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Y1 - Microbio Exam 3 > 3_Protozoa 3 Sporoza > Flashcards

3_Protozoa 3 Sporoza Flashcards

1
Q

life cycle of:

Cryptosporidium parvum

A

2 means of reproduction

  • Asexual
  • Sexual
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2
Q

Asexual reproduction:

in lifecycle of Cyrptosporidium parvum

A
  1. After oocysts are ingested, they released sporozoites
  2. Sporozoites attach to epithelial cells
  3. Transform into trophozoites
    • Trophozoites divide asexually
  4. But they don’t divide by binary fission. They multiply by schizony, which gives what we call merozoites
  5. Schizonts rupture and release the merozoites
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3
Q

SEXUAL reproduction:

in lifecycle of Cyrptosporidium parvum

A
  • Merozoites differentiate into (g, h) micro and macro (male & female) gametocytes
  • Fuse to form zygote and oocysts with sporolated (4 sporozoites) that are released from surface of epithelial cell and (i) passed out in feces and very contagious
  • Some can also release sporozoites in side the intestine of the same host (auto-infection)
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4
Q

transmission of:

Cryptospordiosis parvum

A
  • fecal-oral transmission
  • accidental ingestion of oocysts w/ contaminated water, or by contact w/ infected soil, or crypto-contaminated objects
  • very contagious; can exist even in chlorinated water
  • ETC
    • host: human, sheep, cattle, birds, rodents, primates
    • swallowing the parasite picked up from surfaces such as toys, bathroom fixtures, changing tables, or diaper pails that are infected by stool of infected person
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5
Q

Which patients are susceptabile to:

Cryptospordiosis parvum

A
  • immunocompromised populations
    • malnutrition in poor countries
    • AIDS
    • congenital immunodeficiency (hypoglobulinemia)
    • cancer, organ transplant
    • persistent unless immunological defect is reversed
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6
Q

pathogenesis of:

Crytospordiosis parvum

A
  • Blunting of villi, mild villous atrophy
  • Crypt enlargement, hyperplasia of intestinal crypt cells
  • Infiltration of inflammatory cells into the luminal propria
  • Toxin results in abdominal cramps & severe diarrhea
  • Biliary cryptosporidiosis, inflammation in gall bladder
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7
Q

diagnosis of:

Crytospordiosis parvum

A
  • Identification of oocysts in stool
  • ACID-fast stain
  • Immunofluorescence
  • ELISA for antibodies
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8
Q

prevention for:

Cryptospordiosis parvum

A
  • Hand hygiene,
  • Food safety,
  • Proper diaper changing practices
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9
Q

Life cycle:

Plasmodium species causing malaria

A

2 hosts

  • Sexual reproduction (w/in mosquitoes)
  • Asexual reproduction in liver & RBCs of Humans
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10
Q

describe the INSECT STAGE

in malaria

A

Anopheles species

  1. (1) Feed at dusk or dawn or nocturnal (active at night) feed indoors (endophagic)
  2. A female mosquito probes for a blood meal
  3. Females require a blood meal for the development of eggs
  4. Deposit sporozoites into the avascular tissue of the skin from the salivary glands.
  5. Within one minute, the sporozoites become highly motile, traverse the capillary wall and enter the blood stream.
  6. (2) Migrating to the liver via the bloodstream
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11
Q

Liver stage/ Asexual stage

in Malaria

A

Occurs in Vertebrates

  1. (2) Sporozoites invade hepatocytes
  2. Asexual reproduction occurs
  3. (3) In parasitophorous vacuole (PV) forms the sporozoites undergo asexual reproduction by schizony, repeatedly replicating its nucleus and other organelles
  4. (4) Release thousands of merozoites
  5. The liver-stage of the life cycle is not associated with notable disease in malaria. It allows the parasite to multiply
  6. (5) Once merozoites burst from hepatocytes, they invade red blood cells (RBC)
  7. Enter using surface proteins called merozoite surface protein (MSP)-1 by attachment onto RBC surface molecules, e.g., Duffy antigenMerozoites transform to trophozoites that multiply in RBC Parasites replicate using the amino acids obtained from digesting haemoglobin. Parasite remodels the surface of the RBC and renders them more permeable
  8. (6) The trophozopoites matures and become encased by a PV membrane and form schizonts
  9. (6) Infected RBCs burst releasing merozoites which then invade fresh RBCs to begin a new erythrocytic cycle
  10. (7) Some parasite in infected RBC that goes through differentiate into transmissible male and female gametocytes
  11. This stage is associated with most of the pathologyn
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12
Q

describe the Sexual Reproduction w/in the Anopheles mosquito

(causing Malaria)

A
  • Gametocytes ingested with blood meal develop into male and female reproductive cells (gametes) in the mosquitoes’ gut
  • They fuse to form a zygote
  • The zygote in turn develops into a mobile ookinete, which crosses the wall of the gut and forms a sporozoite-filled oocyst
  • When the oocyst bursts, the sporozoites move to the mosquito’s salivary glands, ready for introduction into the next host
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13
Q

what characterizes uncomplicated malaria?

A
  • shaking chills
  • high fever
  • profuse sweating as body temp falls
  • headache, dry cough, enlarged spleen
  • nausea, vomiting, back pain, muscle fatigue
  • cyclic pattern
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14
Q

cyclic fever:

what generates it?

sxs?

A
  • generated by innate immune response to the RBC cycle; interaction of acute phase response cytokines, such as TNF, w/ the hypothalamus in the brain
  • Sxs: chills and sweats
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15
Q

what characterizes:

severe malaria?

A
  • Severe malarial anaemia (SMA) – Often associated with chronic and repeated infections of malaria due to hemolysis (destruction of the red blood) Hemoglobin in the urine “Black water fever”
  • Metabolic acidosis - Heavy infection (5% of RBC), lysis may cause excessive acidity in the blood and tissue fluids, pH of the blood lowers in association
  • Acute respiratory distress syndrome (ARDS) -Inflammation and accumulation of fluid - inhibits oxygen exchange. Difficult to breathe.
  • Organ failure- Low blood pressure can cause kidneys or liver failure, cardiovascular collapse or spleen to rupture
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16
Q

in which patients do severe life-threatening malaria occur in?

A

mostly in children under 5 years

17
Q

cerebral malaria:

pathogenesis;

symptoms

A
  • Path:
    • infected RBCs autoagglutinate, forming rosettes that accumulate and obstruct microvasculature in the brain
      • Inflammation leads to immune-mediated destruction
        • (infiltration of lymphocytes and NK cells, Release of inflammatory molecules such as TNF, chemokines, expression of adhesion molecules , release of perforin from CD8+ T cells)
      • Contributes to disruption of the blood-brain barrier
  • Sxs: Swelling of the brain or brain damage may occur resulting in impaired consciousness, seizures, coma
18
Q

most advanced malaria vaccine, and how does it work?

A
  • GlaxoSmithKline - RTS,S malaria vaccine
  • Virus-like particles with fusion protein that includes region (R) of the circumsporozoite protein, which contains several T cell epitopes (T), fused to the hepatitis B surface antigen (HBsAg) (S)
  • Prevent the parasite from infecting, maturing and multiplying in the liver, which would allow the parasite to re-enter the bloodstream and infect red blood cells, leading to disease symptoms
  • Protected small babies for as long as 18 months, getting them through the most vulnerable time
  • Tests on more than 15,000 babies aged 6 weeks to 17 months old showed close to half of them — 46 percent — were protected from malaria for 18 months after they got a three-dose series of the vaccine
  • Approved in 2015
19
Q

how does the host adapt for survival AGAINST MALARIA?

A
  • Sickle cells - Variant hemoglobin confers some protective advantage against malaria
  • Glucose-6-phosphate dehydrogenase deficiency –> leads to increased oxidative stress in red blood cells, this may in turn have a negative influence on the parasite. As such, individuals who possess this mutation have some protection against malaria
  • Duffy blood group – if lacking Duffy antigens–> relatively resistant to invasion by P. vivax
20
Q

Who is at greatest risk for acquiring malaria?

How to prevent this?

A
  • At risk:
    • highest risk assoc. w/ 1st and 2nd generation immigrants living in non-endemic countries –> who return to countries of origin to visit friends and relatives
    • pregnant women (1/2 of all cases)
  • Prevention:
    • determine if malaria transmission occurs at travel destination
    • take malaria prophylaxis & buy drug in home country
    • insect repellant, insecticide-treated bed net
      • assess factors such as types of accommodations and activities
21
Q

2 phases of lifecycle for

toxoplasma gondii

A
22
Q

what is the definitive host for toxoplasma gondii?

A
  • the cat in which the sexual reproduction of the parasite occurs and reaches “maturation”
    • rodents have parasites in muscle/brain –> gathered in pseudocysts (containing hundreds of infectious units, which are slow growing parasites - Bradyzoites)
    • cats ingest pseudocysts in rodents
    • parasites infect intestinal epithelial cells; divide and undergo schizony, forming merozoites
    • merozoites differentiate into male/female gametocytes –> fuse to form oocysts
    • w/in oocysts, sporozoites are formed
    • oocysts pass out in cat stool
  • produces oocysts, a sexual cyst w/ infectious units inside (sporozoites0
23
Q

asexual reproduction of toxoplasma gondii

A
24
Q

Tachyzoites infect what cells?

What happens next?

A
  • Tachyzoites infect various types of cell in different organs (Eyes, lung, heart, liver, lymph nodes, etc.).
  • Immune pressure slows down the division of the parasites, turning them in to bradyzoites –> Bradyzoites gather together into pseudocysts
    • pseudocysts in almost any organ of the body (Eyes, lung, heart, liver, lymph nodes, etc.). Brain may contain many.
    • Hosts are chronically infected
25
Q

ACQUIRED toxoplasmosis:

symptoms

A
  • Enlarged lymph nodes
  • Muscle pains
  • Fever (intermittent)
  • General ill feeling
  • Mild symptoms may be relieved by rest or taking over-the-counter medications (Tylenol, Motrin and Advil)
  • Immune systems are able to control the disease in most individuals.
26
Q

CONGENITAL toxoplasmosis:

symptoms

A
  • Early in pregnancy
    • spontaneously abort; stillborn
  • Second to 6th month of gestation
    • blindness, CNS lesions, learning disability
    • death in infancy
  • Last 3 mo of pregnancy
    • prognosis is good
    • baby may not even display any sxs
27
Q

RECRUDESCENT toxoplasmosis:

symptoms

A
  • occurs in individuals immunosuppressed (bone marrow transplant or AIDS)
  • pneumonia
  • blindness, vision disturbances
  • hepatitis and heart
  • muscle spasms
  • papular rash on palms and soles(cutaneous manifestation)
28
Q

CEREBRAL toxoplasmosis:

symptoms

A
  • *MOST COMMON CAUSE OF CNS DISEASE IN PTS W/ AIDS
  • Sxs
    • Encephalitis
    • Severe headaches
    • One-sided weakness or numbness
    • Ataxia and cranial nerve palsies
    • Mood and personality change
    • Leads to coma and death
29
Q

3 stages in life cycle of:

Pneumocystis jirovecii

A
30
Q
A

Y1 - Microbio Exam 3 (13 decks)

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