Parasitic Protozoa Slackers Facts by Mike Ori Disclaimer

Parasitic Protozoa Slackers Facts by Mike Ori

Disclaimer The information represents my understanding only so errors and omissions are probably rampant. It has not been vetted or reviewed by faculty. The source is our class notes. The document can mostly be used forward and backward. I tried to mark questionable stuff with (? ). If you want it to look pretty, steal some crayons and go to town. Finally… If you’re a gunner, buck up and do your own work.

What are three related sporozoans?

Toxoplasmosis Cryptosporidium Plasmodia

What is the definitive host for toxoplasmosis?

What are the routes of acquisition for toxoplasmosis?

1. Ingestion of undercooked meat especially lamb and pork (vive la France) 2. Cat feces 3. Vertical

Explain when toxo is a concern during transplant

When a seropositive donor heart is transplanted into a seronegative recipient

What results from post transplant infection

Myocarditis

What sx would you expect to see in aids pt

Ring enhancing lesions in the brain

Since toxo increases in aids pt, what type of immunity is likely to play a role in toxo control?

Cell mediated immunity

What is the source of toxo in aids pt

Usually reactivated encysted (bradyzoites) organisms

What is a common source of diarrhea in PT with low CD 4+ counts?

Cryptosporidium

Describe the disease course in immunocompetent and immunocompromised pt

Competent: incubation < 2 weeks with 1 week sx. Immunocompromised: long term diarrhea

What is the treatment for cryptosporidium in immunocompromised pt

Raise the CD 4 count.

What organism could cryptosporidium be mistaken for in “regular stains”?

Candida

How do you differentiate cryptosporidium from candida

Crypto is acid fast, Candida is not

Why is crypto hard to treat

The organisms invades the ciliated surface and sits in an intracellular but extracytoplasmic location. This limits access to antimicrobial agents.

Describe Girardia morphology

Flagellated pear shaped organisms with two nuclei and a concave sucking disk

Describe Giardia epidemiology

Outdoorsy people that drink from streams without properly treating the water.

What are girardia’s sx?

Most are asymptomatic. Those that have sx experience loose foul smelling stools, abdominal ramps, bloating, weight loss.

Explain how Girardia attaches to the host

It uses its ventral sucking disk for attachment.

How many nuclei does the encysted Giarardia have

Quattro

Which test is more sensitive, O and P or fluorescent antibodies, or ELISA

O and P is not very sensitive especially if the small intestine is colonized. O and P is repeated three. Three tests are typically done. FA and ELISA are much more sensitive and usually yield results in one test.

What is the string test?

PT’s with small intestinal disease swallow the end of a string overnight in an effort to trap organisms in the string for detection.

What is metabolically unique about anaerobic protozoans?

They do not synthesize nucleotides

Name three anaerobic protozoans

Girardia, Entamoeba, Trichomonas

Describe the SX with Entamoeba infection

Bloody diarrhea

When is Entamoeba infection not a clinical problem

Entamoeba dispar is a frequent colonizer but is not known to cause disease. E. histolytica is only a problem if its invasive.

What is the evidence for invasion with E. histolytica?

RBC’s ingestion

How are E. dispar and E. histolytica differentiated?

By PCR

What colon morphology is indicative of amoebiasis

Inverted flask shaped ulcers.

What is the reservoir for Entamoeba

E. Histolytica = human

What other organs are involved with Entamoeba and what are the findings

Liver can be involved with anchovy paste filled cysts. Organisms will be on the periphery of the cyst.

Describe the sx for trichomonas vaginalis in men and women

Men are usually asymptomatic Women will usually have a foul smelling green discharge

How is Trichmonas vaginalis transmitted?

By sexual contact

Women

How is enamoeba transmitted?

Food > water

How is Girardia transmitted?

Water > food

What is the reservoir for Girardia in the wild

Reservoir = beaver = reservoir builder

What disease does plasmodium cause

Malaria

Name the plasmodium species

P. vivax P. ovale P. malariae P. falciparum

Which species is associated with the most deaths?

P. falciparum

What is the route of transmission for Plasmodium

Anopheles

What is the definitive host for malaria

Mosquitoes

What is injected into humans by said mosquito?

A malaria sporozoite

Where do the sporozoites go

The liver

What is a schizont

The replicating malarial mass in a hepatocyte or RBC

What is a malaria trophozoite?

Something less than a schizont but more than a merizoite.

Why does malaria fever come in 2 -3 day intervals?

The release of the merizoites from RBC’s is fairly well coordinated and occurs in a large burst. This exposes the organism to the immune system and causes a fever. The merizoites then go on to infect more RBC’s thus causing a cycle.

When might the fever cycle degenerate?

P. falciparum tends to degenerate. Multiple infection cycles also tend to degenerate

What are the unique histological features of P. falciparum?

Schizont forms tend to lodge in the microvasculature and so are not seen on routing blood smears. In addition, more ring forms and double infected RBC’s are seen in P. falciparum

What is sequestration

The action of retaining shizonts in the microvasculature. This prevents removal by the spleen.

What is unique about the life cycle of P. vivax and P. ovale?

They can have latent hepatic stages that can release merizoits months to years later. This is in contrast to P. falciparum and P. malariae which release all their merizoites from the liver in a single go.

Which blood cells does P. vivax invade?

It only invades reticulocytes.

What is the role of receptors in malarial disease

Merizoites interact with species specific receptors on the RBC surface. For instance P. vivax required Duffy and reticulocyte receptor

Where are receptors located on merizoites

In a special organelle called the rhoptry

Explain the high incidence of sickle cell trait and the low incidence of Duffy in west Africa

Sickle cell trait is protective for severe malaria. Absence of Duffy prevents P. vivax invasion of reticulocytes. Note there are other examples in the notes.

Explain the belief that the immune response to malaria is incomplete

Mortality is highest in naïve pt (children mostly in endemic areas). Adults can carry a high parasitemia with little sx and thus seem to be protected from severe disease.

What are the run of the mill sx for malaria

High fever (40 -41 c) Chills Headache

What is the typical causative species for severe malaria?

P falciparum

What are the sx of severe malaria

Cerebral malaria – seizures and coma due to cerebral sequestration Severe anemia (Hgb < 5) – falciparum can have very high infectivity General illness – prostration, hypoglycemia, lactic acidosis, ARDS

What is chronic malaria

Continuous parasitemia in contrast to recurring parasitemia

What is the causitive agent for chronic malaria

P. falciparum and P. vivax

What are the methods to prevent malaria

Repellents Mosquito netting Clothing Prophylactic pharmacology

List the malaria time course

Prepatent (hepatic) phase – 2 weeks Red cell phase – 2 -3 days

What is the vector for leishmania

Sand flies

What is an amastigote and a promastigote?

A mastigote = amotile (I. e. no flagella) Promastigote = pretty good swimmer (flagellated)

What cell is invaded by promastigotes

Macrophages

What is the result for the macrophage?

Eventual lysis of the cell due to replication

What are three types of leishmaniasis?

Cutaneous Mucocutaneous Visceral Diffuse cutaneous

Describe cutaneous leishmaniasis

Ulcerative lesions that eventually heal with no sequelae

Describe mucocutaneous leishmaniasis

Cutaneous lesions heal but later destruction of nasal and mucosal tissue occurs

Describe visceral leishmaniasis

Invasion of the liver and other visceral leading to death

Describe diffuse cutaneous leishmaniasis

Treatment resistant non-ulcerative lesions disseminated over the skin surface. Very tx resistant.

Describe the African Trypanosoma brucei species ranges

Roughly divided into east and west african

What is the vector from Trypanosoma brucei

The tsetse fly

Describe the hosts for both species

West = human East = big game animals with humans as incidental

What are the stages of african trypanosomal disease

1. Bite/chancre 2. Hemolymphatic – Lymphadenopathy with relapsing fever 3. Meningoencephalitis – somnolence, coma, death

Why does the immune system fail to clear trypanosomes

The organisms express variant surface glycoproteins that cause antigenic variation

Describe the progression of T. b rhodesiense and T. b. ghambiense

Tbr is east african and is much more acute. Death occurs in months. Tbg is west african and is less acute. Death occurs on years

How is tx complicated with CNS diease

Tx of CNS disease relies on arsenic containing compounds which are toxic to the host.

What is the vector for Trypanosoma cruzi

The reduviid bug

How is T. cruzi spread?

The reduviid bug bites a victim causing a pruritis. The bug also deposits trypanosome laden feces near the bite. The host then scratches the bite, mechanically introducing the organism. The organism can also pass directly across mucosal surfaces.

What is unique about the epithelial invasion of T. cruzi

It invades epithelial cells at point of cell to cell junction.

What are the sx of chagas disease

Nerve destruction Muscle inflammation and hypertrophy Leading to dilated cardiomyopathy, arrhythmia, and GI tract dilation and esophageal impairment (dysphagia, odynophagia)