PARASITOLOGY LECTURE

PROTOZOA
LECTURE

GENERAL CHARACTERISTICS
➔ First observed by Antonie van Leeuwenhoek (1681) ➔ Life cycle stages:
➔ Unicellular eukaryotes o Cyst – covered by thick cyst wall
➔ Aquatic or in moist environments o Merozoite
➔ Maybe free-living, commensal, or parasitic, autotrophic or heterotrophic o Trophozoite – covered by plasmalemma
➔ Body wall is covered by cell membrane or plasmalemma ➔ Cytoplasm is made up of:
o ectoplasm – outer; watery; free from granules
o endoplasm – inner; more viscous; highly granulated
➔ Reproduction
o Asexual: binary fission, schizogony, endodyogeny
o Sexual: gametogony, conjungation
o Balantidum coli

TAXONOMY
➔ 7 phyla
o 4 medically important
 Sarcomastigophora – amoeba and flagellates
• Flagellated stage of amoeba is temporary
• Amoeba:
o Large intestine – Entamoeba histolitica
o Free-living – Naegleria fowleri (CNS); Acanthamoeba (CNS and eye)
• Flagellates
o Hemoflagellates – Trypanosoma, Leishmania
o Gastrointestinal – Giardia lamblia
o Urogenital – Trichomonas vaginalis
 Ciliophora – ciliates
• Gastrointestinal – Balantidium coli
 Apicomplexa – intracellular parasites; no locomotory organelle; have invasive structure known as apical complex
• Blood – Plasmodium, Babesia
• Tissue – Toxoplasma gondii, Sarcocystis
• Gastrointestinal – Cryptosporidium, Cystoisospora, Cyclospora
 Microsporidia
• Gastrointestinal – Enterocytozoan bieneus

PHYLUM SARCODINA

➔ 8,000 spp.
o Mostly free-living, some commensals, few parasitic.
➔ General morphology
o Unicellular
o Cyst stage: uni and multinucleated
o Trophozoite stage: uninucleated
 Body: naked or with external or internal test or skeleton
o Reproduction:
 Asexual: Fission
 Sexual: If present, w/ flagellated or amoeboid gametes
o Locomotory organelle: Pseudopodia, flagella (usually restricted to
developmental/temporary stages)
o Commensal – bacteria are present
o In the case of E. histolytica, RBCs are present.
o Nucleus is used for species identification.
➔ E. histolytica, E. dispar, and E. moshkovskii are identical
o E. moshkovskii is free-living, cannot be seen in stool
o P11/P12 PCR distinguishes E. histolytica and E. dispar
➔ E. hartmanni is identical to E. histolytica but smaller
 Entamoeba histolytica
EPIDEMIOLOGY LIFECYCLE
➔ Zooanthroponotic Infective stage: Cysts and trophozoites
➔ Cosmopolitan distribution Diagnostic stage: Cysts and trophozoites
➔ 3rd world – ingestion of mature Mode of transmission: Ingestion of mature cyst
cysts in contaminated food and Habitat: Large intestine
water
1. Cysts and trophozoites are passes in feces
➔ 1st world – oro-anal sex
o Symptomatic: void trophozoites – fast-moving peristalsis of tract
Morbidity:
o Asymptomatic: void cysts – can withstand the external environment for 6-9 months
➔ 500M 2. Mature cysts are ingested
➔ 3rd to malaria and trichomonas Sexual:
3. Gastric acids in the stomach stimulates the cyst to encyst
Mortality: 4. Excystation occurs in the colon
➔ 3rd to malaria and 5. Cyst produces 4 trophozoites.
schistosomiasis Asexual (fission):
➔ 40,000 – 100,000 deaths from 3. Dehydration stimulate the trophozoite to encyst in the sigmoid rectum
complications 4. Cyst are voided in the stool
o Perforation, peritonitis, MORPHOLOGY
cardiac failure, exhaustion CYST TROPHOZOITE
RISK FACTORS ➔ 10-20 um ➔ 10-40 um
➔ Males ➔ Cigar-shaped/ rod-like chromatoidal bar ➔ Finger-like pseudopodium; unidirectional movement
➔ Tropical and sub-tropical ➔ Mature stage, infective stage, dormant, non-feeding ➔ Active stage, feeding stage
countries o has a huge food reserve inside the cytoplasm ➔ No mitochondrion, golgi apparatus
➔ Institutionalized patients ➔ 4 nuclei; Nuclear envelope is decorated by thin ➔ Uninucleated
➔ Oro-anal sex
layer of chromatin ➔ RBCs may be present in the cytoplasm
➔ Small, centrally located karyosome

SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL & PREVENTION

Disease: Amoebiasis Trophozoite (AC) ➔ Metronidazole ➔ Safe water source
➔ 90% asymptomatic (carriers) ➔ Direct fecal smear ➔ Chemoprophylaxis – mainly on
➔ 10% symptomatic o Observe movement the treatment of chronic cyst
o infected w/ 3 pathogenic o 30% sensitive passers
strains o Collect min. 3 samples to ➔ Education of high-risk groups
Manifestations: increase sensitivity on sexual and other habitual
➔ Amebic Colitis (AC) ➔ Percoll floatation technique practices that promote fecal-
o Most common o Sandwich trophozoites bet. oral transmission.
o Abdominal pain 2 conc. of sugar solution ➔ Thorough washing of fruits and
o Dysenteric stool ➔ P11/P12 PCR vegetables using effective
o Amoebic diarrhea o 100% sensitive, specific disinfectants before
o Bloody diarrhea o Distinguish E. histolytica consumption.
o Mucoid stools and E. dispar ➔ Avoid use of night soil.
o Constipation alternating w/ ➔ RFLP ➔ Improve personal hygiene.
mild diarrhea o Distinguish if virulent or
o Fever avirulent subspecies
o Ulcerations in colon lining ➔ Indirect fluorescent antibody
o Flak-shaped ulcers technique (IFAT)
➔ Amebic Liver Abscess (ALA) o Serology
o Most common o Detect exposure status
extraintestinal Cyst (carriers)
manifestation ➔ DFS
➔ Peritonitis ➔ FECT
➔ Pericarditis o 90-95% sensitive
➔ Recto colitis o Cyst
➔ Cerebral abscess ➔ P11/P12 PCR
➔ Pulmonary abscess ➔ RFLP
➔ Appendicitis ➔ IFAT
 COMMENSAL SPECIES
➔ Commensal species; will no cause sickness but presence may indicate presence of pathogenic species
➔ Due to poor hygiene or contaminated water source
➔ Includes bacteria
Entamoeba coli
EPIDEMIOLOGY MORPHOLOGY
Worldwide: CYST TROPHOZOITE
➔ 10-20% in different populations ➔ 15-30 um (bigger than E. histolytica) ➔ 15-50 um (approx.. same size as Ascaris egg)
➔ High prevalence in rural areas ➔ 4 nuclei (immature); 8 nuclei (mature) ➔ Uninucleated
➔ USA – 4.2% (1987) ➔ Thick peripheral chromatin ➔ Thick peripheral chromatin
➔ Iran – 4.6% hospitalized (2020) ➔ Eccentric karyosome ➔ Blunt pseudopod
– 2.9% gen. pop (1978) ➔ Splinter-shaped chromatoidal body ➔ Multidirectional and sluggish motility
➔ Turkey – 11.5% (2005)
➔ India – 21.8% rural areas
(2014)
➔ Columbia – 25.7-35% rural
school pop (2019)
➔ Ecuador – 34% rural pop (2019)

Endolimax nana
EPIDEMIOLOGY MORPHOLOGY
Worldwide: CYST TROPHOZOITE
➔ Co-infection with E. coli ➔ 5-14 um ➔ 6-15 um
➔ 10-20% in different population ➔ Ovoid shape ➔ Blunt pseudopod
➔ Higher prevalence in areas with ➔ 4 nuclei are found in cluster ➔ Sluggish motility
poor sanitation ➔ Spherical chromatoidal body (not always visible) ➔ Abnormally large, eccentric karyosome
➔ Thin nuclear envelope

Iodamoeba buetschlii
EPIDEMIOLOGY MORPHOLOGY
➔ Zoonotic CYST TROPHOZOITE
o Common in swine and Presence of glycogen vacuole
NHP 5-18 um 6-15 um
➔ Cosmopolitan, 4-8% (2008) 1-2 nuclei Finger-like (freshly voided stool)
Blunt pseudopod (old specimen)
Abnormally large, eccentric karyosome Sluggish motility
with RBC salvaged from environment (freshly voided)

Cyst of I. buetschlii Trophozoite of I. buetschlii

 PHYLUM CILIOPHORA

Balantidium coli
EPIDEMIOLOGY LIFECYCLE
➔ Zoonotic Infective stage: Cyst
o Common among swine Diagnostic stage: Cyst
and NHP Mode of transmission: ingestion of contaminated food or water
Worldwide: Habitat: Colon
➔ 0.02-1% (2019)
➔ Brazil (2008) 1. Excystation occurs in the colon
2. 1 cyst = 1 trophozoite
➔ Venezuela (2008)
3. Trophozoite multiply via transverse binary fission
➔ Philippines (2008) 4. Dehydration in the colon stimulates encystation
➔ Papua New Guinea (2008) 5. Trophozoite and cyst are passed in the feces
➔ West Iran (2008) o Trophozoites dies after 15 mins
➔ Ghana – 10.4 gen. pop; MORPHOLOGY
21.7 farmers (2021) CYST TROPHOZOITE
40-60 um 40-70 um
Outbreaks: Highly granulated Covered with cilia
➔ Belfast – 75% (1979) Thick cyst wall Cytosome: mouth/ gullet; cytopyge: anus
o #1 exporter of pork 2 nuclei with micronucleus
products micronucleus: spherical, sexual reproduction (gametogony/ conjugation)
➔ Caroline Islands (110 cases, macronucleus: kidney-shaped, control vital processes
1973)

RISK FACTOR
➔ Agricultural communities
➔ Piggery workers
➔ Communities engaged in
animal husbandry
➔ Zookeepers and workers

Cyst of B. coli Trophozoite of B. coli

SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL & PREVENTION
Disease: Balantidiasis ➔ Tetracyclines ➔ Boil drinking water and eat
➔ Similar to amoebiasis thoroughly cooked food
➔ Watery diarrhea ➔ Personal hygiene
➔ Blood diarrhea (more blood) ➔ Proper sanitation
➔ Wide-mouth ulcers ➔ Treat infected pigs
➔ Treat positive cases
Extraintestinal
➔ Urinary tract
➔ Vagina
➔ Appendix
 LUMINAL FLAGELLATES

HISTORY
➔ 1681: Discovered by Antony van Leeuwenhoek from his own stool
o Microscope was not well-developed during this time
➔ 1859: Vilem Lambl provided a detailed description of the parasite and named it as “Cercomonas intestinalis”
➔ 1882: "Giardia" was proposed by Kuntsler
➔ 1888: The species was called "Lamblia intestinalis" suggested by Blanchard
➔ 1915: " Giardia lamblia" was recommended by Stiles (Prof. Giard and Dr. Lambl)
➔ 1921: WWI, many soldiers developed Giardiasis exhibiting diarrhea;
o Infected lab. animals developed diarrheal symptoms
o A scientist fed lab animals with the stool specimens from the soldiers, they developed fatty diarrhea
o During this time, they were able to find out that Giardia is zoonotic
➔ 1926: Miller found that Giardia causes fat malabsorption in some children
➔ 1954: Rendroff elucidated its natural history
o Incubation period: 6-15 days
o Minimal # of cysts needed for infection or for the parasite to establish itself to the host: 10-25 cysts
o Certain strains are self-limiting (immunocompetent)

TAXONOMY
Kingdom Protista
o animal-like, plant-like, fungal-like organisms.
o most are unicellular but there are certain species that are multicellular, some are colonial
Subkingdom Protozoa
o animal-like protists; most members are heterotrophic
Phylum Sarcomastigophora (flagellates)
Subphylum Mastigophora
Class Zoomastigophora
o animal-like protozoon; most members are heterotrophic.
Order Diplomonadida
o double-celled; members are tetraploids; bilaterally symmetrical
Family Hexamitidae
o has 6 peripheral mitosomes (comparable to mitochondria but no mitochondrial DNA)

PHYLOGENY
➔ 8 subspecies/ assemblage
o Human infections are caused by Assemblage A and Assemblage B
o Assemblage A is more zoonotic than Assemblage B
➔ Among the most primitive eukaryotes since most of the organelles are missing
➔ Some believe that they are an advance species – loss of organelles are caused by reductive evolution
 Giardia lamblia
EPIDEMIOLOGY LIFECYCLE
➔ Co-infection w/ Cryptosporidium Infective stage: Cyst
Worldwide: Diagnostic stage: Cyst
➔ Cosmopolitan Mode of transmission: ingestion of contaminated food or water
➔ Developing countries – 33%
o Western Nepal – 73.4% 1. Excystation occurs in the duodenum
o Bangladesh – 11% 2. 1 cyst = 2 trophozoite
o India – 0.4-70% 3. Trophozoite multiply via longitudinal binary fission (occurs 6-12 hours)
trophozoites; 50% cysts 4. Dehydration in the small intestine stimulates encystation
o Philippines – 2% 5. Trophozoite and cyst are passed in the feces
 Mindanao – 3.6% o 300M – 14B cysts/ stool
 25-100 out of 100,000 MORPHOLOGY
will acquire giardiasis CYST TROPHOZOITE
➔ 200M Bilateral
➔ Developed countries – 2% 10-12 um length, 5-7 um width
o Primary MOT: oro-anal sex Disc fragments (form the sucking disc) Presence of dome-shaped adhesive/ ventral sucking disc
o Edinburgh – 3% oro-anal (attaches to the villi)
sex Axonemes (microtubule precursor; form flagella) Median/ rigid body (repository of tubulins; maintain
o Portugal – 1.9 children shape of ventral sucking disc)
o USA – most common Peripheral vesicles (combination of endosome and lysosome for metabolizing proteins and lipids)
intestinal parasitic disease 2 nuclei with centrally located nucleolus
Delicate peripheral chromatid
RISK FACTOR 4 pairs of flagella
➔ Travelers (2 anterior, posterior lateral, 2 ventral, 2 caudal)
➔ Children 3 central mitosomes, 6 peripheral mitosomes
➔ Individuals without access to
safe drinking water
➔ Individuals who practice oro-
anal sex
➔ Individuals with Ig deficiency
o Symptomatic

HOST
➔ Beaver
➔ Cats
➔ Dogs

BIOCHEMISTRY
Carbohydrate Nucleic Acid
➔ Main source of energy: glucose ➔ Salvaging pathway: purines, pyrimidines
➔ Energy reserve: glycogen ➔ Uracil -> cytosine (by cytidine triphosphate
synthetase)
Protein ➔ Uptake of pyrimidines are accomplished by carrier-
➔ De Novo Synthesis: alanine and valine; anabolic mediated transport
➔ Salvaging pathway: all other amino acids; catabolic,
from degradation of polypeptides Energy source
➔ Energy source: arginine ➔ Glycolysis
o Site: mitosome
Lipid o Glucose = ATP + ETOH + Acetate + CO2
➔ Competes with the host for the lipid requirement ➔ Respires through a-flavin, Fe-S protein mediated
ETC
➔ Substrate level phosphorylation: Arginine

Other molecules: B vitamins and bile salts

 SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL & PREVENTION
Disease: Traveler’s diarrhea/ ➔ Microscopy ➔ Metronidazole ➔ Provide safe drinking water
Giardiasis o DFS – motile stage ➔ Quinacrine ➔ Practice good hygiene
➔ Common in expats o Zinc-Sulfate Floatation ➔ Furazolidone ➔ Wash all food that is to be
➔ Caused by Cryptosporidium or Technique ➔ Paromomycin eaten raw in running water
o FECT (50-70% sensitive; ➔ Avoid eating raw or uncooked
G. lamblia ➔ Tinidazole
➔ Asymptomatic – 67% cyst stage) food
➔ Symptomatic – 33% ➔ Culture ➔ Prevent direct contact and
➔ Incubation: 1-2 weeks o 6 days to get results contamination with feces during
o Rule out other causative
➔ Bloating oro-anal sex
agents
➔ Malaise ➔ Treat carriers and symptomatic
o Sn: 47.8%; Sp: 100%
➔ Loss of appetite o Monoxenic – w/ E. coli
patients
➔ Sulphureous belching (food source); Robinson’s ➔ Education
➔ Stomach cramps o Axenic - trophozoite only; ➔ Vaccine
➔ Jaundice Diamond’s TP S-1-33 o Cysteine-rich protein
➔ Serology o Variant specific surface
➔ Frothy/ steatorrheic diarrhea
o IgG titter persist after protein responsible for
(fatty and explosive)
eradication – detect antigenic variation
exposure only o Protects trophozoite from
Pathogenesis
intestinal proteases
➔ Trophozoites destroy brush o IgM is useful
o Play a role in immune
border which absorbs fat o ELISA (IgM, IgG) – Sn: 88-
98%; Sp: 95.2 – 96.5% evasion
➔ Fat malabsorption
o Immunoblot (IgM, IgG, IgA)
➔ Direct: release proteinase that
– Sn: 71%; Sp: 78%
attack brush border; release
substance that cause apoptosis ➔ Molecular Diagnosis
o Gold standard
➔ Indirect: most of the damage is
o PCR, RT-PCR, RFLP,
caused by CD8 trying to
Nested PCR
eliminate trophozoites
o 552-bp intergenic spacer
➔ Presence of trophozoites (IGS) region of rRNA gene
prevent nutrient absorption
➔ Rapid Diagnosis
o Copro-antigen diagnosis –
Sn: 87.5%; Sp: 98.6%
o 3 lines – (+) with
Cryptosporidium
o 2 lines – (+) Giardia
➔ Other Methods
o Aspiration of duodenal
contents
o Enterotest/ String test
 Trichomonas vaginalis
EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Trophozoite in urine or genital secretions
➔ Women Diagnostic stage: Trophozoite in vagina or urethra
o 24% prostitutes Mode of transmission: Sexual intercourse or fomites (towels, toilet seats, pool, douching apparatus
➔ 16%, 95% CI 13-32% Mode of reproduction: Longitudinal binary fission
o Wet mount: 15% Habitat: Lower genital tract (female); Urethra and prostate (male)
o Culture: 16%
o Molecular technique: 22% 1. Trophozoite in vaginal and prostatic secretions and urine
➔ Africa: highest, 23%, 95% CI 2. Trophozoite multiplies by longitudinal binary fission
3. Trophozoite in vagina or orifice of urethra
➔ Zambia (2011):
o 25% adolescent due to MORPHOLOGY
sharing of bath water and CYST TROPHOZOITE
inconsistent use of soap NO CYST STAGE ➔ 7-23 um
➔ USA: 2.6M, 2.1% (2018) ➔ 4 anterior flagella
➔ Uninucleated, pear shape
RISK FACTOR
➔ 30-36 y/o (2021)
o 20%, 95% CI 11-30%
➔ Promiscuity
➔ Poor feminine hygiene
➔ Low-income level (2021)
o 23%, 95% CI 14-34%

SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL & PREVENTION

Disease: Trichomoniasis ➔ Urine concentration technique ➔ Metronidazole ➔ Avoid promiscuous behavior
Male: ➔ Vaginal swab o Cure rate: 84-89.8% ➔ Improve personal hygiene
➔ Asymptomatic ➔ Pap smear o Resistant: 4-10% ➔ Safe sex
➔ Prostatitis (pain, burning, or o Reinfection: 17% w/in 3mo
itching penis) o Treat patient and partner/s
➔ Urethritis
➔ Frequent urge to urinate
➔ Discharge from urethra

Females:
➔ Symptomatic
➔ Leukorrhea
➔ Yellow-green, frothy, foul-
smelling discharge
➔ Itching and burning sensation
➔ High vaginal pH
➔ Strawberry cervix
➔ Vaginal bleeding, burning,
swelling
➔ Frequent urge to urinate
➔ Pain during sex
 HEMOFLAGELLATES

Trypanosoma brucei gambiense

EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Trypomastigote (Humans and vector)
➔ Middle and West Africa Diagnostic stage: Trypomastigote in blood (Humans)
o 97% of reported cases of Mode of transmission: Blood meal (vector); Bite, contaminated needle, sexual contact (Humans)
Human African Mode of reproduction: longitudinal binary fission
Trypanosomiasis (HAT)
o 663 cases (2020) Human Stages:
o 24 Sub-Saharan countries 1. Tsetse fly takes blood meal and injects metacyclic trypomastigote
➔ DR Congo: highest, 75% 2. Injected metacyclic trypomastigotes transforms into bloodstream and carried to other sites
3. Trypomastigote reproduce by binary fission in body fluids (blood, lymph, spinal fluid)
RISK FACTOR Tsetse fly Stages:
➔ Rural areas 1. Trypomastigote in blood are ingested by fly during blood meal
2. Ingested trypomastigotes transform into procyclic trypomastigotes in tsetse fly’s midgut
➔ Agricultural communities
3. Procyclic trypomastigote reproduce via binary fission
➔ Fishing communities 4. Procyclic trypomastigote leave the midgut and transform into epimastigote
➔ Animal husbandry 5. Epimastigote multiply in the salivary gland and transform into metacyclic trypomastigote
➔ Hunting communities MORPHOLOGY
EPIMASTIGOTE TRYPOMASTIGOTE
HOST
➔ Kinetoplast and basal body, anterior of nucleus ➔ Longer
Reservoir:
➔ Kinetoplast and basal body, posterior of nucleus
➔ Domesticated animals
➔ Polymorphic
Definitive:
➔ Humans
Vector:
➔ Glossina palpalis
➔ Glossina tachinoides

SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL & PREVENTION

Disease: Gambien Trypanosomiasis ➔ Buffy coat 1st line, 1st stage; non-severe 2nd ➔ Vector control
Chronic African Sleeping Sickness ➔ Peripheral smear stage ➔ Surveillance to detect and treat
Hemolymphatic Phase:15 years ➔ Biopsy ➔ Fexinidazole cases
➔ Chancre ➔ PCR ➔ Avoid streams and waterholes
➔ Nervous impairment ➔ Serology
1st stage: HEMOLYMPHATIC during warm, dry seasons
o Lethargy ➔ Suramin ➔
➔ Xenodiagnosis Restriction to travel to fly-
o Retardation o Nephrotoxicity infested regions
o Tremulous speech o Allergic rx ➔ Apply repellants
o Tremors of tongue/ limbs ➔ Pentamidine ➔ Protective clothing
o Difficulty to rouse o Generally well-tolerated
➔ Chemoprophylaxis
➔ Headaches o Chemoprophylaxis
➔ Fever
➔ Enlarged lymphnodes 2nd stage: CNS
➔ Muscle and joint pain ➔ Melarsoprol
➔ Large sore at bite sites o Reactive encephalopathy
o 3-10% fatality
➔ Rash
o Photophobia
➔ Weight loss o Kidney damage
➔ Malaise o Urticaria
➔ Petechial hemorrhage ➔ Eflornithine
➔ Meningoencephalitis o Less toxic than
Melarsoprol
➔ Nifurtimox (2009)
 Trypanosoma brucei rhodesiense
EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Trypomastigote (Humans and vector)
➔ East Africa Diagnostic stage: Trypomastigote in blood (Humans)
o 12 Sub-Saharan countries Mode of transmission: Blood meal (vector); Bite, contaminated needle, sexual contact (Humans)
➔ More animal cases than human Mode of reproduction: longitudinal binary fission

RISK FACTOR Human Stages:

➔ Rural areas 1. Tsetse fly takes blood meal and injects metacyclic trypomastigote
2. Injected metacyclic trypomastigotes transforms into bloodstream and carried to other sites
➔ Agricultural communities
3. Trypomastigote reproduce by binary fission in body fluids (blood, lymph, spinal fluid)
➔ Fishing communities Tsetse fly Stages:
➔ Animal husbandry 1. Trypomastigote in blood are ingested by fly during blood meal
➔ Hunting communities 2. Ingested trypomastigotes transform into procyclic trypomastigotes in tsetse fly’s midgut
3. Procyclic trypomastigote reproduce via binary fission
HOST 4. Procyclic trypomastigote leave the midgut and transform into epimastigote
Reservoir: 5. Epimastigote multiply in the salivary gland and transform into metacyclic trypomastigote
➔ Wild and domesticated animals MORPHOLOGY
Definitive: ➔ Indistinguishable morphologically from T. b. gambiense
➔ Humans
➔ Animals
Vector:
➔ Glossina morsitans
➔ Glossina swynnertoni
➔ Glossina pallidipes
SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL & PREVENTION
Disease: Rhodesian ➔ Buffy coat 1st line, 1st stage; non-severe 2nd ➔ Vector control
trypanosomiasis, Acute African ➔ Peripheral smear stage ➔ Surveillance to detect and treat
Sleeping Sickness ➔ Biopsy ➔ Fexinidazole cases
Hemolymphatic Phase:shorter ➔ Avoid streams and waterholes
➔ PCR
➔ Weakness 1st stage: Hemolymphatic
➔ Serology during warm, dry seasons
➔ Edema ➔ Suramin ➔ Restriction to travel to fly-
➔ Xenodiagnosis
➔ Rapid weight loss o Nephrotoxicity infested regions
➔ Myocarditis o Allergic rx ➔ Apply repellants
➔ Mania and delusions ➔ Pentamidine ➔ Protective clothing
➔ Irregular fever o Generally well-tolerated
➔ Chemoprophylaxis
o Chemoprophylaxis
➔ Muscle and joint pain
➔ Rash 2nd stage: CNS
➔ Winterbottom’s sign ➔ Melarsoprol
o Reactive encephalopathy
o 3-10% fatality
o Photophobia
o Kidney damage
o Urticaria
➔ Eflornithine
o Less toxic than
Melarsoprol
➔ Nifurtimox (2009)
 Trypanosoma cruzi
EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Amastigote (Vector), Trypomastigote (Human)
➔ 6-8M infected Diagnostic stage: Amastigote
➔ 50,000 deaths yearly Mode of transmission: Blood meal (Vector); Insect bite, vertical, blood transfusion, ingestion of bug (Vertebrate)
➔ 65-100M at risk Mode of reproduction: Binary fission
➔ Latin America
Human Stages:
➔ Southern USA 1. Triatomine bug takes blood meal and passes metacyclic trypomastigotes in feces, trypomastigotes enter
➔ Non-endemic areas w/ cases: bite wound or mucosal membranes
o Canada 2. Metacyclic trypomastigotes penetrate nucleated cells at bite wound site and transforms into amastigotes
o USA 3. Amastigote reproduce by binary fission in cells of infected tissues
o Europe 4. Intracellular amastigotes transform into trypomastigotes, then burst out of the cell and enter the
o Australia bloodstream
o Japan Triatomine bug Stages:
1. Trypomastigote in blood are ingested by triatomine bug during blood meal
RISK FACTOR 2. Epimastigotes in the midgut reproduce via binary fission
➔ Few months – 2 y/o 3. Epimastigotes travel to the hindgut and transforms into metacyclic trypomastigote
o Bugs are attracted to CO2 MORPHOLOGY
emission AMASTIGOTE EPIMASTIGOTE TRYPOMASTIGOTE
➔ Suburban areas Non flagellated stage vector human
➔ Rural areas Human and vector
o Bugs lives on the crevices
of mud huts

HOST
Reservoir:
➔ Domesticated animals
Definitive:
➔ Humans
Vector:
Promastigote temporary stage, kinetoplast and basal body at the anterior side, short anterior flagellum
➔ Reduviid bugs (kissing/
assassin bugs)
SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL & PREVENTION
Disease: American trypanosomiasis, ➔ Buffy coat ➔ Suramin ➔ Vector control
Chagas ➔ Blood smear ➔ Pentamidine ➔ Plaster crevices where reduviid
➔ Chagoma ➔ Biopsy ➔ Nifurtimox lives
o Romana sign – near the ➔ Lymph fluid ➔ Avoid human-vector contact
eye
➔ IFAT
➔ Myocarditis
➔ Xenodiagnosis
➔ Megaesophagus
➔ Megacolon
➔ Hepatosplenomegaly

Pathology
➔ Amastigote destroy the host cell
➔ Lymph nodes are blocked
 Leishmania tropica minor
EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Promastigote
➔ Portugal Diagnostic stage: Amastigote
➔ Spain Mode of transmission: Blood meal (Vector); Insect bite, vertical, blood transfusion, ingestion of bug (Vertebrate)
➔ France Habitat: Macrophage, Reticuloendothelial system of the skin
➔ Italy
Human Stages:
➔ Greece 1. Fly takes blood meal and injects promastigote into the skin
➔ India 2. Promastigotes are phagocytized by macrophage or other mononuclear phagocytic cell
➔ Pakistan 3. Promastigotes transform into amastigotes
➔ Central Asia Sandfly Stages:
➔ West Africa 1. Fly ingest macrophage infected with amastigote during blood meal
2. Parasitized cell are ingested
HOST 3. Amastigotes transform into promastigote in the gut and divide
Reservoir: 4. Migration to proboscis
➔ Dogs MORPHOLOGY
Definitive: AMASTIGOTE PROMASTIGOTE
➔ Humans ➔ Present in human host ➔ Present in vector
Vector: ➔ Non-flagellated ➔ Short flagellum
➔ Phlebotomus
➔ Lutzomia

SYPTOMATOLOGY
Disease: Dry/ Urban Cutaneous
Leishmaniasis, Oriental sore
➔ Lesions/ papules
➔ Nodules
➔ Ulcers
➔ Self-limiting

Pathology
Invades macrophages of skin
(Langerhans’s cells)

Leishmania tropica major

EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Promastigote
➔ Middle East Diagnostic stage: Amastigote
➔ Africa Mode of transmission: Blood meal (Vector); Insect bite, vertical, blood transfusion, ingestion of bug (Vertebrate)
➔ USSR Habitat: Macrophage, Reticuloendothelial system of the skin

HOST Human Stages:

Reservoir: 1. Fly takes blood meal and injects promastigote into the skin
2. Promastigotes are phagocytized by macrophage or other mononuclear phagocytic cell
➔ Gerbils
3. Promastigotes transform into amastigotes
➔ Rodents Sandfly Stages:
Definitive: 1. Fly ingest macrophage infected with amastigote during blood meal
➔ Humans 2. Parasitized cell are ingested
Vector: 3. Amastigotes transform into promastigote in the gut and divide
➔ Phlebotomus 4. Migration to proboscis
MORPHOLOGY
SYPTOMATOLOGY AMASTIGOTE PROMASTIGOTE
Disease: Wet/ Rural Cutaneous
➔ Present in human host ➔ Present in vector
Leishmaniasis
➔ Non-flagellated ➔ Short flagellum
➔ Lesions/ papules
➔ Nodules
➔ Ulcerations with
serosanguineous fluid
➔ Self-limiting but with scarrinh

Pathology
Invades macrophages of skin
(Langerhans’s cells)
 Leishmania donovani
EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Amastigote (Vector), Trypomastigote (Human)
➔ Latin America Diagnostic stage: Amastigote
➔ Mediterranean Mode of transmission: Blood meal (Vector); Insect bite, vertical, blood transfusion, ingestion of bug (Vertebrate)
➔ Middle East Habitat: Macrophage, Reticuloendothelial system of the skin
➔ China
Human Stages:
➔ South Asia 1. Fly takes blood meal and injects promastigote into the skin
2. Promastigotes are phagocytized by macrophage or other mononuclear phagocytic cell
HOST 3. Promastigotes transform into amastigotes
Reservoir: Sandfly Stages:
➔ Wild and domesticated dogs 1. Fly ingest macrophage infected with amastigote during blood meal
Definitive: 2. Parasitized cell are ingested
➔ Humans 3. Amastigotes transform into promastigote in the gut and divide
Vector: 4. Migration to proboscis
➔ Phlebotomus MORPHOLOGY
AMASTIGOTE PROMASTIGOTE
Present in human host Present in vector
Non-flagellated Short flagellum
SYMPTOMATOLOGY TREATMENT
Disease: Kala-azar, Visceral ➔ Miltefosine
Leishmaniasis
➔ Hepatosplenomegaly
➔ Deadly
➔ Post-kalaazar derma
leishmaniasis
o Allergic rx to tx
o Amastigotes migrate to
face

Pathology
➔ Invades macrophages of
internal organs

Leishmania braziliensis
EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Amastigote (Vector), Trypomastigote (Human)
➔ South and Central America Diagnostic stage: Amastigote
Mode of transmission: Blood meal (Vector); Insect bite, vertical, blood transfusion, ingestion of bug (Vertebrate)
HOST Habitat: Macrophage, Reticuloendothelial system of the mucous membrane
Reservoir:
➔ Wild and domesticated dogs Human Stages:
Definitive: 4. Fly takes blood meal and injects promastigote into the skin
➔ Humans 5. Promastigotes are phagocytized by macrophage or other mononuclear phagocytic cell
Vector: 6. Promastigotes transform into amastigotes
Sandfly Stages:
➔ Phlebotomus
4. Fly ingest macrophage infected with amastigote during blood meal
5. Parasitized cell are ingested
SYPTOMATOLOGY
6. Amastigotes transform into promastigote in the gut and divide
Disease: American/ Mucocutaneous
5. Migration to proboscis
Leishmaniasis, Espundia, uta and
chiclero ulcer MORPHOLOGY
AMASTIGOTE PROMASTIGOTE
➔ Extensive oriental sore
➔ Present in human host ➔ Present in vector
Pathology ➔ Non-flagellated ➔ Short flagellum
Invades macrophages of mucous
membrane
 COCCIDIA

Toxoplasma gondii
EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: All stages for human host
➔ France: 85% Diagnostic stage: Amastigote
➔ Vietnam Mode of transmission: Vertical transmission/ transplacental, granulocyte transfusion, organ transplant, ingestion of
➔ US: 22% contaminated food or water
o 15-45 y/o: 10-15%
1. Cyst is ingested by definitive host (cats).
Outbreaks: 2. Unsporulated oocysts are passed in feces and becomes sporulated
3. Oocysts in food, water, or soil are ingested by IH.
➔ Coimbatore, Tamil Nadu, India
(2004): 248 cases HOST
o contaminated water Reservoir: Other Sources of Infection:
➔ Izmir, Turkey (2002): 171 ➔ Wild and domesticated dogs ➔ Sandbox – litterbox of stray cats
boarding school children Definitive: ➔ Unpasteurized milk
o contaminated dining hall ➔ Big and domesticated cats ➔ Meat (poultry and mammalian
➔ Greater Victoria, BC, Canada Accidental Intermediate:
(1998): 2,894-7,718 cases ➔ Humans
o contaminated municipal MORPHOLOGY
water supply due to OOCYST BRADYZOITES TACHYZOITES
cougars & mountain lions ➔ 10x12um ➔ Dormant stage ➔ Invasive stage
➔ Panama (1979): 600 US ➔ 2 sporocyst/ sporoblasts with 4 ➔ Located in the muscle ➔ Can be acquired through
soldiers training in Panama sporozoites vertical transmission
Canal area ➔ Excreted by definitive host ➔ Excreted by host
o Iodine treated semi-
stagnant water
➔ Atlanta, Georgia, USA (1977):
35/37 horse stable patrons
o Contaminated soil
➔ Brazil (1966, 2001, 2009, 2015,
2015, 2016):
o Contaminated food/water
o Hotspot

RISK FACTOR
➔ Preference for raw/ semi-
cooked meat
➔ Unfiltered water source
➔ Unwashed vegetables/ produce
➔ Warm climates
➔ Lower altitudes
➔ Proximity to cats/ felines
➔ 15-25 y/o
SYMPTOMATOLOGY DIAGNOSIS CONTROL AND PREVENTION
Disease: Toxoplasmosis Tachyzoites: ➔ Cook meat properly
➔ Fever o Stool ➔ Stay away from cats
➔ Headache o stain Giemsa ➔ Proper hygiene
➔ Choroiditis Bradyzoites:
➔ Protect sand boxes from cats
o Biopsy
➔ Encephalitis
o H&E stain
➔ Neurologic symptoms
➔ Xenodiagnosis
➔ Respiratory involvement
➔ IFAT
➔ Anemia
➔ PCR
Congenital
➔ 1st trimester
o Spontaneous abortion/
miscarriage
o Congenital defects
 Microcephaly
 Hydrocephaly
 Splenomegaly
 Spastic quadriplegia
 Cryptosporidium parvum
EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Oocyst
➔ Developing countries: 14-41% Diagnostic stage: Oocyst
➔ Developed countries: 0.3-22% Mode of transmission: ingestion of contaminated food or water
➔ Brazil: 90% infants Habitat: Small intestine
➔ China: 75% in 11-13 y/o
4. Cyst is ingested by definitive host (cats).
5. Unsporulated oocysts are passed in feces and becomes sporulated
Cause of Outbreaks:
6. Oocysts in food, water, or soil are ingested by IH.
➔ Water-borne disease
MORPHOLOGY
➔ Food-borne disease OOCYST
➔ HIV-related disease
➔ 10x12um
➔ Travel-related disease ➔ 4 sporozoites
➔ Thin-walled cyst: internal multiplication
RISK FACTOR
➔ Thick-walled cyst: environmental contamination
➔ Young children
➔ Unsafe water source
➔ Agricultural workers
➔ Veterinarians
➔ Travelers
➔ Institutionalized patients

HOST
Reservoir:
➔ Migratory birds
Definitive:
➔ Humans
SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL AND PREVENTION
Disease: Human Cryptosporidiosis ➔ ELISA ➔ Pyrimethamine ➔ Cook meat properly
➔ Watery diarrhea ➔ IFAT ➔ Stay away from cats
➔ Dehydration ➔ PCR ➔ Proper hygiene
➔ Chronic diarrhea ➔ Microscopy using Acid-fast Protect sand boxes from cats
➔ Anorexia stain
➔ Malaise
 Sarcocystis spp.
EPIDEMIOLOGY LIFECYCLE
Worldwide: Infective stage: Oocyst
➔ Asia: 0.4-23.2% Diagnostic stage: Oocyst
➔ Europe: 1.1-10.4% Mode of transmission: ingestion of contaminated food or water
➔ Australia: 0.5-34% Habitat: Small intestine

Cause of Outbreaks: 1. DH ingest contaminated meat.

2. Inside the intestine the sarcocyst will be digested by the gastric acid of the stomach releasing the
➔ Water-borne disease
sporozoites.
➔ Food-borne disease 3. The sporozoites will invade the enterocyte and undergo schizogony releasing the merozoite.
➔ HIV-related disease 4. The merozoite will become macro and micro gametes.
➔ Travel-related disease 5. Fusion will produce the zygote and will eventually become the oocyst.
6. Oocyst and sporocyst are excreted in the stool.
RISK FACTOR 7. The intermediate host will acquire the infection upon ingestion of food and water contaminated with the
➔ Young children oocyst and sporocyst.
➔ Unsafe water source 8. The sporocyst will release the merozoite inside the IH.
➔ Agricultural workers 9. The merozoite will invade the muscle tissue forming the sarcocyst.
➔ Veterinarians MORPHOLOGY
➔ Travelers OOCYST
➔ Institutionalized patients ➔ 15-20 um long x 15-20 um wide
➔ 2 sporocyst with 4 sporozoites
HOST
Reservoir:
➔ Migratory birds
Intermediate:
➔ Prey mammals
Definitive:
➔ Predatory mamm
SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL AND PREVENTION
Disease: Human Sarcosytosis ➔ ELISA ➔ Pyrimethamine ➔ Thorough cooking or freezing of
Human Host ➔ IFAT meat to kill the bradyzoites
➔ 90% asymptomatic ➔ PCR o 60 °C for 20 min
➔ Gastroenteritis ➔ Microscopy using Acid-fast o 70 °C for 15 min
➔ Eosinophilia stain o 100 °C for 5 min
➔ Myalgia o -4 °C for 48 h
o -20 °C for 24 h
➔ Myositis
➔ Chemoprophylaxis for the IH
➔ Vasculitis
(Amprolium, Salinomycin)
➔ Pruritic rashes
➔ Environmental sanitation
Non-Human Host ➔ Provision of safe water source
➔ Death
➔ Abortions
➔ Lower meat yield
 BLOOD APICOMPLEXANS

Plasmodium falciparum
EPIDEMIOLOGY LIFECYCLE
Philippines: Infective stage: Sporozoite (Human); Gametocyte (Mosquito)
➔ 83% of cases Diagnostic stage: Trophozoite, Schizont
➔ 7 provinces with local Mode of transmission: Mosquito bite, Transfusion, Vertical transmission, Contaminated needle
transmission
➔ Palawan: 90% of cases Human Liver Stage
1. Mosquito takes a blood meal and injects sporozoites
HOST 2. Sporozoites will stay in the bloodstream for 30 minutes before entering the exo-erythrocutic phase
3. Sporozoites invades the hepatocytes and undergo schizogony to produce schizont
➔ Anopheles flavirostris: main;
4. Schizont ruptures and releases merozoites into the bloodstream
clean, slow-moving shaded
Human Blood Stage
streams
1. Merozoites enters the erythrocytic phase by invading RBCs
➔ A. mangyanus: open fields 2. Merozoites in the RBC will become trophozoites then undergo schizogony to form new merozoites to
➔ A. balabacensis: forest invade more RBCs
➔ A. litoralis: swampy area 3. Trophozoite transforms to gametocyte
Mosquito Stage
1. Gametocyte will be ingested by mosquito through blood meal
2. Gametocytes will differentiate into micro and macrogametes in the intestine
3. Fusion of micro and macrogametes produce the zygote
4. Zygote elongates producing the ookinete (worm-like) which will invade an enterocyte and become oocyst
5. Oocysts undergo schizogony and release the sporozoites
6. Sporozoites migrates to the salivary glands
MORPHOLOGY
TROPHOZOITE MAURER’S CLEFT ACCOLE
➔ Ring, most common stage ➔ inclusions present in parasitized ➔ trophozoites plasma membrane
➔ RBC is the same size RBC fuses with plasma membrane of
➔ 1/16 of the parasitized RBC ➔ fragmented heme RBC
➔ cytoplasm serves as the band
of the ring while chromatin dots
serve as the gemstone

SCHIZONT GAMETOCYTES
➔ Contains 8-32 merozoites ➔ Banana or crescent-shape
o Highest number among MACROGAMETOCYTES MICROGAMETOCYTES
Plasmodium spp. ➔ Compact nucleus ➔ Diffused nucleus

SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL AND PREVENTION

Disease: Malignant tertian; ➔ Peripheral smear ➔ Chloroquine: RBC stage ➔ Vector control
Falciparum malaria; Cerebral ➔ Buffy coat ➔ With Primaquine: Liver stage ➔ Animal prophylaxis
malaria ➔ IFAT ➔ Quinine: Severe ➔ Detection and Treatment of
➔ Fever ➔ PCR cases
➔ Splenomegaly ➔ Dipstick (Parasight F Test) ➔ Prevent vector-human contact
➔ Anemia
➔ Jaundice
➔ Comma
➔ Hemoglobinuria
➔ Spontaneous bleeding
➔ Anoxia
Recurrence: False relapse
(recrudescence); S&S reappear w/o
reinfection; RBC are sequestered in
the spleen
Prepatent: 6-25 days
 Plasmodium vivax
EPIDEMIOLOGY LIFECYCLE
Philippines: Infective stage: Sporozoite (Human); Gametocyte (Mosquito)
➔ 15-42% of cases Diagnostic stage: Trophozoite, Schizont
Mode of transmission: Mosquito bite, Transfusion, Vertical transmission, Contaminated needle
Worldwide:
➔ Central America Human Liver Stage
➔ India 1. Mosquito takes a blood meal and injects sporozoites
2. Sporozoites will stay in the bloodstream for 30 minutes before entering the exo-erythrocutic phase
➔ Morbidity: 300-500M cases
3. Sporozoites invades the hepatocytes and undergo schizogony to produce schizont
➔ Mortality: 1M 4. Schizont ruptures and releases merozoites into the bloodstream
➔ Cases decline from 2005-2017 Human Blood Stage
1. Merozoites enters the erythrocytic phase by invading RBCs
HOST 2. Some merozoites become hypnozoites that invade other hepatocytes and become dormant
➔ Anopheles flavirostris: main; 3. Merozoites in the RBC will become trophozoites then undergo schizogony to form new merozoites to
clean, slow-moving shaded invade more RBCs
streams 4. Some trophozoite transforms to gametocyte
➔ A. mangyanus: open fields Mosquito Stage
➔ A. balabacensis: forest 1. Gametocyte will be ingested by mosquito through blood meal
➔ A. litoralis: swampy area 2. Gametocytes will differentiate into micro and macrogametes in the intestine
3. Fusion of micro and macrogametes produce the zygote
4. Zygote elongates producing the ookinete (worm-like) which will invade an enterocyte and become oocyst
5. Oocysts undergo schizogony and release the sporozoites
6. Sporozoites migrates to the salivary glands
MORPHOLOGY
TROPHOZOITE SCHIZONT GAMETOCYTES
➔ Amoeboid ➔ Contains 8-24 ➔ Spherical-shape
➔ Enlarged parasitized merozoites MACROGAMETOCYTES MICROGAMETOCYTES
RBC ➔ Compact nucleus ➔ Diffused nucleus
➔ Inclusion: Schuffner’s ➔ Female ➔ Male
dots

SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL AND PREVENTION

Disease: Benign tertian malaria ➔ Peripheral smear ➔ Chloroquine: RBC stage ➔ Vector control
➔ Fever every 3 days ➔ Buffy coat ➔ With Primaquine: Liver stage ➔ Animal prophylaxis
➔ Lassitude ➔ IFAT ➔ Quinine: Severe ➔ Detection and Treatment of
➔ Recurrence ➔ PCR cases
➔ Pains in joints and bones ➔ Dipstick (Parasight F Test) ➔ Prevent vector-human contact
➔ High fever (39-41o)
➔ Lips and nails cyanotic
Prepatent: 6-27 days
 Plasmodium malariae
EPIDEMIOLOGY LIFECYCLE
➔ Only zoonotic species Infective stage: Sporozoite (NHP); Gametocyte (Mosquito)
Philippines: Diagnostic stage: Trophozoite, Schizont
➔ 1% of cases Mode of transmission: Mosquito bite, Transfusion, Vertical transmission, Contaminated needle

HOST Human Liver Stage

Reservoir: 1. Mosquito takes a blood meal and injects sporozoites
➔ NHP 2. Sporozoites will stay in the bloodstream for 30 minutes before entering the exo-erythrocutic phase
Vector: 3. Sporozoites invades the hepatocytes and undergo schizogony to produce schizont
4. Schizont ruptures and releases merozoites into the bloodstream
➔ Anopheles flavirostris: main;
Human Blood Stage
clean, slow-moving shaded
1. Merozoites enters the erythrocytic phase by invading RBCs
streams
2. Merozoites in the RBC will become trophozoites then undergo schizogony to form new merozoites to
➔ A. mangyanus: open fields invade more RBCs
➔ A. balabacensis: forest 3. Some trophozoite transforms to gametocyte
➔ A. litoralis: swampy area Mosquito Stage
1. Gametocyte will be ingested by mosquito through blood meal
2. Gametocytes will differentiate into micro and macrogametes in the intestine
3. Fusion of micro and macrogametes produce the zygote
4. Zygote elongates producing the ookinete (worm-like) which will invade an enterocyte and become oocyst
5. Oocysts undergo schizogony and release the sporozoites
6. Sporozoites migrates to the salivary glands
MORPHOLOGY
TROPHOZOITE SCHIZONT GAMETOCYTES
➔ Band-shaped ➔ Contains 8 ➔ Spherical-shape
➔ Cytoplasm is merozoites MACROGAMETOCYTES MICROGAMETOCYTES
stretched along the ➔ Rosette schizonts ➔ Compact nucleus ➔ Diffused nucleus
diameter of the cell ➔ Female ➔ Male
➔ Normal size
parasitized RBC
➔ Inclusion: Schuffner’s
dots

SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL AND PREVENTION

Disease: Quartan malaria ➔ Peripheral smear ➔ Chloroquine: RBC stage ➔ Vector control
➔ Fever every 4 days ➔ Buffy coat ➔ With Primaquine: Liver stage ➔ Animal prophylaxis
➔ False relapse ➔ IFAT ➔ Quinine: Severe ➔ Detection and Treatment of
Prepatent: 18-50 days ➔ PCR cases
➔ Dipstick (Parasight F Test) ➔ Prevent vector-human contact
 Plasmodium ovale
EPIDEMIOLOGY LIFECYCLE
➔ Only zoonotic species Infective stage: Sporozoite (Human); Gametocyte (Mosquito)
Philippines: Diagnostic stage: Trophozoite, Schizont
➔ 1% of cases Mode of transmission: Mosquito bite, Transfusion, Vertical transmission, Contaminated needle

HOST Human Liver Stage

Reservoir: 1. Mosquito takes a blood meal and injects sporozoites
➔ NHP 2. Sporozoites will stay in the bloodstream for 30 minutes before entering the exo-erythrocutic phase
Vector: 3. Sporozoites invades the hepatocytes and undergo schizogony to produce schizont
4. Schizont ruptures and releases merozoites into the bloodstream
➔ Anopheles flavirostris: main;
Human Blood Stage
clean, slow-moving shaded
1. Merozoites enters the erythrocytic phase by invading RBCs
streams
2. Some merozoites become hypnozoites that invade other hepatocytes and become dormant
➔ A. mangyanus: open fields 3. Merozoites in the RBC will become trophozoites then undergo schizogony to form new merozoites to
➔ A. balabacensis: forest invade more RBCs
➔ A. litoralis: swampy area 4. Some trophozoite transforms to gametocyte
Mosquito Stage
1. Gametocyte will be ingested by mosquito through blood meal
2. Gametocytes will differentiate into micro and macrogametes in the intestine
3. Fusion of micro and macrogametes produce the zygote
4. Zygote elongates producing the ookinete (worm-like) which will invade an enterocyte and become oocyst
5. Oocysts undergo schizogony and release the sporozoites
6. Sporozoites migrates to the salivary glands
MORPHOLOGY
TROPHOZOITE SCHIZONT GAMETOCYTES
➔ Amoeboid-shaped ➔ Contains 6-8 ➔ Spherical-shape
merozoites MACROGAMETOCYTES MICROGAMETOCYTES
➔ Compact nucleus ➔ Diffused nucleus
➔ Female ➔ Male

SYMPTOMATOLOGY DIAGNOSIS TREATMENT CONTROL AND PREVENTION

Disease: Mild tertian ➔ Peripheral smear ➔ Chloroquine: RBC stage ➔ Vector control
➔ Fever every 3 days ➔ Buffy coat ➔ With Primaquine: Liver stage ➔ Animal prophylaxis
➔ Lassitude ➔ IFAT ➔ Quinine: Severe ➔ Detection and Treatment of
➔ Recurrence ➔ PCR cases
➔ Pains in joints and bones ➔ Dipstick (Parasight F Test) ➔ Prevent vector-human contact
➔ High fever (39-41o)
➔ Lips and nails cyanotic
Prepatent: 12-20 days