Isospora belli Cryptosporidium hominis/pavarum

Cyclospora cayetanensis

Sarcocystis hominis Toxoplasma gondii Babesia microti

OBLIGATE

Tax

onom

y

P:Apicomplexa C: Sporozea SbO: EimeriinSbCs:Coccidian

D: EukaryotaK: ChromalveolataSpP: AlveolataP: Apicomplexa(unranked): MyzozoaC: ConoidasidaSbC: CoccidiasinaO: EucoccidioridaSbO: EimeriorinaF: EimeriidaeG: IsosporaS: I. belli

D:EukaryotaK:ChromalveolataSpP:AlveolataP:ApicomplexaC:ConoidasidaSbC:CoccidiasinaO:EucoccidioridaSbO:EimeriorinaF:CryptosporidiidaeG:CryptosporidiumS:C. hominis

C. hominis – anthroponotic pathogen; C. parvum - zoonotic pathogen

K: ProtistaP: SporozoaSbP: Telesporea C: CoccidianO: ApicomplexanG: Cyclospora

K: ChromalveolataSpP: AlveolataP: ApicomplexaC: ConoidasidaSbC: CoccidiasinaO: EucoccidioridaSbO: EimeriorinaF: EimeriidaeG: CyclosporaS: C. cayetanensis

K: ProtistaP: ApicomplexaF: SarcocystidaeG: Sarcocystis

D: EukaryotaK: ChromalveolataSpP: AlveolataP: ApicomplexaC: ConoidasidaSbC: CoccidiasinaO: EucoccidioridaF: SarcocystidaeG: ToxoplasmaS: T. gondii

K: EukaryotaP: AlveolataC: ApicomplexaO: AconoidasidaF: PiroplasmidaG: BabesiidaeS: Over 100 speciesBabesia MicrotiBabesia divergens

DH Man Mammals – C. muris Birds – C. meleagridis Reptiles – C. crotali Fishes – C.nosarum Humans – C. hominis C. parvum

Carnivores/Man [Dogs] Cats (complete [Felidae]) Ixodes scapularisIH Man Omnivores/Herbivores

(Man. rare)

Mammal/bird Man/Animal (reservoir)(reservoir)

Cats, Dogs, RodentsFarm animals, Birds

IS Sporulated oocyst (2 sporocysts, each 4 sporozoites),

Sporulated oocyst (4 sporozoites)

Sporulated oocyst (2 sporocysts, each 2 sporozoite)

Sarcocyst tachyzoite bradyzoite oocyst

Man: Sporozoite [merozoite]Tick: Gametocyte

MO

T Ingestion of an oocyst [Fecal-Oral]

Ingestion of an oocyst [Fecal-Oral]

Ingestion [Fecal-Oral] /Vehicle transmitted

Ingestion of undercooked meat containing sarcocyst

Ingestion of raw meat with infected oocyst

Bite of infected vector (Ixodes scapularis)

Par

asite

Bio

logy

-Oocyst >elongated/ovoid >20-33μm,10-19 μm >Mature in 48hrs (ff. evacuation of stool) >1sporoblast → 2-Sporocyst >12-14μm,7-9 μm

- Cigar shape double layer

-penetration/cell invasion: >microneme, subpellicular tubules, polar rings, conoids & rhoptries

-Asexual/Sexual

-Oocyst >ovoid >4-5 μm (diameter) >4 sporozoites (feces) >bow-shaped >attach: epithelial cells of GI tract

-Trophozoite >“intracellular but extracytoplasmic”

- Long life span on water, not in dry-Immune system reduces the formation of Type 1 merozoites as well as the number of thin-walled oocysts.

>prevent autoinfection. -B cells do not help with the initial response or the fight to eliminate the parasite

-Cyanobactrium-like body (CLB)-Coccidian parasite

-Oocyst: >Non-refractile >Double-walled spheres >8-10µm (diameter) >UNsporulated >(after5days) 2 sporocysts, each 2 sporozoite

-Asexual/Sexual >intestinal tissue

-Cyclospora fluoresces blue under ultraviolet light

-Sporulation is complete in 7-12 days at a "warm" room temperature

Zoite – simplest form >Banana-shaped cell >pointed end – penetration

Sporocysts >Oval, 4 zoites >9-16 μm (length) >survive: ground/infecting host Sporozoite >from SporocystSarcocyst>from Sporozoite>cyst wall present>Macrocyst: naked eye>Microcyst: width as muscle fiber (microscope)

-Sarcocyst in ingested Food -Sarcocyst releases BRADYZOITES -INVADE THE INTESTINAL MUCOSA -Develop into a Oocyst -Develops to a Sporozoite

-Intracellular parasite- Endodyogeny

>Modified Binary Fission >2stg. present in man and other IH

-Typical coccidian LC-Oocyst >ovoid>thin wall >10-13 μm, 9-11 μm >UNsporulated >(3-4days) 2 sporocysts, each 4 sporozoite-Trophozoite>crescent shaped with pointed anterior & rounded posterior>spherical nucleus(post.)

>penetration/cell invasion:>rhoptries & micronemes (anterior)

tachyzoites – quickly multiplying forms and are responsible for initial spread of infection and tissue destructionbradyzoites – slower developing and form into cysts

-blood parasite cause malaria-like infection-intraerythrocytic, pleomorphic, ring forms > Maltese cross. >as P. falciparum.

-become cyclical and develop into a trophozoite ring-morph into merozoites which have a tetrad structure coined a Maltese-cross form-Trophozoite and merozoite growth ruptures the host erythrocyte leading to the release of vermicules, the infectious parasitic bodies, which rapidly spread the protozoa throughout the blood.

Sch

izog

ony

(As)

>Sporozoites>Trophozoites >Merozoite

>Sporozoites>Trophozoites (attach brush border) >Merozoite

Sporozoite (meronts)>Merozoite (8-12 or 4)

Sporocyst>sporozoite>Sarcocyst

(Endodyogeny)Sporozoite> Tachyzoite & bradyzoite>oocyst

(Binary Fission/Budding)Oval from>Gametocytes>Merozoites/ vermicules (invades cells)

Spo

rogo

ny

(S)

Gametocytes (Macro/Micro)>Zygote>Oocyst>Sporocyst>

Gametocytes (Macro/Micro)>Zygote>Oocyst>

Gametocytes (Macro/Micro)>Zygote

Pat

hoge

nesi

s

Asymptomatic-Mild diarrhea/None

Symptomatic-Loose stool-Watery diarrhea (Isosporiasis)-Malabsorption-Weight loss-Malaise -Abdominal pain-Flatuence-Anorexia-Peripheral Eosinophilia

>Mucosal lesions of shortened villi>hypertrophied cryptsInfiltration of the lamina propria w/ polymorphonuclear leucocytes esp. EOSINOPHIL

>acalculous cholecystitis

Asymptomatic-Acute Diarrhea-Persistent Diarrhea -Diarrhea – stool is watery with mucus. -Rare or no leukocytes found in the stool.

Symptomatic-Gastroenteritis-Cryptosporidiosis-Abdominal pains -Low fever-Nausea and Vomiting-Malabsorption -Dehydration -Anorexia -Weight loss-Pancreatitis

>Severe: -Cholecystitis: Bile duct & Gall Bladder>Respiratory: -Chronic coughing -Dyspnea -Bronchiolitis -Pheumonia>Infection: 2-10 days, with an ave. of 7 days  until two weeks.

There are 4 clinical presentations for patients with AIDS.

4% no symptoms, 29% transient

infection 60% chronic diarrhea 8% severe

Symptoms: 12-24hrs after exposure

Asymptomatic: infection occurs

-Gastroenteritis-Constipation-Cyclosporiasis-Loss of appetite-Weight loss-Abdominal bloating -Camping-↑Flatulence-Nausea fatigue-Low-grade fever-D-xylose malabsorption

-Infection:10-100 oocyst

-Cyclosporiasis: average incubation period of about 7 days

>One cause of traveler’s diarrhea

-Gastroenteritis-Diarrhea-Eosinophilic enteritis-Myalgia-Weakness-Mild ↑ creatine kinase-Lack inflammation/degenerative changes (Microscopic exam)

Immunocompromised:-Fever & more severe symptoms

IH:-Damage brain, muscle & kidney tissues-Loss of appetite-Fever-Weight loss-Anemia-Neurological damage -Gait abnormalities -Limbs weakening -Muscle wasting -Head tilt

Abortion in pregnant animal (Cow)-paralysis > death

-Toxoplasmosis-Encephalitis-Myocarditis -Retinochoroiditis -Hepatitis-Splenomegaly -Pneumonia -Failure to gain weight

Bradyzoite when stimulated

>Cysts -Brain, Skeletal & heart muscle, Retina

Immunocompromised: Relapse

Infected babies: -Chorioetinitis -Epileptic seizures -Jaundice -Hydrocephaly -Microcephaly

Normal Host- Approximately 50 % of individuals have antibody and organisms in tissue but are asymptomaticCompromised Host- disease tends to involve the CNS with various neurologic symptoms

-3 dev’t stg: larva, nymph, and adult-requires blood meal

-Asymptomatic-Symptoms: 1-4wks after a tick bite// 6-9wks post-transfusion w/ infected blood products

-Constitutional symptoms-Anorexia-Abdominal pain-Hemoglobinuria w/o RBC-Anemia, ↓HCT-↑ Bilirubin levels-↑Lactate dehydrogenase lvl-Reticuloctosis-Babesiosis --incubation:1-12mon.

(MALARIA-like) -Headache -Fever -Chills -Drenching sweats -Nausea -Vomiting -Myalgia -Altered mental status -Anemia, dyserythropoiesis -Hypotension -Respiratory distress -Renal insufficency

-Jaundice-Hepatomegaly-Splenomegaly

Ha

bita

t Small intestine (distal duodenum, proximal ileum)

Epithelial cells of GI tract (attach); Jejunum

Jejunum Intestinal epithelium Intestinal epithelium(lamina propria)Lymph nodes, Lungs, Liver, Heart, Brain, Eyes

{Intestinal gut} RBC (sporozoite)

Dx specimen

Unsporulated oocyst, stool

Stool Stool Stool (DH), Skeletal muscle, brain tissue (IH)

Biopsies (any tissue), CSF

Blood

Dia

gno

sis

(Dx)

Kinyoun’s Acid fast Auramin-rhodamine stain(+), oocyst-conc. stool=pink (immature)=internal sporocyst (mature)

Direct microscopyor after formalin-ethyl acetate concentration

Concentration Tech- ZnSO4 -Sugar flotation

EnterotestDupdenal aspirate

Sheather’s sugar floatation technique>highly refractile

Kinyoun’s modified acid-fast stainRed-pink doughnut shaped circular organism in blue bg. (cheapest)

Enzyme Immunoassay (EIA) and Indirect Fluorescent Antibody Tests (IFA)

Ziehl-Neelsen mtd.

Formalin-ethyl-acetate concentration technique

Direct microscopyHPO (fecal smear)

Kinyoun’s modified acid-fast stainghost cell

Auto-FluorescentFluorescent microscopy>blue/green circle-screening-(365-450 DM)

-[ Fluorescent DNA probes]

Safranin stain & Microwave heating

Polymerase chain reaction-diff: Cyclospora to Eimeria spp.

DH: SporocystFecal flotation mtd Bright-field microscopy(wet mount)

IH: Schizonts Merozoites -Thick covering containing bradyzoites - elongated dark structure Macrocysts >ducks, sheep, rabbits, mice - grayish to whitish streaks [1-10 mm] -lenghtwise along muscle fiber

Enzyme Immunoassay (EIA) and Indirect Fluorescent Antibody Tests (IFA)

Complement fixation Dermal Sensitive test

Serodiagnostic mtd.- detect antibodies against T. gondii

Sabin-Feldman dye test (for mice) –methylene blue

Toxoplasma skin test –saline extract of mouse peritoneal exudates

Tuberculin skin test – positive rxn: previous exposure or active disease

Enzyme Immunoassay (EIA) and Indirect Fluorescent Antibody Tests (IFA)

Giemsa Stain (Liver)H&E

Polymerase chain reaction

Complete blood cell count (CBC) and erythrocyte sedimentation rate-hemolytic anemia-Howell-Jolly bodies: splenic dysfunction

Lactate dehydrogenase (LDH) and a properly stained peripheral blood smear

Wright or Giemsa stain -Asplenia:greater degrees of parasitemia- Maltese cross

Serum protein electrophoresis (SPEP)

Liver function tests

Urinalysis

Polymerase chain reaction

Tre

atm

ent (

Tx)

Asymptomatic-Bed rest-Bland diet

Symptomatic-Trimethoprim-sulfamethoxazole (std)-co-trimoxazole (1:5)--160/800mg 4x/day, 10days; 2x/day, 3wks

NitazoxanideBovine colostrumsParomomycinClarithromycinAzithromycin

Anti-parasitic drugs. - alleviate diarrhea >attacking the metabolic processes of the cryptosporidium spp.Azithromycin (Zithromax) -compromised immune systems.Anti-motility agents -↓ the movements of your intestines -↑fluid absorption to relieve diarrhea and restore normal stools. loperamide and its derivatives (Imodium, others). Fluid replacement. electrolytes — minerals such as sodium, potassium and calcium >maintain the balance of fluids from persistent diarrhea, either orally or intravenously.These precautions will help keep your body hydrated and functioning properly.Anti-retroviral therapies – for AIDs patients

Trimethoprim and Sulfamethoxazole at 160mg and 800mg, respectively, twice daily for 7 consecutive days.

Clotrimoxazole (trimethoprim plus sulfamethoxazole)

CiprofloxacinNitazoxanide

No effective treatment.

Corticosteroids-muscle inflammation

Trimethropin- sulfamethoxazole -intestinal inflammation

Furazolidone Albendazole Pyrimethamine

Pyrimethamine and sulfadiazine

Clindamycin

SpiramycinAzithromycinClarithromycinDapsoneAtovaquone

Corticosteriods

Trimethoprim-sulfamethoxazole

Prophylactic treatment is often recommended in newborn until it can be demonstrated that IgM antibody is not present

Clindamycin

Clindamycin and quinine

combination of clindamycin with azithromycin and doxycycline

Clindamycin in combination with vancomycin HCl

Pentamidine isethionate (Trypanocide)

Diminazene aceturate

Chloroquine

Epi

dem

iolo

gy

Genus Toispora- Cystoisospora belli

- more frequent in tropical and subtropical countries- can also be acquired by travelers- isosporiasis occurred in 15 percent (20 of 131) of such patients in Haiti- Isospora infections are more commonly observed in Hispanics, foreign-born patients, and HIV-positive homosexual men- December 2006, India: most common parasitic cause of diarrhea in HIV-infected subjects-France: Prevalence of isosporiasis as a cause of diarrhea has increased; seen more frequently in patients originating in sub-Saharan Africa and in children, women and heterosexual individuals-Paris: (2 hospital, 1000 patient) 1995-1996 to (From 0.4) 4.4 per 1000 patients in the year 2001-2003

1993: -400, 000 people developed Cryptosporidium gastroenterititis from the municipal water supply of Milwaukee, Wisconin 2004: 3, 577 cases of cryptosporidiosis were reported to the CDC Cryptosporidium parvu: -reported in six continents and identified in patients aged 3 days to 95 years old (Flanigan, Soave, 1993)Phil: prevalence- 2.6%-among diarrheic patients in San Lazaro Hospital- 8.5%-among diarrheic patients in Philippine General Hospital- 1.7%

-Occur mostly in summer or spring (warm moist)

1996: Llarge outbreak in the spring and summer when it first attracted public attention which involved more than 1400 people from the US and Canada. The cause was traced to eating raspberries imported from Guatemala. 1997: fresh basil in Washington, D.C which more than 200 people were infected. -Outbreaks: Nepal, Peru, Haiti, and other countries of South and Central America, Southeast Asia and Europe.

etymology of the nomentriviale(trivial name) is derived from Cayetano Heredia University in Lima, Peru(1994)

-The infection frequency has not been confirmed and it is estimated at more than 10%, and it affects mostly children.-Infection starts in the oral cavity and gets there with water and food that are poisoned by sporocyst.

--Zoonosis

-northeastern United States such as Nantucket, Martha's Vineyard, and Cape Cod, Mass; Block Island, RI; and Shelter Island and eastern Long Island, NY.

-receiving blood products

-Parasitemia developed in both infants. -Phil: human babesiosis: NO REPORT-Disease could be present in dogs.

Pre

vent

ion

-Good personal hygiene-Sanitary disposal of feces -Sufficient treatment of drinking water -Habitual washing-Eat well cooked-Physical contact with infected person

-Good personal hygiene-Sanitary disposal of feces -Sufficient treatment of drinking water -Water filtration (slow sand filters, diatomaceous earth filters and membranes) -Ultraviolet light treatment at relatively low doses -Chemical treatment (chlorine dioxide and ozone treatment) Prevention of swallowing natural water and swimming pool water

-Personal and food hygiene -Frequent hand washing-Proper waste disposal, use of boiled or filtered drinking water, thorough washing of fruits and vegetables.

-Food animals that are heavily infected should be condemned as unfit for human-Good sanitation & hygiene

Food should be protected from contamination by cat feces.Meat and eggs should be well cooked.Unpasteurized milk should be avoided.Pregnant women should avoid contact with cats.Laboratory workers should be very careful in handling the parasite.

-Decreasing exposure by wearing appropriate, light-colored clothing-Insect/Tick repellents-Detect first babesia spp. Among blood donors