Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
104 Cards in this Set
- Front
- Back
|
symptoms of malaria?
|
Both an acute and a chronic (relapsing) infection characterized by intermittent FEVER, SPLENOMEGALY,
ANEMIA -thrombocytopenia; --> immune complex glomerulonephritis |
|
|
what is malaria caused by?
|
4 Plasmodium species of class Sporozoa
|
|
|
what's malaria transmitted by?
|
mosquito vector of genus Anopheles
(1) exposure to blood or blood products (e.g., blood transfusion or use of shared syringes), (2) congenital infections, or acquired through (3) local mosquito transmission |
|
|
how frequently are there malaria cases?
|
350-500 million cases of malaria occur annually
~ 1-3 million persons die of malaria each year |
|
|
where does malaria outbreak?
|
Worldwide in occurrence
occurs in > 100 countries. Regions include Africa, Asia, islands of the south, west & central Pacific ocean, South America, Latin America, certain Caribbean islands, the middle East and ... *follows Anopheline distribution |
|
|
malaria in US?
|
Was endemic in US in early 1900s
now, scattered cases |
|
|
how was malaria stopped in US?
|
Improved socioeconomic conditions
Water management Vector-control efforts Case management |
|
|
which malaria TYPES are most common in USA?
|
Plasmodium falciparum-613
Plasmodium vivax-275 undetermined- 573 |
|
|
which malaria TYPES are least common in USA?
|
Plasmodium malaria - 46
Plasmodium ovale- 47 mixed -10 |
|
|
what's the life cycle of Plasmodium?
|
1) Sexual Cycle in Mosquito
(Sporogony), 2) Asexual Cycle in Human Host (Schizogony). |
|
|
what form of malaria does mosquito proboscis eject?
|
Plasmodium sporozoites
|
|
|
what happens once mosquito bites person w/ malaria?
|
injected into the human circulation & carried to the liver.
Sporozoites enter liver cells & begin exoerythrocytic cycle |
|
|
which malaria TYPES are most common in USA?
|
Plasmodium falciparum-613
Plasmodium vivax-275 undetermined- 573 |
|
|
which malaria TYPES are least common in USA?
|
Plasmodium malaria - 46
Plasmodium ovale- 47 mixed -10 |
|
|
what's the life cycle of Plasmodium?
|
1) Sexual Cycle in Mosquito
(Sporogony), 2) Asexual Cycle in Human Host (Schizogony). |
|
|
what form of malaria does mosquito proboscis?
|
Plasmodium sporozoites
|
|
|
what happens once mosquito bites person w/ malaria?
|
injected into the human circulation & carried to the liver.
Sporozoites enter liver cells & begin exoerythrocytic cycle. In a liver cell, a sporozoite increases in size & finally develops into a tissue schizont (meront) containing thousands of merozoites. Distended by the meront, the liver cell ruptures, releasing merozoites into the blood stream, where the merozoites invade circulating RBCs |
|
|
how does malaria make malaria babies?
|
by dividing into a number of progeny.
|
|
|
what are rbc invaded by for malaria life cycle?
|
a single parasite, the merozoite
|
|
|
what happens once the malaria is inside the rbc?
|
merozoite is transformed into a ring form, the trophozoite.
As the trophozoite grows, dark malarial pigment may collect within the cytoplasm as the Hgb which the parasite needs for growth is converted into insoluble hematin. When the trophozoite matures, it begins to divide into a segmented form, called a schizont. As a schizont matures, each segment can be recognized as an individual parasitic merozoite, complete with nucleus & cytoplasm. Upon rupture of the RBC, the merozoites are free to infect new RBCs |
|
|
when do you get relapses of malaria?
|
if forms of P. vivax & P. ovale
(hypnozoites) that have been dormant in liver for a year or more are released into blood stream resulting in a new invasion -happens when they're not erradicated from liver -Recrudescences may occur from blood stages of P. malariae & P. falciparum |
|
|
what undergoes schizogony?
|
all malaria species
|
|
|
which forms become hypnozoites?
|
P. vivax
P. ovale |
|
|
how does P. vivax invade rbc?
|
Duffy blood group antigen as its receptor to attach to & invade RBCs
|
|
|
does everyone have the Duffy antigen?
|
RBCs of most West Africans, in contrast to RBCs of Europeans, lack the Duffy Ag.
Thus, West Africans are resistant to P. vivax infections |
|
|
what gives resistance to Plasmodium falciparum?
|
-Sickle hemoglobin (heterozygotes) -Erythrocyte glucose-6-phosphate dehydrogenase deficiency
|
|
|
why do you get fever w/ malaria?
|
Initiated by RBC rupture with release of merozoites (sporulation)
|
|
|
what are the circulatory changes during malaria infection?
|
High fever results in significant vasodilation.
|
|
|
what cytokines are activated during malaria infec?
|
Elevated levels of IL-1 & TNF consistently found in patients with malaria
May aid in destruction of parasite, but increased TNF concentrations may harm the patient |
|
|
what are the circulatory changes during malaria infection?
|
High fever results in significant vasodilation.
-In falciparum malaria, as trophozoites grow -- Infected RBCs become sticky Stick to endothelium of small blood vessels Only early forms in blood films Obstruction of CNS capillaries -- cerebral malaria |
|
|
what cytokines are activated during malaria infec?
|
Elevated levels of IL-1 & TNF consistently found in patients with malaria
May aid in destruction of parasite, but increased TNF concentrations may harm the patient |
|
|
what are circulatory changes during Plasmodium falciparum infec?
|
as trophozoites grow --
Infected RBCs become sticky Stick to endothelium of small blood vessels --> obstruct and cause cell death Only early forms in blood films Obstruction of CNS capillaries -- cerebral malaria |
|
|
what's incubation of malaria?
|
7-30 d (P. falciparum shorter; P. malariae longest)
|
|
|
describe the malaria symptoms in detail:
|
Prodrome - flu like
Early - fever irregular, then cyclic Chills -->fever -->sweats |
|
|
what is the cycle of fever, chills, sweating in malaria?
|
q 48 hours: P. vivax, P. ovale, P. falciparum
q 72 hours: P. malariae |
|
|
do ppl recover from malaria?
|
Gradually develop immunity, less severe symptoms, & finally asymptomatic, but may still have parasites in blood
|
|
|
why do ppl get fever every 48 hours?
|
asexual blood stages in P. falciparum, P. vivax & P. ovale require 48 h to complete their schizogony. Fever is produced when the schizonts mature, ie, at 48 h intervals
|
|
|
why do ppl get fever every 72 hrs?
|
P. malariae requires 72 h, and is associated with “quartan fever, ie, 72 h between paroxysms
|
|
|
what can happen when malaria adheres to CNS blood vessels?
|
Thrombosis
|
|
|
what's your pee like if you have dangerous malaria?
|
dark pee : Kidney damage due to P. falciparum results in “blackwater fever”
Dark blood/plasma b/c of malarial pigment malaria eats hemoglobin from RBC, breaks it down into heme products --> black |
|
|
how do you diagnose malaria?
|
-travel history
-Giemsa-stained smear of patient’s blood should be examined for parasites. -Thick & thin blood smears must be prepared properly. -experienced laboratory personnel. |
|
|
what's the advantage of the thick smear for malaria?
|
-advantage of providing more blood for examination (concentrating any plasmodia that may be present).
|
|
|
how do you prepare a thick smear for malaria?
|
-thin enough so that you can read words on a page underneath the part of the slide that has blood
|
|
|
what's the advantage of the thin smear for malaria?
|
Morphology of intracellular Plasmodia can best be seen in thin smear stained by Giemsa method
|
|
|
why do you need to identify malaria?
|
its increased resistance and rapidly fatal disease
|
|
|
what's parasite density?
|
% of infected RBCs
|
|
|
do any species of Plasmodium have a rbc preference?
|
P. vivax and P. ovale infect young cells (reticulocytes); hence fewer infected cells than for other species
|
|
|
what could identify P. falciparum?
|
banana shaped gametocytes!
infect normal sized rbc Small ring forms, multiple rings/cell and double nuclei are common Appliqué forms are very suggestive Schizonts rarely seen in blood 22 (6 - 32) merozoites |
|
|
what could identify P. vivax?
|
infects big RBC (pale)
Schuffner's dots amoeboid cytoplasm (large trophozoites) 16 (12-24) merozoites in schizonts Round to oval gametocytes fills cell |
|
|
what could identify P. malariae?
|
infects normal sized RBC
compact cytoplasm 8 (6-12) merozoites |
|
|
what could identify P. ovale?
|
infects big RBC
Schuffner's dots compact cytoplasm 8 (6 - 14) Merozoites |
|
|
what's going on if you see schizonts in P. falciparum?
|
sign that patient is about to die b/c rarely see schizonts in P. falciparum
|
|
|
what could identify P. malariae?
|
infects small RBC
compact cytoplasm 8 (6-12) merozoites |
|
|
what could identify P. ovale?
|
infects big RBC
Schuffner's dots compact cytoplasm 8 (6 - 14) Merozoites |
|
|
what's going on if you see schizonts in P. falciparum?
|
sign that patient is about to die b/c rarely see schizonts in P. falciparum
|
|
|
when do you see ring forms in cell for malaria?
|
In falciparum, common to see 2-3 ring forms /cell
Rare to see more than 1 ring form in vivax |
|
|
describe an applique form:
|
Nuclei will stick on outside of cell membrane
|
|
|
how can you identify malaria?
|
MICROSCOPE!!!
Most tests use monoclonal antibodies Low sensitivity for infections with low level parasitemia (microscopy much more sensitive) Tests are rapid, however, and do not require skilled technologist -PCR analysis available for species determination only at CDC: takes days to weeks! |
|
|
how long can you have malaria?
|
months!
|
|
|
how can you prevent malaria?
|
chloroquine
Protective clothing Mosquito netting “DEET” (diethyl toluamide) |
|
|
how can you treat P. vivax if no resistance?
|
primaquine to eradicate hypnozoites in liver
|
|
|
how can you treat P. ovale if no resistance?
|
primaquine to eradicate hypnozoites in liver
|
|
|
how do you treat P. vivax if resistant to chloroquine?
|
primaquine +
1) quinine +, doxycycline, tetracycline, or clindamycin; or 2) atovaquone-proguanil (Malarone®); or 3) mefloquine |
|
|
how do you treat chloroquine resistant P. falciparum?
|
(A) quinine +, doxycycline, tetracycline, or clindamycin; or
(B) atovaquone-proguanil (Malarone®); or (C) mefloquine |
|
|
what malaria drugs are used elsewhere but not legal in US yet?
|
artemisinins (artemether & artesunate)
|
|
|
why must you always use primaquine either by itself or with another med when treating P. vivax and ovale?
|
b/c primaquine specifically gets rid of the liver phase of malaria
|
|
|
who's infected by Babesiosis?
|
A zoonosis infecting deer, cattle & rodents
Man an accidental host |
|
|
how is Babesiosis transmitted?
|
-Ixodes dammini (tick) transmits -transfusion-related infections
|
|
|
where are Babesiosis infections common in US?
|
common in northeastern US (eg, Nantucket, Martha’s Vineyard)
|
|
|
How does Babesiosis look under microscope?
|
Small ring forms in RBC- must differentiate from P. falciparum
|
|
|
what is species name that causes Babesiosis?
|
Babesia microti
|
|
|
Babesia microti symptoms?
|
probably mild
May be headache, malaise, fever, chills, sweating, muscle/joint pain, hepatosplenomegaly -With increased RBC destruction, hemolytic anemia may occur, & patient may develop renal failure |
|
|
what's the drug of choice for a Babesia microti infection?
|
clindamycin combined with quinine
|
|
|
how do Babesia microti grow?
|
Trophozoites in RBCs multiply by binary fission forming small rings and tetrads.
|
|
|
what type of parasite is Toxoplasma gondii?
|
coccidian protozoan
-intracellular parasite |
|
|
what's infected by Toxoplasma gondii?
|
infects many warm blooded animals, including humans
|
|
|
reservoir host of Toxoplasmosis gondii?
|
house cat
|
|
|
how does T. gondii develop in cat?
|
Organisms develop in intestinal cells of cat & also during an extraintestinal cycle with passage to tissues via the blood stream
|
|
|
how do we get infected from cats w/ T. gondii?
|
Organisms from GI tract are passed in cat feces & mature into infective oocysts after 3-4 days in external environment
|
|
|
what are T. gondii oocytes resistant to?
|
disinfectants, freezing, heat, drying, time (years)
|
|
|
how are humans infected by T. gondii?
|
-Ingestion
-Infected undercooked meat (eg, hamburgers) -Oocysts from contaminated cat feces -Organ transplantation (liver) -blood transfusion -Transplacental transmission in pregnancy acquired either from meat or contact with cat feces -Inoculation (rare) |
|
|
what form of T. gondii infects ppl?
|
Infective oocysts (sporozoites)
|
|
|
what's T. gondii life cycle?
|
Tachyzoites released in small intestine and invade mucosa
Tachyzoites (trophozoites) enter circulation and are disseminated to brain, skeletal muscle, myocardium, etc. -go out into poop and are bradyzoites --> 3-4 days later, oocysts |
|
|
what form of T. gondii do cysts have?
|
bradyzoites
|
|
|
what are symptoms of T. gondii in immunocompetant person?
|
Usually asymptomatic, self-limited
May develop flu-like illness, lymphadenopathy |
|
|
what are symptoms of T. gondii in immunocompromised person?
|
affected:
Brain, eyes, skeletal heart muscle |
|
|
what are symptoms of T. gondii congenital infection?
|
Cerebral lesions
hydrocephalus chorioretinitis |
|
|
when is it the worst to get T. gondii?
|
More severe if acquired in 1st or 2nd trimester
|
|
|
how do you diagnose toxoplasmosis?
|
-CAT scan vs. MRI
-Serology (EIA for IgM antibodies or rising IgG titer) -Biopsy of brain, lymph nodes, myocardium or other suspected tissue or body fluid (eg., CSF) -Inoculation of specimen into mouse peritoneum |
|
|
what's the treatment for T. gondii?
|
experimental
pyrimethamine + sulfadiazine or clindamycin + pyrimethamine |
|
|
Describe Acanthamoeba:
|
small free-living water & soil amoebae
|
|
|
what are symptoms of Acanthamoeba?
|
-Granulomatous amebic infections of CNS & other organs in immunocompromised patients,
-Keratitis in soft contact lens wearers |
|
|
what forms of Acanthamoeba are found in infected sites?
|
cysts & trophozoites
|
|
|
what's the treatment for Acanthamoeba?
|
problematic b/c it usually kills ppl
|
|
|
what are Acanthamoeba cysts resistant to?
|
chlorination
|
|
|
how can you avoid an Acanthamoeba infec?
|
-don't wash your contacts w/ tap water
-don't go swimming (even in pool) w/ contacts on: fun fact |
|
|
Describe Naegleria fowleri:
|
free-living water & soil amoeba
an amebo-flagellate |
|
|
symptoms of Naegleria fowleri?
|
-acute, rapidly fatal meningoencephalitis.
-acute hemorrhagic abscesses |
|
|
Naegleria fowleri transmission?
|
Trophozoites enter noses of young swimmers & divers in warm lakes, poorly chlorinated swimming pools, hot tubs
|
|
|
how does N. fowleri get inside you?
|
-gets in nose
-Colonizes nasal mucous membrane (rhinitis) -Invade olfactory nerve, moves along it through cribriform plate into brain -trophozoites invade blood vessel walls |
|
|
are there cysts from N. fowleri?
|
no
|
|
|
how do you diagnose N. fowleri?
|
Purulent CSF with motile trophozoites
|
|
|
how well do ppl recover from N. fowleri?
|
most die within 5-7 days after exposure
|
|
|
Tx of N. fowleri?
|
amphotericin B
|
