Micro U2 L1 pt 2. Flashcards
How does transmission of most parasitic infections spread?
mosquitos, ticks, specific flies, other arthropods
What is human to most parasitic infections?
intermediate host. sexual reproduction occurs in vector associated with transmission of agent
Plasmodium
protozoan parasite - malaria
Which area of the world is most affected by malaria and why?
africa - very efficient mosquito (anophele gambiae complex); predominant parasite species is plasmodium falciparum; warm weather = year round
What transmits malaria?
anopheles mosquitos - usually by female mosquitos
What are the four parasite species that cause malaria in humans?
plamodium falciparum, vivax, malariae, ovale
Plasmodium falciparum
most fatal outcomes - sub saharan africa, SE asia, S america
Plasmodium vivax
most common, seen in US - NOT seen in sub saharan africa
Plasmodium malariae
all malarious areas, but spotty
Plasmodium ovale
tropical areas - africa; SE asia, S america
What are the clinical symptoms of malaria due to?
schizont rupture and destruction of erythrocytes
What are the prodromal symptoms of malaria?
fever, chills, headaches, diaphoresis
What are malarial paroxysms?
febrile attacks following the prodromal symptoms - exhibit periodicities (24 hrs for vivax, ovale, falciparum and 72 hr for malariae)
What are natural protections against malaria?
- hg C, S (sickle cell) 2. Duffy antigen - lack this = low incidence 3. thalassemia
What are the stages of the malaria paroxysm?
- cold stage (lysis of RBC) - intense cold feeling, shivering, 15-20 min 2. hot stage - due to circulating and innate immune response - intense heat, dry burning skin, throbbing headache, 2-6 hr 3. sweating stage due to infection of additional erythrocytes and immune system shutting off - profuse sweating, declining temp, exhausted and weak, 2-4 hr
What are the major complications of severe malaria?
cerebral malaria, pulmonary edema, acute renal failure, severe anemia, bleeding
What are the most common metabolic complications of malaria?
acidosis and hypoglycemia
PfEMP-1 antigen
on 100% of RBCs
What causes stable stationary adherence of the parasitized RBCs?
CD36 and chondroitin sulphate A (CSA) - surface of P falciparum trophozoite and schizont infected RBCs is covered with knob-like excrescences made up of the PfEMP-1 antigen
How does p falciparum modify the surface of RBCs so that asexual parasites and gametocytes can adhere to the endothelium and asexual parasites can adhere to the placenta?
knob-like excresences made up of PfEMP-1 antigen
Cerebral malaria
most severe neurological complication of infection with plasmodium falciparum - breakdown of BBB due to cytoadherence of infected RBCs and vascular sequestration of infected erythrocytes
Placental malaria
accumulation of parasitized erythrocytes and monocytes in the placenta, direct adverse birth outcomes
Malaria relapse
reactivation of infection via hypozoites released from the liver (with vivid and ovale only) - second drug should be given with these types to help prevent relapses
Malaria recrudescence
parasitemia falls below detectable levels and later increases to detectible level = re-attack of malaria due to surviving malaria parasites in RBCs. Due to: 1. incomplete or inadequate treatment 2. antigenic variation 3. multiple infections
Malaria Treatment
chloroquine (RBC stage) and paraquinine (liver stage for ovale and vivax)
American Trypanosomiasis
Chagas disease - chronic, systemic parasitic infection by trypanosoma cruzi - NOT intracellular
Who does Chagas disease affect?
Latin america
What do people with chagas disease develop later on?
cardiomyopathy, digestive megasyndromes (esophagus and colon esp), or both
What transmits Cagas disease to humans?
large, bloodsucking reduviid bugs (tick like) - also by blood transfusion and mother to infant
What is the method of transmission from reduviid bug to human?
bug takes blood meal and releases trypomastigotes in feces near bite wound - enters through wound or intact mucosal membranes (conjunctiva)
What is the classic sign for Chagas infection?
Romana’s sign - swelling of the eyelids near the bite or where the feces was rubbed into eye
What are the clinical manifestations of Chagas disease?
initial infection - acute infection 4-8 weeks, chronic for life
Acute phase of Chagas disease
asymptomatic - might have self-limiting febrile illness - resolve spontaneously in about 90% of infected individuals
Chronic chagas disease
cardiac, diestive, cardidigestive disease usually 10-30 years after initial infection
Chagas heart disease
low intensity, slowly progressive that leads to impairment of contractile function and dilatation of all four chambers. most frequent and serious manifestation of chagas
What are the causes of death in chagas heart disease?
sudden death, refractory heart failure, thromboembolism
Gastrointestinal dysfunction
mainly megaesophagous, megacolon, or both. megacolon = end segments causing abdominal distention, large bowl obstruction, prolonged obstipation. megaesophagus = dysphagia with odynophagia, epigastric pain, regurgitation , ptyalism (excessive saliva), malnutrition (severe)
Diagnosis of chagas
acute: microscopic detection of trypomastigotes in blood. chronic: presence of IgG antibodies against T cruz antigens
Toxoplasmosis
T gondii - coccidian parasite- humans intermediate host so uncommonly cause disease in humans
When does toxoplasmosis cause disease?
usually fetuses and immunologically impaired individuals - typically by food borne transmission (undercooked meat) or CATS MEOW (litter box)
Congenital Toxoplasmosis
Classic triad: chorioretinitis, hydrocephalus, intracranial calcifications. Transmission risk greatest during 3rd trimester, but earlier the infection = more severe symptoms
Pathogenesis of toxoplasmosis in healthy people
often no symptoms - if there are = flu-like - also most common cause of posterior uveitis - parasite remains in body in inactive state
Toxoplasma ocular infection
results from congenital infection or infection after birth. symptoms: eye pain, photophobia, tearing of the eyes, blurred vision
How does reactivation of ocular infection appear on exam?
white fluffy cottony lesions
What is the diagnostic method to determine infection with toxoplasma?
toxoplasma specific antibodies
Lesihmania
found in desert - affect military - usually cause skin lesions and liver shit
