ingested protozoans and Vector-borne Apicomplexans/Kinetoplastids and STI Flashcards
Entamoeba Histolytica
Infective cysts in formed stool, asymptomatic
Transmission: Fecal Oral, anal sex, vectors (flies and cockroaches)
Pathology: Carriers (asymptomatic, shed massive amounts of cysts). Intestinal amebiasis (dysentery) colon, w/ bloody stool. Extraintestinal Amoebiasis (rare-goes to liver, fever)
Diagnosis:cysts in stool+trophozoites in bloody diarrhea, the e.histolytica eat RBCs, aspirate liver abcesses, travel
Treatment: Paromycin for luminal phase, Metronidazole/tinidazole
Giardia duodenalis
you eat cysts from bloody water:
Transmission: Fecal/oral, direct person to person, oral anal sex
Epidemiology: Occurs worldwide
Pathology: Asymptomatic w/ sudden onset. Watery fatty stool, VA, V-B12
Diagnosis: stool examination
Treatment: metronidazole, tinidazole, nitazoxanide For pregnant (paromomycin)
Apicomplexan Parasites
Obligate intracellular
Apical organelle for host cell invasion
Complex lifecycles alternating between asexual (Schizogony) and sexual reproduction (sporultation)
Sexual cycle in intestinal epithelium of the definitive host :
For ingested apicomplexans:
Cryptosporiduem hominis/parvum- humans
Toxoplasma gondii- felines
For vector born apicomplexans:
Plasmodium spp.-mosquitoes
Babesia microti-ticks
Cryptosporidium SPP (Hominis/ Parvum)
Transmission: Fecal/oral, oral/anal
Epidemiology: AIDS pts
Pathology:Syptoms like Giardia, but shorter w/ more fluid loss
Diagnosis: detection of oocysts in stool (acid fast)
Treatment: Nitazoxanide
Toxoplasma Gondii
Transmission: Undercooked meat w/cysts, Fecal oral (from cat or soil oocytes, transplacenta, blood transfusion/organ transplantation
Epidemiology: any animal can be a host (AIDS)
Pathology: intitial infection asymptomatic, Cell mediated immunity
Diagnosis: Serology MRI
Treatment: pyrimethamine/ sulfonamide
Plasmodium (malaria) species
Mosquito will spit in blood, send in spirozoites, then those will live in liver cells, then they will migrate into blood cclls (merozoites) creating trophozoites, the trophozoites reproduce and burst to infect other blood cells. Then a mosquito will bite again to uptake a male or female (sexual)
Africa: falciparum (shortest incubation time) All RBCs
Asia: vivax only reticulocytes
knowlesi: malaysia (rare, humans are accidental host)
definitive host: mosquito
intermediate host: humans
transmission: vector (mosquito) and congenital and needle transfer
Shaking and baking (fevers and chills)
Vivax and Ovale have fever eVery Other day
Pathology of uncomplicated Malaria
Fever, splenomegaly, jaundice, anemia, Shake and Bake, nausea and vomiting, Body aches, just bad shape
Pathology of severe Malaria
almost all deaths resultant from falciparum
Vital organ dysfunction, abnormalities in blood clotting or metaboluc complications (hypoglycemia, acidosis)
Three most common: Cerebral Malaria, Acute REspiratory Distress Syndrome, Sever Anemia
Cerebral Malaria
unarousable coma due to Malaria, its seen in 1% of Falciparum infections. Children older than 2 are at risk (IgG is gone…maternal immunity is gone)
Cause-infected RBCs adhere to the vascular endothelium plugging blood vessels in brain
Acute REspiratory Distress Syndrome (ARDS)
Same concept as cerebral, but pulmonary capillaries and venules are packed with parasitized RBCs and inflamatory cells. Pro inflammatory process increases vascular permeability leading to edema
Severe Anemia
Causes- microbe mediated hemolysis of parasitized RBCs, Ab-mediated destruction of non-parasitized RBCs coated w/ parasite proteins (opsonin or C)
Decrease in erythropoiesis
Diagnosis of Malaria
Microscopy, parasites will be seen on thick and thin smear
Falciparum (multiple rings, stages of maturation, crescent shaped gametocytes, infected RBCs are not enlarged)
PCR, Rapid Diagnostic Test sometimes used
immune evasion: RBCs lack MHC1, malaria can change Ag
immunity is short lived and incomplete
Location: hepatocytes and erythrocytes
Treatment: none
Prevention: Avoidance
Babesiosis
Intracellular sporozoan parasites, resembles Plasmodia
Cause: babesia microti
Cells infected: RBCs only
Hosts: Definitve (deer tick), intermediate (mouse etc), accidental (humans) (north east, midwest)
Transmission: nymph stage of tick bites you, blood transfusions, congenitally (during pregnancy)
incubation: 1-9 weeks
diagnosis: false negative. microscopy (maltese cross differentiates it from malaria)
Kinetoplastids
obligate intracellular parasite, flagellated
Trypomastigote, amastigote, promastigote, epimastigote
Leishmania
Female sandfly (phlebotomus and lutzomyia)
Reservoirs: lots of animals
Causes leishmaniasis:
Cutaneous (oriental sore)-most common
Mucocutaneous/mucosal-least common
Visceral (kalaazar/ black fever)- most serious
Sandfly will infect skin and get into macrophages