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41 Cards in this Set
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Apicomplexan parasites |
Have apical complex of organelles responsible for invasion (construct vacuoles, secrete proteins). Includes Plasmodium and Babesia in this lecture. Also Toxoplasma, Cryptosporidium, Cyclospora, Isospora. |
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Flagellate protozoa |
Includes Trypanosomas, Leishmania, Giardia, Trichomonas |
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Toxoplasma gondii hosts |
Definitive host (where sexual reproduction occurs) is cat. Intermediate host is all mammals and birds. |
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Toxoplasma gondii - forms |
Oocysts - excreted in feces of cats Tissue cyst - contains bradyzoites. Found intracellularly in muscle and various organs. Tachyzoites - Fast replicating. Invade cells, replicate, and go on to other cells. |
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Toxoplasma gondii life cycle |
Humans either: a) Pick up oocyst secreted directly from infected cat. b) Consume cysts from other mammals who have picked up oocyst secreted from cats. |
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Toxoplasma gondii and AIDs |
Toxoplasmosis is an AIDS defining illness. |
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Symptoms of acute acquired toxoplasmosis in healthy host |
Usually subclinical, unrecognized. Occasionally, painless lymphadenopathya, mononucleosus. Rarely severe disease. |
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Chronic acquired toxoplasmosis |
Tachyzoites can be converted to bradyzoites. Leads to mostly asymptomatic life-long infection. Can elicit immune response. Or be reactivated in setting of depressed immunity. |
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Toxoplasmosis in Immunocompromised host |
In case of AIDs, chronic steroid use, etc Reactivated infection more common than new infection. Cerebral complications most common - toxoplasma encephalitis (bradyzoites in brain activated into tachyzoites = encephalitis). Also cardiac, pulmonary complications. |
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Congenital toxoplasmosis |
Typically result of maternal infection during gestation (infection prior to conception only for AIDs, immunosuppressive). Infection early in pregnancy is less likely than later, but more severe outcomes (typically later in child's life) including: - Miscarriage, abortion, stillbirth - Severe neurological, ocular disease - Generalized illness |
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Ocular toxoplasmosis |
Common sequelae of congenital toxoplasmosis, but most commonly seen in patients infected as adults. Acute or reactivated disease includes: Focal necrotizing retinitis, other issues
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Serological diagnosis of toxoplasmosis - acute infection, chronic inactive infection, and congenital infection |
Acute infection - Positive IgM, rising IgG titer Chronic inactive infection - Negative IgM, positive IgG titer Congenital infection - Positive IgM, positive IgG titer Remember that IgG provides long lasting immunity, IgM is during infection. |
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Diagnosis of cerbral toxoplasmosis in persons with AIDs |
Presumptive diagnosis based on clinical picture and MRI/CT imaging, positive serological test Confirmed by clinical and radiographic response to tehrapy. |
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Treatment of Toxoplasmosis |
Pyrimethamine + Sulfadiazine Inhibits folic acid metabolism so supplement with leukovorin (folic acid) |
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Management of toxoplasmosis in pregnancy |
Spiramycin treatment very effective. If amniotic fluiud is negative, continue spiramycin until delivery to prevent congenital infection. If amniotic fluid positive, fetus is infected. Terminate pregnancy or treat with Pyrimethamine + Suldafiazine and leukovorin/folic acid. |
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Toxoplasmosis prevention |
Don't change cat litter if pregnant Don't eat raw meat Wash hands |
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Treatment of HIV/AIDs toxoplasmosis |
Maintenance therapy Preventative therapy with TMP-SMX Get CD4 count up! |
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Toxoplasmosis neurological implications |
Correlation between attempted suicide, depression, schizophrenia and toxoplasma. Intermediate hosts, rats or mice, lose fear of predators. Possibly manipulating host so can be passed on and continue life cycle. |
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Chagas disease agent and vector |
Agent: Trypanosoma cruzi Vector: Triatomine bugs |
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Trypanosoma cruzi life cycle |
When Triatomine takes blood meal, inoculates blood with defecation containing trypomastigote. Trypomastigote infects myocyte, replicates, and ruptures to infect other myocytes. Eventually picked up by another Triatomine taking blood meal to repeat cycle. |
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Trypanosoma cruzi types of inoculation |
Can be vector borne, transfusion/transplantation associated, transplacental to fetus, inoculation via laboratory accident or orally inoculated in juice or fruit. |
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Acute Chagas disease |
High levels of parasitemia, tissue infection. Only symptomatic in 1% of people as febrile illness. Up to 10% mortality with acute myocarditis and meningoencephalitis. Survivors infected for life. |
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Chronic Trypanosoma cruzi infection |
Usually asymptomatic with normal findings. 20-30% have Chronic Chagas Disease, including: - Cardiac abnormalities: congestive heart failure, arrythmias, complete heart block, thromboembolism, sudden death - GI disease - megaesophagus, megacolon |
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Reactivated Trypanosoma cruzi in HIV or immunosuppression |
CNS lesions Acute myocarditis Skin lesions Parasites visualized in peripheral blood, CSF, tissue. |
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Diagnosis of Chaga's disease |
Acute: Direct visualization of parasites in wet mount Serology Chronic: Isolation of parasites by blood culture Serology Xenodiagnosis - inoculate sample in mouse, look for parasites in animals PCR based assay. |
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Chaga's disease treatment |
Nifurtimox and Benznidazole Effective in children and teenagers but not adults. Oral drugs, taken for long period of time. Rapidly clear parasite from acute but not chronic stage. Also use symptomatic treatment for acute disease. |
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Leishmaniasis vector |
Protozoan parasite found in Phlebotomine sand flies. |
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Clinical presentation types of Leishmaniasis |
Cutaneous Mucosal Visceral All caused by different species |
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Life cycle of Leishmania |
Sand fly inoculates promastigote into blood with blood meal. Promastigote taken up by macrophages, prevents macrophage activation so survives in macrophages in spleen, bone marrow, etc. Ruptures macrophages, continue to infect other macrophages. Infected cell produces amastigotes. Cells are eventually taken up by sandfly. Sandfly injects promastigote |
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Immune control of different forms of Leishmaniasis. |
Must activate macrophages to control disease - IFNy is key player but also IL-12, IL-1, TNFa. Visceral - No cellular response. Huge humoral response. Visceral that is subclinical or treated - Lesser humoral response and strong cellular response. Cutaneous - Little humoral, strong cellular response. Mucosal - Little humoral, very strong cellular response causes disease. |
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Visceral leishmaniasis |
Parasites found within macrophages. Subclinical infection more common than clinical infection. Clinical infection (kala azar) - mostly in malnourished or immunocompromised persons. Fatal even with treatment.
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Organisms causing Visceral Leishmaniasis |
Zoonotic organisms - L. infantum, L. chagasi. We are dead end in these organisms. Anthroponotic - L. donovani. Humans are reservoir, so break cycle by treating people. |
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Where is Visceral leishmaniasis seen especially? |
South Asia - Significant number of cases and part of mortality. This is anthropomorphic (L. donovani) War-torn Africa (Sudan, Somalia, Ethiopia) in mid 80s to current. Brazil - moved from rural to city slums |
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Mucosal leishmaniasis - clinical presentation, organism, etc |
Parasites migrate from initial cutaneous lesion to mucus. Results in erosion of hard palate, nose cartilage, mouth. Caused by hyperactive cellular immune response. Frequently present with bacterial and fungal infections that kill them. Caused by L. braziliensis. Mucosal is 1-10% of cases. Treatment is difficult. |
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Disseminated cutaneous leishmaniasis |
Cutaneous lesiosn that resembles sporothrix. No cellular immune response, as oppose to mucosal leishmaniasis. Relapses following treatment and clearance. |
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Cutaneous leishmaniasis cliical presentation |
Raise border with necrotic center. Starts small and grows. |
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Organisms causing cutaneous Leishmaniasis |
Old World cutaneous leishmaniasis - both anthroponotic and zoonotic. Includes L. tropica, L. major. New world cutaneous leishmaniasis - all zoonotic. Includes L. mexicana in Texas, L. amazonensis, L. venezuelensis. |
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Why is speciation of cutaneous Leishmaniasis required? |
Lesions are morphologically indistinguiable. Speciation required to assess risk of disease becoming mucosal because then is difficult to treat. L. braziliensis is example of disease that can become mucosal. |
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Leishmania/HIV coinfection |
Immunosuppression due to HIV can cause reactivation of Leishmaniasis. Can also get via needle sharing. Usually donovani type. HIV increases risk of clinical disease from 10% (imunocompetent). ART can decrease risk. |
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Diagnosis of visceral and cutaneous Leishmaniasis |
Bone marrow aspirate Serological tests - just indicates history Leishmanin skin test - like TB skin test, inject antigen intradermally and look for IgE response. Not positive in active Leishmaniasis, good for tracking if treatment working. If cutaneous, can also scrape from lesion via touch prep. |
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Leishmaniasis treatment |
Antimony Pentostam from CDC - severe cardiac toxicity, great cure rate Liposomal AmB Miltefosine - oral, 90% cure rate. Alternatively can do no treatment for cutaneous (that is not Braziliensis), will self cure eventually. Can excise, heat therapy, topical and intralesional drugs. |
