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Life cycle:

• alternating sexual and asexual generations

Asexual stages
• Schizogony
- schizont: actively dividing form by multiple fission
• Merogony
- merozoite: daughter cell from schizont o
• Gametogony –
- microgametocytes(male); macrogametocytes (female)
Sexual stages
• syngamy: fusion of macrogamete and microgamete
• zygote: product of syngamy
• sporogony: Development of sporozoites

Monoxenous:
Phylum Apicomplexa
• alternation of generations occurs in the same host
Subclass Coccidia Complex
Heteroxenous:
• alternation of generation occurs in different hosts

BLOOD COCCIDIA

Plasmodium species (P. falciparum, P. vivax, P. malariae, P. ovale)

Two hosts: Man (IH) & vector (female anopheles mosquitoes)

Important Blood Group Characteristics


- Resistance to P. Vivax: Fy (A-, B-)
- Resistance to P. falciparum (sickle cell trait, sickle cell anemia, G6PD deficiency, Babesia microti & B.
bigemia)

INTESTINAL COCCIDIA

• Isospora belli
• Cryptosporidium parvum
• Cyclospora cayetanensis
• Sarcocystis hominis
• Sarcocystis lindemanni
Morphology: Disease / Pathogenesis

Ring form: • Black water fever


• Circle configuration (one chromatin dot) or • Malignant tertian malaria
headphone configuration (two chromatin dots) • Aestivoautumnal malaria
• Scant y cytoplasm • Subtertian malaria
• Small vacuole usually visible • Falciparum malaria
• Multiple ring forms
• Accolé forms possible Diagnosis:
• Peripher al Blood Smear (thick and thin smear)
Developing trophozoites:
• Heavy rings common Malaria antigens:
• Fine pigment granules • HRP2(Histidine-rich protein 2)
• Mature forms only seen in severe infections • PLDH (Parasite Lactate Dehydrogenase)
• Antigen Plasmodium Aldolase
Immature schizont:
Plasmodium falciparum
• Multiple chromatin bodies surrounded by cytoplasm Test for malarial antigens:
• Only detected in severe infections • Parasite F: detects HRP-2;(+)
• Optimal test: detects both HRP-2 and pLDH; (+3
Mature schizont: lines)
• Typically consisted of 8-36(average, 24) in cluster • Immunochromatography: detects HRP2 and
arrangement plasmodium aldolase; (3 lines)
• Only detected in severe infections
Resistance to P. falciparum:
Microgametocyte: • Sickle cell trait, sickle cell anemia, G6PD
• sausage or crescent-shaped deficiency
• Dispersed central chromatin with nearby black
pigment usually visible

Macrogametocyte:
• Sausage or crescent-shaped
• compact chromatin
• Black pigment surrounding chromatin may be
visible

Other morphologic characteristics:


• May infect RBCs at any age
• Young infected cells do not enlarge and become
distorted
• Do not contain Schüffner's dots or Ziemann’s dots
• Cytoplasm of infected RBCs may contain Maurer’s
dots

Prepatent period: 11-14 days


Incubation period: 8-15 days

Occurrence of Asexual cycle: Every 36-48hours

Asexual cycle:
• Infected female anopheles mosquito bites and
sucks blood from the human host.

Sporozoites are injected (infective stage).


• Sporozoites are carried immediately to the liver and
enter parenchymal cells.
• Exoerythrocytic schizogony commences which
produces the merozoites in varying duration and
amounts, depending on the species.
• Merozoites proceeds to the peripheral blood to
enter RBCs.
• Within the RBCs, the merozoites grow as ring
forms developing into trophozoites. They also feed
on hemoglobin resulting in pigment production
known as hematin.
• Soon after, the RBCs rupture and merozoites are
released into the blood, ready to enter new red
blood cells. This asexual cycle is synchronous,
periodic and species determined.
• Some merozoites develop into microgametes
(male) and macrogametes (female) which are
picked up by the feeding female mosquitoes

Sexual cycle:
• In the gut of the mosquito, microgametes will
fertilize macrogametes forming zygote.
• Zygote becomes motile, becomes ookinete and
develops into oocysts.
• Oocyst grow and produces sporozoites. These
sporozoites may be injected again into another
human host when the mosquito takes a blood meal.
The entire development cycle in the mosquito takes
8-35 days, depending to some extent on ambient
temperature.

Description: Disease / Pathogenesis


• Most widely disseminated and most prevalent
• enlarged; maximum size (attained with mature MOT:
trophozoites and schizonts) may be 1-12 times • Bite of vector (most common)
normal erythrocyte diameter • Unsterilized hypodermic transfusion
• irregular, ameboid in trophozoites; has “spread-out” • Congenital transfusion
appearance
Infective stage:
Plasmodium vivax Length of asexual cycle: 48-hour cycle • Vector to Man: Sporozoites
(Benign Tertian Malaria) • Man to Vector: Gametocytes
Types of relapse:
Hosts: Man • True relapse Infected RBC’s: young RBC’s Diagnosis:
(Reticulocytes) • Blood film examination
Intermediate host - Harbors • Serologic procedure
asexual stage Stippling: • ELISA
• Schuffner’s dot • IFA
Vector - female anopheles
mosquito - Sexual stage Ring forms: Treatment:
• 1/3 of cell diameter, heavy chromatin dot. -delicate • Antimalarial drugs
ring
Schizonts:
• fills entire RBC
• mature schizont contains 12-24
Merozoites: average is 16

Stages present:
• In circulating blood: all stages; wide range of
stages may be seen on any given films
• In peripheral blood: all stages present

Appearance:
• golden brown, inconspicuous
Description: Disease / Pathogenesis
• Normal -rounded, compact trophozoites with dense
cytoplasm; band form trophozoites occasionally MOT:
seen • Bite of vector (most common)
• Unsterilized hypodermic transfusion
Length of asexual cycle: • Congenital transfusion
• 72-hour cycle (long incubation period)
Infective stage:
Types of relapse: • Vector to Man: sporozoites
• Recrudescence • Man to Vector: gametocytes

Infected RBC’s: Infected RBC (Old RBC) Diagnosis:


Plasmodium malariae • Blood film examination
(Quartan Malaria) Stippling: • Serologic procedure
• Ziemman’s dot • ELISA
Hosts: Man – Intermediate host -
• IFA
Harbors asexual stage Ring forms:
• 1/8 of cell diameter, heavy chromatin dot. Treatment:
Vector: • thick ring, small nucleus • Antimalarial drugs
• Female anopheles
mosquito Schizonts:
• Sexual stage • resembles fruit pie or flowery daisy head or rosette
form
• mature schizont contains 6-12

merozoites:
• average is 8

Stages present:
• In circulating blood: all stages; wide variety of
stages usually not seen; relatively few rings or
gametocytes generally present
• In peripheral blood: few rings forms, mostly mature
trophozoites and schizonts; all stages present
Appearance: dark brown, coarse, conspicuous
Description: Disease / Pathogenesis
• Fringe or irregular edge, oval shape. • Relapses, which occur with vivax and ovale, result
from reactivation of hypnozoite forms of the
Life Cycle: parasite in the liver.
• Cold, fatigue, trauma, pregnancy, and infections
Incubation period: including intercurrent falcifarum malaria by
• 16-18days precipitate reactivation.

An asexual cycle of about 50 hours and persistent MOT:


exoerythrocytic stages (hypnozoites) in the liver which can • Bites of infected Anopheles mosquitoes and sucks
produce relapses of infection. blood from the human host
As in P. vivax infection, red blood cells typically show
Diagnosis:
Schuffner’s stippling: • Microscopic Examination
• Generally, it develops much earlier in young • Thick and Thin Smear (GOLD
trophozoites and the granules tend to be more STANDARD)
Plasmodium ovale prominent.
• All erythrocytic stages are usually present in the Sample:
bloodstream. • Capillary blood most preferred
• If venous blood, use anticoagulant (clotting
HYPNOZOITES: may entrap parasites, preferred:EDTA).
• Inactive sporozoites that can be reactivated and • Prepare within 1 hour of collection to
undergo preerythrocytic schizogony. prevent morphological changes.

Stain: Treatment:
• Giemsa (10% 5-10mins; 3% 40-45mins) • Antimalarial drugs
• Prophylactic drugs
• Blood schizonticidal drugs
* Resistance of P. malariae and P. ovale to
antimalarials is not well characterized, and
infections with these species are still
considered sensitive to chlorophyll.
Description: Disease / Pathogenesis:
• Resembles P. falciparum ring forms, but no • Babesiosis
malarial pigments and no growing trophozoites. • headache, fever, hemolytic anemia with
hemoglobinuria.
Pathogenesis:
• In humans, infections with B. microti or B. microti- Diagnosis:
like species may be asymptomatic or may result in • Serology
Babesia microti mild to severe clinical signs and symptoms. • Giemsa-stained peripheral blood smears
• The severity of infection with possible fatal outcome • Immunofluorescent assay (IFA)
Usual definitive host: Deers is generally associated with the elderly, the
Intermediate host: Ticks (Ixodes) splenectomized and immunocompromised, and
those manifesting evidence of Lyme disease.

MNEMONIC

• Ferdinand Marcos- Falciparum Maurer’s dot


• Manila Zoo- Malariae Ziemman’s dot
• Vilma Santos- Vivax Schuffner’s dot
• Orange Juice- Ovale James’ dot
Phylum Apicomplexa (Algae/Coccidian)

Description: Disease/ Pathogenesis:


• Coccidian and algae, tissue coccidia • Toxoplasmosis: Asymptomatic
• intracellular parasite • Immunocompromised:
• either monoxenous or heteroxenous non-specific flulike symptoms, pneumonia,
• infects macrophages; resist phagolysosome encephalomyelitis, myocarditis,
formation retinochoroiditis
• single-celled eukaryotic protozoan parasite • Congenital toxoplasmosis:
seizure, retinochoroiditis, cerebral
Extraintestinal stages: calcification,
1. Tachyzoites - found during the initial and acute hydrocephalus/microencephalus
stage of the infection. • Cerebral toxoplasmosis
2. Bradyzoites - found in tissue cyst and replicates
slowly. Other modes of transmission:
• Ingestion of zoitocyst in meat of other animals
Life cycle of an animal host: • Blood transfusion: tachyzoite
Toxoplasma gondii • Organ transplantation: zoitocyst, tachyzoite,
Immature oocyst (1 sporoblast) - wall formation (2 bradyzoite
sporocysts) - mature oocyst (8 sporozoites, 4 each) • Mother to fetus: tachyzoite
*infective stage* - schizogony - merogony - gametogony - Diagnosis:
syngamy - zygote - immature oocyst passed out in feces • Serodiagnostic Methods
• Sabin-Feldman methylene blue dye test
Life cycle in man: • Double-sandwich ELISA Method
• Double-sandwich IgM enzyme immunoassay
Ingestion of mature oocyst - release of sporozoites -
• Indirect fluorescent antibody (IFA) Test
penetrates intestinal mucosa - blood circulation - different
• Indirect hemagglutination (IHA) Test
tissues and organs - tachyzoites - endodyogeny -
bradyzoites - zoitocyst - dead-end infection • Latex agglutination test
• Polymerase Chain Reaction (PCR)
Size: Treatment:
• Oocyst: 10-13 um by 9-11 um • Trisulfapyrimidines+pyrimethamine
• Trophozoite:4-8 um in length, 2-3 um width • Spiramycin/azithromycin/dapsone
• Cyst: 4-50um in diameter • Corticosteroids Folinic acid (leucovorin)
• Atovaquone/clarithromycin
Infective stage: Tachyzoite, bradyzoite and oocyst • Prophylaxis + trimethoprimsulfamethoxazole

Diagnostic stage:larvae (affected tissue)


Description: Disease/ Pathogenesis:
• Causative agent of bovine red water fever in • Lyme disease Babesiosis/Texas cattle fever/
cattles. Redwater fever
• Large babesia that infects red blood cells
Immunocompromised:
Sexual stage: • Hemogloblinuria (severe anemia, jaundice, acute
1. Intraerythrocytic stage – parasites were cultured in renal failure)
vitro for 20h using an induction medium
2. Extraerythrocytic stage – first seen in 3h post Diagnosis:
Babesia bigemina induction • Blood smear microscopy
3. Elongated stage with long projection – appeared at • Indirect fluorescent antibody test
Vector: boophilus ticks 6h post induction and forms larger stage at 9h • Polymerase Chain Reaction (PCR
4. Round zygotes – appeared 20h post induction
Treatment:
Life cycle: • Atovaquone + azithromycin Clindamycin + quinine
Ingestion of infectious blood - syngamy - replicate -
develop in salivary glands - ovary - other tissues
Appearance: pear-shaped, it can also be a round, oval or
irregularly shaped

Size:
Large form (4.5um x 2.0um) Round (2-3um in diameter)

Infective stage: sporozoite


Diagnostic stage: larvae (nymphs and adults)
PHYLUM SPOROZOA

Description: Disease / Pathogenesis


• Showed photosynthesizing organelles • Cyclospora cayetanensis infection
• Auto fluorescing particles characteristic of the blue-
green algae Mode of Transmission: ingestion of contaminated water
• Found to be a coccidian parasite or food

Immature oocyst (Unsporulated- noninfective) Initial symptoms


• require at least 1-2 weeks under favorable • malaise and low-grade fever (12-24 hours after
condition to sporulate and become infective exposure)
• Chronic and intermittent watery diarrhea
Mature Oocyst (Sporulated)
• Number of sporocyst: 2 Other symptoms
• Contents of sporocyst: 2 sporozoites • fatigue, anorexia, weight loss, nausea, vomiting,
Cyclospora cayetanensis • Size: 7-10 µm abdominal pain, flatulence, bloating, and dyspnea
may develop
Originally called a Infective Stage and Diagnostic Stage: Oocysts • No death has been associated with
cyanobacterium like body cyclosporidiosis
(CLB) Epidemiology
• Contaminated water is thought to be the main Diagnosis:
source of infection • Direct microscopic examination
• Cyclosporidiosis is presently considered mainly as • Acid-fast staining (Kinyoun’s stain)
a human disease • Fluorescent microscopy- Safranin staining
• Infection caused by C. cayetanensisa have been • Microwave heating
reported in children living in unsanitary conditions • Polymerase chain reaction (PCR) technique
• Contaminated lettuce and fresh fruit (raspberries
have been known to be a source of infection), often Treatment:
imported, have also been associated with C. • Self-limiting and treatment is not necessary if the
cayetanensis infections. symptoms are mild
• Trimethoprim-sulfametoxazole

Prevention and Control


• Good sanitary practices should be followed
• Boiling water seems to be the best method since
chlorination is not effective
Life cycle:
• Ingestion of sporulated oocyst Contains two
sporocysts with two sporozoites each Released
sporozoites invade the epithelial cells of the small
intestines Multiple fissions of these sporozoites
take place inside the cells to produce meronts
Some of the merozoites develop into male (micro)
and female (macro) gametes Microgametes fertilize
the macrogametes to produce oocysts, which are
passed out with feces when the host cells are
sloughed off from the intestinal wall Complete
sporulation 7 to 12 days in a warm environment

• No animal reservoir exists.

Description: Disease/Pathogenesis:
• The wall of S. hominis is up to 6m thick and Sarcocystis infection - asymptomatic
appears radially striated from villar protrusions that two types: a rare invasive form that presents with
are up to 7m long vasculitis and myositis - An intestinal form that presents
• Banana-shaped cell, with a pointed anterior end, with nausea, abdominal pain, and diarrhea -
also apical complex, which possesses micronemes Sarcocystosis, acute fever, myalgias, bronchospasm,
- Simplest form is called a zoite pruritic rashes, lymphadenopathy, subcutaneous nodules
Sarcocystis hominis • Undergoes lysis with concurrent eosinophilia, elevated erythrocyte
• The oval transparent organism consists of two sedimentation rate, and elevated creatine kinase levels
Definitive host: Human mature sporocysts that each average from 10-
Intermediate host: Cattle 18µm in length. Each sporocyst is equipped with MOT: Ingestion
four sausage shaped sporozoites. A double-
layered clear and colorless cell wall surrounds the Diagnosis: - Stool examinations (14 to 18 days after
sporocysts. ingesting beef) - Fecal flotation wet mount - Biopsy -
Microscopic in muscles of cattle - Hematoxylin and eosin
Infective stage and Diagnostic Stage: Oocyst (Sporocyst) stain - Periodic acid-Schiff (PAS) - Polymerase chain
reaction (PCR)
Epidemiology:
• Worldwide, but more common in areas where Treatment: - Albendazole, metronidazole, and
livestock is raised. cotrimoxazole - Corticosteroids
Life Cycle:
• Two host life cycle Prevention and Control:
• The first transmission route occurs when uncooked • Cooking or freezing meat to kill bradyzoites in the
pig or cattle meat infected with Sarcocystis sarcocysts
sarcocysts is ingested. Gametogony usually occurs • Freezing the meat at -5C for several days will kill
in the human intestinal cells. The development of the sporocysts
oocysts and subsequent release of sporocysts thus • Boiling should be considered to ensure disinfection
follow. This sets the stage for continuation of the • Anticoccidial drugs, amprolium and salinomycin
life cycle in a new intermediate host. • Prevention and control in food animals
• The second transmission route occurs when
humans accidentally swallow oocysts from stool
sources of animals other than cattle or pigs. In this
case, the ingested sarcocysts take up residence in
human striated muscle. Under these
circumstances, the human serves as the
intermediate host. It is interesting to note that
Sarcocystis oocysts do not infect the host of their
origin.

Description: Disease / Pathogenesis:


Worldwide, Coccidian Parasite, Obligate parasite, • Isosporiasis
Single-celled
Isospora belli - increase frequency with patients having AIDS Mode of Transmission:
• Fecal-oral contamination Oral-anal sexual contact
Habitat: Small Intestine Size: 25-35µm long, 10-15µm wide
Common Clinical Symptoms:
Appearance/ Characteristic: • Weight loss, Chronic diarrhea, Abdominal pain,
Anorexia, Weakness, Malaise
Shaped:
• Transparent, oval Cell wall: two layered, colorless Charcot-Leyden crystals:
and smootg • response to the eosinophilia
• visible in stool sample
Developing Sporoblast:
• Unicellular with granular cytoplasm Severe infection:
• Malabsorption syndrome
Young oocyst: 2 sporoblast - Foul-smelling stools that are pale yellow and of
loose consistency
Mature oocyst:
• Two sporocyst, each containing sour sausage Diagnosis:
shaped sporozoites • Enterotest
• Direct Microscopy
Infective Stage: Mature oocyst with sporozoites • Duodenal biopsy
Diagnostic Stage: Oocysts in feces • Sheather’s sugar floatation
• Modified acid-fast stain
Life Cycle:
• Ingestion of infective mature oocysts in Specimen: Stool (source: google) (nothing was
contaminated food or water. Sporozoites emerge mentioned)
after excystation of the oocyst in the small
intestine. Treatment:
• Asexual reproduction – merozoites – cells of • Mild Infection:
intestinal mucosa – gametocytes develop – - Bland diet and obtaining plenty of rest
oocysts. • Severe Infection:
- Chemotherapy consisting of trimethoprim and
Epidemiology: sulfamethoxazole or pyrimethamine and
The frequency of contracting I. belli has traditionally been sulfadiazine.
considered rare, even though the organism has worldwide
geographic distribution. An increase in reported cases
began to occur during and following World War II.
Specifically, cases were reported in Africa, Southeast Asia,
and Central America. In addition, countries in South
America, particularly in Chile, have reported I. belli
infections. An increase in frequency was particularly noted
in patients suffering from AIDS. Unprotected oral-anal
sexual contact has been suggested as the mode of
parasite transmission in these patients. The resulting
infections with I. belli are now considered opportunistic.

Description: Disease / Pathogenesis:


Cryptosporidiosis
Worldwide Appearance:
• Roundish shape MOT: Contaminated water or food, person to person
Cryptosporidium parvum • No sporocysts transmission
• 4 (small) sporozoites
• Thick cell wall Clinical Symptoms:
• 1-6 dark granules may be visible • Diarrhea – last approx. 2 weeks fever, Vomiting,
Nausea, Weight loss, Abdominal pain
Size: 4-6 µm

Life Cycle:
• Ingestion of mature oocysts - Sporozoites emerge Severe infection:
after excystation in the upper gastrointestinal tract • Immunocompromised individuals particularly AIDS
– resistance in the cell membrane of epithelial cells patient
– sporozoites rupture – autoinfection by invading - Severe diarrhea and or more symptoms
new epithelial cells – intact oocyst passes through - Malabsorption
the feces. - Infection migrates to other body areas, such as
• Thin-shelled – autoinfection – always rupturing stomach and respiratory tract.
inside the host
• Thick-shelled – autoinfection occasionally – Diagnosis:
remains intact and pass out of the body. • Iodine or modified acid-fast stain
• Enterotest
Epidemiology: • ELISA
Cryptosporidium has worldwide distribution. Of the • Indirect immunofluorescence
20 species known to exist, only C. parvum is • Sheather’s sugar flotation
known to infect humans. Infection appears to
primarily occur by water or food contaminated with Specimen: Stool
infected feces, as well as by person-toperson Treatment: Spiramycin
transmission.

Immunocompromised persons, such as those


infected with the AIDS virus, are at risk of
contracting this parasite. Other populations
potentially at risk include immunocompetent
children in tropical areas, children in day care
centers, animal handlers, and those who travel
abroad.

Description: Disease / Pathogenesis:


• Banana shaped cell with a pointed anterior end Sarcocystis infection
Sarcocystis lindemann (apical complex) - Is often asymptomatic
• Zoite is its simplest form - Two (2) types: a rare invasive form that
Intermediate host: Cattle or pig • Undergoes lysis (once sporogony is completed) presents with vasculitis and myositis
Definitive host: Human • Oval transparent organism consists of two mature - An intestinal form that presents with nausea,
sporocysts abdominal pain, and diarrhea
- Sarcocystosis; acute fever, myalgias,
bronchospasm, pruritic rashes,
lymphadenopathy, subcutaneous nodules with
concurrent eosinophilia, elevated erythrocyte
sedimentation rate, and elevated creatine
Size: kinase levels
• 10-18 µm in length
• Oocyst cell wall appearance: clear, colorless, MOT in 2 ways:
double layered 1. Ingested uncooked meat of cattle or pig infected
with Sarcocystis sarcocysts.
Epidemiology: 2. Human accidentally swallow oocysts from stool
• Relatively low and is worldwide sources of animals other than cattle or pigs.

Diagnosis:
• Fecal flotation wet mount
• Biopsy of an infected muscle
• Hematoxylin and eosin stain
• Confirmatory staining w/ the Periodic Acid-Schiff
(PAS)

Specimen: Stool

Prevention and Control:


• Thoroughly cooking meat to kill bradyzoites in the
sarcocysts
• Freezing the meat at -5°C for several days
• Boiling should be considered to ensure disinfection
• Anticoccidial drugs, amprolium and salinomycin
• Prevention and control in food animals

Treatment:
• combined medications of trimethoprim plus
sulfamethoxazole or pyrimethamine plus
sulfadiazine

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