four sporozoites.

Life Cycle – Isospora belli

• Lab diagnosis methods are similar to that of
Cryptosporidiosis.
• STOOL EXAMINATION:
• Detection and demonstration of
characteristic – Oocyst in pts stool
specimen.
• ACID FAST STAINING:
• The oocyst is uniformly acid fast,
• Oval/elliptical,
• 23-36X12-17um
• Surrounded by a thin, smooth, two layered
cyst wall.
• Other stains like- LPCB and Safranin can be
used.

• FLUORESCENT STAINED SMEARS:
• By Auramine Rhodamine stain.
• AUTO-FLUORESCENCE – can be seen under 330-380 nm ultraviolet
filer.
• However, this property is not consistent like Cyclospora.
• Phase contrast microscopy is also useful.
• If load of oocysts is less – stool samples are conc by Sheather’s Sugar
Flotation technique.
• Examination of small bowel specimens (e.g. duodenal aspirates) may
be helpful if stool examination is negative.

• OTHER METHODS:
• Peripheral Eosinophilia.
• Charcot-leyden crystals in stool.
• Low CD4-T cell count (in HIV infected)
• MOLECULAR METHODS:
• PCR using Isospora belli specific primers – highly sensitive and
specific but not used routinely.
• TREATMENT –
• Cotrimoxazole – 160mg (Trimethoprim) / 800mg
(Sulfamethoxazole) 4 times daily for 10 days.

Microsporidium

Microsporidium
• CLASSIFICATION:
• These are eukaryotic, spore forming obligate intracellular parasite
infecting a broad range of vertebrates and invertebrates.
• In human, they are opportunistic pathogens affecting HIV positive
pts.
• Microsporidia have a unique characteristics of entering into host
cell via a polar tube within a spore.
• Taxonomic classification –
• Previously under Sporozoa.
• Recent reports suggest – Fungus.

Taxonomic Classification
• Kingdom: Fungi
• Phylum : Microspora
• Class: Microsporea
• Order: Microsporidia
• Genus: Microsporidium

Morphology of Spores
• Highly resistant extracellular form (survives in the
environment) and also is the infective stage.
• Oval, variable in size ranging from 1.5-5um in diameter.
• Double layered cyst wall.
• Outer layer (exospore) is proteinaceous and electron-dense.
• Inner layer (endospore) is chitins and electron-luscent.
• Inner side to the cyst wall is lined by plasma memberane.

Morphology of Spores
• Cytoplasm contains various organelles like coiled polar tube,
polar sac, polaroplast, nucleus and a posterior vacuole
• Coiled polar tube has a spring like tubular extrusion mechanism
by which the infective material Sporoplasm is injected into the
host cell.
• The polar tube ends anteriorly into a Polar sac.
• Near the anterior pole, Polaroplast is situated on both the side
of the polar tube, which is a component of the extrusion
apparatus.

Life cycle
• Mode of transmission:
• Humans acquire infection by ingestion of
spores of microsporidia.
• Rarely inhalation.
• Or Ocular contact.
• Infective Form: Spore

Life Cycle – Microsporidia
• EXTRUSION OF SPOROPLASM :
• Infective material of spore (Sporoplasm) is injected into the host
cells (enterocytes).
• A long flexible cylindrical structure a polar tube comes out from
spore and with the extrusion mechanism Sporoplasm is injected in
the host cells.
• Helped by the polar sac, polaroplast, raised pH an calcium ion.
• By punching a hole in host cell plasma membrane for e. g.
Enterocytozoon.
• OR by expansion of host cell plasma membrane to cover the
emerging sporoplasm, for e.g. Encephalitozoon.

• ASEXUAL CYCLE :
• In host cell, sporoplasm multiplies to generate a number of
meronts.
• Multiplication –
• Binary fission (Merogony)
• or Multiple fission (Schizogony) or
• Division of cytoplasm without relation to nuclei produce
multinucleated offspring's (Plasmotomy).
• Meronts are round to elongated.
• Remain free in host cell cytoplasm OR lie inside
parasitophorous vacuole (Encephalitozoon).

• SEXUAL CYCLE :
• Finally meronts develop into sporonts;
• Eventually get surrounded by a double layered cyst wall and directly
transform into sporoblasts OR
• Multinucleated to form sporogonial plasmodia that later transform
into sporoblast.
• Sporoblast – undergo - Sporogony – develop into spores.
• Spores present – free in cytoplasm OR eclosed by sporophorous
vesicle as in Pleistophora & Trachipleistophora.
• Most of the spp. spores are released by lysis of the host cell
except in Encephalitozoon hellem, where the spores are germinate
with out lysing host cells. (Can be asked as MCQ) .

• Microsporidium mainly cause:
• Opportunistic infections in AIDS pts.
• In pts with supressed immunity – Organ recipient of organ transplant :
• ENTERIC INFECTION:
• Immunocompromised individuals:
• Pts are usually co-infected with other coccidian parasites like Crypto,
Cyclospora, Isospora.
• Common features: Diarrhea, Malabsorption and wasting.
• Immunocompetent individuals:
• Traveler’s diarrhea
• Infections in chronically debilitated elderly people.

• OCULAR INFECTION:
• Immunocompromised individuals:
• Involves conjunctival and corneal epithelium –
• Common features: Epithelial Keratopathy and Conjunctivitis.
• Immunocompetent individuals:
• Involves deep corneal stroma may lead to corneal scar and ulcer –
Stromal Keratitis.
• MUSCULOSKELETAL INFECTION:
• Facial myositis with muscle weakness
• Myalgia and fever
• DISSEMINATED INFECTION:
• Rhinitis, sinusitis, cholangitis, bronchitis, hepatitis, peritonitis, UTI,
smooth muscle infection.

Epidemiology
• Recognized as opportunistic infectious agent worldwide
since the advent of HIV AIDS.
• Prevalence ranging from 2 to 50% reported from America,
Europe and Australia in HIV pts.
• In India, few clusters of cases reported.
• First case reported in 2001 - Enteric microsporidiosis.
• Ocular microsporidiosis – 2003.
• In a study from PGI Chandigharh – Microsporidia were the
most common parasite detected 15% in the stool of HIV
pts.

• LIGHT MICROSCOPY:
• SAMPLES:
• Stool
• Small intestinal contents
• Corneal smear or small intestinal biopsies
• Sputum
• Urine
• Etc.

• MODIFIED TRICHROME STAIN
(MTS):
• The recommonded stain for
Microsporidium.
• Appears red oval refractile
spores against a blue
background.
• Various modifications of MTS
are Weber green MTS, Ryan
Blue MTS, Kokoskin Hot
Method of MTS.

• MODIFIED ACID FAST STAIN:
• Modified Acid Fast stain using 1% acid
alcohol – Spores of Microsporidia are acid
fast – red with darkly stained band at the
tip.
• GRAM’S STAIN (BROWN-BRENN
MODIFICATION):
• Spores stains – Gram positive.
• OTHER METHODS:
• Giemsa Stain, PAS, Gram Chromotrope stain
can be used.
Acid fast stain – Red
Mature spores and Blue
unstained immature or
degenerated spores
Duodenal Biopsy –
GM stain shows
spores inside
enterocyte

ELECTRON MICROSCOPY:
• Gold Standard Method for definitive
diagnosis of microsporidiosis.
• Highly specific, lacks sensitivity, time
consuming, labour-intensive and
expensive.
• Microsporidia can be identified upto
genus and species level based on ultra
structure of the spores –No of coils in
polar tubes.
• Method of division and nature of host
cell parasite interface – grow directly or
inside parasitophorous vocuoles.

Culture
• Can be successfully cultivated in
many mammalian cell lines:
• Monkey kidney cells
• Rabbit kidney cells
• Vero and RK131
• Human fetal lung fibroblast –
MRC-5
• Limited use in routine diagnosis.
• Useful for Antigen preparation
and drug susceptibility studies /
tests.

Serology
• ANTIBODY ASSAY:
• Various methods like:
• Immunofluorescence,
• Immunoperoxidase,
• ELISA
• Western Blot
• Can be used to detect Abs.
• Not very useful as lack specificity and give flase positive
• ANTIGEN DETECTION:
• Direct fluorescent Test (DFT): Using fluorescent tagged
monoclonal Abs – Ag on Microsporidia spores – detected.

MOLECULAR METHODS:
• Several PCR based methods are in use.
• Targeting different genes like: Small subunit and
Large subunit genes of Ribosomal Ribonucleic Acid
(rRNA).
• Intergenic spacer region (ISR) gene for diagnosis and
speciation of Microsporidia infecting humans.

TREATMENT
• Albendazole – effective – Enteric, Muscular, Ocular
microsporidiosis- 400mg BD 2-4 wks.
• Relapse may be seen in some cases.
• Other – Octreotide / Nitazoxanide /Fumagillin.
•
• Nutritional Therapy: to reduce malabsorption in enteric.
• Topical agents can be applied for corneal lesions –
Itraconazole, Metranidazole
• Contorl of AIDS by ART is essential to reconstitute
Immune system and to prevent reinfection

Expected Question
• Classify Coccidian parasites ? Describe the
lifecycle, pathogenesis and laboratory
diagnosis of Cryptosporidium.
• Enumerate the opportunistic parasitic
infections in AIDS pts. Describe the lifecycle,
pathogenesis and laboratory diagnosis of
Microsporidium.

Thank you all!

Opportunistic coccidian parasites

More Related Content

What's hot

Similar to Opportunistic coccidian parasites

More from Prasad Gunjal

Recently uploaded

Opportunistic coccidian parasites