Miscellaneous Protozoa

Topic 8

Focusing In i. Toxoplasma gondii

● Cyclospora and Microsporidia are
known to produce human intestinal
disease
○ But they are still to be 3. Blastocystea
learned a. Only contains Blastocystis
hominis (formerly
Miscellaneous Protozoa Classification considered as yeast)
Remaining Four Classes of Protozoa 4. Pneumocystis jiroveci
1. Ciliates (Ciliophora) a. Traditionally, it was a
a. Contains cilia (hairlike protozoa, now considered a
cytoplasmic extensions for fungus.
motility)
b. Ex. Balantidium coli (a Overall, they are unicellular
human pathogen; Phylum
Ciliphora, Class
Kinetofragminophorea,
Intestinal Species: …)
2. Select Sporozoa (Apicomplexa)
a. Except. Plasmodium and
Babesis spp.
b. Intestinal and tissue-
dwelling in nature
c. Belongs to subclass
Coccidia
i. Protozoan parasite
ii. Asexual replication
is outside human
host
iii. Sexual replication is
inside a human host.
d. Referred as coccidian
protozoa
e. Phylum Apicomplexa, Class
Sporozoa, Intestinal
Species:
i. Isospora belli,
Sarcocystis spp.,
Cryptosporidium
parvum
f. Tissue Species:
Balantidium coli
Laboratory Diagnosis
● Disease: Balantidiasis
● Stool examination
Morphology
○ Diarrhoea likely contains
Trophozoites
trophozoites (but not
● Considered as the largest
frequently)
protozoan (28 - 152 μm)
○ Formed stools contain
● Width: 22 - 123 μm (apprx. 40 μm)
cysts.
● Rotary boring motility
● Sigmoidoscopy (if suffering from
● Has 2 nuclei
sigmoid rectal infection)
○ Micronucleus - small dot like
● Wet preparation and permanent
nucleus; usually invisible
stain - Crucial for laboratory test
○ Macronucleus - often
report accuracy
kidney-bean shaped; can
● Multiple samples are needed
appear as hyaline mass
(Usually in unstained preps)
Life Cycle Notes
● Has two contractile vacuoles (in
granular cytoplasm)
○ Usually at least one is
visible
● Cytoplasm may contain food
vacuoles, ingested microbes
(bacteria),
● Has a small cytostome (mouth for
phagocytosis)
● Cilia surround organism for
locomotion
Cyst
● Size: 43 - 66 μm (Avg.: 52 - 55 μm)
● Nucleus
○ Macronucleus - Usually be
revealed in stained prep.
○ Micronucleus - may not be
observed in wet/permanent
prep.
● Has 2 contractile vacuoles (may 1 or
both be visible, especially in young ● Similar to that of Entamoeba
unstained cysts) histolytica (but B. coli does not
● Has double protective cyst wall multiply in cyst phase)
● Cilia may be visible in between the
cyst walls in unstained young cysts ● Infective stage: Cyst
○ Mature tends to lose their ● Diagnostic Stage: Cyst and
cilia Trophozoite
 ● Ingestion of cysts from ● Colon abscess and ulcers (in the
contaminated food and water mucosa and submucosa)
● Excystation in small intestine ○ With secondary bacterial
● Trophozoites stays and feeds in infections
cecal and terminal ileum (including Acute infections
lumen, mucosa, and submucosa of ● 15 liquid stools daily with pus,
small intestine) mucus, and blood
● Multiplication via transverse binary
fission Chronic infection
○ Trophozoites are fragile ● Tender colon
from outside environment ● Anaemia
● Encystation in lumen ● Cachexia
● Mature cyst as an infective stage ● Frequent diarrhoea with alternating
for new hosts. constipation
○ Cysts survives for weeks
outside ● B. coli can be extraintestinal: liver,
lungs, pleura, mesenteric nodes,
Epidemiology urogenital tract (rare)
● Distributed worldwide
○ With known outbreaks Treatment
● Low human infection incidence ● Important factors for prognosis:
● Transmitted by ingesting severity and response to treatment
contaminated food and water by ● Good recovery chance for
oral-faecal/person-person routes Asymptomatic and chronic
○ Recent days presumed ● Effective: Oxytetracycline
faecal-submerged water of (Terramycin), Iodoquinol
pigs (a reservoir host) plays ● Metronidazole (Flagyl) can be used
in important source of as well
infection
○ Due to high pig-human Prevention and Control
contact shows low ● Effective: Personal hygiene and
incidence of infection, so it Proper sanitary conditions
could be infected food ● Proper pig handling with their
handlers faeces

Clinical Symptoms: Asymptomatic Notes of Interest and New Trends

● Similar to E. histolytica, some ● Trophozoite is seen as a sac in
patients are carriers and shape
asymptomatic ○ Balantidium means “little
bag”
Clinical Symptoms: Balantidiasis ● 63% - 91% of pigs harbour B. suis
● Mild colitis
● Diarrhoea
● Clinical balantidiasis (through ○ Apparently non-pathogenic
amoebic dysentery) but morphologically similar
to B. coli
 ○ There were attempts to be For visibility/identification
infected, but unsuccessful ● Visible in direct wet preps and
● Suggestion that humans have high concentration/flotation procedure
natural resistance to this organism ● Sheather’s sugar flotation
procedure can obtain promising
results
Isopora Belli ● Oocysts may be transparent and
hard to identify if in saline wet prep.
● Disease: Isosporiasis ○ They are identified easily via
iodine prep
Morphology ● Dim microscope light and proper
Oocysts contrast for favourable conditions
● 25 - 35 μm x 10 - 15 μm of parasite recovery
○ Average: 30 x 12 μm ○ Especially when screen
● Sporoblast (developing morphologic tested by zinc sulphate
form in the oocyst technique/other
○ Roundsh immature sac concentration + polyvinyl
○ Small nucleus alcohol preservation
○ Granular cytoplasm ● Unlikely to diagnose successfully:
● Maturing young oocyst splits into 2 Auramine rhodamine permanent
sporoblast stain for preparation and
● Maturing Sporocyst splits until examination.
sporocyst/mature oocyst (mature ● Recommendedpermanent stain:
stage) Modified acid-fast stain.
○ Rounding sac with four ○ Shows organism
sausage-shaped characteristic (same with
sporozoites Cryptosporidium)
● Confirmatory test: Wet preps
NOTE
Both sporocyst and sporoblast have a
double-layered, smooth, colourless cell wall

Laboratory Diagnosis
Retrieving
● Specimens: fresh faeces, duodenal
contents
○ Stools may have premature,
partially matured, and
mature oocysts
● Entrotest for getting oocysts
● Intestinal biopsies for finding
intracellular morphologic stages
● A biopsy may contain oocysts, but
the stool will not due to small
numbers present.
 ● Excystation in small interesting
(oocyst to reveal sporozoites)
● Schizogony in intestinal mucosa
cells to turn into merozoites
● Making of macrogametocyte and
microgametocyte (via gametogony)
● Macro and microgametocytes unite
Life Cycle Notes to oocysts to be excreted in stool
● Immature oocyst complete
development outside environment
● Mature sporulated oocysts for next
infection, repeating cycle

Epidemiology
● Rare, but worldwide
○ Rare infection may be
because of false-negative
results due to difficulty in
recognising
● Increase reported cases during and
after WWII (Africa, SEA, Central
America, South America esp. Chile)\
● Increase infection due to AIDS
○ Therefore, Unprotected
oral-anal sexual contact as
Mode of Transmission
○ Therefore, infections are
opportunistic

Clinical Symptoms
Asymptomatic
● Self-limited
● Thought to be typical coccidal Isosporiasis
parasite ● Mild GI discomfort - severe
● No intermediate hosts dysentery
○ Believed Intermediate host: ● Common
Pigs and cattle ○ Weight loss
● Definitive hosts: Humans (for ○ Chronic diarrhoea
asexual and sexual reproduction) ○ Abdominal pain
○ Asexual: Schizogony ○ Anorexia
● Ingestion of infective mature (a.k.a. ○ Weakness
sporulated) oocysts via ○ Malaise
contaminated food/water. ● Eosinophilia (leading to Charcot-
○ Can be transmitted via oral- Leyden crystals)
anal sex ● Severe
○ Malabsorption syndrome
 ○ Foul-smelling, pale yellow,
loose stools
○ May increase faecal fat
levels

○ Shedding of oocysts in stool

as long as 120 days
○ Death

Treatment
● Bland diet and plenty of rests for
asymptomatic or mild
● Chemotherapy (of a
trimethoprim,sulfamethoxazole/pyri
methamine, sulfadiazine mix) for
severe
○ Lower dosage for longer
period for AIDS-infected

Prevention and Control

● Similar with E. histolytica
● Proper personal hygiene
● Protected sex especially for gays
Sarcocystis Species
● Disease: Sarcocystic infection
● Sarcocystis hovihominis/hominis for
cows
● Sarcocystis suihominis for pigs
● Sarcosystis lindemanni - an
umbrella term as potentially
pathogenic to humans

Morphology
Mature Oocysts
● Originally classified and considered
as genus Isospora member, but now
genus Sarcocystis member. (due to
differences such as life cycle)
● Hs 2 mature sporocysts with 4
sausage-shaped sporozoites
(Average size: 10 - 18 μm)
● Double-layered, clear, colourless
cell wall surrounding sporocysts NOTE
Asexual reproduction happens in
Laboratory Diagnosis intermediate hosts
● Specimen: Stool
○ May contain fully developed Ways of Human infection 1
oocysts ● Ingestion of uncooked pig/cattle
● Mature oocysts are seen in wet meat that’s infected with
preps, but has ruptured with only its Sarcocystis sarcocysts
sporocysts visible ● Definitive Hosts: Humans
○ Sporocysts may be seen 1 ○ Sexual reproduction via
or 2 cemented together gametogony in intestinal
● Routine histologic methods for cyst cells
stage (sarcocyst) identification via ● Oocysts -> sporocysts release for
muscle samples next cycle in another host

Life Cycle Notes

Ways of Human infection 2
● Human swallow oocysts from stool
of animals (except cattles and pigs)
● Sarcocysts stay in striated muscle
○ Therefore, Intermediate
Host: humans
Epidemiology
● Low frequency, but worldwide
● Sarcocystis are found in other
animals than cattles and pigs

Clinical Symptoms
Sarcocystis Infection
● Fever
● Severe diarrhoea
● Weight loss
● Abdominal pain
● Muscle tenderness (presumably
from Sarcocystis invading striated
muscle)

Treatment
● Similar to Isospora belli
(Trimethoprim +
sulfamethoxazole/pyrimethamine +
sulfadiazine chemotherapy) except
for those in striated muscle
(unknown)

Prevention and Control

● Humans as Direct Host: Proper
cooking of beef and pork
● Humans as Intermediate Host:
Proper stool care and stool disposal
Cryptosporidium
parvum
Life Cycle Notes
● Disease: Cryptosporidiosis

Morphology
Oocysts
● 4 - 6 μm
● Often confused with yeast
● Mature oocysts has 4 small
sporozoites surrounded by thick
cell wall (often invisible)
● Cryptosporidium oocysts has no
sporocysts
● Has visible 1- 6 granules

Schizonts and Gametocytes

● Schizonts contain 4 - 8 merozoites,
microgametocytes, and
microgametocytes (2 - 4 μm; not
routinely seen) ● Ingestion of mature oocyst
● Excystation in upper GI ->
Laboratory Diagnosis Sporozoites emerge to stay in
● Specimen: Stool epithelial cells
● Oocysts can be seen using ● Asexual and Sexual replication
○ Iodine stain ● Sporozoites rupture (from oocysts)
○ Modified acid-fast stain -> invading new epithelial cells
○ Formalin-fixed smear + ● Some oocysts remain and pass
Giemsa stain through faeces as infective for new
○ Enterotest hosts
○ Enzyme-linked
immunosorbent assay Oocyst types
(ELISA) ● Thin-shelled - responsible for auto
○ Indirect fluorescence. infections (due to rupturing inside
○ Concentration vis modified host)
zinc sulphate floatation or ● Thick-shelled - Intact and passed
Sheather’s sugar flotation out of body; starts auto infections
(especially when examined occasionally
under phase-contrast
microscopy) Epidemiology
● Intestinal biopsy for merozoites and ● Worldwide
gametocytes recovery ● 1/20 of Cryptosporidium species
can infect humans
(Cryptosporidium parvum)
 ● MoT: Water/food contaminated with Prevention and Control
infected faeces ● PPE
● Immunocompromised (e.x. AIDS), ● Proper water supply treatment
Immunocompetent children in ● Proper handwashing
tropical region, children in daycare ● Proper disinfection of equipment via
centres, animal handlers, who commercial bleach or 5 - 10%
travels abroad are at risk of ammonia
infection ● Enteric precautions (for those
infected)
Clinical Symptoms
Cryptosporidiosis Notes of Interest and New Trends
● Diarrhoea (for 2 weeks) ● C. spp. Was first associated with
○ 1 - 4 weeks for those in poultry and cattle, now as an agent
some daycare centres responsible for neonatal diarrhoea
○ Fatal for young children if in cattle and lambs (life-
severe (due to fluid loss) threatening)
○ Severe diarrhoea for ● First reported 1976
immunocompromised ● Several outbreaks in water supply
(particularly AIDS) including due to Cryptosporidium oocysts
1 or more of other contamination
symptoms mentioned below ○ Carroll County, Georgia -
● Fever 1987
● Nausea ○ June 2011 - Indiana first
● Vomiting station workers after barn
● Weight loss fire on nearby Michigan
● Abdominal pain farm (due to local hydrant
● Malabsorption (for those with AIDS) water for Cryptosporidium
● Extraintestinal Routes: Stomach, contaminated swimming
Respiratory Tract pond water by calf faeces
○ Causing weakening leading ● Modified stool processing
to death technique involving layer and
floatation of hypertonic sodium
● AIDS with Cryptosporidiosis chloride solution for separating
Statistics Cryptosporidium oocysts.
○ 3 - 20% US
○ 50 - 60% Africa and Haiti
○ Cryptosporidium infection is
considered to be a cause of
morbidity and mortality
Treatment
● None so far (after countless
experiments and researches)
● Spiramycin (although in
experimental stage; for ridding of
Cryptosporidium)
Blastocystis hominis Life Cycle Notes
● Disease: Blastocystis hominis
infection

Morphology
● Common and easiest to recognise:
Vacuolated form

Vacuolated form
● 5 - 32 μm
○ Average: 7 - 10 μm\
● Large central, fluid-filled vacuole
(90% of the cell)
● 10% - Periphery of the organism
○ Ring of cytoplasm with 2 - 4
nucleus

Laboratory Diagnosis ● Reproduction by sporulation or

● Specimen: stool binary fission
● Iodine wet prep ● Has a lot of morphologic forms to
○ Light yellow peripheral pass
cytoplasm with 1 - more ● Does sexual and asexual
nuclei reproduction
○ Unstained central vacuole ● Has pseudopods extension and
(clear and transparent) retraction
● Permanent stain prep ● Detailed discuss has not been
○ Central vacuole may vary in widely presented
visibility
○ Nuclei in peripheral Epidemiology
cytoplasm is dark ● Epidemic in subtropical countries
● Saline stain lyses the organism, ● 10 - 25 years ago - articles show B.
giving false-negative result hominis to be found ranging from
Saudi Arabia to British Columbia
NOTE: ○ Study in Saudi Arabic shows
Sceen suspicious samples via iodine wet no conclusion of travelling
prep and permanent stain (for confirmation being a risk factor
of parasite) ● MoT: ingestion of faecally
contaminated food and water

Clinical Symptoms
Blastocystis hominis infection ○ Thus it is placed into
● Unclear pathogenicity Stramenopiles (a line of
● Diarrhoea eukaryotes) after
● Vomiting undergoing so much
● Nausea reviews
● Fever
● Abdominal Pain
● Cramping

● Other say that undetected

pathogen is responsible for
discomfort indicated above

● B. hominis + other pathogens

○ B. hominis is believed to be
the pathogen
○ Severe symptoms as said
above

Treatment
● Iodoquinol
● Metronidazole
○ Both are suggestions for
those infection with
Blastocystis who has no
reason for diarrhoea

Prevention and Control

● Proper faecal material treatment
● Thorough hand washing
● Subsequent proper handling of food
and water
○ Those 3 are critical for
halting spread

Notes of Interest and New Trends

● B. hominis as name given by Emile
Brumpt in 1912
● Has been a subject of controversy
○ Algae -> harmless intestinal
yeast -> protozoan
parasite(since 1970s)
● 1966 - Genetic analyses shows
Blastocystis is not fungal or
protozoan
 Life Cycle Notes
Cyclospora
cayetanensis
● Disease: Cyclospora cayetanensis
infection

Morphology
Oocyst
● Similar to cryptosporidiosis
● Intestinal coccidal organism
● 7 - 10 μm in diameter
● Maturation -> 2 sporocysts (with 2
sporozoites each)

Laboratory Diagnosis
● Can be diagnosed through
concentration of stool samples
even without formalin fixative
● Oocyst sporulation (making spores)
● Similar that of Isospora
is best at room temperature
● Floatation method + phase-
● Ingestion of oocyst (contains 2
contrast/bright field microscopy for
sporocysts, enclosing with 2
isolation
sporozoites)
● Modified acid-fast stain
● Small intestine as place for
● Oocysts auto fluoresce under UV
sporozoites emergence
microscopy
● Asexual and sexual reproduction for
sporozoites, making many
merozoites, and macrogametocyte
and microgametocyte production
respectively
● Micro and macrogametocyte unites
-> Oocysts
● Passing of immature oocysts in
stool
● In optimal conditions, oocysts
continue to develop and mature
outside human body (takes 1-more
weeks)
● Maturation complete, Oocysts are
good to make a new cycle
● There are no animal reservoir
Epidemiology
● May countries
○ US
○ Canada
○ Lima, Peru
(where children live in
unsanitary condition)
○ Nepal and other parts of
Asia (as
travellers/foreigners)
○ 1990 mini outbreak of
Chicago (in a physician’s
dormitory)
● Source of infection: Imported
(sometimes) contaminated lettuce
and fresh fruit (raspberries as
known source of infection)

Clinical Symptoms
Cyclospora cayetanensis infection
● Similar to Cryptosporidiosis (as to
seen in children)
○ But C. cayetanensis causes
longer diarrhoea time
● No known connection between C.
cayetanensis infection and
immunocompromised patients

Prevention and Control

● Treating water properly before
using (for handling and processing
food)

Notes of Interest and New Trends

● May not be recovered using
standard/traditional specimen
processing techniques
● See laboratory diagnosis section for
future containing.
 ● Uses transmission electron
Microsporidia microscopy for identification of
microsporidia
● Disease; Microsporidia infect,
● Molecular diagnostic methods are
microsporidial infection
currently developed
● Classified as protozoa by WHO, but
Fungi from DNA testing results
Life Cycle Notes
● 3/5 cause human disease are
observed for those with AIDS
○ Most well known:
Enterocytozoon bieneusi
(causing enteritis)
○ Encephalitozoon and
Pleistophora is known to
infect AIDS, causing severe
tissue infections
○ Microsporidium and Nosema
● Maybe have direct or indirect hosts
(a fatal infection for
● Infection starts with spores
immunocompromised
injecting sporoplasm into cell
infants) is known for corneal
● Complex reproductive process ->
infections
new spores emerge + new infected
cells
Morphology
● Spores dispersed via faeces, urine,
Spores
death of host (for direct
● There are different morphological
transmission cycle)
forms, but spores are only
● Spores may be ingested by
described
carnivorous animal
● 1 - 5 μm
● Unlike other protozoans, it has
Epidemiology
extruding polar filaments (tubules)
● E. bieneusi founded in AIDS
to initiated infection via injecting
patients of Haiti, Zambia, Uganda,
sporoplasm (infectious) into host
UK, US, and Netherlands
cell
● Those without AIDS are also
mentioned
Laboratory Diagnosis
● Vary through species
Clinical Symptoms
● Serologic test for detection of some
Microsporidial Infection
species
● Enteritis
● Some will grow in cell culture
● Keratoconjunctivitis
● Couple of stains to detect all or part
● Myositis
of the spore microscopically
● Peritonitis (rare)
● Trichrome/Acid-fast-stained thin
● Hepatitis (rare)
smears to show desired spores
● Partial positive stain for acid-fast
stain or PAS (periodic acid-Schiff)
● Giemsa-stained biopsy and faecal
concentration shows spores
Treatment
● Albendazole or oral fumagillin for E.
bieneusi
● Albendazole + fumagillin eye drops
for Nosema

Notes of Interest
● C. cayetanensis and Microsporidia
are somewhat common
● Recently, Microsporidia is in US’
EPA (Environment Protection
Agency) Candidate Contaminant
List as emerging water-borne
pathogen needing monitorial
attention
● Microsporidia is common for those
immunocompromised (including
AIDS), while AIDS continue to
increase in incidence
Toxoplasma gondii
Laboratory Diagnosis
● +Disease: Toxoplasmosis,
● Specimen: blood (via serological
congenital toxoplasmosis, cerebral
tests)
toxoplasmosis
● Double Sandwich ELISA method for
immunoglobulin M (IgM) antibody
Morphology
detection in congenital infections
● Morphologies seen by humans:
● Indirect fluorescent antibody (IFA)
tachyzoites and bradyzoites
test Immunoglobulin G and M
● Infective stage: oocyst
detection
(encountered especially in
● ELISA and indirect hemagglutination
veterinary parasitological
test (IHA) for only immunoglobulin G
techniques)
● Human tissue samples microscopic
examination or inoculation of lab
Oocyst
animals for observation of
● Infective form
demonstration of trophozoites
● Similar look with I. belli
(tachyzoites) and cysts (filled with
○ Difference: T. gondii is
bradyzoites)
smaller
○ Tedious, and impractical
● Round - slightly oval
(not easy and effectively)
● 10 - 15 μm x 8 - 12 μm wide
● Contains two sporocysts (4
Life Cycle Notes
trophozoites each)
● Border by clear, colourless, 2-
layered cell wall

Tachyzoites
● Actively multiplies
● Crescent-shaped
● 3 - 7 μm x 2 - 4 μm
● One end is rounder
● Has 1 contrary located nucleus,
surrounding a cell membrane
● Organelles may be present (ex.
Mitochondrion, Golgi apparatus)

Bradyzoites ● Accidental life cycle is complicated

● Same look as tachyzoite, but (involving many animals and
smaller humans)
● Gather in clusters in a cell
● Develop in surrounding membrane Natural Cycle
● Forms a cyst in varied ● Definitive host: cat, other felines
extraintestinal tissues and muscles ● Intermediate hosts: rodents (mice
● A cyst may have 50 - several and rats; they ingest mature T.
thousand bradyzoites (12 - 100 μm) gondii)
 ○ Mature oocyst -> d. IgM does not cross the
tachyzoites (growing) in placenta, but infants may
intestinal epithelium present anti-T. gondii IgM
○ Tachyzoites goes to from birth - several months
brain/muscle old
● Cat eats brain/muscle tissue of 4. Contaminated blood transfusion
rats/mice to release enclosed (rare)
bradyzoites into cat
● Bradyzoites -> tachyzoites ● In humans, tachyzoites emerge
● Asexual and sexual reproduction in from cyst to grow and divide
cat gut ● Tachyzoites - tissue damage and
○ Sexual reproduction results initial infection
in immature oocytes, and it ● Tachyzoites transfer to tissues and
to shed in stool organs (ex. brain) to form cyst-filled
● Complete oocyst matures outside (1 bradyzoites
- 5 days)
● Cycle repeats (rat <-> cat) Epidemiology
● Worldwide (due to various animals
Accidental Infection: Humans harbouring it)
● Has many ways ● Anyone and anything and contract
T. gondii
1. Ingesting mature oocysts of ○ Especially those with AIDS
infected cat faeces via hand-to-
mouth transmission Epidemiologic considerations
a. Primary source From litter 1. T. gondii infection occur in 15 - 20%
boxes, children’s sandboxes of population in US
2. Undercooked contaminated 2. 93% and 50% of of Parisian women
cattle/pig/sheep/other animals meat and children (respectively) via
a. Via ingesting oocyst in cat eating undercooked meat
faeces 3. Around 4,000 infects are infected
b. Sporozoites released transplacentally in US annually
c. Same with natural cycle 4. Oocysts survives under uncommon
d. Cyst formed in animal conditions for a long time
muscle a. Kansas - survived for 18
e. Parasites are active for months (with winter
years seasons)
3. Transplacental 5. Humans infections in Us are caused
a. Asymptomatic mother by hand-to-mouth, eating oocysts
passes infection to unborn of cat faeces, eating contaminated
foetus meat, transplacentally, and
b. Mother produces IgG and contaminated blood transfusion
IgM to parasite (although rare)
c. IgG crosses to placenta to
be present in circulation of
foetus for several months
Clinical Symptoms ○ Age of foetus and time of
Asymptomatic infection
● Many especially children (after ● Subsequent retinochoroiditis (after
newborn) years)
● Conditions for T. gondii to cause ● Typical symptoms for children
diseases ○ Hydrocephalus
○ Organism’s virulent strain in ○ Microcephaly
the body ○ Intracerebral calcification
○ Host in susceptible state ○ Chorioretinitis
(ex. AIDS) ○ Convulsions
○ Particular site where tissue ○ Psychomotor Disturbances
destruction is most likely to ■ All of them results to
occur mental retardness,
severe visual
Toxoplasmosis: General Symptoms impairment/blindnes
● Typical infected show mild s
symptoms, mimicking infectious ● Infant results
mononucleosis ○ 5 - 15% of infected patients
● Acute die
○ Fatigue ○ 10 - 13% of infants will have
○ Lymphadenitis moderate - severe
○ Chills handicaps
○ Fever ○ Around 8 - 10% infants will
○ Headache have brain and eye damage
○ Myalgia ○ Remaining 58 - 72% infants
● Chronic are asymptomatic at birth
○ Maculopapular rash ○ Small percentage of infants
○ Encephalomyelitis will have mental retardation
○ Myocarditis and retinochoroiditis later in
○ Hepatitis life (children/young adult
○ Retinochoroiditis (with stage)
subsequent blindness; rare)
Toxoplasmosis in Immunocompromised
Congenital Toxoplasmosis Patients
● Severe and often fatal ● Known contractors:
○ Occasionally mild (leading to Immunosuppressed due to organs
complete recovery) transplantation or having neoplastic
● Occurs in around 1/5 of 1000 disease (ex. Hodgkin’s disease)
pregnancies ● Note screening potential donor
● Transmission occurs via units for toxoplasmosis before
transplacental of unknowingly transfusion
asymptomatic mother
● Degree of severity factors Cerebral Toxoplasmosis in AIDS Patients
○ Antibody protection of ● Focus of attention
mother ● Toxoplasmic encephalitis
(significant since 1980)
 ○ First clinical symptom ● Folinic acid (leucovorin) - for AIDS
involves the central nervous patients (to counteract bone
system by T. gondii marrow suppression by
● Headache pyrimethamine.)
● Fever ● AIDS with toxoplasmic encephalitis
● Altered mental status (ex. - atovaquone
confusion)
● Lethargy
● Subsequent focal neurologic
deficits Prevention and Control
● Brain lesions ● Avoidance of cat faeces (via
● Convulsions protective gloves especially when
● T. gondii in AIDS-infected patients cleaning litter boxes; especially for
don’t spread, but stay in CNS those pregnant)
● Diagnostic: rise in spinal fluid IgG ● Protect cover for children’s
antibody levels, tachyzoites in CSF sandboxes
on microscopic examination ● Hand washing after handling
○ Serum and CSF IgG levels contaminated meat
does not respond ● Ingesting/tasting raw/contaminated
○ There are no serum IgM meat (especially for those
antibodies (with no changes pregnant)
of serum IgG levels ● Keeping cats away from infected
suggests T. gondii infection rodents
occurs because of ● Feeding cats dry/cooked canned
reactivation of chronic cat food
latent infection, not ● No cats
acquired primary infection)
Notes of Interest and New Trends
Treatment ● 1908: Ctenodactylus gondii (African
● Symptomatic: Trisulfapyrimidines rodent) - first discovered with T.
and pyrimethamine (Deprapim) gondii
combination ● 1939: T. gondii as cause of
● Infected pregnant women should be transplacental infections
given pyrimethamine, but ● Techniques using PCR assay has
spiramycin been developed
○ Spiramycin is used in ● Successful results for analysing
Europe, Canada, and Mexico samples of venous (for AIDS) and
○ Spiramycin is an amniotic fluid (for pregnant)
experimental drug in US ● Immunocapture essay - a research
(but can be obtained by to detect specific IgE of
permission from FDA for toxoplasmosis-infected patients
toxoplasmosis in the first ○ Using CSF, foetal blood,
trimester of pregnancy) umbilical cord, blood, sera,
● Corticosteroids - anti-inflammatory amniotic fluid
agent
 ○ Easy to perform and helpful
for diagnosis (especially for
those pregnant)
● “T. gondii tachyzoites, both
invasive, and intracellular, have
been successfully demonstrated in
AIDS patients suffering from
pulmonary toxoplasmosis.

○ Bronchoalveolar lavage on
collected on each patient
(which were Giemsa-stained
and microscopically
examined)
 ○ Mature cyst rupture to
Pneumocystis produce trophozoites

jiroveci (actively growing,

multiplying, feeding form)
○ Trophozoites -> pre cysts
● Disease: Pneumocystis, atypical
and cysts
interstitial plasma cell pneumonia
● Other sites: spleen, lung, lymph
nodes, bone marrow
Morphology
● Former name: Pneumocystis carinii
Epidemiology
● Considered as fungus
● Many parts
○ US
Trophozoites
○ Asia
● Most commonly seen form
○ Europe
● Simple ovoid and ameboid organism
● MoT presumably: transfer of
● Single nucleus
pulmonary drools via person-to-
● 2 - 4 μm
person contact
● Immunosuppressed are at risk
Cysts
(specifically AIDS)
● Has 4 - 8 intracystic bodies (some
○ Highly at risk: Children
say nuclei/trophozoites)
(especially malnourished
○ Nuclei may be arranged
infants, those with
specifically (rosette) or
predisposing conditions like
randomly (scattered)
malignancy)
● Small: 4 - 12 μm
● Can be transplacental
○ May cause stillbirth
Laboratory Diagnosis
● Giemsa and iron hematoxylin
Clinical Symptoms
● Successful diagnosis using
Pneumocystosis: Atypical Interstitial Plasma
histological procedures (Gomori’s
Cell Pneumonia
methenamine silver nitrate stain)
● For immunosuppressed adults and
● Serologic techniques are developed
children
but not appropriate for clinical
○ Nonproductive cough
diagnosis
○ Rapid reparations
● Monoclonal immunofluorescence
○ Cyanosis
stain for organism identification
■ All occur for a few
● Specimen: varied (but include
days
sputum; sputum often for those
● Cause of Death for AIDS patients
immunocompromised)
○ AIDS patients can suffer
from Kaposi’s sarcoma
Life Cycle Notes
(malignant skin disease)
● Unknown
● Theory
○ May stay in alveolar spaces
in lung tissue
 ● For malnourished infacts
○ Poor feeding
○ Energy loss
○ Rapid respiration rate
○ Cyanosis
■ All last for several
weeks
● Infiltrate on chest e-ray
● Difficulty breathing
○ Causing low PO2 (arterial
oxygen tension) and
normal-low PCO2 (carbon
dioxide tension)
○ Death if lacking of O2 and
CO2 exchange in lungs

Treatment
● Trimethoprim-sulfamethoxazole
(Bactrim) -first line treatment
● Pentamidine isethionate
● Cotrimoxazole

Prevention and Control

● Life cycle is uncertain by some, so
preventions and control are difficult
to determine
● Mask - assumed that MoT is
through person-to-person contact
via pulmonary droplets
 Merozoite
Babesia Species ● Develops in RBC as trophozoite
matures
Historical Perspective
● “Resembles 4 trophozoites attacked
● Infects wild and domestic
together by their respective
● First described in 1880s
chromatin dots in a shape of a
○ Responsible for Texas cattle
cross” (Like a maltese cross)
fever/Red water fever
● Undergoes binary fission in human
○ Almost decimated cattle
to make more sporozoites
production industry
○ Several species infects
Life Cycle
humans (mostly as
accidental host)
● Common isolated from clinical
specimens: B. microti (Theileria
microti) and B. divergens
○ Other species also exist but
rare
● B. microti is is more related into
Theileria genus due to ribosomal
RNA comparisons, thus it is now
called Theileria microti

Morphology and Life Cycle Notes

● Has sexual and asexual phase
● Involves several morphological
(biphasic)
forms
○ Sexual phase - in ticks
○ 2 forms are commonly
Ixodes (vector)
encountered in humans
○ Asexual phase - animals and
humans
Trophozoite
● MoT: bite of Ixodes tick
● Developed after sporozoite infects
○ Must be fed at least 12
RBC to form something similar to
hours prior to transmission
Plasmodium
○ Its saliva must be in contact
○ Blue cytoplasmic circle
for 12 hours or more for
connected with or to a red
transmission
chromatin dot (some say
● Ixodes tick transmit sporozoites into
nucleus)
host
○ Space inside the ring is a
● (Can be multiple) sporozoites
vacuole
invade (a single) RBC to turn into
● Ring form: most commonly seen
trophozoites
diagnostic feature
● Trophozoites -> merozoites ->
● Difference between malaria: No
gametocytes (usually not seen in
malaria pigment/hemozoin and
accidental human host)
Shüffner, Zieman’s, James’,
● For humans:
Maurer’s dots
Merozoites –binary fission->
sporozoites
 ● RBC ruptures (due to overleaf of ● Patients are exposed 1 - 4 weeks
sporozoites) to infect more RBCs before symptoms are felt
● Gametocytes travels to gut to unite ● Infects are presented in late
and turn into ookinete summer - early fall
● Ookinete goes to salivary glands to ● Correlated with the breeding cycle
start sporogony (spore and of the ixodid tick
sporozoite production via sexual ● Common to see those with co-
reproduction) for many sporozoite existing Lyme disease and or
to be transmitted to another host human granulocytic ehrlichiosis

Laboratory Diagnosis ● Asymptomatic (rare)

● Specimen: Blood ● Prodrome-like symptoms
○ In giemsa-stained peripheral ○ Fever - no periodicity/not
blood films recurrent
● Giemsa stain - recommended to ○ Headache
stain for all blood films for parasite ○ Chills
study ○ Sweating
● Wright’s stain - alternative ○ Arthralgias
● Thick and thin smear ○ Myalgia
○ Thick - for screening slides ○ Fatigue
○ Thin - for differentiating ○ Weakness
Babesia from Plasmodium ○ Hepatosplenomegaly
■ All blood firms are ○ Hemolytic anaemia (from
studied in OIO mild - severe)
configuration ○ Elevated bilirubin levels
● Crucial for correct identification, ○ Elevated transaminase
reporting, and treatment: Careful levels
and thorough screening of all ● Worse to those splenectomised and
smears immunocompromised
○ Timing is no concern as they
don’t show periodicity (as Bablesia Classification
compared to Plasmodium) ● Phylum Apicomplexa -> Class
● Serologic tests and PCR Aconoidasia -> Order Piroplasmida
○ For diagnosing low -> Family Babesiidae
parasitemia/in donor blood (Blood Species: Babesia microti,
supply screening and Babesia divergens)
epidemiologic studies
○ For speciation (since this is
a limitation of blood film
tests)

Pathogenesis and Clinical Symptoms of

Babesia
Babesiosis
● Self-limiting infections
 Treatment
Babesia microti ● In combinations of drugs

(Theileria microti) ● Common

○ Clindamycin + quinine
○ Atovaquone + azithromycin
and Babesia ● Diminazene + pentamidine (either
singly or in combination)
divergens ● Pyrimethamine + quinine
○ Some of the medications (as
● No common disease/condition
said in the last 2) may have
name(s)
side effects
Life Cycle
● Role of choice and choice of
Bebesia microti/Theileria microti
treatment
● B. microti’s most associated vector
○ Patient age
- Ixodes dammini
○ Immune status
● Reservoir host - Peromyscus
○ G6PD status
leucopus (white-footed mouse)

Prevention Control
Babesia divergens
● Avoid tick infested areas
● B. divergens most associated
○ If otherwise, it’s crucial to
vector - Ixodes ricinus
examine the body before
● Reservoir host - cattle and rabbits
leaving the area
● Insect repellants
Epidemiology
● Eradicating tick population
B. microti
● Southern New England
○ Nantucket
○ Martha’s Vineyard
○ Shelter Island
○ Long Island
○ Connecticut
● (Isolated) New Jersey, Wisconsin,
Missouri, Georgia, North Carolina,
Mexico

B. divergens
● Yugoslavia
● Russia
● Ireland
● Scotland
● Nantucket, New England

Clinical Symptoms Difference

● B. divergens is more severe,
therefore fatal if untreated
● B. microti is benign and self-limiting