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Author: Amelia Virostko

1. Toxoplasma gondii

1.1. Introduction

  1. Intracellular sporozoa that infects vertebrates
  2. Sexual cycle and oocyst production only occurs in cats, while proliferative stages and tissue cysts develop in animals that acquire the infection
    1. Ingestion of oocysts, tissue cysts from meat, organ transplantation or transplacental migration

1.2. Life Cycle

  1. Infected cats excrete oocysts in feces
  2. Oocysts are ingested by any mammalian host and sporozoites are released in the gut
  3. Sporozoites enter epithelial cells and replicate and release tachyzoites
  4. Tachyzoites disseminate throughout the body via macrophages, and form cysts that contain bradyzoites
  5. Bradyzoite cysts can persist indefinitely and can “reactivate” if the immune system becomes compromised

1.3. Pathology

  1. Infection is usually asymptomatic in immunocompetent host
    1. Can occasionally cause symptoms similar to infectious mononucleosis
  2. Congenital toxoplasmosis can cause retinochoroiditis, encephalomyelitis, and hydrocephalus or microcephaly
  3. In immunocompromised hosts, can cause multifocal cerebral toxoplasmosis

1.4. Diagnosis

  1. Detected by elevated antibody titer, particularly of IgM
  2. In immunocompromised hosts, positive brain scans and anti-Toxoplasma IgG are more helpful
  3. Screen women for anti-Toxoplasma antibody when pregnancy is detected
    1. Avoid changing cat litter during pregnancy

1.5. Treatment

  1. AIDS patients with CD4 counts below 100 receive Bactrim (or dapsone plus pyrimethamine in patients with sulfa allergies) prophylaxis
  2. Corticosteroids may decrease inflammation of CNS infections in immunocompromised hosts or in retinochoroiditis

2. Leishmania

2.1. Introduction

  1. Protozoa that live in human macrophages as intracellular amastigotes or extracellular promastigotes
  2. Risk factors include: malnutrition, cell-mediated immunity suppression
  3. Sandflies transmit the parasite between humans and from canines or rodents to humans
  4. Troops are coming back from Iraq with infection

2.2. Life Cycle

  1. Infected sandflies inject Leishmania promastigotes into host while feeding
  2. Promastigotes attach to macrophages via complement receptors, stimulating phagocytosis of the promastigote
  3. In phagosome, promastigote loses its flagellum and transforms into amastigote
    1. Survives phagosomal-lysosomal fusion via production of superoxide dismutase, resistance to lysosomal enzymes, and use of low pH environment to increase uptake of nutrients

2.3. Pathology

  1. Cutaneous Leishmaniasis
    1. Small red papule that itches intensely, grows to 2 cm and ulcerates
    2. Lesions usually heal spontaneously
  2. Mucocutaneous Leishmaniasis
    1. Similar to cutaneous form, but also develop ulcers on the oral or nasal mucosa
    2. Slow progression, but need treatment to prevent hard and soft palate destruction
    3. Death usually occurs from secondary infection
  3. Visceral Leishmaniasis
    1. Parasites found throughout the body
    2. Non-specific symptoms
    3. Can lead to post-kala-azar dermal leishmaniasis
    4. Immunity involves induction of Th1 response
      1. Parasite can induce Th2 response that does not lead to protection

2.4. Diagnosis/Identification

  1. Demonstration of amastigotes by light microscopy with Wright or Giemsa stain
  2. Serologic tests have cross-reactivity with leprosy, Chagas disease, malaria, and schistosomiasis

2.5. Treatment

  1. 1st line therapy = pentavalent antimonials, stibogluconate sodium, or meglumine antimoniate
  2. Miltefosine is anew oral drug that has up to 94% cure rate, but may be teratogenic
  3. Amphotericin B is alternative therapy for antimony failures
  4. Pentamidine, allopurinol, ketoconazole, and itraconazole are alternative therapies