Introduction to Parasitology Flashcards

1
Q

Protozoans

A

Single cell microorganisms; microscopic; the size of a yeast

  • Four groups: rhizopods, ciliates, flagellates and sporozoans
  • Most protozoans are free living; those causing disease are obligate parasites with hosts being vertebrates and arthropods
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2
Q

Helminths

A

Macroscopic; millimeter to longer than a meter; multicellular worms

  • Round worms: dimorphic sexes; found in digestive tract of humans
  • Cestodes: flat, ribbons of proglottids (both sexes and no digestive tract)
  • Flukes: flattened parasites; some in the blood, others in the biliary tree
  • Filarial worms: reside in the lymph system and circulate in the blood
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3
Q

Strategies of a Successful Parasite

A
  • Chronicity
  • Means of transmission to a new host
  • Immune evasion
  • Environmental resistance (e.g. cyst)
  • Human, animal or environmental reservoir
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4
Q

Ectoparasites

A
  • Parasites living on the outside of the host
  • May be vectors of infectious diseases and include:
  • Lice
  • Mites
  • Ticks
  • Fly larvae
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5
Q

Diagnosis of Parasitic Diseases

A
  • Collection of fecal specimens; 3 specimens are optimal; recheck 5-6 weeks after treatment of Taenia.
  • Fresh observation and preservative.
  • Direct observation of stool for trophozoites.
  • Urine test for Schistosoma hematobium.
  • Sputum for: Paragonimus, Strongyloides
  • Blood smear for Babesia, Plasmodium, Chagas
  • PCR (Biofire 20): available as a combo test for multiple protozoans and helminths in Biofire 20
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6
Q

Drugs for Protozoan Infection: Antimalarial Quinolines

A
  • Three major classes analogs of quinine; chloroquine, primaquine and mefloquine.
  • Mechanism: Destroy intracellular parasites by accumulating in parasitized host cells. Inhibit heme polymerase that allows buildup of toxic hemoglobin metabolites within the parasite.
  • Chloroquine and mefloquine: active in erythrocytes
  • Primaquine: Accumulates in tissue cells and destroys hepatic parasites
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7
Q

Drugs for Protozoan Infection: Quinones

A
  • Atovaquone works against malaria and toxoplasmosis by blocking pyrimidine biosynthesis.
  • Effective in patients with chloroquine-resistant P. falciparum malaria.
  • Coformulate “Malarone” is used for malaria prophylaxis. Not active against malarial liver infection.
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8
Q

Drugs for Protozoan Infection: Artemisinin

A
  • Natural extract of the plant Artemisia annua was used for fevers in China.
  • Active against both chloroquinesensitive/resistant Plasmodium falciparum.
  • These compounds concentrate in parasitized erythrocytes, decompose and release free radicals that damage parasitic membranes.
  • They act more rapidly than other malarial drugs.
  • They should not be used in pregnancy because of their tetratogenic properties.
  • Relapses occur so they have to be combined with another malarial drug.
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9
Q

Drugs for Protozoan Infection: Nitroimidazoles

A
  • Metronidazole (nitroimidazole) is effective against trichomoniasis, giardiasis, amebiasis and several obligate anaerobic bacteria.
  • These agents cause DNA alkylation.
  • A newer agent in this group is Tindazole.
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10
Q

Drugs for Helminths: Benzimidazoles

A

•for larval and adult nematodes, inhibits fumarate reductase (a mitochondrial enzyme of the helminths)

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11
Q

Drugs for Helminths: Avermectins

A

•paralysis of worms

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12
Q

Drugs for Helminths: Praziquantil

A

•cestodes and trematodes

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13
Q

Toxoplasma gondii

A
  • Toxoplasma gondii – Sporozoan (Protozoa)
  • Definitive hosts are felines, sexual stage of reproduction
  • Thick walled oocysts are passed in cat feces, mature and are swallowed
  • Oocyst wall is digested releasing trophozoites
  • Enter macrophage, trafficked through the lymphohematogenous route and infect: brain, heart, retina and skeletal muscle turning into pseudocysts
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14
Q

How is Toxoplasmosis Acquired?

A
  • Human is an incidental host
  • Common worldwide, prefers moist climate, rare in desert regions of Arizona
  • Transmitted to humans from:
  • Contaminated soil (78 million cats in US in houses)
  • Cat feces
  • Eating infected meat (pork or lamb)
  • Vertical (congenital toxoplasmosis - part of TORCHS)
  • Waterborne
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15
Q

Toxoplasma: Pathogenesis

A
  • Invade host cells with local and hematogenous spread, all nucleated cells are susceptible
  • Tissue necrosis, infiltration of mononuclear cells
  • Phagocytosed by macrophages (phagosome-lysosome fusion) is blocked by trophozoites, preventing acidification and killing,
  • Killing of T. gondii by macrophages is enhanced by IFN-γ
  • Development of effective cell-mediated immunity, TH1 response  Tissue cysts formation, numerous trophozoites with markedly decreased their metabolic activity to become bradyzoites
  • They are walled off by the host into a collection called a pseudocyst (a true cyst would be walled by parasite-produced material). This becomes a latent infection, but may be reactivate in the event of immunosuppression.
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16
Q

Immunity in Toxoplasmosis

A
  • Humoral immunity
  • Cell immunity is paramount
  • Transplant patients
  • AIDS Patient
17
Q

Clinical Diseases of Toxoplasmosis

A
  • Congenital infection: 1/500 pregnancies; 20% of infected fetuses with severe disease resulting in microcephaly, hydrocephalus, abortion, stillborn; usually with organomegaly; calcified brain lesions; chorioretinitis
  • Infection in a normal host: lymphadenopathy (cervical) or generalized and presenting as “mononucleosis” syndrome
  • Infection in the immunocompromised host: declining cell immunity: pneumonitis, myocarditis, serositis, encephalitis; common in AIDS patients (brain)
18
Q

Toxoplasmosis Diagnosis

A

•Biopsy, serology, PCR

19
Q

Toxoplasmosis Treatment

A

•Sulfa plus pyrimethamine for AIDS and immunocompromised patients

20
Q

Cryptosporidium partum

Cryptosporidium hominis

A
  • Two species Cryptosporidium partum and C. hominis, sporozoa (Protozoa)
  • Found in cattle and humans, 2-6 micron in size
  • Obligate intracellular parasite (epicellular: looks like a yeast)
  • Acid-fast oocyst membrane
  • In Milwaukee (1994), 400,000 people were infected
  • Recent outbreak in England; water contaminated by rabbit species
21
Q

Cryptosporidium Infection: The Pathogen

A
  • Oocysts are fully mature when shed from feces
  • When swallowed attach to the small intestinal villi
  • Form schizonts, then gametocytes and then oocyst
  • ~20% of the oocysts lack the thick protective wall and immediately begin a cycle of autoinfection
22
Q

Cryptosporidium Pathogenesis and Immunity

A
  • Fecal oral spread (water, probably food)
  • Day care centers and parents of children with acute disease
  • Common in AIDS patients with diarrhea (<50 CD4 cells/mL)
  • Replicates in an intracellular, but extra-cytoplasmic location, which may be part of the reason why drug treatment works so poorly.
  • Superficial patchy infection of small intestine with mild histologic changes is found.
  • The mechanism by which Cryptosporidium causes diarrhea is unknown.
  • Animal studies in addition to the common occurrence in AIDS patients indicate that the cell-mediated immune response is of primary importance in preventing and controlling infection
23
Q

Clinical Disease: Cryptosporidiosis

A
  • Most common cause of diarrhea in AIDS patient
  • Rarely it can disseminate beyond the intestine, primarily to the gall bladder
  • Villous atrophy, lymphocytic infiltrate in lamina propria
  • In normal hosts, the incubation period is 2-14 days and illness typically lasts about 2-7 days, and then resolves without complication
  • Frequent, watery stools—enterotoxin?
  • Some people develop chronic diarrheal illness with frequent , foul smelling, bulky stools associated with significant weight loss
24
Q

Foodborne Cryptosporidiosis

A
  • 8% of cases (most waterborne; remain viable in ice for days); 7 day incubation period
  • Minimum inoculum of 10-100 oocysts (as many as 30 billion oocysts are shed by a calf in 2 weeks)
  • Remain viable on fruits and vegetables usually spread by contaminated irrigation water or water used to spray insecticides
25
Q

Cryptosporidiosis Diagnosis

A
  • Biofire 20 (a PCR) test
  • Acid-Fast Stain
26
Q

Cryptosporidiosis Treatment

A
  • No treatment for immunocompetent host
  • Restore the CD4 cell count in AIDS
  • Nitazoxanide is the only therapy (not effective in immunocompromised patients)
  • Paromomycin (aminoglycoside)
27
Q

Cyclospora cayetanensis

A
  • Apicomplexa (Sporozoa)
  • Life cycle like Cryptosporidium
  • Gastroenteritis syndrome—watery diarrhea
  • Occurs in US due to imported berries, usually from Guatamala
  • Also cause of traveler’s diarrhea
  • Trimethoprim-sulfamethoxazole treatment
28
Q

Cyclospora cayetanensis Clinical Picture

A
  • Symptoms: Watery diarrhea (most common)
  • Loss of appetite/weight loss
  • Cramping/Bloating/Gas
  • Nausea/Fatigue
  • If not treated, symptoms can persist for several weeks to a month or more.
29
Q

Cyclospora cayetanensis Diagnosis

A
  • Acid-fast
  • Biofire 20 (PCR), fluorescent under UV light
30
Q

Cystisopora (Isospora) belli

A
  • Humans are the only known reservoir of Cystisospora
  • Can be serious cause of diarrhea in infants because of dehydration
  • PCR of stool, Biofire 20 detect disease.
  • Otherwise a short 2-3 days of diarrhea
  • Found throughout Africa, Latin America and Asia
  • Treated with trimethoprim-sulfamethoxazole and prevented by Pneumocystis jiroveci pneumonia prophylaxis