MEDICAL PROTOZOOLOGY

• Cryptosporidiosis

• Amoebiasis

• Isospora belli
• Free living amoeba

• Cyclospora
• Balantidium coli
• G. lamblia
• Trichomonas vaginalis
• Leishmaniasis

• Trypanosomiasis

• Malaria

• Babesiosis

• Toxoplasmosis 


1
Introduction
Protozoa are unicellular, and can be considered a single celled animal.

Cytoplasm consists of

• Ectoplasm (protection, motion, nutrition, respiration, excretion)

• Endoplasm (granular,metabolism, food, volutin, excretory granules)

Nucleus, like any other :)

Reproduction
-Asexual: simple division, binary or multiple

-Sexual: gametes unite to form zygote

Classification based on organs of locomotion

Examples

Amoeba: Entamoeba and Acanthamoeba. (Phylum Rizopoda)

Ciliates: Balantidium (The only medically relevant one). (Phylum Ciliophora)

Flagellates: Giardia &Trichomonas (Metamonada) / Leishmania, Trypanosoma, and

Naegleria (Kinetoplasta).

Sporozoa: Cryptosporidium, Toxoplasma, Isospora, Cyclospora (Class Coccidea)

/ Plasmodium (Class Haemosporidea) and Babesia (Class Piroplasmea).

all Sporozoa (Phylum Apicocomplexa). They all move by gliding. 


2
AMOEBIASIS (E. histolytica)
Entamoeba histolytica is the only human pathogen in this group

Dist: World wide more common in developing countries

Hbit: Large intestines mainly in caecum and sigmoidorectal region

Transmission:

Definitive host: Man is the only host

Infective stage: Quadrinucleate cyst
Diagnostic stage: Trophozoites
Mode of Infection: Ingestion of contaminated water mainly, also food,
and autoinfection

Amoebiasis 3
 Notes on life cycle, morphology, and pathogenesis.

1. Excyst in lower part of small intestines.

2. Quadrinucleate amoeba
emerges

3. trophozoite is 20-40 μm

4. Encyst in large intestines 12-15 μm

5. Immediately infective upon excretion and viable for months

-Classic flask shaped ulcer

-May perforate

-Granuloma (amoeboma)

-Liver abscess with chocolate colored necrotic tissue

-Pulmonary abscess by extension from liver

Immunity
ABs appear one week after infection, however, have very little role in
protection and reinfection is common. Parasite continuously sheds surface
antigens.

Clinical manifestations: 


A) Intestinal

1. Asymptomatic cyst passers

2. Symptomatic non dysenteric (colic, anorexia, nausea, diarrhea with no blood)

3. Acute amoebic dysentery (starts slow, tenesmus, then diarrhea + blood) (no
fever or general manifestation)

4. Fulminating amoebic colitis (20+ evacuations/day. like dysentery + fever and

systemic manifestations, may cause intestinal perforation)

5. Amoeboma (painful abdominal mass in cecum and asc colon.mistaken for

tumor)

B) Extra intestinal

1. Amoebic hepatitis and abscess (most common) (upper right quad. pain)

2. Pulmonary amoebiasis (sputum may contain trophozoites)

3. Other organs (brain, spleen, and pericardium) rare

4. Cutaneous amoebiasis (perianal or around fistula)

Amoebiasis 4
Diagnosis:
1. Motile trophozoite in fresh stool sample

2. Concentration stool tech. (Zinc sulphate flotation) detects cysts

3. Stained stool (w iodien, eosin, or trichrome)

4. Culture of stool on special media (difficult but very sensitive)

5. detection of coproantigen by ELISA

6. Sigmoidscopy

7. Hepatic lesions detected by imaging (ultrasonography, CT, MRI,) or

aspiration in selected cases

8. examination of sputum in pulmonary cases (trophozoite)

9. Serology (ELISA, IFAT, IHAT, etc.) used for epidemiology as ABs persist for
years

Bacillary (shigella) dysentery is differentiated by

-Sudden onset

-Epidemic

-Ulcers are serpiginous

-Stool is less offensive, watery, alkaline, contains PMNL, and no cysts or

trophozoites

Treatment:
-Asymptomatic patients --> luminal drugs which include

- Iodoquinol
- Diloxanide
- Paromomycin

-Symptomatic --> Tissue drugs (Metronidazole or Tinidazole) + luminal

-Drainage of liver abscess only for large abscesses that may rupture

Prevention:
1. Strict hygiene, washing hands before eating and after defecation

2. Treatment of cases and carriers especially food handlers

3. Safe water supply and sanitary sewage disposal

4. control of insects that may transmit the infection 


Amoebiasis 5
PATHOGENIC FREE LIVING AMOEBA
Naegleria fowleri causes Acute Primary Amoebic Meningoencephalitis (PAM)
Acanthamoeba causes chronic Granulomatous Amoebic encephalitis (GAE)

Naegleria fowleri Acanthamoeba

Habitat Fresh water and swimming pools soil/fresh/salt water may contaminate
contact lens sol.

Morphology troph 10-15 μm with single 25-40 μm with spine like pseudopodia
pseudopod

Transmission INF: Trophozoites INF: Trophozoites

MOI: Through olfactory nerve while MOI: Lower respiratory tract, broken
swimming skin, invade CNS hematogenously
Clinical -PAM rapidly fatal with sudden -Opportunistic (pneumonitis and dermal
manifestation headache, fever, stiff neck, and coma. ulcers)

-GAE slow and fatal

-Keratitis (lens solution)

Diagnosis -Postmortem
microscopic identification of trophozoite
-identifying trophozoite in CSF or and cyst
brain section and culturing
Treatment Amphotericen B Only keratitis can be treated

w propamidine

Control -Chlorination of swimming pools

-Sterilize contact lenses properly

-Health education -Treat skin lesions early

-Health education

Free living Amoeba 6

INTESTINAL PROTOZOA
Balantidium coli (Balantidiasis) Giardia lamblia (Giardiasis)

Geo. Dist Central and south America and Asia World wide, more in warm countries

Habitat Large intestines, Cecum, and terminal ileum Upper small intestines (duodenum & jejunum)

* Free in lumen or attached to mucosa

TRANSMISSION

Def. Man Man

Reservoir Pig Not certain

Inf. Cyst Cyst

MOI Auto-infection or ingestion of food or water Ingestion of contaminated food or water, or

contaminated with pig feces, also man to auto-infection. It's more prevalent in children.
man transmission exists.

Dia. Trophozoite or cyst in stool Trophozoite or cyst in stool

Morph. Troph: Ovoid, 70x45 μm, covered with cilia, Troph: Pear shaped, two nuclei, two median
two nuclei (large kidney shaped, small bodies, fibrils along its length (axonemes),
spherical)
sucking disc, and fours pairs of flagella.

Cyst: Spherical, 55 μm, covered by cilia, has two

nuclei, and thick walled.

Clinical 1- Asymptomatic infectious carriers

1- Asymptomatic
manifest. 2- Acute dysentery
2- Acute: Explosive foul smelling diarrhea
3- Chronic alterations between diarrhea 3- Chronic: Alterations with marked distention
and constipation (mucoid but rarely bloody)
4- Malabsorption (Steatorrhea)
4- Complications: appendicitis, perforation, 5- Gall bladder involvement + jaundice
peritonitis, and dehydration.

Diagnosis 1- Direct fresh stool examination shows
trophozoite with characteristic rotatory
movement.
2- Stool concentration reveals cysts
3- Biopsy of ulcers by sigmoidoscope
4- Culture rarely needed
1- Repeated samples of stool show tropho.
2- Aspiration of duodenal fluid --> Tropho.
3- Tissue biopsy may be needed to confirm
4- Immunofluorescence (stool sample)
5- Coproantigen by ELISA

Treatment - Tetracycline
- Metronidazole

- Metronidazole - Tinidazole

Prevention 1- Avoid pig excreta and treat pigs

Same as B. coli but no pig control, instead
& control 2- Safe water supply and sanitary sewage
protect food from insects which may transmit
3- Proper hygiene the parasite.

N.B. B. coli is the only pathogenic ciliate to man.

Intestinal protozoa 7
 B. coli
G. lamblia

Intestinal protozoa 8
TRICHOMONIASIS
The only human pathogen of the flagellated group, Trichomonads.

Geo: Worldwide but more in developed countries

Habitat:
Female: Attached to epithelium of vulva and vagina, less commonly urethra
and uterus.

Male: Urethra and prostate.

Transmission

Def: Man is the only host

MOI: Sexual intercourse (mainly), in childbirth to the
neonate, and very rarely from contaminated towels
Inf: Trophozoite (no cyst stage)
Diag: Trophozoite

Clinically:

Female: Copious foul smelling mucoid grayish yellow vaginal discharge,

occasionally blood tinged. There's diffuse vulvar erythema. Rarely there's
dysuria and minimal urethral discharge. strawberry Cervix due to
hemorrhage.

Male: Often asymptomatic. Urethral discharge and dysuria and pruritus may
occur.

Diagnosis:
1- Fresh wet mount of discharge shows troph. (morph + rapid jerky motion)
2- Fixation and staining with Giemsa
3- Immunohistochemistry
4- Culture on special media (Sensitive but time consuming)

5- PCR

Treatment:
- Metronidazole

- Tinidazole

- Metronidazole (vaginal)

Prevention: Simultaneous treatment of both partners, Safe practices

(condom).

Trichomoniasis 9
Trichomoniasis 10
HEMOFLAGELLATES

Trypomastigote: Kinetoplast (kt) is posterior to the nucleus. The flagella folds

back along the whole length of the cell forming undulating membrane (um).

Epimastigote (Crithidial form): Kt is central with shorter um.

Promastigote: Anterior kt
with no um.

Amastigote (Leishmania
form): No flagellum.
Rounded and found
intracellularly. still has kt.

Leishmania Trypanosoma

Trichomoniasis 11
Leishmaniasis
Habitat: Cells of reticuloendothelial system, mainly the macrophages.

tropica / major / aethiopica braziliensis / mexicana donovani / infantum

Cutaneous Cutaneous & muco-cutaneous Visceral

North & Central Africa, Middle Central and South America Africa, Southern Europe, and India
East, and Southern Asia & Iran.

Transmission

Def: Man, in some areas man is the only host

Vector: Phlebotomus (sand fly) in old world,
and Lutzomyyia in new world
Inf: Promastigote
MOI: Bite of vector
Diag: Clinical / Direct / Indirect
Reservoir: 'Doge' in many parts of the world :)

Trichomoniasis 12

Cutaneous (Oriental sore)
Wet lesion by L. major (multiple
nodules, rapid, ulcerates, severe,
heal in few months, leave
characteristic scar)
Dry lesion by L. tropica (single,
large, slow, mild inflammation,
also enlarged lymph nodes.
Clinical picture
Muco-cutaneous
(Espundia)
Caused by braziliensis & mexicana Caused by donovani & infantum
Begins by simple skin lesion on
face --> gradually enlarge then
metastasize by blood and
lymphatics to the mucosa of
mouth and nose.
Visceral ( Kala azar,
Black fever,
Dumdum fever)
It is a serious generalized disease
affecting the RES all over the
body. There's fever, general pain,
splenomegaly & hepatomegaly,

heals slowly leaving permanent

scar) Continue for years causing Other possible manifestations
Diffuse Cutaneous (DCL) Rare, disfigurement. Regional lymph include edema, dysentery,
caused by L. aethiopica allover nodes may be enlarged . anemia, lymphocytosis, and
the body, doesn't ulcerate and thrombocytopenia.

resemble leprosy.
If not treated may lead to post
(LR) Recidivans Rare type caused kala azar (like DCL but easier to
by tropica (chronic, non treat)
ulcerating, extends gradually,
disfiguring, lasts for life,
resembles cutaneous TB. LR and
DCL are difficult to cure.

There's solid life-long immunity (cutaneous --> Cell mediated) (Visceral --> Humoral)

Diagnosis:
1- Clinical manifestation in endemic areas

2- Direct: Obtain sample from margin of 3- Indirect:

cutaneous lesion, or slit smear or needle - Intradermal Leishmanin (Montenegro) test

biopsy of muco-cutaneous. In visceral, take used for epidemiology as it remains positive

lymph node aspirate, splenic puncture, or for years.

bone marrow smears.

- IFAT / ELISA / DAT

Examine as follows

A- Direct stain with Giemsa or Leishman to - PCR

demonstrate amastigote inside macrophage.
B- Culture on NNN (rabbit blood agar) to see
promastigote
C- Inoculate in hamster, very sensitive but
time consuming

Treatment:

- Pentavalent antimonials (glucantime or pentostam)

- Amphotericin B

- Miltefosin

Control: Personal protect. from sand flies / euthanize stray dogs / insecticide spray
areas of sand fly breeding / treatment of cases

Trichomoniasis 13
TRYPANOSOMIASIS

Monomorphic:
American

Polymorphic:

African sleeping sickness

cruzi brucei gambiense:

brucei rhodesiense:

Chronic,Western and Acute, Eastern and

central Africa Southern Africa

African trypanosoma

Transmission:

Def: Man only (west) zoonotic (east)

Vec: tsetse flies (glossina) only found in Africa
MOI: Vector's bite / Transplacental / accidental in laboratory.
Inf: Trypomastigotes
Diag: Trypomastigotes in blood

Notes on pathogenesis:

Stage 1 Hemolymphatic: Painless chancre,

generalized lymphadenopath, cervical is more
commonly observed (west) giving the
characteristic Winterbottom sign (enlarged,
non-tender, mobile posterior cervical node)

*If patient is pregnant abortion might happen.

Stage 2 CNS stage:

1- Persistent headaches 2- Loss of appetite

3- Seizures (rare in adults) 4- (west) slower Tsetse fly

onset

5- Kerandel sign (delayed pain upon compressing soft tissue)

6- Behavior changes 7- Coma giving rise to the name sleeping sickness

Trichomoniasis 14
 Diagnosis:
1- Mainly clinical

2- Direct (found in buffy coat of centrifuged blood/CSF/LN aspirate/scraping from chancre/BM)

-Wet stains examined for motility -Fixation with Giemsa to visualise -Inoculation into rats

-Culture on NNN media

3- CSF assay: elevated WBC, increased IgM, elevated protein, morula cells (altered plasma cells).

4- Immunodiagnosis: CATT, IFAT, IHAT, and ELISA.

5- PCR

6- Imagin: CT or MRI --> cerebral edema and white matter enhancement respectively.

Treatment:
- In acute stage: Pentamidine (Pentacarinat)
- In late stage: Melarsoprol

Prevention & control:

1- Control vector

2- Chemoprophylaxis: Pentamidine --> gambinese Suramin --> rhodesiense

3- Treatment of infected cases.

Trichomoniasis 15
American T (CHAGAS DISEASE)

Geo: Central and south America

Morphology and habitat:

1- Trypomastigote: in blood, doesn't

replicate.
2- Amastigote: intracellular, divides by
binary fission, affects RES, sk. muscles,
heart, CNS.

Kissing bug

Transmission:

Def: Man
Vec: Kissing bug (Triatoma)
MOI*: Contact of bug feces with wound or conjunctiva
Inf: Metacyclic trypomastigote
Diag: Trypomastigote in blood

*Other MOI:
• Touching eyes or wounds with Triatoma feces-contaminated
fingers.

• Bugs directly depositing feces in eyes.

• Eating food contaminated with their feces.

• Congenital or from breast feeding.

• In laboratories (accidental).

• Blood transfusion or transplant.

Notes on pathogenesis:
- Unlike the African type, blood trypomastigotes here do not divide

clinical picture

Acute stage Chronic stage

Local skin nodule (Chagoma) at site of bite Neurological: dementia.

Romana's sign is unilateral periorbital Dilated cardiomyopathy

edema, conjunctivitis, and preauricular
lymphadenitis. It's present when the infection
is transmitted to the eye.
Fatigue, fever, hepatosplenomegaly, and Megacolon and or megaesophagus
myocarditis
- The intracellular dividing amastigote damages autonomic neurons leading to
megacolon, and or dilated cardiomyopathy.

Trichomoniasis 16
Diagnosis:

• History of possible exposure to T. cruzi is considered.

• In acute cases direct diagnosis is preferred.

• In chronic cases indirect diagnosis is better due to scanty parasites in blood.

Direct:
1. Direct microscopic examination of buffy coat for motile trypanosomes.

2. Thin or thick blood film with Giemsa to visualize parasites.

3. Biopsy from LN or SK. muscle to detect amastigotes.

4. Culture on NNN media to obtain epimastigotes.

5. Animal inoculation.

6. Xenodiagnosis by letting bugs feed on patient's blood then examining their gut
contents after a month.

Indirect:
1. Hemagglutination

2. Complement fixation

3. Immunoblot

4. PCR

Treatment: Acute stage (Benzonidazole or nifurtimox), Chronic cases can only be

managed symptomatically.

Prevention: Insecticides to kill bugs / be wary of blood trans. in some countries /

no vaccine or prophylactic drug available. 


Trichomoniasis 17
MALARIA
This is a disease caused by the genus Plasmodium, which belongs to the
class Haemospridea of the phylum Sporozoa. Only 4 of around 156 species
infect humans, these are:

1. vivax causing benign tertian malaria in many parts of the world.

2. ovale causing ovale tertian malaria in Africa.

3. malariae causing quartan malaria in temperate zones.

4. falciparum causing malignant tertian malaria in tropical Africa.

Geo: Tropical and subtropical areas below altitudes of 1500 m. These are the
conditions in which mosquito vectors survive best.

Notes on life cycle:

Transmission:

Def: Female anopheles mosquito where parasite reproduces sexually.

Int: Human where Asexual reproduction of parasite occurs.

Inf: Sporozoite.

MOI:

1- Bite of infected female anopheles.

2- Erythrocytic stage through blood trans.
3- Congenital transplacental.

Malaria 18
In man:

-Two stages occur (Liver & blood) Exo- and Erythrocytic schizogony respectively.

-In liver phase

- sporozoites reach liver in 1h, lose sickle shape and divide into thousands of
merozoites, which enclose into schizont (Primary tissue phase).

-Merozoites liberated from ruptured schizont to reinfect other liver cells (secondary
tissue phase) or attack RBCs to start the the erythrocytic stage.

-P. vivax and P. ovale form hypnozoites which are dormant merozoites in liver. They
can be reactivated causing relapses weeks or even years later.

-Recurdescence may occur with falciparum and malariae. This is reactivation of

inactivated erythrocytic schizont when immunity is low after incomplete treatment.

-In blood phase

-When merozoites enter RBCs they become ring shaped

-Ring form (trophozoite) feeds on Hb and release a pigment toxic to itself

-Some merozoites after being released from RBC schizont differentiate into sexual
male and female microgametocytes. Others reinvade RBCs to form new blood
schizonts.

In mosquito:

-In blood meal the female mosquito takes all stages of malaria. all will be digested
except gametocytes.

-Exflagellation of gametes takes place where they grow flagellae and divide into
smaller microgametocytes.

-Fertilizations makes a zygote which elongates into an ookinete.

-Ookinete penetrate epithelium of midgut and turns into spherical Oocyst.
-Oocyst expands and ruptures releasing fusiform motile sporozoites (Inf.stage).

-This process of sexual reproduction is called 'Sporogony'

N.B. Parasitic or prepatent incubation period is the time between entry of sporozoyte and
invasion of blood

Clinical incubation period is the time between mosquito bite and clinical manifestations

Check page 21 for an important diagram of part of the life cycle!

Malaria 19
Clinical picture:
It varies according to the infecting species, level of parasitemia,

and immunity of host. but all have influenza like prodromal symptoms.

Malarial attack (malarial paroxysms):

1- Cold stage, lasts up to 1 h.

There'sfeeling of extreme cold,
shivering, pallor, and elevated temp.

2- Hot stage, high fever with flushed

dry skin, headache & vomiting (2-6 h).

3- Sweating stage, temp. falls back to

normal, sweating, exhaustion (hours).

Tertian (every 48 h) vivax & ovale.

Quartan (every 72 h) malariae.
Every 36-48 h falciparum.
N.B in vivax irregular paroxysm might
occur when there's overlapping infection,
and this might cause misdiagnosis.

Other clinical findings include: Anemia/

thrombocytopenia/hypoglycemia/
splenomegaly/pulmonary or renal failure.

Complications:
vivax & ovale are relatively benign, but may cause mild anemia and splenomegaly.

malariae causes massive nephrotic syndrome it responds to corticosteroids but not anti-
malarials.

falciparum is often fatal (40,000 merozoites in each liver schizont) (malignant)

parasitized RBCs adhere to one another + to the intima of capillaries --> ischemia
of different organs:

1-Cerebral ischemia causing headaches and ataxia and might lead to convulsions

2-Algid: adrenal failure with hypothermia and no fever

3-Acute pulmonary edema

4-Hypoglycemia <40 mg/dl

5-Acute renal failure

6-Dysentery

7-DIC

8-Anemia

9-Black water fever in G6PD def patients, hypersensitivity to quinine and hemolysis --> black urine.

10-Tropical (Hyperactive malarial) spleno

Malaria 20
Malaria and pregnancy:
In non-endemic areas there's risk of abortion or stillbirth.

In endemic areas there's transplacental transport of IgG --> no paroxysms in new

borns.

Diagnosis:
1- Clinical picture and history must be considered

2- Blood examination of thin and thick smears. Thin film differentiates species.
Sample taken in febrile period.

3- Antibody detection by IFAT. Not practical for diagnosis but useful for screening
blood donations, or for suspected cases with negative smears.

4- Antigen detection by RDTs .

5- Molecular diagnosis like PCR.

6- Immunologic/Biochemical of malarial products.

Treatment: It varies according to the species and where it was contracted.

1- Clinical cure by Chloroquine which destroys blood schizonts.

2- Radical cure by Primaquine which destroys tissue stages and prevents relapses.

3- Casual prophylaxis with Daraprim.

4- Sporonticidal Proguanil arrests mosquito stages --> infection control.

N.B. In resistant cases new drugs like Fansidar and Artemesinin are used.

Control:
1- Recognition of cases.

2- Treatment of patients to avoid mosquito infection.

3- Chemoprophylaxis.

4- Mosquito control.

5- Vaccination is still under trials.

Malaria 21
BABESIOSIS
Mainly B. microti and B. divergens cause human infection among these hemoptozoans.

Geo: Worldwide (divergens in Europe) and (microti in USA).

Transmission:

Def: Hard ticks

Int: Humans and other mammals
MOI: Through tick bite (man is dead end host) but
man-man infection occurs with blood transfusion
Inf: Sporozoites

Clinical pic:

May be asymptomatic. There maybe constitutional symptoms.

It's more severe in immunocompromised patients, splenectomized, and/or elderly

(opportunistic infection)

Diagnosis:
1- Microscopic examination of thin and thick blood smears stained with Giemsa repeated
smears may be needed and must be differentiated from malaria.

There's No Change in shape or size of RBC / Malarial pigment / Stippling.

2- Antibody detection by IFAT.

3- Molecular tech. PCR.

4- Isolation and inoculation in hamsters.

Treatment:
Clindamycin
+ Quinine. /
transfusion to
severely ill
patient.

Control:
Tick control.

Screen trans.
blood.

Malaria 22
TOXOPLASMOSIS
Geo: Worldwide and one of the most common human infections.

Habitat: Toxoplasma gondii is an obligate intracellular parasite.

Clinical pic:
Transmission:
1- Congenital
Def: Cat (Sexual cycle is completed in cat gut) 2- Acquired
Int: Man, mammals, and birds. (any nucleated cell) 3- Immunocompromised
MOI: 4- Ocular

1- Food contam. w Tropho. or tissue cyst in raw meat.

2- Ingestion of oocyst passed in cat feces.

3- Organ transplantation or blood trans.

4- Transplacental

Congenital toxoplasmosis:

- If the woman is infected before pregnancy the baby is usually not affected.

- If infected during pregnancy, or prior then became immunocomp. (baby is affected).

- If early in pregnancy it leads to stillbirth or abortion.

- If later on: classic triad of hydrocephalus / chorioretinitis / intracranial calcifications.

- Other symptoms: hepatosplenomegaly, hepatitis, encephalitis, and hydrops fetalis.
N.B. At birth most infants appear normal. Symptoms appear later if not treated.

Toxoplasmosis 23
Acquired toxoplasmosis:
- Usually subclinical

- Rarely develop fever and lymphadenopathy. It is self limiting.

In immunocompromised:
- Life threatening pneumonitis, myocarditis, encephalitis, and sever retinochoroiditis.

Ocular toxoplasmosis:
- Necrotizing retinochoroiditis which can be primary or recurrent.

Lab diagnosis:

-Direct:
1. Detection of parasite in patient samples such as BAL or LN aspirate.

2. Identify trophozoite in impression smears of LN, bone marrow, or spleen.

3. Isolation from body fluids, and inoculate in mice.

-Indirect:
1. Sabin-Feldman dye test sample from infected mice is taken and mixed with
patient serum, if patient has antibodies trophozoites won't take up methylene blue.

2. IFAT

3. IHAT

4. Complement fixation.

5. Intradermal (Toxoplasmin) test of Frenkle.

6. Amniocentesis if a case is pregnant.

7. Ultrasound on fetus.

8. Test for antibodies in new borns.

9. MRI in encephalitis.

10. Rarely brain biopsy.

Treatment:
1- Most healthy individuals require no treatment as it is self limited

2- Pyrimethamine (Daraprim).

3- Sulfadiazine.

4- In pregnancy use Spiramycin.

5- For babies use the drugs above but switch from one to one to reduce toxicity.

Prevention and control:

1- Don't feed raw meat to pet cats. 2- Thorough cooking of meat.

3- Wash hands after handling raw meat. 4- Wash fruits and vegetables before eating.

5- Freezing meat for a few days before cooking. 6- Wash kitchen utensils/cutting boards.

7- Wear gloves on cleaning cat litter box. 8- Wear gloves when gardening.

9- Test women at beginning and during pregnancy.

Toxoplasmosis 24
OTHER COCCIDEA

Cryptosporidiosis (C. parvum) Isospora belli Cyclospora

Geo Worldwide more in tropics

Habitat Surface epithelium of small Enterocytes of proximal small Small intestines

intestines, it's intracellular intestines
extracytoplasmic. Might affect
other parts of GIT in immunocomp

Transmission

Def Man Man Man

Reservoir Calves -

Inf Sporulated oocyst (4 sporozoites) Sporulated oocyst Sporulated oocyst

(Di-sporocystic tetrazoic) (Di-sporocystic

dizoic)

MOI Ingestion of inf. in water and less Ingestion of oocyst

Ingestion of oocyst.

commonly food
No autoinfection due to non- No autoinfection as
can be man-man or from calves.
sporulated sporoblasts unsporylated oocyst
Internal auto infection leads to (diagnostic) forming first then (diag) must mature
super infection sporulating after being excreted outside host first

C/P 1- Watery diarrhea with no blood.

1- self limited gastroenteritis in Severe diarrhea
2- Transient in healthy ppl.
healthy ppl

3- Life threatening in immuocomp.

2- In chronic cases
and may cause extra intestinal malabsorption and diarrhea.

symptoms like pancreatitis, 3- In immunocomp. might be

hepatitis, and cholangitis.
self limited or resemble
cryptosporidiosis.

Diag. - Direct detection of oocyst in Sporoblast detected after stool Florescent

stool by modified Ziehl-Neelsen.
concentration techniques when microscopy of stool
stained by modified Ziehl- sample

- Indirect
Neelsen.
ELISA

Coproantigen

Immunoblots

Treat. - Paromomycin Trimethoprim-sulfamethoxazole

- Nitazoxanide
- Symptomatic

Prevention Safe water supply and hygiene

25
Life cycle of cryptosporidium

Notice how it sits inside the cell but separate from the cytoplasm. 


26
Life cycle of Isospora belli Cyclospora life cycle

27