Parasitology II: Protozoa

Question 1

Characteristics of protozoa:

Answer 1

Single-celled eukaryotic organisms.
All protozoa that cause disease must multiply in humans.
Eosinophilia is not a usual sign of protozoal infection.

Question 2

*Entamoeba histolytica (amebiasis) life cycle:

Answer 2

Life cycle involves only humans.
Humans ingest cysts (human fecal contamination or sexual intercourse).
Cysts open in the intestine, progeny parasites multiply as TROPHOZOITES (actively multiplying stage of parasitic infection) in the large intestine.
As the bowel contents lose water and become formed stools, the trophozoite changes to a cyst. Cysts are resistant to most environmental conditions.

Question 3

*Entamoeba histolytica (amebiasis) diagnostic stage:

Answer 3

Cysts in formed stools or trophozoite in diarrhea. A monoclonal antibody is usually used for diagnosis now.

Question 4

*Entamoeba histolytica (amebiasis) signs and symptoms:

Answer 4

May be symptomatic or asymptomatic. Symptomatic disease involves invasive disease of the colonic mucosa with pain and dysentery (blood and mucous stools). ULCERATED lesion is visible endoscopically.
Lesions are “flank shaped ulcers” histologically.
May cause amoebic abscesses in the liver, and rarely brain or lung.

Question 5

*Entamoeba histolytica (amebiasis) treatment:

Answer 5

Metronidazole

Question 6

*Amebic meningoencephalitis (naegleria) pathogenesis:

Answer 6

Caused by swimming in stagnant warm water. Amoebae reach the brain via the cribriform plate.

Question 7

Giardia (giardiasis) life cycle:

Answer 7

Cysts are ingested from fecal contamination.
Cysts open in the small intestine, releasing trophozoites into the duodenum and jejunum. As the stool mass is dehydrated, trophozoites are encysted and are excreted in the feces.

Question 8

Giardia (giardiasis) diagnostic stage:

Answer 8

Cysts in formed stools or trophozoites in diarrhea. Can be visualized by microscopy or fluorescent antibody detection.

Question 9

Giardia (giardiasis) signs and symptoms:

Answer 9

Acute infection involves diarrhea, foul-smelling greasy stools, abdominal discomfort, and nausea. More common in individuals with IgA deficiency. PARASITE DOES NOT SPREAD FROM THE GI TRACT, unlike entamoeba.
Chlorination does not kill the organism, but filtration removes it from water.

Question 10

Giardia treatment:

Answer 10

Metronidazole

Question 11

Trichomonas vaginalis life cycle:

Answer 11

Trophozoites exist in the female vagina and male urethra, prostate. Transmitted by sexual contact or poor hygiene. THERE IS NO CYST STAGE. Increases risk of HIV infection, due to inflammatory process.

Question 12

Trichomonas vaginalis diagnostic stage:

Answer 12

Motile trophozoite in vaginal secretions and in urine. Also, pap stain, rapid EIA, MOLECULAR ASSAYS (most sensitive).

Question 13

Trichomonas vaginalis treatment:

Answer 13

Metronidazole. Must involve PARTNERS too.

Question 14

Toxoplasma gondii life cycle:

Answer 14

Humans are ACCIDENTAL, intermediate hosts.
The cat is the definitive host, which release Toxoplasma cysts in their stool.
At ambient temperature, the cysts become infectious in about 2 days.
A non-feline animal ingests infectious cysts, and survives acute infection to have tissue cysts that infest the brain and muscles (a different kind of cyst than the one that is excreted from cat feces).
Humans are infected by:
1) ingesting undercooked meat that contains tissue cysts.
2) feline fecal contamination (i.e., cleaning a litterbox).

Question 15

Toxoplasma gondii diagnosis:

Answer 15

Serological. Anti-toxoplasma IgG (establishes infection at some point in life) and IgM (establishes recent infection) or PCR of toxoplasma DNA.

Question 16

Toxoplasma gondii treatment:

Answer 16

Pyrimethamine (blocks DHFR) and sulfadiazine (blocks dihydrofolate synthesis).

Question 17

Toxoplasma gondii signs and symptoms:

Answer 17

Most patients are asymptomatic.
Some primary infections present with lymphadenitis, myalgia, headache, fatigue, fever, ENCEPHALITIS, MYOCARDITIS. May develop retinitis.
Toxoplasmic encephalitis is common in HIV patients (CD4 < 100): headache, confusion. Diagnosis and treatment is with pyrimethamine-sulfadiazine.
Transplacental toxoplasmosis: microcephaly, hydrocephalus, intracerebral calcifications, mental retardation, blindness.

Question 18

Cryptosporidium pathogenesis:

Answer 18

Intracellular parasites that protrude from plasma membranes of intestinal epithelial cells. Infectious cysts are excreted in the feces of humans and animals (fecal-oral transmission).
Results in a self-limited diarrhea in normal patients, and a severe diarrhea in AIDS patients. Unlike toxoplasma, there is no chronic infectious stage.

Question 19

Cryptosporidium diagnosis:

Answer 19

Acid-fast cysts in feces. Also, immunofluorescent detection.

Question 20

Characteristics of “…spor…” organisms (cryptosporidium, cyclospora, isospora, microsporidia):

Answer 20

Obligate intracellular parasites.
Produce mild-to-moderate diarrhea in patients with normal immunity, and severe diarrhea in patients with AIDS.
Transmitted via fecal-oral pathway.
Resistant to chlorination at the concentration used for municipal water supplies.

Question 21

Malaria life cycle:

Answer 21

Human is intermediate host, Anopheles mosquito is definitive host.
The mosquito injects SPOROZOITES into humans.
Sporozoites enter the liver and divide to form MEROZOITES. This is asymptomatic.
Merozoites enter the circulation and infect red cells.
The merozoites first enter a “ring stage,” and then grow (cytoplasmic synthesis) and divide (nuclear replication).
The merozoites are release from lysing RBCs, and infect more cells.
Some merozoites become GAMETOCYTES, which are taken up by mosquitos.
Male and female gametocytes fuse, and eventually become sporozoites.
May be transmitted via BLOOD TRANSFUSIONS or TRANS-PLACENTALLY.

Question 22

Species of human malaria:

Answer 22

Plasmodium falciparum (most virulent)
P. vivax
P. ovale
P. malariae

Question 23

P. falciparum malaria signs and symptoms:

Answer 23

Very serious. Incubation period is 2 weeks. Infects red cells of all ages. Fever spikes occur every 48 hours. P. falciparum stimulates RBCs to adhere to vascular endothelium, which can lead to infarcts and CEREBRAL MALARIA. Infarcts of the GI tract and kidney are not uncommon.

Question 24

P. falciparum diagnosis:

Answer 24

Histologically, some cells have multiple ring forms.

GAMETOCYTES ARE BANANA-SHAPED. Other stages are not visualized, as these cells are adhered to the vascular endothelium.

Question 25

P. vivax malaria signs and symptoms:

Answer 25

Fever spikes seen every 48 hours. RETICULOCYTES are preferentially infected (thus lower parasitemia than P. falciparum). Initial symptoms may be delayed for several months due to HYPNOZOITE. Because of this, P. vivax can survive in temperate zones.

Question 26

P. vivax diagnosis:

Answer 26

On blood smear, one can observe:

1) large-size infected RBCs
2) all stages are observed
3) SCHUFFNER’S DOTS are prominent in some late stage infected cells.

Question 27

P. malariae signs and symptoms:

Answer 27

Incubation 5 weeks. Fever spikes seen every 72 HOURS. Parasitemia is low, as OLDER RED CELLS are preferentially infected.
Relapse is common, probably due to a low-level continuous infection.

Question 28

P. malariae diagnosis:

Answer 28

On blood smear, one can observe:

1) smaller, older infected RBCs
2) all stages are observed
3) BAND FORMS are visible
4) yellow-brown malarial pigment is visible

Question 29

Malaria treatment:

Answer 29

CHLOROQUINE, atovaquone-proguanil, mefloquine.

PRIMAQUINE is used to eradicate the hypnozoite form of P. vivax and P. ovale.

Question 30

Babesia microti life cycle:

Answer 30

Transmitted by the same tick that causes Lyme disease. Tick houses the sexual stage.
Infectious stage penetrates RBCs and multiplies (forming TETRADs).
RBCs release merozoites, which infect more RBCs.
Merozoites can also be taken up by mosquitos.
This disease can be problematic in asplenic patients.

Question 31

Babesia microti diagnosis and treatment:

Answer 31

Diagnosis is by visualization of trophozoites (“tetrads”) in red cells. Most infections are subclinical, but may present with hemolytic anemia, fever, and chills.
Treatment is atovaquone plus azithromycin OR clindamycin plus quinine.

Question 32

*Hemoflagellate characteristics:

Answer 32

All are found in blood at some stage of the life cycle, have flagella, and have an insect host in their life cycle.
Some species also have an intracellular AMASTIGOTE stage.

Question 33

*African trypanosomiasis life cycle:

Answer 33

An infected tsetse fly bites a human and transmits the trypanosome via saliva.
In humans, typanosomes multiply in the blood, lymph, and CSF.
An uninfected tsetse fly bites a human with parasitemia, and the trypanosome begins to multiply in the gut of the fly.

Question 34

*African trypanosomiasis diagnosis:

Answer 34

Visualization of flagellated form in blood, lymph node, or CSF.

Question 35

*African trypanosomiasis signs and symptoms:

Answer 35

A local, ulcerated lesion appears at the bite site a few days after infection.
Two weeks after infection: parasitemia, fever, lymphadenopathy (WINTERBOTTOM’S SIGN = posterior cervical node enlargement). Invasion of the CNS results in lethargy, coma, and death.
Immunity is almost impossible to achieve, due to changing antigen presentation by the parasite.

Question 36

*Leishmaniasis life cycle:

Answer 36

Sandflies regurgitate extracellular flagellated forms at the site of a bite.
This flagellated form enters mononuclear phagocytes, loses its flagellum, and multiplies as an INTRACELLULAR AMASTIGOTE.
Amastigotes are released by host cell lysis, and infect more cells.
An uninfected sandfly ingests macrophages that are infected, which release organisms that become flagellated.

Question 37

*Leishmaniasis diagnosis:

Answer 37

Intracellular amastigote is diagnostic stage.

A type IV hypersensitivity reaction may develop (Montenegro test).

Question 38

*Visceral leishmaniasis signs and symptoms:

Answer 38

Insidious onset with fever (twice daily), enlarged spleen and lymph nodes, and hypergammaglobulinemia. FATAL IF UNTREATED. Diagnosis is by marrow biopsy.

Question 39

*Visceral leishmaniasis treatment:

Answer 39

Antimony containing drugs. AMPHOTERICIN B is best current treatment.

Question 40

*Cutaneous leishmaniasis signs and symptoms:

Answer 40

Papule at bite site enlarges and becomes an ulcer that lasts 6 months to several years. Results in scar formation.
May progress to mucocutaneous leishmaniasis, and produce progressive, massive necrotizing lesions that the junction of the nose and mouth.

Question 41

*Chagas’ disease (Trypanosoma cruzii) life cycle:

Answer 41

Infected reduviid bug takes a blood meal and defecates. The feces contains the extracellular flagellated form which enter the body and invade macrophages, skeletal muscle, and cardiac muscle, where they multiply intracellularly as AMASTIGOTES. An uninfected reduviid bug ingests extracellular flagellated forms with a blood meal.

Question 42

*Chagas’ disease signs and symptoms:

Answer 42

Painful swollen lesion near eye at the site of the bite (Romana’s sign). Some people may die during acute infection due to heart failure or meningitis.
Chronic Chagas’ disease results in cardiac enlargement and CHF, destruction of autonomic ganglia in the GI tract (leading to mega-colon and mega-esophagus). Transplacental infection is possible.

Question 43

Trichomonas vaginalis signs and symptoms:

Answer 43

Vaginitis with frothy purulent discharge. Urethritis, prostatitis, low birth weight, infertility. Most are asymptomatic.