4/14 Parasitology and Travel Med II + Ch 8 Flashcards
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?
Trophozoite
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?
Giardia
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?
why?
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?
Cryptosporidium:
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?
-Metronidazole
(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
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)
This is an acid-fast stain from a patient with profuse watery diarrhea.
Dx? Tx?
Cryptosporidium
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)
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
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?
(falciparum)
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)
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.
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?
Babesia
tetrad (sort of); rings are of varying sizes, never see brown areas (as with malaria since malaria breaks down Hgb)
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)
