Trif Protozoa and Helminths
Terms in this set (41)
two successive bites of ANOPHELES mosquito.
Plasmodium falciparum, vivax, malarie, ovale.
Pathogenesis of malaria:
1. mosquito inoculates hosts with SPOROZOITES living in gut
2. sporozoites go to liver of host and infect liver cells
3. parasite divsion in liver causing MEROZOITES
4. merozoites leave live and go to blood to infect RBC
5. RBCS: parasites grow in membrane bound digestive vacuole hydrolyzing HGB with enzymes-->now called trophozoites (single chromatin mass)-->schizonts (multiple chromatin masses)-->new merozoites
6. RBC lyses: new merozoite infect other RBCs
7. parasites develop int sexual GAMETOCYES that infect the mosquio when it takes a meal
8. mature in mosquito gut until infective stage
What are the host defenses against malaria?
1. antibodies to sporozoites prevent hepatocyte invasion
2. interfoeron gamma inhibit liver stage
3. CTL lyse hepatocytes
4. ABs to merozoites prevent RBC invasion
5. P. vivax requires a DUFFY ANTIGEN to enter RBC
6. Antibodies to antigens on infected RBC can eliminate cells
7. cytokines destroy RBC that is infected
8. sickle cell provide a poor environment
Morphology for P. falcipurm
infected RBC gets to endothelium---foci of ischemic necrosis.....RES is stimulated and produces HEPATOSPLENOMEGALY....spleen becomes fibrotic and brittle.
P. vivax ovale and malaria cause
low parasitemia, mild anemia, rare splenic rupture
P. falciparum causes
BLACK WATER FEVER ! intravascular hemolysis= jaundice, hemoglobinuria, acute renal failure
Microscopy of malaria
p. falciparum in the walls of blood vessels in brain/retinal arteries....clinical: paroxysmal crises of fever, chills, HA, malaise....encephalopathy.
Diagnosis of p. falciparum
demonstrate parasite in thin/thick blood smears.....SEAL-RING CELLS (trophozoites)
sand fly bite ....vector= sand fly Phlebotomus papatacii (Old ) and Lutzomia longpapi (New World)
mexicana.....cutaneous form causing indolent ulcers ...middle east= "Baghdad Boil"
muco-cutaneous form....nose destroying ulcers (reservoir= rodents and sloths)
visceral form..KALA AZAR...humans, dogs, jackals, foxes.
Clinical aspects of L. donovani
Kala azar is Hindu for black fever....no symptoms in the begninning but severe systemic disease (hepatosplenomegaly, lymphadenopathy, BM suppresiion, fever, hyperpigmentation of skin in the extremties)....pancytopenia from BM suppresion causes death through thrombocytopenia and predisposition to secondary infections.
Macroscopy of L. donovani
spleen weight is 3 kg...LN size is 5cm in diameter
microscopy of L. donovani
LNs with macrophages loaded with parasites
"sleeping sickness"....T. rhodensi = acute dz and kill patient in 3-6 months.....T. gambiense= evolve more than 1 year......transmission from Tsetse fly, reservoir: humans ONLY.........pathogenesis: blood and lymph, disseminate into BM and invade the CNS......CLINICAL: lethargy, apathy, coma..DIAGNOSIS: demonstrate parasite in blood or CSF
Chagas Disease and American Trypanosomiasis.....flagellate protozoa penetrate human skin through scratches (from shit of blood sucking bugs).....endemic in rats, cats, dogs, armadillos
T. cruzi info
vector= kissing reduviid bug....Acute manifestation: subQ inflammatory nodule "chagoma" and unilateral palpebral edema "Romana's sign".
Chronic manifestations of T. cruzi
1. heart: destroy conductive system and myocytes....chronic myocarditis ....complete heart block, ventricular aneurysms....most important cause of death from heart disease in Latin American countries...
2. esophagus/colon= myenteric plexus destruction loss of autonomics (megacolon)
caused by ingestion of OOCYSTS....Paris because of eating raw-undercooked meat and having CATS as pets.......zoonotic hosts= CATS....intermediate hosts= chicken sheep pig that ingest cyst, meat is infection. contaminated food water
Pathogenesis of T. gondii in immune competent
mild and self-terminating.....lymphadenopathy in upper cervical LN, fever, malaise, and CHORIORETINITIS
Pathogenesis of T. gondii in immunosuppressed, fetus, baby
serious...reactivation of latent infection causes pneumonia and encephalitis
Non immune pregnant mothers, warning:
incection can be transmitted to fetus, causing congenital toxoplasmosis:: abortion, still birth, abrnomalities
Three clinical forms:
1. Lymphadenopathy syndrome
2. Devastating form: HIV/AIDS
3. congenital toxoplasmosis
necrotizing encephalitis from T. gondii:
loss of brain parenchyma- atrophy....cerebral calcifications marked hydrocephalus
What is a host response to Helminth infestation?
1. eosinophilia= peripheral blood and in tissues invaded in larva
2. inflammatory rxn= produced by larva/egg deposits in tissue
3. hypersensitivity rxn= when migratory larvae invade tissues
Cestodes are intestinal Tapeworms
1. Taenia saginata (beef); Taenia solium (pork)= Cysticercosis
2. Diphylobothrium latum= fish
ingestion of larvae in undercooked meat/fish
*cystic larvae of T. solium found in any part of body, eye, muscle or brain
**D. latum sucks blod absorbing B12 and causes megaloblastic anemia
Echnococcus granulosis- Cestode
Causes HYDATID Disease
- dog tapework: endemic in sheep, goats, cattle.....larvae ingested with infested food....penetrade bowel wlal and carry to liver, lung, kidney, muscle.....develop into hyatid cysts
domestic dogs and cats....alveolar hyatid dz...pulmonary cysts
T. spiralis info
encysted larva in muscle of PIG BOAR RAT BEAR WALRUS......mmost common source is raw pork or boar meat.......invade intestinal tract, blood and STRIATED SKELETAL MUSCLES with richest blood supply (diaphragm, extraocular, larynx, deltoid, gastroc)
Morphology of T. spiralis
coiled larvae of 1 mm surrounded by VACUOLES WITHIN NURSE CELLS ....around are new blood vessles and infiltrate with eosinophils and mononuclear cells....calcifications cause scars......clinical froms: asymptomatic. S
Symptoms of T. spiralis:
periorbital edema, vasculitis (splinter hemorrhages), diarrhea, myositis, eosinophilia
Schistosoma hematobium, S. masoni, S. japonicum cause blood flukes: Schistosomiasis (Bilharziasis)
Transmission of Flukes
wading in water containing infective larvae stage....penetrate human skin...enter blood stream and inhavit lung, liver, intestine, urinary bladder........FEMALE WORMS deposit eggs in colon and liver (mason and japon). and bladder (haematobium)....ALL casue GRANULOMATOUS inflammation
Clinical manifestations of fluke
hematuria, hepatic fibrosis, portal HTN, pulmonary fibrosis..
**S. haematobium determines high incidence of squamous carcinoma of bladder!
Brugia malayi and Wucheria bancrofti....human hosts...vectors are 80 species of mosquitos. Adult worms inhabit LYMPHATICS, EPIDIDYMIS, TESTIS = granulomatous reaction
Symptoms of Filariasis
1. acute: fever, malaise.....pulmonary eosinophilia
2. late: lymphadenopathy, lymphangitis, lymph obstruction, lymphedema, ELEPHANTIASIS, warty skin.