Parasites Flashcards
ingesting solid food particles
Cytostome
protozoa secrete a protective coat and shrink into a round armoured form
Cyst
when ingested into humans, this is the motile form of the bacteria.
trophozoite
creeping projections = pseudopodia
asymptomatie most of the time inside the host carrier
fecal-oral transfer
more common in homosexual men.
chromotoid bodies = ribosomes
10% of the time they invade the intestinal mucosa causing erosions. results in abdominal pain, a couple of loose stools a day with fecks of blood and mucus in the stool. can become severe, with bloody, voluminous diarrhea.
can cause liver abcesses, followed by spreading to the diaphram into the lung. pulmonary abscesses lead to death.
trophozites with RBC in the cytoplasm suggest active disease, while cycts or trophozites without internalized red cells suggest asymptomatic carriage.
diagnosis = antigen assays or CAT scan
prevention by good sanitation.
Entamoeba histolyca
microscopy cannot differentiate between H. histolytica and non-pathogenic intestinal protozoa Entamoeba dispar
looks like a kite.
reservour = rodents and beavers or clear mountain water.
adheres to the small intestine and interferes with fat absorbtion. leads to fatty poops with a
HORRIFIC ODOR
NO BLOOD IN STOOL
Diagnosis: stool with cysts, immunoassay kit to detect antigens in stool samples, or sanitation measures
Giardia Lamblia
is everywhere, causes diarrhea outbreaks, round oocyst that contain 4 motile sporozoites. list cycle within the intestianl epithelium causing diarrhea and abdominal pain. self-limiting. immunocompromised = life threatening due to losing 3-17 liters of stool per day.
Crytosporidium
severe diarrhea in immunocompromised pts. fecal-oral route. contaminated rasberries, ACID FAST STAIN, flurescent microscopy is alternative.
Isospora and cyclospora
STD, lives in vagina and male urethra.
itching, burning on urination, copious vaginal secretions. thin, watery, frothy, malodorous discharge in the vaginal vault. males are asymptomatic.
diagnosis: microscopic examination reveals highly mobile parasites. urine will reveal T. vaginalis.
Trichomonas vaginalis
Free-living meningitis causing amoebas?
Naegleria fowleri, Acanthamoeba, and Balamuthia mandrillis live in fresh water and soils
In fresh water, when they penetrate the cribiform plate into the brain and spinal fluid, they cause sudden deadly infection. most die within a week.
FOWL PLAY
fever, stiff neck, nausea, vomiting, history of swimming a week earlier, CSF: high N, low Glucose, High protein (just like bacteria) but NO GRAM STAIN AND CULTURE. microscopic examination shows amoeba.
Acute meningoencephalitis in normal hosts
mature amoeba ONLY in brain tissue (no cyst)
no corneal infection.
Nageria Foeleri
chronic, granulomatous, brain infection in immunocompromised pts. headache, fever, seizures, focal neurologic deficits. CSF show cyst stage and trophozoite stage.
CHRONIC meningoemcephalitis in immunocompromised
cyst and mature amoeba found in brain tissue
corneal infection: diagnose by scraping the cornea.
Acanthamoeba
CHRONIC meningoencephalitis in normal and immunocompromised hosts
cysts and mature amoeba found in brain tissue
granulomatous skin lesions - diagnose by skin biopsy.
Balamuthia mandrillaris
infects animals and within raw pork and cats.
sexual division within the cat and secretes live cysts. leads to fetal infections
fever, lymph nodes, liver, and spleen enlargment, meningies can be infected too. most common CNA infection in AIDS pts. symptoms like a tumor with a headache and focal neurologic defecits. retina reveal yellow-white, fluffy (like cotton) patches that stand out from the surrounding red retina. TORCHES
diagnosis: CAT of brain shows a contrast enhancing mass. , retinas will be inflammed, serology: elevated Ig titers suggest that the pt has at some tie been exposed to this organisim.
Toxoplasma gondii
in AIDS pts and fetus Toxoplasma gondii is TOXIC to the brain and eyes.
Major infections in AIDS patients?
Toxoplasma gondii and pneumocytstis carinii
flying saucer appearing FUNGUS. invades the lungs. most people have it by age 4. causes severe intersital pneumonia called pneumocystis carinii pneumonia (PCP)
chest x-ray shows bilatering intersitual infiltrates or can be normal.
Pneumocystis carinii (PCP)
timing of different Malaria bursts
Pf = 36-48 hr Pv = 48 hr Po = 48 hr Pm = 72 hr Know the life cycle!
Two malaria parasites that can be dormant in the liver? and what one is more aggressive? clinical signs?
Pv and Po can be dorment in the liver
high fever, chills, and profuse sweating at 48-72 hr intervals.
Pf is the most agressive invading so many RBC causing anemia and sickle cell, kidney, lung, and brain damage. death occurs in less than 5 years in sub-Saharan Africa due to cerebral malaria = seizures and impared conciousness, leading to coma.
pts will have HSM and spleen can rupture.
strains of malaria africans are immune to? how?
some africans are immune to Pv and Pf. Pf due to RBC membrane antigens DUFFY a and b. pF becuase of sickle cell anemia trait.
Diagnosis and control of malaria?
Diagnosis: thin and thick smears (1000X) of blood, under oil-immersion magnification, reveals the trophozoites and schizonts within RBS. rapid antigen based diagnostics are higly sensitve and specific.
Control: pestisides, DEET, chemical prophylazis of travelers, vaccination isnt ready.
Anopheles mosquito carries them within their salivary glands and infects while feeding. grow in the liver and spread to the human RBC, when they reproduce. once RBC are filled with protozoa they burst. causing fever.
Malaria: caused by Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, Plasmodium malarie and the more recently recognized Plasmodium konlesi.
like malaria, but from a tick. causes fever and hemolysis.
causes disease in cattle, do not infect liver cells.
spreads by Ixodes scapularis with Lyme disease. leave the salivary glands of ticks and invade RBC. look like a pear or rings shaped trophozoite. asexual budding forming a cross or X-shaped tetrad.
Babesiosis
babesia microti and Babesia divergens
transfered by a blood sucking insect
round cells without flagella called amastigotes. or with flagella called promastigotes, epimastigotes, and trymastigotes. initial skin ulcer, followed by systemic infection.
Leishmania and trypanosoma
carried by rodents, dogs, and foxes. transmited to humans by the SANDFLY
south and central america, Africa, and Middle east. replicates with MQ in the lymph nodes, spleen, liver, and bone marrow. can get anything from a single ulcer that will heal without treatment, to a widley disseminated ulcer, to severe systemic infection in the spleen and liver. cell-mediated defences result in a varied severity of diseases.
Diagnosis and Parasites?
Leichmaniiasis
caused by L. tropica, L. chagagasi, L. major, L. braziliensis, and L. donovani
bite causes a skin ulcer. invokes cell-mediated immunity. like PPD there is a test that will show if ever infected.
Diagnosis?
Clinical Leishmaniasis
nodular skin lesion that does ulcerate. seen in Ethiopia and Venezuela. due to defect in cell-mediated immunity. skin test will be negative.
Diagnosis?
diffuse cutaneous Leschmaniasis
sandfly bite heals quick, ulcers in nose and mouth with erosion of the nasal septum over a course of 20-40 years. diagnose with skin scrapings. Diagnosis?
Mucocutaneous Leishmaniasis
only with L. donovani or L. chagasi in malnourished children. abdominal discomfort and distension, low grade fever, anorexia, weight loss, massive splenomegaly, severe anemia and high WBC. titers for IgG, skin test is negative during the active disease as cell mediated immunity is deficient. Diagnosis?
Viceral Leishmaniasis (Kala-azar)
vector = testse fly
trypomastigote = motile and spreads in the blood to the lymph and CNS.
hard, red, painful ulcer that heals in 2 weeks. followd with fever, headache, dizzineaa, and lymph node swelling. followed by fever intervals that can occur for months. drowsiness during the day, behavioral changes, difficulty walking, slurred speach, and finally coma and death.
Diagnosis and Parasite?
African Sleeping Sickness
Tryanosoma bruceli rhodesience and Trypanosoma bruceli gambiense
WEST vs EAST African sleeping sickness?
parasites?
WEST African = slowly progressing, fevers, wasting, and late neurologic symptoms
west = T. brucei GAMBIENSE
EAST African = more severe with death in weeks
east = T. brucei rhodesiense.
reocuring fever due to variable surface glycoproteins (VSG) - changes coats.
southern US (texas), Mexico, Central America, and South America. lives in wild rodents, opossums, and armadillos. vector = reduviid bug (kissing bug) invade local skin, MQ, lumph nodes, and spread to distant organs through blood.
Chagas’ Disease
Trypanosoma cruzi, the american Trypanosome
Acute vs Chronic Chagas’?
acute = chagoma
fever, malaise, swollen lymph,
organs infected include the heart (tachycardia and severe meningoencephalitis, can enter an intermediate phase. low levels of Abs can be detected.
Chronic = cardiomyopathy, megacolon, constipation.
diagnosis: directly from blood. or Xenodiagnosis: a sensative test is concucted as follows: foty lab-grown reduviid bugs are allows to feed on the pt for one month and later the bugs intestinal contents are examines for the parasite.
serologic evidence for chronic can be used with cardiac and megadisease.
Intestinal protozoa ?
Entamoeba histolytica (bloody diarrhea), Entamoeba lamblia and cyclospora (non-bloody diarrhea in normal individuals), Cryptosporidium and Isospora belli (severe diarrhea in immunocompromised individuals)
