Infectious Disease (Block 6): Blood/tissue Protozoa

Front 1

which type of plasmodium is the #1 killer? what makes it particularly lethal?

Back 1

p. falciparium; can lead to severe clinical manifestations like brain and kidney failure, jaundice with NORMAL ALT (compared to hepatitis)

Front 2

what is the general pathogenesis of plasmodium (malaria)? how does this lead to clnical manifestations?

Back 2

sexual dviision in ANOPHELES mosquitoes, then enters humans by bite (sporozoite), invade liver and then RBCs (trophozoite --> schizont --> merozoites), release of merozoites from RBCs stim immune resp (fevers, chills, sweat)

Front 3

P. vivax and P. ovale produce chills and fever followed by drenching sweats (caused by burst of red cells at different intervals) every __ hours.

Back 3

48 (tertian malaria)

Front 4

P. malariae bursts every 72 hours (3 day cycle). what is this called?

Back 4

quartan malaria

Front 5

where is P. ovale usually found compared with P. vivax?

Back 5

P. ovale: W. Africa

P. vivax: Asia, latin America, some parts of Africa

"It's Vivid in Asia..."

Front 6

what is the incubation period of malaria? how do you Dx and Tx it?

Back 6

incubation = 1-4 weeks

Dx: Wright stain (blood smear under microscope for ring forms in RBCs)

Tx: chloroquine for most malaria (including P. falciparum)

chloroquine (followed by primaquine) for P. vivax/P. ovale
- must do G6PD testing prior to primaquine treatment (contraindication)

Front 7

Name the 2 types of plasmodium that have a latent liver stage that could lead to continual reproductionin the liver. name it as well.

Back 7

P. vivax & P. ovale

hypnozoites

Front 8

name the protozoan that is commonly found in undercooked meat (raw pork) or food contaminated with household cat feces

Back 8

Toxoplasma gondii (ingestion of either is common source of transmission)

DON'T FORGET TOXO IS ONE OF THE CONGENITALLY TRANSMITTABLE AGENTS (TORCHES!!)

Front 9

clinical manifestation of toxo

Back 9

ACUTE = usually asymptomatic; can cause mono-like illness (this is what the case is in immunocompetent pts)

CONGENITAL= CNS (hydrocephaly, microcephaly) and systemic dz; survivors can have cerebral calcifications/mental retardation/retinochoroiditis later in life (this is when toxo is acquired by mom DURING pregnancy

REACTIVATION= this is what AIDS pts usually have ==> CNS disorders

Front 10

most common cause of intracranial mass lesions in AIDS patients

Back 10

toxoplasmosis gondii

BIG PICTURE: in AIDS pts and fetuses Toxoplasma gondii is TOXIC to the BRAIN and the EYES!!!

Front 11

Dx and Tx of toxoplasma gondii

Back 11

Dx: SEROLOGY + "CAT" scan for brain lesions

Tx: none needed for immunocompent pts.
- Pyrimethamine + sulfadiazine for pregnant & immunocompromised
- P/S (for 1 year) in congenitally infected newborns

Front 12

what is the importance of Babesia?

Back 12

it can be easily confused with P. falciparum (so epidemiology is key= it's found in NE united states)

Front 13

what are the 3 clinical forms of Leishmaniasis? what is the severity of this dz based upon?

Back 13

1. cutaneous: single painless ulcer (at site of inoculation) that will heal w/o Tx
2. mucocutaneous: widely disemminated ulcerations of skin/mucous membranes
3. visceral: very sever infection depp in the reticuloendothelial organs (spleen/liver)

based on strength host cell-mediated defenses

Front 14

in terms of pathogenesis of leishmaniasis, it is tranmitted by bite of the _______. what actually multiples within the macrophages found witihin lymph nodes, spleen, liver, and bone marrow?

Back 14

sandfly; amastigotes (nonmotile without flagella)

Front 15

what protozoa can lead to hyperparasitemia (>5% RBCs infected), which eventually gives hypoglycemia and metabolic acidosis?

Back 15

P. falciparium (malaria)

Front 16

differentiate bw simple and diffuse cutaneous leishmaniasis

Back 16

simple = large painless, ulcer at site of sandfly bite (heals on its own)

diffuse = chronic form of cutaneous leishmaniasis that occurs in immunocomproised pts; shows up as numerous nodular lesions (W/O ULCERATION) across the body

Front 17

manifestations of mucocutaneous vs. visceral leishmaniasis

Back 17

ML= initially dermal ulcer; months to years later, ulcers arise in mucous membrane of nose and mouth

VL= more commonly found in malnourished children and HIV pts (lack of intact cellular immunity); pt will have huge abdominal enlargement due to massive SPLENOMEGALY and hepatomegaly, fever, pancytopenia (abnormal deficiency in all blood cells)

Front 18

Dx and Tx of leishmaniasis

Back 18

Dx: direct microscopy; diffrentiate complexes by molecular/Ab assays

Tx: anitmonials
- amphotericin B for visceral leishmaniasis (due to resistance to antimonials)

Front 19

Name the bugs that transmit:
Leishmania = _______
T. brucei (African sleeping sickness) = ________
T. cruzi (Chagas) =______

Back 19

sandfly
Tsetse fly
Reduvid bug

Front 20

Where can Trypanosoma cruzi (Chagas dz) be found? what is it usually transmiited by?

Back 20

Texas, Mexico, S. America

transmitted by feces of reduviid bug while person is sleeping (tryptomastigotes from feces goes into human host, organism invades local skin, macrophages, lymph nodes, spread in blood to distant organs)

Front 21

characterize the 3 stages of Chagas (T. cruzi)

Back 21

1. acute dz = CHAGOMA (inflammed area of skin at site of oculation), fever, muscles heavily infected (myocarditis) and encephalitis

2. intermediate stage = asymptomatic but seropositive (lasts decades)

3. chronic stage= enlarged esophagus and colon (mega!), cardiomyopathy (dilated heart)

Front 22

Dx of T. cruzi and Tx...

Back 22

Dx:
- microscopy in acute dz (can see parasites); can't see parasites in chronic dz => must use ELISA (IgG for T. cruzi).

Tx for acute=Nifurtimox
there's no Tx for chronic Chagas dz

Front 23

epidemiology and pathogenesis of T. brucei (African trypanosomiasis -- sleeping sickness)

Back 23

Sub-Saharan Africa; spread by Tsetse fly bite; spreads via bloodstream to lymph nodes and then CNS

Front 24

what's the difference bw T. brucei rhodesiense vs. T. brucei gambiense

Back 24

rhodesiense = acute dz with CNS involvment; death occurs within weeks (more severe)

gambiense = slowly progressing fevers, wasting, late neurologic symptoms

Front 25

clinical presentation of African trypanosomiasis

Back 25

initially = nonspecific (malaise, headache, fever, rash) + trypanosomal chancre (at inoculation site) + enlarged cerviacal lymph nodes (Winterbottom's sign) with "gambiense"

later = CNS problems (sleep disorders, mental status changes, loss of appetite)

Front 26

Dx and Tx of Trypanosomiasis (T. brucei)

Back 26

Dx:
- trypanosomes on a blood smear (direct microscopy)
- CNS dz presumed when parasites are seen or when lymphocytes increase by >5 cells/mL (in absence of parasites)
- detection of intrathecal IgM synthesis also sensitive marker for CNS dz

Tx: early = suramin
late stage = melarsoprol (crosses blood-brain barrier)