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Lecture 4

Tissue Protozoa II (Leishmania, Trypanosomes, and Pneumocystis)

Which species of Leishmania cause visceral leishmaniasis? Leishmania donovani, L. infantum/L. chagasi
What's another name for visceral leishmaniasis? kala-azar means black fever
What diseases do Leishmania donovani, L. infantum/L. chagasi cause? visceral leishmaniasis, post-kala-azar dermal leishmaniases, occasionally cutaneous leishmaniasis
Which leishmania species cause Old World cutaneous leishmaniasis? Leishmania tropica, L. aethiopica and L. major
Which leishmania species affected the American troops in the Gulf War and what did it cause? L. major cause visceral or viscerotropic leishmaniasis
Which leishmania species cause New World cutaneous leishmaniasis, diffuse cutaneous leishmaniasis, and sometimes visceral leishmaniasis? L. mexicana, L. amazonensis and other related species
Which leishmania species cause New World cutaneous and mucosal leishmaniasis? L. (Vianna) braziliensis and related L (Vianna) species
Which cells do the intracellular amastigotes infect? mammalian macrophage
Where do the extracellular promastigote proliferate? In the gut of the sand fly
What is the vector of leishmania species? Female sand fly
Which stage of leishmania spp. are inoculated into mammals? metacyclic promastigotes
Which animals are the reservoir for the Leishmania spp.? Canines, rodents, humans, other (incl foxhounds in the US) (varies with species)
Which immune cells confer protection against leishmania spp.? leishmania-specific Th1 CD4+ T cells which secrete gamma interferon. Progressive disease correlates with lack of a Th1 response
Which two markers are high in humans with visceral leishmaniasis? Interleukin-10 and TGF-beta
Describe the characteristics of visceral leishmaniasis hepatosplenomegaly, fever, anemia, leukopenia, hypergammaglobulinemia and progressive weight loss
What is the normal cause of death in visceral leishmaniasis? secondary bacterial or viral infection
What is different about the presentation of visceral leishmaniasis in immunocompromised individuals? splenomegaly may be absent, amastigotes may be seen in macrophage in any organ.
Describe post-kala-azar dermal leishmaniasis? Macular, papular or nodular skin lesions after successful treatment of visceral leishmaniasis in India or Africa
Which forms of leishmaniasis demonstrate elevated anti-leishmania antibodies? visceral and mucosal leishmaniasis
When are the anti-leishmania antibodies not elevated in an infected person? cutaneous and some patients with AIDS
Describe cutaneous leishmaniasis Chronic skin lesion(s), frequently ulcerative, may be single or multiple, and typically heal spontaneously after months to years leaving a flat, atrophic scar.
Describe Mucosal (mucocutaneous) leishmaniasis. Months to years after skin lesions of L.(V.) braziliensis or related Leishmania spp. heal, metastatic mucosal lesions develop in the nose, mouth or upper airway. There is a tissue damaging TH1 response.
describe Diffuse cutaneous leishmaniasis A rare, anergic variant with widespread skin nodules, but no ulceration. It is similar to lepromatous leprosy – there is no apparent TH1 response.
What are the five methods for diagnosing leishmaniasis? 1. Identification of amastigotes in aspirates or biopsies 2.Culture of aspirates or biopsies 3. ELISA or immunofluorescence antibody assays 4. PCR based assays 5. Montenegro (leishmanin) skin test
Which tissues are needed to identify leishmania amastigotes? Visceral: splenic or bone marrow Cutaneous: punch biopsy and aspirate of a skin lesion (Trypanosoma cruzi has amastigote stage in tissue)
Which form of leishmania grow in media? promastigotes
Which organism can give a false positive antibody assay for leishmania? Trypanosoma cruzi
Which form of leishmaniasis have the highest antibody titer? visceral or mucosal leishmaniasis. low or no titers in cutaneous leishmaniasis
list treatments for leishmaniasis: Liposomal amphotericin B, pentavalent antimony, milteosine (not approved), itraconazole (+/-)
What disease does Trypanosoma cruzi cause? Chagas disease
Describe the life cycle of leishmania spp. 1. sandfly give mammal metacyclic promastigote 2. promastigotes enter mononuclear phagocytes in skin 3.Amastigotes develop and multiply ->asymptomatic or leishmaniasis 4.Sandfly takes up amastigotes 6.Amastigotes convert to promastigotes in sandfly gut
Where is Trypanosoma cruzi endemic? Rural Central and South America
What factors have helped to decrease the incidence of Chagas dz? economic improvement, better housing and urban migration
What are the methods of transmission of T. cruzi? arthropod vector, contaminate blood, organ transplantation or lab exposure
How is T. cruzi spread in the US and Canada (and other placees?) Usually immigrants with chronic infection who donate blood or organs.
What is the vector for Trypanosoma cruzi? Triatomidae (reduviid bugs, “kissing bugs”, “barbeiros”)
Describe how T. cruzi is inoculated. Bugs defecate infected feces when taking a blood meal. victim scrates trypomastigote into bite site or invastion through conjunctiva or mucous membranes
What is the reservoir for T. cruzi? Many animals including humans
what are the three phases of Chagas dz? Acute, Indeterminate and Chronic
Describe the acute phase of Chagas dz. Indurated papule at the site of inoculation (periorbial edema=Romana's sign), fever, anorexia, carditis, hepatomegaly, adenopathy
What is the outcome of the acute phase of Chagas dz? Most resolve spontaneously, small % are fatal
Which phase of Chagas disease is asymptomatic? Intermediate phase
What percentage of infected persons develop chronic Chagas disease? 20-30% years after acute symptoms
Describe Chagasic cardiomyopathy Congestive heart failur, arrhythmias, emboli or sudden death
Describe the Chagas Megadisease megaesophagus with progressive dysphagia, pain and aspiration and megacolon with chronic constipation, volvulus
How is the diagnosis of chagas disease made? 1. ID of trypanosomes in blood 2. Antibody test 3. PCR assays 4. Xenodiagnosis 5. Animal inoculation 6. Axenic culture
How is Chagas dz treated? Acute: nifurtimox or benznidazole Intermediate: benznidazole Chronic: no curative therapy available, supportive treatment and surgery
Describe how infection by Trypanosoma cruzi occurs. Reduviid bug spreads metacyclic trypomastigotes and infect bite site, mucosal surfaces or conjunctiva. They enter local cells, multiply and spread systemically
Which form of Trypanosoma cruzi causes acute disease? Trypomastigotes enter local cells and become intracellular amastigotes to cause acute dz: fever, local swelling (chagoma), periorbital edema, myocarditis
How does T. cruzi cause chronic disease. bloodstream trypomastigotes circulate to smooth muscle and autonomic ganglia in heart esophagus colon and convert to amastigotes
What is the form that multiplies within the midgut of the Reduviid vector? Epimastigotes
Describe the life cycle of T. cruzi within the Reduviid bug. Trypanosomes are taken up by bug and transform into epimastigotes. Epimastigotes multiply in midgut ad migrate to hindgut. Here they differentiate into trypomastigotes which are shed in bug feces to infect the mammal.
Which Trypanosoma species causes West African sleeping sickness? Trypanosoma brucei gambiense
Trypanosoma brucei rhodesiens causes which disease? East African sleeping sickness
Which trypanosoma species causes sleeping sickness in animals? T. brucei brucei
Where is T. b. gambiense located? West and central Africa
In which part of Africa is T. b. rhodesiense found? East Africa
What is the vector for human African Trypanosomiasis? Glossina species (tsete fly)
Humans are the main reservoir for which Trypanosoma species? T. b. gambiense
Which Trypanosoma species has mainly large animals as its reservoir? T. b. rhodesiense. humans are infected when they enter endemic areas
How does West African sleeping sickness manifest? Hemolymphatic stage (early):local lesions at the site of inoculation, may heal spontaneously. later fever and lymphadenopathy (LAD) develop esp. posterior cervical LAD (Winterbottom's sign) and CNS stage (late)
What is the late stage of West African sleeping sickness? CNS stage: subacute or chronic with fever, headache and later, signs of meningoencephalitis
How does infection with T. b. rhodesiense maniefest? East African sleeping sickness: acute illness with fever, constitutional symptoms and merging of hemolymphatic stage and meningoencephalitis
How is human african trypanosomiasis diagnosed? 1. ID of trypanosomes in blood, cerebrospinal fluid or lymph node aspirates 2. Positive antitrypanosomal antibody 3. Brain biopsy with Morula or Mott cells
What are the treatment options for human african trypanosomiasis? Eflornithine (DFMO), suramin or pentamidine, melarsoprol
Which serological tests are there for antitrypanosomal antibodies (Abs)? immunofluorescent Ab test, hemagglutination and card agglutination test (may be falsely positive for T. b. gambiense)
Describe the Trypanosoma spp. life cycle. Tsetse fly bites and metacyclic trypanosomes enter site. 2.trypanosomes mature/divide in blood/lymph then invade CNS 3.fly picks up trypanosomes with blood meal 4.Crithidia develop into epimastigotes and metacyclic trypanosomes in fly salivary gland.
What form of Trypanosoma spp cause painless trypanosomal chancre? Trypomastigotes at the bite site.
Which trypanosoma species manifests CNS symptoms earlier? T. b. rhodesiense (T. b. gambiense may take months to years)
What is the causative agent for pneumocystis pneumonia? Pneumocystis jiroveci
What is the distribution for Pneumocystis jiroveci? Worldwide
What is the likely route of infection for Pneumocystis jiroveci? Pulmonary
What is Pneumocystis jiroveci closer to: fungi or protozoa? fungi by DNA hybridization and electron microscopy
Which patients are most often affected by PCP? Immunocompromised patients due to 1.AIDS, lymphocytic leukemia, lymphoma or other neoplasms 2.Immunosuppression for transplant or collagen vascular dz 3. Severe malnourishment
Pneumocystis jiroveci attaches to which cells? type I pneumocytes
Describe the pathogenesis of Pneumocystis jiroveci. Attachment to type I pneumocytes, proliferation causes disease and formation of foamy alveolar exudate. Proliferation and immune response cause tissue destruction and symptoms
How do patients present with PCP? Patients with AIDS have subacute cough, fever, tachypnea and slowly progressive respiratory distress. With other patients (and some AIDS), progression to hypoxia may be rapid
How is PCP diagnosed? Gomor methenamine silver or Giemsa stains of sputum (in AIDS), bronchoalveolar lavage or lung biopsy
How is PCP treated? Pyrimethoprim plus sufamethoxazole, pentamidine isethionate, atovaquote, primaquine plus clindamycin or other. Steroids for mod to severe hypoxia
What are the side effects of pyrimethoprim plus sulfamethoxazole? fever, rash, neutropenia (high incidence in AIDS pts)
What is used for PCP prophylaxis? Trimethoprim/sulfamethoxazole (Dapsone is an alternative)
Who should receive PCP prophylaxis? HIV infected pt with CD4 count <200, pt with history of PCP, children with acute lymphocytic leukemia
Created by: UVAPATH4