Microbiology: proteozoa Flashcards
Giardia Lamblia
Giardiasis
Flagellated water-based protozoan that is either in a multinucleated tropozoite form or a cyst form in the human body
Produces giardiasis which is a diarrheal disease from drinking the cyst forms from contaminated/untreated water
Giardiasis:
1) acute symptoms: (7-14 days after exposure)
- diarrhea
- malaise
- ab pain
- extreme flatulence
- nausea/vomiting
- malodorous stool (foul smelling stool)
- steatorrhea (fatty stools that float in water)
2) chronic symptoms: (>18 days)
- all of #1 symptoms
- weight loss
- borborygmus (fluid/gas moving upon listening to Bowels
- malaise
- depression
- can cause electrolyte deficiency symptoms as well and growth delay in children*
Treatment:
- Metronidazole*
- paromomycin (in pregnant/lactating patients only)
Entamoeba histolytica
Amoebasis
A anaerobic protozoan dysentery infection
- causes symptoms via trophozoites binding to intestinal epithelial cells in the colon and releasing lytic enzymes -> epithelial cell damage
endemic to Africa/Central America/Asia and is found in contaminated/untreated water consumption. is highly infectious (even through sexual contact in some cases). Most cases are in immunocompromised individuals
Amebasis: destruction of GI and blood vessel epithelial tissues.
- 20% cases are asymptomatic*
- ulcerative colitis
- GI ulcers that are “flask-shaped”
- sepsis
- blood diarrhea
- distention
- ab pain
- fever/weight loss
- right upper quadrant pain
- jaundice
- coughing
Treatment:
- metronidazole*
- paromonmycin/iodoquinol for liver cysts
- broad spread antibiotic (if sepsis is suspected)
- surgery (if heavy bleeding, toxic megacolon or ruptured liver abscesses are present)
Cryptosporidium
Intracellular protozoan that causes either mild diarrhea (immunocompetent) or life-treating blood diarrhea (immunocompromised)
endemic to tropical countries and is infectious especially though children and through sexual partners. Infects humans via oocyte form
Treatment:
- immunocompetent = nitazoxanide
- immunocompromised = azithromycin and other antimicrobial therapies in combination
Naegleria Fowleri
Primary amebic Meningoencephalitis
Thermophilic free-living ameba found in stagnant freshwater. Super rare infection that is 95% fatal.
3 life cycle phases:
1) cyst:
- dormant survival immobile phase
- is a smooth single-layer cell wall w/ a single nucleus pathogen
- form in unfavorable conditions for life
* almost never seen in humans
2) trophozoite
- *feeding/reproductive phase
- *infectious phase also
- can transform from 1->2 at around 25C with habitual conditions
- reproduction occurs via binary fission at around 42C
- is the most commonly seen form in humans
3) Bifagellate
- motile and highly infectious stage*
- pear shaped body with two flagella
- can transform from 2 -> 3 when changes in fluid ionic concentration occurs
- is only seen in humans when it is in the CNS
- enters humans via swimming in infected water, attaches to olfactory epithelium, and crosses through the cribiform plate -> olfactory bulbs -> brain*
Primary amebic meningioencephaltiis: (symptoms appear 1-9 days after exposure)
- fowleri ameoba feeds on RBCs/WBCs and astrocytes in the brain
- meningitis symptoms w/
- change in smell/taste sensation (sometimes complete loss)
- headache
- seizures
- fever/nausea
- subarachnoid hemorrhages w/ multiple infarcts on imaging
- CSF shows amebas
- can be grown on agar w/ E. Coli already on it. Put 1 drop of CSF on agar, incubate at 37C and look for clearing tracts through the E.coli colonies (amoeba eating the E. Coli)*
Treatment:
- amphotericin + fluconazole (if possible)
- Milteofosine
- 95% chance the patient dies even with correct treatment
Toxoplasma Gondii
Toxoplasmosis
Obligate intracellular amoeba that can infect all animals, but is primarily found in cats and their feces or improperly cooked meat
is the sole reason for why pregnant women shouldn’t be near cats or change cat litter. The amoeba can cross the placenta and infect the baby, even if the mother is asymptomatic
Life cycle:
1) sexual reproduction
- human/animal consumes infected animal meat or inhales animal feces
- parasite gets to the stomach and infects intestinal epithelial cells.
- parasites undergo sexual reproduction and form millions of zygote oocytes.
2) Felid shedding
- infected epithelial cells rupture and release oocytes into intestinal lumen and shed in feces and spread into soil/water/food
3) infection of intermediate host
- ingestion of oocytes by warm blood ed animals
- oocytes dissolves in stomach and small intestines, releasing sporozoites
- these cells invade intestinal epithelium and turn into tachyzoites and undergo asexual reproduction
4) formation of tissue cysts
- rupture of intestinal epithelium causes hematogenous spread and immune response
- turn into bradyzoites (slow dividing dormant cells that cant be killed by normal immune system and implant on tissues, usually brain/eyes or striated muscles)
- forms tissue cysts that occasionally rupture and spill Bradyzoites out and cause infection
Toxoplasmosis symptoms:
1) immunocompetent hosts
- active = mild flu symptoms,
- latent = asymptomatic
2) immunosuppressive hosts
- active = headache/AMS/ ataxia/ seizures/ dyspnea. (Life threatening)
- latent = asymptomatic (but is rare in immunosuppressive populations)
3) congenital toxoplasmosis(chorioretinitis)
- unilateral decrease in visual acuity
- hydrocephalus
- intracranial calcifications on imaging
- seizures
- lymphadenopathy
- hepatosplenomegaly
Diagnosis
- CT or T2-MRI shows lesions in basal ganglia/corticomedullary junction
- PCR shows toxoplasma gondii DNA in blood/serum/CSF
- IgG is stupid high (past infection)
- IgM is stiupid high (acute infection)
Treatment:
- prophylaxis = TMP-SMX
- acute = pyrimethamine + sulfadiazine/clindamycin/spiramycin therapy
- latent = atovaquone + clindamycin
- Chorioretinitis = pyrimethamine + sulfadiazine + foilnic acid (triple therapy)
Trypanosoma Brucei
African sleeping sickness
Protozoa transmitted via the tsetse fly that is endemic to Africa (is also a really painful bite)
shows trypomatigotes in blood smears and CSF (only in stage 2 for CSF though)
Has two stages: hemolympahtic stage and meningoencephalic stage
Symptoms:
1) hemolymphatic stage
- headache
- malaise
- pruritis and arthralgia throughout body
- hepatosplenomegaly
- weight loss
2) meningoencephalic stage
- recurrent fever
- reversed sleep cycle (somnolence)*
- mental delirium and hallucinations
- ataxia/tremors
- paresthesia, anesthesia or hyperasthesia
- seizures
- ultimately coma and death
Treatment:
- suramin = 1st stage only
- melarsoprol and suramin = 2nd stage only
Acanthamoebas
Single-celled eukaryotes that can be found in almost all water sources other than saltwater. Also hospitals and air conditioners.
- cans be metabolically active trophozoite or a dormant stress resistant cyst (the former form is in mostly immunocompromised, the later in immunocompetent)
really only dangerous in immunocompromised individuals
Granulomatous amoebic encephalitis (GAE)
- ONLY seen in immunocompromised, cirrhosis, renal failure or acute lupus patients.
- paradise enters body through inhalation or cutaneous lesions and through hematogenous spread enters the CNS.
- causes mass neuronal damage and immune response in the brain. Also forms granulomas, but the shear number of new things in the brain in such a small amount of time causes encephalitis
- 95% fatal
- headaches/seizures/AMS/ataxia/delirium.
Endosymbiosis: * can increase seocondary infection resistance and virulence
- most common endosymbiosis = legionella, A.aureus and pseudomonas aeruginosa
Treatment:
- pretty much all anti-fungal meds + TMP-SMX + macrolides
- surgical resection of cerebral lesion
Leishmania species
(Visceral leishmaniasis “Kala-azar ”)
(Cutaneous leishmaniasis)
Flagellated parasitic protozoan that is commonly transmitted to humans via *sandfly bites
- endemic to Africa/Asia and India
- Can also be caused by infected dog bites
Cutaneous leishmaniasis: most common
- skin ulcers that look similar to leprosy
- very disfiguring
Mucocutaneous leishmaniasis:
- same as cuteness but also mucosal ulcers usually on th nose
- often causes mid facial destruction
- hoarse voice/gingivitis/periodontitis are all present
- very rarely hits genitals, in which case can destroy them*
Visceral leishmaniasis (Kala-azar disease)
- most severe and is systemic
- disables NK cells so can often reappear even with proper treatment
- spiking Fever/weight loss/ hepatosplenomegaly/ pancytopenia/ ab tenderness
- often shows symptoms of ML/CLabove
diagnosis is blood smear showing macrophages containing amastigotes for all three possible forms
Treatment:
- CL = paromomycin, mitefosine and fluconazole.
- ML = liposomal amphotericin B, mitefosine and pentamidine
- VL = liposomal amphotericin B, mitefosine
Trypanosoma Cruzi
Chagas’ disease
Protozoan disease transmitted to humans via the kissing bug “triatomine insect” feces/bites
- endemic to central/South America
- this parasite can cross the placenta
Chagas Disease (takes 2 weeks after infection onset)
Acute phase possible symptoms
- romana sign* (eye swelling (not always present though))
- pericardial effusions
- flu-like symptoms
- hepatosplenomegaly
Chronic phase possible symptoms:
- usually asymptomatic
- dilated cardiomyopathy W/ apical atrophy
- ataxia
- ventricular fib. W/ CHF
- megacolon/esophagus
- meningioencephalitis (late stage chronic)
diagnosis is blood smear shows trypomastigotes
Treatment:
- Benzindiazole or/and Nifurtimox
Trichomonas vaginalis
Vaginitis
A protozoan parasite that cannot form cyst life forms (so it has to live inside a human or other vector)
Symptoms: Men: * usually asymptomatic - pain while peeing or having sex - increased urination - swelling and redness around the glands of the penis Women: - foul odor - green discharge e - puritis, urethritis and burning sensation - pain while peeing or having sex
diagnosis is made with the presence of trophozoites on wet mount from vaginal swab
Treatment:
- metronidazole (for both patient and any partner they have had or have)
Babesia microti
Babesiosis
An ameoba that is spread by the Ixodes tick (tick that also spreads Lyme disease and anaplasma species)
- hence why Babesiosis and Lyme disease are often seen as co-infections in 66% cases of either.
Risk factors:
- endemic area (northeast/Midwest and western US)
- May-September months (summer)
- 50 years old or older
- being male
- asplenia* (very common in these people)
- immunosuppressive patients
- premature birth
- having Lyme disease or anaplasma infections
Babesiosis symptoms: is often misdiagnosed since it looks like flu in non-severe, and malaria in severe
1) acute (nonsevere)
- fatigue/chills/sweats
- Fever
- headache, myalgia, arthralgia
- anorexia and nause
- non productive cough
2) chronic (severe) more common in immunocompromised
- intense fever/malaise and fatigue
- presence of hemolytic anemia
- diagnosis is the “Maltese cross” formation in erythrocytes that are seen under microscope w/ low hematocrit*
Treatment:
- *azithromycin + atovaguone (symptomatic only)
- if asymptomatic give nothing
- DONT GIVE ANTIBIOTICS AS PROPHYLAXIS*
Cycle fever patterns with each plasmodium species (malaria)
P. Knowlesi = 24 hrs
P. Viviax = 48 hrs
- “tertian fever”
P. Ovale = 48 hrs
- “tertian fever”
P. Malariae = 72 hrs
- “quatrain fever”
P. Falciparum = irregular and varies
- “malignant tertiary fever”
Plasmodium species
malaria
Protozoa that is spread via anopheles mosquito.
- primarily endemic to sub-Saharan Africa, South Asia, and Latin America but there are isolated cases in South America and south-eastern US
Most common/risky populations:
- pregnant women
- immunocompromised people
- young children under 5 yrs
- travelers to endemic regions that have no prior exposure or drinking of tonic water
- people who have G6PD
Signs/symptoms:
- extreme fatigue
- Jaundice
- headaches
- splenomegaly
- recurrent fever in varying hrs based on subspecies
- organ failure (usually P. Falciparum only)*
- AMS/seizures and coma (cerebral malaria ONLY (caused by P. falciparum))
- diarrhea
- vomiting
- sepsis (usually on P. Falciparum only)*
Diagnosis
- through thick (shows the parasite “schizont and ring apperance”)in RBCs and thin (shows specific species)
- if % of RBCs are 5% or greater = parasitemia w/ malaria and causes the worst outcomes if not using blood dialysis*
Treatment:
- chemoprophylaxis = atovaquone/proguanil or chloroquine
- active treatment:
1) chloroquine/hydroxychloroquine (first line for all species that are not P. Falciparum)
2) artesunate + mefloquine or amodiaquine (1st line for P.falciparum and 2nd line for all others)
3) atovaquone + proguanil (1st line for all drug resistant strains) - radical treatment (kills hypnozoites) =
1) atovaquone + primaquine + proguanil/doxycycline - cerebral malaria/ disseminated malaria
1) quinidine + doxycycline + Clindamycin + artesunate
CANT USE SAME MEDICATION FOR
TREATMENT THAT WAS USED FOR PROPHYLAXIS
- MUST TEST FOR G6PD BEFORE TREATMENT*
Life cycle stage of plasmodium species
1) blood stage
- gametocytes in host are eaten by female anopheles suckling blood from the host
- gametocytes multiply and growth in 10-18 day cycle
- at this point they become sporozoites
2) infectious stage
- sporozoites conjugate in female anopheles salvia
- female anopheles feeds on another human and the sporozoites spill into the blood stream
- sporozoites hemotogenously head to the liver and undergo rapid hepatic parenchymal cell invasion
- undergo asexual reproduction at this point for 7-14 days and become meroxoites
2b) exoerythrocytic phase (ONLY P. Vivax/Ovale)
- meroxoites go into dormancy in hepatocytes for months to years (Hypnozoites)
- eventually they go into blood RBC phase
* this is why some malarial cases have a long delay from exposure -> symptoms*
3) erythrocytic stage:
- meroxoities invade RBCs and undergo asexual reproduction for 2-3 days
- meroxoties transforms into schizonts (presence can diagnose malaria w/ “ring form” in the RBC or Schizont)
- symptoms become prevalent at this point
What is the “Duffy antigen”?
A specific RBC antigens that P. Vivax needs to bind to get into RBCs and multiply
- patient who have sickle cell disease DONT have this receptor, so they are effectively immune to P. Vivax malaria (also P. Falciparum)
