SUBKINGDOM: PROTOZOA (“first animal”)

SUBKINGDOM: PROTOZOA (“first animal”)
KINGDOM: PROTISTA SUBKINGDOM: PROTOZOA (“first animal”)

Reminder Your group project plates have to be inoculated this Thursday or else wait until after the holiday break. If you inoculate this Thursday, you need to go and observe them this Saturday. Remember to bring a good quality camera for photos that you might want to blow up and put on your poster. Cell phones don’t have good quality for this.

CHARACTERISTICS OF PROTOZOA
1. Unicellular 2. Chemoheterotrophs (get their energy by breaking down organic matter). 3. Most ingest their food; thus, they have special structures for this. 4. Trophozoites: any stage in a protozoa’s life cycle which can ingest food. In practice it refers to the motile form (pseudopods, cilia, flagella). 5. Cyst: Non-motile form, protected by a membrane. This is usually the infective stage. Cysts have a thick cell wall that allows for survival in harsh environments better than the trophozoite form. Excystation: process of emergence of the trophozoite from the cyst. 7. Capable of reproduction A. Asexual: fission, budding, or schizogony (produces a large number of trophozoites) B. Sexual: conjugation

PROTOZOA CYSTS Cysts are not as resistant as a bacterial endospore.
You can kill cysts by boiling them. They can live in the soil or water for months. A cyst is not motile, so it is not trophozoic. A cyst does not go and seek its nutrients or ingest food, but it can absorb nutrients. It has no organelles to ingest food.

Classification Domain: Eukaryotes Kingdom: Protista

TERMS: Host Types The definitive host is the one in which the parasite completes its sexual life cycle. For instance, in Plasmodium, the definitive host is the tropical mosquito anopheles and the intermediate host is the human. Some organisms use the human as the definitive host.

Mosquito

Kingdom Protista Subkingdom: Protozoa
Phylum: Sarcomastigophora Subphylum: Sarcodina (amoebas) Amoeba spp. Entamoeba histolytica Naegleria fowleri Subphylum: Mastigophora (flagellates) Giardia lamblia Trichomonas vaginalis Trypanosoma brucei and cruzi Phylum: Ciliata (ciliates) Paramecium spp Balandtidium coli Phylum: Apicomplexia (Sporozoa; non-motile obligate parasites) Plasmodium spp Toxoplasma gondii Cryptosporidium

Phylum: Sarcomastigophora (amoebas and flagellates)
Amoebas (move by pseudopods) Flagellates (move by flagella)

Subphylum: Sarcodina (amoebas)
All amoebas have pseudopods (false foot) Amoeba spp (free living; not parasitic) Entamoeba histolytica (parasitic) Naegleria fowleri (parasitic)

Amoeba Pseudopods Nucleus Food vacuole

Amoeba Pseudopods Nucleus Food vacuole p

Amoeba Pseudopods Nucleus Food vacuole

Entamoeba histolytica
Disease: Amoebiasis This is a global disease that any traveler can get. As soon as you cross the border into Mexico, you are exposed to it. Entamoeba histolytica consume red blood cells. In a fresh diarrheal specimen, you can see RBCs in the cytoplasm of the amoebas.

Entamoeba histolytica, as its name suggests, can actually bore through the enteric walls (histolysis = destroying tissue) and reach the blood stream. From there, it can reach different vital organs of the human body, like the liver, lungs, brain, eyes etc. A typical effect is a liver abscess caused by such migrating Entamoeba histolytica, which can be fatal.

Entamoeba histolytica infection can lead to amoebiasis or amoebic dysentery. Symptoms include dysentery (diarrhea), weight loss, fatigue, and abdominal pain. It can be diagnosed by stool samples. Trophozoites should be seen in a fresh fecal smear and cysts in an ordinary stool sample.

Treatment Metronidazole Diagnostic Features Ingested RBC Bull’s eye Karyosome

Entamoeba histolytica Trophozoites

Trophozoites of Entamoeba histolytica with ingested erythrocytes

Cysts

Teen nearly blinded after parasite latches onto contact lens
A rare parasite had grown on her contact lens and was trying to eat its way through her cornea. Had they not discovered it in time, Ashley could have lost the use of her eyesight. Ashley had what is called an acanthamoeba infection. A tiny parasite, commonly found in fresh water and soil, acanthamoeba are capable of spreading through contact lens infections, cuts or being inhaled into the lungs. Acanthamoeba infections are just one possible side effect of improper cleaning of contact lenses. Many ophthalmologists recommend using daily disposable contact lenses, to better avoid contracting infection and disease.

Naegleria fowleri “Brain-eating amoeba“
Found in the soil and in freshwater lakes in the Southern part of the United States during the summer. Infections usually occur when it is hot for prolonged periods of time It can also survive in inadequately chlorinated swimming pools or dirty tap water, and can infect the brain when someone gets water up the nose. Causes primary amoebic meningoencephalitis (PAM)

Naegleria fowleri Boy, 9, Dies of Rare Amoeba Infection After Swimming in a Lake

Girl contracts brain eating amoeba after swimming at Arkansas water park. July 29, 2013
A 12-year-old Arkansas girl has contracted parasitic meningitis, a rare and deadly disease caused by a brain-eating amoeba, Naegleria fowleri, typically found in freshwater or soil. It enters the human body through the nose, where it then moves to the brain, typically causing death. "I couldn't get her fever down. She started vomiting," Hardig told the Christian Post. "She'd say her head hurt really bad. She cried, and she would just look at me and her eyes would just kind of roll." Doctors put Kali into a coma, in order to stabilize her condition.

Subphylum: Mastigophora (Flagellates)
Giardia lamblia (intestinal parasite) Trichomonas vaginalis (urogenital parasite) Trypanosoma brucei and cruzi (blood parasite) Undulating membrane (for movement) Kinetoplast (circular mass of DNA)

Mastigophora: Flagellates
Giardia lamblia Disease: Giardosis Trichomonas vaginalis Disease: Trichomoniasis (an STD) Trypanosoma brucei Disease: African Trypanosomiasis African Sleeping Sickness Trypanosoma cruzi Disease: American Trypanosomiasis Chaga’s disease

TERMS Mastigote = flagella Promastigote: has single flagella
Amastigote: has no flagella Kinetoplast: round mass of circular DNA

Giardia lamblia Disease: Giardosis
Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces. Infection occurs by the ingestion of cysts in contaminated water, food (includes undercooked meat), or by the fecal-oral route.

Life Cycle of Giardia lamblia

Giardia lamblia Trophozoite form: piroform (pear or teardrop shape), looks like a happy face. Discovered by Anton Van Leuwenhoek when he examined his own feces when he had this infection. You won’t see the flagella in lab because you need a special stain for that. Cyst form: oval shaped. Nuclei looks like two eyes.

Giardia lamblia Trophozoite

Giardia lamblia Trophozoites

Giardia lamblia trophozoite

Giardia lamblia Cysts

Giardosis Abdominal pain Diarrhea Gas or bloating Headache
Loss of appetite Low-grade fever Nausea Swollen or distended abdomen Vomiting

Trichomonas vaginalis
Disease: Trichomoniasis Trichomonas vaginalis resides in the female lower genital tract and the male urethra and prostate. The parasite is a trophozoite only; it does not have a cyst form, and does not survive well in the external environment. Trichomonas vaginalis is transmitted among humans, its only known host, primarily by sexual intercourse.

Trophozoite Undulating membrane

Trichomoniasis Usually asymptomatic in men, or mild itching
In women, vagina is extremely pruritic, with vaginal odor and discharge.

Trypanosomiasis African Trypanosomiasis American Trypanosomiasis
(African Sleeping Sickness) American Trypanosomiasis (Chaga’s Disease)

Trypanosoma brucei Disease: African Trypanosomiasis
“African Sleeping Sickness” Trypanosomiasis has a biological vector, the tsetse (pronounced “set-see”) fly. Wild animals may also be a reservoir (Zoonotic is when a disease is transmitted to animals as well as humans.) The tsetse fly bites a human and injects the trypanomastigotes into the skin. This causes a chancre (pronounced “shanker”), which is an ulcer on the skin. Then it enters the lymphatic system.

Trypanosomiasis It is characterized by Winterbottom’s Sign: swelling of the cervical lymph nodes in the head and neck area. CNS symptoms include a shuffling gait (like a stroke victim), slurred speech, and malaise (needing to sleep longer and longer each day). They are also restless at night.

Winterbottom’s Sign

Trypanosomiasis CNS symptoms Shuffling gait Slurred speech
Malaise (sleeping all day) Treatment Melarsoprol: which has dangerous side-effects like chemotherapy. This drug requires administration with a substance called ethylene glycol, which will break down regular plastic tubing, so the drug must be administered with special plastic iv tubing.

Trypanosoma brucei Trypomastigote stages are the only form found in patients. Blood-saliva route Posterior kinetoplast Centrally located nucleus Undulating membrane Anterior flagellum

Trypanosoma brucei

Trypanosoma brucei Trypomastigote

Trypanosoma

Tsetse Fly

Trypanosoma cruzi Disease: American Trypanosomiasis “Chaga’s Disease”
A zoonotic disease (can infect animals) that can be transmitted to humans by blood-sucking bugs. This organism is a little smaller than T. bruceii and has a larger kinetoplast.

“Chaga’s Disease” This disease is NOT found in Africa.
The vector is a large bug called the “Kissing Bug”. It is found in warm regions and crowded areas, especially in the cracks of adobe huts. It comes out at night and crawls on a human while they sleep.

Kissing Bug

Trypanosoma cruzi Triatomine bug, Trypanosoma cruzi vector, defecating on the wound after taking a blood meal. Fecal-blood route

“Chaga’s Disease” It is called the kissing bug because it prefers the lips because the blood supply is close to the surface and also it is attracted to the CO2 emissions. It sucks the blood there, but they don’t transmit the organism this way. When they suck the blood, they also defecate, and the organism is in the feces. When the human wakes up to scratch the itch, feces get into the tiny wound. This is a fecal- blood route.

Romana’s sign Swollen eye, seen in Chaga’s disease.
LA Times article on Chaga’s Disease

“Chaga’s Disease” Symptoms include fever, anorexia, swollen lymph nodes, hepatosplenomegaly (enlarged liver and spleen), and myocarditis (inflammation of the heart), which usually causes death. They also have megacolon (large colon) and megaesophagus (large esophagus).

Trypanosoma cruzi

Trypanosoma brucei and cruzi
Smaller posterior kinetoplast Trypanosoma cruzi Larger posterior kinetoplast American Trypanosomiasis “Chaga’s Disease” African Trypanosomiasis “Sleeping sickness”

Trypanosoma cruzi

Trypanosoma cruzi large kinetoplast

Leishmania donovani Disease: Leishmaniasis
Vector-borne disease transmitted by sandflies.

Leishmania Life Cycle It starts out as a spindle-shaped, single flagellated cell called a promastigote (mastigote means flagella). You can also see the nucleus and a kinetoplast (mass of circular DNA). Kinetoplast

Leishmania rosette In prepared slides you can see promastigotes align their nose in a circle, called a rosette.

Leishmaniasis rosette

Leishmania Life Cycle It reproduces in the gut of a female sandfly, and migrates to her proboscis (mouth part). It is introduced into the human by her bite. It then enters a macrophage and becomes intracellular. Here, it loses its flagella and is now known as an amastigote.

Leishmaniasis These amastigotes multiply in various organs including the spleen, liver, and lymph nodes. Symptoms include hepatosplenomegaly, lymph adenopathy, fever, weight loss, and a decrease in all blood cells: WBC, RBC, and platelets. The treatment is almost as bad as the disease because of the side effects. It is best to catch it early.

Leishmania Life Cycle The female sandflies inject the infective stage, promastigotes, during blood meals. Macrophages phagocytize them and they transform into amastigotes. Other sandflies become infected during blood meals when they ingest infected macrophages. In the sandfly's midgut, the parasites differentiate into promastigotes, which multiply and migrate to the proboscis.

Leishmaniasis Life Cycle

Leishmania donovani (Promastigote)
Single flagellum found in sand flies

Leishmaniasis Macrophage rupturing Amastogotes
Amastogotes with nucleus and kinetoplast

Leishmania Amastigotes

Sand Fly This looks like a mosquito, except its body is hairy and the wings are feathery.

Leishmaniasis Geographic Distribution: More than 90 percent of the world's cases of visceral leishmaniasis are in India, Bangladesh, Nepal, Sudan, and Brazil. Leishmaniasis is also found in Mexico, Central America, and South America, southern Europe, Asia, the Middle East, and Africa. More and more cases are reported in the US, especially Texas and surrounding areas.

Cutaneous Mucocutaneus Visceral Leishmaniasis
There are three forms of Leishmaniasis: Cutaneous Mucocutaneus Visceral

Cutaneous Leishmaniasis
The disease is only at the site of the bite. This form is seen in Texas, Mexico, Asia, and the Middle East (our Iraq troops are coming down with this form). It manifests as a large, wet sore with raised edges. It looks like a volcano with weepy serum coming out of the center. The wound is not contagious, just the sandfly bite. Dogs can get this disease, too.

Leishmaniasis (cutaneous)

Leishmaniasis (mucocunateous)
This is when the disease located in the mucous membranes of the nose and mouth. The most gruesome photos are of this form.

Leishmaniasis (mucocunateous)

Leishmaniasis (visceral)
This is the most serious form. It occurs especially in immunocompromised people, especially HIV patients. The amastagotes reproduce inside macrophages. Only T-cells can kill infected macrophages, but HIV is a disease that infects T-cells. This form is known as Kala Azar.

Kala Azar Hepatosplenomegaly

Kala Azar (duodenum)

Phylum: Ciliata (ciliates)
Paramecium spp (free living; non-parasitic) Oral groove (mouth) Balantidium coli (intestinal parasite) Cytostome (mouth)

Phylum: Ciliata (Ciliates)
Ciliates (move by cilia)

Paramecium

Balantidium coli Disease: Balantidiosis
The animal reservoir is the pig. Its geographical distribution is world-wide, wherever humans and pigs live nearby each other. This is the only ciliated protozoan that causes disease in humans.

Balantidiosis This is almost identical to Entamoeba histolytica.
The cyst form is infective. It has a thick wall to protect it from stomach acid. It enters the human (and dogs) by ingestion of fecal contaminants on food, water, and hands. In the trophozoite form, they reproduce in the large intestine, invade the colon wall, and cause ulcerations in the colon. Like Entamoeba, it leaves a flask-shaped ulcer. Symptoms include diarrhea and GI discomfort.

Balantidium coli Trophozoites characterized by:
Large size (40 µm to more than 70 µm). Presence of cilia on the cell surface A cytostome (where they take in food) A bean shaped macronucleus which is often visible and a smaller, less conspicuous micronucleus.

Balantidium coli Trophozoites Cytostome

Balantidium coli Trophozoites

Balantidium coli Trophozoite

Balantidium coli Cyst

Balantidium coli Cysts

Balantidium coli

APICOMPLEXA Characteristics: has an organelle called an apical complex which allows the organism to attach to the host. They all require a biological vector for transmission (to get into the blood of the host). Organisms Plasmodium Disease: Malaria Toxoplasma gondii Disease: toxoplasmosis Cryptosporidium parvum Disease: Cryptosporidiosis

Phylum: Apicomplexia (Non-motile obligate parasites)
Plasmodium spp (blood and liver parasite) Sporozoite stage: Sporozoites Hepatic stage: Merozoites Blood stage: Ring stage trophozoites

Plasmodium spp Disease: Malaria 200-300 million infections a year
2-3 million deaths a year Affects mostly young people and teenagers 2/3 of the cases are in Africa

Malaria The term “malaria” comes from “mal air”, which means “bad air”. They used to think malaria was caused from the bad air of a foul-smelling swamp. Later it was discovered that the disease was caused by the protozoa inside the mosquito.

Malaria Sporozoites migrate into the salivary gland of the mosquito, and they are injected into the blood of the human. They immediately go to the liver. This is the only way to get malaria; you can’t get it from a blood transfusion because the transmission form is the sporozoite. As soon as they get to the liver, they change into a merozoite and are no longer contagious. They go right to the liver quickly to begin their next cycle.

Terms Sporozoite: formed by sexual reproduction
Trophozoite: motile form of protozoa Cyst: non-motile form of protozoa Merozoite: Special name of the trophozoite form of Plasmodium after it hatches from a schizont. Schizont: sack of Plasmodium organisms formed by sporozoites that have entered the liver. They metamorphasize into merozoites within the schizont (sack), multiply until they rupture the sack and spread. Schizogony: the process of forming a schizont. Gametocyte: some merozoites differentiate into a male or female gamete. These are taken up by the mosquito, and they combine into a zygote (sporozoite) in the mosquito.

Plasmodium The malaria parasite life cycle involves two hosts.
Sporogenic Stage During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host. Hepatic Stage Sporozoites infect liver cells, form schizonts, metamorphasize into merozoites and multiply until the schizont ruptures and releases the merozoites into the bloodstream. Blood Stage Merozoites infect red blood cells The parasites undergo asexual multiplication in the erythrocytes. The ring stage trophozoites form another schizont, which ruptures, releasing merozoites. Some parasites differentiate into male and female gametocytes. Blood stage parasites are responsible for the clinical manifestations of the disease.

Schizont: Hepatic Stage

Blood Phase: Rings

Malaria Merozoites being released from lysed RBC.

Gametocyte: Blood Stage

Malaria Symptoms Fever, chills, sweating, headaches, muscle pains
Severe complications (cerebral malaria, anemia, kidney failure) can result in death.

Plasmodium - Malaria endemic malaria has been eradicated from U.S.
occurs in developing countries current problems with drug resistance by the protozoan and insecticide resistance by vector estimated that 40% of world’s population is at risk of acquiring malaria

Malaria death rates (1900-1997)
Mandell, Figure 275-1

Malaria (the problem) ~3000 children die of malaria/day in Africa
1946 the CDC was founded to combat malaria millions of cases of malaria in the U.S. in 1930s in the U.S. the species of Anopheles that transmitted the parasite preferred to feed on cattle rather than humans disease eradicated in U.S. in the 1950s 2009 report in Emerging Infectious Disease that there are ~3,000 cases of non-endemic malaria in the U.S. each year

Plasmodium – Life Cycle
Mosquito (Anopheles) takes blood meal and injects sporozoites sporozoites travel to liver cell (metamorphosis into trophozoite form, called merozoites) They reproduce in the liver in a sack called a schizont (process is called schizogony) and transform into merozoites. They multiply rapidly until the sack ruptures, releasing the merozoites. merozoites leave liver and enter RBCs (ring stage) merozoites kill RBC and then: infect more RBCs to make more merozoites OR gametocytes gametocytes taken up by mosquito gametes join to form zygote, which develops into a sporozoite sporozoites move to salivary glands

Plasmodium – Life Cycle
once mosquito infected, infected for life mosquito LC ~10 days (depending on temperature) Anopheles bites many times

Plasmodium spp. life cycle.

Plasmodium

Human malaria 4 (major) species that infect humans P. vivax
P. falciparum P. malariae P. ovale Pathology bursting RBCs – release of “toxins” “sticky” RBCs can cause blockage in blood vessels (especially in lungs, kidney, spleen and CNS) Sickle-cell patients resistant to falciparum malaria Glucose-6-phosphate dehydrogenase deficiency patients have milder falciparum symptoms (parasite needs this enzyme)

Malaria paroxysm presents as acute febrile illness often followed by chills and rigors, then fever spikes (up to 40C/104F) and sweating severity depends on species of Plasmodium age of patient (more severe in children under 5) other pathological conditions (superimposed bacterial infections, malnutrition, etc)

Malaria pathology symptoms due to: host response
fever – waste products of RBCs overproduction of cytokines (e.g. TNFa) paroxysm – sudden appearance of symptoms that come and go. chills first, then fever, then back to normal until next attack (symptoms last ~8-12 hours) falciparum has no stage where patient feels good anemia destruction of RBCs; cannot recycle iron fast enough infected cells can stick to un-infected RBCs which are then lysed ↓ RBC production by bone marrow (TNFa ↓ erythropoietin) Cerebral malaria - P. falciparum - ~10% of cases thought to be due to infected RBCs sticking to endothelial cells (including in the CNS) Relapse (Recrudescence) (P. vivax/P. ovale /P. malariae)

Treatment Quinine multi-drug resistance (P. falciparum) vaccination
Synthetic drugs: chloroquine, primaquine, etc multi-drug resistance (P. falciparum) vaccination difficult because infection doesn’t provide effective life-long immunity organisms shed protein coats different antigens during infectious cycle

Anopheles Mosquitoes Female mosquitoes need blood meals to nourish their eggs.

Bacteria-infected mosquitoes may halt malaria
Scientists have infected mosquitoes with a bacteria known as Wolbachia, which sabotages malaria-causing parasites in the bugs, limiting their ability to spread malaria to humans.

Toxoplasma gondii Disease: Toxoplasmosis
Infects most species of warm blooded animals, including humans. Cats are the only known definitive hosts for the sexual stages of T. gondii and thus are the main reservoirs of infection. Cats become infected by eating infected wild animals (e.g. birds) Tissue cysts or oocysts are excreted in the feces. Oocysts can survive in the environment for several months and are remarkably resistant to disinfectants. Pregnant women who clean the litter box can catch the mild disease, but the fetus has severe symptoms.

Toxplasmosis Most primary infections produce no symptoms. The time between exposure to the parasite and symptom development is weeks. The disease can affect the brain, lung, heart, eyes, or liver. Symptoms are mild illness with fever, muscle pain, sore throat, headache, enlarged lymph nodes. This organism prefers nerve tissue, so it travels to the CNS. Pregnant women should avoid cleaning cat litter boxes, because the fetus can develop mental retardation, blindness and epilepsy, and stillbirths.

Toxplasmosis Cyst Cyst in brain tissue

Toxplasmosis Trophozoites

Toxoplasmosis Trophozoites

Toxoplasma Trophozoites sometimes form rosettes

Toxplasmosis Oocyst

Toxplasmosis Ocular toxoplasmosis

Toxplasmosis Cats causing suicide?

Cats causing suicide? Toxoplasma antibodies (proof of exposure to the parasite) are elevated in patients with schizophrenia. There is also an increased rate of suicide attempts in those with the infection. A Dutch study looked at 45,000 pregnant women and found that 27% had antibodies to toxoplasma. In those 27%, self-destructive violence was more common by about 50%. And the higher the antibodies to toxoplasm (presumably showing a more significant exposure), the greater the risk. Those with the highest level of antibodies were at almost 100 percent higher risk for self-harm.

Cats causing suicide? The actual completed suicide rate was over twice as high in women who had been exposed to toxoplasma compared to those who had not. One reason toxoplasma could trigger severe psychiatric symptoms—including suicides—is that it causes inflammation in the central nervous system, raising the levels of inflammatory compounds like interleukin-6. Those inflammatory compounds may be neurotoxic.

Cryptosporidium parvum
Disease: Cryptosporidiosis Spread through the fecal-oral route, often through contaminated water Causes self-limiting diarrhea in people with intact immune systems. In immunocompromised individuals (such as AIDS patients), symptoms are severe and often fatal. AIDS patients have been known to have 50 stools a day, with tremendous water and weight loss. In these patients, the disease may persist for years.

Cryptosporidium

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