Stages: Tropososite (feeding stage),

Cyst (protective resistant stage)

Motility: Pseudopod (mobility & feeding),

Flagella present in some

Characteristic: Karyosome=Dx ring around nucleus 

Clinical signs:

aymptomatic carriers, 

intestine: abdominal pain, cramping, dysentery, perforated colon.

hepatic disease: abdominal pain, fever, weakness, weightloss

can move to brain 

dignostic test: karyosome fecal smear

vector/transmission: contaminated water/food, ingestion of cyst

1. longitudinal binary fission
2. transverse binary fission 
3. budding
4. multiple fission 
5. endodyogeny 
6. endopolyogeny

1. conjugation 
2. syngamy
3. anisogamy
4. isogamy

1. unicellular eukaryotes
2. possesses organelles that often function similarly to organs and systems of multicellular  organisms 
3. parasistic forms with holozoic nutrition (ingest complex organic material)
4. basic forms of locomotion: flagella, cilia, pseudopodia, and gliding

Sacromastigophora

and

Apicomplexa

equal division of organism into 2 across longitudinal axis

ex. lumen dwelling flagellates

merogony: schizogony; multiple karyokinesis followed by multiple cytokinesis

Ex. malaria

fusion of gametes

ex. Malaria

entamoeba histolytica 

giardia lamblia duodenalis

trichomonas vaginalis 

balantidium coli

isospora sp.

cryptosporidium parvum

cyclospora sp.

microsporidia

“Once Smelled Never Forgotten”

Classification: Protozoa, Flagellate

Structure: Giardia has endoplasmic reticula and two separate nuclei, but lack mitochondria. Kite shaped with 2 nuclei giving it appearance of “monkey face.” Flagella for motility.

Life Cycle: Has two stages, a trophozoite (feeding stage) which is the only form found in tissues and the cyst form, which is the infectious stage (contains 4 nuclei).

Basic concepts of infection and Pathology: Cyst form is ingested, and matures to trophozoite. It adheres to intestinal wall and limits fats absorption. That’s causes fat in stool, which causes horrific odor and floating feces. Diagnosed by cysts in fecal smear.

Mode of locomotion: Rodents, deer, cattle, cats, dogs may act as Zoonosis for humans

Sites of Infection: Adheres to and coats intestinal wall.

Medicine: Metronidazole.

Classification: Protozoa, Flagellate

Structure: No mitochondria, has flagella for motility.

Mode of reproduction: Binary Fision. No cyst stage.

Basic concepts of infection and Pathology: Parasites invade vagina and urethra and cause infection, irritation and profuse discharge of leukocytes. Diagnosis is made of smear of urine, semen or discharge with flagellated parasites. 

Mode of locomotion: Sexual contact

Sites of Infection: In vagina in females and urethra in males. Labia will be red.

Treatment: Metrondazole

Key Facts: Sexually transmitted disease 7 million cases annually in US, 180 million worldwide. Discharge gives off bad odor.

Classification: Protozoa. Ciliate.

Structure: Ciliated (only infectious ciliatd protozoa). Very large. Cyst form lacks cilia.

Mode of reproduction: Binary Fision of trophozoite. Conjugation may occur.

Basic concepts of infection and Pathology: Cyst enters mouth and goes though excystation in small intestines becoming trophozoite in large intestines. Then goes through encystations to produce infected cyst which is passed with feces.

Mode of locomotion: Fecal-Oral. Spread thru H2O and food through reservoirs, monkeys, rats, guinea pigs, dogs and pigs.

Sites of Infection: In large intestines and colon. Causes chronic diarrhea and ulcers in intestines.

Treatment: tetracycline, iodoquinol or metronidazole

Key Facts: known as Balantidiosis, balantidiasis, or balatidial dysentery. Prevention of contamination more useful than treatment. Verify is parasite is absent in stool after 1 month.

Classification: Protozoa, Apicomplexa

Life Cycle: Excreted as oocyst containing sporoblast. Sporoblast divides into 2. Sporoblasts secrete cyst wall becoming sporocysts. They divide twice producing 4 sporozoites each.

Mode of reproduction: Both asexual and sexual development in new epithelial cells.

Basic concepts of infection and Pathology: A sporocyst is eaten, and excysts in S.Intestines releasing sporozoite. It initiates schizogony and the schizonts rupture, releasing marozoites. Invade epi and do asexual multiplication. Trophozoites develop schizonts with contain merozoites. Sexual development of male and female gametes occur. Fertilization à oocysts

Mode of locomotion: Fecal-oral.

Sites of Infection: Small intestines causing diarrhea.

Treatment: Trimethoprim-sulfamethoxazole

Key Facts: Diagnosis by identigication of oocysts in feces using concentration techniques. Eosinphilia. 

Cyclospora – “Tourist Diarrhea”

Classification: Protozoa, Apicomplexa

Life Cycle: Oocysts.

Basic Concepts of infection and pathology: Cyst form is eaten. Causes prolonged diarrhea (4-10 water stools a day). Non-inflammatory reaction (No WBCs). Causes anorexia, fatigue, weight loss.

Locations: Napal and S. America.

Mode of locomotion: Oocysts from stool contaminate fruits (most strawberries and raspberries) and vegetables.

Diagnosis: Fast Acid fecal stain or UV light.

Treatment: Trimethoprim/Sulfamethoxazole.  

Key Facts: Should be considered diagnosis in the differential if prolonged diarrhea especially in pts with Hx of travel. Cause of endemic diarrhea in Peru. Also, share common epidemiology with cryptosporidium, and in fecal smear oocysts have to be measured to distinguish the two. 

Classification: Protozoa, Apicomplexa

Structure: Each oocysts contain 4 sporozoites.

Life Cycle: Oocysts sporolates in hosts with infective agent (4 sporozoites). Life cycle occurs within infected epi cells.

Mode of reproduction: Both asexual and sexual cycle.

Basic concepts of infection and Pathology: Water

Mode of locomotion: Fecal-oral. Found in drinking water, auto-infection  cycle is possible

Sites of Infection: Small intestines causing diarrhea, vomiting and abdominal pain. Crypto develops in the microvilli border.

Diagnosis: Fecal smear with acid fast red stain. Oocysts are ~4-5um in diameter.

Treatment: Nothing good, supportive therapy, nitazoxinide, spiramycin and paromomycin in severe cases.

Key Facts: Risks factor: Exposure to untreated or inadequately treated water.Oocysts extremely resistence to breakdown

Classification: NOW fungus!

Structure: Unicellular spore, 1-2 nuclei, extrustion apparatus (polar caps, polar tube). Resistant spore is infective form. No mitochondria.

Life Cycle: Spore and microspore.

Sites of Infection: Small intestines causing diarrhea

Mode of Reproduction: Binary or multiple Fission.

Basic Concepts of infection and pathology: Spore extrudes polar tubule and infects host cell. Once inside cell, sporoplasm multiples extensively.  The microsporidia develop by sporogony to mature spores. A thick wall forms around spores for protection. Spores keep multiply until cell bursts, and sports infect new cells.

Sites of Infection: Intestines lung and liver depending on the species.

Key Facts: Obligatory intracellular parasites. 

Trichurius Trichura

Whipworm(Trichurius Trichura)

Classification: Nematode, Geohelminth

Clinical: Chronic diarrhea often with frank blood, Anemia, Growth retardation.

Life Cycle: Infected egg in swallowed. Larva hatch in small intestines and mature as an adult in cecum.

Diagnosis: Detection of characteristic football shaped eggs with bipolar plugs. May require more than 1 sample.

Treatment: Mebendazole, Albendazole

Key Fact:Ice Man's rectum infected with whipworm. People are often co-infected with Ascaris because they have similar distribution. World prevalence 900 million, U.S. prevalence about 1%. Infection in population, food preparation and toilet facilities in same area.  Albendazole does not work.

Paragonimus westermani 

Paragonimus westermani (Lung Fluke)

Classification: Trematode, Helminth

Mode of Locomotion: Found in carnivores, pigs, rodents and man but is acquired by eating uncooked crab.

Location: Mostly seen in Southern and Eastern Asia.

Pathogenesis: Adult worms live in fibrotic capsules in lungs. Eggs are trapped within the lung tissue.

Clinical Signs: Hemoptysis (spiting blood sputum), chronic cough, Seconary bacterial infection.

Diagnosis: Eggs in sputum or feces, radiolocal changes like white cloud in lung.

Life Cycle: Eggs hatch releasing miracidium, which infects first intermediate host (snail). Parasite reproduces asexually and cercariae are produced. They infect secondary intermediate host (crab). Cercariae encyst in host, forming matacercarie which is ingested by definitive host. Metacercaria “excysts” in the small intestines and immature worms penetrate gut wall to lungs. Adult parasites reside in lungs

Schistosoma

Schistosoma (Blood Fluke)

Classification: Trematode, Helminth

Structure: Have sharp pointers that help pierce intestines to get into venous system. Cercicaria have forked tail and can penetrate human skin in water. NO METACERCARIAL STAGE

Mode of Locomotion: Fecal contaminated water, human water contant, human feces used as fertilizer.

Life Cycle: Egg hatches in fresh water. Larva infect snail, cercaraie leave snail and are now infectious to humans. In the water then penetrate through skin and travel to hepatic vein. Here the male and females mature and mate. Then, they go to either the small intestines or the bladder to lay their eggs ensuring the eggs will be released from the body.

Key Fact: Can practice molecular mimicry, by incorporating host antigens on surface to fool immune system into thinking its “self”. Eosinophilia. 200 million people infected w/ 1million deaths/year. Adult worms, separate sexes,permanent copulation

3 Species: S. Mansoni, S. Japonicum, S. Haematobium.

Enterobius Vermicularis

Pinworm (Enterobius Vermicularis)

Classification: Nematode, Helminth

Structure: Male worm is much smaller than female.

Life Cycle: Egg is ingested, mature worms live in large intestines. Larva is passed in feces.

Mode of Transmission: Self-infection/auto-infection may occur.

Site of Infection: Adults in the cecum, appendix, colon

Clinical: Pruritus and anal irritation, especially at night.

Diagnosis: Scotch tape on anal.

Treatment: Pyrantel, Albendazole or Mebendazole

Key Facts: Clean house to remove eggs

Heat bedclothes in hot dryer. 

Hymenolepis nana

Hymenolepis nana

Classification: Cestode, Helminth

Structure: Small tapeworm (4 cm)

Life Cycle: Insect intermediate host

Mode of locomotion: Accidental ingestion in food,                                                              Tribolium beetle in cereal 

Site of infection: Autoinfection possible with metacestode forming in intestine

Clinical: Heavy infection cause diarrhea, abdominal pain

Diagnosis: Identification of egg

Treatment: Praziquantel

Most common in children and institutionalized

Diphyllobothrium Latum

Diphyllobothrium Latum

Classification: Cestode, Helminth

Structure: No spines on scolex.

Key Fact: Infection, presents a variable range of pathology, but is not commonly the cause of serious disease in man.

Clinical: abdominal pain and loss of weight, and are often similar to the symptoms displayed during infection with adult Taenia. However D. latum differs from Taenia in absorbing much more vitamin B12, (between ten and fifty times more) than other tapeworms. Infection may result in a macrocytic hypochromic anemia in some cases, vitamin B12 having an important role in formation of blood cells.

Location: Baltic region, particularly in Finland.

Life Cycle: Egg hatches and is eaten by copepod as 1^st intermediate. Procercoid develops, and copepod is eaten by fish (2^nd intermediate). Plerocercoid develops in fish muscle, and is eaten by human and matures to worm.

Taenia solium

Taenia solium

Classifaction: Cestode, Helminth

Mode of Locomotion: Eggs passed in gravid segments from host. Intermediate host ingests eggs.

Life Cycle: Egg is feces  is eaten by animal. Matures to bladder worm and attaches to muscle. Infect occurs by eating cysticerci larvae in un/undercooked meat. T. saginata is beef tapeworm, T. solium is pork. Bladder worm attach to intestines and segments.

Clinical Sign: Diarrhea, Indigestion.

Diagnosis: Identification of eggs or segments.

Treatment: Praziquantel and niclosamide.

Epidemiology: Found worldwide, but Seen primarily in Latin America (common public health problem in Mexico), Middle East, Asia, Africa T. Solium is seen mostly in travels and immigrants.

Key Facts: Humans can also act as intermediate host

Causes “Cysticercosis” in eye, brain and muscle. Death of cysticerci in NS often precipitates disease.

Ascaris lumbricoides

Ascaris lumbricoides

Classifaction: Nematode, Helminth

Mode of Locomotion: Eggs passed in gravid segments from host. Intermediate host ingests eggs. Passed in comtaminated water or pigs.

Life Cycle: Ingested eggs hatch, and larva migrate to liver and lung. Coughed up, swallowed and after 60 days, matures to worm in S.I.

Clinical Sign: Bloating, vomiting, abdominal pain, asthma like reachtion in lunch, obstruction of bile duct and bowel.

Diagnosis: Identification of eggs or adult worm in feces.

Treatment: Albendazole, mebendazole or pyrantel.

Toxoplasma gondii

Toxoplasma gondii

Classification: Apicomplexa, Protozoa

Structure: Infection oocyst and trophozoites.

Mode of locomotion: Parasite is found in animal feces (inhalation, direct contant) or undercooked meat. Oocysts are shed in a cat's stool and can survive in kitty litter and for up to 18 months in the soil. From mother to fetus through placenta usually results in still born. Blood transfusion.

Mode of reproduction: Oocysts are only produces in cell lining of the intestine of cats.  

Basic Concepts of infection and pathology: Sporozoites emerge from oocyst, leave gut and begin rapid division in cells called tachyzoites. ivision slows and bradyzoite (cyst) is formed.

Key Facts: Severe illness generally develops only in fetuses and people with a weakened immune system (HIV/AIDS). Also seen with hydrocephalus.

Diagnosis: blood smear.

Treatment: Clindamycin.

Babesiosis

Babesiosis

Classification: Protozoa, Apicomplexa

Structure: 4 buds from 1 blood cell. Resemble Cross.

Mode of locomotion: Transmitted by same deer tick that transmits Lyme Disease or blood transfusion.

Mode of reproduction: Undergoes asexual replication by budding in RBC. Multiplication in blood causes clinical manifestations of the diease.

Basic Concepts of infection and pathology: Sporozoites from tick cause infection. Then matures into trophozoites and infects the red blood cells. Resembles malaria, high fever, jaundice, dark urine, kidney failure.

Key Facts: In people whose spleen has been removed, the risk of sever disease and death is high. Also, easy to confuse with malaria. Immunocompetent usually asymptomatic.

Diagnosis: Positive blood smear.

Treatment: Quinine and clindamycin.

Cutaneous Leishmania (Leishmania Tropica)

Classification: Protozoa, flagellate parasite

Life Cycle: Promastigote – flagellated in fly. Amastigote – intracellular and nonflagellated in phagocytic cells (macrophage)

Mode of locomotion: Through Sandfly vector.

Basic Concepts of infection and pathology: Promastigote enters skin. Phagocytized by macrophages, where transform and multiple to Amastigote. Stays in skin becase lower temp than viscera. Lesion begins as papule at bite site, and grows into ulcer as WBCs destroy skin tissue.

Sites of Infection: Ulcers on skin at site of bite.

Key Facts: Multiple lesions on ears in L.America. Often designated as New and Old World Forms. US military sites.

Diagnosis: Blood smear, biopsy of skin lesion.

Treatment: Stibugluconate, Amphotericin B

Also known as: Oriental Sore, Baghdad or Dehli Boil.

Location: 90% of cases in Middle East and South America.

Plasmodium

Malaria (Plasmodium)

Classification: Apicomplexa Protozoa

Life Cycle: Sporozoites, Merozoites, Trophozoites, Gametocytes.

Mode of locomotion: Through mosquito vector. Found in warm tropical areas: S. America, Africa, South Asia and Middle East.

Mode of Reproduction: Sexual reproduction in vector and asexual reproduction in human. Can pass to fetus.

Basic Concepts of infection and pathology: Mosquito transfers sporozoites to human. They travel to liver and multiply asexually in hepatocytes. Hepatocyte ruptures (6-16days) and merozoites enter blood to become trophozoites.

Sites of Infection: Liver and blood (RBC) infection.

Key Facts: 4 types. P. Falciparum (most serious), P vivax, P. ovale, P. malaria. Falciparum 24hr fever. Vivax and Ovale 48 hr fever. Malaria 72 hr fever.Cyclic symptoms: cold, hot, sweating.

Clinical Signs: Flu-like, headache, vomiting, anemia, myalgia.

Diagnosis: Blood smear and dipstick technique.

Treatment: Quinine and clindamycin.

Trypanosoma cruzi 

Trypanosoma cruzi (American Trypanosomiasis)

Chagas Disease

Classification: Trypanosoma Protozoa

Life Cycle: Trypomastigote, Amistogote and Epimastigote.

Mode of locomotion: Triatomine Bug (Kissing Bug, Reduviid Bug) or contaminated blood transfusion. Found in rodent, opossums and armadillos are reservoirs.

Basic Concepts of infection and pathology: Kissing bug defecates on skin. Trypomastigotes in feces tunnel into skin.

Clinical Signs: Healthy person is asymptomatic, hepato- and spleenomegaly, acute inflammation at bite site (Romanas Sign), mostly seen in children.

Sites of Infection: Bite is usually eye or lip but trypomastigote is found in circulation.

Location: Mostly S. American. Transmission by blood transfusion has become very important in some areas;Up to 50% of blood infected in some blood banks.

Diagnosis: Xenodiagnosis (Kissing Bug feeds on patient, then its intestines are examined for parasite) or blood smear. 

Visceral leishmaniasis (kala azar)

Classification: Protozoa, flagellate parasite

Modes of transmission: Sandfly vector.

Sites for infection: Parasites not restricted to skin. Usually seen is reticuloendothelial cells (fixed phagocytic cells in spleen and lymph nodes).

Key Facts: Most serious form of leishmaniasis. STRONG relationship between AIDS and visercel leishmaniasis.

Clinical Signs: Hepatomegaly, low grade fever, progressive anemia.

Diagnosis: Microscopy of blood and bone marrow samples.PCR antigen test.

Treatment: Stiboguconate.

Dipylidium Caninus

Dipylidium Caninus

Classification: Cestode, Helminth

Modes of transmission: Most common in dogs or cats, because flea is intermediate host.

Sites for infection: Children occasionally become infected with adult tapeworm.

Key Facts:. Juveniles in flea and louse.

Diagnosis:  Two genital pores and reproductive system in each proglottid.

Treatment: Praziquantel

Clonorchis sinensis 

Clonorchis sinensis (Chinese liver Fluke)

Classification: Helminths, Trematodes.

Structures: Oral sucker, intestine, uterus, yolk gland, testes, ovary, Perculum and seminal receptacle.

Living Cycle: Cercaria infects fish. Fish is eaten raw and metacercaria in fish tissue is ingested.

Clinical Signs: Cirrhosis of liver, Diarrhea, Edema, abdominal Pain, biliary fibrosis and obstruction, hepatitis and hepatomegaly  

Diagnosis: Detection of eggs in fecal samples, may require repeated samples.

Pathogenesis: Light infections asymptotic. Heavy infections up to 21,000 worms (can completely block bile passages.

Treatment: Several drugs used

Fasciolopsis buski

Fasciolopsis buski (intestinal Fluke)

Classification: Helminth, Trematode

Diagnosis: Hemorrhage and abscesses of small intestines.

Affects: 10 million people (man and pig).

Life Cycle: Egg hatches producing miracidium. Infects intermediate host, a snail. Parasite reproduces asexually making cercariae. The cercarie encyst on edible vegetable into metacercariae. Then, once ingested by pig or human (definitive host) it excysts in the small intestines. The sexual mature adult resides on small intestines. 

Fascioloa hepatica 

Fascioloa hepatica (Sheep Liver Fluke)

Classification: Helminths, Trematodes

Mode of locomotion: Eat vegetation with contaminated metacercaria. Usually raw water plant.

Life Cycle: Egg in water becomes meracidium and goes in snail. Matures to sporocyst and further to Redia. Leaves snail as cercaria and becomes metacarcia where it is eaten on plants.

Pathogenesis: Migratory phase is to ectopic locations. Juveniles in liver, causing liver damage and anemia. 

Leishmania Braziliensis

Mucocutaneous Leishmanaisi (Leishmania Braziliensis)

Classification: Protozoa, flagellate parasite

Mode of transmission: Sandfly vector or carried zoonotically in rodents, dogs and foxes.

Clinical Signs: Lesion that spreads through skin to mucosal area (Nasal, Pharyngeal, Buccal mucosa).

Key Facts: Much less common that cutaneous form.

Random fact: Initial cutaneous ulcer heals, and months to years later ulcers in mucous membrane arise. 

Schistosoma

1.    Schistosoma mansoni

Common in African, Middle East, S. America and Caribbean.

Infection site: Inferior Mesenteric Veins

Repoduction: Females release ~200 eggs a day.

2.    Schistosoma hematobium

Common in African, Middle East, India and Portugal

Egg morphology: conspicuous terminal spine.

Pathology: Mostly in urinary tract, eggs passed by urine.

Infection siteL Venous plexus surrounding urinary bladder.

Clinical: Leads to calcification of bladder wall à Hydronephrosis,

Which leads to Squamous Cell Carcinoma.

3.    Schistosomajaponicum

Common in Asia.

Structure – Inconspicuous lateral spine.

Infection site – Superior Mesenteric Veins

Pathology – Worse, due to a higher egg production

Repoduction – females release ~2000 eggs a day.

Classification: Trypanosoma Protozoa

Mode of locomotion: Tsetse Fly bite (vector) and contaminated blood transfusion.                (NO AMASTIGOTE STAGE)

Life Cycle: Trypomastigote is flagellated in extracellular form. Trypomastigote and epimastigote are found in vector.

Mode of Reproduction: Binary fission in human and fly stages.

Basic Concepts of infection and pathology: Tsetse fly deposits trypomastigote when feeding. It divides and lives in circulation.

Key Facts: 2 Stages- 1. Acute Stage and 2. Neurologic Stage. Neurologic stage is “sleeping sickness” when parasite enters CNS. People eventually slip into coma and die.

Clinical Signs: 1.) fever, joint pain, headache //2.)  confusion, seizures sensory disturbances, coma.

Diagnosis: Trypomastigotes in blood, CSF and LN.

Treatment: Suramin (doesn’t penetrate CNS), Melarsoprol.

Interesting: Can change antigen sequence as defense to immune

Flat, usually pretty big as adults

Segmented

All are parasites of the intestinal tract as adults

Life cycles involve 1 intermediate host

General term for the larval stage is a “metacestode”

Different kinds of metacestodes:

    1. Cysticercus--invaginated scolex in fluid filled bladder

    2. Cysticercoid--scolex without fluid filled bladder

    3. Hydatid--like cysticercus only bladder can generate                  many scoleces with potential for large size

Scolex: Attachment organ with suckers, some also

                  have hooks

Neck:  Right behind the scolex, gives rise to segments

Segments: Each segment a separate reproductive unit.

Most posterior segments are most mature.

Once egg development is complete the segment is called “gravid”

Echinococcus multilocularis

Echinococcus multilocularis

Classification: Helminth, Cestode.

Key: Multilocular Hydatid cyst, More serious disease because difficult to remove surgically. 

Life Cycle: Sheeps eat eggs on vegetation. Dogs eat entrails of sheep, and then human comes in contact with infected dogs feces. Egg becomes oncosphere, matures to hydatid cyst, then protoscolex, and finally a scolex to adult.

Clinical: Protoscolicies, Hydatid Sand and laminated cyst wall.

Site of Infection: Hydatid cyst in lungs and liver. Adult worm in small intestines.

Location: Europe, Asia, Alaska, Canada, northern U.S.

Possibly expanding south in U.S.

Echinococcus granulosus

Echinococcus granulosus

Classification: Helminth, Cestode.

Structure: only 3 proglottids; Scolex/immature, Mature, Gravid

Size: Very small adults

Mode of Locomotion: Zoonotic, Canine definitive host. Humans and sheep both intermediate hosts.

Mode of Reproduction: Metacestode and cysts undergoes asexual

Key: Unilocular Hydatid cyst (cysticercus)- many protoscolices.

Life Cycle: Sheeps eat eggs on vegetation. Dogs eat entrails of sheep, and then human comes in contact with infected dogs feces. Egg becomes oncosphere, matures to hydatid cyst, then protoscolex, and finally a scolex to adult.

Clinical: Protoscolicies, Hydatid Sand and laminated cyst wall.

Site of Infection: Hydatid cyst in lungs and liver. Adult worm in small intestines.

Location: Worldwide, but commonly seen in Utah. 

Hookworm(Ancylostoma duodenale)

Classification: Geohelminth, Nematode

Structure: Hookworms have mouths used to bite in intestinal wall and suck blood.

Mode of Locomotion: Egg is excreted, turns into larva, then worm which penetrates skin and goes to Blood, then heart, then coughed up, swallowed and the worm stays in intestines. Other routes are:Ingestion, Transmammary, and Meat.

Clinical: Anemia (bloodsucking parasites), diarrhea with melena, Vomiting, Weakness, Edema and pallor, “Ground itch”--papular rash and pruritus from sensitization to skin penetration of larvae, Stunted growth.

Diagnosis: Detectiong of eggs in fecal sample.

Treatment: Albendazole, mebendazole, pyrantel. Treatment will not remove arrested larvae

Key Facts: Seen mostly in Europe, N.Africa, China, SE Asia, India.

Total daily blood loss would exsanguinate 1.5mill. Important cause of anemia in developing countries. Higher in females.

Baylisascaris procyonis

Baylisascaris procyonis

Classication: Helminth, Nematode.

Life Cycle: These eggs can survive for months to years in the environment. The parasite is transmitted when the eggs are ingested by another animal. Humans generally become infected from accidentally ingesting eggs from soil, water, hands, or other objects which are contaminated with raccoon feces.

Site of Infection: Eggs hatch into larvae which then cause disease by migrating through the central nervous system, eyes, and other organs.

Characteristic diagnostic features: prominent lateral alae and excretory columns

Clinical: nausea, lethargy, liver enlargement, incoordination, loss of muscle control, coma, and blindness.

Treatment: There are no consistently effective treatment regimens available at this time.

At greater risk: Hunters, trappers, taxidermists, and wildlife rehabilitators are also at increased risk if they handle raccoons or items contaminated with raccoon feces.

Trichinella spiralis

Trichinella spiralis

Classification: Helminth, Nematode.

Site of Infection: Larvae encyst in muscles of humans and other mammals

Mode of transmission: Ingesting larvae in undercooked meat

 “cycle of carnivorism” among hogs and rats.

Life Cycle: humans ingest encysted larvae in infected, undercooked pork. Larvae exist in stomach and burrow into small intestinal mucosa.  Adult males and female reemerge and produce larvae which penetrate intestine and circulate in bloodstream. Larvae enter skeletal muscle cells and encyst

Treatment: Mebendazole to kill adults worms

Strongyloides stercoralis

Strongyloides stercoralis

Classification: Helminth, Nematode.

Mode of Infection: Autoinfection; Infective larvae in gut must penetrate mucosa and go though migration to lungs and be coughed up and swallowed.

Clinical: Pneumonitis from migrating larvae, diarrhea, vomiting, epigastric pain, hyperinfection syndrome(in GI tract and Lungs).

Diagnosis:  Detection of larvae in feces. May be difficult to find, repeated sampling required

Treatment: Ivermectin.

Key Facts: Of greatest concern in immunocompromised patients because no immunity to control larval production. Uncommon infection in dogs, but unclear how easily humans infected with canine strains.

Entamoeba histolytica

Karyosome

fecal smear

Giardia

"monkey face"

Balantidium coli

cyst

Cyclospora

oocyst

Isospora sp.

oocyst with sporoblasts

Cyrptospordium parvum 

acid fast stain

1. infect cells in one of these surfaces (the skin, respiratory mucosa, the alimentary tract, genital tract, and the conjuctiva) 
2. otherwise breach the surface (by trauma, the bite of an arthropod or animal, or injection, transfusion or transplantation)
3. be transmitted congenitally.

1. contact 

-direct 

-indirect

-droplet

2 vechicle 

-water borne

-airborne

-foodborne

3 vector

-mechanical 

-biological

4 fecal-oral

5 iatrogenic

phoresis

commensalism

mutualism

predation

parasitism

1. multiple fission
2. hermaphrodism
3. parthenogenesis
4. strobilation
5. high ova/larval output

1. loss of digestive tract
2. loss of wings
3. loss of many sensory structures
4. tegument
5. special holdfasts organs
6. anti-coagulants 

1. antigenic variation
2. tough tegument
3. intracellular habitat
4. antigen acquisition/mimicry
5. suppression eosinophil or neutrophil
6. encystment
7. ability to cleave antibodies
8. trigger immune response

1. physical trauma
2. nutritional diversion
3. toxins/excretory products/immune complexes
4. blood loss

1. ingestion 
2. vectors
3. direct penetration

1. fecal specimen collection
2. collection of material other than fecal
3. blood films/smears

1. biochemical (first generation)
2. immunological (antibodies)
3. nucleic acid

isoenzymes: perform same functions but diferent

movement on gels. 

genetically controlled: parasites with different gel patterns genetically distanct. 

enzymes separated by size: SDS-PAGE

advantages: 

1. rapid easy field-based test
2. both individual & mass population screening
3. Ig subclases-to improve specificity & sensitivity

1. ribosomal DNA/RNA
2. specific sequences of genomic DNA
3. random primer amplification (RADP) PCR

1. cryptosporidium
2. isospora
3. cyclospora
4. toxosplasma
5. plasmodium
6. babesia

small blood meals-many hosts

short period on host 

characteristics: 

-capillary location 

-specialization mouthparts

-anti-coagulants

anaesthetic

types of ticks

hard ticks

Ixodid ticks

-contains most of the common ticks 

soft ticks

-much less common, not important in U.S.

rocky mt. spotted fever

lyme disease

babesia

ascending flaccid paralysis

caused by attachment of female tick, usually near spinal cord, and release of toxins

reversed by removal of ticks