Protozoal Infections Flashcards
Protozoal Overview
single celled eukaryotes
three classes: amebae (pseudopoda), flagellates (flagella), sporozoites (nonmotile)
Malaria
mosquito-borned, hemolytic febrile illness
P. falciparum (most severe/deaths), P. vivax, P. ovale, P. malariae
EPIDEMIOLOGY: underdeveloped countries, from female anopheles mosquito bite, Fal/viv most common,fal/ovale - africa, malariae- least common, mild
ETIOLOGIC: bug releases sporozoites -> liver (merozoites) -> young rbc -> rupture -> problems (fever, chills, anemia, HSM); falciprum ->MALIGNANT MALARIA (no exoerythrocytic stage, all rbc ages, more blood vessel obstruction)
PATHOLOGY: slate grey liver, spleen, LN; rbc stick to walls -> little circulating parasites, organ ischemia; giemsa stain blood smears stain malaria
CLINICAL FEATURES: recurrent paroxysms of chills and high fever, ischemic damage differs based on organ is effected; Rx chloroquine, primaquine, differs for falciprum
Babesiosis
malaria like disease transmitted by hard bodied ticks
EPIDEMIOLOGY: rare, organism invades erythrocytes-> hemoglobinemia, hemoglobinuria, renal failure
Babesia spp. resistant to most antiprotozoal drugs
Toxoplasmosis
Toxoplasma gondii
asymptomatic unless immunocomprimised (necrotizing disease)
EPIDEMIOLOGY/ETIOLOGIC: France, cat is only final host, two forms: tachyzoites (intracellular vacuoles cause rupture, spread through lymphatics) and bradyzoites (chronic infection, cysts causing nucleus to be pushed peripherally), fecal oral with oocytes, congenital transplacental from asymptomatic mother;
LATENCY: dormant tissue cysts in cells, can emerge if human becomes immunocomprimised
IMMUNOCOMPETENT: lymphadenopathy with epithelioid macrophages surrounding reactive germinal centers, associated symptoms: fever, sore throat, HSM, atypical lymphocytes; self limited, therapy not needed
CONGENITAL: necrotizing meningoencephalitis, cerebral calcifications, hydrocephalus, chorioretinitis, usually spon abortion results, when born - symptoms can vary, Rx with antiprotozoal therapy
IMMUNOCOMPRIMISED - usually reactivation, multifocal necrotizing encephalitis, fatal is not Rx with antiprotooal agents
Amebiasis
Entamoeba histolytica
lytic actions on tissue, usually colon and liver
EPIDEMIOLOGY: only known reservoir - human, reproduced in colon and passes in feces, places with poor sanitization
ETIOLOGIC: three stages- 1) amebic trophozoites - spherical/oval with thin cell membrane, PAS+, in colon transform into 2) precyst, stop eating, round, nonmotile, one nucleus, form glycogen masses and chromatoidal bodies then become 3) amebic cysts - infecting stage, in stools, do not invade tissues, spherical with thick walls, four nuceli, divide into 4 trophozoites in new host, attach to colonic epithelial cell and lytic protein breaches cell membrane, cell death leads to ulcer
PATHOLOGY: small foci of necrosis -> ulcers with irregular and sloughing mucosa (flask or bottle neck shaped), trophozoites present throughout ulcer, inflamm response only when ulcer enlarges, AMEBOMA - napkin ring constriction, invasion of wall, made of granulation tissue, fibrosis, trophozoites; if reach liver - necrotic cavity filled with semisolid material (anchovy paste) brown and odorless, can be contained or rupture with distant infestation
CLINICAL FEATURES: asymptomatic to dysenteric disease, 8-10 incubation period, abdominal discomfort, tenderness, cramps, malodorous flatus, liquid stools with bloody mucus, no dehydration, can last for years, Rx metronidazole (trophozoites) and diloxanide (cysts)
Liver abscess presents with severe RUQ pain, fever, weight loss, few have diarrhea or trophozites in stool, Dx made from imaging, Rx drainage and antiamebic drugs
Cryptosporidiosis
enteric infection, diarrhea in immunocomprimised
ETIOLOGIC/PATHOLOGY: fecal oralof oocytes, person to person; attach to small bowel microvilli, remain EXTRACELLULAR, progeny also attach, self limited in immunocompetent, can spread to local structures in immunocomprimsed
CLINIAL FEATURES: profuse watery diarrhea, cramping abdominal pain with low grade fever sometimes, severe dehydration fatal in immunocomprimised
Giardiasis
Giardia lamblia
small intestine infection with abdominal cramping and diarrhea
EPIDEMIOLOGY: children more than adults, fecal oral of cysts, epidemic outbreaks have occured
ETIOLOGIC/PATHOLOGY: trophozoites (flat, pear shaped, binucelate with 4 pairs of flagella, proximal small intestine, sucker plate helps with attachment) and cysts (2 or 4 nuclei, revert to trophozoite when reach intestine), stools have only cysts, trophozoites present with diarrhea, no gross alterations, microscopic: mucosal changes with crescentic or semilunar shaped trophozoites on villous surfaces and within crypts)
CLINICAL FEATURES: usually harmless commensal, but can be acute or chronic; acute: cramping, frequent bad smelling stools; chronic: malabsorption, weight loss, retarded growth; Rx antibiotics, including metronidazole
Leishmaniasis
EPIDEMIOLOGY: from phlebotomus sandflies, subtropical and tropical areas
ETIOLOGIC: sandfly bite -> mononuc phagocytosis -> transform into amastigotes and reproduce ->rupture and spread -> cluster of macrophages at inoculation site, three possible outcomes:
1)Localized cutaneous - “oriental/tropical sore,” leishman-donovan bodies, itchy solitary papule sore becomes granuloma and ulcerates, ulcer heals spontaneous, diffuse cutaneous develops in immunocompromised (multiple modules, resembles leprosy)
2) mucocutaneous - Leishmania braziliensis, complication of cutaneous leishmaniasis, solitary ulcer appears, expands, resolves, years later ulcer develops at mucocutaneous junction and erodes mucousal surface and cartilage ex. tapir nose, Rx antiprotozoal agents
3) visceral (Kala Azar) - Leishmania donovani, potentially fatal, reservoir differs in different places, HSM, LN enlargement, fever, weight loss, anemia, thrombocytopenia, leukopenia, skin darkening, cachectic, Rx systemic antiprotozoal therapy
Chagas Disease (american trypanosomiasis
insect borne zoonotic infection of heart and GI tract by T. cruzi
EPIDEMIOLOGY: central and south america, reduviid/kissing bug
ETIOLOGIC: bug poops on you -> you scratch -> trypomastigotes penetrate -> lose flagella and undulating membranes round up and become amastigotes -> go in macrophages and replicate -> enter cells and reduviid bug also eats during feeding -> chagomas form-> disseminates-> organ disfunction
ACUTE CHAGAS -> FATAL MYOCARDITIS: heart enlarges with pale focally hemorrhagic myocardium, pseudocysts in myofibers, fever, malaise, lymphadenopathy, HSM
CHRONIC CHAGAS -> HEART AND GI: after years, no protozoa present, just chronic progressive inflammation, heart is dilated, CHF, megaesophagus from achalasia/parasympathetic ganglia, megacolon with constipation from myenteric plexus destruction
CONGENITAL: transplacental, spon abortions, if born die of encephalitis after a few days
TREATMENT: antiprotozoal chemo effective for acute but not chronic, heart transplant has been effective
African Trypanosomiasis
Sleeping sickness, life threatening meningoencephalitis
Trypanosoma brucei gambiense (year infection) or trypanosoma brucei rhodesiense (3-6 months)
EPIDEMIOLOGY: hemoflagellate protozoa, glossina tsetse flies, humans only important reservoir
ETIOLOGIC: fly ingests trypomastigotes-> lose surface antigen coat -> multiply in gut -> salivary gland -> epimastigote stage ->multiply -> infect human lymphatics and blood vessels
PATHOPHYSIOLOGY: involves immune complex formation, can change glycoprotein antigen coat to evade immune system
PATHOLOGY: primary chancres are localized nodular lesions, lymphocyte and macrophage hyperplasia, brucei - destructive vasculitis in brain rhodesiense - brain and heart vasculitis
CLINICAL FEATURES: three stages 1) primary chancre - papillary swelling with central red spot at inoculation site, resolves within 3 weeks; 2) systemic infection - bloodstream invasion, intermittent fever, large spleen, myocarditis (rhodesian), sometimes other organdys function; 3) brain invasion - early in rhodesian, late in gambian, apathy, somnolence, coma, can be diffuse or focal
Primary Amebic Meningoencephalitis
Naegleria fowleri
fatal meningoencephalitis
