4/14 Parasitology and Travel Med II + Ch 8 Flashcards Preview

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Flashcards in 4/14 Parasitology and Travel Med II + Ch 8 Deck (66)

General characteristics of protozoa:

number of cells?

where do they multiply?

do they cause eosinophilia?

number of cells? --> single-celled eukaryotes

where do they multiply? --> multiply in host; growth can be intracellular or extracellular

do they cause eosinophilia? --> protozoa RARELY cause eosinophilia.

(connect eosinophilia more with helminths (worms))

Pic: I just needed a picture. 


General characteristics of protozoa:

number of cells?

where do they multiply?

do they cause eosinophilia?

number of cells? --> single-celled eukaryotes

where do they multiply? --> multiply in host; growth can be intracellular or extracellular

do they cause eosinophilia? --> protozoa RARELY cause eosinophilia.

(connect eosinophilia more with helminths (worms))

Pic: I just needed a picture. 


Giardia lamblia: 

characteristics of the protozoa?

what are the reservoirs?

what can new infections cause?

Flagellated extracellular protozoan

several animal reservoirs; human and animal feces contaminate water

New infections cause GI sx, malabsorption, steatorrhea, weight loss (characteristic = floating foul-smelling stool)


Giardia: how does water have to be treated in order to avoid this?

Giardia's infectious cysts resist chlorine, leading to municipal water outbreaks.

Have to FILTER water rather than just chlorinate it. Boiling also works.

May have focal outbreaks due to contaminated water supplies.


Giardia: what do we call the stage that multiplies and adheres to the wall of the small intestine?



Giardia: describe the life cycle briefly

-Human or animal ingests a cyst from a water source.

-Cysts open in the small intestine. Released parasites multiply as trophozoites in duodenum and jejunum

-Trophozoites adhere to the villi of the small bowel, causing problems!

-As the stool mass is dehydrated, the trophozoites become encysted and excreted in feces

(pic = cyst)


what is this beastie?

what is it doing?

Giardia (trophozoite)

has a sucker that adheres to the small bowel. Thousands of these guys cover the villi, leading to malabsorption and foul stools.


Giardia: what does the clinical presentation of a chronic infection look like?

chronic infections more likely in what people?

Clinical presentation of acute infections?


Chronic infections may be asymptomatic.

Chronic infection more likely in ppl with lack of mucosal IgA.

Acute infection may cause severe diarrhea, and usually abdominal discomfort, floating stools, weight loss



Giardia: what is treatment? 


Treatment = metronidazole

because Giardia lacks mitochondria


Giardia: how do we diagnose?

What is the diagnostic stage of the life cycle?

Two ways:

-Microscopy of stool ("Ova and parasite")

-Immunofluorescent antibody detection

Diagnostic stage = cyst (in formed stools) or trophozoite (in diarrhea)

(IF pic: giardia = oval, round = cryptosporidia)


Cryptosporidium: how is it transmitted?

How do we keep it from the municipal water supply?


Fecal-oral transmission via fecal cysts getting into water

Water borne disease: like giardia, not killed via chlorination. therefore have to filter water.


Generally, what does cryptosporidium cause clinically?

Diarrhea! High volume and watery. (contrast with steatorrhea from giardia)

Will be self-limited in pts with normal immune systems

Can be protracted/debilitating in AIDS pts 


Cryptosporidium has a complex life cycle that we don't need to know everything about.

What is the form of the protozoa that we ingest? How is it introduced into the water supply?

What are the hosts/reservoirs?

Humans ingest cysts, which cause problems in the small bowel (--> diarrhea)

Then excreted in feces & gets into water supply

Animals = reservoirs --> cysts get into water supply via their feces as well

(pic = cryptosporidium cyst from acid-fast stain of watery diarrhea)


Cryptosporidium: where within the small bowel does it reside in humans?

Sets up shop just beneath the plasma membrane of intestinal epithelial cells. Looks like they are just adhered to the epithelial surface, but in fact they are underneath.


Cryptosporidium: how is it diagnosed?

As with Giardia, can diagnose 2 ways:

-O and P examination of stool (pic on other side of card: stained with acid fast stain)

-Immunofluorescence detection of antibodies to Cryptosporidium antigen (round = crypto; oval = giardia trophozoites)


Cryptosporidium: drug treatment?

No great drug for this, and we don't treat normo-immune patients since Crypto is generally self-limited.

Give Nitazoxanide if the patient has severe or protracted disease; has some efficacy but not great.

For AIDS patients it will resolve by giving them HAART therapy.


Trichomonas vaginalis: describe the protozoan? 

What stage causes disease?

What is the host?

How is it transmitted?

(pic: part of lifecycle; note no cyst form!!)

Flagellated protozoan

There's only one stage: Trophozoite! Trophozoite causes disease (rather than the cyst stage, as with giardia and crypto)

Transmitted person to person as an STD.


Trichomonas vaginalis: symptoms? (M and F)

F: Vaginitis with frothy purulent discharge. Urethritis. Many will be asymptomatic

M: 75% are asymptomatic. If sx: urethritis, prostatitis, epididymytis


Trichomonas: what can it cause beyond the immediate inflammatory effects?

-Increases risk of HIV acquisition

-Correlation with early delivery, low birth weight

-May cause infertility


Trichomonas: treatment?


(trich has no mitochondria)

-Treat patient and all sexual partners


Trichomonas vaginalis: prevention?

Barrier contraceptives: condoms

(does anyone use dental dams anymore???)


Trichomonas vaginalis: how to diagnose?

(pic: the red smudge in the middle is Trich)

-Microscopy of wet prep from frothy vaginal discharge (pic this side. Note the Trich will be swimming around!!)

-Microscopy from PAP stain (pic on other side)

-Rapid EIA (whatever that is) looking for Trich antigens

-Molecular assays: most sensitive


Toxoplasma Gondii: describe the protozoan?


Obligate intracellular protozoan

Lots of organelles, mitochondria

The apical organelles (pointy end) allow parasite to enter host cells. 


Toxoplasma: what is the reservoir?

what are the important parts of the life cycle?

Reservoir = domestic cats.

Within the cat, Toxoplasma produces cyst, which is shed in feces and gets into soil. Very stable there and can infect people, animals, birds.

Also an asexual life cycle occurring in the tissue of animals. The cyst can get into the tissue, and if we eat undercooked meat, we get infected.

Note: two cyst stages: fecal and tissue


Toxoplasma gondii: how prevalent is it?

what are the symptoms in people with normal immune systems?

15-90% of population is infected; higher rate in cultures that eat undercooked meat

most infections are asymptomatic

if there are symptoms, they range from mononucleosis-like to myocarditis, hepatitis, pneumonia, encephalitis.


What is "reactivation disease?"

aka Toxoplasma Encephalitis

Historically a disease that defined AIDS: Toxoplsma gondii can cause encephalitis in immunocompromised patients

These patients were infected with Toxoplasmosis many years ago and had parasites encysted in their brain. These cysts reactivate when they become immunocompromised.

Symptoms: headache, focal neuro deficits


If a woman is infected with Toxoplasma while pregnant, what can happen to the fetus?

There can be transplacental infection with mild to severe damage to the fetus. 

Mild: visual defects

Severe: microcephaly, hydrocephalus, blindness....


Toxoplasma: treatment?

Pyrimethamine - sulfadiazine combination


Toxoplasma: what can happen to a patient's eye?

this is a result of what kind of transmission?

(Pic: the red blob = toxoplasma cyst. breaks down to release rapidly dividing forms which destroy surrounding tissue)

Toxoplasmic retinitis

Either congenital transmission or acute infection in adults (seen as outbreaks in Brazil, Canada)



Toxoplasmosis: diagnosis?

Dx based on serology for antibody

(NOT standard O & P)

IgG antibody establishes that there has been an infection at some point in the past

IgM (+ others) used to date the infection --> esp important in pregnancy


Giardia: where in the world is it prevalent? 


Giardia is prevalent wherever there are mammals (ie, basically everywhere).

Prevention requries avoiding human and animal fecal contamination of water. Hanover has an open reservoir - Beavers can be a problem.

When Jen was hiking in Wyoming, we were worried about the elk and marmots. You don't want to get this when you're 7days walk from a flushing toilet. 


This is an acid-fast stain from a patient with profuse watery diarrhea.

Dx? Tx?


This is the diagnostic stage: acid-fast (red-stained) cysts in feces.

(not sure if we need to know Tx. But tx = Nitazoxanide. Not effective in severely immunocompromised patients. in AIDS patients, this will resolve with HAART therapy)


Toxoplasma: life cycle?

-Member of the cat family eats the intermediate host (ie a bird or something) that has dormant Toxoplasma cysts.

-In the cat's intestine, Toxoparasites grow intracellularly & produce male and female gametes.

-Gametes -> zygote, excreted in feces as noninfectious cyst with protective outer coat

-2 days (if at ambient temp) later the cyst has become infectious

-Non-feline animal ingests infectious fecal cysts -> acute infection with trophozoites. The infected animal/person now has tissue cysts as well. (different from the cysts that the cat shat out)


For an AIDS patient with a CD4 count of <100, which of these protozoa are we concerned about? what will be the s/s?

Concerned for Toxoplasma -> Toxoplasmic encephalitis

(reactivation disease)

s/s: headache, confusion with focal neuro deficits

-> ring-enhancing lesion on MRI or CT


For an AIDS patient with a CD4 count of <200, which of these protozoa are we concerned about? what will be the s/s?

Concerned for Cryptosporidium -> profuse, watery diarrhea


What is the life cycle of Malaria?

-Lodge in the salivary glands of Anopheles mosquito

-Mosquito bites human, transmits spore

-Infectious form travels to liver really quickly. 

-Liver = asymptomatic stage: each spore infects one hepatocyte, divides rapidly (may stay in liver for months)

-Symptomatic stage: breaks out of liver, infects/lyses RBCs. This is the RING STAGE.

-More divisions, break out of RBCs, some form gametes

-Mosquito bites again; gametes taken up & mosquito can infect someone else.


What species is the definitive host for the Anopheles mosquito?
What species is the intermediate host?

(Anopheles carries malaria)

Definitive host = mosquito

Intermediate host = human


There are 3 types of malarial parasites (that they told us about; there are actually 5): which is the most virulent? What are the others?

Plasmodium falciparum is most virulent.

Other spp: Plasmodium vivax, Plasmodium Malariae


What is this?

Malarial ring stage. Note dot of condensed chromatin, blue ring of malarial cytoplasm.

Blood smear designed to allow us to see intracellular parasites (here, intra-RBCs).


What is this?

What are the brown areas?

Malaria (P vivax)

can see parasite multiplying within RBCs. Still only one area of nuclear chromatin. 

Brown: breakdown of Hgb.



P vivax gametocyte




P falciparum gametocyte

Classic diagnostic form for P falciparum

Elongated, single nuclear mass, still inside RBC.

***Remember this one: likely to be on test!


How many days post-infection will we likely see this on the blood smear?


10-14d post infection


General global distribution of malaria?

Equatorial and tropical

Red areas:

Central Africa, southern India, center of South America.


Where is the bulk of mortality due to malaria occurring?

in what patients?

if someone in the US has malaria, how did they likely get it?

Subsah Africa in kiddos under 5yrs old.

(90% malaria death = <5y)

US: most cases are in travelers

(pic: sad map of relative malaria mortality)


Malaria clinical presentation: what is the incubation period?

Incubation = 10-40 d

(rarely, vivax may incubate in the liver up to 12m)


Malaria clinical presentation: what do the first sx look like?

can be mistaken for influenza.

fever, headache, joint pain, prostration

(non-specific - note fever though)


Malaria clinical presentation: after the first sx, how does it present?

Periodic febrile episodes of shaking chills followed by sweats.

Classically the sx are periodic, as the stages of infection of RBCs become synchronized with progression of disease


A little more about the febrile pattern of malaria: do the patterns differ among the types of malaria? how long is the periodicity?

Generally the erythrocytic cycle = 48h

Fever spikes, then pt will be afebrile for 48 hrs, then temp spikes again. 

the patterns are largely similar: but for falciparum the fever may not completely resolve in between spikes.

(graphs: top= vivax. middle= malariae (dntk). bottom= falciparum)


What is cerebral malaria?

What process causes it? 

How serious is it?

Caused by many RBCs adhering to epithelial linings, and clogging small venules.

This occurs in lung, kidney, GI tract -- but what will kill you is the cerebral malaria.

May get small hemorrhage due to ischemia. Also release of TNF, IL-1.

Can go from conscious to coma in a few hours. If treated, may still not fully regain neuro function. Lethal if not treated.


What are some new diagnostic techniques for detecting malaria?Where are they most useful?

Classic diagnosis is blood film (as we have seen)

New techniques:

-Immunochromotographic: a dipstick assay. Good in places where microscopy is not available or is of poor quality. Used in US also

-Lab-developed PCR: most sensitive, available only at references labs. Not very quick. 


Is there a vaccine for malaria?

Are some people resistant/why?

No vaccine.

Some pts are resistant due to genetic factors:

-Sickle cell dz is partially protective against P falciparum (involvement of RBC hemoglobin)

-G6PD deficiency in RBCs also partially protects against P falciparum

-Duffy blood antigen is partially protective against P vivax



Can a person develop immunity to malaria?


but it is slow to develop

and reinfection is common due to antigen variability of the parasite surface.


Malaria: treatment?

Chloroquine (resistance is common) 

Atovaquone-proquanil (malarone) if patient is there is resistance to 1˚ treatmetn or if the patient has eczema (chloroquine is contraindicated in these patients)

add Primaquine (for latenet form of P. vivax)


Malaria: prevention?

Insecticide-treated bed nets

mosquito control


Babesia: what causes it?

what dz is it related to?

transmitted how?

Where is it endemic?

Caused by Babesia microti

Related to malaria (both erythrocytic infections)

Transmitted via tick (same tick as Lyme disease: deer tick)

Found in Europe and US, esp northeast coastal islands like Martha's Vineyard! (seen in New England)


Babesia: what other parasite/dz does the RBC cycle resemble?

What patients are at risk for serious disease from Babesia?

RBC cycle resembles that of P falciparum (48h febrile cycles)

Causes serious dz in asplenic patients (there's no way for them to filter out the infected RBCs)


Babesia life cycle:

we don't need to know the (complex) tick part of the cycle, but what is the life cycle within humans?

Human bitten by tick.

Babesia enters RBC, goes through cycle in RBC (including phase that looks like a tetrad). 

Then RBC bursts open; some parasites infect other TBCs.


What's this?

How can we distinguish it from a very similar parasite?

Babesia on blood film.

Distinguish from malaria because Babesia has intracellular and extracellular rings. Malaria: we hardly ever see extracellular parasites.


What's this?

Diagnostic tetrad (trophozoite) stage for Babesia.

There are also extracellular forms as below, but the tetrad is classic.

(Tetrad is unique and a result to the way Babesia replicates: entire ring structure at once, rather than expanding cytoplasm then replicating nuclear material, as with malaria)


P falciparum or Babesia?

P falciparum

rings are of consistent size. May see brown areas due to breakdown of Hgb within RBCs


P falciparum or Babesia?


tetrad (sort of); rings are of varying sizes, never see brown areas (as with malaria since malaria breaks down Hgb)


Babesia: treatment?

Depends on severity.

Mild or asx: may not treat

Symptomatic: Combination therapy (atovaquone/azithromycin; clindamycin/quinine)

Severe: blood transfusion possible


Co-infection: if you have a patient from the coast of Maine, what 2 diseases might you think they are infected with?

Borrelia burgdorferi (-> Lyme disease)

Babesia microti

also: Anaplasma (-> dystentery - we didn't need to know this one)


Three (sort of 2) parasitic diseases in AIDS patients?

1. Pneumocystis pneumonia (not a parasite but historically was thought to be)

2. Toxoplasmosis (encephalitis)

3. Cryptosporidiosis (diarrhea)

4. Amebiasis (dysentery) dntk but just in case.


oversimplified: treatment of anaerobic protozoa (Giardia, Trichomonas)?